Unit 11 and 9 Complete
Unit 11 and 9 Complete
Unit 11 and 9 Complete
Key Players:
HIV stands for “Human Immunodeficiency Virus” and AIDS stands for “Acquired Immunodeficiency Syndrome”.
CD4 cells – also known as T cells, are white blood cells that fight infection and play an important role in your immune system.
DEFINITION
HIV is a virus that attacks the human body’s immune system, specifically the CD4 positive cells.
targets the immune system and weakens people's defense against many infections and some types of cancer that people with healthy
immune systems can fight off.
PATHOPHYSIOLOGY
HIV is a retrovirus that cannot grow or multiply by itself.
It finds the helper t cell and other cells that have a CD4 receptor on its surface as the perfect host cell.
HIV uses this receptor to gain access to the cell, which allows the virus to reproduce and destroy its host cell.
Life Cycle of HIV
Step 1: Attachment: GP120 protein projections make contact and bind with a CD4 receptor.
Step 2: Fusion: dumps the viral RNA and other enzymes
Step 3: Reverse transcription: Viral RNA releases reverse transcriptase, an enzyme that causes the viral RNA to turn into double stranded
DNA
Step 4: Integrate: HIV DNA strand releases another enzyme called integrase, which allows it to become part of the cell’s DNA.
Step 5: Replicate: HIV’s DNA is in control of the hijacked cell and make long chains of the virus.
Step 6: Assembly: These long chains and other viral material are being assembled and start to move toward the cell’s surface.
Step 7: Budding: The assembled parts start to grow off the cell wall.
Step 8: Maturity: Grown off the cell’s surface, it pops off. Hijacked cell dies and this new mature HIV virus has a mission of finding another
cell victim with a CD4 receptor and start the whole process again.
STAGES: Acquired Immunodeficiency Syndrome
Acute Stage: Chronic Stage (Asymptomatic Stage) (AIDS)
DEFINITION: DEFINITION DEFINITION
Begins about a couple of weeks to a Lower viral load but the virus is still Last Stage
month after becoming infected replicating and destroying the cells. Immune system will be completely
CD4 count is more than 200 to about destroyed by the virus and without
500 cell/mm3 medications survival time is only a few
years
CD4 count drops to less than 200 cells
per millimeter or
Opportunistic disease is present
CLINICAL MANIFESTATIONS CLINICAL MANIFESTATIONS CLINICAL MANIFESTATIONS
Flu-like that last for a few weeks May not have signs and symptoms Sweats
Aches Fever Chills
joint pain Fatigue Recurring fever
headache Swollen lymph nodes — often one of Chronic diarrhea
fever the first signs of HIV infection Swollen lymph glands
fatigue Diarrhea Persistent white spots or unusual
sore throat Weight loss lesions on your tongue or in your
swollen lymph nodes Oral yeast infection (thrush) mouth
GI upset Shingles (herpes zoster) Persistent, unexplained fatigue
Rash Pneumonia Weakness
Diarrhea Weight loss
Weight loss Skin rashes or bumps
Cough
Night sweats
RISK FACTORS
having unprotected anal or vaginal sex;
having another sexually transmitted infection (STI) such as syphilis, herpes, chlamydia, gonorrhoea and bacterial vaginosis;
sharing contaminated needles, syringes and other injecting equipment and drug solutions when injecting drugs;
receiving unsafe injections, blood transfusions and tissue transplantation, and medical procedures that involve unsterile cutting or
piercing; and experiencing accidental needle stick injuries, including among health workers
DIAGNOSTIC
Seroconversion – it detects antibodies against the virus
Combination test: tests for the antigen and antibodies of HIV
Antibody HIV test
Nucleic acid test (NAT): measures the amount of virus in the blood (viral load)
CD4 count: used to measure the helper t cells
ELISA Test – which stands for enzyme-linked immunosorbent assay, is used to detect HIV infection.
MOT
Unprotected sexual contact
Drug use (needle sharing)
Blood product transfusion
Needle stick injury or unclean needle from a piercing or tattoo
During pregnancy (pregnancy itself, birthing process, or via breastmilk)
Non-sterile tools
COMPLICATION
Infections common to HIV/AIDS
Pneumocystis pneumonia (PCP).
Candidiasis (thrush).
Tuberculosis (TB).
Cytomegalovirus.
Cryptococcal meningitis
Toxoplasmosis
Cancers common to HIV/AIDS
Lymphoma.
Kaposi's sarcoma.
HPV-related cancers.
Other complications
Wasting syndrome.
Neurological complications.
Kidney disease.
Liver disease.
MEDICATION:
PrEP: Pre-Exposure Prophylaxis
Prevents becoming infected with HIV BEFORE an encounter with HIV
Truvada (emtricitabine/tenofovir disoproxil fumarate)
Descovy (emtricitabine/tenofovir alafenamide)
PEP: (Post-Exposure Prophylaxis)
HIV medications taken AFTER an encounter with an HIV infected person to help prevent HIV.
Truvada and Isentress (Raltegravir)
Truvada and Dolutegravir (Tivicay)
Antiretroviral Treatment (ART):
Goal of ART: limit the virus’ ability to replicate by interfering with parts of the HIV life cycle
decreases the amount of virus in the blood
increases CD4 numbers (>500)
six Classes of ARTs
1. Attachment Inhibitors:
- Post-attachment Inhibitors: binds with the CD4 receptors and inhibits the HIV’s glycoprotein (gp120 knob) from being able to
activate and engage the co-receptors CXCR4 and CCR5. Trogarzo (ibalizumab)
- Attachment Inhibitors: binds to the glycoprotein on HIV (gp120) and inhibits it from engaging with the CD4 receptor Rukobia
(Fostemsavir) (pill)
2. Entry Inhibitors:
- Chemokine Receptor Antagonists (CCR5 Antagonist): blocks the co-receptor CCR5 on the cell so HIV can’t engage the
receptor and enter the cell Maravirco (Selzentry) (pill)
3. Fusion Inhibitors:
- stops HIV from entering the cell (the virus must fuse with the CD4 cell in order to enter and inject its viral material into the
cell) Enfuvirtide (Fuzeon)
4. Inhibits Reverse Transcriptase:
- prevents the enzyme reverse transcriptase from turning viral RNA into viral DNA
- Non-nucleoside Reverse Transcriptase Inhibitors (NNRTIs): stops the enzyme reverse transcription from working by BINDING
to it. Doravirine, Efavirenz, Etravirine, Nevirapine, Rilpivirine
- Nucleoside/Nucleotide Reverse Transcriptase Inhibitors (NRTIs): modifies reverse transcriptase’s role when it tries to convert
viral RNA into viral DNA. This will alter the development of the HIV’s DNA so the virus can’t recreate itself. Abacavir,
Emtricitabine, Lamivudine, Zidovudine, Tenofovir disoproxil fumarate
5. Integrase Inhibitors:
- prevents the enzyme integrase from allowing HIV to insert its DNA into the cell’s DNA. Raltegravir (PEP), Dolutegravir,
Cabotegravir
6. Protease Inhibitors:
- stops the enzyme protease from cutting the long chains of virus. This process is stopped so the immature virus can’t be
assembled and mature. Atazanavir, Darunavir, Fosamprenavir
NURSING MANAGEMENT
Screening patients for possible HIV infection,
Educating (testing, transmission, preventing OIs, antiretroviral therapy),
Monitoring labs, patient’s signs/symptoms for opportunistic diseases (progression of the disease)
SYPHILIS
Key Players:
Treponema pallidum – is a spirochaete bacterium with various subspecies that cause the diseases syphilis, bejel (also known as endemic
syphilis), and yaws.
DEFINITIONS
- Bacterial infection caused by the spirochete treponema pallidum, and is considered a sexually transmitted disease.
- Also known as “the great imitator”, as it mimics a large number of different condition.
STAGES IN ACQUIRED SYPHILIS:
PRIMARY STAGE – 3-90 days after infection
Single chancre – sore at the original site of infection
Painless
Firm
Open sore
SECONDARY STAGE – 4-20 weeks after infection
Rash
Fever
Swollen lymph nodes
Wartlike sores in mouth, armpits, genital anus
Headache
Sore throat
Jaundice
Hair loss
LATENT STAGE – no symptom
TERTIARY – 3-15 years of infection if untreated
Lesion sometimes appear
Develops quarter of untreated cases
- Gummatous syphilis – presence of soft lumps of inflammatory tissues called gummas, which can infiltrate and destroy
any organ.
- Cardiovascular syphilis – affects the aorta and the heart valves, causing aortic aneurysm and aortic valve disease.
- Neurosyphilis – number of problems in the nervous system: meningitis, seizures, stroke, hearing loss, visual
impairment, speech disorder, dementia and other mental disorders.
PATHOPHYSIOLOGY
Primary stage – after the treponema pallidum lands on the skin or mucous membrane, the spirochetes destroy the soft tissue in the body and that
results in the formation of ulcers called syphilitic chancre. It heals on their own in a few months. But during that time some spirochetes go to
nearby lymph nodes where they cause lymph adenopathy which has lymph node enlargement and then they get into the lymph and finally into
the blood stream. If the syphilis is acquired through blood transfusion, then there may not be an early localized stage at all and no primary
chancre.
Second stage – the dissemination stage. Spirochetes enter into the bloodstream which is called spirochetemia. This causes generalized
lymphadenopathy, which is when the spirochetes can be found in the lymph nodes throughout the body. The spirochetes like to attach to and
infect endothelial cells and small capillaries near the skin. This causes non-itchy maculopapular rash which has small bumps that are either flat
or raised. The rash starts from the trunk and then spreads out to the arms and legs and eventually to the palms, soles, genitalia and other mucous
membranes. These rashes can sometimes be pustular which means they’re filled with the white fluids pus or they can be popular squamous
which is when they’re scaly and hard. In addition, there can be something called condyloma lata which are smooth, white, painless wart like
lesions and they appear in moist areas like genitals around the anal region and the armpits. So these various rashes can erupt all over the body
and the lesions are chock-a-block full of spirochetes which makes the secondary syphilis the most infectious stage. The rashes from the
secondary syphilis usually resolve within the few weeks or months.
Latent phase – this is when the disease enters a dominant or asymptomatic phase. During this phase, the spirochetes can mostly be found in the
tiny capillaries of various body organs and tissues. Latent phase can be further divided into an early phase and the late phase. Early latent
syphilis occurs within a year of infection, and during that time, the spirochetes can re-enter the blood so this means that during early latent
syphilis, they can still be found circulating in large numbers in the blood causing symptoms of secondary syphilis. However, the late latent
phase is generally after a year, and that’s because spirochetes generally stay within the tiny capillaries of various body organs and tissues. As it
turns out, there are actually only very few spirochetes which are found in the capillaries, tissues and organs. But there is a severe immune
response, so severe that it causes a tremendous amount of damage to the cells there and that triggers the next stage.
Tertiary syphilis – in this phase, there’s a type 4 hypersensitivity reaction. Which means that there’s an immune response that’s mainly led by t
cells and they recruit phagocytes like macrophages and cause the release of pro-inflammatory cytokines such as tumor necrosis factor
interleukin 1 and interleukin 6. All of these leads to local swelling or edema as well as redness, warmth and systemic symptoms like fever. T
pallidum has three main antigens these include groups specific antigen which is present on ultra-panama’s. species-specific antigen which is
specific to t pallidum and cardiolipin which is a lipid antigen which interestingly is present within the spirochetes as well as cells in our body.
Now plasma cells like to get themselves involve in the immune reaction by producing antibodies against these antigens.
MOT
Acquired syphilis – t pallidum enters via body fluids
Sexual contact (oral, anal, vaginal)
Cuts/breaks in skin or mucous membranes
Contaminated needles
Direct contact with skin lesion
Blood transfer (transfusion, need sharing)
Non-sexual direct contacts with infected skin lesion
Congenital syphilis – mother has syphilis
CAUSES
Treponema pallidum
DIAGNOSTIC
Serological tests – for antibodies against the bacteria in blood or cerebrospinal fluid samples.
Dark-field microscopy – used to visualize spirohetes from chancre exudates or lymph node aspirates.
Silver nitrate – a dieterie stain, it can stain the bacteria in grey or black and background yellow
Treponema pallidum particle agglutination test (TPPA) –
MANAGEMENT
Penicillin g benzathine
NURSING MANAGEMENT
Educate patient on safe sex practice
Encourage the use of condoms
Encourage treatment of a partner
Administer benzathine penicillin
Educate patient on avoiding sex with an infected partner
Listen to the heart for the murmur of aortic regurgitation
Check the chest x-ray report (syphilis can cause aortic aneurysms)
Assess neurologic and mental status (rule out tertiary syphilis)
Assess genitals to ensure healing has occurred
GONORRHEA
Key Players:
Neisseria gonorrhoeae is a bacterial pathogen responsible for gonorrhoea and various sequelae that tend to occur when asymptomatic infection
ascends within the genital tract or disseminates to distal tissues.
DEFINITIONS
- Gonorrhea is a sexually transmitted infection (STI) caused by the bacterium Neisseria gonorrhoeae.
CAUSES
Neisseria gonorrhoeae
MOT
oral, anal, or vaginal sex.
birthing parent to baby during delivery.
CLINICAL MANIFESTATIONS
Gonorrhea infection in men include:
Painful urination
Pus-like discharge from the tip of the penis
Pain or swelling in one testicle
CHLAMYDIA
Key Players:
Chlamydia trachomatis bacterium – bacteria that is most commonly spread through vaginal, oral and anal sex.
– an obligate intracellular bacterium that infects human mucosal epithelial cells of the oropharynx, genital tract,
anorectal area and conjunctiva.
Mucosal epithelial cells – (mucosal epithelia) are the initial responders that control and regulate immune responses to viral infections.
DEFINITIONS
- Chlamydia is a common sexually transmitted infection (STI) caused by bacteria. People who have chlamydia often don’t have outward
symptoms in the early stages.
CAUSES
Chlamydia trachomatis bacterium
CLINICAL MANIFESTATIONS
Painful urination
Vaginal discharge in women
Discharge from the penis in men
Painful sexual intercourse in women
Bleeding between periods and after sex in women
Testicular pain in men
RISK FACTOR
Being sexually active before age 25
Having multiple sex partners
Not using a condom consistently
History of sexually transmitted infection
COMPLICATIONS
Chlamydia trachomatis can be associated with:
Pelvic inflammatory disease (PID). PID is an infection of the uterus and fallopian tubes that causes pelvic pain and fever. Severe
infections might require hospitalization for intravenous antibiotics. PID can damage the fallopian tubes, ovaries and uterus, including
the cervix.
Infection near the testicles (epididymitis). A chlamydia infection can inflame the coiled tube located beside each testicle
(epididymis). The infection can result in fever, scrotal pain and swelling.
Prostate gland infection. Rarely, the chlamydia organism can spread to a man's prostate gland. Prostatitis can cause pain during or
after sex, fever and chills, painful urination, and lower back pain.
Infections in newborns. The chlamydia infection can pass from the vaginal canal to your child during delivery, causing pneumonia or
a serious eye infection.
Ectopic pregnancy. This occurs when a fertilized egg implants and grows outside of the uterus, usually in a fallopian tube. The
pregnancy needs to be removed to prevent life-threatening complications, such as a burst tube. A chlamydia infection increases this risk.
Infertility. Chlamydia infections — even those that produce no signs or symptoms — can cause scarring and obstruction in the
fallopian tubes, which might make women infertile.
Reactive arthritis. People who have Chlamydia trachomatis are at higher risk of developing reactive arthritis, also known as Reiter's
syndrome. This condition typically affects the joints, eyes and urethra — the tube that carries urine from your bladder to outside of your
body.
DIAGNOSTIC
Urine test
Swab test
MANAGEMENT
MEDICATION
doxycycline – taken every day for a week
azithromycin – one dose of 1g, followed by 500mg once a day for 2 days
NURSING MANAGEMENT
Educate the patient about chlamydia infections
Encourage patient to practice safe sex
Encourage the use of condoms
Encourage patient to remain compliant with medications
Check labs for culture results
Administer antibiotics as ordered
Check labs to ensure female is not pregnant as doxycycline cannot be given in pregnancy
Encourage the patient to notify the partner to come in for a screening test
Encourage patient to follow up in the STD clinic
AJ - Smaller Joints in the hands and feet - Weight-bearing joint (pain mugawas - Big toe followed by the foot and
after activity) the knee
JA - Pannus Formation (is a type of - osteophyte formation( nipis to - Tophus Formation (plural:
extra growth in your joints that can gabok) tophi) happens when crystals of
cause pain, swelling, and damage to the compound known as sodium
your bones, cartilage, and other urate monohydrate, or uric acid,
tissue. builds up around your joints.
N - Ulnar Drift (occurs when your - Heberden's nodes (are small, pea- -
knuckle bones, or sized bony growths that occur on the
metacarpophalangeal (MCP) joints, joint closest to the tip of the finger,
become swollen and cause your also called the distal interphalangeal
fingers to bend abnormally toward joint)
your little finger.) - Bouchard nodes?
- Swann Neck Deformities (a bending -
in (flexion) of the base of the finger,
a straightening out (extension) of the
middle joint, and a bending in
(flexion) of the outermost joint.)
CM - Weight loss - Obese - Elevated ESR (Erythrocytes
- Splenomegaly Sedimentation Rate) during
- Hepatomegaly purine food intake
- Lymphadenopathy - Renal Problem/damage
DX - Rheumatoid factor - X-RAYS - Blood Uric Acid Level (BUC) =
- ANA Normal ‹6 mg/dL
- ASO (present on GABHS patient)
T - Corticosteroids - NSAIDS - Anti-gout Medications
- NSAIDS (compli. Develop gastric - Colchicine (leads to
ulcer) - DIET: Control obesity gastrointestinal problems)
- COX-2 Inhibitor (inhibit pain) (leads - Allopurinol (increase fluid intake)
to heart problem) - Probenecid (blocks reabsorption
- DMARDS of uric acid in the body)
DIET:
- DIET: no diet (since autoimmune) - -control purine intake
PO - *Joint pain early in the morning, - Negative morning stiffness - 2 hours after ingestion of purine
decreased with activity - Pain after activity food
- Night time
HEMORRHAGIC SHOCK
Key Players:
Hypo: low
Vol: volume
Emic: blood
“low blood volume”
DEFINITIONS
When the fluid loss occurs exclusively as a result of severe blood loss, a more specific term is used to describe the condition. This is
called “hemorrhagic shock.”
It occurs when there is LOW fluid volume in the intravascular system.
Hypovolemic shock resulting from hemorrhage is more frequently noted in trauma patients with pelvic fractures and in patients with a
displaced or open femoral fracture in which the femoral artery is torn by bone fragments.
CAUSES
Causes of hypovolemic shock that involve bleeding include:
Broken bones around your hips
Cuts on your head and neck
Damage to organs in your belly, including your spleen, liver, and kidneys, because of a car accident or a bad fall
A tear in your heart or a large blood vessel, or a weakened spot in a large blood vessel that could burst
Problems with your digestive tract, such as ulcers
An embryo growing outside a woman’s uterus (ectopic pregnancy)
The placenta peeling away from the wall of a pregnant woman’s uterus (placental abruption)
A ruptured ovarian cyst
Heavy bleeding during labor or delivery, or in the following 24 hours
A disorder in which the tissue that usually lines a woman’s uterus grows outside it (endometriosis)
Causes that don’t involve bleeding include:
Dehydration
Diarrhea and vomiting
High fever
Severe sweating
Other gastrointestinal problems like stoma or fistulas
Kidney disease and diuretics
Fluids getting stuck in one part of your body because of a condition like pancreatitis or intestinal blockage
CLINICAL MANIFESTATIONS
thirst
muscle cramps
decrease in blood pressure, or poor blood supply throughout the body
RISK FACTORS
Car accident
Aneurysm
Dehydrated – risk if they lose salt that lead to a loss in blood volume
COMPLICATION
dehydration, which can be both a cause and a complication
damage to organs such as your kidneys or brain
metabolic acidosis
hypoxia
heart attack
diabetes
previous stroke
heart disease
previous lung disease
kidney disease
taking blood thinners like warfarin (Coumadin) or aspirin
DIAGNOSTIC
blood testing to check the severity of the hypovolemic loss
trauma ultrasound known as Focused Assessment with Sonography for Trauma (FAST)
CT scan to visualize body organs
echocardiogram, an ultrasound of the heart
MANAGEMENT
stabilizing the fracture to prevent further hemorrhage,
restoring blood volume and circulation,
relieving the patient’s pain,
providing proper immobilization,
protecting the patient from further injury and other complications
PHARMACOLOGIC THERAPY
dopamine
dobutamine
epinephrine
norepinephrine
NURSING MANAGEMENT
Monitor oxygenation and perfusion status of patient
If bleeding, hold firm, direct pressure.
place in modified Trendelenburg position
Obtain IV access
Collect labs
Fat Embolism Syndrome (FES)
Key Players:
EMBOLISM – a blocked artery caused by a foreign body, such as a blood clot or an air bubble.
DEFINITIONS
A fat embolism (FE) is a piece of intravascular fat that lodges within a blood vessel and causes a blockage of blood flow. Fat emboli
commonly occur after fractures to the long bones of the lower body, particularly the femur (thighbone), tibia (shinbone), and pelvis.
While fat emboli are common and generally resolve on their own, they can lead to a serious condition called fat embolism syndrome
(FES). FES can cause inflammation, multi-organ dysfunction, and neurological changes that can be deadly.
According to research, FES can be seen in 3 to 4 percent of those with one long-bone fracture and up to 15 percent of those with
multiple long-bone traumas.
describes the clinical manifestations that occur when fat emboli enter circulation following orthopedic trauma, especially long bone
(e.g., femur) fractures.
CAUSES
being male
being between the ages of 20 and 30
having a closed fracture (the broken bone doesn’t penetrate the skin)
having multiple fractures, especially in the lower extremities and pelvis
CLINICAL MANIFESTATIONS
rapid breathing
shortness of breath
mental confusion
lethargy
coma
pinpoint rash (called a petechial rash), often found on the chest, head, and neck area, which occurs due to bleeding under the skin
fever
anemia
RISK
young age,
closed fractures,
multiple fractures,
conservative therapy for long-bone fractures.
COMPLICATION
No long term complication
DIAGNOSTIC
physical examination
medical history
Gurd’s criteria
MANAGEMENT
intravenous fluids and drugs that will increase blood volume – this helps remove damaging free fatty acids from the body.
steroids and the blood thinner heparin
NURSING MANAGEMENT
oxygen levels will be monitored and may be given oxygen, if needed
help in breathing with mechanical ventilation
COMPARTMENT SYNDROME
Key Players:
COMPARTMENT – A separate division; specifically, a structural or biochemical portion of a cell that is separated from the rest of the cell
DEFINITIONS
Compartment syndrome occurs when pressure rises in and around muscles. The pressure is painful and can be dangerous. Compartment
syndrome can limit the flow of blood, oxygen and nutrients to muscles and nerves. It can cause serious damage and possible death.
Compartment syndrome occurs when too much pressure is exerted within the muscle compartments found within the fascia.
CAUSES
serious injury or too much physical exertion
fascia won’t expand
CLINICAL MANIFESTATIONS
6 P’s
Pain
Pallor
Pulselessness
Paresthesia (burning or tingling sensation) is an early sign of nerve involvement.
Paralysis
Poikilothermia
RISK FACTOR
Older adults
Patient who exhibit floating elbow fracture pattern
neurovascular injury patient
open radius/ulna fractures patient
high-energy trauma patient
humerus fractures sustained concurrently with forearm fractures patient
tibia fractures patient
COMPLICATION
serious damage
possible death.
DIAGNOSTIC
Physical exam
X-ray
Compartment pressure measurement test
Repeat pressure test
Doppler ultrasonography
MANAGEMENT
vacuum dressing to remove fluids and hasten wound closure
The affected arm or leg is splinted in a functional position and elevated to heart level, and prescribed intermittent passive ROM
exercises are usually performed.
when the swelling has resolved and tissue perfusion has been restored, the wound is débrided and closed
SURGICAL MANAGEMENT
Fasciotomy
NURSING MANAGEMENT
The nurse should frequently assess pain and neurovascular status of the affected limb and report any negative changes
The limb should be maintained in a functional position at the level of the heart to promote optimal blood flow.
Pain management as prescribed
Careful assessment of intake and output and urinalysis could alert the nurse to the development of rhabdomyolysis
Education for those patients discharged to home-based or community settings
Give instructions when to contact the primary provider for emergent follow-up.
Key Players:
"Thrombo" means blood clot
"embolism," means a circulating particle that causes an obstruction.
"Venous" means in the veins.
VTE – Venous thromboembolism (VTE), also known as blood clots, is a disorder that includes deep vein thrombosis (DVT) and pulmonary
embolism (PE). A deep vein thrombosis (DVT) occurs when a blood clot forms in a deep vein, usually in the lower leg, thigh, or pelvis. A
pulmonary embolism (PE) occurs when a clot breaks loose and travels through the bloodstream to the lungs.
DEFINITIONS DEFINITIONS
Deep Vein Thrombosis (DVT) – Deep vein thrombosis (DVT) Pulmonary Embolism (PE) – a blockage in one of the pulmonary
occurs when a blood clot (thrombus) forms in one or more of the arteries in your lungs. In most cases, pulmonary embolism is caused by
deep veins in the body, usually in the legs. Deep vein thrombosis blood clots that travel to the lungs from deep veins in the legs or, rarely,
can cause leg pain or swelling. Sometimes there are no noticeable from veins in other parts of the body (deep vein thrombosis).
symptoms.
PATHOPHYSIOLOGY PATHOPHYSIOLOGY
Reduced blood flow. Venous stasis occurs when blood Obstruction. When a thrombus completely or partially obstructs
flow is reduced, when veins are dilated, and when skeletal the pulmonary artery or its branches, the alveolar dead space is
muscle contraction is reduced. increased.
Damage. Damage to the intimal lining of blood vessels Impairment. The area receives little to no blood flow and gas
creates a site for clot formation. exchange is impaired.
Phlebitis. Formation of a thrombus frequently Constriction. Various substances are released from the clot and
accompanies phlebitis, which is an inflammation of the surrounding area that cause constriction of the blood vessels and
vein walls. results in pulmonary resistance.
Platelet aggregates. Venous thrombi are aggregates of Consequences. Increased pulmonary vascular resistance due to
platelets attached to the vein wall that have a tail-like regional vasoconstriction leading to increase in pulmonary
appendage containing fibrin, white blood cells, and many arterial pressure and increased right ventricle workload are the
red blood cells. consequences that follow.
Tail. The “tail” can grow or can propagate in the direction Failure. When the workload of the right ventricle exceeds the
of the blood flow as successive layers of the thrombus limit, failure may occur.
form.
Fragmentation. Fragmentation of the thrombus can occur
spontaneously as it dissolves naturally, or it can occur with
an elevated venous pressure.
Recanalization. After an acute episode of DVT,
recanalization or reestablishment of the lumen of the vessel
typically occurs.
CAUSES CAUSES
damage to a vein from surgery or inflammation and Fat from the marrow of a broken long bone
damage due to infection or injury. Part of a tumor
Air bubbles
RISK FACTOR RISK FACTOR
Age. Heart disease.
Lack of movement. Cancer.
Injury or surgery Surgery.
Pregnancy. Disorders that affect clotting.
Birth control pills (oral contraceptives) or hormone Coronavirus disease 2019 (COVID-19).
replacement therapy. Prolonged immobility
Being overweight or obese Smoking.
Smoking. Being overweight.
Cancer. Supplemental estrogen.
Heart failure. Pregnancy.
Inflammatory bowel disease.
A personal or family history of DVT or PE.
Genetics.
CLINICAL MANIFESTATIONS CLINICAL MANIFESTATIONS
Swelling. Chest pain.
Redness. Shortness of breath.
Warmth. Rapid heart rate.
Pain. Rapid breathing.
Lightheadedness.
Loss of consciousness.
Sweating or clamminess.
Coughing up blood.
COMPLICATION COMPLICATION
Pulmonary embolism (PE). pulmonary hypertension,
Postphlebitic syndrome. Cardiogenic shock.
Treatment complications. Right ventricular failure.
DIAGNOSTIC DIAGNOSTIC
medical history medical history
Blood tests Pulse oximetry
Vascular ultrasound Chest X-ray
MR venography CT pulmonary angiography (CTPA)
Contrast venography Pulmonary angiogram
MANAGEMENT MANAGEMENT
Prevent the clot from getting bigger.
Prevent the clot from breaking loose and traveling to the
lungs.
Reduce the chances of another DVT.
Blood thinners.
Clot busters (thrombolytics).
Filters.
Support stockings (compression stockings).
PHARMACOLOGIC THERAPY PHARMACOLOGIC THERAPY
Unfractionated heparin. Anticoagulation therapy.
Low-molecular-weight heparin (LMWHs). Thrombolytic therapy.
Oral anticoagulants.
Factor Xa inhibitor.
Thrombolytic therapy.
NURSING MANAGEMENT NURSING MANAGEMENT
Demonstrate increased perfusion as individually Increase perfusion
appropriate. Verbalize understanding of condition, therapy regimen, and
Verbalize understanding of condition, therapy, regimen, medication side effects.
side effects of medications, and when to contact the Display hemodynamic stability.
healthcare provider. Report pain is relieved or controlled.
Engage in behaviors or lifestyle changes to increase level Follow prescribed pharmacologic regimen.
of ease.
Verbalize sense of comfort or contentment.
Maintain position of function and skin integrity as
evidenced by absence of contractures, footdrop, decubitus,
and so forth.
Maintain or increase strength and function of affected
and/or compensatory body part.
Delayed union- occurs when healing does not occur within the expected time frame
DEFINITIONS
-
CAUSES
- Bone fracture
CLINICAL MANIFESTATIONS
Delayed healing
Misaligned bone
DIAGNOSTIC
xray
MANAGEMENT
ultrasound stimulation
electrical bone stimulation
SURGICAL
bone graft and autograft
NURSING MANAGEMENT
Monitor for possible complication
Patient safety
AVASCULAR NECROSIS
Key Players: THE BONE LOSE ITS BLOOD SUPPLY AND DIES
DEFINITIONS
- Tbone tissue death
CAUSES
Dislocation/fracture
Long term used of corticosteroids
Radiation therapy
Sickle cell disease
Rheumatoid arthritis
CLINICAL MANIFESTATIONS
Pain with movement that progress to pain at rest
DIAGNOSTIC
Xray/CT Scan/bone scans
MANAGEMENT
NSAIDs
Exercise
Limiting weight bearingof the affected region
Total replacement surgery
NURSING MANAGEMENT
Patient safety
HETEROTROPIC OSSIFICATION
Key Players: ABNIRMAL GROWTH OF BONE IN THE NON-SKELETAL TISSUES INCLUDING MUSLCE,TENDONS OR OTHER
SOFT TISSUE
DEFINITIONS
-
CAUSES
- Trauma/injury
- genetics
CLINICAL MANIFESTATIONS
decrease ROM
swelling or warmth of joint area
fever
increase spcity
joint pain,muscle pain, autonomic dysreflexia
DIAGNOSTIC
CT Scan/ UTZ/ xray
Three phase bone scan
MANAGEMENT
Provide ROM
Pain management
NURSING MANAGEMENT
Provide ROM