Semiology is the study and the interpretation of the signs and symptoms aiming to

establish the diagnosis, prognosis and treatment for the patient.

A symptom is a departure from normal function or feeling which is noticed by a
patient, indicating the presence of disease or abnormality.
A symptom is subjective, observed by the patient and cannot be measured directly.
The 7 attributes of a symptom:
1.Location. Where is it? Does it radiate?
2.Quality. What is it like?
3.Quantity or severity. How bad is it? (For pain, ask for a rating on a scale of
1 to 10.)
4.Timing and duration. When did (does) it start? How long did (does) it last? How
often did (does) it come?
5.Setting in which it occurs. Include environmental factors, personal activities,
emotional reactions, or other circumstances that may have contributed to the
illness.
6.Remitting or exacerbating factors. Does anything make it better or worse?
7.Associated manifestations. Have you noticed anything else that
accompanies it?
There are 3 main types of symptoms:
-Chronic symptoms - long lasting or recurrent symptoms. Examples: bone pain
(osteoarthritis), cough.
-Relapsing symptoms - symptoms which had occurred in the past, disappeared, and
then come back, and the person is affected by them once again, as may be the case
with asthma, depression, multiple sclerosis, and also cancer.
-Remitting symptoms - when symptoms improve, and sometimes go away
completely
Symptoms may also progressively get worse, or get better.
Diseases and conditions can also be described as:
-Asymptomatic diseases/conditions - the disease is present but there are no
symptoms. For example, high blood pressure is often asymptomatic.
An asymptomatic infection is also called a subclinical infection. An infected
individual may not develop symptoms during the incubation period (also known as
the period of subclinical infection). This is often the case with sexually transmitted
diseases such as AIDS.
Many cancers are asymptomatic during their early stages. Prostate cancer, for
example, is mainly asymptomatic until it has advanced to a certain point. This is
why regular testing for higher risk groups for some cancers is so important.
-Symptomatic diseases/conditions - the disease is present and there are symptoms.
Some diseases/conditions are always symptomatic, such as COPD, heart failure.
-Constitutional symptoms - also known as general symptoms. These are symptoms
which are related to the systemic effects like fever, weight loss, or altered appetite.
-Presenting symptom - also known as chief complain. This is a term used by doctors
which refers to the initial symptom(s) that brought the patient to see the doctor.
-Cardinal symptom - a term used by medical professionals referring to the symptom
that ultimately leads to a diagnosis.
A medical sign is an objective feature indicating some medical fact detected by a
physician, nurse or medical/laboratory device during a physical examination of a
patient.
Sometimes a sign may not be noticed by the patient, and have no meaning at all for

Mor Halgoa 1
the patient, but is meaningful for the physician. Signs can help the doctor in his/her
diagnosis. For example high blood pressure (may indicate a cardiovascular problem),
clubbing of the fingers (may point to lung disease), palor skin (anemia), jaundice
(hepatic diseases).
There are different types of signs:
-Prognostic signs - signs that point to the future. Rather than indicating the name of
the disease they predict the outcome for the patient, what is likely going to happen
to him/her.
-Anamnestic signs - signs that always point to the past. Some skin scars may point
to severe acne in the patient's past. An anamnestic sign of polio during childhood
may be observed as a distorted limb during adulthood.
-Diagnostic signs - signs that help the doctor recognize and identify what the
patient has.
-Pathognominic signs - "a sure sign". This is step further from a diagnostic sign.
This sign leaves the physician certain that a particular disease is present.
The difference between a sign and a symptom
Sign” and “Symptom” are both medical terms with different medical meanings. While
symptoms are problems that a patient notices or feels, signs are whatever a physician
can objectively detect or measure.
A feature might be sign or a symptom, or both, depending on the observer(s).
Some features, such as pain, can only be symptoms, because they cannot be directly
observed by other people. Other features can only be signs, such as a blood cell count
measured in a medical laboratory.
A syndrome is a set of symptoms or conditions that occur together and suggest the
presence of a certain disease. This is the aggregate of symptoms and/or signs that
have a common mechanism from the physiological point of view.
A disease is the actual diagnosed impairment of health or a condition of abnormal
functioning. This is a transitory of permanent deviation from the parameters defined
as health.
Health is the status of general well-being that determines one to complete his/her
tasks, conditioned by an optimal status of all the skeletal structures, body systems,
thus accomplishing homeostasis and the capacity of adapting physically, psychically
and socially.
Anamnesis is the totality of information gathered by the physician from the patient,
from the persons accompanying him or from medical papers, claiming to establish the
diagnosis, prognostic or treatment.
During anamnesis there may be some difficulties: physician’s experience, knowing
patient’s psychology, medical information, amount of available time, patient’s mental
status, adapting the language, patient’s ability.

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ANAMNESIS
1.Personal and preliminary data
A.Name
B.Age
C.Gender
D.Place of birth
E.Place of living
F.Ethic or racial apartenence
G.Profession and employment history
In case of previous hospitalizations:
A.Date of admission
B.Date of discharge
C.Medical letter after discharge
D.Referral diagnosis
E.Diagnosis at admission/24/48/72 hours
F.Diagnosis at discharge
G.Patient's status at discharge
2.Chief complaint (reason for admission)
A list of symptoms and/or signs that the physician considers to be the most relevant.
This is not a diagnostic step!
We ask the patient to describe, in his own words, the reason for seeking medical care.
Although patients may have many reasons for initiating a visit to the physician, they
should be encouraged to select the single or two most important concerns they have.
The patient should be reassured that the physician will not ignore other concerns but
wants to understand what is most important to the patient.
Sometimes patients have no overt complaints, in which case you should report their
goals instead.

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3.Present illness
There is an immediate actual illness and history of actual illness.
Immediate actual illness MUST obtain:
A.Description of all symptoms and signs
B.Their evolution
C.Pharmacologic treatment and dosing
D.Paraclinical investigations already done
E.Medical consultations
F.Patient’s accomplishment to the medical recommendations
G.Relationship between the symptoms and medical gests
Previous established diagnosis can be used.
The physician needs to obtain a chronological, detailed description of all the
symptoms and/or signs presented by the patients as related with the present illness,
from the moment of their start or worsening until the contact with the physician (that
is taking the history) or until the hospital admission.
Other information, except symptoms, is frequently relevant, such as risk factors or
current medications.
History of actual illness needs to consist of a general description of the principal
moments of patient’s illness from its start until the moment when immediate
symptoms occurred.
Previous diagnosis can be used.
4.Past history - physiological data
In children: Pediatric data.
In women:
A.Age at menarche
B.Last menstrual period
C.Periods: regularity, duration, amount of bleeding
D.Number of pregnancies
E.Number of abortions-spontaneous or induced
F.Number and type of deliveries
5.Past history - pathological data
Pathologies that MUST be noted:
A.Infectious diseases of childhood
B.Acute viral hepatitis
C.Tuberculosis
D.Sexually transmitted diseases
E.Major trauma
F.Surgical interventions
G. Epilepsy/ convulsions
Pathologies that are noted only if they were present:
Most important diseases that are not related with the actual illness, nor represent
moments of its evolution.
6.Family history
Most important illnesses of the siblings, brothers/sisters, parents and grandparents are
noted, but also for the persons living in the same home.
For deceased persons, age and cause of death are noted.
Review each of the following conditions and record if they are present or absent in the
family: hypertension, coronary artery disease, elevated cholesterol levels, stroke,
diabetes, thyroid or renal disease, cancer (specify type), arthritis, tuberculosis, asthma

Mor Halgoa 4
or lung disease, headache, seizure disorder, mental illness, suicide, alcohol or drug
addiction and allergies, as well as symptoms reported by the patient.
7.Social data
A.Alcohol consumption
B.Tobacco use (type, frequency)
C.Illicit drug abuse
D.Working environment
E.Intensity of physical activity and exercise habits
F.Allergy history

GENERAL SYMPTOMS
A general symptom can be present in many syndromes and diseases, not necessarily
related.
Fever
Elevation of body temperature above the normal circadian range. It is based on
individual situation, someone can keeps a relative low or high body temperature.
In fever, the balance is shifted to increase the core temperature
It can be measured orally, rectally or in the axillary region.
It has a diurnal variation, with oral temperature ranging between 36.8o C  0.4o C to
37.2o C.
During fever, early morning oral temperature is >37.2o C. at noon it is >37.7o C (or
>38o C in the axillary region).
The rectal temperature is about 0.6o C higher than the oral temperature.
Hyperthermia (hyperpyrexia) - an elevation of body temperature above the
hypothalamic set point (>41o C), due to insufficient heat dissipation.
This is a vital state that has to be treated.
There are 3 staged in fever development:
- Stadium incrementi is the least dangerous stage, in which the body
temperature increases. It is accompanied by vasoconstriction and increased
muscle tome (feeling cold, goosebumps and shivering).
- Fastigium is the highest point in the course of a fever and the body
temperature is maintained at a new level. In this stage the body gets tired.
- Stadium decrementi is the most dangerous stage, in which the severity of the
disease decreases. It is accompanied by vasodilation and sweating.
The fever may resolve suddenly, by crisis where the body can enter into a shock, or
gradually, by lysis, returning to the normal body temperature.
Depending on what's causing the fever, additional fever symptoms may include:
sweating, shivering, headache, myalgias (muscle pain), arthralgias (joint pain), lack of
appetite, dehydration, malaise (general discomfort or uneasiness) and somnolence (a
strong desire for sleep).
Very high fevers, between 40-41o C may cause hallucinations, confusion, irritability,
convulsions (‫ פרכוסים‬,‫)עוויתות‬.

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Fever patterns (temperature is measured twice a day - morning and evening):

- Remittent - the fluctuations are above the hypothalamic set point.

- Intermittent - the fluctuations are ranging above and below the hypothalamic set
point.

Fever pattern cannot be considered pathognomonic (characteristic for a particular

disease).
Fever pattern can be altered by antipyretics, antibiotics and corticosteroids.

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Hypothermia (hypopyrexia) - an abnormally low temperature, below 35°C rectally.
It may occur in various situations: reduced movement, water immersion and near-
drowning, prolonged unconsciousness in low ambient temperatures, especially in
combination with alcohol intoxication (which causes peripheral vasodilatation), drug
overdosage, stroke or head injury, and in severe hypothyroidism.

J or Osborn wave:

Headaches (cephalalgia), migraines

Tension headaches - most common. Usually bilateral, may be generalized or localized
to the back of the head and upper neck or to the frontotemporal area.
Mild and aching or a sense of tightness and pressure.
Gradual onset, variable duration: hours or days, but often weeks or months, often
recurrent or persistent over long periods.
Associated symptoms: anxiety, tension, and depression.
Aggravated by sustained muscular tension; emotional.
May be relieved by massage, relaxation.
Cluster headache - one-sided, located high in the nose, and behind and over the eye.
Abrupt onset, often 2-3 hours after falling asleep, and 1-2 hours in duration.
Its course is typically clustered in time, with several each day or week and then relief
for weeks or months
Associated with unilateral stuffy, runny nose, and reddening and tearing of the eye.
May be provoked by alcohol during a cluster.

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Migraines - unilateral, typically frontal or temporal pain, but also may be occipital or
generalized.
Throbbing or aching, variable in severity.
Fairly rapid, reaching a peak in 1-2 hours, lasts several hours to 1-2 days.
It often begins between childhood and early adulthood. Typically recurrent at
intervals of weeks, months, or years, usually decreasing with pregnancy and
advancing age.
Associated with: nausea and vomiting, visual disturbances (local flashes of light,
blind spots) or neurological symptoms (local weakness, sensory disturbances).
May be provoked by alcohol, certain foods, or tension.
More common premenstrually.
Aggravated by noise and bright light.
May be relieved by quiet, dark room, sleep.
Other headaches -
Face pains - associated with acute paranasal sinusitis, trigeminal neuralalgia.
Acute illness with very severe headache - in meningitis, subarachnoid hemorrhage.
Following head trauma - post-concussion syndrome, chronic subdural hematoma.
Brain tumor.
Hunger and appetite
Hunger is a sensation that promotes food consumption
Appetite is the desire for a specific food. It is stimulated by the sight, smell or thought
of food and accompanied by the flow of saliva in the mouth and gastric juice in the
stomach. Appetite is psychological, dependent on memory and associations.
Dizziness and vertigo
Vertigo refers to the perception that the patient is rotating or spinning. These
sensations point primarily to a problem in the labyrinths of the inner ear, peripheral
lesions of CN VIII or lesions in its central pathways,or nuclei in the brain.
Dizziness is the feeling that the environment and everything around us is rotating or
spinning.
Dyspnea, asthenia and fatigability
Dyspnea is the shortness of breath. It can be either cardiac or pulmonary.
Asthenia is the lack or loss of strength and energy, weakness, even before the
beginning of an activity.
Fatigability is the tendency to become tired or exhausted quickly or easily, right after
the beginning of an activity, and it can be caused by many resons.

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GENERAL SURVEY

Apparent state of health

- Vigorous, robust (‫ חזק‬,‫ עירני‬,‫)נמרץ‬
- Frail, feeble (‫ שברירי‬,‫ עדין‬,‫)חלש‬
- Acutely or chronically ill.
for the daily evaluation of the patients use: ameliorated, stable, worsen (reffering to
the previous day/admittance as comparison).

Decubitus
The patient's position in bed.
It can be indifferent for the patient, or it can be preferred.
In case of a preferred position, the reason can be either physiological or pathological.
Pathological postures:
Orthopnea - the patient is propped up in bed. This position may be performed for
calming pain, calming cough or calming dyspnea.
Extreme orthopnea - pillow sign (sleeping in seat), squatting.
Lateral decubitus - in pleural diseases.
In pleuritis the pain is sharp and increases with every movement. Therefore the
patient will prefer to lie on the affected side, where the pressure will limit the
movement of the lung while breathing.
In pleural effusion there is a fluid accumulation in the pleural space, and we need
to move it to allow the lung dilation. In this case the patient will prefer to lie on the
healthy side.
Opisthotonus - severe hyperextension and spasticity in which an individual's head,
neck and spinal column enter into a complete "bridging" or "arching" position.
It occurs in tetanus and meningism.
Ulcer - pressing the epigastrium.
Colic is a form of pain which starts and stops abruptly.
Biliary colic - right sided decubitus, slightly curved.
Acute renal colic - there is no position that can relief the pain. The patient will be
uncomforted.
Abdominal colic - curling, hips and knees flexed.
Peritoneal irritation - set of abdominal examination findings that indicate
inflammation of the visceral or parietal peritoneum.

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 - Involuntary guarding - pressure of the parietal peritoneum onto the inflamed
area results in a reflex contraction of the overlying muscles.
- Board-like rigidity - in generalized peritonitis. The anterior abdominal wall
does not move with respiration and breathing becomes increasingly thoracic.

Facies
The appearance or expression of the face, typical of a certain disorder or disease.
The face is the anatomical region, and the physiognomy are the facial features held to
show qualities of mind or character by their configuration or expression.

Cardiovascular facies:
Mitral facies - starts as “mitral beauty” (red cheecks) due to
vasodilation, then becomes “mitral mask” (gray-blue cheecks)
since not enough blood is reaching the face, and eventually it
develops into Shattuck facies (yellow-blue) due to jaundice
and cyanosis.
Associated with mitral stenosis and is due to low cardiac output,
and therefore low perfusion of the facial skin.
It includes rosy cheeks, while the rest of the face is bluish due to
cyanosis.
Plethoric facies - includes red face, with fine teleangiectasias
(small dilated blood vessels near the surface of the skin or
mucous membranes).
It can occur in Cushing syndrome or polycythemia vera,
hypertensive disease and alcoholism.

Hippocratic facies:
Present in severe and prolonged diseases, indicative of
approaching death.
It includes concavity of the cheecks and temples,
pinched nose, sunken eyes, cold and retracted ears,
livid (‫כחול‬-‫ )אפור‬skin color.

Cirrhotic facies:
Jaundiced sclerae, pinched nose and shiny red lips.

Chronic obstructive pulmonary disease (COPD) facies:

Pink puffer - in patients with predominant emphysema
(type A). They have an increased redness of the skin,
leading to the 'pink puffer' description. There will be less
hypoxemia than in type B, and less storage of CO2. 
Blue bolater - in patients with predominant chronic bronchitis
(type B). They may experience cyanosis related to a lack of
oxygen in the blood.

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Facies in nephrotic syndrome:
This is a nonspecific disorder in which the
kidneys are damaged, causing them to leak
large amounts of protein.
The face is edematous and often pale, swelling
usually appears first around the eyes and in the
morning, and the eyes may become slitlike when edema is severe.
Lips may be swollen.

Facies in autoimmune diseases:

Scleroderma facies - scleroderma is a systemic autoimmune disease
(primarily of the skin) characterized by fibrosis, vascular alterations
and autoantibodies.
Peri-oral fibrosis leads to a taut (‫ )מתוח‬skin around the mouth, thin
lips, small mouth, beaking of the nose, mask like face.
Systemic lupus erythematosus - a type III hypersensitivity reaction
that can act against any part of the body.
It includes a ”butterfly” or malar rash, and normal colored
nasolabial folds.
Dermatomyositis - an inflammation of the muscles and the
skin. It is associated with patches of slightly raised reddish
rash which can be on the bridge of the nose or around the eyes.
Heliotrope (‫ )עוקץ העקרב‬rash.

Facies in endocrine disorders:

Grave's disease - an autoimmune disease where the thyroid is
overactive. It includes bilaterally, slightly asymmetric
exophthalmos, startled (‫ )מבהיל‬expression, widened palpebral
fissure , infrequent and incomplete blinking (Stellwag sign),
fine tremor of the eyelids (Rosenbach sign) and a prominent
hyperpigmentation of the lids (Jellinek s.).
Myxedema - caused by a decreased activity of the thyroid gland.
The patient has dull, puffy facies. The edema is often pronounced
around the eyes, and it does not (!) pit with pressure.
there are also thin lateral eyelids (Hertoghe sign)
and decreased mobility. Dry, coarse, and thinned hair and
eyebrows, and the skin is dry.
Congenital hypothyroidism - inadequate thyroid hormone
production in newborn infants.
It includes hypertelorism (abnormal distance between two
paired organs), dental abnormalities , macroglossia and
“clover” (‫ )תלתן‬nose.

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Acromegaly - the excess of growth hormoes produces
Enlargement of both bones and soft tissues. The head is
elongated with a bony prominence of the forehead, nose and
lower jaw (prognathism).
Soft tissues of nose, lips and ears are also enlarged.
It also includes macroglossia.
The facial features appear generally coarsened.

Facies in Cushing disease:

This syndrome describes the signs and symptoms associated with
prolonged exposure to inappropriately high levels of the hormone
cortisol.
The increased adrenal production causes a round or “moon” face
with red cheeks. Excessive hair growth in the mustache and
sideburn areas, and on the chin.

Facial paralysis:
Peripheral lesion (Bell's palsy) - paralyzes the entire
right side of the face, including the forehead. CentralPeripheral
In this case the contralateral facial nerve is damaged.
The forehead does not wrinkled and the eyebrow is
not raised. The eye does not close due to palpebral
ptosis (dropping of the eyelid).
It also includes epiphoras (overflow of tears due to
obstruction of lacrimal duct), flat nasolabial fold and
drooping of the corner of mouth.
Central lesion - paralyzes the lower part of the face.
In this case there are nuclei that are affected and have
a bilateral innervation of the lower half of the face.
The upper part of the face is unharmed.
The Forehead wrinkled and the eyebrow is raised.
The eye closes, perhaps with slight weakness.
It also includes flat nasolabial fold and drooping of
the corner of mouth.

Facies in tetanus:
Risus sardonicus (abnormal, sustained spasm of the facial
muscles). It also includes raised forehead and eyes half closed.

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Height
Tall stature:
Can be physiological or pathological.
The pathological causes can be:
 Gigantism - excessive growth hormones.
 Hypogonadism - diminished functional activity of the gonads.
 Delayed puberty.
 Marfan's syndrome - a genetic disorder of the connective tissue.
The people have long slender fingers (arachnodactyly), narrow
feet, a high-arched palate, upward dislocation of the lenses of the
eyes, and cardiovascular abnormalities: mitral valve prolapse,
dilatation of the aortic root.

Short stature
Intrinsic shortness - familial (genetic) short stature, turner's syndrome (females
with one of the two defective or absent X-chromosomes).
Delayed growth - constitutional delay in growth (adult height often normal), subtle
undernutrition, physical and/or psychological abuse or child neglect, underlying
systemic diseases of mild to moderate severity.
Attenuated growth - chronic renal failure, metabolic acidosis, malignancy
(including effects of chemotherapy and radiotherapy), glucocorticoid excess,
pulmonary disease (e.g. cystic fibrosis and severe asthma), congenital heart
disease,
gastrointestinal disease (e.g. coeliac disease and Crohn's disease), hypothyroidism,
advanced HIV infection, severe protein and calorie malnutrition.

Weight and nutritional status

Body mass index (BMI):
Weight in pounds, height in inches:
weight (lbs)
2
700
[height (inches)]
Weight in kilograms, height in meters:
weight (kg)
¿¿
Underweight < 18.5
Normal 18.5-24.9
Overweight 25-29.9
Obese 30-39.9
Morbid obesity  40

Underweight < 18.5

Can be caused by: malnutrition, avitaminosis, dieting, anorexia nervosa, bulimia and
other psychiatric disorders, hyperthyroidism, hypoproteinemias, diabetes
(ketoacidosis), chronic consumptive diseases, panhypopituitarism (Simmonds d.,
Sheehan sd), hyperparathyroidism.

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Overweight > 25
Can be caused by: dietary intake exceeds energy expenditure, Cushing’s disease or
syndrome, type 2 diabetes, psychiatric disorders, hypothyroidism, insulinoma,
Pickwickian syndrome.
The waist circumference correlates with visceral fat and indirectly measures central
adiposity
The circumference is measured at the level equidistant between the costal margin and
iliac crest.
In overweight individuals the waist circumference is > 94 cm (37 inches) in men and
> 80 cm (34 inches) in women.
Types of obesity:
-Android (central, abdominal) obesity - located in the abdomen, cervical region,
“buffalo hump”, “apple shape”.
Waist circumference > 102 cm (40 inches) in men, and > 88 cm (35 inches) in
women.
The waist-hip ratio is > 0.9 in men and > 0.85 in women.
It is associated with: cardiovascular diseases, gout (‫)דלקת פרקים‬, biliary lithiasis (
‫)אבנים‬, type 2 Diabetes mellitus, sleep apnoea, hyperlipidemias, shortens life
expectancy.
-Gynoid (gluteal) obesity - rounded hips. Fat accumulation in the upper part of the
body, buttocks, thighs and subumbilical abdomen. “Pear shape”.
It is associated with: varicose veins, arthrosis, intervertebral disc disorders,
digestive disorders.
-Generalized obesity

Speech and mental status

Level of consciousness:
Lethargy - the patient appears drowsy but opens the eyes and looks at you,
responds to questions, and then falls asleep.
Obtundation - the patient opens the eyes and looks at you, but responds slowly and
is somewhat confused. Alertness and interest in the environment are decreased.
Stupor - the patient arouses from sleep only after painful stimuli. Verbal responses
are slow or even absent. The patient lapses into an unresponsive state when the
stimulus ceases. There is minimal awareness of self or the environment.
Coma - the patient remains unarousable with eyes closed. There is no evident
response to inner need or external stimuli.

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Level of consciousness Glasgow coma scale

Speech and language:

Quantity
Rate
Loudness
Articulation of Words
Fluency - word comprehension, repetition, naming, reading comprehension,
writing.
Disorders of speech are affecting the voice, the articulation of words and the
production and comprehension of language.

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Aphonia - a loss of voice seen in diseases affecting the larynx or its nerve supply.
Dysphonia - less severe impairment in the volume, quality, or pitch of the voice.
For example: hoarse (‫ )צרוד‬or only able to speak in a whisper.
It can be caused by laryngitis, laryngeal tumors, and a unilateral vocal cord
paralysis.
Dysarthria - a defect in the muscular control of the speech apparatus. Words may
be nasal, slurred (‫)נבלעות‬, or indistinct, but the central symbolic aspect of language
remains intact.
It can be caused by motor lesions of the central or peripheral nervous system,
parkinsonism, and cerebellar disease.
Aphasia - a disorder in producing or understanding language.
It is often caused by lesions in the dominant cerebral hemisphere (usually the left).
Two common types of aphasia: are Wernicke's (a fluent, receptive, aphasia) and
Broca's (a nonfluent, expressive) aphasia.
Paraphasia - in which words are malformed, wrong or invented.
Mood:
Sadness and deep melancholy.
Contentment, joy, euphoria, and elation.
Anger and rage.
Anxiety and worry.
Detachment and indifference.
Thoughts and perception:
Assess the logic, relevance, organization, and coherence of the patient’s thought
processes as they are revealed in words and speech throughout the interview.
Abnormalities of thoughts:
Compulsions - repetitive behaviors or mental acts that a person feels driven to
perform in order to produce or prevent some future state of affairs, although
expectation of such an effect is unrealistic.
Obsessions - recurrent, uncontrollable thoughts, images, or impulses that a person
considers unacceptable and alien.
Phobias - persistent, irrational fears, accompanied by a compelling desire to avoid
the stimulus.
Anxieties - a general sense of ill-defined dread or impending doom.
Feelings of unreality - sense that things in the environment are strange, unreal,
remote.
Feelings of depersonalization - a sense that one’s self is different, changed, or
unreal, or has lost identity or become detached from one’s mind or body
Delusions - false, fixed, personal beliefs that are not shared by other members of
the person’s culture or subculture.
Abnormalities of perception:
Illusions - misinterpretations of real external stimuli.
Hallucinations - subjective sensory perceptions in the absence of relevant external
stimuli (auditory, visual, olfactory, gustatory, tactile, or somatic).
Cognitive function:
Orientation - time, place, person.
Remote and recent memory.
Information and vocabulary - if considered in the context of cultural and
educational background, information and vocabulary are fairly good indicators of
intelligence. They are relatively unaffected by any but the most severe psychiatric

Mor Halgoa 16
 disorders, and may be helpful for distinguishing mentally retarded adults (whose
information and vocabulary are limited) from those with mild or moderate
dementia (whose information and vocabulary are fairly well preserved.
Calculating ability
Abstract thinking
Constructional ability

Orthostatism (standing) and gait (walking)

Depends upon vision, lower motor neurones , spinal reflexes, musculoskeletal system,
and on proprioceptive, corticospinal, extrapyramidal and cerebellar pathways.
Ataxia is an abnormal orthostatic posture/gait that lacks coordination, with a wide-
base standing and instability.
Maneuvers:
Romberg test - with the eyes open, three sensory systems provide input to the
cerebellum to maintain truncal stability: vision, proprioception, and vestibular
sense. If there is a mild lesion in the vestibular or proprioception systems, the
patient is usually able to compensate with the eyes open. When the patient closes
their eyes, however, visual input is removed and instability can be brought out. 
Ask the patient to stand up with his heels close together and toes
apart (preferably with bare feet), with both arms and hands extended toward the
examiner, first with his eyes open. Then ask the patient to close his/hers eyes for
20-30 sec without support.
- Positive Romberg sign: loss of steadiness with the eyes closed, but no or
minimal swaying when eyes are open.
Caused by sensory (proprioceptive) ataxia.
In case of a positive Romberg sign, we need to check if the patient is tending
towards one side (a problem in the inner ear of the same side) or tilting to both
sides (damaged structure above).
- Negative Romberg sign: loss of balance with the eyes opened.
Caused by cerebellar ataxia.
- Indifferent Romberg sign: no loss of balance with the eyes closed and open.
Tandem walking - ask the patient to walk heel-to-toe in a straight line.
Types of ataxia:
Cerebellar ataxia - wide-bases, staggering and unsteady gait, difficulty on taking
turns and impossible tandem walking, negative Romberg sign.
Caused in cerebellar syndrome (disease of cerebellum and associated tracks).
Sensory ataxia - unsteady and wide-based gait, positive Romberg sign: the swaying
begins as soon as the eyes are closed, occurs in all directions, and is rapid.
Occurs due to proprioceptive sensory loss: polyneuropathy, damage of the dorsal
column spinal cords or central areas that integrates proprioceptive information -
cerebellum, thalamus, parietal lobes.
Vestibular ataxia - positive Romberg sign: the imbalance appears after an interval,
consists of a slow lateral inclination of the body, is of small amplitude, always in
the same direction and may vary with the position of the head.
Caused by labyrinthine disorders.
Types of gaits:
Parkinson gait - posture is stooped, with head and neck forward and
hips and knees slightly flexed. The arms are flexed at elbows and
wrists. The hands are usually shaking.

Mor Halgoa 17
 Initiation of walking may be delayed, the steps short and shuffling
and there is loss of arm swing. Rapid short-stepped hurrying (festinant) gait.
Caused by Parkinson disease (defect in basal ganglia).

Hemiplegic gait - the leg being extended at the knee with plantar
flexion of the foot. The patient walks by either dragging the foot,
often scraping the toe, or circles it stiffly outward and forward
(circumduction).
Ipsilateral arm is held immobile and close to the side, with elbow,
wrist, and interphalangeal joints flexed.
Caused by a unilateral upper motor neurone lesion (stroke).

”Scissors” (diplegic) gait - walking is stiff with short steps and

each leg is advanced slowly with effort. The thighs tend to cross
forward on each other at each step.
Caused by bilateral upper motor neurone damage of the lower
limbs (bilateral spastic paresis).
It is usually caused after sever hypoxia in childhood or before
birth, which produces an irreversible damage.

”Steppage” (neuropathic) gait - the patient either drag the damaged

feet or lift it high, with knee flexed, and bring it down with a slap
onto the floor.
It is associated with the inability to walk on its heels.
Caused by peroneal nerve injury (sciatica), multiple sclerosis.

Myopathic gait - “waddling” gait due to proximal muscular weakness.

The lower limb is not controlled due to lack or less muscle tonus.
Caused by muscle disease.

”Drunken sailor" (ataxic) gait - a wide-based gait, with uncertain

start and stop, lateral deviations, and unequal steps.
Caused by cerebellar ataxia, alcohol intoxication.

”Dancing” gait - bizarre walking patterns associated with choreic movements of

the arms. Usually in women.
Caused by Huntington disease, psychogenic.

Mor Halgoa 18
SKIN EXAMINATION
Skin exanimation is being performed in parts (head, thorax, abdomen, limbs) while
examining body's systems.
Elementary skin lesions can be divided into:
1. Primary - first appear on the skin:
Circumscribed color changes
Elevated (palpable) solid masses
Elevated masses with fluid content
2. Secondary - a consequence or an evolution of a primary lesion:
Loss of skin surface
Material on the skin surface
Scars

Primary skin lesions:

Circumscribed color changes
Macule is a small, flat spot with a dimension < 1 cm.
For example:
- Pigmented (freckles, lentigo,”café au lait” spots).
- Depigmented (after superficial burns).
- Purpuric (‫)סגלגל‬.
- Erythematous (syphilis rash) - appers in
secondary syphilis as symmetrical,
reddish-pink, non-itchy rash on the trunk
and extremities, including the palms and soles.
Patch is a macule with size > 1 cm.

Elevated (palpable) solid masses

Papule is a protuberant, well-defined, of various colors, superficial, solid, and of
small size (< 1 cm).
Plaque is a papule with size > 1 cm.
For example:
- Urticaria (hives) - an acute or chronic disorder, characterised
by wheal (‫ )חבורה‬rash (recurrent transient oedematous dermal
papules, persisting less than 24 hours. It may be
asymptomatic but are often intensely itchy or sting and burn).
It is caused by food, drugs allergies, insect bites or physical factors (scratching
which leads to dermatographia).
- Naevi - a pigmented spot or mark on the skin, such as a mole or birthmark.
- Seborrheic keratoses (senile warts) - a benign skin growth that
originates in keratinocytes. These are slightly raised, light brown
spots with rough, warty surface.
Lesser-trelat sign is an abrupt erruptive seborrheic keratoses that
may denote underlying internal malignancy.

- Warts - well-defined papules with rough surface (on the

hands, knees, face), which has a viral etiology (verruca

Mor Halgoa 19
 vulgaris), which is very congagious.

Nodule is a rised skin mass, going deeper in the skin. It is larger (> 1cm), firmer
and deeper than papule.
For example:
- Epithelioid granulomas - small size nodule (~ 1-2cm),
caused by a dermic collection of mixed inflammatory
cells.
In sarcoidosis it is non-caseating , and in tuberculosis
(scrofuloderma) it is caseating (‫)פצע פתוח‬.
- Osler nodules - red, tender, small nodules (1-3mm)
on the finger pads, palms and soles.
Seen in infective endocarditis.
- Maynet nodules - small, non-tender, skin colored nodules on extension
surfaces.
Seen in rheumatic fever.
- Gouty tophi - a desposit of monosodium uric acid crystals in
people with high urate levels in blood. It is formed in the
joints, cartilage, bones and other places throughout the body.
Sometimes, it breaks through the skin and appears as white
or yellowish-white, firm, non-tender nodules.
It may ulcerate.
It may be present in the ear, elbow, fingers and feet,
mainly on small and not large joints.
- Xanthomas - a deposition of yellowish cholesterol-rich
material in tendons or other body parts in various disease
states. They are cutaneous manifestations of lipidosis in
which there is an accumulation of lipids in large foam
cells within the skin. It is caused by the accumulation
of fat in macrophages.
Xanthelasma is a distinct condition, only being called a
xanthoma when becoming larger and nodular, assuming
tumorous proportions.
Xanthoma tuberous is characterized by xanthomas
located over the joints (knees, elbows, heels, buttocks).
Eruptive xanthoma is clinically characterized by small,
yellowish-orange to reddish-brown papules that appear
all over the body (hypertriglyceridaemia).
Skin tumors are large masses (> 2 cm) that involve all the layers of the skin.
For example:
- Benign nevus
- Melanoma, other skin carcinomas. It may appear by it self or as a development
of a beuty mark.
Malignant melanoma is characterized by the ”ABCDEs” of melanoma:
Asymmetry
irregular Borders
variation in Color
Diameter > 6 mm
Elevation
- Metastatic tumors.

Mor Halgoa 20
Elevated masses with fluid content
Vesicle is a serous fluid accumulation, small sized (< 0.5 cm). It can be in the
epidermis (not scaring) or in dermis (scaring).
There are two types of vesicles:
Localized:
- Herpes eruption (cold sores) - small, closely grouped
vesicles on a red base face (lips), genitals (type 2 HSV).
When it appers all over the mouth, this is a primary
contagion. In later eruptions the viruses are locacalized
in one side.
- Herpes zoster (shingles) - closely-grouped red bumps
in a continuous band on the area of skin. It is supplied
by one, occasionally two, and rarely more
neighbouring spinal nerves. The virus does not
invade the blood.
The serous fluid, containing the veriscella zoster virus is very contagious.
An intense, persistent pain (neuralgia) precedes, accompany and often persists
after the healing of the eruption.
Generalized:
- Varicella (chickenpox) - an itchy rash of red papules
(small bumps) progressing to vesicles (blisters).
Different stages of lesions are present simultaneously.
Appers on the stomach, back and face, and then
spreading to other parts of the body.
- Dermatitis - itchy, vesicle eruption caused by skin
inflammation.
For example: atopic dermatitis, irritant contact dermatitis,
allergies.
Bulla is a vesicle (serous fluid) larger than 1-2 cm.
For example: second , bullous pemphogoid, porphyria
cutanea tarda.

Pustule is a vesicle/bulla with purulent (‫ )מוגלתי‬exudate

(sterile or not).
For example: acne.

Secondary skin lesions:

Loss of skin surface
-Excoriation is a linear loss of epidermis. It may penetrates to
dermis, with or without scarring. It is caused by scratching, skin
abrasion.
-Fissure is a deap linear split in the skin which penetrates in to
dermis.
-Erosion is a loss of the superficial epidermis. It doesn‘t
bleed and can be with or without scarring. For example
after vesicle ruptures.

Mor Halgoa 21
-Ulcer is a focal loss of epidermis and dermis and is always
scarring.
- Venous (varicose) ulcer - well defined edges, bottom
covered with crusts, adjacent skin with stasis eczema.
It ic casued due to chronic venous insufficiency.
- Syphilis chancre - round, sharp edges, erythematous
bottom, nontender hard base, highly infective.

Material on the skin surface

Crust is a deposit caused by the died residue of serum, pus, or
blood.
It can be hematic (brown-red) or melicerice (yellow-golden).
Scale is an exfoliated fragment of the keratinic layer of the
Epidermis (like after sun burns).
It is produced by abnormal keratinization or sheeding,
and can overly macules, papules or plaques.
Psoriasis is a chronic, common disease (2% of population).
It contains a non-tender, non-itchy red scaly patches with
well-defined edges.
Scratching the scales produces a silvery white powder,
and if continued a drop of blood appears (Auspitz sign).
It is localized in the elbow, knee, sacrum and scalp.
Associated features are nail pitting and psoriatic arthritis.
After the psoriasis patch remission (‫)הפוגה‬, either
Spontaneous or posttreatment, it may leave post-inflammatory of
hyper/hypopigmentation.
Psoriasis does not cause true scarring.
Keratosis (keratoderma) is marked thickening of the skin.
For example:
- Palmoplantar keratoderma - hereditary (26 syndromes),
acquired.
- Ichthyosis - persistently dry, thickened, rough,
fish scale skin.
There are 20 forms (inherited and acquired).
Acquired ichthyosis: cancer (lymphoma, generalised),
thyroid disease, sarcoidosis, HIV infection, drugs:
hydroxyureea.

Scars
Scar is a fibrous tissue that replace a destroyed focal area of the skin. It can be:
- Linear (after cuts, surgical sutures) or irregular (after ulcers, profound
wounds).
- Hypertrophic (thick and pink) or atrophic (thin and white).
Keloids has the same consistency and composition of scars,
but they grow beyond the border of the injury that incited them.
Skin atrophy is a focal depression of the skin resulting from
thinning of epidermis and/or dermis.
It can be caused by senile (aging) and arterial insuficciency.

Mor Halgoa 22
Stria is a linear skin atrophy (white/red) due to tear of the elastic fibers of the
subdermic layers. It can be caused due to pregnancy, growth spurs, obesity or
hypercorticism (cushing syndrome).
Skin sclerosis is the thickening and thighting of the skin and the subcutaneous tissue
to form hard plaques, due to excessive activation of the fibroblasts. It can be:
- Localized - also called morphea.
It is secondary to an inflammatory process.
- Generalized (systemic scleroderma) - sclerodactyly
(in fingers and toes), bizantin facies, skin calcinosis
(formation of calcium deposits in soft tissues),
raynaud syndrome (discoloration, mostly of the fingers and
toes), ulcers, esophagial and cardiac disorders.

Hemorrhagic skin lesions:

Petechia is a small (1-3 mm), reddish-purple macule,
persists when pressed, not pulsatile.
In case of multiple or conflated it is called purpura.
It appers due to small intradermic hemorrhage, and
is caused by vascular disorders, platelet disorders
or coagulation disorders.
Ecchymosis is a patch, various shape and size,
with color that changes in time.
First it is purplish-blue → green (days) → yellow-brown (weeks).
It is not pulsatile and is persists when pressed.
It appers due to a dermic hemorrhage, and can be caused by
bruising, traumas.
It can also be spontaneous, due to bleeding disorders.
Hematoma is a nodule of various size and shape, tender/nontender with the same
color changes in time as petechia and ecchymosis.
It appers due to large hemorrhage or blood accumulation in the subcutaneous
tissue.

Vascular skin lesions:

Apper due to overgrowth and dilation of dermic blood vessels, and they fade away
when pressed over.
Angiomas are reddish-purple patch/papule.
For example:
- Cherry angiomas - the most common angiomas. These are
cherry red papules on the skin, containing an abnormal
proliferation of blood vessels.
- Spider angiomas - a type of telangiectasis found slightly
beneath the skin surface, often containing a central red
spot and reddish extensions which radiate outwards like
a spider's web.
When pressed it blanches from the central area to periphery.

Mor Halgoa 23
 It is caused by hyperestrogenism, chronic liver failure.

- Venous lake - bluish angiomas on the lip, face and ears.

- Telangiectasias (spider vein) - bluish, irregular,
linear macule on the limbs and anterior chest.
These are small vessels (venules, arterioles or capillaries)
which are dilated due to increase pressure in the
superficial veins.
It is not pulsatile and diffuse pressure blanches the veins.

EXAMINATION OF SKIN AND MUCOSAE

Tegumentum (skin) is the outer covering of living tissue, with complexes functions:
sensation, adaptive immune system, heat regulation, storage and synthesis, excretion.
The skin thickness is 0.2-0.5 mm (at the level of the eyelids), and up to 4-8 mm (at the
level of the heels). Its surface is 1.5-2 m2 and it presents:
- Folds: coarsely (inframammary, intergluteal, inguinal), more discreet (the
flexion face of joints) and fine (fingerprints). The palmary and plantar folds
mark the limits of papillary crests.
- Infundibular depressions: correspond to the openings of sudoriferous glands
channels or to sebaceous follicles.
The skin is made out of 3 layers:
1. Epidermis - superficial, no blood vessels, contains layers of cells –
melanocytes that produce melanin.
2. Dermis - consists of connective tissue (collagenic, elastic and reticular fibers,
fibroblasts, mast cells), nerves, blood vessels, lymphatic vessels, muscles,
sebaceous glands, the channels of sebaceous glands.
The roles of this layer are dermis nutrition and skin analyzer.
3. Hypodermis - consists of adipose lobules separated by fibrous tracts, nerves,
receptors, blood and lymphatic vessels, sudoriferous glands, the deeper portion
of bulb of hair.
The role of this layer is tegument support.
Skin glands:
- Sudoriferous glands (merocrine glands) - produce sweat: water, chloride,
sodium, potassium, lactic acid, urea, fat acids, mucopolysaccharides,
glycoproteins, hydrosoluble vitamins.
- Sebaceous glands (holocrine glands) - open at the level of hair follicle,
produce sebum (oxycholesterin, cholesterin, unsaturated fat acids, soaps).
Androgens increase their secretion and estrogens decrease it.
Annexes of skin:
Visible from the outside.
- Hair - the enlarged basal part of a hair within the skin is the root, and the part
of a hair projecting beyond the skin is the shaft.
A hair consists: hair shaft, sebaceous gland, hair follicle, hair bulb and papilla.
- Nails - corneous thin sheets on the surface of the distal phalanges. Their
source is the nail matrix. The lunula is a part of the nail matrix.

Mor Halgoa 24
Cutaneous symptoms - pruritus (itches)
Pruritus is a cutaneous symptom produced by subliminal irritation of nervous
terminations by the mediators (histamine, acetylcholine) which determines an
“attenuated pain”.
In producing pruritus are involved genetic factors and psychological factors
(emotional pruritus).
Secondary lesions might be: excoriations (‫)קילוף של העור‬, lichenification (thickening
and hardening of the skin), cutaneous infections, local pigmentations, degraded nails.
 DO NOT confuse between pruritus and prurigo, which are papulous,
pruriginous lesions, determining local pruritus).

Secondary
(Determined by cutaneous affections)

Pruritus Generalized

Primitive
("sine materia")

Localized
Systemic pruritus
Appears in:
Jaundice syndromes (billiary salts retention, pre-jaundice phase leading to
neoplasia and increases in night or in heat conditions).
Paraneoplasic pruritus (lymphoma, lymphosarcoma, carcinoma).
Diabetes mellitus (one of the early signs).
Uremia (calcium deposits in the tegument - irritation of nervous terminations).
Gout (teenagers).
Parasitic infections.
Hyperthyroid, hypothyroid, cushing syndrome, acromegaly, menopauses.
Senile (due to elasticity changes and increased capillary fragility).
Drugs allergy (usually along with urticarial eruption).
Scabies - intensive, especially during the night (increased scratching (‫מגורד‬
‫ )בפומפיה‬lesions).
Other causes (psychological, gastric hypoacidity, iron deficiency anemia,
pernicious anemia, avitaminosis).

Local pruritus
Have preferential localization in several affections:
Vulvar - diabetes mellitus (associated to candidiasis - fungal infection),
menopause (“widow pruritus”), iron deficiency, lack of vitamins, uterine or anexial
neoplasia, psychogenic.
Scrotal / penile - diabetes mellitus, prostate carcinoma, urinary tract infections
(frequent urethritis), psychogenic.
Abdomen, hips, extremities - hepatitis, cirrhosis.
Nasal - asthma, allergic rhinitis (‫)דלקת אף‬, giardiasis (children), uremia,

Mor Halgoa 25
 morphinomania (abitual and uncontrollable craving for morphine)
Hyperfoliculinemia.
Auricular - diabetes mellitus.
Scalp - alcohol abuse, pre-/postmenstrual.
Anal - parasitic infections, hemorrhoids, intestinal diseases, nearby infections.

Skin color changes

Skin color results from 4 natural pigments with or without other pathologic ones.
The 4 natural pigments are:
- Melanin (brown).
- Oxyhemoglobin (bright red), mainly within arteries/capillaries.
- Deoxyhemoglobin (more bluish), present in venous blood.
- Carotene (yellow).
Special or pathological conditions may be hemosiderin, bilirubin and metals.
This depends on skin thickness and light (artificial light distorts colors).
The examination of skin color must be done in sunlight!
Skin color changes can be classified:
- Pallor
- Cyanosis
- Jaundice
- Hypercarotenemia
- Changes of skin pigmentation
- Hyperemia (redness of the skin)

Pallor
A lighter color of the skin and visible mucosae, caused by a reduced amount of
oxyhemoglobin.
Pallor is best appreciated where the epidermis is thinnest: the fingernails, the lips,
tongue, palpebral conjunctiva, palmar skin.
Main causes are:
- Thickening of the skin (myxedema, edema).
- Lack of development of dermal capillaries (hypogonadism in men - “egyptian
picture” aspect).
- Vasoconstriction (strong emotions, acute circulatory failure).
- Anaemia (in association with tiredness and fatigue).
Different colors associated with pallor could be correlated with the causes of
the anemia: Flavinic shade - hemolytic anemia
Yellowish shade - pernicious anemia
Verdinic shade - young girls chlorosis (“green sickness”) =
hypochromic anemia
Lighter yellow shade - gastric neoplasia
“Cafe au lait” shade - bacterial endocarditis
“White like paper” shade - acute hemorrhagic anemia
Pallor is associated with “clue” signs that could ascertain the origins of anemia:
- (“spoon nails”) - anemia due to iron deficiency
(the nails are flattened and have concavities).
- Hunter glossitis - pernicious anemia.
- Inappetence and loss of weight - neoplasia.
- Cutaneous hemorrhagic manifestations (petechia, ecchymosis, hematomas) -
acute leukemia, loss of blood.

Mor Halgoa 26
Cyanosis
A bluish color of the skin and mucosal surfaces, which appears from 2 reasons:
- Due to an increased quantity of reduced hemoglobin (more than 5g/dl) in the
arterial blood.
- Due to abnormal hemoglobin or rare type of hemoglobin (”kansas” Hb,
methemoglobin, sulphuretted Hb).
Cyanosis disappears with digital pressure.
False cyanosis is a discoloration of the skin induced by deposition of gold salts
(chrysiasis), silver salts (argyria), arsenic or other compounds.
False cyanosis doesn’t disappear with digital pressure.
Cyanosis due to abnormal or rare Hb
These are rare conditions which appear in patients without cardiac and pulmonary
disease.
Methemoglobinemia – presence of higher than normal level of metHb (ferric
[Fe3+], rather than ferrous [Fe2+] Hb).
Can occur due to:
- Oxidative substances - intoxication with nitrites, phenacetin, potassium
chloride, aniline derivatives.
- Congenital or genetic.
- Idiopatic methemoglobinemia.
Sulfhemoglobinamia.
Can occur due to:
- Presence of sulphuretted hydrogen in the intestine (Hijmans van der bergh
toxic cyanosis).
- Administration of drugs like phenacetin or sulphamides.
Cyanosis due to an elevated quantity of reduced Hb
The bluish color appears when the quantity of reduced Hb in the arterial blood is more
than 5 g/dl (normally it is < 3g/dl).
Cyanosis indicates a bad oxygenation of the arterial blood (hypoxemia).
The degree of cyanosis depends on quantity of Hb. Therefore we need to pay attention
to the anemic patients. Because of the small quantity of Hb, cyanosis appears when
hypoxemia is extremely severe.

Localized
Pulmonary
Cyanosis Central Right-left shunt

Generalized

Peripheral Cardiac / stasis

Generalized central cyanosis
Pulmonary central cyanosis - this is the sign of respiratory insufficiency, bad
oxygenation (low arterial saturation) of arterial blood in the lungs.
It is caused by low alveolar oxygen pressure, disturbances in gas exchange,
ventilation/perfusion mismatch.

Mor Halgoa 27
 This type of cyanosis has several characteristics:
- Generalized (even the tongue is cyanotic).
- Warm (hypoxia induces vasodilatation).
- Negative Lewis test (rubbing the ear lobe with the fingertips does not make
cyanosis to disappear).
- Oxygen supplementation of the inspired air may correct cyanosis.
Central cyanosis with right-to-left shunt - also called “the blue syndrome”.
It is caused by congenital heart disease with right-to-left shunt (fallot tetralogy),
associated with retarded growth and physical development, dyspnea on exertion,
clubbing of the fingers and toes.
The typical position is squatting. The patient suffers from anoxic episodes (lack of
oxygen), and its state is not influenced by oxygen administration.
Generalized peripheral cyanosis (stasis)
This is the sign of right heart failure, accompanied by gravitational edema.
This type of cyanosis has several characteristics:
- Respects blood peripheral circuits.
- Doesn’t affect the tongue.
- Cold (because of the low velocity of blood which leads to stasis and
vasoconstriction).
- Positive Lewis test (rubbing the ear lobe with the fingertips makes cyanosis to
disappear becoming red).
In cardiogenic shock patient presents “pale cyanosis” due to vasoconstriction,
marmoreal teguments, which remain cold and cyanotic when adopting a declined
position.
Localized cyanosis
Due to an increased tissue oxygen extraction of arterial blood.
It is produced by 2 mechanisms: decreased arterial supply and slowing down of
venous-capillary circulation.

Thrombophlebitis
Acute
Arterial embolus
Localized
cyanosis
Peripheral chronic ischemia syndrome
Chronic
Acrocyanosis

Erythrocyanosis- also called “red cyanosis”, appears in

polycythemia vera.
It was described by osler as “red like roses in summer and
blue like indigo in winter“.
Color changes are more obvious in the areas exposed to
temperature variations (face and hands).
It is associated with pruritus “sine materia” which commonly
starts after a bath.

Acrocyanosis - refers to a persistent blue or cyanotic

discoloration of the digits, most commonly occurring
in the hands although also occurring in the face and

Mor Halgoa 28
 feet as well.
It appears in cold exposure, phlebitis, chronic venous
failure, raynaud syndrome, and is caused by functional
anomalies in capillary circulation.
Livedo reticularis - a “lace-like” purplish discoloration.
It has a particular aspect: racemos livedo - permanent red-violet
arborizations (‫)הסתעפויות‬.
It occurs in the abdomen in acute pancreatitis.

Face cyanosis - venous thrombosis, superior cave vein syndrome.

Jaundice
Better seen on the bulbar conjunctives, under the tongue, on the hard palate and on the
lips (after digital pressure).
When bilirubin value is > 7 mg, the jaundice is visible for the patient and its
entourage.
In hyperpigmented patients, jaundice is put in evidence by plasma aspect and urine
color changes.
The differential diagnosis of jaundice is done with hypercarotenemia and chronic
renal failure.
Xanthopsia is a visual disturbance in which objects apper yellow due to dyeing of the
ocular media.
Jaundice can be classified depending on shade:
-Orange - hepatocellular jaundice.
-Flavin - hemolytic jaundice.
-Rubin - leptospirosis.
-Verdin - mechanical jaundice. Critical hepatocellular jaundice, due to the
conversion of bilirubin into biliverdin, associated with pruritus.
-Melas - pancreatic head cancer. Increased tegumentum amount of biliary salts and
biliverdin.

Hypercarotenemia
Carotenoids give yellow to yellow-orange discoloration of the
skin (adipose tissue). It is prominent in regions of increased
sweating (face), palms and soles.
Primery hypercarotenemia (carotenoderma) is due to increased
dietary food intake or nutritional supplements.
Conditions associated with hypercarotenemia include myxedema, diabetes and
chronic renal failure.

Pigmentation disorders
Melanocytes produce melanin which has a yellow-soil color. Melanocytes number is
the same for all races, but the number of melanin granules varies.
Melanocytes are predominantely located in the axilla, genital region, elbow and knee.
Rare locations are the mucosa, palms and soles.
Melanogenesis is hormonally controlled.
Pigmentation disorders can be classified as follows:
Hypopigmentation - can be generalized or local.
1. Generalized hypopigmentation:

Mor Halgoa 29
 Albinism is a genetic disorder, which can be total (amelanosis) or partial (only
the eyes lack of pigment).
Total oculocutaneous albinism is also a genetic disorder, that includes white
tegument, white hair and decolorized iris, through which the eye fundus (the
back portion of the interior of the eyeball) is seen.
2. Local hypopigmentation:
- Phenylketonuria - accumulation of phenylalanine and metabolites in the
blood. This is an inherited metabolic disorder, caused by an enzyme
deficiency.
It includes decolorized hair and iris, severe mental retardation and urine
smelling like mouse.
- Others - burns, scars, Simmonds disease (atrophy or destruction of the
anterior lobe of the pituitary gland), Biermer disease (lack of vitamin
B12), menalocytes deficiency in protein deficiencies, shadows around the
nevi.
Discolorations:
Vitiligo (leukoderma) - loss of pigment, resulting in
Irregular pale patches of skin, areas of hyopigmentation
with surround hyperpigmentation and migration of
melanocytes to the border of the affected area.

Hyperpigmentation - can be generalized (melanoderma), local or circumscribed.

1. Generalized hyperpigmentation (melanoderma):
An abnormally intense pigmentation of the skin, caused by increased deposits
of melanin, hemosiderin and metals (pseudocyanosis).
- Addison disease - most typical melanoderma. It covers all the tegument
(except the palms and soles), mucosae, areas submitted to frictions or
pressure, scars, axilla, white linea, folds, palmary crests, nipples genitalia.
- Hemochromatosis - hyperpigmentation with "metal shade" iron deposits
(hemosiderin), due to pathological increase in total body iron (skin, liver,
pancreas, "bronzed diabetes").
Distribution areas include: face, forearms (the extension region), belly,
nipples, genitalia, scars.
It includes atrophic tegument with hair loss.
2. Local hyperpigmentation:
- Pregnancy mask - irregular symmetric patches like a mask. Appears in
pregnant women, after the 5th month.
- Face - thalassemia, malabsorption syndrome, contraceptives.
- Periocular pigmentation - hepatic diseases, ovarian tumors, Graves-
Basedow disease.
- Rihel disease - pigmentary patches at the level of the face and thorax.
Regional hyperpigmentation:
- Leg - chronic venous insufficiency.
- Mammar areola - pregnant women, estrogen
treatment in men.
- Axillas - "acantosis nigricans".

- Not coated part of body - porphyria pellagra.

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 - Different region - gratilage lesions, frequent
heat contact.
3. Circumscribed hyperpigmentation:
- Freckles
- Lentigo (moles)
- "Café au lait" patches - Recklinghausen neurofibromatosis.
- Peutz-Jeghers syndrome - periorificial lenticulosis, colon polyposis.
- Fixed drug erythema - entemato pigmented plaques.
- Urticaria - enhanced mast cells degranulation.
- Malignant melanoma

SKIN APPENDAGES
Including hair, nails, sebaceous glands and sweat glands.

Hair
A protein filament that grows through the epidermis from follicles deep within the
dermis.
Body hair is racial, genetical and hormonally influenced.
Lanugo - fine black hair that covers the entire body of the fetus and newborn.
Vellus - short, fine, inconspicuous, and relatively unpigmented, covers most of the
body of the females and children.
Terminal hair - coarser, thicker, more conspicuous, usually pigmented (scalp,
eyebrows, eyelashes, axillary, pubic, beard).
Axillary and pubic pelage - appears on puberty in both sexes. It is fully developed
after the 20s, and is dependent on androgens.
Excessive hair growth
Hypertrichosis is an increase in the amount of hair growth in areas that are normal
for the sex and age of the patient. Extensive cases of hypertrichosis have
informally been called werewolf syndrome.
Causes for hypertrichosis:
1. Physiological - men, limbs of some brunet women.
2. Pathological -
- Congenital: generalized (“werewolf syndrome”) or localized
(on the back - "faun tail" due to neural abnormalities and spinal
defect, and on the pinna - in old men, AIDS patients and diabetic
patients).
- Acquired: due to a variety of injuries like trauma, irritation or inflammation,
after plaster casts, drugs (phenytoin, cyclosporine a and minoxidil), porphyria
cutanea tarda (problems with heme synthesis), malignancy, anorexia nervosa,
malnutrition.
Hirsutism is an excessive hairiness on women or children (premature pubarche) in
those parts of the body where terminal hair does not normally occur or is minimal.
(for example, a beard or chest hair). It refers to a male pattern of body hair (thick
or dark terminal hair).
- Virilisation is an abnormal development of male sexual characteristics in a
female.

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 Signs of virilisation: enlarged clitoris, deep voice, seborrhea (chronic
inflammatory disease of the skin characterized by the accumulation of scales
of greasy skin), acne, android features.
- Signs of defeminisation (removal of female characteristics): atrophy of the
uterus, breast, amenorrhea (absence of a menstrual period), secondary sterility,
male behavior.
Causes for hirsutism:
- Idiopathic: end-organ hypersensitivity to androgens.
- Acromegaly.
- Cushing’s syndrome, virilizing tumours (a functional tumor that produces
virilization in girls and women or precocious (‫ )מוקדם‬sexual development in
boys), congenital adrenal hyperplasia.
- Drugs: androgens, progesterone.
- Polycystic ovary syndrome (causing fertilities problems), tumours.
- Paraneoplastic syndrome of the lung, pancreas, colon. This is a collective term
for disorders arising from metabolic effects of cancer on tissues remote from
the tumor.
Hair loss
Baldness occurs when the terminal scalp hairs undergo miniaturization to vellus hairs.
This is an aging phenomenon with an inherited component, dependent on androgens.
Women may show age-related hair loss that is more diffuse.
Alopecia is a pathological hair loss. It can be:
Diffused - in hypothyroidism, hypopituitarism and iron deficiency, or it may be
drug induced (cytotoxic agents).
Localized. It may be:
- Non- scarring - alopecia areata (lost of hair from some or all areas of the body,
usually from the scalp "spot baldness"), fungal infection, secondary syphilis,
hertzoghe syndrome (alopecia of the external half of the eyebrow), loss of
axillary and pubic hair (old age, cirrhosis, hypopituitarism).
- Scarring - burns, severe infections (like herpes zoster), lichen planus (a
chronic mucocutaneous disease that affects the skin, tongue, and oral mucosa),
systemic lupus erythematosus.
Hair texture and color
- Premature graying - Basedow (Graves) disease, cushing’s syndrome,
emotional shock, iron deficiency.
- Hypothyroidism - dry, coarse, thinned hair.

Nails
Nails are a plate of hardened densely packed keratin, which protects the fingertip and
facilitate grasping and tactile sensitivity in the finger pulp.
Nail matrix contains dividing cells that mature, keratinize and move forward to form
the nail plate.
The lunula is the visible distal part of the matrix

Mor Halgoa 32
Nail color changes:

Nail changes:
Onychauxis - thickening of the nail.
Onychogriphosis - clawlike nails, due to genetic causes,
ill-fitting shoes, injury, poor blood flow to the feet, diabetes
or nutritional deficiency.
Onychocryptosys - ingrown nail (‫)ציפורן חודרנית‬.
Onychorrhexis - brittle (‫ )שברירי‬nails, due to the effect of
water and detergent, iron deficiency, hypothyroidism or
digital ischaemia.

Onycholysis - separation of nail from nail bed, due to psoriasis,

fungal infection, trauma, thyrotoxicosis or tetracyclines.

Onychomycosis - thickening, whitening, ridging of the nail.

Paronychia - inflammation of the proximal and lateral nail

folds. The folds are red, swollen, and often tender.
The cuticle may not be visible.

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Nail fold erythema and telangiectasia - due to vasculitis, systemic lupus
erythematosus systemic sclerosis, dermatomyositis.

Koilonychia - spoon-shaped depression of nail plate.

It occurs in iron deficiency anemia.

Beau’s lines - transverse grooves. May be caused by any

severe systemic illness which affects growth of the nail
matrix.

Pitting nails - fine, small pits, due to psoriasis.

Leukonychia - white nails, due to an injury to the base of

the nail (the matrix) where the nail is formed, or by a diet
low in potassium.

Half and half nails - the proximal portion of the nail is

white and the distal half is red, pink, or brown, with a sharp
line of demarcation between the two halves.
Common in hemodialysis patients.

Splinter hemorrhages - tiny blood clots that tend to run

vertically under the nails. They are a nonspecific finding
and can be associated with subacute bacterial endocarditis,
scleroderma, trichinosis, systemic lupus erythematosus,
rheumatoid arthritis, psoriatic nails, antiphospholipid
syndrome and trauma.
Clubbing of the fingers:
A deformity of the fingers and fingernails associated with a number of diseases,
mostly of the heart and lungs.
The nail plate is more convex, the proximal nail fold, when palpated, feels spongy or
floating, and the distal phalanx of each finger is rounded and bulbous.
Pierre marie’s hypertrophic pulmonary osteoarthropathy includes clubbing of the
fingers, thickening of periosteum and synovium, and paraneoplastic syndrome: lung
cancer.
Causes for clubbing of the fingers:
Lung disease
- Lung cancer.
- Interstitial lung disease.
- Tuberculosis.
- Suppurative (‫)מוגלתי‬: lung abcess, empyema,
bronchiectasis, cystic fibrosis.
- Pulmonary hypertension.
- Mesothelioma.
Heart disease
- Congenital cyanotic heart defect.

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 - Subacute infective endocarditis.
- Any disease featuring chronic hypoxia.

Gastrointestinal or hepatobilliary disease

- Malabsortion.
- Crohn’s disease, ulcerative colitis.
- Cirrhosis.
Others
- Graves’s disease.
- Unilateral: subclavian/axillary artery aneurism.

Sweat glands
Located in the dermis layer of the skin.
There are two types of sweat glands:
Eccrine - widely distributed, open directly onto the skin surface.
Their sweat production help to control body temperature.
Apocrine - present in the axillary and genital regions, usually open into hair
follicles. They are stimulated by emotional stress.
Bacterial decomposition of apocrine sweat causes an adult body odor.

Hyperhidrosis

Quantitative
modifications
Anhidrosis

Chromhidrosis

Qualitative
modifications Bromhidrosis

Increased chloride level

Hyperhidrosis (diaphoresis) is the sweating in excess of that required for normal
thermoregulation. It can be:
Generalized:
- Neurologic or neoplastic diseases.
- Metabolic disorders (thyrotoxicosis, diabetes mellitus, hypoglycemia, gout,
pheochromocytoma, menopause).
- Febrile illnesses.
- Medications (propranolol, tricyclic antidepressants).
- Chronic alcoholism.
- Hodgkin disease or tuberculosis (night sweats).
Localized:
- Emotional induced in the palms, soles, and/or axillae.
- Associated with vascular abnormalities, peripheral neuropathy.
Anhidrosis is the lack of sweating. It can be:

Mor Halgoa 35
Generalized:
- Autonomic neuropathy.
- Extensive burns.
- Sclerodermia.
- Haloperidol.
Localized:
- Face: Claude-Bernard-Horner syndrome.
- Lower half of the body: diabetes (xerosis diabetica).

Sebaceous glands
Located in dermis layer of the skin. They produce a fatty substance sebum that is
secreted to the skin surface through the hair follicles.
Palms and soles are the only region without sebaceous glands.
Seborrhea is an excessive secretion of sebum. It occurs mainly in puberty (associated
with acne), pregnancy, menopause, hypercortisolism (in cushing’s syndrome, drug
induced), Parkinson’s disease.
Sebaceous cyst (epidermoid cyst)
This cyst is the result of the implantation of epidermal elements in the dermis, which
are NOT of sebaceous origin.
Many cysts originate from the infundibular portion of the hair follicle.
The cysts are firm, round, of variable size and painless subcutaneous nodules. They
are mobile from profound layers but attached to skin.
It may be flesh-colored to yellow or white or even pigmented.
It contains a central pore or punctum from which a thick cheesy material can
sometimes be expressed.
They are usually present on the face, the trunk, the neck, the extremities, and the
scalp.
Rhinophyma
Describe thickening of the skin on the nose and the presence of many oil glands.
The nose appears thick, bulb shape, reddish, with a waxy, yellow surface.
It usually occurs in old men and in patients with COPD.

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SUBCUTANEOUS TISSUE EXAMINATION
The lower most layer of the skin, of variable thickness. It contains:
- Loose connective fibers (elastic, fibrous bands)
- Lobules of fat
- Hair follicle roots
- The glandular part of some sebaceous glands
- Blood vessels, lymphatic vessels, nerves
- Bursae, in the space overlying joints in order
- Fine, flat sheets of muscle (the scalp, face, hand, nipple, and scrotum)
The main role of the subcutaneous tissue is fat storage.
Any lump or swelling should be assessed by these characteristics:
1. Position, location
2. Size and shape
3. Surface, edge
4. Consistency
5. Attachments
6. Adjacent skin → signs of inflammation (with/without redness (erythema),
tenderness, heat.
7. Thrills, bruits and noises
Lipoma
Is a benign tumor of adipose tissue where adipocytes have increased size and number.
Lipomas are:
Well-defined mass with smooth edge
Of variable dimensions and locations
Painless
Its consistency can be soft, fluctuant or hard (fibrolipoma) with ossifications.
Movable on superficial and profound layers.
Lipoma can be:
Capsulated
Difusse - fatty tissue mass occupying a region of variable dimensions, seldom
symmetrically: shoulders, neck, thorax.
Unique
Multiple (lipomatosis):
- Multiple familial lipomatosis
- Adiposis dolorosa (dercum’s disease) - multiple painful lipomas located on the
trunk and limbs, affects mostly postmenopausal women.
Lipodystrophies
Is a group of diseases characterized by abnormalities of fat distribution, and is
associated with metabolic, autoimmune or renal disorders.
Congenital lipodystrophies:
- Generalized/partial (the residual fat undergoes compensatory hypertrophy).
- Appears from birth → total or partial absence of fat tissue.
- Associated with insulin resistance and diabetes, hypertriglyceridemia.
Acquired lipodystrophies :
- Acquired partial lipodystrophy (barraquer-simons syndrome).
- Acquired generalized lipodystrophy

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 - HIV-associated lipodystrophy.
- Localized lipodystrophy (lipoatrophy) - insulin injection sites, “buffalo
hump”.
Inflammatory lesions in the adipose tissue
Panniculitis
Tender skin nodules with/without weight loss, and with/without fever. It can be:
- Unique or multiple nodules
- Of variable sizes
- Tender spontaneously or when palpated
- Of firm consistency then fluctuant
- Discoloration of adjacent skin: reddening-brownish-darker pigmentation
- Due to the fat necrosis
Evolution: resorbtion (lipoatrophy) or suppuration (oily fluid).
Examples: posttraumatic, cold exposure, Weber-christian
disease, associated with connective tissue disorders
(like scleroderma), erythema nodosum.
Cellulitis
Regional, diffuse, severe inflammation of the skin and Erythema Weber-christian
subcutaneous tissues due to acute bacterial infection Nodosum disease
(streptococci or staphylococci).
Clinical findings:
- Unilateral redness, swelling, increased warmth, tenderness.
- Usually with indistinct borders, except in erysipelas (a type of cellulitis with
sharply demarcated margins).
- Lymphangitis and regional lymphadenopathy.
- With/without systemic manifestations (fever, chills, hypotension, tachycardia).
Evolution: blistering, abscesses, ulceration, erosion or after successful treatment,
the skin may flake or peel off as it heals.
Complication: septicaemia, necrotising fasciitis, endocarditis.
Differential diagnosis: deep venous thrombosis.

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Subcutaneous tissue - assessment of hydration
In adults water comprises 60-65% of body mass: 2/3 is intracellular and from the
resting 1/3, 2/3 is in the interstitial fluid and 1/3 is volemia.
Assessing the hydration state:
- Detailed history of the nature and the quantity of fluid loss (vomiting,
diarrhoea, sweating, burns and polyuria, raised ambient temperature).
- Check the skin turgor: gently pinch of fold of skin on the neck or the
subclavicular area. Hold it for a few seconds then release it.
Normal skin turgor - well-hydrated skin springs back into position
immediately.
Decreased turgor - abnormally slow skin turgor seen in dehydration.
- Examine the patient tongue and mouth mucosae.
- Look for weight loss (if previous weight is known).
- Check the pulse and blood pressure (supine and erect).
- Check for edema.
- Examine the jugular venous pulse.

EDEMA
Edema is an increase in interstitial volume, localized or generalized, due to sodium
and water accumulation in the subcutaneous tissue.
The normal anatomic profile disappears and pits appear under pressure.
Edema results from either increased movement of fluid from the intravascular to the
interstitial space, or from decreased movement of water from the interstitium to
capillaries/lymphatics. The onset may be abruptly or develop in time.
Types of edema:
1. Local edema (inflammatory and allergic edemas). It is asymmetrical, and is
localized to a single area/extremity/part of an extremity.
2. General edema (cardiac and renal edemas). Mandatory generalized
hydrosaline retention, leading to weight gain.
It is symmetrical, and is usually dependent (fluid overload) or nondependent in
areas with lax conjunctive tissue (eyelid, face, scrotum).
Clinical features:
The normal anatomical profile disappears and appears swelling of the affected
area.
Initially the skin is under tension and shiny. In resolution phase fine longitudinal
folds appear, together with thickening of the teguments. Other skin lesions or
discolorations may also occur, as well as hair or nails changes
Color:
- White in renal edema.
- Cyanotic in cardiac and venous edemas.
- Red in inflammatory or allergic edemas.
Local temperature:
- Increased temperature in inflammatory edema.
- Normal temperature in renal edema and in venous/lymphatic obstruction.
- Decreased temperature in cardiac edema.

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Consistency:
- Soft, easy pitting in renal or starvation edema.
- Pits appear very hard, or not at all in inflammatory and venous edema.
- No pitting in myxedema and lymphedema.
- Skin thickening in chronic edema.
Pain: inflammatory edema is painful, but the other types of edema are generally
not painful.
Severity of edema is graded on a 4-point scale, from slight to very marked
Anasarca
Clinical syndrome characterized by pronounced water and sodium retention, casing an
extreme generalized edema, leading to fluid accumulation in the serous spaces of the
body (hydrothorax, ascites, hydropericardium).
The fluid is usually transudate, it is clear with a green-yellow tan, and has a low
content of proteins.
Where to look for edema?
Retromaleolar region: by applying digital pressure on the area until a pit is formed.
Anterotibial.
Over the knee articulation.
Anterior abdominal wall: when you fold the skin pits and orange like surface
appears.
Sacral region: in bed immobilized patients.
Breast edema: infero-external aspect.
Upper limbs: infero-internal and posterior aspect, over the elbow.
Face edema: compare the aspect with a recent photo.
Mechanisms of edema
Local factors: the fluid volume which leaves the capillary at the arterial end is
higher than the resorbed volume at the venous extremity.
Local factors that influence the onset of edema:
- Increased capillary hydrostatic pressure (vs. colloid-osmotic pressure).
- Decreased plasma osmotic pressure (vs. tissue mechanical pressure).
- Increased capillary permeability.
- Obstruction of the lymphatic system and drainage.
Water and sodium retention: when the local mechanism of water transudation
becomes secondary, this is associated with a decrease in sodium, and secondary,
water excretion.
Cardiac edema
- Symmetrical, painless, pitting edema
- Gravitation dependent.
- In bedridden patients lumbosacral edema is dominant.
- Untreated edema develops in a cranial direction (downup), until anasarca
appears.
- Edema is cyanotic and cold (stasis cyanosis) due to low cardiac output.
- The presence of dyspnea is mandatory.
- Increased levels of BNP (B-type Natriuretic Peptide) are mandatory. This
substance is secreted from the ventricles in response to changes in pressure that
occur when heart failure develops and worsens.
- Edema is much more frequent in right heart failure.
- It is produced by an increase in central venous pressure.

Mor Halgoa 40
- There is marked sodium and water retention due to reduced glomerular filtration
rate.

Renal edema
- Nephrotic edema is due to protein loss after basal membrane damage
(albuminuria > 4g/24hr.).
- In nephritic edema, on the other hand, protein loss not so important to justify
edema. It is caused due to sodium retention.
- Symmetrical, painless, white, soft, easy pitting edema with normal temperature.
- Mostly is visible in the face, eyelids, dorsal aspect of feet, external genitalia.
Starvation edema
- Generalized, soft, pits appear easy.
- Localized at the legs and face.
- General aspect similar to renal edema.
- Main mechanism is hypoalbuminemia, due to malabsorbtion, hepatocellular
failure or serumalbumin synthesis failure.
Hepatic edema
- White, soft, located in the inferior limbs.
- Appears in decompensated liver cirrhosis.
- Ascites is not proportional with edema.
- Jaundice and spider nevi are present.
- Reduced liver aldosterone turnover.
- Mechanisms: hypoalbuminemia, hyperaldosteronism.
Pregnancy edema
- Moderate, symmetrical, painless, white, soft, easy pitting edema with normal
temperature.
- Localized at the inferior limbs, mostly on the dorsum of the feet and on the
ankles.
- Determined by several factors: humoral, inferior vena cava compression.
- Generalized edema may occur after the 20th pregnancy week, including
hypertension and proteinuria. Presence of these factors is called preeclampsia,
which can lead to eclampsia - an acute and life-threatening complication
of pregnancy, characterized by the appearance of seizures. It may develop into
coma and even death.
Catamenial or cyclic edema
- Discreet and moderate edema of the legs, which appears predominantly in the
second half of the menstrual period.
- They are dependent on secondary hyperaldosteronism.
Mixedema
- Appears in severe hypothyroidism.
- It is determined by infiltration of the subcutatenous tissue with
mucopolysaccharides.
- Periorbital edema that does not pit with pressure.
- The skin is dry and thickened.
- The hair and eyebrows are dry, coarse, and thinned.
Iatrogenic edema
Resulting from treatment by a physician or surgeon.
- Excessive water and sodium administration.
- Corticoids.

Mor Halgoa 41
- Estrogens.
- Other drugs.

Inflammatory edema
- Due to infection, trauma, burns, capillary leak syndrome.
- Localized edema accompanied by the other features of inflammation (redness,
heat and pain)
- Pits do not appear.
Quincke edema
- Pruriginous, pink, easy painful.
- Located in the eyelid and the superior lip.
- Glotic edema can appear, and results in a bad prognosis because of respiratory
obstruction.
Venous edema
- Acute, white, non-pitting edema in a single, usually lower extremity.
- Usually painful
- Present redness, warmth, and tenderness (less marked than in cellulitis).
- Initially it is moderate, but later it can be important.
- In superficial thrombophlebitis the edema is limited beyond the thrombosed vein.
- In deep thrombophlebitis the edema can be found in either inferior or superior
limbs.
- It sometimes has a predisposing factor (recent surgery, trauma, immobilization,
hormone replacement, cancer).
Chronic venous failure
- Due to chronic obstruction or valvular incompetence of the deep veins.
- Soft, pits on pressure, and later may become hard.
- Skin thickening especially near ankle.
- Occasionally bilaterally and non painfull.
- Skin is often cyanotic, with brown pigmentation, varicose veins, ulcerations.
- Consecutive to recurrent deep venous thrombosis - posthrombotic syndrome.
- Increased in orthostatic position.
Lymphedema
- Caused by a lymphatic obstruction.
- Located in the legs, external genitalia, the female breast most frequently
involved.
- Soft swelling in early stages → indurated, hard, nonpitting.
- Normal skin in early stages → rough and thick (elephantiasis).
- Unilateral or bilateral.
- Normal color, no brown pigmentation of the skin.
Allergic edema
- The affected area is red and itchy but not painful.
- Angioedema - Affects the face, lips and mouth.
Diffuse, nonpitting, tense, pink or skin-colored swelling.
Does not itch .
Develops rapidly typically disappears over subsequent
hours/days.
May be life-threatening if glottic edema appears.

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LYMPH NODES EXAMINATION
The lymphatic system an extensive vascular network that drains lymph, from organs
and tissues and returns it to the venous circulation.
From the blind lymphatic capillaries, the lymphatic fluid moves into thin vascular
vessels, then to the collecting ducts and eventually into the major veins at the root of
the neck.
Roles of the lymphatic system:
1. Vascular function
2. Body’s defense system
3. Lipid metabolism
The lymph nodes are the “filtration stations” along these vessels.
They are round, oval, or bean-shaped structures and they vary in size according to
their location.
There are 2 types of lymph nodes: superficial and deep.

Lymph nodes description

Location: localized/generalized, palpable/non-palpable lymph node
Size: 0.5-1cm.
Adenopathy is when the size of a lymph node is > 1-1.5 cm.
Consistency: soft, rubbery/”craggy”/”matted”/”stony”.
Tenderness: normally they are non-tender.
Surface: regular/irregular.
Fixation: normally they are mobile to the skin and deep structures.
Adjacent skin: normal/red, warm, swollen, tender/infiltrated.

Head and neck lymph nodes

Occipital lymph nodes.
- Location: at the base of the skull.
- Drainage: the occipital region of the scalp.
- Palpation: from the front of the patient, using the pads
of the 2nd and the 3rd fingers, with a gentle rotary motion.
- Occipital lymphadenopathy: can be caused by tinea capitis
(superficial fungal infection of the scalp), seborrheic
dermatitis (inflammatory skin disorder affecting the scalp),
pediculosis (infestation (‫ )שריצה‬with lice), insect bites,
orbital cellulitis (inflammation of eye tissues), rubella,
roseola infantum.
Posterior auricular lymph nodes.
- Location: superficial to the mastoid process.
- Drainage: the posterior part of the temporoparietal
region, the back of the external acoustic meatus.
- Palpation: from the front of the patient, using the
pads of the 2nd and the 3rd fingers, with a gentle rotary motion.

Mor Halgoa 43
Preauricular lymph nodes.
- Location: in front of the tragus.
- Drainage: the conjunctivae, skin of the cheek, eyelids,
the temporal region of the scalp.
- Palpation: from the front of the patient, using the pads
of the 2nd and the 3rd fingers, with a gentle rotary motion.
- Preauricular lymphadenopathy: can be caused by viral
infections, chlamydia trachomatis, gonococcus conjunctivitis.
Tonsillar lymph nodes.
- Location: at the angle of the mandible.
- Drainage: the tonsillar and posterior pharyngeal
regions.
- Palpation: from the front of the patient, using the
pads of the 2nd and the 3rd fingers, with a gentle
rotary motion.
- Tonsillar lymphadenopathy: can be caused by pharyngitis.
Submandibular and submental lymph nodes.
- Location: midway between the angle and the tip of the
mandible/in the midline, behind the tip of the mandible.
- Drainage: the teeth, tongue, gums, and buccal mucosa.
- Palpation: from the front of the patient, using the pads of
the 2nd and the 3rd fingers, with a gentle rotary motion.
- Submandibular and submental lymphadenopathy: can be
caused by oral and dental infection, acute lymphadenitis.
Cervical lymph nodes.
- Location: superficial - superficial to the sternocleidomastoid.
posterior - along the anterior edge of the trapezius.
deep cervical - deep to the sternocleidomastoid.
- Drainage: the tongue, external ear, parotid gland, deeper
structures of the neck (larynx, thyroid, trachea).
- Palpation: from the back of the patient - superficial nodes.
from the front of the patient - posterior and deep
nodes.
- Cervical lymphadenopathy:
1. Viral infections: infectious mononucleosis, adenovirus, herpesvirus
coxsackievirus, and CMV.
2. Bacterial infection: streptococcal infection, atypical mycobacterium,
mycobacterium tuberculosis, “catscratch” disease (bartonella henselae).
3. Hodgkin’s and non-hodgkin lymphoma, neuroblastoma, leukemia.
4. Kawasaki disease (an autoimmune disease in which the medium-sized
blood vessels throughout the body become inflamed).
Supraclavicular lymph nodes
- Location: deep in the angle formed by the clavicle and the
sternocleidomastoid.
- Drainage: the head, neck, arms, superficial thorax, lungs,
mediastinum, and abdomen (left supraclavicular node).

Mor Halgoa 44
 - Palpation: from the front of the patient, using the pads of
the 2nd and the 3rd fingers, with a gentle rotary motion.
- Supraclavicular lymphadenopathy:
1. Infections: tuberculosis, histoplasmosis, and coccidioidomycosis.
2. Mediastinal or lung tumors.
3. Occult abdominal neoplasm (abdominal cancer, especially gastric).
It is indicated by enlarges Virchow-Troisier’s node in the supraclavicular
fossa.

Axillary lymph nodes

- Location: there are 5 groups of lymph nodes.
1. Central - high in the axilla.
2. Lateral - along the upper humerus.
3. Pectoral - along the lower border of
pectoralis major, inside the anterior axillary fold.
4. Infraclavicular.
5. Subscapular - along the lateral border of the
scapula, inside the posterior axillary fold.
- Drainage: the hand, arm, lateral chest, abdominal
walls, breasts.
- Palpation: from in front of the patient.
Support the arm on the side under examination and
palpate the right axilla with your left hand and vice versa.
- Axillary lymphadenopathy:
1. Recent immunization in arm (bacilli,
Calmette-Guerin vaccine).
2. Silicone implants.
3. Infections: catscratch disease, brucellosis, s. aureus,

Mor Halgoa 45
 streptococcus.
4. Lymphoma.
5. Breast cancer.
6. Metastatic melanoma.
Epitrochlear lymph nodes
- Location: on the medial surface of the arm ~3 cm above the elbow.
- Drainage: the ulnar surface of the forearm and hand, the
little and ring fingers, the adjacent surface of the middle
finger.
- Palpation: support the patient's right wrist with your left
- hand, grasp the patient's partially flexed elbow with your
right hand and use your thumb to feel for the epitrochlear
gland.
Examine the left epitrochlear gland with your left thumb.
- Epitrochlear adenopathy: can be caused by repeated minor
trauma and infections, cat scratch disease, tularemia,
sarcoidosis, secondary syphilis, lymphoma, chronic lymphocytic leukemia.

Inguinal lymph nodes

- Location: there are 2 superficial groups.
1. Horizontal - below the inguinal ligament.
2. Vertical - near the upper part of the saphenous vein.
- Drainage: the horizontal group drains into the superficial
portions of the lower abdomen and buttock, the external
genitalia (but not the testes), the anal canal and perianal
area, and the lower vagina.
The vertical group drains into the corresponding region
of the leg.
- Palpation: from the front of the patient, using the pads
of the 2nd and the 3rd fingers, with a gentle rotary motion.
- Inguinal adenopathy: can be caused by cellulitis, sexually
transmited diseases (treponema pallidum, herpes simplex
virus, h. ducrey, c. trachomatis), lymphoma, metastatic
melanoma or squamous cell carcinoma.

Popliteal lymph nodes

- Location: deep within the popliteal fossa.
- Drainage: the heel and the outer aspect of the foot.
- Palpation: use both hands to examine the popliteal
fossa with the knee flexed and limb muscles relaxed.

Generalized lymphadenopathy
Viral (adenovirus, ebv, hiv, cmv, rubella, varicella, measles).
Bacterial (septicemia, typhoid fever, tuberculosis, syphilis, plague).
Protozoal - toxoplasmosis.
Fungal - coccidioidomycosis.
Autoimmune disorders rheumatoid arthritis, lupus erythematosus.
Hypersensitivity states (serum sickness: phenytoin, allopurinol.
Storage diseases gaucher disease, niemann-pick disease.
Malignancy: acute/chronic leukemia, lymphoma.
Mor Halgoa 46
MUSCLES AND BONES EXAMINATION
Examination of muscles
Muscular diseases are important cause for invalidity, and may be temporary or
permanent. They are determined by loss of functionality of muscular fibers,
innervations, blood supply and adjacent connective tissues.
The motor unit is composed of a neuron and the totality of muscle fibers innervated
by it.
Mechano-receptors are the ones that maintain the muscular tonus.
The causes for muscular diseases may be:
- Primary muscular: dystrophies, infections or inflammatory diseases, trauma.
- Neurological: central and lower neuron syndromes, pyramidal syndrome, extra-
pyramidal syndrome, dysfunction of the neuro-muscular connection.
It is important to review the history of the symptoms appearance according to the
seven attributes of a symptom.
Symptoms can be:
Subjective:
- Pain = myalgia.
- Weakness = myasthenia.
Objective:
- Disturbances of muscular mass.
- Disturbances of muscular tonus.
- Involuntary movements.
- Diminution of muscular straight.
Clinical examination
Inspection - can be:
- Passive (static time) - distribution and symmetry.
- Active (dynamic time) - tonus and kinetics.
Palpation - passive or active.
Lab and procedures:
- Lab determinations: CK (creatine kinase), LDH (lactate dehydrogenase),
TGO, calcium, other electrolytes.
- EMG (electromyography).
- Muscle biopsy.
- Immunological and genetic testing.
Myalgia is a muscular pain. It can be:
Diffuse:
- Acute - Febrile syndrome, infectious (influenza, bacterial and parasitic) or by
vaccinations, electrolyte disturbances (hypokalemia), alcoholism, adverse
reaction of drugs (statins, interferon), exercise: over-use or over-stretching.
- Chronic - autoimmune (multiple sclerosis), metabolic myopathies
(glycogenosis), chronic fatigue syndrome.
Localized: trauma, intermittent (claudication).
Trichinosis is a parasitic disease, caused by trichinella spiralis.

Mor Halgoa 47
Criteria for diagnosis: non-specific gastro-enteritis, fever, muscle soreness or pain,
facial edema, eosinophilia, subungual, splinter hemorrhage, conjunctival or retinal
hemorrhage.
Lab test that need to be done are for: Eosinophils, CK, IgG, antibodies.
Myasthenia ("lack of strength") is a direct term for the inability to exert force with
one's muscles to the degree that would be expected given the individual's general
physical fitness.
Force of contraction will decrease with repeated exercise. It can be perceived or true.
It can be:
- Proximal: bilateral - myopathies.
- Distal: bilateral - neuropathies.
- Myasthenia gravis.
Myasthenia gravis
An autoimmune neuro-muscular disease, in which auto-antibodies block acetylcholine
receptors at the postsynaptic neuromuscular junction.
Symptoms include muscle weakness in a sudden onset, often intermittent, of the eye
muscles, face muscles (affecting mimicking, talking, chewing, swallowing), neck and
limbs muscles.
Applying ice improves muscle strength.
Disturbances of muscular mass
Atrophy is a reduction in muscle(s) mass. It is appreciated
by the disappearance of muscle contour (‫ )מתאר‬and better
visibility of bony contours.
It is more easily seen when is asymmetrical.
There are several types of dystrophy:
Primary: neurological - poliomyelitis, lateral amyotrophic
sclerosis, pyramidal syndrome, mononeuritis.
Secondary: part of cachexia (cancer, AIDS, organ failure:
heart, liver), disuse atrophy (inactivity, bed rest , cast), starvation.
Muscular dystrophy (MD)
A group of muscular diseases that are genetically determined (dystrophin-Duchenne
MD), affecting mostly boys.
Symptoms include progressive muscular wasting (the location depend on the type of
MD), poor balance, inability to walk, frequent falls, scoliosis, calf deformation, joint
contractures, respiratory difficulties, cardiomyopathies, arrhythmias.
MD is multisystemic, involving the heart, GI system, nervous system, endocrine
glands, eyes and brain.
In case of MD-like group of diseases, there are not affected behavioral, intellectual,
sexual individuals. Other patients may have cognitive and behavioral, speech, visual
problems.
Muscular hypertrophy is an increase of muscle mass. It can be:
Secondary to chronic overuse - either because of occupational reasons (body-
builders) or because of pathology - myotonia (Thomsen / Becker’s diseases).
Pseudo-hypertrophy - replacement of muscle mass by fat due to parasitic
infiltration (cysticercosis).
Localized tumefaction: amyloidosis, sarcoidosis, neoplasia, hematomas.
Disturbances of muscular tonus
Muscle tone (tonus) is the ability of muscles to respond to abrupt straight. It is an
involuntary response. Not to be confused with mass/force.
Muscle tone is responsible for maintaining body posture.

Mor Halgoa 48
Diminished muscular tonus - hypotonia.
- Congenital: genetic disorders (Down syndrome), congenital hypothyroidism.
- Acquired: infectious (meningitis, encephalitis, polio), hypothyroidism, vitamin
D overdose, hypocalcaemia.
Increased muscular tonus - hypertonia.
- Spasticity: lesion of the upper motor neuron (pyramidal syndrome), "pocket
knife".
- Rigidity: extra-pyramidal syndrome, "cog-wheel".
- Localized: antalgic (analgesic) contracture.
- Trismus (lockjaw): temporo-mandibular arthritis, pericoronitis, peri-tonsillar
abscesses.
- Torticolis: movement disorder in which the muscles controlling the neck cause
sustained twisting or frequent jerking (‫)טלטול‬.
- Tetanic contractions: alkalosis, hypocalcaemia, adverse drug reactions.
Involuntary movements
Seizures - paroxysmal (‫ )התקף פתע‬events that interest whole muscles.
The seizure can be tonic (contracture) or clonic (rhythmic movements).
It appears in epilepsy, tumor or head trauma or intracranial hypertension,
hypoglycemia, cardiac or circulatory arrest, any profound metabolic imbalance.
Myoclonus - a brief, involuntary twitching of a muscle or a group of muscles.
Contractions are called positive myoclonus, while relaxations are called negative
myoclonus.
It appears in epilepsy, head or spinal cord injury, brain tumors, essential
myoclonus (benign, sometimes inherited), post-hypoxemia.
Hemiballismus - a unilateral wild, large amplitude, movements of the arm and leg,
normally causing falls and preventing postural maintenance. It is caused by a
lesion, usually an infarct, around the contralateral subthalamic nucleus.
Chorea - a non-rhythmic, jerky, rapid, non-suppressible involuntary movements,
mostly of distal muscles or the face. Movements may merge imperceptibly into
purposeful or semipurposeful acts that mask the involuntary movements.
Athetosis - a non-rhythmic, slow, writhing (‫)עיוות‬, sinuous movements
predominantly in distal muscles, often alternating with postures of the proximal
limbs to produce a continuous, flowing stream of movement.
Choreoathetosis - a condition marked by abnormal movements of the body that
have a combined choreic and athetoid pattern.
Huntington’s disease - common cerebellar, autosomal dominant disorder.
Sydenham’s chorea - rheumatic fever.
Tremor is a rhythmic, alternating or oscillatory movements.
Resting tremor - maximal at rest and decreases with activity, “counting money” -
Parkinson's disease.
Postural tremor - maximal when a limb is maintained in a fixed position against
gravity.
Essential - gradual onset.
Abrupt onset - metabolic, drug adverse reactions.
Intention tremor - maximal during movement toward a target, as in finger-to-nose
testing. Cerebellar disorder, multiple sclerosis, Wilson's disease.

Mor Halgoa 49
Diminution of muscular straight
This is the difficulty or the impossibility of conducting specific movements. It can be:
Total - paralysis or partial - paresis.
- Hemiplegia: paralysis of one side of the body.
- Paraplegia: paralysis of the lower part of the body, including the legs.
- Quadriplegia: paralysis of all four limbs.
Generalized or localized.
Acute or chronic.

Examination of bones
Clinical examination
Inspection can be:
- General or on each segment.
- By steps - static (appreciates integrity and symmetry) and dynamic (finds
abnormal movements).
Palpation - follows inspection’s steps, confirms observations, determines
relationship with neighbouring tissues for modifications.
Percussion - detects/elicit sensibility (low-grade pain) and can appreciate
consistency and tissue structure composing deformations.
Auscultation - can detect bones crackles.
As a rule: uniloculate modifications (‫ )ממוקמים באזור אחד‬are orthopedic or trauma, and
multiloculate affectation are due to another cause.
Symptoms include:
1.Pain - easy to be recognized, confined to the affected region. The pain is
permanent and getting worse with movement and percussion.
It associates systemic symptoms:
- Pain + fever = acute osteomyelitis
- Pain + low grade fever, asthenia, loss of appetite = chronic osteomyelitis
- Neuralgic type + deformation of plain bones = syphilis
- Localized to cranium, tibia, clavicle, sternum ribs (spares the pelvis) =
multiple myeloma
2.Tumefaction / tumors - an action or process of swelling or becoming tumorous.
 Callus: a new growth of osseous matter at the ends of a fractured bone, serving
to unite them. Vicious callus can determine functional disturbances or
compress / include anatomical structures.
 Osteomyelitis: an infection of the bone or bone marrow. It has a discrete
tumefaction, with imprecise margins and is extremely painful.
 Benign tumors / cysts: palpable after they reach certain dimensions, well
delimitated. They are more easily palpable when it is superficial. On the skin
above is evident venous circulation. It is not adherent to superficial structures.
 Malignant tumors: if they are palpable it means they surpassed bone’s cortex,
painful spontaneous, worsen with palpation, adherent, imprecise delimited,
thick external layer, with a fluctuant (‫ )בעל תנועה‬content - multiple myeloma.
3.Bone deformation - does not affect bone’s integrity. It occurs in:
- Scimitar (curved) tibia, due to congenital syphilis.
- Scimitar femur and diaphysis hypertrophy - Paget’s disease
of bone.

Paget’s disease of bone

Mor Halgoa 50
 - Rickets - a deficiency disease resulting from a lack of vitamin D
or calcium and from insufficient exposure to sunlight,
characterized by defective bone growth and occurring chiefly in
children.
It results in twisting of long bones and genu valgum
(a deformity of the thigh or leg, or both, in which the knees are
abnormally close together and the space between the ankles is
increased) or genu varum (an outward curvature of one or both
legs near the knee), Harrison’s groove (an evidence horizontal
groove along the lower border of the thorax corresponding to
Genu varum
the costal insertion of the diaphragm), ribs rosary (prominent
knobs of bone at the costochondral joints).
- Acromegaly.
4.Fractures - a break in the continuity of the bone. The fracture cab be
on normal bone or on pathological bone, determined mainly by history.
Fractures are favored by:
Osteoporosis - a skeletal disease in which the bone mineral density
(BMD) is reduced and bone architecture is disrupted. Genu valgum
For positive diagnosis: BMD < 2.5 standard deviations below peak bone mass.
It may appear post-menopausal, due to glucocorticoid treatment or Cushing
syndrome.
Protein depletion (cirrhosis, nephrotic syndrome).
Lack of physical exercise.
Hypogonadism, menopause, hyperparathyroidism, hypercorthicism.
Symptoms of fractures include intense pain in a localized point, loss of
functionality,
deformations of the region, eventually shortening of a limb, abnormal mobility,
crackles, ecchymosis or hematoma, vicious position (for example a fracture of the
head of femur).

JOINTS - CLINICAL EXAMINATION

A joint is the location at which two or more bones make contact. They allow
movement and provide mechanical support.
Functional classification:
- Synarthrosis - permits little or no mobility, fibrous joint (skull).
- Amphiarthrosis - permits slight mobility, cartilaginous joints (vertebrae).
- Diarthrosis - permits a variety of movements. All diarthrosis joints are
synovial joints (shoulder, hip, elbow, knee).
We should recall the key elements of the history: mechanism of injury - trauma, the
time course of symptoms and limitations in function.
Prior to palpating, we should ask the patient if experiencing any pain.
Joints examination should be systematic, and it includes:
1.Inspection:
- Joint symmetry.
- Alignment.
- Bony deformities.
2.Inspection and palpation of bony landmarks, related joint and soft-tissue structures.
- Surrounding tissues for skin changes.

Mor Halgoa 51
 - Nodules.
- Muscle atrophy.
- Crepitus = audible and/or palpable crunching during movement of tendons or
ligaments over bone.
3.Assessment of range of motion, joint function and stability, and the integrity of
ligaments, tendons and bursae.
This assessment is necessary especially if there are pain or trauma.
4.Special maneuvers to test specific movements and range of motion.
We should always compare one side with the other.
We need to assess:
- Active movements (i.e. movements performed by the patient on their own).
- Passive movements (i.e. movements performed by the examiner).
- Resisted movements (i.e. movements against resistance).
A general rule of thumb is:
Reduced active movements, that improve on passive movement, suggest muscular or
tendon problems.
Reduced range of both active and passive movements suggest intraarticular disease.
We should be alert to signs of inflammation and arthritis: swelling, warmth,
tenderness, redness.

The Temporomandibular Joint (TMJ)

1.Inspection and palpation - place the tips of your index fingers just in front of the
tragus of each ear and ask the patient to open his or her mouth. The fingertips
should drop into the joint spaces as the mouth opens.
2.Range of motions - opening / closing, protrusion / retraction, lateral / side to side
motion.
Pathological findings
Swelling, tenderness and decreased range of motion are indication to arthritis
(inflamed joint).
Dislocation of the TMJ is a trauma.
Palpable crepitus / clicking are indication for meniscus injury or synovial swelling
from trauma.

The shoulder
1.Inspection and palpation -
- Note any swelling, deformity, muscle atrophy or fasciculations (fine tremors
of the muscles).
- Identify the bony landmarks of the shoulder:
1) The acromion process.
2) Acromioclavicular joint.
3) The greater tubercle of the humerus.
4) The coracoid process of the scapula.
- Palpate the painful area and identify the structures involved:
1) Sternoclavicular joint.
2) Clavicle.
3) Acromioclavicular joint.
4) Humeral head.
5) Coracoid process.
6) Deltoid muscle.
7) Spine of scapula.

Mor Halgoa 52
 8) Supraspinatus muscle.
9) Infraspinatus muscle.
10) Trazpezius muscle.
Then repeat on the other side.

2.Range of motions
- Flexion normal range usually 180 degrees.
- Extension normal range usually ~ 50 degrees.
- Abduction normal range usually ~ 180 degrees.
- Adduction normal range usually ~ 45 degrees.
- External rotation normal range usually ~ 90 degrees.
- Internal rotation normal range usually ~ 50 degrees.

Mor Halgoa 53
Pathological findings
Pain, pinching and stiffness when raising the arm.
Pain in the upper arm which:
- May radiate into the forearm, hands and fingers.
- Worse at night, making sleeping a painful and difficult event.
Remember there are many other conditions that can cause shoulder pain (e.g. pain
radiating from the neck, gallbladder disease, cardiac pain), so depending on the
circumstances you may want to perform other relevant clinical examinations.
Examination of all other areas is necessary.
Muscle atrophy is a lesion in the cervical nerves.
The rounded lateral aspect of the shoulder appears flattened = anterior dislocation.
Inability to perform movements may reflect weakness or soft-tissue changes from
bursitis (excess fluid and swelling), capsulitis, rotator cuff tears or sprains, or
tendinitis (irritation of the tendons leading to inflammation).

The elbow
1.Inspection and palpation -
- Identify the medial and lateral epicondyles and the olecranon process of the
ulna.
- Press on the epicondyles for tenderness.
- Note any displacement of the olecranon.
- Palpate the grooves between the epicondyles and the olecranon, noting any
tenderness, swelling, or thickening.
2.Range of motion -
- Flexion / extension at the elbow.
- Pronation / supination of the forearm.
Pathologic finding
Swelling over the olecranon process in olecranon bursitis, inflammation or
synovial fluid in arthritis.
Tenderness in lateral epicondylitis (tennis elbow) and in medial epicondylitis
(pitcher’s or golfer’s elbow).
The olecranon is displaced posteriorly in posterior dislocation of the elbow and
supracondylar fracture.

The wrist and hand

1.Inspection - of the palmar and dorsal surfaces of the wrist and hand (for swelling
over the joints).
- Note any deformities of the wrist, hand, or finger bones, as well as any
angulation from radial or ulnar deviation.
- Observe the thenar and hypothenar eminences.
- Note any thickening of the flexor tendons or flexion contractures in the
fingers.
2.Palpation - look for tenderness and swelling when examining the:
- Wrist / distal ulna and radius.
- Anatomic snuffbox.
- 8 carpal bones, each of the 5 metacarpals and the proximal, middle, and distal
phalanges.
3.Range of motions - flexion / extension.

Mor Halgoa 54
 The thumb range of motions:
- Flexion / extension.
- Abduction / adduction.
- Opposition.

Pathologic finding
Dupuytren’s contracture - fixed flexion contracture of the hand where the fingers
bend towards the palm and cannot be fully extended (straightened).
Herbeden’s nodes.
Bouchard’s nodes.

Rheumatoid Arthritis:
- Early rheumatoid arthritis -
1) Swollen, warm and red MCP (metacarpophalangeal) joints.
2) Squeezing causes a lot of pain.
3) The MCP joints are tender to touch.
4) The patient is unable to make a tight fist.
- Late rheumatoid arthritis -
1) Boutonniere deformities present.
2) Swan neck deformity of the thumb.
3) Ulnar deviation of the MCP joints.
4) Subluxation of the PIP joints.
The spine
1.Inspection -
From the side → the spinal curvatures:
1) Cervical lordosis.
2) Thoracic kyphosis.
3) Lumbar lordosis.
4) Sacral kyphosis.
From behind:
1) "vertebra prominens" (spinous process of C7).
2) 2nd lumbar vertebra.
3) L4-5 inter-vertebral space.
4) Iliac crests.
5) Dimples of venus / sacroiliac joints.
Abnormalities include scoliosis.
2.Palpation - of the spinous process / the paraspinal
muscles / the sacroiliac joints.
Look for tenderness.
3.Range of motions -
 The cervical spine:

Mor Halgoa 55
 - Flexion / extension.
- Lateral flexion.
- Lateral cervical rotation.
 The thoracolumbar spine
- Flexion / extension.
- Lateral flexion.
- Thoracolumbar rotation.
Schober’s test
Measures the degree of flexion of the spine.
Mark the spine at the lumbosacral junction, then 10 cm above
and 5 cm below this point. A 4-cm increase between the two
upper marks is normally seen.

Hip
1.Inspection -
- Exam the patient standing (both stationary and walking) and lying supine.
- Inspect for the level of the iliac crests. Assess if there are any scar, muscle
wasting or any obvious discrepancy in leg length.
2.Palpation -
- Note if there is any tenderness / heat / swelling around the inguinal areas and
the greater trochanter area.
- Measurement of length of legs between the anterior iliac spine to the tip of the
medial mallous, with the anterior spines lying at the same transverse level.
Compare one side to the other.
3.Range of motions
- Flexion normal range of movement ~ 120 degree.
- Extention.
- Adduction normal range of movement ~ 30 degrees.
- Abduction normal range of movement ~ 45 degrees.
- External rotation normal range of movement ~ 60 degrees.
- Internal rotation normal range of movement ~ 45 degrees.

Mor Halgoa 56
The knee and lower leg
1.Inspection - observe the patient both walking & standing.
- Does he walks with a limp or appear to be in pain?
- Is there any evidence of muscle wasting?
- Is there any evidence of bowing (varus) or knock-kneed (valgus) deformity?
- Does the knee appear red or swollen?
- Any rashes present?
2.Palpation -
- Palpate the knee for temperature.
- Feel systematically around the knee joint for tenderness including the patella,
quadriceps tendon, and the prepatellar and collateral ligaments.
- Bend the knee to 90 degrees & feel around the medial & lateral joint lines for
tenderness
- Remember to feel at the back of the knee for a popliteal (Bakers) cyst.
There are 3 tests to assess fluid in the knee join:
The Bulge Sign (for minor effusions).
 Milk downward
 Apply medial pressure
 Tap and watch for fluid wave.

The Balloon Sign (for major effusions).

Compress the suprapatellar pouch against the femur.
Feel for fluid entering (or ballooning into) the spaces
next to the patella under your right thumb and index
finger. This is a pathological finding.
Ballotting the patella-large effusions.
Compress the suprapatellar pouch and “ballotte”
or push the patella sharply against the femur.
Watch for fluid returning to the
suprapatellar pouch.
3.Range of motions -
- Flexion/extension.
- Internal/external rotation.
- Active flexion of the knee.
- Passive flexion of the knee.
Crepitus is usually indicative of degenerative
knee disease (osteoarthritis). Active flexion

Passive flexion

Mor Halgoa 57
The ankle and foot
1.Inspection - noting any deformities, nodules, or swellings and any calluses or
corns.
2.Palpation - looking for spontaneous tenderness or on compression, swelling,
nodules, when examining:
- The anterior aspect of each ankle joint.
- Achilles tendon.
- The heel: the posterior and inferior calcaneus and the plantar fascia.
- The metatarsophalangeal joints.
3.Range of motions -
- At the ankle (tibiotalar) joint: flexion / extension.
- At the foot: inversion / eversion.
Abnormalities
Localized tenderness and pain on mobilization in arthritis, ligamentous injury, or
infection of the ankle.
Rheumatoid nodules in Achilles tendon, tenderness in Achilles tendinitis, bursitis,
or partial tear from trauma.
Bone spurs may be present on the calcaneus; pain over the plantar fascia suggests
plantar fasciitis.
Tenderness on compression is an early sign of rheumatoid arthritis.
Acute inflammation of the first metatarsophalangeal joint is associated with gout.
Heel spurs are spikes of bone seen on the x-ray of the foot
Inflammation (irritation and swelling) of the plantar fascia can cause heel pain and
make walking difficult.

JOINTS - SIGNs, SYMPTOMS AND DISEASES

Gathering information regarding the history of the patient is necessary:
- What the patient means when describing symptoms.
- The sequence and severity of symptoms.
- The patterns of the progression, exacerbation and remission.
- Assessment of functional impact of the disease.
- The effects of current or previous therapy on the course of the illness.
- Assessment of compliance to therapy.

Main symptoms
1.Pain - a complex, subjective sensation that is difficult to define, explain, or
measure. This is the most common complaint.
Localization:
Pain needs to be localized anatomically. Since patients use terms in a non-anatomic
manner, ask the patient to point to the area of pain with a finger. If the pain is in a
joint, an articular disorder is likely to be present.
 Pain between joints may suggest bone or muscle disease or referred pain.
 Pain in bursal areas, in fascial planes, or along tendons, ligaments, or nerve
distributions suggests disease in these structures.
 Pain arising from deeper structures is often less focal than pain originating
from superficial tissues.

Mor Halgoa 58
  Pain in small joints of the hands or feet tends to be localized more accurately
than pain in larger joints (shoulder, hip, or spine).
 When pain is diffuse, variable, poorly described, or unrelated to anatomic
structures, fibromyalgia, malingering, or psychologic problems should be
suspected.
The character of pain:
"Aching" in a joint area suggests an arthritic disorder.
"Burning" in an extremity may indicate a neuropathy.
The intensity of pain:
It is important to ask about the severity of pain. Ask the patient to describe it on a
numeric scale from 1 to 10.
It is also necessary to assess the pain during activity and rest.
 Joint pain at rest and with movement is suggestive of an inflammatory process.
 Pain mainly during Activity can indicate a mechanical disorder (degenerative
arthritis).
Assessment the time of day:
When the pain or stiffness occurs.
2.Stiffness - discomfort perceived by the patient attempting to move joints after a
period of inactivity. It is usually develops after several hours of inactivity. It may
resolve within a few minutes (mild stiffness), or it may persist for many hours (RA
or polymyalgia rheum).
Morning stiffness:
A prodromal symptom of rheumatoid arthritis, and is a criterion for the diagnosis
of RA. If it is associated with non-inflammatory joint diseases:
 It is almost always of short duration (usually less than one-half hour).
 Less severe than stiffness of inflammatory joint disease.
 It is related to the extent of overuse of the damaged joint (mechanical or
degenerative joint disease).
 Usually responds within a few days to adequate limitation of the use of the
affected joint.
3.Limitation of motion - true limitation in motion is fixed and does not vary.
This complaint must be distinguished from stiffness (which is usually transient).
It is important to know:
 The extent of limitation.
 Degree of active and passive motion limitation.
 Type of onset -
- Abrupt  suggestive of a mechanical derangement (tendon rupture).
- Gradual  more common with inflammatory joint disease.
4.Swelling - we need to determine where and when the swelling occurs, and get the
information about:
 The factors that influence it.
 The onset and persistence of the swelling -
- Developed acutely → is most painful.
- Developed slowly (at a similar degree) → is often much more tolerable.
The patient can describes a feeling of swelling even if when an actual effusion is
not present.
An obese person may interpret normal collections of adipose tissue over the medial
aspect of the elbow or knee and lateral aspect of the ankle as swelling.

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5.Weakness - a loss of motor power or muscle strength. It can be objectively
demonstrated on physical examination
There are specific patterns to the distribution and duration of weakness:
 Musculoskeletal disorders: usually persistent rather than intermittent.
 Neuromuscular disorders (myasthenia gravis): initially good strength with
subsequent weakness.
 Inflammatory myopathies: weakness occurs in a proximal distribution
(shoulders and hips rather than hands and feet).
 Neurologic disorder: significant distal involvement.
6.Fatigue - an inclination to rest due to a sense of exhaustion, not because of muscle
weakness or pain. It is a common complaint of patients with musculoskeletal
disease. In rheumatic diseases, fatigue may be prominent even when the patient has
not been active.
Differentiation of fatigue from stiffness and weakness may be facilitated by
remembering that:
- Stiffness is a discomfort during movement.
- Weakness is an inability to move normally, especially against resistance.
Fatigue is a normal phenomenon after variable degrees of activity but should
resolve after rest.
Malaise is an indefinite feeling of lack of health that frequently occurs at the onset
of an illness. It often occurs with fatigue.
Both fatigue and malaise can be seen in the absence of identifiable organic disease,
and anxiety, tension, stress, and emotional factors can play a role.

Patient profile may provide important clues to the diagnosis:

1.Age -
 Young: SLE, rheumatic fever, and Reiter's syndrome.
 Middle age: fibromyalgia.
 Old age: osteoarthritis, polymyalgia rheumatic.
2.Sex -
 Men: Gout, spondyloarthropathies.
 Women: rheumatoid arthritis, fibromyalgia.
3.Race -
 Whites: giant cell arteritis, and Wegener.
 Blacks: sarcoidosis and systemic lupus erythematosus.
4.Family history - familial aggregation: ankylosing spondylitis, gout, RA,
Heberden's nodes of osteoarthritis.

Joint pain can be induced from:

Extrinsic lesions - cellulitis, bursitis, tendonitis, non-articular rheumatism or
fibromyositis.
Intrinsic lesions - VINDICATE:
- Vascular: aseptic bone necrosis, hemophilia, scurvy.
- Inflammation/Infections: gonorrhea, streptococcus organisms, tuberculosis,
syphilis.
- Neoplastic disorders: osteogenic sarcoma, giant cell tumors.
- Degenerative disorders: osteoarthritis.

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 - Intoxications: uric acid (gout), calcium pyrophosphate (pseudogout), "gout
syndrome" of diuretics.
- Congenital: congenital and acquired malformations - the joint deformities of
tabes dorsalis and syringomyelia, congenital dislocation of the hip,
alkaptonuria.
- Autoimmune: rheumatoid arthritisthe most prevalent, serum sickness, lupus
erythematosus, ulcerative colitis, regional ileitis, psoriatic arthritis.
- Trauma: traumatic synovitis, tear/rupture of the collateral or cruciate
ligaments, subluxation/Laceratin of the meniscus, dislocation of the joint or
patella, sprain of the joint, fracture of the bones of the joint.
- Endocrine: acromegaly (GH → growth in bone & soft tissues), diabetes
(pseudogout).

Arthritis
A group of conditions where damage is caused to the joints of the body.
Arthritis can be classified into:
1. Osteoarthritis
2. Autoimmune diseases (rheumatoid arthritis, psoriatic arthritis, reactive arthritis)
3. Septic arthritis
4. Gouty arthritis
5. Pseudogout

1.Osteoarthritis - degeneration and progressive loss of cartilage within the joints,

damage to underlying bone and formation of new bone at the margins of the
cartilage. It occurs following:
- Trauma to the joint
- An infection of the joint
- As a result of aging
Abnormal anatomy may contribute to early development of osteoarthritis.
Common locations: knees, hips, hands (distal, sometimes PIP), cervical and lumbar
spine, wrists (the 1st CMC joint) and joints previously injured or diseased.
Pattern of spread: additive or only 1 joint may be involved.
Onset: usually insidious.
Progression and duration: slowly progressive, with temporary exacerbations after
periods of overuse.
Associated symptoms:
- Swelling - small effusions in the joints may be present, especially in the knees,
as well as bony enlargements.
- Redness, warmth, and tenderness - possibly tender, seldom warm, and rarely
red.
- Stiffness - after inactivity.
- Limitations of motions - often develops.
- Generalized symptoms - absent.

2.Autoimmune diseases
Rheumatoid arthritis - chronic inflammation of synovial membranes with
secondary erosion of adjacent cartilage and bone and damage to ligaments and
tendons.
Common locations: hands (PIP / MCP joints), feet (MTP joints), wrists, knees,
elbows, ankles.

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 Pattern of spread: symmetrically additive - progresses to other joints while
persisting in the initial ones.
Onset: usually insidious.
Progression and duration: often chronic, with remissions and exacerbations.
Associated symptoms:
- Swelling - of synovial tissue in joints or tendon sheaths, and subcutaneous
nodules.
- Redness, warmth and tenderness: tender, often warm, but seldom red.
- Stiffness: prominent, often for an hour or more in the morning, also after
inactivity.
- Limitation of motion: often develops.
- Generalized symptoms: weakness, fatigue, weight loss, and increased fever are
common.
Early rheumatoid arthritis:
- Swollen, warm and red MCP joints.
- Squeezing causes a lot of pain.
- The MCP joints were tender to touch.
- The patient is unable to make a tight fist.
Late rheumatoid arthritis:
- Boutonniere deformities present.
- Swan neck deformity of the thumb.
- Ulnar deviation of the MCP joints.
- Subluxation of the PIP joints.
Psoriatic arthritis - a type of inflammatory arthritis that affects around 10-30% of
people suffering from psoriasis
Associated signs:
- Psoriatic nail lesions → splitting of nails → onycholysis.
- Tendinitis - ‘sausage-like’ swelling of digits ~ dactylitis.
There are 5 types of psoriatic arthritis:
- Symmetric - affects joints on both sides of the body simultaneously is most
similar to rheumatoid arthritis.
- Asymmetric - does not occur in the same joints on both sides of the body, and
it usually only involves less than 3 joints.
- Arthritis mutilans - a severe, deforming and destructive arthritis.
- Spondylitis - stiffness of the spine or neck, and can also affect the hands and
feet, in a similar fashion to symmetric arthritis.
- Distal interphalangeal predominant - inflammation and stiffness in the joints
nearest to the ends of the fingers and toes. Nail changes are often marked.
Reactive Arthritis - an autoimmune condition that develops in response to an
infection in another part of the body (genitourinary or gastrointestinal infections).
It includes a combination of 3 symptoms - Reiter´s syndrome:
- An inflammatory arthritis of large joints.
- Inflammation of the eyes (conjunctivitis and uveitis).
- Urethritis.

3.Septic arthritis - caused by joint infection by:

- Dissemination of pathogens via the blood, from abscesses or wound
infections.
- Dissemination from an acute osteomyelitic focus.
- Dissemination from adjacent soft tissue infection.

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 - Entry via penetrating trauma.
- Entry via iatrogenic means.

The bacteria which are commonly involved: Staphylococcus aureus, Streptococci,

Haemophilus influenzae, Escherichia coli, M. tuberculosis, Salmonella spp. and
Brucella spp.

4.Gouty arthritis - gout is caused by deposition of uric acid crystals in the joint that
results in subsequent inflammation. It is characterized by:
- Severe, sudden, unexpected, burning pain.
- Swelling, redness, warmth, and stiffness in the affected joint.
- Occurs commonly in men in their toes.
- Low-grade fever may also be present.
Patients with longstanding hyperuricemia can have uric acid crystal deposits,
called tophi in other tissues such as the helix of the ear, the kidneys or bladder
(leading to uric acid kidney stones), knees, elbows, hands.

5.Pseudogout - less common form of gout, and is caused by the formation of

rhomboidal shaped crystals of calcium pyrophosphate.
Inflammation of one or more joints often resulting in pain in the affected joint(s).
It is associated with chondrocalcinosis:
- Hyperparathyroidism
- Hemochromatosis
- Hypophosphatemia
- Renal osteodystrophy

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PHYSICAL EXAMINATION OF CHEST AND LUNGS
Anatomical reference points
Anterior:
- Sternal lines - midsternal, laterosternal,
parasternal
- Midclavicular line
Lateral:
- Axillary lines - anterior, midaxillary, posterior
Posterior
- Vertebral line
- Interscapulovertebral space
- Scapula - scapular line, medial margin, spinal line
Anatomical projections
- Pulmonary apices
- Lobes and fissures
- Heart
- Traube space of the stomach
- Liver
- Spleen
With the patient sitting, examine the posterior thorax and lungs. The patient’s arms
should be folded across the chest with hands resting, if possible, on the opposite
shoulders. This position moves the scapulae partly out of the way and increases your
access to the lung fields. Then ask the patient to lie down.
With the patient supine, examine the anterior thorax and lungs. The supine position
makes it easier to examine women because the breasts can be gently displaced.
Furthermore, wheezes, if present, are more likely to be heard.
For patients unable to sit up without aid, try to get help so that you can examine the
posterior chest in the sitting position. If this is impossible, roll the patient to one side
and then to the other. Percuss the upper lung, and auscultate both lungs in each
position. Because ventilation is relatively greater in the dependent lung, your chances
of hearing wheezes or crackles are greater on the dependent side.

Inspection
Can be static or dynamic.
Static inspection of the chest (cage):
- Skin
- Breasts / mammary glands
- Shape of the thorax. Modification in thorax shape include:
1) Long
2) Pyknic - large chest and abdomen
3) Athletic
4) Sthenic - strong, active
5) Emphisematous (barrel chest)
6) Pectus carinatum (gallinaceum) - protrusion of
the sternum and the ribs.
7) Pectus excavatum - the sternum and the ribs
grow abnormally, producing sunken chest.

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 8) Kyphotic - curved spine
9) Pottic
Modifications can be generalized or localized, and symmetrical or asymmetrical.

Dynamic inspection of the content:

During normal breathing -
- Type: superior thoracic in children
inferior thoracic in men
abdominal in women
- Frequency
During deep breathing -
- Retractions
- Bulging
Observe the rate, rhythm, depth, and effort of breathing. A normal resting adult
breathes quietly and regularly about 14-18 times a minute. An occasional sigh is to be
expected. Note whether expiration lasts longer than usual.
Always inspect the patient for any signs of respiratory difficulty.
- Assess the patient’s color for cyanosis. Recall any relevant findings from earlier
parts of your examination, such as the shape of the fingernails.
- Inspect the neck. During inspiration, is there contraction of the sternomastoid or
other accessory muscles, or supraclavicular retraction? Is the trachea midline?
Inspiratory contraction of the sternomastoids at rest signals severe difficulty
breathing. Lateral displacement of the trachea occurs in pneumothorax, pleural
effusion, or atelectasis.
- Audible stridor, a high-pitched wheeze, is an ominous sign of airway obstruction
in the larynx or trachea.

Mor Halgoa 65
Also observe the shape of the chest. The anteroposterior diameter may increase with
aging.
From a midline position behind the patient, note the shape of the chest and the way in
which it moves, including:
- Deformities or asymmetry.
- Abnormal retraction of the interspaces during inspiration. Retraction is most
apparent in the lower interspaces. Supraclavicular retraction is often
associated. Retraction in severe asthma, COPD, or upper airway obstruction.

Palpation
Can be static or dynamic.
As you palpate the chest, focus on areas of tenderness and abnormalities in the
overlying skin, respiratory expansion, and tactile fremitus.
Chest expansions.
Of the apices, bases and postero-anterior.
To test chest expansion, place your thumbs at about the level of the
10th ribs, with your fingers loosely grasping and parallel to the lateral
rib cage. As you position your hands, slide them medially just enough
to raise a loose fold of skin on each side between your thumb and the
spine.

Mor Halgoa 66
 Ask the patient to inhale deeply. Watch the distance between your thumbs as they
move apart during inspiration, and feel for the range and symmetry of the rib cage
as it expands and contracts.
Causes of unilateral decrease or delay in chest expansion include:
- Chronic fibrotic disease of the underlying lung or pleura
- Pleural effusion
- Lobar pneumonia
- Unilateral bronchial obstruction
Tactile fremitus.
Fremitus refers to the palpable vibrations transmitted through the
bronchopulmonary tree to the chest wall when the patient speaks.
To detect fremitus, use the ball (the bony part of the palm at the
base of the fingers). Ask the patient to repeat the words
“ninety-nine” or “one-one-one”. If fremitus is faint, ask the
patient to speak more loudly or in a deeper voice.
Palpate and compare symmetric areas of the lungs.
Identify and locate any areas of increased, decreased, or absent
fremitus.
Fremitus is typically more prominent in the interscapular area than in the lower
lung fields, and is often more prominent on the right side than on the left. It
disappears below the diaphragm.
Tactile fremitus can be normal, accentuated, decreased or absent.
Accentuated fremitus:
- Consolidation syndromes with free bronchi (pneumonia, atelectasis)
- Cavitary syndrome
Decreased or absent fremitus:
- Consolidation syndromes with obstructed bronchi
- Hyperinflation syndromes
- Pulmonary edema
- Pleural diseases (pneumothorax, pleurisy, pleural thickening)
Fremitus is decreased or absent when the voice is soft or when the transmission of
vibrations from the larynx to the surface of the chest is impeded. Causes include:
- An obstructed bronchus
- COPD
- Separation of the pleural surfaces by fluid (pleural effusion), by fibrosis
(pleural thickening), by air (pneumothorax)
- An infiltrating tumor
- A very thick chest wall

Percussion
Percussion is one of the most important techniques of physical examination. It helps
to establish whether the underlying tissues are air-filled, fluid-filled, or solid.
However, it penetrates only about 5-7 cm into the chest, and therefore will not help to
detect deep-seated lesions.
To perform percussion, hyperextend the middle finger of your left hand, and press its
distal interphalangeal joint firmly on the surface to be percussed.
With a quick sharp but relaxed wrist motion, strike the finger with the right middle
finger. Aim at your distal interphalangeal joint. Strike using the tip of the finger, not
the finger pad. The striking finger should be almost at right angles to the other finger.

Mor Halgoa 67
This is a trying to transmit vibrations through the bones of this joint to the underlying
chest wall.

When comparing two areas, use the same percussion technique in both areas.
Percuss or strike twice in each location. It is easier to detect differences in percussion
notes by comparing one area with another than by striking repetitively in one place.
Learn to identify five percussion notes. These notes differ in their basic qualities of
sound: intensity, pitch, and duration.
Percuss one side of the chest and then the other at each level.
Skip the areas over the scapulae - the thickness of muscle and bone
alters the percussion notes over the lungs. Identify and locate the
area and quality of any abnormal percussion note.
Percussion can be direct, on the clavicle, or mediated (posterior,
lateral, anterior, hirtz).
Normal lungs are resonant.
Modifications of percussion:
Hyper-resonance - hyperinflation syndrome, cavitary syndrome, pneumothorax.
Generalized hyperresonance may be heard over the hyperinflated lungs of
emphysema or asthma.
Unilateral hyperresonance suggests a large pneumothorax or possibly a large air-
filled bulla in the lung.
Tympani - cavitary syndrome, massive pneumothorax.
Methalic sound - superficial cavities larger than 6 cm with no bronchial
communication.
Dullness - replaces resonance when fluid or solid tissue replaces air-containing
lung or occupies the pleural space beneath your percussing fingers.
- Pulmonary - consolidation syndrome
- Pleural -
1) Syndrome of pleural effusion.
It can be large - Pitres, Δ garland, Δ Grocco-Rauchfuss.
It can be medium Damoiseau-Ellis curve, Skodism, Dull traube space.
2) Pleural thickening
Other examples include: lobar pneumonia, in which the alveoli are filled with fluid
and blood cells, blood (hemothorax), pus (empyema), fibrous tissue or tumor.

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Auscultation
Auscultation involves listening to the sounds generated by breathing, listening for any
adventitious (added) sounds, and if abnormalities are suspected, listening to the
sounds of the patient’s spoken or whispered voice as they are transmitted through the
chest wall.
Sounds from bedclothes, paper gowns, and the chest itself can generate confusion in
auscultation. Hair on the chest may cause crackling sounds. Either press harder or
wet the hair.
If the patient is cold or tense, you may hear muscle contraction sounds - muffled, low
pitched rumbling or roaring noises. A change in the patient’s position may eliminate
this noise.
Normal breath sounds are:
Vesicular, or soft and low pitched.
Bronchial, or louder and higher in pitch, with a short silence between inspiratory
and expiratory sounds. Expiratory sounds last longer than inspiratory sounds.
Bronchovesicular, with inspiratory and expiratory sounds about equal in length, at
times separated by a silent interval. Differences in pitch and intensity are often
more easily detected during expiration.

After instructing the patient to breathe deeply through an open mouth, listen to the
breath sounds with the stethoscope. Use the pattern suggested for percussion, moving
from one side to the other and comparing symmetric areas of the lungs.
If you hear or suspect abnormal sounds, auscultate adjacent areas so that you can fully
describe the extent of any abnormality. Listen to at least one full breath in each
location.
Note the intensity of the breath sounds. Breath sounds are usually louder in the lower
posterior lung fields and may also vary from area to area. If the breath sounds seem
faint, ask the patient to breathe more deeply. You may then hear them easily.
When patients do not breathe deeply enough or when they have a thick chest wall, as
in obesity, breath sounds may remain diminished.

Mor Halgoa 69
Breath sounds may be decreased when air flow is decreased (as by obstructive lung
disease or muscular weakness) or when the transmission of sound is poor (as in
pleural effusion, pneumothorax, or emphysema).
Is there a silent gap between the inspiratory and expiratory sounds? A gap suggests
bronchial breath sounds.
Listen for the pitch, intensity, and duration of the expiratory and inspiratory sounds.
Are vesicular breath sounds distributed normally over the chest wall?
Adventitious (added) sounds
Detection of adventitious sounds: crackles (rales), wheezes and rhonchi, is an
important part of your examination, often leading to diagnosis of cardiac and
pulmonary conditions. The most common kinds of these sounds are:

Crackles may be due to abnormalities of the lungs (pneumonia, fibrosis, early

congestive heart failure) or of the airways (bronchitis, bronchiectasis).
If you hear crackles, especially those that do not clear after cough, listen carefully for
the following characteristics, which are clues to the underlying condition:
- Loudness, pitch, and duration (summarized as fine or coarse crackles)
- Number (few to many) timing in the respiratory cycle.
- Location on the chest wall.
- Persistence of their pattern from breath to breath.
- Any change after a cough or a change in the patient’s position.
Fine late inspiratory crackles that persist from breath to breath suggest abnormal lung
tissue.
In some normal people, crackles may be heard at the lung bases anteriorly after
maximal expiration. Crackles in dependent portions of the lungs may also occur after
prolonged recumbency.
Wheezes suggest narrowed airways, as in asthma, COPD, or bronchitis.
Rhonchi suggest secretions in large airways.
If you hear wheezes or rhonchi, note their timing and location, and if they change
with deep breathing or coughing.

Mor Halgoa 70
Clearing of crackles, wheezes, or rhonchi after cough suggests that secretions caused
them, as in bronchitis or atelectasis.

Auscultation can be direct or mediated.

Direct auscultation is the transmitted voice.
Transmission of voice (normal speaking, “ninety-nine”).
- Normally - muffled and indistinct
- Bronchophony - loud, clear. It can be caused by:
Consolidation syndrome, with free bronchi
Cavitary syndrome, with free bronchi
Mediastinal syndrome (déspine sign)
Transmission of “ee” sound.
- Normally - long, muffled “ee”
- Egophony - e-to-a change. It can be caused by:
Consolidation syndrome.
Pleural effusion, medium quantity
Pectoriloquy - pneumothorax.
Amphoric voice
- Pneumothorax
- Cavitary syndrome (outward, big cavities with peripheral consolidation and
small free bronchi).
Whispered pectoriloquy
- Pneumothorax
- Pleural effusion, medium quantity
- Consolidation syndrome, with free bronchi
Mediated auscultation can be assessed by:
1.Inspiration/expiration ratio
 Prolonged inspiration - in (superior) obstructive syndrome, in which the
larynx, trachea or principal bronchi are involved.
 Prolonged expiration - in hyperinflation syndrome, bronchospasm, pulmonary
edema, bronchopneumonias.
2.Breath sounds (or sounds that replace them)
Vesicular sound can be:
 Exagerated - compensatory hyperfunction of one lung. It can occur in pleural
effusion, massive atelectasias, important infiltrative lesions.
 Harsh can occur in diminution of the caliber of bronchi, edema of the
bronchial mucosa, adherent bronchial secretions.
 Diminuated can occur in larynx stenosis, bronchial stenosis, limitation of
pulmonary expansion (pleurisy, pleuritis), consolidation syndrome, permanent
hyperinflation syndrome, pleural effusion in small or medium quantity.
 Abolished - respiratory silentium. It can occur in massive pleural effusion,
pneumothorax, massive consolidation syndrome, bronchial foreign bodies.
Replacement of vesicular sounds - murmurs, can be:
 Tubar (broncho-vesicular sound) - in consolidation syndrome rounding one
big, free bronchi.
 Pleuretic (bronchial sound) - pleurisy, medium quantity.
 Amphoric (i) - cavitary syndrome (superficial big cavities with smooth inner
walls).

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  Cavernous (i+e) - cavitary syndrome (>6 cm, profound).

3.Added sounds
Can be broncho-pulmonary (rales) or pleural (pleural rub).
 Rales:
- Dry, continuous -
1) Ronchi - low pitch, harsh quality, “snorring”, insiration + expiration,
modification with coughing: in localization, pitch and intensity, big
caliber bronchi.
2) Wheezes - high pitch, musical quality, “whistling”, insiration +
expiration, modification with coughing: in localization, pitch and
intensity, medium and small caliber bronchi.
- Moist, discontinuous
1) Crackles - uneven: small, medium, coarse, high pitch, “blowing air
through a straw in a glass of water”, small (fine), medium, large
(coarse), inspiration + the first part of expiration, modification with
coughing: in localization, pitch and intensity, small (4th order) bronchi
and bronchioles.
 Fine crackles - “the most dry of moist rales”, high pitch, “rubbing
the hair near the ear”, in the second half of inspiration, increases
after coughing, alveoli.
→ “Backwards” crackles - more moist, uneven, coarse-fine
crackles: can be confounded with coarse crackles,
inspiratory, pneumonia- regresion phase.
→ Recumbency crackles - after prolonged bed rest, disappears
after ample breathing.
2) Cavernous - resembles coarse crackles, coarse, uneven, few in
number.
 Pleural friction rub - superficial (near the ear), dry quality, inspiration +
expiration, no modification after coughing, becomes louder when pressing the
stethoscope, can have an equivalent on palpation, pleural inflamatory
disorders.
4.Tracheal sound
Over the larynx and superior retrosternal region, less “vesicular”, expiration
follows immediately inspiration.
I/E=1, expiration > 4 sec= prolonged.
Summarizes all non-alveolar rales.
If present in other area, this is a tubar murmur.

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RESPIRATORY SYSTEM SYMPTOMS
Dyspnea
Conscious perception of difficult respiration, “air thirst”. This is a subjective
component which is not measurable.
The objective, measurable components are: rhythm, rate and amplitude of breath
movements.
Dyspnea is caused by alterations of the lungs, pleura, respiratory muscles, rib cage
and nervous coordination of respiration.
When tidal volume equals 40% of total respiratory capacity, dyspnea appears.
Dyspnea can occur with polypnea (tachypnea) or with bradypnoea.
 Dyspnea with tachypnea.
> 14-18 respirations per minute (in children 30-40 rpm) with acute conditions of
the respiratory system.
Severe chest pain, which is associated with superficial breathing.
It is very similar to dyspnea in cardiovascular conditions.
 Dyspnea with inspiratory bradypnea.
Airway obstruction by heterodense material which blocks the air inflow. This is a
foreign material in larynx, trachea, main bronchi, endoluminal tumor or external
compression by tumor or lymphadenopathy.
Accompanied by inspiratory wheezing, epigasrtic region depression, suprasternal
region depression.
 Dyspnea with expiratory bradypnea.
Due to difficulty in expelling the air from the lung. It may occur in pulmonary
emphysema, COPD, bronchiolitis in children, asthma in crisis.
Associated with expiratory wheezing.
Conditions of appearance:
- Acute dyspnea: bronchial obstruction (tumors, compression), larynx obstruction,
asthma, spontaneous pneumothorax, acute pulmonary embolism
(ventilation/perfusion mismatch).
- Chronic dyspnea: COPD, pure emphysema, extensive pulmonary fibrosis, agonic
status.
- Psychogenic dyspnea: deep respiratory effort at variable intervals, no objective
diagnostic features.
Changes in the respiratory cycle
Cheyne-Stokes respiration: alternating of acceleration and deceleration periods,
with apnea periods, of variable duration (15-60 sec).
In tachypnea periods the patient is anxious, while during apnea is somnolent (‫)רדום‬.
When Apnea is longer, seizures can occur. This situation is caused due to
depression of the excitability in the respiratory centers.
Signs of central nervous system depression include left ventricular failure with low
output, brain hemorrhages and brain tumors. It can appear in normal subjects at
high altitudes.
Sleep apnea syndrome: Normal ventilation alternating with periods of apnea,
during the sleep. Associated with COPD, obesity and hypertension. The patients
feel dizzy during the day and they can get asleep very easy even in daytime.

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Kussmaul respiration: cycles of high amplitude respiratory movements, separated
by short pauses. It appears in metabolic acidosis.
Biot respiration: brain tumors, meningitis, agonic status, periods of apnea and
normal respiration.
Cough
Cough is reflex which either blocks foreign body penetration into the airways, or
expels mucus or pus accumulation in the bronchial tree.
Excitation comes from special receptors whos stimulation provokes deep inspiration
followed by glottic shut down and then sudden and strong expiration.
There are several types of cough:
 Dry cough - no expectoration, acute inflammatory airway conditions, airway
compression.
 Wet cough - expectoration present, acute and chronic conditions.
 Aphonic cough - laryngeal conditions, deep weakness, laryngeal cancer.
 Barking cough - tracheobronchial compression.
 Bitonal cough - left vocal cord paralysis, due to left recurrent laryngeal nerve.
(lymph nodes in mediastinum, aneurysm, tumor).
 Cavernous cough - metallic sound, in caverns at least 6 cm in diameter with free
drainage bronchi.
 Convulsive cough - appears in paroxismal crisis starts with a deep breath,
followed by short and rapid coughs until all the air is evacuated from the lungs.
At the end of the crisis inspiration is deep and associated with wheezing due to
glottic spasm. The patient becomes cyanotic and vomits can occur.
 Emesis generating cough - appears in tuberculosis after stomach distension,
which provokes cough and its evacuation by vomiting. It can also appear in
esophageal-bronchial fistulae.
 Irritation cough - it can appear in acute and chronic lung diseases, chronic
bronchitis in smokers.
Conditions of appearance:
- Morning cough - due to secretions evacuation in chronic bronchitis and
bronchiectasis.
- Evening fever - concomitant with fever increase in the evening in tuberculosis.
- Night fever - left ventricular dysfunction.
- Effort cough - appears in both pulmonary and cardiac diseases.
- Continous cough - pulmonary tuberculosis associated with laryngitis, or
tracheobronchial compression.
- Positional cough - determined by position changes in pleural effusions, lung
abscess, bronchiectasis.
- Cough in massive pleural effusion - drainage can appear when the visceral pleura
makes contact with the needle.
Sputum
 Mucous sputum - transparrent.
 Serous sputum - white coloured.
 Purulent sputum - cremous, yellow-green colored.
 Bloody or blood streaked cough.
 Blood sputum - hemoptysis.
 Seromucous sputum, mucopurulent sputum, mucous-bloody sputum.
 Rusty sputum - mucofibrinous, aerated, viscous - pneumococus pneumonia.
 Pearled sputum - at the end of asthma crisis.

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 Pseudomembranous sputum - high amount of mucus and fibrin, appearance of
bronchial tree cast.
 Vomica - sudden elimination after cough effort of pulmonary collection which
has penetrated the airways and include pus, serous liquid, blood.
It can appear from the pulmonary parenchyma, pleural cavity, mediastinum, sub-
diaphragmatic region. The evacuation can be associated with intense, tearing
chest pain, dyspnea and anxiety.
Conditions of appearance:
- Vomica - large: 1-2 liters, medium 250-300 ml.
- Fractioned vomica: 60-100 ml.
- Pseudovomica - abundant sputum.
- Origin: Mediastinal vomica - mediastinitis.
Pleural vomica - serofibrinous, pus, hemorrhagic.
Pulmonary - abscess, hidatidosis
Abdominal: under-diphragmatic abscess.
Hemoptysis
Evacuation of fresh, bright-red, aerated blood after cough, from the tracheobronchial
tree or pulmonary tissue.
Retrosternal heat sensation appears before the onset of hemoptysis. Sometimes the
patient has a special metallic taste, he is anxious, pale and dyspneic.
- Small hemoptysis <100 ml.
- Medium - 100-500 ml.
- Large > 500 ml.
Fractioned: hour or days, small amounts of blood.
In sudden, massive hemoptysis death by asphyxiation can occur. The patient should
not be moved.
At the end expectoration becomes black in color.
Differential diagnosis:
Blood from the oral cavity, pharynx, epistaxis.
Causes:
- Pulmonary tuberculosis: from the onset of the disease as a first sign, or in
evolution, it can be massive.
- Chronic bronchitis and bronchiectasis - small hemoptysis.
- Acute bronchitis - very rare due to bronchial mucosa hyperemia - viral etiology
or irritant gases.
- Bronchopulmonary cancer.
- Cardiac causes: mitral stenosis, LV failure (rare), pulmonary embolism with
infarction, ruptured aortic aneurysm (very rare).
- Thoracic trauma.
- Hematologic bleeding disorders.
- Endometriosis.
Chest pain in pulmonary disorders
Stitch - similar to a pointed knife hit, acute, accentuated with respiration, it appears
in various respiratory conditions:
- Lobar pneumonia - under the nipple, if its accompanied by shivering and
temperature raise its almost pathognomonic.
- At the nipple or subscapular - penumothorax.
- Pulmonary embolism with pulmonary infarction - associated with blood streak
sputum.
- Purulent pleural effusions - skin hyperesthesia.

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 - Other pleural effusions.
Pleural pain - very intense, sudden onset, over a variable surface, accentuated with
respiratory movements. It appears in some viral infections, especially due to
Coxackie B virus.
RETRACTILE CONSOLIDATION SYNDROME
Atelectasis
Lack of gas exchange within alveoli, due to alveolar collapse or fluid consolidation.
It simply means collapse of one or part of a lung.
Causes:
Post-surgical - most common.
Postoperative atelectasis is the main cause for post-operative respiratory failure.
Symptoms include vague thoracic pain, dry cough, symptoms of respiratory failure
(dyspnea with tachypnea, cyanosis). No fever caused by atelectasis itself, frequent
infections. Treatment with antibiotics is recommended.
Blockage of a bronchiole or bronchi, which can be within the airway (foreign
body, mucus plug), from the wall (tumor) or compressing from the outside (tumor,
lymph node, tubercle).
Poor surfactant spreading during inspiration, causing the surface tension to be at its
highest which tends to collapse smaller alveoli. This causes newborn respiratory
distress syndrome.
This syndrome is caused by pulmonary surfactant deficiency in the lungs of
neonates, most commonly in those born at < 37 week gestation.
Surfactant are a mixture of phospholipids and lipoproteins secreted by type II
pneumocyts. It diminishes the surface tension of the water film that lines alveoli,
thereby decreasing the tendency of alveoli to collapse and the work required to
inflate them.
Absent surfactant  diffuse atelectasis  blood goes out not oxygenated from
atelectatic region  hypoxemia  increases work of breathing  hypercapnia 
acidosis.
During suction, as along with sputum, air is withdrawn from the lungs.
Oxygen therapy. Atelectasis determined by oxygen supplementation is also called
absorption atelectasis. The air composed of 78% nitrogen + 21% oxygen.
Since oxygen is exchanged at the alveoli-capillary membrane, nitrogen is a major
component for the alveoli's state of inflation.
Nitrogen is replaced with oxygen (oxygen supplementation)  oxygen is absorbed
into the blood  alveoli volume reduce  alveolar collapse.
Symptoms include dyspnea and lower pO2 despite supplementation.
Treatment is done with PEEP.
Collapse of lung by massive pneumothorax do not fit into the definition of
atelectasis.
Clinical symptoms:
1.Inspection -
 Static: localized, asymmetric modifications.
- Affected hemi thorax smaller.
- Retractions of supraclavicular area and intercostal spaces.
 Dynamic: not typical.
- Tachypneea as a sign of respiratory failure or distress.
- Retraction remains fixed with deep breathing.

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2.Palpation -
 Static:
- Confirms the asymmetry and retractions remarked at I.
- Confirms the smaller diameter of involves hemi thorax.
- Passive mobility ↓ or absent where are retractions.
 Dynamic:
- ↓ or absent tactile fremitus.
- ↓ expansions of apices/ bases of lung in affected region.
3.Percussion -
 Dullness in the affected area.
 Hyper-resonance, even tympanic sounds in area surrounding it or in the
opposite lung.
4.Auscultation -
 No modification in transmission of voice, normal or whispered.
 ↓ or abolished vesicular sound.
 Eventually rales, as with etiology, most common bronchial rales (ronchi).
Etiological treatment:
Measures to improve ventilation include:
- Incentive spirometry.
- Ensuring adequate analgesia for chest and abdominal incisions.
- Physical measures: upright positioning.
- Early mobilization.
- Diminution of abdominal distension: nasogastric suction for excessive
intraluminal air, paracentesis to evacuate tense ascites.
- PEEP/ mechanical ventilation.
Chest X ray
- Homogenous density with concavity towards the exterior, involving one
segment / one lobe / the entire lung, with a smaller extension than the respective
region (in normal conditions).
- Narrow and oblique intercostal spaces.
- Mediastinum shifted toward involved side.
- Ascended diaphragm.
- Inspiratory movement of mediastinum toward the involved side.
Airways obstruction - bronchial obstruction and broncho-pulmonary cancer
Most of the lung tumors are malignant.
There are 2 major categories:
 Small cell lung cancer - aggressive, smoking present in practically all patients,
perihilar mass.
 Non-small cell lung cancer - smoking 85%.
Squamous: central, endobronhial
Adenocarcinoma and large cell are present as peripheral nodules or masses.
Symptoms:
25% are asymptomatic, detected at routine X-rays.
Localized symptoms include:
- Vague chest pain
- Cough, dry
- Dispnea
- Hemoptysis: rare, minor; massive, if cancer erodes an artery, can be fatal by
exsanguination or asphyxiation

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- Post-obstructive atelectasis
- Recurrent pneumonia
Syndromes determined by lung cancer:
 Consolidation syndrome -
- Obstructive - retractile, with obstructed bronchi, atelectasis.
- With free bronchi - repeated pneumonias, in area of affected bronchi.
 Pleural effusion -
- Transudation - in the context of atelectasis.
- Exudative - malignant (hemorrhagic).
 Mediastinal syndromes
 Cavitary syndrome
 Paraneoplasic syndromes - occur distant from the tumor or its metastases.
- Hypercalcemia (squamous cell carcinoma: parathyroid hormone-related
protein production).
- Inappropriate antidiuretic hormone secretion (SIADH).
- Finger clubbing with or without hypertrophic pulmonary osteoarthropathy.
- Hypercoagulability with migratory superficial thrombophlebitis (Trousseau's
syndrome).
- Myasthenia (Eaton-Lambert syndrome).
- Various neurologic syndromes that involve tumor expression of autoantigens
with production of autoantibodies.
 Regional spread / symptoms -
- Recurrent laryngeal nerve - hoarseness.
- Phrenic nerve - diaphragm paralysis, pain.
- Esophagus - dysphagia.
- Vagus - dyspnea, constipation.
- Cervical sympathetic chain - Claude-Bernard- Horner syndrome (ptosis,
miosis, enophthalmos, and anhidrosis).
- Trachea - stridor, dyspnea.
- Superior vena cava - facial and upper limbs edema, turgid jugular veins,
headache, flush, supine breathlessness.
- Pericardium - pericarditis / cardiac temponade.
- Heart - arrhythmias.
- Upper thoracic ring - Pancoast syndrome. (shoulder and upper extremity pain
and weakness or atrophy of the ipsilateral hand, lysis of first and second rib).
Airway obstruction - upper obstruction
Causes:
 Aspiration of foreign bodies.
 Infections: croup, epiglottitis, retropharyngeal abscesses, bacterial tracheitis.
 Severe allergic reaction.
 Post-extubation complications.
 Laryngeal spasm (recurrent).
 Vocal cords paralysis.
 Laryngeal or tracheal tumors.
Signs and symptoms:
- Nasal flaring (children).
- Retractions of supraclavicular areas, suprasternal, subcostal, even intercostal
spaces (symmetrical).

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- Stridor - high-pitched, predominantly inspiratory sound produced by the rapid,
turbulent flow of air through a narrowed or partially obstructed segment of the
extrathoracic upper airway (pharynx, epiglottis, larynx, and the extrathoracic
trachea). Prolonged inspiration.
- Cough.
- Drooling.
- Sore throat, dysphagia, odynophagia.
- Dyspnea, cyanosis, fatal asphyxia.

HYPERINFLATION SYNDROME
Hyperinflation syndromes can be permanent - COPD or transient - asthma attack.
Transient hyperinflation syndrome - asthma
A common chronic disorder of the airways that is complex and characterized by
variable and recurring symptoms, airflow obstruction, bronchial hyperresponsiveness,
and an underlying inflammation. The interaction of these features of asthma
determines the clinical manifestations and severity of asthma and the response to
treatment.
It is necessary to collect the information regarding to the patients history of asthma,
but also other allergies (food, eczema, allergodermia), as well as personal history of
respiratory and cardiovascular diseases.
Pathological pathway:

Pathogenesis
Interaction host-environment:
- Host - innate imbalance of immune response (Th1/Th2). Cytokine response
profile determining the capability of smooth muscle activation and fibroblast
production
- Environment - allergens and respiratory infections, diet, perinatal factors.
Onset in childhood (earlier in boys, girls after puberty).
Bronchoconstriction
The dominant physiological event leading to clinical symptoms. It is determined by
bronchial smooth muscle contraction that occurs quickly to narrow the airways in
response to exposure to a variety of stimuli.
Typically, stimulus (allergen)  IgE mediated activation of mast cells  release of
mediators (histamine, tryptase, leukotrienes, prostaglandins)  bronchoconstriction.
Airway inflammation/ mucus hyper-secretion:

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Intervenes in narrowing of airways.
Cell migration / activation  inflammatory infiltration of epithelia release of
mediators  epithelial edema.
The number of goblet cells increases, as well as mucus production, forming mucus
plugs.

Airway remodeling:
Are permanent modifications, diminishing the response to drugs and increasing
hyperresponsiveness. This process includes:
- Thickening of the sub-basement membrane.
- Subepithelial fibrosis.
- Airway smooth muscle hypertrophy and hyperplasia.
- Blood vessel proliferation and dilation.
- Mucous gland hyperplasia and hypersecretion.
Hyperresponsiveness
Is an exaggerated bronchoconstrictor response to a wide variety of stimuli that do not
(necessarily) determines clinical expressed bronchoconstriction to a healthy person.
This is a major, but not necessarily unique, feature of asthma.
Mechanisms: inflammation, dysfunctional neuroregulation and structural changes.
When it is not related to asthma, it is normally present in the convalescence of the
viral respiratory infection.
Diagnosis of asthma:
To establish a diagnosis of asthma, the clinician should determine that:
- Episodic symptoms of airflow obstruction or airway hyperresponsiveness are
present.
- Airflow obstruction is at least partially reversible.
- Alternative diagnoses are excluded.
Recommended methods to establish the diagnosis are:
- Detailed medical history.
- Physical exam focusing on the upper respiratory tract, chest, and skin.
- Spirometry to demonstrate obstruction and assess reversibility, including in
children 5 years of age or older.
Reversibility is determined either by an increase in FEV1 of ≥12% from baseline
or by an increase ≥10% of predicted FEV1 after inhalation of a short-acting
bronchodilator.
- Additional studies as necessary to exclude alternate diagnoses.
Triggers of asthma attack:
 Environmental and occupational allergens (numerous)
 Infections (viruses-syncytial resp, rhino, parainfluenza; pneumonia)
 Exercise, rapid changes in environmental temperature
 Inhaled irritants (perfumes, cleaning products)
 Emotions
 Aspirin/ AINS
 Gastroesophageal reflux
 Menstrual cycle
 Domestic triggers
- Home- related allergens: dust-mite (dermatophagoides sp), cockroach, pets.
- Irritants: environmental tobacco smoke, air pollution (Si dioxide, ozone).

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Asthma in its “steady-state”:
- Eventually no symptoms or signs appear
- Nighttime coughing, a chronic “throat-cleaning” type cough
- Dyspnea with exercise (not at rest)
- Tight feeling in the chest

Symptoms of asthma attack:

 Dyspnea and wheezing.
Expiratory dyspnea starts abruptly, usually during nighttime (4 am - vagal
predominance) / temporal relationship to the exposure to trigger.
Classically is bradypnea with wheezing, predominantly during expiration.
 Cough.
Dry at the beginning, then becomes productive.
The sputum has a pearl appearance - mucous, clear, adherent.
On microscopical examination we can see Curshman spirals and Charcot Leyden
crystals.
Cough-variant asthma - no dyspnea.
 Chest tightness.
Between attacks, patients with mild asthma are typically asymptomatic.
Physical examination:
- Anti-dyspneic decubitus
- Anxiety
- Tachycardia, mild hypertension, pulsus paradoxus
- Diaphoresis
- No cyanosis
Respiratory examination:
1.Inspection - tachypnea, hyperinflation, barrel chest effort of breathing (use of neck
and suprasternal muscles), pursed lips, inability to speak.
2.Palpation - diminished chest expansion, diminished elasticity, diminished tactile
fremitus.
3.Percussion - diffuse hyperresonance.
4.Auscultation -
- Important prolongation of expiration (usually > 1:3).
- Diminished vesicular sounds, diffuse.
- Rales: bronchial, wheezes predominate, plus ronchi, coarse crackles.
- Wheezes persistent after the end of the attack.
Paraclinical examination:
- Chest X-ray not mandatory, shows hyperinflation.
- Lab: mild leucocitosis with eosinofilia, elevated IgE.
- Sputum microscopic examination.
- Pulmonary function tests- spirometry, PEF.
Classification of asthma severity:

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Classification of asthma control:

Status asthmaticus:
A very severe asthma attack, symptoms lasting > 24 hours.
It includes loud wheeze that slowly diminishes and disappears  auscultatory
silentium.
Agitation (‫ )סערה‬starts from severe and then stops  confusion and drowsiness
intervenes. There is also complete inability to speak, bradycardia, cold, moist
extremities, and decreased PO2 (under 60 mmHg), leading to cyanosis and imminent (
‫ )קרב ובא‬respiratory arrest.
Differential diagnosis of asthma attack:
- “Cardiac asthma”- acute heart (LV) failure, in which dyspnea episodes have a
cardiogenic etiology, clinically dominated by the bronchoconstriction.
DD is easy if careful history is taken (starts with exertion, progressive worsening
of respiratory status), as well as history of cardio-vascular disease(s)
- Upper airway obstruction: STRIDOR.
Permanent hyperinflation syndrome - COPD
Chronic Obstructive Pulmonary Disease (COPD) is a preventable and treatable
disease with some significant extra-pulmonary effects that may contribute to the
severity in individual patients.
Its pulmonary component is characterized by airflow limitation that is not fully
reversible. The airflow limitation is usually progressive and associated with an
abnormal inflammatory response of the lung to noxious particles or gases.
Pathogenesis of COPD:

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Changes in lung parenchyma in COPD include alveolar wall destruction, epithelial
dysplasia, loss of elasticity, destruction of pulmonary capillary bed, macrophages,
CD8+ lymphocytes.
Pulmonary Emphysema:
A destruction of lung parenchyma leading to loss of elastic recoil and loss of alveolar
septa and radial airway traction, which increases the tendency for airway collapse.
Lung hyperinflation, airflow limitation, and air trapping follow. Airspaces enlarge and
may eventually develop bullae.
It is defined pathologically, and it describes one kind of many structural changes
present in COPD.
Pathological changes -
- Centro-lobular: common. In smokers, modifications starts and are more
pronounced in the central portion of the lobule.
- Pan-lobular: common in α-1 antitrypsin deficiency.
- Distal lobular: peripheral, can associate with giant bullae.
- Near scarring areas: complicates diseases associated with fibrosis (TB,
silicosis).
Pulmonary symptoms - productive, mucous sputum, shortness of breath.
Dyspnea - progressive, persistent, exertional, expiratory, with polypnea, with
wheezing, worsens during respiratory infections.
Exacerbation - worsening of symptoms, determining factors not always identified,
but infections presumed, in severe cases > 3/year.
Chronic bronchitis:
Is a chronic inflammation of the lower airways, characterized by chronic productive
cough, as a result of low-grade exposure to respiratory irritants of a person without
hyperresponsiveness of bronchials.
Mandatory symptoms are cough with mucous expectoration for repeated days, more
than 3 months/year in at least 2 consecutive years (if bronchiectasias and TB are
excluded).
Etiology:
- Smoking - major cause.
- In-house pollution: smoke from biomass fuels.
- Genetic: severe hereditary deficiency for α-1 antitrypsin.
- Occupational: mineral dust, cotton dust.
- Socio-economic status, nutrition, outdoor pollution, infections.
Pathological changes:
- Inflammatory infiltrate
- Hyperplasia of mucous glands
- Localized area of scuamous metaplasia
- Smooth muscle hypertrophia
- Peribronchial fibrosis
- Distruction of elastin fibers

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 Type B:
Type A: emphysema,
chronic bronchitis, “blue
“pink puffer”
bloater”
Age: 50-70 Age: 40-60

Dyspnea is the predominant Cough and sputum production

symptom are the predominant symptoms

Long thorax Pyknic thorax

Cyanosis develop lately Cyanotic from early stages

Any nutritional status, can be

Weight loss, muscle wasting
obese
Marked impairment of diffusing
Marked obstruction
capacity

α-1 antitrypsin deficiency:

A congenital lack of α-1 antitrypsin, a neutrophil elastase inhibitor.
Emphysema develop before age 45 (rarely before 25) or in non-smokers, no
occupational risk.
Clinically associated with liver impairment (cirrhosis in childhood or early in
adulthood), panicullitis.
Extra-pulmonary manifestations:
- Cachexia, loss of fat-free mass
- Muscle wasting: apoptosis, disuse atrophy
- Osteoporosis
- Apoptosis
- Depression
- Chronic normocytic anemia
Complications:
Pulmonary hypertension and cor pulmonale.
Pulmonary hypertension is a consequence of:
- Hypoxemia - arterial smooth muscle constriction, in time hypertrophies and
vasoconstriction becomes permanent.
- Destruction of pulmonary vasculature.
Right-sided heart failure is called cor pulmonale, and it includes:
- Systemic congestion.
- ECG: clockwise rotation, RA enlargement (P pulmonale), eventually RBBB.
- Right A and V dilation, tricuspid regurgitation.
Respiratory failure.

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 Defined as an arterial partial pressure of O2 (PaO2) less than 8.0 kPa (60 mm Hg),
with or without arterial partial pressure of CO2 (PaCO2) greater than 6.7 kPa (50
mm Hg) while breathing air at sea level.
The components of respiratory failure include hypoxemia and hypercapnia.
The symptoms include morning headaches, central cyanosis, Chemosis, flapping
tremor.

Clinical examination:
1.Inspection -
 Static: barrel chest.
- Short neck
- Filled supraclavicular fossae
- Horizontal ribs, large intercostal spaces
- The ant-post diameter is larger than the lateral one.
 Dynamic:
- Small amplitude inflations; retraction of inferior intercostal spaces in
inspiration (Hoover’s sign)
- Prolonged expiration
- Eventually, usage of accessory respiratory muscles
2.Palpation -
 Static:
- Confirms modification observed before
- Reduced passive mobility
 Dynamic:
- Reduced excursion of apices and bases
- (Slightly) reduced tactile fremitus
3.Percussion -
- Resonance extended to the lateral third of clavicle.
- Diffuse hyperresonance.
- Tympanic sounds over bullae.
- Hirtz maneuver can be negative if hyperinflation is extreme.
4.Auscultation -
- Prolonged expiration.
- Diffuse diminishing of vesicular sounds.
- Wheezes, ronchi, crackles - symmetrical.
- Asymmetrical auscultation - into exacerbations can signal
condensation/effusions/pneumothorax.
Diagnosis of COPD:
By symptoms: cough, sputum, shorten of breath.
By exposure to risk factors: tobacco, occupation, indoor/outdoor pollution.
The patient's respiration is measured by spirometry.
Criteria for diagnosis in spiromety:
- FEV1/FVC < 70%
- FEV1: classifies the severity:
Mild: >80%
Moderate: <80%
Severe: 30<FEV1<80%
Very severe: <30%, respiratory failure intervenes

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 Asthma COPD
Evolution Variable Worsens progressively
Most important etiologic
Smoking Not directly linked
factor
Permanent, exacerbations
Symptoms Periodical
exists
Obstructive ventilator Permanent, worsens
Periodical, reversible
syndrome progressively
Appears earlier in
Hypoxemia Episodical, if any emphysema, worsens
progressively

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Mor Halgoa 87