PROPEDEUTICS OF

INTERNAL DISEASES –
FIRST PART
3rd year – 4th and 5th semester

18 JUNE 2018

CRISTINA RIBERA SOLER 1

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 TOPIC 1. HISTORY TAKING –
COMMUNICATION WITH THE PATIENT
HEADINGS.

SCOPE OF ASSESSMENT

COMPREHENSIVE EXAMINATION

• Does more than assess body systems.

• It is a source of fundamental and personalized knowledge about the patient that

strengthens the clinician–patient relationship.

• Provides a more complete basis for assessing these concerns and answering patient
questions.

FOCUSED EXAMINATION

• Selection of methods relevant to thorough assessment of the targeted problem.

• The patient’s symptoms, age, and health history help determine the scope of the
focused examination, as does your knowledge about diseases

For patients you are seeing for the first time in the office or hospital, you will usually choose
to conduct a comprehensive assessment, which includes all the elements of the health history
and the complete physical examination.

Nevertheless, in many situations, a more flexible focused or problem-oriented assessment is

appropriate, particularly for patients you know well who are returning for routine office care
or for patients with specific “urgent care” concerns like sore throat or knee pain.

You will adjust the scope of the history and physical examination to the situation at hand,
keeping several factors in mind: the magnitude and severity of the patient’s problems; the
need for thoroughness; the clinical setting—inpatient or outpatient, primary or subspecialty
care; and the time available.
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Mastery of all the components of a comprehensive assessment allows you to select the
elements that are most pertinent to the patient’s concerns yet meet clinical standards for best
practice and diagnostic accuracy.

SUBJECTIVE OR OBJECTIVE DATA

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COMPREHENSIVE ADULT HEALTH HISTORY

Be aware of the date (moment when

Date and time of history
you evaluate the patient)
Initial Includes age, gender, marital status,
Identifying data
information and occupation.
Document information must be
Reliability
relevant.
Chief The one or more symptoms or concerns causing the patient to seek
complaints care.
Amplifies the Chief complaint → describes how each symptom
developed.
Includes patient’s thoughts and feelings about the illness.
Present illness Pulls in relevant portions of the Review of systems, called
“pertinent positives and negatives”
May include: medications, allergies, and habits of smoking and
alcohol, which are frequently pertinent to the present illness
List childhood illnesses
Medical
List adult illnesses with
Surgical
dates for at least four
Past history Obstetric/Gynecologic
categories
Psychiatric
Includes health maintenance practices such as: immunizations,
screening tests, lifestyle issues, and home safety.
Outline or diagram the age and health, or age and cause of death, of
each immediate relative, including parents, grandparents, siblings,
Family history children, and grandchildren.

Documents presence or absence of specific illnesses in family, such as

hypertension or coronary artery disease.
Personal and Describes educational level, family of origin, current household,
social history personal interests and lifestyle.
Documents presence or absence of common symptoms related to each
Review of major body system.
symptoms Series of “yes-no” questions that should come at the end of the
interview which go from “head to toe.”
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 TOPIC 2. HISTORY TAKING –
HEADINGS, OFTEN ASKED
QUESTIONS.

OFTEN ASKED QUESTIONS

Chief complaints What are your complains? (Note patient’s own words)

Principal symptoms should be well-characterized:

• Location (Where does it hurt?)
• Quality (How does it hurt?)
• Quantity (severity) (How much does it hurts?)

Risk factors for coronary heart diseases

• Do you or did you had chest pain?
• Do you currently take any pills?

Medications
• What kind of medication are you currently taking?
• What is the dosage of the medication?
• How frequent do you are taking that medication?
Present illness Allergies
• Do you have any kind of allergy?

Tobacco use
• Do you smoke?
• Which kind of tobacco do you use?
• How much cigars per day? (Often reported in pack-years)
• Have you quit smoking? For how long?

Alcohol and drug use

• Do you drink alcohol? / Do you take drugs?
• Which kind of alcohol do you drink? / Which kind of
drugs?
• How much per day?

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 Childhood illness
• Did you have any serious infection during your childhood?
• Was the infection viral or bacterial?
• Do you remember the name of it?

Medical:
• Do you suffer from diabetes?
• Do you suffer from high blood pressure?
• Do you suffer from hepatitis?
• Do you suffer from asthma?
• Do you suffer from HIV?
• Have you ever been hospitalized? / Why?
• Are you married / Do you have a
girl/boyfriend?
• Do you have any risky sexual behavior?

Surgical:
Past history
• Did you have any kind of operations?
Adult • To what have you been operated?
illness Obstetric/Gynecologic:
• Any problems with menstruation? \ Pain? /
Duration?
• Any pain during sexual intercourse? / Any
bleeding?

Psychiatric:
• Do you suffer from any kind of
psychological problem?
• Do you take currently any medication?

Health Maintenance:
• Have you ever and screening tests?
Do you follow the current vaccination program?

• Do you have family? / Who are they? / They died from

Family history what?
• Do they suffer/died from:
o Hypertension
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 o Coronary artery disease
o Elevated cholesterol levels
o Stroke
o Diabetes
o Thyroid or renal disease
o Arthritis
o Tuberculosis
o Asthma or lung disease
o Headache
o Seizure disorder
o Mental illness
o Suicide
o Substance abuse
o Allergies
o Symptoms reported by the patient.
o History of breast, ovarian, colon, or prostate cancer
o Other genetically transmitted diseases

• How do you feel in the society?

• Do you feel sad or alone?
• Do you feel accomplished?
Personal and social • What is the most important thing for you?
history • Do you work? Do you like what you do?
• Do you practice sport?
• Do you smoke?
• Do you drink?

• Do your head/neck/arm/ands/legs/feet/articulation hurts?

Review of symptoms
• Are you able to perform determined movement?

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TOPIC 3. ROUTINE EXAMINATION OF
THE PATIENT.

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 TOPIC 4. PHYSICAL METHODS FOR
EXAMINATION OF THE PATIENT.

The physical examination relies on four classic techniques: inspection, palpation, percussion,
and aus- cultation.

CARDINAL TECHNIQUE OF EXAMINATION

Close observations of the details of the patient’s appearance, behavior and

movement such as:
• Facial expression
• Mood
• Body habitus and conditioning
• Skin conditions (petechiae or echymoses)
Inspection • Eye movements
• Pharyngeal color
• Symmetry of the thorax
• Height of jugular venous pulsations
• Abdominal contours
• Lower extremity edema
• Gait

Tactile pressure from the palmar fingers or finger-pads to assess areas of:
• Skin elevation, depression, warmth, or tenderness
Palpation • Lymph nodes
• Pulses
• Contours and sizes of organs and masses
• Crepitus in the joints

Use of the striking or plexor finger, usually the third, to deliver a rapid tap
or blow against the distal pleximeter finger, usually the distal third finger
of the left hand laid against the surface of the chest or abdomen, to evoke
Percussion a sound wave such as resonance or dullness form the underlying tissues or
organs.
This sound waves also generates a tactile vibration against the pleximeter
finger.
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 Use of the diaphragm and bell of the stethoscope to detect the
characteristics of heart, lung and bowel sounds, including:
• Location
• Timing duration
• Pitch
Auscultation • Intensity

For the heart → sounds form closing the four valves and flow into the
ventricles + murmurs.
It also can detect bruits or turbulence over arterial vessels.

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TOPIC 5. GENERAL CONSIDERATIONS.

“Head-to-toe” sequence of the techniques for examining each region of the body, and how to
optimize patient comfort and minimize changes in the patient position:

GENERAL SURVEY

• Observe the patient’s general state of health, height, build, and sexual development.

• Obtain the patient’s weight.

• Note posture, motor activity, and gait; dress, grooming, and personal hygiene; and any
odors of the body or breath.

• Watch the patient’s facial expressions and note manner, affect, and reactions to people
and things in the environment.

• Listen to the patient’s manner of speaking and note the state of awareness or level of
consciousness.

VITAL SIGNS

• Measure the blood pressure.

• Count the pulse and respiratory rate.

• If indicated → measure the body temperature.

The patient is sitting on the edge of the bed or examining table → Stand in front of the
patient, moving to either side as needed.

HEAD

• Examine the hair, scalp, skull, and face.

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EYES

• Check visual acuity and screen the visual fields.

• Note the position and alignment of the eyes.

• Observe the eyelids and inspect the sclera and conjunctiva of each eye.

• With oblique lighting, inspect each cornea, iris, and lens.

• Compare the pupils and test their reactions to light.

• Assess the extraocular movements.

• With an ophthalmoscope, inspect the ocular fundi.

The room should be darkened for the ophthalmoscopic examination → This promotes
pupillary dilation and visibility of the fundi.

EARS

• Inspect the auricles, canals, and drums.

• Check auditory acuity.

• If acuity is diminished, check lateralization (Weber test) and compare air and bone
conduction (Rinne test).

NOSE AND SINUSES

• Examine the external nose; using a light and a nasal speculum, inspect the nasal
mucosa, septum, and turbinates.

• Palpate for tenderness of the frontal and maxillary sinuses.

THROAT (MOUTH AND PHARYNX)

• Inspect the lips, oral mucosa, gums, teeth, tongue, palate, tonsils, and pharynx.

(You may wish to assess the cranial nerves during this portion of the examination).

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 NECK

• Inspect and palpate the cervical lymph nodes.

• Note any masses or unusual pulsations in the neck.

• Feel for any deviation of the trachea.

• Observe the sound and effort of the patient’s breathing.

• Inspect and palpate the thyroid gland.

Move behind the sitting patient to feel the thyroid gland and to examine the back,
posterior thorax, and lungs.

BACK

• Inspect and palpate the spine and muscles of the back.

• Observe shoulder height for symmetry.

POSTERIOR THORAX AND LUNGS

• Inspect and palpate the spine and muscles of the upper back.

• Inspect, palpate, and percuss the chest.

• Identify the level of diaphragmatic dullness on each side.

• Listen to the breath sounds; identify any adventitious (or added) sounds, and, if
indicated, listen to the transmitted voice sounds.

BREASTS, AXILLAE AND EPITROCHLEAR NODES

• In a woman, inspect the breasts with her arms relaxed, then elevated, and then with her
hands pressed on her hips.

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 • In either sex:

o Inspect the axillae and feel for the axillary nodes.

o Feel for the epitrochlear nodes.

By this time, you have made some preliminary observations of the musculoskeletal system.
You have inspected the hands, surveyed the upper back, and, at least in women, made fair
estimate of the shoulders’ range of motion.

Use these and subsequent observations to decide whether a full musculoskeletal examination
is warranted.

If indicated, with the patient still sitting, examine the hands, arms, shoulders, neck, and
temporomandibular joints → Inspect and palpate the joints and check their range of
motion.

ANTERIOR THORAX AND LUNGS

The patient position is supine. Ask the patient to lie down. You should stand at the right
side of the patient’s bed.

• Inspect, palpate, and percuss the chest.

• Listen to the breath sounds, any adventitious sounds, and, if indicated, transmitted
voice sounds.

CARDIOVASCULAR SYSTEM

Elevate the head of the bed to approximately 30 degrees for the cardiovascular
examination, adjusting as necessary to see the jugular venous pulsations.

• Observe the jugular venous pulsations and measure the jugular venous pressure in
relation to the sternal angle.

• Inspect and palpate the carotid pulsations.

• Listen for carotid bruits.

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 • Inspect and palpate the precordium.

• Note the location, diameter, amplitude, and duration of the apical impulse.

• Listen at each auscultatory area with the diaphragm of the stethoscope.

• Listen at the apex and the lower sternal border with the bell.

• Listen for the first and second heart sounds and for physiologic splitting of the second
heart sound.

• Listen for any abnormal heart sounds or murmurs.

ABDOMEN

Lower the head of the bed to the at position. The patient should be supine.

• Inspect, auscultate, and percuss the abdomen.

• Palpate lightly, then deeply.

• Assess the liver and spleen by percussion and then palpation.

• Try to feel the kidneys and palpate the aorta and its pulsations.

o If you suspect kidney infection, percuss posteriorly over the costovertebral

angles.

LOWER EXTREMITIES

Examine the legs, assessing three systems while the patient is still supine. Each of these
three systems can be further assessed when the patient stands.

In supine:

• Peripheral vascular system:

o Palpate the femoral pulses and, if indicated, the popliteal pulses.

o Palpate the inguinal lymph nodes.

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 o Inspect for lower extremity edema, discoloration, or ulcers.

o Palpate for pitting edema.

• Musculoskeletal system:

o Note any deformities or enlarged joints.

o If indicated, palpate the joints, check their range of motion, and perform any
necessary maneuvers.

• Nervous system:

o Assess lower extremity muscle bulk, tone, and strength; also assess sensation
and reflexes.

o Observe any abnormal movements.

Now the patient is standing. You can sit on a chair or stool.

• Peripheral vascular system:

o Inspect for varicose veins.

• Musculoskeletal system:

o Examine the alignment of the spine and its range of motion, the alignment of
the legs, and the feet.

• Genitalia and hernias in men:

o Examine the penis and scrotal contents and check for hernias.

NERVOUS SYSTEM

The complete examination of the nervous system can also be done at the end of the
examination.

It consists of the five segments: mental status, cranial nerves (including funduscopic
examination), motor system, sensory system, and reflexes.

• Mental Status:

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 o If indicated and not done during the interview, assess the patient’s orientation,
mood, thought process, thought content, abnormal perceptions, insight and
judgment, memory and attention, information and vocabulary, calculating
abilities, abstract thinking, and constructional ability.

• Cranial Nerves:

o If not already examined, check sense of smell, strength of the temporal and
masseter muscles, corneal re exes, facial movements, gag reflex, and strength
of the trapezia and sternocleidomastoid muscles.

• Motor System:

o Muscle bulk, tone, and strength of major muscle groups.

• Cerebellar function:

o Rapid alternating movements (RAMs), point-to-point movements, such as

finger-to-nose (F → N) and heel-to-shin (H → S), gait.

• Sensory System:

o Pain, temperature, light touch, vibration, and discrimination. Compare right

with left sides and distal with proximal areas on the limbs.

• Reflexes → biceps, triceps, brachioradialis, patellar, Achilles deep tendon reflexes;

also, plantar reflexes or Babinski reflex.

ADDITIONAL EXAMINATIONS

The rectal and genital examinations are often performed at the end of the physical
examination.

• Rectal Examination in Men:

The patient is lying on his left side for the rectal examination (or standing and bending
forward).

o Inspect the sacro-coccygeal and perianal areas.

o Palpate the anal canal, rectum, and prostate.

If the patient cannot stand, examine the genitalia before doing the rectal examination.

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• Genital and Rectal Examinations in Women:

The patient is supine in the lithotomy position. You should be seated during
examination with the speculum, then standing during bimanual examination of the
uterus, adnexa (and rectum as indicated).

o Examine the external genitalia, vagina, and cervix.

o Obtain a Pap smear.

o Palpate the uterus and adnexa bimanually.

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TOPIC 6. TEMPERATURE, TYPES OF
FEVER

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TOPIC 7. EXAMINATION OF THE SKIN,
NAILS AND HAIR.

EXAMINATION OF THE SKIN

COLOR

Patients may be the first to notice a change in their skin color. Ask them about it. Look for
increased brown pigmentation, loss of pigmentation, redness, pallor, cyanosis, and yellowing
of the skin.

Assess the red color of oxyhemoglobin and the pallor in its absence where the horny layer of
the epidermis is thinnest and causes the least scatter: the fingernails, the lips, and the mucous
membranes, particularly those of the mouth and the palpebral conjunctiva. In dark-skinned
people, inspecting the palms and soles may also be useful.

Pallor results from decreased red- ness in anemia and decreased blood flow, seen in fainting
or arterial occlusion.

Central cyanosis is best identified in the lips, oral mucosa, and tongue. The lips can also turn
blue in the cold, and melanin in the lips may simulate cyanosis in darker-skinned people.
Causes of central cyanosis include advanced lung disease, congenital heart disease, and
hemoglobinopathies.

Cyanosis of the nails, hands, and feet may be central or peripheral in origin. Anxiety or a cold
examining room may cause peripheral cyanosis. The cyanosis of heart failure is usually
peripheral, reflecting deoxygenation or impaired circulation. In COPD and pulmonary edema,
hypoxia may give rise to central cyanosis.

Look for the yellow color of jaundice in the sclera. Jaundice may also appear in the palpebral
conjunctiva, lips, hard palate, undersurface of the tongue, tympanic membrane, and skin. To
see jaundice more easily in the lips, blanch out the red color by pressure with a glass slide.
Jaundice suggests liver disease or excessive hemolysis of red blood cells.

For the yellow color that accompanies high levels of carotene, look at the palms, soles, and
face. It is seen in carotenemia.

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MOISTURE

Examples are dryness, sweating, and oiliness. Dryness in hypothyroidism; oiliness in acne.

TEMPERATURE

Use the backs of your fingers to assess skin temperature. In addition to identifying generalized
warmth or coolness of the skin, note the temperature of any red areas. Generalized warmth in
fever, hyperthyroidism; coolness in hypothyroid- ism. Local warmth if inflammation or
cellulitis

TEXTURE

Examples are roughness and smoothness. Roughness in hypothyroidism; velvety texture in

hyperthyroidism.

MOBILITY AND TURGOR

Lift a fold of skin and note how easily it lifts up (mobility) and how quickly it returns into
place (turgor). Decreased mobility in edema, scleroderma; decreased turgor in dehydration.

LESIONS

Closely inspect any lesions, noting important features such as:

1. Anatomic location and distribution over the body: Are the lesions generalized or
localized? Do they, for example, involve the exposed surfaces, the intertriginous or
skin-fold areas, extensor or flexor areas, or acral areas (such as the hands and feet)?
Do they involve areas exposed to specific allergens or irritants, such as wristbands or
rings?

2. Types of skin lesions (e.g., macules, papules, vesicles, nevi). If possible, find
representative and recent lesions that have not been traumatized by scratching or
otherwise altered. Inspect them carefully and feel them.

3. Color

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 EXAMINATION OF THE HAIR

Inspect and palpate the hair. Note its quantity, distribution, and texture.

Alopecia refers to hair loss—diffuse, patchy, or total.

Sparse hair is seen in hypothyroidism; fine, silky hair in hyperthyroidism.

EXAMINATION OF THE NAILS

Inspect and palpate the fingernails and toenails. Note their color and shape, and any lesions.

Longitudinal bands of pigment may be seen in the nails of normal people who have darker
skin.

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 TOPIC 8. CUTANEOUS
MANIFESTATIONS OF INTERNAL
DISEASES.

DISEASES AND RELATED SKIN CONDITIONS

Addison’s disease: Hyperpigmentation of skin and mucous membranes

AIDS:

• Hairy leukoplakia, Kaposi’s sarcoma, herpes simplex virus (HSV), human

papillomavirus (HPV), cytomegalovirus (CMV), molluscum contagiosum,
mycobacterial skin infections, candidiasis and other cutaneous fungal infections.
• Oral and anal squamous cell carcinoma, acquired ichthyosis, bacterial abscesses,
psoriasis (often severe), erythroderma, seborrheic dermatitis (often severe).

Chronic renal disease: Pallor, xerosis, pruritus, hyperpigmentation, uremic frost, metastatic
calcification in the skin, calciphylaxis, “half and half” nails, hemodialysis-related skin disease

CREST syndrome: Calcinosis, Raynaud’s phenomenon, sclerodactyly, telangiectasias.

Crohn’s disease: Erythema nodosum, pyoderma gangrenosum, enterocutaneous fistulas,

aphthous ulcers.

Cushing’s disease: Striae, skin atrophy, purpura, ecchymoses, telangiectasias, acne, moon
facies, buffalo hump, hypertrichosis.

Dermatomyositis: Heliotrope rash, Gottron’s papules, periungual telangiectasias, alopecia,

poikiloderma in sun-exposed areas, Raynaud’s phenomenon.

Diabetes: Necrobiosis lipoidica diabeticorum, diabetic bullae, diabetic dermopathy,

granuloma annulare, acanthosis nigricans, candidiasis, neuropathic ulcers, eruptive
xanthomas, peripheral vascular disease.

Disseminated intravascular coagulation: Skin necrosis, petechiae, ecchymoses,

hemorrhagic bullae, purpura fulminans.

Dyslipidemias: Xanthomas (tendon, eruptive, and tuberous), xanthelasma (may occur in

healthy people).

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Gonococcemia: Erythematous macules to hemorrhagic pustules; lesions in acral distribution
that can involve palms and soles

Hemochromatosis: Skin bronzing and hyperpigmentation.

Hypothyroidism: Dry, rough, and pale skin; coarse and brittle hair; myxedema; alopecia
(lateral third of the eyebrows to diffuse); skin cool to touch; thin and brittle nails.

Hyperthyroidism: Warm, moist, soft, and velvety skin; thin and fine hair; alopecia; vitiligo;
pretibial myxedema (in Graves’ disease); hyperpigmentation (local or generalized).

Infective endocarditis: Janeway lesions, Osler nodes, splinter hemorrhages, petechiae.

Kawasaki disease: Mucosal erythema (lips, tongue, and pharynx), strawberry tongue, cherry
red lips, polymorphous rash (primarily on trunk), erythema of palms and soles with later
desquamation of fingertips.

Liver disease: Jaundice, spider angiomas and other telangiectasias, palmar erythema, Terry’s
nails, pruritus, purpura, caput medusa.

Leukemia/lymphoma: Pallor, exfoliative erythroderma, nodules, petechiae, ecchymoses,

pruritus, vasculitis, pyoderma gangrenosum, bullous diseases.

Meningococcemia: Pink macules and papules, petechiae, hemorrhagic petechiae,

hemorrhagic bullae, purpura fulminans.

Neurofibromatoses 1 (von Recklinghausen’s syndrome): Neurofibromas, café-au-lait

spots, freckling in the axillary and inguinal areas, plexiform neurofibroma.

Pancreatitis (hemorrhagic): Grey Turner sign, Cullen’s sign, panniculitis.

Pancreatic carcinoma: Panniculitis, migratory thrombophlebitis.

Peripheral vascular disease: Dry, scaly, shiny atrophic skin; dystrophic, brittle toenails; cool
skin; hairless shins; ulcers; pallor; cyanosis; gangrene.

Pregnancy (physiologic changes): Melasma, increased pigmentation of areolae, linea nigra,

palmar erythema, varicose veins, striae, spider angiomas, hirsutism, pyogenic granuloma.

Reiter’s syndrome: Psoriasis-like skin and mucous membrane lesions, keratoderma

blennorrhagicum, balanitis circinata.

Rheumatoid arthritis: Vasculitis, Raynaud’s phenomenon, rheumatoid nodules, pyoderma

gangrenosum, rheumatoid papules, erythematous to salmon-colored rashes.

Rocky Mountain spotted fever: Erythematous rash that begins on wrists and ankles, then
spreads to palms and soles; becomes more purpuric as it generalizes.
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Scleroderma: Thickened, taut, and shiny skin; ulcerations and pitted scars on fingertips;
sclerodactyly; telangiectasias; Raynaud’s phenomenon.

Sickle cell: Jaundice, leg ulcers (malleolar regions), pallor.

Syphilis:

First-degree: Chancre (painless)

Second-degree: Rash (“the great imitator”)—generalized, maculopapular rash that involves

the palms and soles, pustules, condylomata lata, alopecia (“moth-eaten”), white plaques on
oral and genital mucosa

Third-degree: Gummas, granulomas

Systemic lupus erythematosus: Photosensitivity, malar (butter y) rash, discoid rash,

alopecia, vasculitis, oral ulcers, Raynaud’s phenomenon.

Thrombocytopenic purpura: Petechiae, ecchymoses.

Tuberous sclerosis: Adenoma sebaceum (angio bromas), ash-leaf spots, shagreen patch,
periungal fibromas.

Ulcerative colitis: Erythema nodosum, pyoderma gangrenosum.

Coxsackie A (hand, foot, and mouth): Oral ulcers; macules, papules, and vesicles on hands,
feet, and buttocks.

Erythema infectiosum (fifth disease): Erythema of cheeks (“slapped cheeks”) followed by

erythematous, pruritic, reticulated (net- like) rash that starts on trunk and proximal extremities
(rash worsens with sun, fever, and temperature changes).

Roseola infantum (HSV 6): Erythematous, maculopapular, discrete rash (often fever
present) that begins on head and spreads to involve trunk and extremities, petechiae on soft
palate.

Rubella (German measles): Erythematous, maculopapular, discrete less confluent rash

(often fever present) that begins on head and spreads to involve trunk and extremities,
petechiae on soft palate.

Rubeola (measles): Erythematous, maculopapular rash that begins on head and spreads to
involve trunk and extremities (lesions become confluent on face and trunk, but are discrete
on extremities), Koplik spots on buccal mucosa.

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Varicella (chickenpox): Generalized, pruritic, vesicular (vesicles on an erythematous base,
“dewdrop on a rose petal”) rash begins on trunk and spreads peripherally, lesions appear in
crops and are in different stages of healing.

Herpes zoster (shingles): Pruritic or painful vesicular rash (vesicles on an erythematous

base) in a dermatomal distribution.

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TOPIC 9. PHYSICAL EXAMINATION OF
THE HEAD.

THE HAIR

Note its quantity, distribution, texture, and any pattern of loss. You may see loose flakes of
dandruff.

THE SCALP

Part the hair in several places and look for scaliness, lumps, nevi, or other lesions.

THE SKULL

Observe the general size and contour of the skull. Note any deformities, depressions, lumps,
or tenderness. Learn to recognize the irregularities in a normal skull, such as those near the
suture lines between the parietal and occipital bones.

THE FACE

Note the patient’s facial expression and contours. Observe for asymmetry, involuntary
movements, edema, and masses.

THE SKIN

Observe the skin, noting its color, pigmentation, texture, thickness, hair distribution, and any
lesions.

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 TOPIC 10. PHYSICAL EXAMINATION
OF THE NECK.

Inspect the neck, noting its symmetry and any masses or scars. Look for enlargement of the
parotid or submandibular glands, and note any visible lymph nodes.

THE LYMPH NODES

Palpate the lymph nodes. Using the pads of your index and middle fingers, move the skin over
the underlying tissues in each area. The patient should be relaxed, with neck flexed slightly
forward and, if needed, turned slightly toward the side being examined. You can usually
examine both sides at once. For the submental node, however, it is helpful to feel with one
hand while bracing the top of the head with the other.

Feel in sequence the following nodes:

1. Preauricular—in front of the ear

2. Posterior auricular—superficial to the
mastoid process
3. Occipital—at the base of the skull
posteriorly
4. Tonsillar—at the angle of the mandible
5. Submandibular—midway between the
angle and the tip of the mandible. These
nodes are usually smaller and smoother
than the lobulated submandibular gland
against which they lie.
6. Submental—in the midline a few
centimeters behind the tip of the mandible
7. Superficial cervical—superficial to the
sternocleidomastoid
8. Posterior cervical—along the anterior edge of the trapezius
9. Deep cervical chain—deep to the sternocleidomastoid and often inaccessible to
examination. Hook your thumb and fingers around either side of the
sternocleidomastoid muscle to find them.
10. Supraclavicular—deep in the angle formed by the clavicle and the sternocleidomastoid
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Note their size, shape, delimitation (discrete or matted together), mobility, consistency, and
any tenderness. Small, mobile, discrete, nontender nodes, sometimes termed “shotty,” are
frequently found in normal people.

Palpate the anterior superficial and deep cervical chains, located anterior and superficial to
the sternocleidomastoid. Then palpate the posterior cervical chain along the trapezius
(anterior edge) and along the sternocleidomastoid (posterior edge). Flex the patient’s neck
slightly forward toward the side being examined. Examine the supraclavicular nodes in the
angle between the clavicle and the sternocleidomastoid.

Enlarged or tender nodes, if unexplained, call for:

• re-examination of the regions they drain

• careful assessment of lymph nodes elsewhere so that you can distinguish between
regional and generalized lymphadenopathy.

Occasionally you may mistake a band of muscle or an artery for a lymph node. You should
be able to roll a node in two directions: up and down, and side to side. Neither a muscle nor
an artery will pass this test.

TRACHEA AND THE THYROID GLAND

To orient yourself to the neck, identify the thyroid and cricoid cartilages and the trachea below
them.

Inspect the trachea for any deviation from its usual midline position. Then feel for any
deviation. Place your finger along one side of the trachea and note the space between it and
the sternocleidomastoid. Compare it with the other side. The spaces should be symmetric.

Inspect the neck for the thyroid gland. Tip the patient’s head back a bit. Using tangential
lighting directed downward from the tip of the patient’s chin, inspect the region below the
cricoid cartilage for the gland. The lower shadowed border of the thyroid glands shown here
is outlined by arrows.

30
Observe the patient swallowing. Ask the patient to sip some water and to extend the neck
again and swallow. Watch for upward movement of the thyroid gland, noting its contour and
symmetry. The thyroid cartilage, the cricoid cartilage, and the thyroid gland all rise with
swallowing and then fall to their resting positions.

Confirm your visual observations by palpating the gland outlines as you stand facing the
patient. This helps prepare you for the more systematic palpation to follow:

1. Ask the patient to flex the neck slightly forward to relax the sternocleidomastoid
muscles.
2. Place the fingers if both hands on the patient’s neck so that your index finger are just
below the cricoid cartilage.
3. Ask the patient to sip and swallow water before. Feel for the thyroid isthmus rising up
under your finger pads. It is often, but not always, palpable.
4. Displace the trachea to the right with the fingers of the left hand; with the right-hand
fingers, palpate laterally for the right lobe of the thyroid in the space between the
displaced trachea and the relaxed sternocleidomastoid. Find the lateral margin. In a
similar fashion, examine the left lobe.

o The lobes are somewhere harder to feel than the isthmus, so practice is needed.
The anterior surface of a lateral lobe is approximately the size of the distal
phalanx of the thumb and feels somewhat rubbery.

31
 5. Note the size, shape, and consistency of the gland and identify any nodules or
tenderness.
6. If the thyroid gland is enlarged, listen over the lateral with a stethoscope to detect a
bruit, a sound similar to a cardiac murmur but of noncardiac origin.

CAROTID ARTERIES AND JUGULAR VEINS

Defer a detailed examination of the neck vessels until you begin examining the cardiovascular
system when the patient is supine with the head elevated to 30 degrees.

Jugular venous distention may be visible when the patient is in the sitting position and should
be promptly assessed.

Also. be alert to unusually prominent arterial pulsations.

32
 TOPIC 11. RESPIRATORY FAILURE –
DEFINITION, CLASSIFICATION,
COMMON CAUSES OF ACUTE AND
CHRONIC RESPIRATORY FAILURE.

DEFINITION

RESPIRATORY FAILURE → pulmonary gas exchange fails to maintain normal arterial

oxygen and carbon dioxide levels.

CLASSIFICATION

It is classified into types I and II by the absence or presence of hypercapnia (raised PaCO2).

COMMON CAUSES OF ACUTE AND CHRONIC RESPIRATORY FAILURE.

Type 1 Type 2
Hypoxia (PaO2 < 8.0 kPa (60
mmHg)) Hypoxia (PaO2 < 8.0 kPa (60 mmHg))
Normal or low PaCO2 (< 6.6 kPa Raised PaCO2 (> 6.6 kPa (50 mmHg))
(50 mmHg))
Acute Chronic Acute Chronic
H+ → → ↑ → or ↑
HCO3- → → → ↑
Acute severe asthma
Acute asthma
Acute exacerbation of
Pulmonary
COPD COPD
oedema Sleep apnea
Lung fibrosis Upper airway obstruction
Pneumonia Kyphoscoliosis
Lymphangitis Acute
Lobar collapse Myopathies/muscular
carcinomatosa neuropathies/paralysis
Pneumothorax dystrophy
Causes Right-to-left Narcotic drugs
Pulmonary Ankylosing spondylitis
shunts Primary alveolar
embolus
hypoventilation
ARDS
Flail chest injury
ARDS= Acute Respiratory Distress syndrome
COPD= Chronic Obstructive Pulmonary diseases

33
 TOPIC 12. DYSPNOEA – CHANGES IN
THE RATE AND RHYTHM OF
RESPIRATION.

DEFINITION

Dyspnoea can be defined as the subjective feeling of an uncomfortable need to breathe.

CAUSES

RESPIRATORY SYSTEM DYSPNEA:

• Airway disease:
o Asthma and chronic obstructive pulmonary disorder (COPD) are common
causes of dyspnea associated with increased work of breathing. Broncho- spasm
can cause chest tightness and hyperventilation. Hypoxemia and hypercapnia
can result from ventilation-perfusion mismatch.
• Chest wall disorders:
o Chest wall stiffness (e.g., kyphoscoliosis) and neuromuscular weakness (e.g.,
myasthenia gravis) cause increased work of breathing.
• Lung parenchymal disorders:
o Interstitial lung diseases cause reduced lung compliance and increased work of
breathing. Ventilation-perfusion mismatch and pulmonary fibrosis may lead to
hypoxemia. Stimulation of lung receptors can cause hyperventilation.

CARDIOVASCULAR SYSTEM DYSPNEA:

• Left heart disorders:

o Elevations of le -ventricular end-diastolic and pulmonary capillary wedge
pressures lead to dyspnea related to stimulation of pulmonary receptors and
hypoxemia from ventilation-perfusion mismatch.
• Pulmonary vascular disorders:

34
 o Pulmonary emboli, primary pulmonary arterial hypertension, and pulmonary
vasculitis stimulate pulmonary receptors via increased pulmonary artery
pressures. Hyperventilation and hypoxemia also may contribute to dyspnea.
• Pericardial diseases:
o Constrictive pericarditis and pericardial tamponade cause increased intracardiac
and pulmonary arterial pressures, leading to dyspnea.

DYSPNEA WITH NORMAL RESPIRATORY AND CARDIOVASCULAR SYSTEM:

• Anemia can cause dyspnea, especially with exertion.

• Obesity is associated with dyspnea due to high cardiac output and impaired ventilatory
function.
• Deconditioning may also cause dyspnea in patients with normal respiratory and
cardiovascular systems.

PATHOPHYSIOLOGY

35
 EXAMINATION OF CHRONIC DYSPNEA

KEY QUESTIONS

• How is your breathing at rest and overnight?

o In COPD, there is a fixed, structural limit to maximum ventilation, and a
tendency for progressive hyperinflation during exercise. Breathlessness is
mainly apparent when walking, and patients usually report minimal symptoms
at rest and overnight.
o Patients with significant asthma are often woken from their sleep by
breathlessness with chest tightness and wheeze.

• How much can you do on a good day?

o The approximate distance the patient can walk on the level should be
documented, along with capacity to climb inclines or stairs.
o In mild asthma, the patient may be free of symptoms and signs when well.
o In COPD, gradual, progressive loss of exercise capacity over months and years,
with consistent disability over days, is typical.
o Relentless, progressive breathlessness that is also present at rest, often
accompanied by a dry cough, suggests interstitial fibrosis.
o History of angina, hypertension or myocardial infarction raises the possibility
of a cardiac cause.

• Did you have breathing problems is childhood or at school?

o When present, a history of childhood wheeze increases the likelihood of asthma,
although this history may be absent in late-onset asthma. A history of atopic
allergy also increases the likelihood of asthma.

• Do you have other symptoms along with your breathlessness?

o Digital or perioral paraesthesiae and a feeling that ‘I cannot get a deep enough
breath in’ are typical features of psychogenic hyperventilation, but this cannot
be diagnosed until investigations have excluded other potential causes.
o Additional symptoms include light- headedness, central chest discomfort or
even carpopedal spasm due to acute respiratory alkalosis. These alarming
symptoms may provoke further anxiety and exacerbate hyperventilation.

36
 o Psychogenic breathlessness rarely disturbs sleep, frequently occurs at rest, may
be provoked by stressful situations and may even be relieved by exercise.
o Pleuritic chest pain in a patient with chronic breathlessness, particularly if it
occurs in more than one site over time, should raise suspicion of
thromboembolic disease.
o Morning headache is an important symptom in patients with breathlessness, as
it may signal the onset of carbon dioxide retention and respiratory failure.

EXAMINATION OF ACUTE DYSPNEA

CONDITION HISTORY SIGNS CXR ABG ECG

Chest pain,
Central cyanosis, Sinus
Palpitations, Cardiomegaly,
Pulmonary ↑JVP, sweating, ↓PaO2 tachycardia,
Orthopnea, oedema/pleural
oedema cool extremities, ↓PaCO2 ischemia,
Cardiac effusions
basal crackles arrhythmia
history
Central cyanosis, Sinus
Risk factors, Often normal
↑JVP, absence of tachycardia,
Massive chest pain, Prominent hilar
signs in the lung, ↓PaO2 RBBB,
pulmonary pleurisy, vessels,
shock ↓PaCO2 S1Q3T3
embolus syncope, oligaemic lung
(tachycardia, pattern
dizziness fields
hypotension) ↑T(V1–V4)
Tachycardia,
↓PaO2
History of pulsus Hyperinflation Sinus
↓PaCO2
asthma, paradoxus, only (unless tachycardia
Acute severe (↑PaCO2
medications, cyanosis (late), complicated by (bradycardia
asthma in
wheeze JVP →, ↓peak pneumothorax) in extremis)
extremis)
flow, wheeze
↓ or ↓↓
PaO2
Previous
Cyanosis, ↑PaCO2
episodes,
hyperinflation, Hyperinflation, in type II Normal, or
Acute smoker. If in
signs of CO2 bullae, failure ± signs of right
exacerbation type II
retention complicating ↑H+, ventricular
of COPD respiratory
(flapping tremor, pneumothorax ↑HCO3 in strain
failure, may
bounding pulses) chronic
be drowsy
type II
failure

37
 ↓or ↓↓
PaO2
↑PaCO2
Fever,
in type II
Prodromal confusion, Normal, or
illness, pleural, rub, Pneumonic signs of right
failure ±
Pneumonia fever, rigors, consolidation, consolidation ventricular
↑H+,
pleurisy cyanosis (if strain
↑HCO3 in
severe)
chronic
type II
failure
Evidence of
diabetes
Fetor (ketones),
mellitus or
hyperventilation PaO2
renal
Metabolic without heart or normal
disease, Normal -
acidosis lung signs, ↓↓PaCO2,
aspirin or
dehydration, air ↑H+
ethylene
hunger
glycol
overdose
Previous No cyanosis, no
episodes, heart or lung
PaO2 ↓↓PaCO2,
digital or signs, Normal
Psychogenic normal ↓H+
perioral carpopedal
dysaesthesia spasm
ABG = Arterial Blood Gases
RBBB = Right Bundle Branch Block

38
 TOPIC 13. CYANOSIS.

DEFINITION

Bluish discoloration of the skin and/or mucous membranes are usually due to elevated
quantity of reduced hemoglobin (>40 g/L [>4 g/dL]) in the capillary blood vessels.

EPIDEMIOLOGY

Findings are most apparent in the lips, nail beds, ears, and malar eminences.

CENTRAL CYANOSIS

Results from arterial desaturation or presence of an abnormal hemoglobin. Usually evident

when arterial saturation is ≤85%, or ≤75% in dark-skinned individuals.

ETIOLOGY

• Decreased arterial oxygen saturation

o Decreased atmospheric pressure—high altitude
o Impaired pulmonary function
o Alveolar hypoventilation
o Inhomogeneity in pulmonary ventilation and perfusion (perfusion of
hypoventilated alveoli)
o Impaired oxygen diffusion
• Anatomic shunts
o Certain types of congenital heart disease
o Pulmonary arteriovenous fistulas
o Multiple small intrapulmonary shunts
o Hemoglobin with low affinity for oxygen
• Hemoglobin abnormalities
o Methemoglobinemia—hereditary, acquired
o Sulfhemoglobinemia—acquired
o Carboxyhemoglobinemia (not true cyanosis)
39
 PERIPHERAL CYANOSIS

Occurs with normal arterial O2 saturation with increased extraction of O2 from capillary
blood caused by decreased localized blood flow.

Contributors include:

• Vasoconstriction due to cold exposure

• Decreased cardiac output (e.g., in shock)
• Heart failure
• Peripheral vascular disease with arterial obstruction or vasospasm.

Local (e.g., thrombophlebitis) or central (e.g., constrictive pericarditis) venous hypertension

intensifies cyanosis.

40
 TOPIC 14. COUGH AND SPUTUM.

COUGH

Cough is the most frequent symptom of respiratory disease and is caused by stimulation of
sensory nerves in the mucosa of the pharynx, larynx, trachea and bronchi.

ORIGIN COMMON CAUSES CLINICAL FEATURES

Pharynx Post-nasal drip History of chronic rhinitis
Voice or swallowing altered, harsh or painful
Laryngitis, tumor,
Larynx cough Paroxysms of cough, often associated
whooping cough, croup
with stridor
Trachea Tracheitis Raw retrosternal pain with cough
Bronchitis (acute) and Dry or productive, worse in mornings
COPD Asthma Usually dry, worse at night
Eosinophilic bronchitis Features similar to asthma but AHR absent
Bronchi Bronchial carcinoma Persistent (often with haemoptysis)
Tuberculosis Productive (often with haemoptysis)
Pneumonia Dry initially, productive later
Productive, changes in posture induce
Bronchiectasis
sputum production
Often at night (may be productive of pink,
Pulmonary edema
Lung frothy sputum)
Parenchyma Interstitial fibrosis Dry and distressing
Drug side
ACE inhibitors Dry cough
effects
ACE = Angiotensin-converting Enzyme
AHR = Airway Hyper-Reactivity
COPD = Chronic Obstructive Pulmonary Diseases

41
TYPES OF COUGH

ACUTE COUGH

ACUTE COUGH → duration <21 days, usually related to respiratory infection, aspiration, or
inhalation of respiratory irritants.

• Subacute cough (present for 3–8 weeks) is often related to persistent inflammation
from a tracheobronchitis episode.

CHRONIC COUGH

CHRONIC COUGH → >8 weeks in duration, can be caused by many pulmonary and cardiac
diseases.

• Chronic bronchitis related to cigarette smoking is a common cause.

• If the chest radiograph and physical examination are unremarkable, other common
causes of chronic cough include cough-variant asthma, gastroesophageal reflux
disease (GERD), postnasal drip related to sinus disease, and medications including
ACE inhibitors.
• Irritation of tympanic membranes and chronic eosinophilic bronchitis also can cause
chronic cough with a normal chest radiograph.

SPUTUM (EXPECTORATIONS)

DEFINITION

Tracheobronchial secretion mixed with saliva.

PHYSIOLOGY

Under normal circumstances, a thick mucus layer covers the airways and protects the
bronchial epithelium against inhaled noxious substances.
42
This continuously renewed mucus is transported by the respiratory cilia towards the
oropharynx.

• It will be swallowed under normal circumstances and coughed up, if its quantity is
increased.
• The normal amount of secretion is about 100 mL per day.

PATHOPHYSIOLOGY

Sputum production is increased by any injury of the bronchial tree or the lung parenchyma
due to inhaled noxious substances or by inflammation.

Enhanced sputum production is a hallmark for airway injury or inflammation.

Most inflammatory diseases of the bronchi (e. g., bronchitis, asthma, and bronchiectasis) and
of the lung parenchyma (pneumonia) are associated with sputum production.

COMPOSITION

Sputum consists of 95% water and only 5% organic components, e.g., substances such as high
molecular weight mucins, secretory IgA, etc.

• It contains substances that transude or exude from the blood, such as fibrinogen or
albumin.
• In addition, it contains cells from the blood or exfoliated epithelial cells.
• Cell products and mediators are further components.

APPEARANCE

According to the color of the sputum a distinction is made between mucous (whitish),
mucopurulent, and purulent (yellowish) expectoration.

• The yellow or green color of the sputum is due to leucoproteins and leucoverdins,
which mainly originate from decaying inflammatory cells, i. e., neutrophils and
eosinophils and only partially from bacterial products.
• If sputum contains blood its color turns from faint red to dark brown according to the
amount of blood and the time course of bleeding.

43
TOPIC 15. CHEST PAIN – DIAGNOSTIC
APPROACH TO THE PATIENT WITH
CENTRAL OR PERIPHERAL CHEST
PAIN.

CHARACTER DURATION LOCATION

Center of chest,
over sternum or just
to the left of it
Stable → 5 min
Sometimes ring-
Angina pectoris Chest heaviness, Unstable → 5−10
like
(Myocardial tightening, constricting, min (sometimes
Radiation to
ischemia) choking, burning lasting hours with
shoulder/arms,
changing intensity)
neck/jaw,
epigastrium
(seldom back)
Excruciating, severe Building up over Precordial,
Myocardial
constriction and minutes radiating as in
infarction
tightening, dyspnea Persistent = 30 min angina pain
Sharp, severe, stabbing,
tearing,
Varying with
Often precordial
respiration, position,
Infrequently
Pericarditis and motion Persistent
radiating to neck
Increasing in
and shoulders
recumbence and with
deep inspiration or
coughing
Exercise-induced chest
heaviness or tightening, Similar to angina
Aortic stenosis 5−10 min
often accompanied by pectoris
dyspnea
Ending with stop of Precordial
Arrhythmias Sharp pain at rest
arrhythmia Radiating to throat
Mitral valve
Sharp Long duration Left side of chest
prolapse

44
 Precordial and/or
Aorta Excruciating pain, Abrupt onset
interscapular
Aortic dissection ripping, tearing Persistent
Often migrating
Sharp, tearing, often
Functional chest Precordial
associated with
pain Often persistent Localized
hyperventilation
Lungs/Pleura
Massive, Blunt, chest heaviness,
pulmonary accompanied by Abrupt onset,
Precordial
embolism dyspnea persistent
Tearing, rubbing,
varying with respiration
Pulmonary
Occasionally resembles
embolism + lung Persistent Center of chest
angina pectoris
infarction and/or affected
Associated with
chest side
tachycardia, hemoptysis
Sharp, tearing, variable
with respiration, Sudden onset
Unilateral
accompanied by Persistent
Pneumothorax
dyspnea, tachycardia
Persistent Unilateral, radiating
Sharp, tearing, variable
(sometimes for to shoulder or
Pleuritis with respiration
days) epigastrium
Sharp, variable with
Unilateral, radiating
respiration,
to shoulder or
Pneumonia accompanied by fever, Persistent
epigastrium
cough
Esophagus
Burning, dull,
Gastro-esophageal
tightening, mimicking
reflux Lasting minutes to Precordial,
angina
Esophagitis hours epigastrium
Provoked by bending,
Esophageal spasm
straining, or lying down
Excruciating, sharp
Rupture of the Usually after vomiting Precordial
Persistent
esophagus Followed by fever and Radiating to back
shock

45
 Musculoskeletal apparatus
Vertebral pain
Varying, dull to sharp Unilateral
Rib fracture
(more often sharp) Sometimes
Intercostal muscle Variable
Often provoked or localized
injury Often beginning
worsened by motion, Occasionally along
Tumors of chest after exercise/move
position, pressure intercostal space
wall
Nervous system
Intercostal
neuralgia Tearing, burning,
Spinal cord electrifying.
Persistent
compression Accompanied by Dermatome
Resistant to therapy
Herpes neuralgia sensory disorders
Thoracic outlet (paresthesia, numbness)
syndrome

46
 TOPIC 16. INSPECTION OF THE CHEST
– POSSIBLE PATHOLOGICAL
CHANGES.

INSPECTION OF THE CHEST

From a midline position behind the patient, note the shape of the chest and how the chest
moves, including:

× Deformities or asymmetry in chest expansion

× Abnormal retraction of the interspaces during inspiration. Retraction is

× most apparent in the lower interspaces.

× Impaired respiratory movement on one or both sides or a unilateral lag (or delay) in
movement.

POSSIBLE PATHOLOGIC CHANGES.

NORMAL ADULT

The thorax in the normal adult is

wider than it is deep.

Its lateral diameter is larger than its

anteroposterior diameter.

47
FUNNEL CHEST (PECTUS EXCAVATUM)

Note depression in the lower portion of

the sternum.

Compression of the heart and great

vessels may cause murmurs.

BARREL CHEST

There is an increased anteroposterior

diameter.

This shape is normal during infancy,

and often accompanies aging and
chronic obstructive pulmonary
disease.

PIGEON CHEST (PECTUS CARINATUM)

The sternum is displaced anteriorly,

increasing the anteroposterior
diameter.

The costal cartilages adjacent to the

protruding sternum are depressed.

48
TRAUMATIC FLAIL CHEST

Multiple rib fractures may result in

paradoxical movements of the thorax.

As descent of the diaphragm decreases

intrathoracic pressure, on inspiration the
injured area caves inward; on expiration, it
moves outward.

THORACIC KYPHOSCOLIOSIS

Abnormal spinal curvatures and vertebral

rotation deform the chest.

Distortion of the underlying lungs may

make interpretation of lung findings very
difficult.

49
 TOPIC 17. PALPATION OF THE CHEST.
VOCAL FREMITUS; PATHOLOGICAL
CHANGES.

POSTERIOR CHEST

As you palpate the chest, focus on areas of tenderness and abnormalities in the overlying skin,
respiratory expansion, and fremitus.

1. Identify tender areas

Carefully palpate any area where pain has been reported or where lesions or bruises are
evident. Look for bruises over a fractured rib.

2. Assess any visible abnormalities

Such as masses or sinus tracts (blind, inflammatory, tubelike structures opening onto the
skin). Although rare, sinus tracts indicate infection of the underlying pleura and lung (as in
tuberculosis, actinomycosis).

3. 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.

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. This is sometimes termed lung excursion.

Unilateral decrease or delay in chest expansion occurs in chronic fibrosis of the underlying
lung or pleura, pleural effusion, lobar pneumonia, pleural pain with associated splinting, and
unilateral bronchial obstruction.

50
4. Feel for tactile fremitus

Fremitus refers to the palpable vibrations transmitted through the bronchopulmonary tree to
the chest wall as the patient is speaking. To detect fremitus, use either the ball (the bony part
of the palm at the base of the fingers) or the ulnar surface of your hand to optimize the
vibratory sensitivity of the bones in your hand. 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.

Use one hand until you have learned the feel of fremitus. Some clinicians find using one hand
more accurate. Using both hands to compare sides increases your speed and may facilitate
detection of differences.

Fremitus is decreased or absent when the voice is higher pitched or soft or when the
transmission of vibrations from the larynx to the surface of the chest is impeded by a thick
chest wall, an obstructed bronchus, COPD, or pleural changes from effusion, fibrosis, air
(pneumothorax), or an infiltrating tumor.

5. Palpate and compare symmetric areas of the lungs

Follow the pattern shown in the photograph. 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.

Asymmetric decreased fremitus occurs in unilateral

pleural effusion, pneumothorax, neoplasm due to
decreased transmission of low frequency sounds;
asymmetric increased fremitus occurs in unilateral
pneumonia from increased transmission through
consolidated tissue.

Tactile fremitus is a somewhat imprecise assessment tool, but as a scouting technique, it

directs your attention to possible abnormalities. Later in the examination, confirm any
suggested findings by listening for underlying breath sounds, voice sounds, and whispered
voice sounds. All these attributes tend to increase or decrease together.

51
 ANTERIOR CHEST

Palpation has four potential uses:

1. Identification of tender areas

• Tender pectoral muscles or costal cartilages suggest, but do not prove, that chest pain
has a musculoskeletal origin.

2. Assessment of observed abnormalities

3. Further assessment of chest expansion

• Place your thumbs along each costal
margin, your hands along the lateral rib
cage.
• As you position your hands, slide them
medially a bit to raise loose skin folds
between your thumbs.
• Ask the patient to inhale deeply.
• Observe how far your thumbs diverge as
the thorax expands and feel for the extent
and symmetry of respiratory movement.

4. Assessment of tactile fremitus

• Compare both sides of the chest, using the
ball or ulnar surface of your hand.
Fremitus is usually decreased or absent
over the precordium. When examining a
woman, gently displace the breasts as
necessary.

52
TOPIC 18. PERCUSSION OF THE CHEST
– NORMAL FINDINGS.

POSTERIOR CHEST

Percussion is one of the most important techniques of physical examination.

• Percussion sets the chest wall and underlying tissues in motion, producing audible
sound and palpable vibrations.
• Percussion helps you establish whether the underlying tissues are air-filled, fluid-
filled, or solid.
• It penetrates only 5 cm to 7 cm into the chest, so it will not help you to detect deep-
seated lesions.

The key points for good technique, described for a right-handed person, are as follows:

1. Hyperextend the middle finger of your left hand, known

as the pleximeter finger. Press its distal interphalangeal
joint firmly on the surface to be percussed. Avoid surface
contact by any other part of the hand because this
dampens out vibrations. Note that the thumb and 2nd,
4th, and 5th fingers are not touching the chest.

2. Position your right forearm quite close to the surface,

with the hand cocked upward. The middle finger should
be partially flexed, relaxed, and poised to strike.

3. With a quick, sharp but relaxed wrist motion, strike the

pleximeter finger with the right middle finger, or plexor
finger. Aim at your distal interphalangeal joint. You are
trying to transmit vibrations through the bones of this
joint to the underlying chest wall. Use the same force for
each percussion strike and the same pleximeter pressure
to avoid changes in the percussion note related to your
technique rather than patient findings.

53
 4. Strike using the tip of the plexor finger, not the finger
pad. Your finger should be almost at right angles to
the pleximeter. A short fingernail is recommended to
avoid injuring your knuckle.

5. Withdraw your striking finger quickly to avoid

damping the vibrations you have created.

In summary, the movement is at the wrist. It is directed, brisk yet relaxed, and a bit bouncy.

NOTES

A thick chest wall requires stronger percussion than a thin one. However, if a louder note is
needed, apply more pressure with the pleximeter finger (this is more effective for increasing
percussion note volume than tapping harder with the plexor finger).

When percussing the lower posterior chest, stand somewhat to the side rather than directly
behind the patient. This allows you to place your pleximeter finger more firmly on the chest
and your plexor is more effective, making a better percussion note.

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

PERCUSSION CHARACTERISTICS

Relative Relative Relative

Example of location
intensity pitch duration
Flat Soft High Short Thigh
Dull Medium Medium Medium Liver
Resonant Loud Low Long Healthy lung
Hyper
Very loud Lower Longer Usually none
resonant
Gastric air bubble or
Loud High Long
Tympanic puffed-out cheeck

54
PATTERN FOR PERCUSSION

IDENTIFY THE DESCENT OF THE DIAPHRAGM, OR DIAPHRAGMATIC

EXCURSION.

First, determine the level of diaphragmatic dullness during quiet respiration. Holding the
pleximeter finger above and parallel to the expected level of dullness, percuss downward in
progressive steps until dullness clearly replaces resonance. Confirm this level of change by
percussion near the middle of the hemothorax and also more laterally.

Note that with this technique, you are

identifying the boundary between the
resonant lung tissue and the duller structures
below the diaphragm. You are not
percussing the diaphragm itself. You can
infer the probable location of the diaphragm
from the level of dullness.

Now, estimate the extent of diaphragmatic

excursion by determining the distance
between the level of dullness on full
expiration and the level of dullness on full
inspiration, normally about 3 to 5.5 cm.

55
 ANTERIOR CHEST

Percuss the anterior and lateral chest, again

comparing both sides. The heart normally produces
an area of dullness to the left of the sternum from the
3rd to the 5th interspaces. Percuss the left lung lateral
to the area of dullness.

In a woman, to enhance percussion, gently displace

the breast with your left hand while percussing with
the right. Alternatively, you may ask the patient to
move her breast for you.

Identify and locate any area with an abnormal percussion note.

With your pleximeter finger above and parallel to

the expected upper border of liver dullness, percuss
in progressive steps downward in the right
midclavicular line. Identify the upper border of liver
dullness. Later, during the abdominal examination,
you will use this method to estimate the size of the
liver. As you percuss down the chest on the left, the
resonance of normal lung usually changes to the
tympany of the gastric air bubble.

56
TOPIC 19. PERCUSSION OF THE CHEST
– PATHOLOGICAL CHANGES.

POSTERIOR CHEST

PATHOLOGICAL CHANGES – SOUND

Dullness replaces resonance when fluid or solid tissue replaces air- containing lung or
occupies the pleural space beneath your percussing fingers. Examples include: lobar
pneumonia, in which the alveoli are filled with fluid and blood cells; and pleural
accumulations of serous fluid (pleural effusion), blood (hemothorax), pus (empyema), fibrous
tissue, or tumor. Dullness makes pneumonic and pleural effusion 5 and 18 times more likely,
respectively.

Generalized hyperresonance may be heard over the hyperinflated lungs of COPD or asthma.
Unilateral hyperresonance suggests a large pneumothorax or possibly a large air-filled bulla
in the lung.

PATHOLOGICAL CHANGEES – DIAPHRAGMATIC EXCURSION

An abnormally high level suggests pleural effusion, or a high diaphragm as in atelectasis

or phrenic nerve paralysis.

57
 ANTERIOR CHEST

PATHOLOGICAL CHANGES – SOUND

Dullness replaces resonance when fluid or solid

tissue replaces air-containing lung or occupies the
pleural space. Because pleural fluid usually sinks to
the lowest part of the pleural space (posteriorly in a
supine patient), only a very large effusion can be
detected anteriorly.

The hyperresonance of COPD may totally replace

cardiac dullness.

In a woman:

The dullness of right middle lobe pneumonia

typically occurs behind the right breast. Unless you
displace the breast, you may miss the abnormal
percussion note.

PATHOLOGICAL CHANGES – LIVER POSITION

A lung affected by COPD often displaces the upper

border of the liver downward and lowers the level
of diaphragmatic dullness posteriorly.

58
 TOPIC 20. AUSCULTATION OF THE
LUNGS (BREATH SOUNDS) –
MECHANISM OF FORMATION.

AUSCULTATION

ANTERIOR CHEST

Auscultation involves:

(1) listening to the sounds generated by breathing,

(2) listening for any adventitious (added) sounds,

(3) if abnormalities are suspected, listening to the sounds of the patient’s spoken or
whispered voice as they are transmitted through the chest wall.

PATTERN FOR AUSCULTATION

POSTERIOR CHEST

Listen to the chest anteriorly and laterally as the patient breathes with mouth open, and
somewhat more deeply than normal. Compare symmetric areas of the lungs, using the pattern
suggested for percussion and extending it to adjacent areas if indicated.
59
Listen to the breath sounds, noting their intensity and identifying any variations from normal
vesicular breathing. Breath sounds are usually louder in the upper anterior lung fields.
Broncho-vesicular breath sounds may be heard over the large airways, especially on the right.

Identify any adventitious sounds, time them in the respiratory cycle, and locate them on the
chest wall. If indicated, listen for transmitted voice sounds.

BREATH SOUNDS

NORMAL BREATH SOUNDS

INTENSITY LOCATIONS
DURATION PITCH OF
OF WHERE
OF THE EXPIRATORY
EXPIRATORY HEARD
SOUNDS SOUND
SOUND NORMALLY
Inspiratory
sounds last
Over most of
longer than Soft Relatively low
both lungs
expiratory
sounds.
Often in the 1st
Inspiratory and and 2nd
expiratory interspaces
Intermediate Intermediate
sounds are anteriorly and
about equal. between the
scapulae
Expiratory Over the
sounds last manubrium,
longer than Loud Relatively high (larger
inspiratory proximal
ones. airways)
Inspiratory and
Over the
expiratory
Very loud Relatively high trachea in the
sounds are
neck
about equal.

60
MECHANISM OF FORMATION

61
 TOPIC 21. AUSCULTATION OF THE
LUNGS (ADDED SOUNDS) –
MECHANISM OF FORMATION.

AUSCULTATION OF THE LUNGS

ANTERIOR CHEST

Auscultation involves:

1. listening to the sounds generated by breathing,

2. listening for any adventitious (added) sounds,
3. if abnormalities are suspected, listening to the sounds of the patient’s spoken or
whispered voice as they are transmitted through the chest wall.

PATTERN FOR AUSCULTATION

POSTERIOR CHEST

Listen to the chest anteriorly and laterally as the patient breathes with mouth open, and
somewhat more deeply than normal. Compare symmetric areas of the lungs, using the pattern
suggested for percussion and extending it to adjacent areas if indicated.
62
Listen to the breath sounds, noting their intensity and identifying any variations from normal
vesicular breathing. Breath sounds are usually louder in the upper anterior lung fields.
Bronchovesicular breath sounds may be heard over the large airways, especially on the right.

Identify any adventitious sounds, time them in the respiratory cycle, and locate them on the
chest wall. If indicated, listen for transmitted voice sounds.

ADDED (ADVENTITIOUS) SOUNDS

CRACKLES (OR RALES) WHEEZES AND RHONCHI

Discontinuous Continuous
≥250 msec, musical, prolonged
Intermittent, nonmusical, and
(but not necessarily persisting
brief
throughout the respiratory cycle)
Like dots in time Like dashes in time
Fine crackles: soft, high-pitched, very brief Wheezes: relatively high-pitched
(5–10 msec) (≥400 Hz) with hissing or shrill quality
Coarse crackles: somewhat louder, lower in Rhonchi: relatively low-pitched (≤200 Hz)
pitch, brief (20–30 msec) with snoring quality

MECHANISM OF FORMATION

CRACKLES

Crackles have two leading explanations:

• They result from a series of tiny explosions when small airways, deflated during
expiration, pop open during inspiration.
o This mechanism probably explains the late inspiratory crackles of interstitial
lung disease and early heart failure.
• Crackles result from air bubbles flowing through secretions or lightly closed airways
during respiration.
o This mechanism probably explains at least some coarse crackles.

63
LATE INSPIRATION CRACKLES

• May begin in the first half of inspiration but must continue into late inspiration
• Usually fine, fairly profuse, and persist from breath to breath
• Appear first at the bases of the lungs, spread upward as the condition worsens, and
shift to dependent regions with changes in posture.
• Causes include:
o Interstitial lung disease (such as pulmonary fibrosis)
o Early heart failure.

EARLY INSPIRATION CRACKLES

• Appear and end soon after the start of inspiration

• Often coarse and relatively few in number
• Expiratory crackles are sometimes associated
• Causes include:
o Chronic bronchitis
o Asthma

MIDINSPIRATORY CRACKLES

• Midinspiratory and expiratory crackles are heard in bronchiectasis but are not specific
for this diagnosis.
• Wheezes and rhonchi may be associated.

WHEEZES AND RHONCHI

Wheezes occur when air flows rapidly through bronchi that are narrowed nearly to the point
of closure.

• They are often audible at the mouth as well as through the chest wall.
• Causes of wheezes throughout the chest include asthma, chronic bronchitis, COPD,
and heart failure (cardiac asthma).
o In asthma, wheezes may be heard only in expiration or in both phases of the
respiratory cycle.

64
Rhonchi suggest secretions in the larger airways.

• In chronic bronchitis, wheezes and rhonchi often clear with coughing.

Occasionally in severe obstructive pulmonary disease, the patient is unable to force enough
air through the narrowed bronchi to produce wheezing → silent chest → immediate attention.

Persistent localized wheezing suggests partial obstruction of a bronchus, seen with a tumor or
foreign body. It may be inspiratory, expiratory, or both.

STRIDOR

• Wheeze that is entirely or predominantly inspiratory

• Often louder in the neck than over the chest wall
• Indicates a partial obstruction of the larynx/trachea and demands immediate attention.

PLEURAL RUB

• Inflamed and roughened pleural surfaces grate against each other as they are
momentarily and repeatedly delayed by increased friction.
o These movements produce creaking sounds known as a pleural rub (or pleural
friction rub), usually during expiration.
• Resemble crackles acoustically, although they are produced by different pathologic
processes.
• The sounds may be discrete, but sometimes are so numerous that they merge into a
seemingly continuous sound.
• Usually confined to a relatively small area of the chest wall, and typically is heard in
both phases of respiration.
• When inflamed pleural surfaces are separated by fluid, the rub often disappears.

MEDIASTINAL CRUNCH

• Series of precordial crackles synchronous with the heartbeat, not with respiration.
• Best heard in the left lateral position→ due to mediastinal emphysema
(pneumomediastinum).
65
TOPIC 22. LUNG FUNCTION TESTING –
VENTILATORY CAPACITIES; LUNG
VOLUMES; BLOOD GASES –
PATHOLOGICAL CHANGES IN
DIFFERENT LUNG DISEASES.

LUNG FUNCTION TESTING

Respiratory function tests are used to aid diagnosis, assess functional impairment, and
monitor treatment or progression of disease.

Airway narrowing, lung volume and gas exchange capacity are quantified and compared with
normal values adjusted for age, gender, height and ethnic origin.

• In diseases characterized by airway narrowing (e.g. asthma, bronchitis and

emphysema), maximum expiratory flow is limited by dynamic compression of small
intrathoracic airways, some of which may close completely during expiration, limiting
the volume that can be expired (‘obstructive’ defect).
o Hyperinflation of the chest results and can become extreme if elastic recoil is
also lost due to parenchymal destruction, as in emphysema.
• In contrast, diseases that cause interstitial inflammation and/or fibrosis lead to
progressive loss of lung volume (‘restrictive’ defect) with normal expiratory flow
rates.

VENTILATORY CAPACITIES

Ventilation involves the delivery of gas to the alveoli → Pulmonary function tests are used to
assess ventilatory function.

To distinguish large airway narrowing (e.g. tracheal stenosis or compression) from small
airway narrowing, flow/volume loops are recorded using spirometry.

• Spirometry involves forced exhalation from total lung capacity (TLC) to residual
volume (RV); key measurements from a spirogram are the forced expiratory volume
in 1 s (FEV1) and the forced vital capacity (FVC).

66
Expiratory flow rates may be plotted against lung volumes to yield a flow-volume curve.

LUNG VOLUMES

Lung volumes can be measured by spirometry.

67
BLOOD GASES

DISTURBANCE IN PULMONARY CIRCULATION

The pulmonary vasculature normally handles the right ventricular output (~5 L/min) at a low
pressure.

• Normal mean pulmonary artery pressure (PAP) is 15 mmHg.

• When cardiac output increases, pulmonary vascular resistance (PVR) normally falls,
leading to only small increases in mean PAP.

Assessment of the pulmonary vasculature requires measuring pulmonary vascular pressures

and cardiac output to derive PVR.

• PVR rises with hypoxemia (due to vasoconstriction), intraluminal thrombi (due to

diminished cross-sectional area from obstruction), or destruction of small pulmonary
vessels (due to scarring or loss of the alveolar walls).

DISTURBANCE IN GAS EXCHANGE

The primary functions of the respiratory system are to remove CO2 from blood entering the
pulmonary circulation and to provide O2 to blood leaving the pulmonary circulation.

• Normal tidal volume is approximately 500 mL and normal respiratory rate is

approximately 15 breaths/min, leading to a total minute ventilation of approximately
7.5 L/min.
• Because of anatomic dead space, alveolar ventilation is approximately 5 L/min.
• Gas exchange depends on alveolar ventilation rather than total minute ventilation.

Partial pressure of CO in arterial blood → PaCO2 = 0.863 × VCO2/V A

• VCO2 – Amount of CO2 produced each minute

• VA – Alveolar ventilation

Assessment of gas exchange is commonly performed with arterial blood gases, which provide
measurements of the partial pressures of O2 and CO2.

68
 • The actual content of O2 in blood is determined by both PO2 and hemoglobin
concentration.
• In order to calculate the (A-a) gradient, the alveolar PO2 (PaCO2) must be calculated:

PaO2 = [FIO2 × (PB – PH2O)] – (PaCO2/R)

FIO2 – fractional concentration of inspired O2 (0.21 while breathing room air)
PB – barometric pressure (760 mmHg at sea level)
PH2O – water vapor pressure (47 mmHg when air is saturated at 37°C [98.6°F])
R – respiratory quotient (the ratio of CO2 production to O2 consumption, usually assumed to be 0.8)

The measurement of hydrogen ion concentration, PaO2 and PaCO2, and derived bicarbonate
concentration in an arterial blood sample is essential to assess the degree and type of
respiratory failure, and for measuring acid-base status.

TRANSFER FACTOR

To measure the capacity of the lungs to exchange gas, patients inhale a test mixture of 0.3%
carbon monoxide, which is taken up avidly by hemoglobin in pulmonary capillaries.

After a short breath-hold, the rate of disappearance of CO into the circulation is calculated
from a sample of expiate and expressed as the TLCO or carbon monoxide transfer factor.

Helium is also included in the test breath to allow calculation of the volume of lung examined
by the test breath.

• Transfer factor expressed per unit lung volume is termed KCO.

69
 PATHOLOGICAL CHANGES IN DIFFERENT LUNG
DISEASES.

ALTERATION OF RESPIRATORY FUNCTION (BY DIAGNOSIS CATEGORIES)

ALTERATION IN RESPIRATORY FUNCTION (MOST COMMON DISEASES)

FEV1 – Force Expiratory Volume KCO – Transfer factor

FVC – forced vital capacity TLC – Total Lung Capacity
VC – Vital capacity RV – Residual volume
TLCO – Carbon monoxide transfer N – normal
factor

70
 TOPIC 23. PLEURAL ASPIRATION AND
EXAMINATION OF THE PLEURAL
FLUID.

Core biopsy of the pleura, guided by either ultrasound or CT, has largely replaced the
traditional ‘blind’ method of pleural biopsy using an Abram’s needle.

Thoracoscopy, which involves the insertion of an endoscope through the chest wall,
facilitates biopsy under direct vision and is performed by many surgeons and an increasing
number of physicians.

• This is particularly important in suspected malignancy or in characterizing the

pathological changes in interstitial lung disease.
• Important causative organisms, such as M. tuberculosis, Pneumocystis jirovecii or
fungi, may be identified in bronchial washings, brushings or transbronchial biopsies.

Cytological examination of exfoliated cells in pleural fluid or bronchial brushings and

washings, or of fine needle aspirates from lymph nodes or pulmonary lesions, can support
a diagnosis of malignancy but, if this is indeterminate, a larger tissue biopsy is often
necessary.

71
 TOPIC 24. ACUTE CIRCULATORY
FAILURE – SHOCK, SYNCOPE, SUDDEN
DEATH.

SHOCK

DEFINITION

Condition of severe impairment of tissue perfusion leading to cellular injury and dysfunction.

CLINICAL MANIFESTATIONS

× Hypotension (mean arterial bp <60 mmHg), tachycardia, tachypnea, pallor, rest-

lessness, and altered sensorium.

× Signs of intense peripheral vasoconstriction, with weak pulses and cold clammy
extremities. In distributive (e.g., septic) shock, vasodilation predominates and
extremities are warm.

× Oliguria (<20 mL/h) and metabolic acidosis common.

× Acute lung injury and acute respiratory distress syndrome (ARDS) with

noncardiogenic pulmonary edema, hypoxemia, and diffuse pulmonary infiltrates.

CATEGORIES OF SHOCK

• Hypovolemic shock
o Hemorrhage
o Intravascular volume depletion (vomiting, diarrhea…)
o Internal sequestration (ascites, pancreatitis…)
• Cardiogenic shock
o Myopathic (acute MI, fulminant myocarditis)
o Mechanical (acute mitral regurgitation, ventricular septal defect…)
o Arrhythmic
72
 • Extracardiac obstructive shock
o Pericardial tamponade
o Massive pulmonary embolism
o Tension pneumothorax
• Distributive shock = profound decrease in systemic vascular tone
o Septic shock
o Toxic overdoses
o Anaphylaxis
o Neurogenic shock (e.g. in spinal cord injury)
o Endocrinologic shock (Addison’s disease, myxedema)

PHYSICAL EXAMINATION

• Jugular veins:
o Flat → oligemic or distributive (septic) shock
o Jugular venous distention (JVD) → cardiogenic shock
o JVD in presence of paradoxical pulse → cardiac tamponade
• Check for asymmetry of pulses
• Assess for evidence of heart failure, murmurs of aortic stenosis, acute mitral or aortic
regurgitation, and ventricular septal defect
• Tenderness or rebound in abdomen may indicate peritonitis or pancreatitis
• High-pitched bowel sounds suggest intestinal obstruction.
• Perform stool guaiac to rule out GI bleeding.

Septic shock:

• Fever and chills typically accompany septic shock.

o Sepsis may not cause fever in elderly, uremic, or alcoholic pts.
• Skin lesions may suggest specific pathogens in septic shock: petechiae or purpura
(Neisseria meningitidis or Haemophilus influenzae), ecthyma gangrenosum
(Pseudomonas aeruginosa), generalized erythroderma (toxic shock due to
Staphylococcus aureus or Streptococcus pyogenes).

73
LABORATORY DIAGNOSIS

CVP – Central venous pressure

PCWP – Pulmonary Capillary Wedge Pressure

SYNCOPE

DEFINITION

Syncope is a transient, self-limited loss of consciousness due to acute global impairment of

cerebral blood flow.

It may occur suddenly, without warning, or may be preceded by presyncopal symptoms such
as light-headedness or faintness, weakness, fatigue, nausea, dimming vision, ringing in ears,
or sweating.

ETIOLOGY

• Neurally mediated syncope

o Vasovagal syncope
§ Provoked fear, pain, anxiety intense emotion, sight of blood, unpleasant
sights and odors, orthostatic stress.

74
 o Situational reflex syncope
§ Pulmonary:
• Cough syncope
• Wind instrument player’s syncope
• Weightlifter’s syncope
• “Mess trick” and “Finting lark”
• Sneeze syncope
• Airway instrumentation
§ Urogenital:
• Postmicturition syncope
• Urogenital tract instrumentation
• Prostatic massage
§ Gastrointestinal:
• Swallow syncope
• Glossopharyngeal neuralgia
• Esophageal stimulation
• Gastrointestinal tract instrumentation
• Rectal examination
• Defection syncope
§ Cardiac:
• Bezold-Jarisch reflex
• Cardiac outflow obstruction
§ Ocular:
• Ocular pressure
• Ocular examination
• Ocular surgery

• Orthostatic hypotension
o Primary autonomic failure due to idiopathic central and peripheral
neurodegenerative diseases – the “synucleinopathies”
§ Lewy body diseases:
• Parkinon’s disease
• Lewy body dementia
• Pure autonomic failure
§ Multiple system atrophy (the Shy-Drager syndrome)

o Secondary autonomic failure due to autonomic peripheral neuropathies

§ Diabetes
75
 § Hereditary amyloidosis
§ Idiopathic immune-mediated autonomic neuropathy
§ HIV neuropathy
§ Sjögren’s syndrome

o Postprandial hypotension

o Iatrogenic (drug-induced)

o Volume depletion

• Cardiac syncope
o Arrhythmias
§ Sinus node dysfunction
§ Atrioventricular dysfunction
§ Ventricular tachycardia
§ Inherited channelopathies

o Cardiac structural disease

§ Valvular disease
§ Myocardial ischemia
§ Obstructive and other cardiomyopathies
§ Atrial myxoma
§ Pericardial effusions and tamponade
•

SUDDEN DEATH

Unexpected cardiovascular collapse and death most often result from ventricular fibrillation
in pts with acute or chronic atherosclerotic coronary artery disease.

Arrhythmic causes may be provoked by electrolyte disorders (primarily hypokalemia),

hypoxemia, acidosis, or massive sympathetic discharge, as may occur in CNS injury.
Immediate institution of cardiopulmonary resuscitation (CPR) followed by advanced life
support measures (see below) is mandatory. Ventricular fibrillation, or asystole, without
institution of CPR within 4–6 min is usually fatal.

76
CONTRIBUTORY FACTORS

• Structural associations and causes

o Coronary heart disease
o Myocardial hypertrophy
o Dilated cardiomyopathy
o Inflammatory or infiltrative disorders
o Valvular heart diseases
o Electrophysiological abnormalities
o Inherited disorders associated with electrophysiological abnormalities

• Functional contributing factors

o Transient ischemia
o Low cardiac output states (heart failure, shock)
o Systemic metabolic abnormalities:
§ Electrolyte imbalance
§ Hypoxemia
§ Acidosis
o Neurologic disorders
o Toxic responses:
§ Proarrhythmic drug effects
§ Cardiac toxins

77
 TOPIC 25. HYPERTENSION.
MEASUREMENT OF BLOOD PRESSURE.

HYPERTENSION

Hypertension, or high blood pressure, is probably the most common of all cardiovascular
disorders.

Blood Pressure Classification SBP DBR

Normal 120-129 80-84

Prehypertension 130-139 85-89

Stage I 140-159 90-99

Stage II 160-179 100-109

Stage III ≥180 ≥110

CLASSIFICATION

Hypertension is divided into:

• Primary (essential) hypertension = 80 – 90% cases→ the chronic elevation in blood

pressure occurs without evidence of other disease
• Secondary (symptomatic) hypertension = 10 – 20% cases → the elevation of blood
pressure results from some other disorder, such as kidney disease
Malignant hypertension, as the name implies, is an accelerated form of hypertension.

EPIDEMIOLOGY

“Rule of half”

• About 50% of people do not know about an increase of their blood pressure!!!
o Of those who know → 50% are untreated!
• Thus, only about 25 % of patients taking medications to lower blood pressure.
o Effective antihypertensive therapy → only 12-13 % of patients.

78
REGULATION OF ARTERIAL PRESSURE

MECHANISMS OF BLOOD PRESSURE ELEVATION

79
 MEASUREMENT OF BLOOD PRESSURE

STEPS TO ENSURE ACCURATE BLOOD PRESSURE MEASUREMENT

• In ideal situations, instruct the patient to avoid smoking or drinking caffeinated

beverages for 30 minutes before the blood pressure is measured.
• Check to make sure the examining room is quiet and comfortably warm.
• Ask the patient to sit quietly for at least 5 minutes in a chair with feet on the floor,
rather than on the examining table.
• Make sure the arm selected is free of clothing.
o There should be no arteriovenous fistulas for dialysis, scarring from prior
brachial artery cut-downs, or signs of lymphedema (seen after axillary node
dissection or radiation therapy).
• Palpate the brachial artery to confirm that it has a viable pulse.
• Position the arm so that the brachial artery, at the antecubital crease, is at heart level
roughly level with the 4th interspace at its junction with the sternum.
• If the patient is seated, rest the arm on a table a little above the patient’s waist; if
standing, try to support the patient’s arm at the mid-chest level.

MEASURING OF BLOOD PRESSURE

80
 TOPIC 26. HEART FAILURE –
PATHOPHYSIOLOGY. TYPES OF
HEART FAILURE.

HEART FAILURE

HEART FAILURE → heart is unable to generate an adequate cardiac output, causing

inadequate perfusion of tissues or increased diastolic filling pressure of the left ventricle, or
both → pulmonary capillary pressures are increased.

EPIDEMIOLOGY

• It affects nearly 10% of individuals older than age 65 and is the most common reason
for admission to the hospital in that age group.

PREDISPOSING RISK FACTORS

• Ischemic heart disease and hypertension → most important

• Others: age, obesity, diabetes, renal failure, valvular heart disease, cardiomyopathies,
myocarditis, congenital heart disease, and excessive alcohol use.
• Genetics:
o Numerous genetic polymorphisms have been linked to an increased risk for
heart failure, including genes for cardiomyopathies, myocyte contractility, and
neurohumoral receptors.
o Recently, genetic changes in kinases, phosphatases, and cellular calcium
cycling are being explored.

CLASSIFICATION

Heart failure has been classified according to the side of the heart (right ventricular or left
ventricular) that is primarily affected.

Although the initial event that leads to heart failure may be primarily right or left ventricular
in origin, long-term heart failure usually involves both sides.
81
COMPENSATORY MECHANISMS

In heart failure, the cardiac reserve is largely maintained through compensatory mechanisms,
the most important of which are:

• Frank - Starling mechanism

• Increased sympathetic nervous system activity
• Renin-angiotensin mechanism
• Atrial natriuretic peptide
• Myocardial hypertrophy

The healthy and the failing heart may use the same compensatory mechanisms. In the failing
heart, early decreases in cardiac function may go unnoticed because these compensatory
mechanisms maintain the cardiac output. This state is called compensated heart failure.

Unfortunately, these mechanisms were not intended for long-term use. In severe and
prolonged decompensated heart failure, the compensatory mechanisms may themselves
worsen the failure.

82
 TYPES OF HEART FAILURE

LEFT -SIDED HEART FAILURE

The left side of the heart pumps blood from the low-pressure pulmonary circulation into the
high-pressure arterial side of the systemic circulation.

With impairment of left heart function, there is a decrease in cardiac output; an increase in
left atrial and left ventricular end-diastolic pressures; and congestion in the pulmonary
circulation.

When the pulmonary capillary pressure (normally about 10 mm Hg) exceeds the capillary
osmotic pressure (normally about 25 mm Hg), there is a shift of intravascular fluid into the
interstitium of the lung and development of pulmonary edema.

RIGHT SIDED HEART FAILURE

The right heart pumps deoxygenated blood from the systemic circulation into the pulmonary
circulation.

Consequently, when the right heart fails, there is accumulation or damming back of blood in
the systemic venous system.

• This causes an increase in right atrial, right ventricular end-diastolic, and systemic
venous pressures.
• The clinical result is manifested in development of edema in the peripheral tissues and
congestion of the abdominal organs.

Cor pulmonale → right ventricular enlargement (hypertrophy, dilation, or both) caused by

pulmonary hypertension.

HIGH-OUTPUT FAILURE

Inability of the heart to adequately supply the body with blood-borne nutrients, despite
adequate blood volume and normal or elevated myocardial contractility.

83
84
 TOPIC 27. LEFT-SIDED HEART
FAILURE – CLINICAL FEATURES.

The left side of the heart normally pumps blood from the low-pressure pulmonary circulation
into the high-pressure arterial side of the systemic circulation → left-sided heart failure
impairs it.

With impairment of left heart function:

• Decrease in cardiac output to the systemic circulation.

• Blood accumulates in the left ventricle, left atrium, and pulmonary circulation →
elevation in pulmonary venous pressure

pressure in the pulmonary capillaries (normally approximately 10 mm Hg) >

capillary osmotic pressure (normally approximately 25 mm Hg)
→ there is a shift of intravascular fluid into the interstitium of the lung →
development of pulmonary edema

85
CAUSES

The most common causes of left ventricular dysfunction are:

• Hypertension
• Acute myocardial infarction
o LVHF + Pulmonary congestion → develop very rapidly in people with acute
myocardial infarction.
o Even when the infarcted area is small, there may be a surrounding area of
ischemic tissue → may result in large areas of ventricular wall hypokinesis or
akinesis → rapid onset of pulmonary congestion and edema

Stenosis or regurgitation of the aortic or mitral valve also creates the level of left-sided
backflow that results in pulmonary congestion.

• As pulmonary pressure rises as a result of congestion, it may progress to produce right-

sided heart failure.

MANIFESTATIONS

• Dyspnea
• Orthopnea-shortness of breath occurs when a person is supine
• Cough
• Blood - tinged sputum
• Cyanosis
• Elevation in pulmonary capillary wedge pressure
• Pulmonary edema
→ occurs at night, after the person has been reclining for some time and the
gravitational forces have been removed from the circulatory system
→ edema fluid that had been sequestered in the lower extremities during the
day is returned to the vascular compartment and redistributed to the pulmonary
circulation

86
87
 TOPIC 28. RIGHT-SIDED HEART
FAILURE – CLINICAL FEATURES.

The right heart pumps deoxygenated blood from the systemic circulation into the pulmonary
circulation → light-sided heart failure impairs it.

When the right heart fails:

• Reduction in the amount of blood moved forward into the pulmonary circulation
and then into the left side of the heart → reduction of left ventricular cardiac
output.
• Acumulation or damming back of blood in the systemic venuos system. This causes:
o increase in right atrial pressure
o right ventricular end-diastolic pressure
• systemic venous pressure

The clinical result (major effect) is manifested in development of:

• Edema in the peripheral tissues

o More pronounced in the dependent part of the body:
§ When in upright position → lower extremities
§ When supine position → area over sacrum
o Accumulation of fluid → evidenced by a gain of weight
• Congestion of the abdominal organs
o Liver congestion → hepatomegaly and pain.
o Spleen engorgement → ascites
o GIT congestion → anorexia and abdominal discomfort

CAUSES

The causes of right ventricular dysfunction include conditions that impede blood flow into
the lungs or compromise the pumping effectiveness of the right ventricle.

• Left ventricular failure → most common

• Sustained pulmonary hypertension
o It occurs in patients with: chronic pulmonary disease, severe pneumonia,
pulmonary embolus, or aortic or mitral stenosis.
o When it occurs from chronic pulmonary disease → cor pulmonale.
88
 • Other common causes include stenosis or regurgitation of the tricuspid or pulmonic
valves, right ventricular infarction, and cardiomyopathy.
• It is also caused by congenital heart defects → tetralogy of Fallot and ventricular
septal defect.

MANIFESTATIONS

• Fatigue
• Dependent edema
• Distention of the jugular veins
• Liver engorgement
• Ascites
• Anorexia and complaints of gastrointestinal distress
• Cyanosis
• Elevation in peripheral venous pressure

89
 TOPIC 29. SUPRAVENTRICULAR
ARRHYTHMIAS – SINUS, ATRIAL AND
JUNCTIONAL.

90
TOPIC 30. VENTRICULAR
TACHYARRHYTMIAS.

91
 TOPIC 31. DISORDERS OF
CONDUCTION – TYPES OF HEART
BLOCKS.

92
 TOPIC 32. INSPECTION AND
PALPATION OF THE PRAECORDIUM –
POSSIBLE PATHOLOGICAL FINDINGS.

93
 TOPIC 33. AUSCULTATION OF THE
HEART – MECHANISM OF FORMATION
OF THE HEART SOUNDS.

AUSCULTATION OF THE HEART

In a quiet room, listen to the heart with your stethoscope, starting at either the base or apex.
Either pattern is satisfactory:

• Some experts recommend starting at the apex and inching to the base: Move the
stethoscope from the PMI medially to the left sternal border, superiorly to the 2nd
interspace, then across the sternum to the 2nd interspace at the right sternal border.
• Alternatively, you can start at the base and inch your stethoscope to the apex: with
your stethoscope in the right 2nd interspace close to the sternum, move along the left
sternal border in each interspace from the 2nd through the 5th, and then to the apex.

TIMING S 1 AND S 2

Regardless of the direction you move your stethoscope, keep your left index and middle
fingers on the right carotid artery in the lower third of the neck to facilitate correct
identification of S1, just before the carotid upstroke, and S2, which follows the carotid
upstroke. Be sure to compare the intensities of S1 and S2 as you move your stethoscope
through the listening areas above.
94
 • At the base, you will note that S2 is louder than S1 and may split with respiration. At
the apex, S1 is usually louder than S2 unless the PR interval is prolonged.
o By carefully noting the intensities of S1 and S2, you will confirm each of these
sounds and thereby correctly identify systole, the interval between S1 and S2,
and diastole, the interval between S2 and S1.

As you will observe when listening to the extra sounds of S3 and S4 and to murmurs, timing
systole and diastole is an absolute prerequisite to the correct identification of these events in
the cardiac cycle.

MECHANISM OF FORMATION OF THE HEART SOUNDS.

Right-sided events usually occur slightly later than those on the left. Instead of a single heart
sound, you may hear two discernible components, the first from left-sided aortic valve
closure, or A2, and the second from right-sided closure of the pulmonic valve, or P2.

Consider the second heart sound, S2, and its two components, A2 and P2, caused primarily by
closure of the aortic and pulmonic valves, respectively.

• During inspiration, the right heart filling time is increased, which increases right
ventricular stroke volume and the duration of right ventricular ejection compared with
the neighboring left ventricle.
o This delays the closure of the pulmonic valve, P2, splitting S2 into its two
audible components.

95
 • During expiration, these two components fuse into a single sound, S2. Note that
because walls of veins contain less smooth muscle, the venous system has more
capacitance than the arterial system and lower systemic pressure.
o Distensibility and impedance in the pulmonary vascular bed contribute to the
“hangout time” that delays P2.

Of the two components of the S2:

• A2 is normally louder, reflecting the high pressure in the aorta. It is heard throughout
the precordium.
• P2, in contrast, is relatively soft, reflecting the lower pressure in the pulmonary artery.
o It is heard best in its own area, the 2nd and 3rd left interspaces close to the
sternum. It is here that you should search for the splitting of S2.

S1 also has two components, an earlier mitral and a later tricuspid sound.

• The mitral sound, its principal component, is much louder, again reflecting the high
pressures on the left side of the heart. It can be heard throughout the precordium and
is loudest at the cardiac apex.
• The softer tricuspid component is heard best at the lower left sternal border; it is here
that you may hear a split S1.

The earlier, louder mitral component may mask the tricuspid sound, however, and splitting is
not always detectable.

• Splitting of S1 does not vary with respiration.

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TOPIC 34. ABNORMAL HEART SOUNDS
AND MURMURS – TYPES AND
MECHANISM OF FORMATION.

ABNORMAL HEART SOUNDS AND MURMURS

Heart murmurs are distinguishable from heart sounds by their longer duration.

• They are attributed to turbulent blood flow and may be diagnostic of valvular heart
disease, or “innocent” flow murmurs, especially in young adults.

A stenotic valve has an abnormally narrowed valvular orifice that obstructs blood flow, as in
aortic stenosis, and causes a characteristic murmur.

So does a valve that fails to fully close, as in aortic regurgitation or insufficiency.

• It allows blood to leak backward → regurgitant murmur.

TYPES AND MECHANISMS OF FORMATION

BY TIMING

A midsystolic murmur begins after S1 and stops before S2. Brief gaps are audible between
the murmur and the heart sounds. Listen carefully for the gap just before S2. It is heard more
easily and, if present, usually confirms the murmur as midsystolic, not pansystolic.

A pansystolic (holosystolic) murmur starts with S1 and stops at S2, with- out a gap between
murmur and heart sounds.

97
A late systolic murmur usually starts in mid- or late systole and persists up to S2.

An early diastolic murmur starts immediately after S2, without a discernible gap, and then
usually fades into silence before the next S1.

A middiastolic murmur starts a short time after S2. It may fade away, as illustrated, or merge
into a late diastolic murmur.

A late diastolic (presystolic) murmur starts late in diastole and typically continues up to S1.

A continuous murmur begins in systole and extends into all or part of diastole.

98
BY SHAPE

A crescendo murmur grows louder.

A decrescendo murmur grows softer.

A crescendo–decrescendo murmur first rises in intensity, then falls.

A plateau murmur has the same intensity throughout.

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BY INTENSITY

GRADATIONS OF MURMURS
GRADE DESCRIPTION
Very faint, heard only after listener has “tuned in”; may not be heard in all
Grade 1
positions
Grade 2 Quiet, but heard immediately after placing the stethoscope on the chest
Grade 3 Moderately loud
Grade 4 Loud, with palpable thrill
Very loud, with thrill. May be heard when the stethoscope is partly off the
Grade 5
chest
Grade 6 Very loud, with thrill. May be heard with stethoscope entirely off the chest

BY PITCH

• High
• Medium
• Low

BY QUALITY

• Harsh
• Rumbling
• Musical

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TOPIC 35. DIFFERENTIAL DIAGNOSIS
BETWEEN FUNCTIONAL AND
ORGANIC CARDIAC MURMURS.

101
TOPIC 36. PHYSICAL EXAMINATION
OF THE ARTERIES AND ARTERIAL
PULSES.

102
TOPIC 37. PHYSICAL EXAMINATION
OF THE VEINS AND VENOUS PULS.

103
TOPIC 38. ELECTROCARDIOGRAPHY –
NORMAL ECG. METHOD OF READING
AND INTERPRETING THE ECG.

104
 TOPIC 39. FUNCTIONAL AND OTHER
METHODS FOR EXAMINATION OF THE
HEART.

ECHOCARDIOGRAPHY

Visualizes heart in real time with ultrasound; Doppler recordings noninvasively assess
hemodynamics and abnormal flow patterns. Imaging may be compromised in pts with chronic
obstructive lung disease, thick chest wall, or narrow intercostal spaces.

CHAMBER SIZE AND VENTRICULAR PERFORMANCE

Assessment of atrial and ventricular dimensions, global and regional systolic wall motion
abnormalities, ventricular hypertrophy/infiltration, evaluation for pulmonary hypertension:
RV systolic pressure (RVSP) is calculated from maximum velocity of tricuspid regurgitation
(TR):

RVSP = 4 × (TR velocity)2 + RA pressure

CLINICAL USES OF ECHOCARDIOGRAPHY

Transesophageal Doppler Stress

2-D Echo
Echocardiography Echocardiography Echocardiography
Cardiac chambers:
size, hypertrophy, Superior to 2-D echo to Valvular stenosis and
wall motion identify: regurgitation
abnormalities
Valves:
morphology and Infective endocarditis Intracardiac shunts
Assess myocardial
motion
ischemia and viability
Pericardium: Cardiac source of Diastolic
effusion, tamponade embolism filling/dysfunction
Aorta: aneurysm, Prosthetic valve Approximate
dissection dysfunction intracardiac pressures
Assess intracardiac
Aortic dissection
masses
105
 NUCLEAR CARDIOLOGY

Uses nuclear isotopes to assess LV perfusion and contractile function.

VENTRICULAR FUNCTION ASSESSMENT

Contractile function can be assessed during gated single-photon emission computed

tomography (SPECT) myocardial perfusion exercise test imaging. Occasionally, blood pool
imaging is obtained by injecting IV 99m Tc-labeled albumin or RBCs to quantify LV ejection
fraction.

NUCLEAR MYOCARDIAL PERFUSION ASSESSMENT

SPECT imaging, most commonly using 99m Tc-labeled compounds (sestamibi or

tetrofosmin), or PET imaging (82Rb or 13NH3), obtained at peak stress and at rest, depicts
zones of prior infarction as fixed defects and regions of inducible myocardial ischemia as
reversible defects.

Nuclear imaging is more sensitive, but less specific, than stress echocardiography for
detection of ischemia.

For pts who cannot exercise, pharmacologic perfusion imaging with adenosine,
regadenoson, dipyridamole, or dobutamine is used instead.

• For pts with LBBB, perfusion imaging with adenosine or dipyridamole is preferred to
avoid artifactual septal defects that are common with exercise imaging.

Pharmacologic PET scanning is especially useful in imaging obese pts and to assess
myocardial viability. Thallium-201 SPECT imaging can also be utilized to assess viability.

MAGNETIC RESONANCE IMAGING

Delineates cardiac structures with high resolution without ionizing radiation.

Excellent technique to quantitate LV mass, to characterize the pericardium, great vessels,

anatomic relationships in congenital heart disease, abnormal cardiac masses, and to evaluate
valvular heart disease as a complement to echocardiography.

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MRI with delayed gadolinium enhancement (avoid in pts with renal insufficiency)
differentiates ischemic from nonischemic cardiomyopathy and is useful in assessing
myocardial viability.

Pharmacologic stress testing with MR identifies significant CAD and detects subendocardial
ischemia with higher sensitivity than SPECT imaging.

COMPUTED TOMOGRAPHY

Provides high-resolution images of cardiac structures (including the pericardium and cardiac
masses) and detects coronary calcification in atherosclerosis with high sensitivity.

• CT angiography (CTA) delineates abnormalities of the great vessels, including aortic

aneurysms and dissection, and pulmonary embolism.
o CTA is also helpful in assessing the patency of bypass grafts.

• Multislice spiral CT provides high-resolution images of coronary anatomy.

o It is most useful in evaluation of suspected coronary anatomic anomalies and to
exclude high-grade coronary stenosis in pts with chest pain and intermediate
pretest probability of coronary artery disease.
o Its greatest accuracy is in detection of left main and proximal LAD and
circumflex disease.

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a
Relative contraindication: pacemakers, metallic objects, claustrophobic.
b
When not seen on TTE.
Abbreviations: Echo, echocardiography; SPECT, single-photon emission CT; TEE,
transesophageal echocardiography; TTE, transthoracic echocardiogram.

108
 TOPIC 40. ACUTE RENAL FAILURE -
PATHOGENESIS AND CLINICAL
FEATURES.

RENAL FAILURE → condition in which the kidneys fail to remove metabolic end
products from the blood and to regulate the fluid, electrolyte, and pH balance of the
extracellular fluids.

Types:

• Acute renal failure → abrupt in onset and often is reversible.

• Chronic renal failure is the end result of irreparable damage to the kidneys.

ACUTE RENAL FAILURE

ACUTE RENAL FAILURE → sudden decrease in renal function sufficient to increase

nitrogenous wastes and impair fluid and electrolyte balance.

• The term azotaemia is used to describe an abnormally high blood level of nitrogenous
wastes (i.e., urea, nitrogen, uric acid, and creatinine) related to acute renal failure.
o It is due to a decrease in the glomerular filtration rate (GFR) and the
inability of the kidneys to filter nitrogenous waste products from the blood.

The causes of acute renal failure can be categorized as prerenal, postrenal, and intrarenal.

PRERENAL FAILURE

Prerenal failure results from impaired renal blood flow that, if sustained, predisposes to
tubular necrosis.

• Reversible if the cause of renal hypofunction can be identified and corrected before
damage to the renal cells occurs.

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CAUSES

• Shock (anaphylactic, septic)

• Hypovolemia: hemorrhage, diarrhea, vomiting, GI disorders (pancreatitis, intestinal
obstruction, peritonitis), burn injury…
• Heart failure
• Drugs inducing renal hypoperfusion: NSAIDs, ACE-inhibitors + diuretics,
radiocontrast agents, antibiotics, cytostatics

PATHOGENESIS

¯ GFR → ¯ urine output → ­ tubule reabsorption of urea, creatinine in tubules → ­ blood

urea/creatinine = 20/1 (normal 10/1 in mg/ml)

INTRARENAL FAILURE

Intrarenal causes of acute renal failure are categorized according to the primary site of injury:
tubular, interstitium, or glomerulus.

Injury to the tubules is most common and is often ischemic or toxic in origin.

CAUSES

• Acute renal disorders (glomerulonephritis, pyelonephritis)

• Acute tubule necrosis resulting from:

o Prolonged renal ischemia
o Nephrotoxic drugs (antibiotics, cytostatics)
o Heavy metals (mercury…)
o Organic solvents
Pathogenesis:
o Tubular cells’ necrosis → obstruction, ­ intraluminal pressure, urine in the
interstitium → vasoconstriction of vas afferens (tubule-glomerular feedback)
→ ¯ GFR

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 • Intratubular obstruction resulting from:
o Hemoglobin (incompatible blood transfusion)
o Myoglobin (“crush syndrome”, seizures)
o Myeloma proteins
o Uric acid crystals (tumor destruction, leukemia treatment)

POSTRENAL FAILURE

Postrenal failure results from obstruction of urine outflow from the kidneys.

The obstruction can occur in:

• ureter → calculi and strictures

• bladder → tumors or neurogenic bladder
• urethra → prostatic hyperplasia, strictures, calculi

PHASES OF ACUTE RENAL FAILURE

The course of acute tubular necrosis usually has four successive phases: onset or initiating
phase; oliguric or anuric phase, diuretic phase, and recovery or convalescent phase.

1. Initiating/Onset phase → 1 – 3 days from the onset of the precipitating event until
tubular injury occurs
2. Oliguric/Anuric phase → represented by a decrease in urine output (urine output <
400 ml/day). The oliguric phase of acute tubular necrosis is characterized by:
o Marked decrease in GFR → sudden retention of endogenous metabolites such
as urea, potassium, sulfate, and creatine that normally are cleared by the
kidneys → metabolic acidosis
o Fluid retention → edema, water intoxication, and pulmonary congestion
3. Diuretic phase → begins within a few days to 6 weeks after oliguria, indicating that
the nephrons have recovered to the point where urine excretion is possible
o Polyuria → dehydration, decreased K+
4. Recovery/Convalescence phase → renal function recovers slowly (after 6 – 12
months)
o The GFR usually returns to 70% to 80% of normal within 1 to 2 years.
§ Increased urine output
§ Blood urea and creatinine → normal
o In some cases, mild to moderate kidney damage persists.
111
112
TOPIC 41. CHRONIC RENAL FAILURE –
AETIOLOGY, PATHOGENESIS,
CLINICAL FEATURES.

RENAL FAILURE → condition in which the kidneys fail to remove metabolic end
products from the blood and to regulate the fluid, electrolyte, and pH balance of the
extracellular fluids.

Types:

• Acute renal failure → abrupt in onset and often is reversible.

• Chronic renal failure is the end result of irreparable damage to the kidneys.

CHRONIC RENAL FAILURE

CHRONIC RENAL FAILURE → progressive and irreversible destruction of kidney

structures.

Chronic renal failure can result from a number of conditions that cause permanent loss
of nephrons, including:

• Uncontrolled hypertension
• Urinary tract obstruction and infection (chronic pyelonephritis)
• Hereditary defects of the kidneys (polycystic renal disease)
• Disorders of the glomeruli
• Systemic diseases such as: diabetes mellitus and systemic lupus erythematosus.

Regardless of cause, chronic renal failure results in progressive deterioration of glomerular

filtration, tubular reabsorptive capacity, and endocrine functions of the kidneys.

STAGES OF PROGRESSION

The rate of nephron destruction differs from case to case, ranging from several months to
many years.

The progression of chronic renal failure usually occurs in four stages: diminished renal
reserve, renal insufficiency, renal failure, and end-stage renal disease.
113
DIMINISHED RENAL RESERVE

• GFR drops to about 50% of normal (normal = 120 – 130 ml/min)

• Creatinine level and serum blood urea nitrogen (BUN) are normal
• No symptoms of impaired renal function

Because of the diminished reserve, the risk of developing azotaemia increases with an
additional renal insult such as that due to nephrotoxic drugs.

RENAL INSUFFICIENCY

• GFR decreases to about 20% to 50% of normal.

• During the stage, azotaemia, anaemia, and hypertension appear.
• As nephrons are destroyed, the remaining nephrons undergo changes to compensate
for those that are lost.
o In the process, each of the remaining nephrons must filter more solute particles
from the blood.
o Because the solute particles are osmotically active, they cause additional water
to be lost in the urine.
o One of the earliest symptoms of renal failure is isosthenuria, which is polyuria
that is almost isotonic with plasma.

Conservative treatment → avoid/prevent renal infections, no neprhortoxic drugs, decreased

proteins in diet, no alcohol, no smoking.

RENAL FAILURE

• GFR is less than 20% to 25% of normal.

• The kidneys cannot regulate volume and solute composition, and edema, metabolic
acidosis, and hypercalcemia develop.
• Overt uremia may ensue with neurologic, gastrointestinal, and cardiovascular
complications.

114
END-STAGE RENAL DISEASE

• GFR is less than 5% of normal.

• Histologic findings of an end-stage kidney include a reduction in renal capillaries
and scarring in the glomeruli.
o Atrophy and fibrosis are evident in the tubules.
• The mass of the kidneys usually is reduced.

At this final phase of renal failure, treatment with dialysis or transplantation is necessary
for survival.

CLINICAL MANIFESTATIONS

• Accumulation of nitrogenous wastes

o Urea
o Creatinine
o In azotemia → without symptoms
o In uremia → extreme weakness, frequent vomiting, lethargy, confusion, coma,
death.

• Sodium and water imbalance

o ¯ concentration of urine (hypo- or Isosthenuria) → polyuria, nocturia →
dehydration
o ­ sensitivity to external water and sodium loss (vomiting, diarrhea, sweating)
o Hydration → result of ¯ GFR → water and sodium retention

• Potassium imbalance
o Hyperkalemia (90% of potassium excretion → through the kidneys)
o ‼ Potassium-containing foods and medications

• Acid-base imbalance
o Metabolic acidosis
o Buffering capacity of bone

• Bone disorders
o Renal osteodystrophy → bone tenderness, fractures, muscle weakness.

115
 Pathogenesis:
§ ­ PO43- → ¯ plasma Ca2+ → ­ PTH → ­ bone resorption
§ ¯ active vitamine D → ¯ plasma Ca2+
§ Acidosis → bone Ca2+ → osteomalacia

• Hematologic disorders
o Anemia → normal size of RBCs, normal MHC
Causes:
§ ¯ erythropoietin
• Recombinant human erythropoietin treatment (rhEPO) →
hypertension (­ renin), convulsion
§ Uremic toxins → bone marrow
§ Bone disorders → bone marrow fibrosis
§ Hemodialysis → hemolysis and hemorrhage
§ Iron deficiency (­ iron loss + ¯ iron intake)
o Bleeding disorders in CRF
§ Epitaxis, menorrhagia, skin, GI and brain bleedings
Causes:
• Coagulopathy
• Thrombocytopathies → platelet adhesion and aggregation,
dispersed platelet in anemia
o Leukocyte function
§ ¯ granulocytes, ¯ phagocytosis
§ ¯ humoral and cell-mediated immunity

• Cardiovascular disorders
o Secondary (renal) hypertension
o Cardiomyopathy
o Congestive heart failure
o Pericarditis

• Gastro-intestinal disorders
o Nausea, vomiting → early-morning, ­ NH3 in GIT (decomposition of urea by
intestinal flora)
o ¯ appetite, metallic taste in the mouth
o ­ PTH → ­ gastric acid secretion → ulcerations → bleeding

• Central nervous system disorders

o Uremic encephalopathy
116
 Causes: uremic toxins, fluid-electrolyte imbalance
Manifestations:
• Loss of memory, attention, disorientation
• Seizures, delirium, coma

• Skin disorders
o Pale, yellow-brownish skin
o Itching → ­ phosphates
o Dryness
§ ¯ sweat glands → ¯ perspiration
§ ¯ oil glands
o Urea crystals

• Elimination of drugs disorders

o ¯ drug absorption in GIT
o ­ free drugs in plasma due to ¯ plasma proteins
o ¯ elimination of drugs and toxic substances by kidneys

117
 TOPIC 42. PHYSICAL EXAMINATION
OF THE KIDNEYS AND URINARY
SYSTEM – INSPECTION, PALPATION,
PERCUSSION.

INSPECTION

Starting from your usual standing position at the right side of the bed, inspect the abdomen.
Inspect the surface, contours.

PALPATION

PALPATION OF THE LEFT KIDNEY

• Move to the patient’s left side.

• Place your right hand behind the patient, just below and parallel to the 12th rib, with
your fingertips just reaching the costovertebral angle. lift, trying to displace the kidney
anteriorly.
• Place your left hand gently in the left upper quadrant, lateral and parallel to the rectus
muscle.
• Ask the patient to take a deep breath.
• At the peak of inspiration, press your left hand firmly and deeply into the left upper
quadrant, just below the costal margin.
• Try to “capture” the kidney between your two hands.
• Ask the patient to breathe out and then to stop breathing briefly.
• Slowly release the pressure of your left hand, feeling at the same time for the kidney
to slide back into its expiratory position.
• If the kidney is palpable, describe its size, contour, and any tenderness.

Alternatively:

• Standing at the patient’s right side, with your left hand, reach over and around the
patient to lift up beneath the left kidney, and with your right hand, feel deep in the left
upper quadrant.
• Ask the patient to take a deep breath and feel for a mass.
• A normal left kidney is rarely palpable.
118
PALPATION OF THE RIGHT KIDNEY

• To capture the right kidney, return to the

patient’s right side.
• Use your left hand to lift up from the
back, and your right hand to feel deep in
the right upper quadrant.
• Proceed as before.

A normal right kidney may be palpable,

especially when the patient is thin and the
abdominal muscles are relaxed.

• It may be slightly tender.

• The patient is usually aware of a capture and release.
• Occasionally, a right kidney is located more anteriorly and must be distinguished from
the liver.
• The edge of the liver, if palpable, tends to be sharper and extend farther medially and
laterally. It cannot be captured.
• The lower pole of the kidney is rounded.

PERCUSSION

If you find tenderness when examining the abdomen, also check

each costovertebral angle.

Pressure from your fingertips may be enough to elicit tenderness;

if not use fist percussion.

• Place the ball of one hand in the costovertebral angle and

strike it with the ulnar surface of your fist.
• Use enough force to cause a perceptible but painless jar
or thud.

To save the patient from repositioning, integrate this assessment

into your examination of the posterior lungs or back.

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 TOPIC 43. PROTEINURIA. NEPHROTIC
SYNDROME.

PROTEINURIA

PHYSIOLOGY

Of the different proteins that can be found in urine, albumin represents the most important
because of its significance in the early detection of renal diseases. The occurrence of a
pathologic albuminuria is routinely detected by screening with test strips.

The GBM is a filter whose pores retain higher molecular weight proteins, e.g., albumin,
transferrin, and immunoglobulins, due to a sieving effect, but conversely, are permeable for
low molecular weight proteins, e. g., free light chains (κ or λ) or peptide hormones.

The sieving effect of the glomerular capillaries is dependent on molecular radius and charge
of the respective proteins.

The proteins advancing in the tubule lumen are reabsorbed and catabolized in the proximal
tubular cells, so that proteinuria becomes manifest only after exceeding the reabsorption
capacity of the proximal tubules.

TYPES OF PROTEINURIA

BENIGN AND ORTHOSTATIC PROTEINURIA

The normal (physiologic) total protein excretion in urine amounts to 40− 150 mg/day.

• In physical effort or fever, this limit may occasionally be exceeded, but the rate should
always be < 0.5 g/24 hours (benign proteinuria).

GLOMERULAR PROTEINURIA

Glomerular proteinuria is caused by damage to the glomerular filtering system and is a

frequent cardinal symptom in primary and secondary renal diseases.

120
The glomerular proteinuria can also be classified schematically into selective and
nonselective.

• Selective means → predominantly anionic proteins of medium size with a molecular

weight of 50 000−80 000 Da (e. g., albumin) are identified, an indication that the
GBM is only minimally damaged, e.g., in minimal change glomerulonephritis (lipoid
nephrosis).
• Nonselective means → in addition to albumin, proteins with a molecular weight of >
50 000−80 000 Da are also found in the urine (e.g., IgG), which indicates more
extensive damage of the glomeruli, e. g., in more inflammatory
glomerulonephritides.

When the proteinuria is < 3.5 g/24 h, it normally produces no or only minimal clinical signs.

When it is in the nephrotic range > 3.5g/24h

• The urine can become foamy.

• In addition, there can be lipiduria, which makes the urine milky and cloudy.
• In parallel with the extent of proteinuria patients develop a more or less distinctive
edema.
• A severe nephrotic syndrome → massive edema + pleural effusions + ascites
(anasarca) goes with an albuminuria > 10 g/day and a hypoalbuminemia < 20−30 g/L.

OVERFLOW PROTEINURIA

An overflow proteinuria occurs without primary glomerular damage but in the presence of
abnormal levels of proteins in blood, that are normally glomerularly filtered.

When the filtration of these proteins (in particular Bence Jones protein, hemoglobin, and
myoglobin) exceeds the tubular reabsorption capacity, an overflow proteinuria is produced.

Bence Jones proteinuria is found in the following diseases:

• Multiple myeloma
• Waldenström disease
• AL amyloidosis
• Light-chain deposition disease
• Lymphoma
• Fanconi syndrome in adults.

121
TUBULAR PROTEINURIA

Tubular proteinuria results from an insufficient ability to resorb normal levels of glomerularly
filtered protein.

An increased amount of low molecular weight plasma proteins are found in the urine, e. g.,
a1- and b2-microglobulins.

Underlying diseases are usually interstitial nephropathies or Fanconi syndrome.

NEPHROTIC SYNDROME

DEFINITION

Characterized by albuminuria (>3.5 g/d) and hypoalbuminemia (<30 g/L) and accompanied
by edema, hyperlipidemia, and lipiduria.

DIAGNOSIS

Protein excretion should be quantified by 24-h urine collection but can be monitored by
measurement of the urine protein/creatinine ratio or albumin/creatinine ratio on a random spot
urine.

The measurement of creatinine excretion helps define the adequacy of 24-h urine collections.
Daily creatinine excretion should be:

• 20–25 mg/kg lean body weight in men

• 15–20 mg/kg lean body weight in women

For random urine samples, the ratio of protein or albumin to creatinine in mg/dL approximates
the 24-h urine protein excretion, since creatinine excretion is only slightly greater than 1000
mg/d per 1.73 m2.

A urine protein/creatinine ratio of 5 is thus consistent with 5 g/d per 1.73 m2.
122
Quantification of urine protein excretion on spot urines has largely supplanted formal 24-h
urine collections for monitoring or screening, due to the greater ease and the need to verify a
complete 24-h collection.

The total protein/creatinine ratio does not detect microalbuminuria, a level of albumin
excretion that is below the level of detection by tests for total protein; urine albumin/creatinine
measurement is therefore preferred as a screening tool for lesser proteinuria.

CLINICAL MANIFESTATIONS

In addition to edema, the complications of NS can include:

• Renal vein thrombosis and other thromboembolic events

• Infection
• Vitamin D deficiency
• Protein malnutrition
• Drug toxicities due to decreased protein binding

CAUSES

Abbreviations: GN, glomerulonephritis.

Source: Modified from RJ Glassock, BM Brenner: HPIM-13.

123
 TOPIC 44. HAEMATURIA,
BACTERIURIA, LEUKOCYTURIA.

HAEMATURIA

When increased numbers of erythrocytes occur in the urine, a microhematuria or even a

macrohematuria is present.

• Eumorphic erythrocytes originate mostly in the lower urinary tract and are passed into
the urine by tumors, stones, or infections.
• Dysmorphic erythrocytes indicate a glomerular origin, and the percentage of
dysmorphic erythrocytes should be > 70% with glomerular hematuria.

However, the specificity of this finding is not very high.

Acanthocytes are a special type of dysmorphic erythrocytes with bubblelike extrusions.

• If acanthocytes constitute > 5 % of the total erythrocytes in the urine, this is highly
suspicious of a glomerulonephritis.

If one or several erythrocyte casts are found in the sediment together with dysmorphic
erythrocytes, the diagnosis of a glomerular disease (mostly a glomerulonephritis) is
confirmed.

BACTERIURIA, LEUKOCYTURIA

An increased number of leukocytes in the urine can indicate a urinary tract infection.

• In an established infection, the leukocytes often cumulate in clusters.

• In addition, bacteria are found and the nitrite and leukocyte esterase tests are positive
in the dipstick test.

The additional presence of squamous cells is suggestive of a vaginal contamination.

If leukocyte casts are found in the sediment as well, this indicates that the infection is localized
in the kidneys (pyelonephritis).

124
 • An increased excretion of eosinophilic leukocytes is predominantly observed in drug-
induced acute interstitial nephritis.

A sterile leukocyturia (negative bacterial growth on conventional immersion culture media)

can indicate an infection by atypical pathogens, e. g., Chlamydia or mycobacteria (urogenital
tuberculosis).

• A sterile leukocyturia is also observed in tubulo-interstitial diseases (acute and chronic

interstitial nephritis, analgesic nephropathy).

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 TOPIC 45. MEASUREMENT OF THE
RENAL FUNCTION – CONCENTRATION
OF UREA AND CREATININ IN THE
BLOOD; MEASUREMENT OF
GLOMERULAR FILTRATION RATE;
RENAL CONCENTRATING ABILITY.

126
TOPIC 46. RADIOLOGICAL AND OTHER
INVESTIGATION OF THE URINARY
SYSTEM – INTRAVENOUS
UROGRAPHY; ULTRASOUND
EXAMINATION, CT ETC.

127
 TOPIC 47. PHYSICAL EXAMINATION
OF THE ABDOMEN.

INSPECTION

Starting from your usual standing position at the right side of the bed, inspect the abdomen.
As you look at the contour of the abdomen, watch for peristalsis.

• It is helpful to sit or bend down so that you can view the abdomen tangentially.
• An arched back thrusts the abdomen forward and tightens the abdominal muscles.

Inspect the surface, contours, and movements of the abdomen, including the following:

• The skin
o Scars. Describe or diagram their location.
o Striae. Old silver striae or stretch marks are normal
o Dilated veins. A few small veins may be visible normally.
o Rashes or ecchymoses

• The umbilicus.
o Observe its contour and location and any inflammation or bulges suggesting a
ventral hernia

• The contour of the abdomen

o Is it flat, rounded, protuberant, or scaphoid (markedly concave or hollowed).
o Do the flanks bulge, or are there any local bulges? Also survey the inguinal and
femoral areas.
o Is the abdomen symmetric?
o Are there visible organs or masses? look for an enlarged liver or spleen that has
descended below the rib cage.

• Peristalsis
o Observe for several minutes if you suspect intestinal obstruction. Normally,
peristalsis may be visible in very thin people.

• Pulsations
o The normal aortic pulsation is frequently visible in the epigastrium.

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 AUSCULTATION

Place the diaphragm of your stethoscope gently on the abdomen.

• Listen for bowel sounds and note their frequency and character.
o Normal sounds consist of clicks and gurgles, occurring at an estimated
frequency of 5 to 34 per minute.
o Occasionally you may hear borborygmi = prolonged gurgles of hyper-
peristalsis, the familiar “stomach growling.”
Because bowel sounds are widely transmitted through the abdomen, listening in one
spot, such as the right lower quadrant, is usually sufficient.

ABDOMINAL BRUITS AND FRICTION RUB

If the patient has high blood pressure,

listen in the epigastrium and in each
upper quadrant for bruits.

Later in the examination, when the

patient sits up, listen also in the
costovertebral angles.

Epigastric bruits confined to systole are

normal.

Listen for bruits over the aorta, the iliac

arteries, and the femoral arteries, as
illustrated.

Listen over the liver and spleen for friction rubs.

PERCUSSION

Percussion helps you to assess the amount and distribution of gas in the abdomen, possible
masses that are solid or fluid-filled, and the size of the liver and spleen.

• Percuss the abdomen lightly in all four quadrants to assess the distribution of tympany
and dullness.
129
 o Tympany usually predominates because of gas in the gastrointestinal tract, but
scattered areas of dullness from fluid and feces are also typical.
• Note any large dull areas suggesting an underlying mass or enlarged organ.
o This observation will guide your palpation.
• On each side of a protuberant abdomen, note where abdominal tympany changes to
the dullness of solid posterior structures.
• Briefly percuss the lower anterior chest above the costal margins.
o On the right, you will usually find the dullness of the liver
o On the left, the tympany that overlies the gastric air bubble and the splenic
flexure of the colon.

PALPATION

LIGHT PALPATION

Gentle palpation is especially helpful for eliciting abdominal tenderness, muscular resistance,
and some superficial organs and masses. It also serves to reassure and relax the patient.

• Keeping your hand and forearm on a horizontal plane, with fingers together and flat
on the abdominal wall, palpate the abdomen with a light, gentle, dipping motion.
• As you move your hand to different quadrants, raise it just off the skin.
• Gliding smoothly, palpate in all four quadrants.

Identify any superficial organs or masses and any area of tenderness or increased resistance
to your hand.

• If resistance is present, try to distinguish voluntary guarding from involuntary

muscular spasm. To do this:
o Try all the methods you know to help the patient relax
o Feel for relaxation of abdominal muscles that normally accompanies
exhalation.
o Ask the patient to mouth-breathe with the jaw dropped open.

Voluntary guarding usually decreases with these maneuvers.

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DEEP PALPATION

This is usually required to delineate abdominal masses.

• Again, using the palmar surfaces of your fingers, press down in all four quadrants.
• Identify any masses:
o Note their location, size, shape, consistency, tenderness, pulsations, and any
mobility with respiration or pressure from the examining hand.
• Correlate your palpable findings with their percussion notes.

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 TOPIC 48. EXAMINATION OF A
PATIENT WITH ASCITES – DETECTION
OF ASCITES, ASPIATION OF
PERITONEAL FLUID.

ASCITES

ASCITES → Accumulation of fluid within the peritoneal cavity.

• Small amounts may be asymptomatic

• Increasing amounts cause abdominal distention and discomfort, anorexia, nausea,
early satiety, heartburn, flank pain, and respiratory distress.

DETECTION OF ASCITES

PHYSICAL EXAMINATION

Bulging flanks, fluid wave, shifting dullness, “puddle sign” (dullness over dependent
abdomen with patient in position over hands and knees).

• May be associated with penile or scrotal edema, umbilical or inguinal herniation,

pleural effusion.
• Evaluation should include rectal and pelvic examination, assessment of liver and
spleen.
• Palmar erythema and spider angiomata seen in cirrhosis.
• Periumbilical nodule (Sister Mary Joseph’s nodule) or supraclavicular node
(Virchow’s node) suggests an abdominal malignancy.

ULTRASONOGRAPHY/CT

Very sensitive; able to distinguish fluid from cystic masses.

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DIFFERENTIAL DIAGNOSIS

• Cirrhosis counts for 84% of cases of ascites.

• Cardiac ascites, peritoneal carcinomatosis, and “mixed” ascites resulting from
cirrhosis and a second disease account for 10–15%.

DISEASES OF PERITONEUM:

• Infections (bacterial, tuberculous, fungal, parasitic)

• Neoplasms
• Connective tissue disease
• Miscellaneous (Whipple’s disease, familial Mediterranean fever, endometriosis, starch
peritonitis, etc.)

DISEASES NOT INVOLVING PERITONEUM:

• Cirrhosis
• CHF
• Budd-Chiari syndrome
• Hepatic venoocclusive disease
• Hypoalbuminemia (nephrotic syndrome, protein-losing enteropathy, malnutrition)
• Miscellaneous (myxedema, ovarian diseases, pancreatic disease, chylous ascites)

ASPIRATION OF PERITONEAL FLUID

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 TOPIC 49. SYMPTOMS OF
OESOPHAGEAL DISEASE. METHODS
FOR EXAMINATION OF THE
OESOPHAGUS.

134
TOPIC 50. SYMPTOMS OF STOMACH
DISEASE. METHODS FOR
EXAMINATION OF THE STOMACH.

135
 TOPIC 51. DIARRHOEA AND
CONSTIPATION.

DIARRHOEA

DIARRHOEA → fecal output >200 g/d on low-fiber (western) diet.

• Also, frequently used to connote loose or watery stools.

TYPES

OSMOTIC DIARRHEA

Non-absorbed solutes increase intraluminal oncotic pressure, causing outpouring of water;

usually ceases with fasting; stool osmolal gap >40 (see below).

Causes include:

• Disaccharidase (e.g., lactase) deficiencies

o Lactase deficiency can be either:
§ Primary (more prevalent in blacks and Asians, usually presenting in
early adulthood)
§ Secondary (from viral, bacterial, or protozoal gastroenteritis, celiac or
tropical sprue, or kwashiorkor).
• Pancreatic insufficiency, bacterial overgrowth
• Lactulose or sorbitol ingestion
• Polyvalent laxative abuse
• Celiac or tropical sprue
• Short bowel syndrome.

SECRETORY DIARRHEA

Active ion secretion causes obligatory water loss → Diarrhea is usually watery, often profuse,
unaffected by fasting. Stool Na+ and K+ are elevated with osmolal gap <40.

136
Causes include:

• Viral infections (e.g., rotavirus, Norwalk virus)

• Bacterial infections (e.g., cholera, enterotoxigenic Escherichia coli, Staphylococcus
aureus)
• Protozoa (e.g., Giardia, Isospora, Cryptosporidium)
• AIDS-associated disorders (including mycobacterial and HIV-induced)
• Medications (e.g., theophylline, colchicine, prostaglandins, diuretics)
• Zollinger-Ellison syndrome (excess gastrin production)
• Vasoactive intestinal peptide (VIP)-producing tumors
• Carcinoid tumors (histamine and serotonin)
• Medullary thyroid carcinoma (prostaglandins and calcitonin)
• Systemic mastocytosis
• Basophilic leukemia
• Distal colonic villous adenomas (direct secretion of potassium-rich fluid)
• Collagenous and microscopic colitis
• Choleraic diarrhea (from ileal malabsorption of bile salts)

EXUDATIVE DIARRHEA

• Inflammation, necrosis, and sloughing of colonic mucosa

• May include component of secretory diarrhea due to prostaglandin release by
inflammatory cells
• Stools usually contain polymorphonuclear leukocytes as well as occult or gross blood.

Causes include:

• Bacterial infections (e.g., Campylobacter, Salmonella, Shigella, Yersinia, invasive or

enterotoxigenic E. coli, Vibrio parahaemolyticus, Clostridium difficile colitis
[frequently antibiotic-induced])
• Colonic parasites (e.g., Entamoeba histolytica)
• Crohn’s disease
• Ulcerative proctocolitis
• Idiopathic inflammatory bowel disease
• Radiation enterocolitis,
• Cancer chemotherapeutic agents
• Intestinal ischemia

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ALTERED INTESTINAL MOTILITY

Alteration of coordinated control of intestinal propulsion → Diarrhea often intermittent or

alternating with constipation

Causes include:

• Diabetes mellitus
• Adrenal insufficiency
• Hyperthyroidism
• Collagen-vascular diseases
• Parasitic infestations
• Gastrin and VIP hypersecretory states
• Amyloidosis
• Laxatives (esp. magnesium-containing agents)
• Antibiotics (esp. erythromycin)
• Cholinergic agents
• Primary neurologic dysfunction (e.g., Parkinson’s disease, traumatic neuropathy)
• Fecal impaction
• Diverticular disease
• Irritable bowel syndrome

Blood in intestinal lumen is cathartic, and major upper GI bleeding leads to diarrhea from
increased motility.

DECREASED ABSORPTIVE SURFACE

Usually arises from surgical manipulation (e.g., extensive bowel resection or rearrangement)
that leaves inadequate absorptive surface for fat and carbohydrate digestion and fluid and
electrolyte absorption.

Occurs spontaneously from enteroenteric fistulas (esp. gastrocolic).

PHYSICAL EXAMINATION

• Signs of dehydration are often prominent in severe, acute diarrhea.

• Fever and abdominal tenderness suggest infection or inflammatory disease but are
often absent in viral enteritis.
138
 • Evidence of malnutrition suggests chronic course.
• Certain signs are frequently associated with specific deficiency states secondary to
malabsorption (e.g., cheilosis with riboflavin or iron deficiency, glossitis with B12,
folate deficiency).

STOOL EXAMINATIONS

Culture for bacterial pathogens, examination for leukocytes, measurement of C. difficile

toxin, and examination for ova and parasites are important components of evaluation of pts
with severe, protracted, or bloody diarrhea.

• Presence of blood (fecal occult blood test) or leukocytes (Wright’s stain) suggests
inflammation (e.g., ulcerative colitis, Crohn’s disease, infection, or ischemia).
• Gram’s stain of stool can be diagnostic of Staphylococcus, Campylobacter, or Candida
infection.
• Steatorrhea (determined with Sudan III stain of stool sample or 72-h quantitative fecal
fat analysis) suggests malabsorption or pancreatic insufficiency.
• Measurement of Na+ and K+ levels in fecal water helps to distinguish osmotic from
other types of diarrhea:
o Osmotic diarrhea is implied by stool osmolal gap > 40, where stool osmolal gap
= osmolserum [2 × (Na+ + K+) stool].

LABORATORY STUDIES

• Complete blood count may indicate anemia (acute or chronic blood loss or
malabsorption of iron, folate, or B12), leukocytosis (inflammation), eosinophilia
(parasitic, neoplastic, and inflammatory bowel diseases).
• Serum levels of calcium, albumin, iron, cholesterol, folate, B12, vitamin D, and
carotene; serum iron-binding capacity; and prothrombin time can provide evidence of
intestinal malabsorption or maldigestion.

139
 CONSTIPATION

CONSTIPATION → decrease in frequency of stools to less than one per week or difficulty
in defecation; may result in abdominal pain, distention, and fecal impaction, with consequent
obstruction or, rarely, perforation.

Constipation is a frequent and often subjective complaint.

Contributory factors may include inactivity, low-fiber diet, and inadequate allotment of time
for defecation.

CAUSES

• Altered colonic motility due to neurologic dysfunction (diabetes mellitus, spinal cord
injury, multiple sclerosis, Chagas’ disease, Hirschsprung’s disease, chronic idiopathic
intestinal pseudoobstruction, idiopathic megacolon)
• Scleroderma
• Drugs (esp. anticholinergic agents, opiates, aluminum- or calcium-based antacids,
calcium channel blockers, iron supplements, sucralfate)
• Hypothyroidism
• Cushing’s syndrome
• Hypokalemia
• Hypercalcemia
• Dehydration
• Mechanical causes (colorectal tumors, diverticulitis, volvulus, hernias,
intussusception)
• Anorectal pain (from fissures, hemorrhoids, abscesses, or proctitis) leading to
retention, constipation, and fecal impaction.

140
 TOPIC 52. MALABSORPTION.

DEFINITION

Intestinal malabsorption of ingested nutrients may produce:

• Osmotic diarrhea
• Steatorrhea
• Specific deficiencies (e.g., iron; folate; B12; vitamins A, D, E, and K)

Protein-losing enteropathy may result from several causes of malabsorption.

• It is associated with hypoalbuminemia and can be detected by measuring stool α1-

antitrypsin or radiolabeled albumin levels.

CAUSES

141
 TOPIC 53. GASTROINTESTINAL
BLEEDING – HEMATEMESIS AND
MELENA.

HEMATEMESIS → vomiting of blood or altered blood (“coffee grounds”) indicates bleeding

proximal to ligament of Treitz.

MELENA → Altered (black) blood per rectum (>100-mL blood required for one melenic
stool) usually indicates bleeding proximal to ligament of Treitz but may be as distal as
ascending colon; pseudomelena may be caused by ingestion of iron, bismuth, licorice, beets,
blueberries, and charcoal.

HEMATOCHEZIA → Bright red or maroon rectal bleeding usually implies bleeding beyond
ligament of Treitz but may be due to rapid upper GI bleeding (>1000 mL). Positive fecal
occult blood test with or without iron deficiency.

CLINICAL FEATURES

SYMPTOMS OF BLOOD LOSS

• Light-headedness
• Shortness of breath.

HEMODYNAMIC CHANGES

Orthostatic drop in bp >10 mmHg usually indicates >20% reduction in blood volume (±
syncope, light-headedness, nausea, sweating, thirst).

SHOCK

BP <100 mmHg systolic usually indicates <30% reduction in blood volume (± pallor, cool
skin).

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LABORATORY CHANGES

Hematocrit may not reflect extent of blood loss because of delayed equilibration with
extravascular fluid. Mild leukocytosis and thrombocytosis. Elevated blood urea nitrogen is
common in upper GI bleeding.

ADVERSE PROGNOSTIC SIGNS

Age > 60 years, associated illnesses, coagulopathy, immunosuppression, presentation with

shock, rebleeding, onset of bleeding in hospital, variceal bleeding, endoscopic stigmata of
recent bleeding (e.g., “visible vessel” in ulcer base).

UPPER GI BLEEDING

COMMON CAUSES

• Peptic ulcer (accounts for ~50%)

• Gastropathy (alcohol, aspirin, NSAIDs, stress)
• Esophagitis
• Mallory-Weiss tear (mucosal tear at gastroesophageal junction due to retching)
• Gastroesophageal varices

LESS COMMON CAUSES

• Swallowed blood (nosebleed)

• Esophageal, gastric, or intestinal neoplasm
• Anticoagulant and fibrinolytic therapy
• Hypertrophic gastropathy (Ménétrier’s disease)
• Aortic aneurysm
• Aortoenteric fistula (from aortic graft)
• Arteriovenous malformation
• Telangiectases (Osler-Weber-Rendu syndrome)
• Dieulafoy lesion (ectatic sub-mucosal vessel)
• Vasculitis

143
 • Connective tissue disease (pseudoxanthoma elasticum, Ehlers-Danlos syndrome)
• Blood dyscrasias
• Neurofibroma
• Amyloidosis
• Hemobilia (biliary origin)

LOWER GI BLEEDING

CAUSES

• Anal lesions (hemorrhoids, fissures)

• Rectal trauma
• Proctitis
• Colitis (ulcerative colitis, Crohn’s disease, infectious colitis, ischemic colitis,
radiation)
• Colonic polyps
• Colonic carcinoma
• Angiodysplasia (vascular ectasia)
• Diverticulosis
• Intussusception
• Solitary ulcer
• Blood dyscrasias
• Vasculitis
• Connective tissue disease
• Neurofibroma
• Amyloidosis
• Anticoagulation

BLEEDING OF OBSCURE ORIGIN

Often small-bowel source.

• Consider small-bowel enteroclysis x-ray (careful barium radiography via peroral

intubation of small bowel), Meckel’s scan, enteroscopy (small-bowel endoscopy), or
exploratory laparotomy with intraoperative enteroscopy.

144
TOPIC 54. SYMPTOMS OF DISEASES OF
THE COLON. METHODS FOR
EXAMINATION OF THE COLON.

145
 TOPIC 55. HEPATIC
ENCEPHALOPATHY, ACUTE AND
CHRONIC HEPATIC FAILURE.

LIVER FAILURE

The most severe clinical consequence of liver disease is hepatic failure → may result from:

• Sudden and massive liver destruction (e.g. fulminant hepatitis)

• Progressive damage to the liver (e.g. alcoholic cirrhosis)

Whatever the cause, 80% to 90% of hepatic functional capacity must be lost before liver
failure occurs.

CLINICAL MANIFESTATIONS

The manifestations of liver failure reflect the various synthesis, storage, metabolic, and
elimination functions of the liver.

146
HEMATOLOGIC DISORDERS

Liver failure can cause:

• Anemia → due to blood loss, excessive RBC destruction and impaired formation of
RBCs
• Thrombocytopenia → often occurs as a result of splenomegaly
• Coagulation defects
o Because factors V, VII, IX, and X, prothrombin, and fibrinogen are synthesized
by the liver, their decline in liver disease contributes to bleeding disorders.
o Malabsorption of the fat-soluble vitamin K contributes further to the impaired
synthesis of these clotting factors.
• Leukopenia

ENDOCRINE DISORDERS

The liver metabolizes the steroid hormones → particularly disturbances in gonadal (sex
hormone) function, are common accompaniments of cirrhosis and liver failure.

• Women → menstrual irregularities (usually amenorrhea), loss of libido, and sterility

• Men (testosterone levels fall) → testes atrophy, loss of libido, impotence, and
gynecomastia
A decrease in aldosterone metabolism → salt and water retention by the kidney, along with
a lowering of serum potassium resulting from increased elimination of potassium.

SKIN DISORDERS

• Vascular spiders
• Telangiectases
• Spider angiomas
• Spider nevi

They are seen most often in the upper half of the body + consist of a central pulsating arteriole
from which smaller vessels radiate

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HEPATORENAL SYNDROME

HEPATORENAL SYNDROME → functional renal failure → seen during the terminal

stages of liver failure when no functional causes of renal disease exist.

Characterized by:

• Progressive azotemia
• Increased serum creatinine levels
• Oliguria

It is believed to occur due to a decrease in renal blood flow.

• When renal failure is superimposed on liver failure → azotemia + elevated levels of

blood ammonia → hepatic encephalopathy and coma.

HEPATIC ENCEPHALOPATHY

HEPATIC ENCEPHALOPATHY → totality of CNS manifestations of liver failure.

Hepatic encephalopathy (portal-systemic encephalopathy) is a complex neurologic

syndrome characterized by impaired cerebral function, flapping tremor (asterixis), and
electroencephalogram (EEG) changes.

The syndrome may develop:

• Rapidly during acute fulminant hepatitis

• Slowly during the course of chronic liver disease and the development of portal
hypertension

PATHOPHYSIOLOGY

Hepatic encephalopathy results from a combination of biochemical alterations that affect

neurotransmission.

148
Liver dysfunction and the development of collateral vessels that shunt blood around the liver
to the systemic circulation permit toxins absorbed from the gastrointestinal tract to
accumulate and circulate freely to the brain.

• The accumulated toxins alter cerebral energy metabolism, interfere with

neurotransmission, and cause edema.

The most hazardous substances are end products of intestinal protein digestion, particularly
ammonia, which cannot be converted to urea by the diseased liver.

• Other substances include inflammatory cytokines, short-chain fatty acids, serotonin,

tryptophan, and manganese.

Infection, hemorrhage, and electrolyte imbalance (including zinc deficiency) as well as the
use of sedatives and analgesics can precipitate hepatic encephalopathy in the presence of
liver disease.

CLINICAL MANIFESTATIONS

Characterized by neural disturbances ranging from: lack of mental alertness to confusion,

coma and convulsions.

• Very early sign → asterixis (flapping tremor)

• Memory loss + personality changes (euphoria, irritability, anxiety, lack of concern
about personal appearance and self).
• Impaired speech
• Inability to perform certain purposeful movements

The encephalopathy may progress to decerebrate rigidity → terminal deep coma.

EVALUATION

Diagnosis of hepatic encephalopathy is based on a history of liver disease and clinical

manifestations.

• Electroencephalography and blood chemistry tests provide supportive data. Tracking

levels of serum ammonia assesses treatment effective- ness and liver function.

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 TOPIC 56. JAUNDICE – AETIOLOGY,
PATHOGENESIS, CLINICAL FEATURES,
INVESTIGATIONS.

Jaundice (i.e., icterus) results from an abnormally high accumulation of bilirubin in the
blood, as a result of which there is a yellowish discoloration to the skin and deep tissues.

• The normal levels of serum bilirubin → 1.2 mg/dl.

• Jaundice → bilirubin levels rise above 2.0 to 2.5 mg/dl.

The four major causes of jaundice are:

• Excessive destruction of red blood cells

• Impaired uptake of bilirubin by the liver cells
• Decreased conjugation of bilirubin
• Obstruction of bile flow

Jaundice can be categorized as prehepatic, hepatic, and posthepatic.

PREHEPATIC (HEMOLYTIC) JAUNDICE

The major cause of prehepatic jaundice is excessive hemolysis of red blood cells.

• Hemolytic jaundice occurs when red blood cells are destroyed at a rate in excess of the
liver’s ability to remove the bilirubin from the blood.

CHARACTERISTICS

• Normal stool and urine color

• Mild jaundice
• Indirect hyperbilirubinemia → no bilirubin in the urine

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CAUSES OF PREHEPATIC JAUNDICE

• Hemolytic blood transfusion reaction

• Hereditary disorders of the red blood cells
o Sickle cell anemia
o Thalassemia
o Spherocytosis
• Acquired hemolytic disorders
• Autoimmune hemolytic anemias

151
INTRAHEPATIC (HEPATIC) JAUNDICE

Intrahepatic jaundice is caused by disorders that directly affect the ability of the liver to
remove bilirubin from the blood or conjugate it so it can be eliminated in the bile.

• Conjugation of bilirubin is impaired whenever liver cells are damaged, when transport
of bilirubin into liver cells becomes deficient, or when the enzymes needed to
conjugate the bile are lacking.

CHARACTERISTICS

• Affected persons have no symptoms other than:

o Slightly elevated unconjugated bilirubin
o Mild jaundice.

• Associated with:
o Dark urine
o Elevated alkaline phosphate (produced by the liver and excreted with the bile)
§ When flow is obstructed → blood alkaline phosphate is elevated

CAUSES OF INTRAHEPATIC JAUNDICE

• Decreased bilirubin uptake by the liver

o Gilbert’s disease → inherited as a dominant trait and results in a reduced
uptake of bilirubin; the disorder is benign and fairly common.

• Decreased conjugation of bilirubin

o Hepatocellular liver damage
§ Hepatitis
§ Cancer of liver
§ Cirrhosis

o Drug-induced cholestasis
§ Drugs → especially the anesthetic agent halothane
§ Oral contraceptives, estrogen, anabolic steroids are all possible causative
factors.

152
POSTHEPATIC (OBSTRUCTIVE OR CHOLESTATIC) JAUNDICE

Posthepatic or obstructive jaundice, also called cholestatic jaundice, occurs when bile flow
is obstructed between the liver and the intestine.

CHARACTERISTICS

• Conjugated and unconjugated bilirubin levels are usually elevated → blood levels of
bilirubin are often elevated
o As the bile acids accumulate in the blood, pruritus develops.
• Stools are clay colored because of the lack of the bilirubin in the bile

153
 • Urine is dark because of the increased elimination of bilirubin in the urine
• Serum levels of alkaline phosphate are elevated

CAUSES OF POSTHEPATIC JAUNDICE

• Structural disorders of the bile ducts (strictures)

• Cholelithiasis (gall bladder stones)
• Congenital atresia of the extrahepatic bile flow
• Bile duct obstruction caused by tumor (pancreatic tumor…)

154
 TOPIC 57. PORTAL HYPERTENSION.

PORTAL HYPERTENSION

Portal hypertension is abnormally high blood pressure in the portal venous system. Pressure
in this system is normally 3 mm Hg; portal hypertension is an increase to at least 10 mm Hg.

PATHOPHYSIOLOGY

Portal hypertension is caused by any condition that increases resistance to flow in the
portal-venous system.

• Prehepatic causes → from portal vein

o Thrombosis

o External compression due to cancer or enlarged lymph nodes

• Intrahepatic causes → conditions that cause obstruction of blood flow within the liver

o Shunts

o Thrombosis

o Inflammation

o Fibrosis of the sinusoids, as occurs in cirrhosis of the liver, biliary cirrhosis,

viral hepatitis, or schistosomiasis (a parasitic infection).

• Posthepatic causes → from hepatic vein

o Thrombosis

o Cardiac disorders that impair the pumping ability of the right heart (severe right-
sided heart failure)

The most common cause of portal hypertension is fibrosis and obstruction caused by
cirrhosis of the liver.

155
Long-term portal hypertension causes several pathophysiologic problems that are difficult to
treat and can be fatal: varices, splenomegaly, ascites, hepatic encephalopathy, and
hepatopulmonary syndrome.

• Varices → distended, tortuous, collateral veins.

o Prolonged elevation of pressure in the portal vein → opening of collateral

veins between the portal vein and systemic veins → transformation into
varices:

§ Esophageal and gastric varices → most common

§ Over the abdominal wall (caput medusae)

§ Over the rectum (hemorrhoidal varices)

o Rupture of varices can cause life-threatening hemorrhage.

• Splenomegaly → enlargement of the spleen caused by increased pressure in the

splenic vein, which branches from the portal vein.

o Thrombocytopenia is the most common symptom of congestive splenomegaly.

o The enlarged spleen can be palpated.

156
 • Hepatopulmonary syndrome (vasodilation, intrapulmonary shunting, and hypoxia)
and portopulmonary hypertension (pulmonary vasoconstriction and vascular
remodeling) are complications of liver disease and portal hypertension.

The pathophysiology is complex and involves different effects of vasoactive substances.

CLINICAL MANIFESTATIONS

There may be no clinical manifestations, although dyspnea, cyanosis, and clubbing may
occur.

Vomiting of blood (hematemesis) from bleeding esophageal varices is the most common
clinical manifestation of portal hypertension.

• Slow, chronic bleeding from varices causes anemia and the presence of digested
blood in the stools.

• Usually the bleeding is from varices that have developed slowly over a period of years.

• Rupture of esophageal varices causes hemorrhage and voluminous vomiting of

dark-colored blood.

o The ruptured varices are usually painless.

o Rupture is caused by a combination of erosion by gastric acid and elevated

venous pressure.

o Mortality from ruptured esophageal varices ranges from 30% to 60%.

• Recurrent bleeding of esophageal varices indicates a poor prognosis.

o Most individuals die within 1 year.

EVALUATION AND TREATMENT

Portal hypertension is often diagnosed at the time of variceal bleeding and confirmed by
endoscopy and evaluation of portal venous pressure.

• The individual usually has a history of jaundice, hepatitis, or alcoholism.

• Upper gastrointestinal endoscopy is commonly used to diagnose varices.

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 TOPIC 58. EXAMINATION OF THE
LIVER – INSPECTION, PERCUSSION,
PALPATION.

INSPECTION

Starting from your usual standing position at the right side of the bed, inspect the abdomen.

• As you look at the contour of the abdomen, watch for peristalsis.

• It is helpful to sit or bend down so that you can view the abdomen tangentially.

Inspect the surface, contours, and movements of the abdomen, including the following:

• The skin.
o Scars. Describe or diagram their location.
o Striae. Old silver striae or stretch marks are normal.
o Dilated veins. A few small veins may be visible normally.
o Rashes or ecchymoses

• The umbilicus.
o Observe its contour and location and any inflammation or bulges suggesting a
ventral hernia.

• The contour of the abdomen

o Is it flat, rounded, protuberant, or scaphoid (markedly concave or hollowed)?
o Do the flanks bulge, or are there any local bulges? Also survey the inguinal and
femoral areas.
o Is the abdomen symmetric?
o Are there visible organs or masses? look for an enlarged liver or spleen that has
descended below the rib cage.

• Peristalsis.
o Observe for several minutes if you suspect intestinal obstruction. Normally,
peristalsis may be visible in very thin people.

• Pulsations.
o The normal aortic pulsation is frequently visible in the epigastrium.
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 PERCUSSION

Measure the vertical span of liver dullness in the right midclavicular line.

• First locate the midclavicular line carefully to avoid inaccurate measurement.

o Use a light to moderate percussion strike because examiners with a heavier
strike underestimate liver size.
• Starting at a level below the umbilicus in the right lower quadrant (in an area of
tympany, not dullness), percuss upward toward the liver.
o Identify the lower border of dullness in the midclavicular line.
• Next, identify the upper border of liver
dullness in the midclavicular line.
o Starting at the nipple line, lightly
percuss from lung resonance down
toward liver dullness.
o Gently displace a woman’s breast
as necessary to be sure that you
start in a resonant area.

Now measure in centimeters the distance between your two points – the vertical span of liver
dullness.

• Normal liver spans, are generally greater in men than women and in tall people
compared to short people.
• If the liver seems enlarged, outline the lower edge by percussing medially and laterally.

Measurements of liver span by percussion are more accurate when the liver is enlarged with
a palpable edge.

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 PALPATION

• Place your left hand behind the patient,

parallel to and supporting the right 11th
and 12th ribs and adjacent soft tissues
below.
o Remind the patient to relax on
your hand if necessary.
o By pressing your left hand
upward, the patient’s liver may be
felt more easily by your other
hand.
• Place your right hand on the patient’s right abdomen lateral to the rectus muscle, with
your fingertips well below the lower border of liver dullness.
o Some examiners like to point their fingers up toward the patient’s head, whereas
others prefer a somewhat more oblique position, as shown on the next page. In
either case, press gently in and up.
• Ask the patient to take a deep breath.
o Try to feel the liver edge as it comes down to meet your fingertips.
§ If you feel it, lighten the pressure of your palpating hand slightly so that
the liver can slip under your finger pads and you can feel its anterior
surface.
§ Note any tenderness.
o If palpable at all, the normal liver edge is soft, sharp, and regular, with a smooth
surface.
§ The normal liver may be slightly tender.

On inspiration, the liver is palpable about 3 cm below the right costal margin in the
midclavicular line.

• Some people breathe more with the chest than with the diaphragm.
• It may be helpful to train such a patient to “breathe with the abdomen,” thus bringing
the liver, as well as the spleen and kidneys, into a palpable position during inspiration.

In order to feel the liver, you may have to alter your pressure according to the thickness and
resistance of the abdominal wall.

• If you cannot feel it, move your palpating hand closer to the costal margin and try
again.

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Try to trace the liver edge both laterally and medially.

• Palpation through the rectus muscles, however, is especially difficult.

• Describe or sketch the liver edge and measure its distance from the right costal margin
in the midclavicular line.

The “hooking technique” may be helpful, especially when the patient is obese.

• Stand to the right of the patient’s chest.

• Place both hands, side by side, on the
right abdomen below the border of liver
dullness.
• Press in with your fingers and up toward
the costal margin.
• Ask the patient to take a deep breath.
• The liver edge, is palpable with the
fingerpads of both hands.

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 TOPIC 59. SPECIAL TECHNIQUES IN
THE EXAMINATION OF THE LIVER –
FUNCTIONAL TESTS, IMAGING
TECHNIQUES, SPECIAL TESTS.

FUNCTIONAL TESTS

Blood tests function → Used to detect presence of liver disease, discriminate among different
types of liver disease, gauge the extent of known liver damage, and follow response to
treatment.

BILIRUBIN

Provides indication of hepatic uptake, metabolic (conjugation) and excretory functions.

• Conjugated fraction (direct) distinguished from unconjugated by chemical assay.

AMINOTRANSFERASES (TRANSAMINASES)

Aspartate aminotransferase (AST; SGOT) and alanine aminotransferase (ALT; SGPT) →

sensitive indicators of liver cell injury.

• Greatest elevations seen in hepatocellular necrosis (e.g., viral hepatitis, toxic or

ischemic liver injury, acute hepatic vein obstruction), occasionally with sudden,
complete biliary obstruction (e.g., from gallstone)
• Milder abnormalities in cholestatic, cirrhotic, and infiltrative disease

Poor correlation between degree of liver cell damage and level of aminotransferases:

• ALT more specific measure of liver injury, because AST also found in striated muscle
and other organs

Ethanol-induced liver injury usually produces modest increases with more prominent
elevation of AST than ALT.

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ALKALINE PHOSPHATASE

Sensitive indicator of cholestasis, biliary obstruction (enzyme increases more quickly than
serum bilirubin), and liver infiltration.

• Mild elevations in other forms of liver disease

• Limited specificity because of wide tissue distribution.
• Elevations also seen in normal childhood, pregnancy, and bone diseases.
• Tissue-specific isoenzymes can be distinguished by fractionation or by differences in
heat stability (liver enzyme activity stable under conditions that destroy bone enzyme
activity).

5′-NUCLEOTIDASE (5′-NT)

Pattern of elevation in hepatobiliary disease similar to alkaline phosphatase.

• Has greater specificity for liver disorders

• Used to determine whether liver is source of elevation in serum alkaline phosphatase,
esp. in children, pregnant women, pts with possible concomitant bone disease.

Γ-GLUTAMYL TRANSPEPTIDASE (GGT)

Correlates with serum alkaline phosphatase activity.

• Elevation is less specific for cholestasis than alkaline phosphatase or 5′-NT.

COAGULATION FACTORS

Measure of clotting factor activity.

• Prolongation results from clotting factor deficiency or inactivity.

o All clotting factors except factor VIII are synthesized in the liver, and
deficiency can occur rapidly from widespread liver disease as in hepatitis, toxic
injury, or cirrhosis; single best acute measure of hepatic synthetic function;
helpful in diagnosis and prognosis of acute liver disease.
o Clotting factors II, VII, IX, X function only in the presence of vitamin K
§ PT prolongation from fat malabsorption distinguished from hepatic
disease by rapid and complete response to vitamin K replacement.
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ALBUMIN

Decreased serum levels result from decreased hepatic synthesis (chronic liver disease or
prolonged malnutrition) or excessive losses in urine or stool.

• Insensitive indicator of acute hepatic dysfunction, because serum half-life is 2–3

weeks; in pts with chronic liver disease, degree of hypoalbuminemia correlates with
severity of liver dysfunction.

GLOBULIN

• Mild polyclonal hyperglobulinemia often seen in chronic liver diseases.

• Marked elevation frequently seen in autoimmune chronic active hepatitis.

AMMONIA

Elevated blood levels result from deficiency of hepatic detoxification pathways and portal-
systemic shunting, as in fulminant hepatitis, hepatotoxin exposure, and severe portal
hypertension (e.g., from cirrhosis).

• Elevation of blood ammonia does not correlate well with hepatic function or the
presence or degree of acute encephalopathy.

IMAGING TECHNIQUES

ULTRASONOGRAPHY (US)

Rapid, noninvasive examination of abdominal structures.

Advantages:

• No radiation exposure
• Relatively low cost
• Equipment portable

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Disadvantages

• Images and interpretation strongly dependent on expertise of examiner

Uses:

• Particularly valuable for detecting biliary duct dilation and gallbladder stones (>95%)
• Much less sensitive for intraductal stones (~60%)
• Most sensitive means of detecting ascites
• Moderately sensitive for detecting hepatic masses
• Excellent for discriminating solid from cystic structures
• Useful in directing percutaneous needle biopsies of suspicious lesions

Doppler US useful to determine patency and flow in portal, hepatic veins and portal-systemic
shunts.

• Imaging improved by presence of ascites but severely hindered by bowel gas

Endoscopic US less affected by bowel gas and is sensitive for determination of depth of tumor
invasion through bowel wall.

CT

Particularly useful for detecting, differentiating, and directing percutaneous needle biopsy of
abdominal masses, cysts, and lymphadenopathy.

• Imaging enhanced by intestinal or intravenous contrast dye and unaffected by intestinal

gas
• Somewhat less sensitive than US for detecting stones in gallbladder but more sensitive
for choledocholithiasis
• May be useful in distinguishing certain forms of diffuse hepatic disease (e.g., fatty
infiltration, iron overload).

RADIONUCLIDE SCANNING

Using various radiolabeled compounds, different scanning methods allow sensitive

assessment of biliary excretion (HIDA, PIPIDA, DISIDA scans), parenchymal changes
165
(technetium sulfur colloid liver/spleen scan), and selected inflammatory and neoplastic
processes (gallium scan).

• HIDA and related scans particularly useful for assessing biliary patency and excluding
acute cholecystitis in situations where US is not diagnostic
• CT, MRI, and colloid scans have similar sensitivity for detecting liver tumors and
metastases
• CT and combination of colloidal liver and lung scans sensitive for detecting right
subphrenic (suprahepatic) abscesses.

CHOLANGIOGRAPHY

Most sensitive means of detecting biliary ductal calculi, biliary tumors, sclerosing cholangitis,
choledochal cysts, fistulas, and bile duct leaks; may be performed via endoscopic
(transampullary) or percutaneous (transhepatic) route

• Allows sampling of bile and ductal epithelium for cytologic analysis and culture
• Allows placement of biliary drainage catheter and stricture dilation
• Endoscopic route (endoscopic retrograde cholangiopancreatogram [ERCP]) permits
manometric evaluation of sphincter of Oddi, sphincterotomy, and stone extraction.

ANGIOGRAPHY

• Most accurate means of determining portal pressures and assessing patency and
direction of flow in portal and hepatic veins.
• Highly sensitive for detecting small vascular lesions and hepatic tumors (esp. primary
hepatocellular carcinoma)
• “Gold standard” for differentiating hemangiomas from solid tumors; most accurate
means of studying vascular anatomy in preparation for complicated hepatobiliary
surgery (e.g., portal-systemic shunting, biliary reconstruction) and determining
resectability of hepatobiliary and pancreatic tumors.

Similar anatomic information (but not intravascular pressures) can often be obtained
noninvasively by CT- and MR-based techniques.

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 SPECIAL TESTS

PERCUTANEOUS LIVER BIOPSY

• Most accurate in disorders causing diffuse changes throughout the liver

• Subject to sampling error in focal infiltrative disorders such as metastasis
• Should not be the initial procedure in the diagnosis of cholestasis.

Contraindications to performing a percutaneous liver biopsy include:

• Significant ascites
• Prolonged international normalized ratio (INR)

In such settings, the biopsy can be performed via the transjugular approach.

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 TOPIC 60. EXAMINATION OF
GALLBLADDER AND BILE DUCTS.

The bladder normally cannot be examined unless it is distended above the symphysis pubis.

PALPATION

On palpation, the dome of the distended bladder feels smooth and round.

• Check for tenderness.

PERCUSSION

Use percussion to check for dullness and to determine how high the bladder rises above the
symphysis pubis.

• Bladder volume must be 400 to 600 ml before dullness appears.

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 TOPIC 61. PHYSICAL EXAMINATION
OF THE SPLEEN. SPLENOMEGALY.

When a spleen enlarges, it expands anteriorly, downward, and medially, often replacing the
tympany of stomach and colon with the dullness of a solid organ.

It then becomes palpable below the costal margin.

• Percussion suggests but does not confirm splenic enlargement.

• Palpation can confirm the enlargement but often misses large spleens that do not
descend below the costal margin.

PERCUSSION

Two techniques may help you to detect splenomegaly, an enlarged spleen:

1. Percuss the left lower anterior chest wall roughly from the border of cardiac dullness
at the 6th rib to the anterior axillary line and down to the costal margin, an area termed
Traube’s space.

o As you percuss along the routes suggested by the arrows in the following
figures, note the lateral extent of tympany.
o Percussion is moderately accurate in detecting splenomegaly (sensitivity, 60%–
80%; specificity, 72%–94%).

If tympany is prominent, especially laterally, splenomegaly is not likely. The dullness of a

normal spleen is usually masked by the dullness of other posterior tissues.
169
 2. Check for a splenic percussion sign.

o Percuss the lowest interspace in the left anterior axillary line, as shown next.
o This area is usually tympanitic.
o Then ask the patient to take a deep breath, and percuss again.
o When spleen size is normal, the percussion note usually remains tympanitic.

If either or both of these tests is positive, pay extra attention to palpation of the spleen.

PALPATION

• With your left hand, reach over and around the patient to support and press forward
the lower left rib cage and adjacent soft tissue.
• With your right hand below the left costal margin, press in toward the spleen.
• Begin palpation low enough so that you are below a possibly enlarged spleen.
o If your hand is close to the costal margin, it is not sufficiently mobile to reach
up under the rib cage.
• Ask the patient to take a deep breath.
o Try to feel the tip or edge of the spleen as it comes down to meet your fingertips.

Note any tenderness, assess the splenic contour, and measure the distance between the
spleen’s lowest point and the left costal margin.

• In approximately 5% of normal adults, the tip of the spleen is palpable.

• Causes include a low, flat diaphragm, as in chronic obstructive pulmonary disease, and
a deep inspiratory descent of the diaphragm.
170
The spleen tip, illustrated at the right side, is just palpable deep to the left costal margin.

Repeat with the patient lying on the right side with legs somewhat flexed at the hips and
knees.

• In this position, gravity may bring the spleen forward and to the right into a palpable
location.

This enlarged spleen is palpable about 2 cm below the left costal margin on deep inspiration.

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TOPIC 62. ANAEMIA – PHYSICAL AND
LABORATORY EXAMINATION OF THE
PATIENT.

172
 TOPIC 63. METHODS FOR
INVESTIGATION OF THE PITUITARY
GLAND.

173
 TOPIC 64. METHODS FOR
INVESTIGATION OF THYROID GLAND.

TRACHEA AND THE THYROID GLAND

To orient yourself to the neck, identify the thyroid and cricoid cartilages and the trachea below
them.

Inspect the trachea for any deviation from its usual midline position. Then feel for any
deviation. Place your finger along one side of the trachea and note the space between it and
the sternocleidomastoid. Compare it with the other side. The spaces should be symmetric.

Inspect the neck for the thyroid gland. Tip the patient’s head back a bit. Using tangential
lighting directed downward from the tip of the patient’s chin, inspect the region below the
cricoid cartilage for the gland. The lower shadowed border of the thyroid glands shown here
is outlined by arrows.

Observe the patient swallowing. Ask the patient to sip some water and to extend the neck
again and swallow. Watch for upward movement of the thyroid gland, noting its contour and
symmetry. The thyroid cartilage, the cricoid cartilage, and the thyroid gland all rise with
swallowing and then fall to their resting positions.
174
Confirm your visual observations by palpating the gland outlines as you stand facing the
patient. This helps prepare you for the more systematic palpation to follow:

1. Ask the patient to flex the neck slightly forward to relax the sternocleidomastoid
muscles.
2. Place the fingers if both hands on the patient’s neck so that your index finger are just
below the cricoid cartilage.
3. Ask the patient to sip and swallow water before. Feel for the thyroid isthmus rising up
under your finger pads. It is often, but not always, palpable.
4. Displace the trachea to the right with the fingers of the left hand; with the right-hand
fingers, palpate laterally for the right lobe of the thyroid in the space between the
displaced trachea and the relaxed sternocleidomastoid. Find the lateral margin. In a
similar fashion, examine the left lobe.

o The lobes are somewhere harder to feel than the isthmus, so practice is needed.
The anterior surface of a lateral lobe is approximately the size of the distal
phalanx of the thumb and feels somewhat rubbery.

5. Note the size, shape, and consistency of the gland and identify any nodules or
tenderness.
6. If the thyroid gland is enlarged, listen over the lateral with a stethoscope to detect a
bruit, a sound similar to a cardiac murmur but of noncardiac origin.

175
TOPIC 65. METHODS FOR
INVESTIGATION OF THE
PARATHYROID.

176
 TOPIC 66. METHODS FOR
INVESTIGATION OF THE ADRENAL
GLANDS.

177
 TOPIC 67. METHODS FOR
EXAMINATION OF THE JOINTS.
INVESTIGATION OF PATIENTS WITH
DISEASES OF THE JOINTS.

178