Unit 11 and 9 Complete

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HIV/AIDS

Key Players:

HIV stands for “Human Immunodeficiency Virus” and AIDS stands for “Acquired Immunodeficiency Syndrome”.

HIV – the virus

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

Gonorrhea infection in women include:


 Increased vaginal discharge
 Painful urination
 Vaginal bleeding between periods, such as after vaginal intercourse
 Abdominal or pelvic pain
SITES OF INFECTION
 Rectum. Signs and symptoms include anal itching, pus-like discharge from the rectum, spots of bright red blood on toilet tissue and
having to strain during bowel movements.
 Eyes. Gonorrhea that affects your eyes can cause eye pain, sensitivity to light, and pus-like discharge from one or both eyes.
 Throat. Signs and symptoms of a throat infection might include a sore throat and swollen lymph nodes in the neck.
 Joints. If one or more joints become infected by bacteria (septic arthritis), the affected joints might be warm, red, swollen and
extremely painful, especially during movement.
RISK FACTOR
 Sexually active women younger than 25
 men who have sex with men
 Having a new sex partner
 Having a sex partner who has other partners
 Having more than one sex partner
 Having had gonorrhea or another sexually transmitted infection
COMPLICATION
 Infertility in women. Gonorrhea can spread into the uterus and fallopian tubes, causing pelvic inflammatory disease (PID). PID can
result in scarring of the tubes, greater risk of pregnancy complications and infertility. PID requires immediate treatment.
 Infertility in men. Gonorrhea can cause a small, coiled tube in the rear portion of the testicles where the sperm ducts are located
(epididymis) to become inflamed (epididymitis). Untreated epididymitis can lead to infertility.
 Infection that spreads to the joints and other areas of your body. The bacterium that causes gonorrhea can spread through the
bloodstream and infect other parts of your body, including your joints. Fever, rash, skin sores, joint pain, swelling and stiffness are
possible results.
 Increased risk of HIV/AIDS. Having gonorrhea makes you more susceptible to infection with human immunodeficiency virus (HIV),
the virus that leads to AIDS. People who have both gonorrhea and HIV are able to pass both diseases more readily to their partners.
 Complications in babies. Babies who contract gonorrhea from their mothers during birth can develop blindness, sores on the scalp and
infections.
DIAGNOSTIC
 Urine test. This can help identify bacteria in your urethra.
 Swab of affected area. A swab of your throat, urethra, vagina or rectum can collect bacteria that can be identified in a lab.
MANAGEMENT
 Gonorrhea treatment in adults
 ceftriaxone — given as an injection
 oral azithromycin (Zithromax).
If you're allergic to cephalosporin antibiotics, such as ceftriaxone, you might be given:
 oral gemifloxacin (Factive)
 injectable gentamicin
 oral azithromycin.
 Gonorrhea treatment for partners
 Gonorrhea treatment for babies – treated with antibiotics.
NURSING MANAGEMENT

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

RHEUMATOID ARTHRITIS OSTEOARTHRITIS GOUTY ARTHRITIS


D - An autoimmune disease - Wear and tear theory - Purine foods intake
- exposure to previous infection
C - Infection – GABHS INFECTION - (the more you use it, the more it - Purine Foods (produce a
deteriorates) byproduct of uric acid that
crystallize/store in the joints)
RF - Common in 30’s – 60s - Common in 40s - Increasing age - Improper diet
- Obesity
S/ - Symmetrical (if its present in the - BOTH - Asymmetrical (affects the part
AS right part of the knee, it is present in - It depends what area of joints kung aha lang na deposit ang uric
the left part) ginalihok/ginagamit nimo permi. acid)

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.

OTHER EARLY COMPICATION

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.

DIC IN FRACTURES – result in widespread hemorrhage


 DELAYED COMPLICATIONS

Key Players: DELAYED UNION – NONUNION – MALUNION

Delayed union- occurs when healing does not occur within the expected time frame

Nonunion- results from failure of ends of fractured bone to unite

Malunion- the healing of fractured bone in a misaligned position

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

COMPLEX REGIONAL PAIN SYNDROME

Key Players: NEUROPATHIC PAIN INVOLVING LONG TERM PAIN

Abbormal impilse continue to travel stimulating inflammatory response


DEFINITIONS
- Regional dysfunction of autonomic destruction
CAUSES
- Unknown
- Triggered by fractures or surgery
CLINICAL MANIFESTATIONS
 prolonged pain burning or stinging
DIAGNOSTIC
 buddapest criteria
MANAGEMENT
 Pain management
 Physical therapy
NURSING MANAGEMENT

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

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