Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Complex patient MGMT > Hepatic disorders > Flashcards

Hepatic disorders Flashcards

1
Q

Portal Hypertension: Definition of Pathology and etiology

A

Increase inhepatic pressure greater than 6 mm Hg that causes venous BF to go back into the stomach, esophagus, umbilicus, and rectum.

Pre-hepatic:
- most common cause: Portal vein obstruction 2/2 thrombus.

Intra-hepatic causes:
cirrhosis (most common); schistosomiasis, flatworm infection of the liver, and Sarcoidosis

Post-hepatic:
right-sided heart failure, constrictive pericarditis (restriced blood flow from heart to lungs), and budd-chiari syndrome

most common case of portal hypertension is cirrhosis caused by an increase of intrahepatic vasoconstriction and incr, BF thus making pressure even higher. Cylces of inflammation & healing lead to fibrous bands of connective tissue that replace normal liver cells, -> abnormal liver architecture forming a mechanical barrier to blood flow and increasing resistance

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Portal Hypertension: Risk Fxs , gender and age

A
  • cirrhosis
  • intravenous drug use
  • unsanitary tattooing or piercing/ needlestick injury
  • blood transfusion before 1992
  • viral hepatitis
  • unprotected sexual intercourse.
  • Thrombus, tumor, or an

Males> Females with the exception of non-cirrhotic portal hypertension which Females get more than males

Idopathic: 43-56
Non-cirrhotic portal hypertension 25-35

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Portal Hypertension: Clinical impression

A
  • maybe asymptomatic until complications occur
  • distended abdomen for ascites
  • visibly engorged superficial abdominal veins (caput medusae)
    -GI bleeding, bloody stools, or vomiting blood for esophageal varices
  • jaundice for liver impairment
  • hand tremors with extended wrist
  • altered consciousness, lethargy, seizure, or coma
    A for Ascites
    B for bleeding(GI and/or esophageal varices)
    C for Caput Medusae
    D for diminished liver function(Jaundice)
    E for enlarged spleen(Splenomegaly, Anemia, Pallor)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Portal Hypertension: Diagnostic Tests/Screens

A

Gold standard: hepatic Venous Pressure Gradient Measurement (Differences btwn pressures in inferior vena cava and hepatic portal vein)

  • MRI CT/ Lab tests to see if there are other complications such as, ascites, cirrhosis, splenomegaly
  • Upper GI Endoscopy to ID esophageal varices
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Portal Hypertension: Med MGMT

A
  • Propranolol (Beta blocker) can decrease portal venous pressure
  • Diuretics + sodium restriction are implemented to reduce the fluid overload (ascites )
  • TIPS (Transjugular Intrahepatic Portosystemic Shunt) is the preferred procedure to decrease hepatic portal pressure
  • if untreated can lead to coma and death
  • Transplant with liver failure
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Portal hypertension: Physical TherapyTests and Measures and Implications for evaluation

A
  • MoCA is designed to detect mild cognitive dysfunction
  • DGI for balance deficits or gait impairments poss. attributed to peripheral edema, proprioceptive or sensation deficits
  • Neurologic for nassociated neuro deficts
  • Ab screen; palpation and ausculatation
  • Increased heart rate and decreased blood pressure indicates decreased venous return

Educate

  • less alcohol ; alcohol-related osteoporosis and areobic capacity
  • decr ab pressure methods
  • refer to PCP if unmanaged
  • nutrtion
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Hepatitis definition and etiology

A

Inflamation of the liver.
exists in A, B, C, D E with D & E being the most rare forms.
can be contractd via virus, a chemical or drug reaction, or alcohol abuse

Hep A - acute liver infection spread by fecal-oral transmission-spread by:-feces-saliva-contaminated food and water

Hep B / Hep C can be acute or chronic and can lead to sevre liver issues, failure or death if untreated. Can be spread by -Parenteral-Sexual contact-Unidentified exposure1-Perinatal

Hep cells do not destroy, they cause severe infmation that generally most can fight off expcept for immuno compromised, young and old

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Hepatitis risk fxs, gender and age

A

Hepatitis A
-Direct contact with someone with hepatitis A-Traveling to or adopting a child from countries where hepatitis A is common-Men who have sex with men-Injection or non-injection drug use-Homelessness-Clotting factor disorders-Working with nonhuman primates.-Tattoos or body piercings with unsterile or shared needles

Hepatitis B- Born to infected mother-Sexual partners or household contacts of infected persons-Men who have sex with men-Injection drug use-Health care and public safety workers at risk for exposure to blood-Hemodialysis patients.

Hepatitis C
Injection drug use-Specific types of health care exposures-HIV-positive-Born to infected mother-
generally males 18-50

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Hepatitis clinical presentation

A

Generally Fever•Fatigue•Loss of appetite•Nausea•Vomiting•Abdominal pain•Dark urine, joint pn and jaundice Clay-colored stool
Hep A - Diarrhea, Symptoms begin up to 28 days after exposure
Hep B - 90 days after exposure
Hep C- 2-26 weeks

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Hepatitis Diagnostic tests

A

Hep A - elevated levels of bilirubin or jaundice
Hep B- screening seromarker
Hep C- Screening tests for antibody to HC

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Hepatitis med MGMT

A

A- Vaccine and use ofImmune globulinbefore or within2 weeks of exposure
B Vaccine and treatment (no cure) α-Interferon andantiviral agents
C no vaccine - interferon and ribaviron

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Hepatitis Physical TherapyTests and Measures and Implications for evaluation and best prax

A

ROM/MMT to address joint pain and fatigue, but mus weakness is not an issue according to study cept’ for older sedentary adults, but every benefits from exercise

  • EDU on mental health and how the disease spreads
  • Fulminant Hepatic Failure- strenuous exercise should be avoided
  • watch for: signs of anemia (includes low hemoglobin, weakness, dyspnea upon exertion, skin pallor, tachycardia, and increased fatigability), infection, and GI bleeding (easy bruising).
  • clean surfaces
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Pancreatitis etiology and definition

A

Acute inflamation of the pancreas that can be acute or chronic.
Leads to auto digestion (self digestion)
- Acute is mild and can lead to systemic dysfxn
- 15% of acute cases can turn into chronic cases
- etio: excess levels of trypsin (responsible for activating other pancreatic enzymes) are made and are unable to be cleared by the body which leads to acinar cell damage and vascular damage -> inflammation and edema
Chronic cases caused by gene mutation, fam Hx and alcohol consumption

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Pancreatitis Risk fxs gender and age

A

long term alcohol use

  • gallstones
  • medications (oral estrogens, antibiotics, AZT, thiazide diuretics, corticosteroids)
  • blunt or penetrating trauma
  • family history
  • autoimmune diseases
  • cystic fibrosis
  • hypercalcemia -lipidemia (hypertriglyceridemia)
  • infection (bacterial, viral)
  • ischemia
  • neoplasm (pancreatic tumors)
  • peptic ulcers
  • postoperative inflammation
  • pregnancy (third trimester)
  • vasculitis -smoking
  • obesity
  • hereditary (2+ relatives with chronic pancreatitis or cystic fibrosis diagnosis)
  • Acute same for men and women, risk increased with age - chronic: more common in men (35-45)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Pancreatitis Clinical Presentation:

A

Acute:

  • abdominal pain (both upper quadrants)
  • nausea / vomiting
  • anorexia
  • light headed/dizziness
  • shortness of breath
  • symptoms can be triggered or increased by drinking alcohol and eating fatty meals.1

*red flags of worsening condition include: tachycardia, hypoxia, tachypnea, and changes in mental status.

Chronic:

  • epigastric abdominal pain radiating to the back
  • meals can aggravate symptoms
  • positional changes such as flexing knees to chest of flexing trunk can ease symptoms
  • nausea/vomiting (same as acute)
  • signs of disease progression and increased tissue damage includes diarrhea, steatorrhea, and diabetes mellitus
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Pancreatitis diagnostic tests

A

-increased serum amylase levels (3x normal levels), lipase, ALT (indicative of diagnosis related to gallstones)
-abdominal CT scan (assess for necrotizing pancreatitis)
- ultrasound for gallstones
-

17
Q

Pancreatitis Med MGMT

A

Acute: usually resolves within 3-5 days

  • IV fluids -medications for pain control
  • NPO
  • if related to Gallstones a laparoscopic cholecystectomy
  • if fluid collections are present surgery is postponed and fluid is drained
  • antibiotics if infected

Chronic:

  • alcohol intake and smoking cessation
  • pain management; nonnarcotics,
  • pancreatic duct sphincterotomy
  • drainage of pseudocysts
  • Pancreatectomy with islet cell autotransplantation (last resort option)
  • *Complications following the procedure include the development of pseudocysts, pseudoaneurysm bleeding, splenic vein thrombosis, and fistula formation
18
Q

Pancreatitis Physical Therapy Tests and Measures and Implications for evaluation and best prax

A
  • chief complaint of upper thoracic back pain
  • rule up pancetitis with change in bowel pattern
  • tenderness, guarding, dissension and rigidity in LUQ, epigastric and umbilical region
  • peripheral neuropathy for chronic cases
  • Red Flags - hypoxia, tachypnea, tachycardia, fever, hypotension, hypovolemia, or changes in mental status. - REFERAL TO ER
  • educate of Sx complication
  • adhere to NPO
  • scar mobilzation
  • promote back extenesion if decr
19
Q

Rhabdomyolysis Definition and etiology

A

rapid breakdown of striated skeletal muscle that results in intracelluar leakage and myoglobin is excreted and may lead to renal failure
- crushing type of injury is often the cause
- common causes include:
prolonged immobility,
use of alcohol,illicit (cocaine, heroin) prescription (statins) drugs,
strenuous exercise,
electrical burns, hyperthermia
,infections such as HIV and influenza (viral)
herbal supplements taken by athletes
Legionella (bacterial)

20
Q

Rhabdomyolysis Risk fxs, gender and age

A

-Acute exacerbation can occur with hot and humid -conditions
-prolonged immobility,
-trauma,
- recent overexertion of muscular activity especially for -the untrained individual
-untreated hypothyroidism
-higher dosages of statins,
-renal insufficiency, hepatic insufficiency,
- female sex,
-diabetes
Age/ gender
-typically seen in african american males
-occurs in pts over 60 and in children under 10 2/2 infection

21
Q

Rhabdomyolysis Clinical Presentation:

A

The classictriad of symptoms include: muscle weakness, myalgia (muscle pain), and tea-colored urine.
Not all patients present with triad, and less than 3% have urine color

22
Q

Rhabdomyolysis Diagnostic tests

A

Gold standard=serum creatine kinase levels
No standard is set for level of lab values, estimated that 5x the amount is enough to dx
myoglobin not tested 2/2 short 1/2 life

23
Q

Rhabdomyolysis Med MGMT

A

maintaining hydration, electrolyte balance, andalkalization of the urine to prevent deposition of myoglobin in the kidneys with the goal of preventingof acute renal failure.
Monitor blood lab levels
goal to urinate 200ml / hr

24
Q

Rhabdomyolysis Physical TherapyTests and Measures and Implications for evaluation

A
  • gather from subjective exam if ot participates in extreme exercise
  • nueroscreen
  • check msk system via MMT, ROM, strength, AROM,PROM areobic capacity 6MWT, TIRE test
  • stay hydrated
    -Phase 1:
    oRest for 72 hours
    o8 hours of sleep
    oWait for creatinine kinase levels to drop below 5 times upper limit

-Phase 2:
oBegin light activities, no strenuous activity, and physical activity must be done at own pace
oFollow-up with care provider after one week
oIf no symptoms can progress to phase 3

-Phase 3:
oGradual return to regular sport and referal out if needed

25
Q

Sarcoidosis Definition and Etiology

A

accumulation of immune cells such as macrophages and T lymphocytes that aggregate to form granulomas in parts of the body speifcally in the lungs. Etiology is most likely due to an autoimmune disorder

26
Q

Sarcoidosis Risk fxs gender and age

A
  • African and Scandinavian descendants are at great risk than Caucasians
  • Females at greater risk than Males
  • People 20-40 years old compared to other age range
27
Q

Sarcoidosis clinical presentation

A
  • can be asymptomatic
  • can be unnoticed till chest x-ray is taken is taken for other reasons
  • respiratory symps:
    -Shortness of breath (dyspnea), nonproductive cough
    •Constitutional Symptoms: fever, malaise, weight loss, and fatigue
    depending on where granulomas are:
    Integumentary: Skin rashes/lesions, multiple, tender, non-ulcerating nodules
    •Ophthalmic: Eye irritation, dry eyes, and occasionally blurry vision
    •Cardiovascular: Tachycardia, heart palpitations and/or lightheadedness
    •Orthopedic: Arthralgia (joint pain), myopathy, chronic tissue swelling, tenosynovitis, and otherinflammatory changes in the musculoskeletal system
    •Renal: Kidney Stones
    •Hepatic: Abnormal liver function
28
Q

Sarcoidosis Dx tests

A 
Other dsx must be ruled out 
Blood Tests,
 Chest X-ray, 
Pulmonary function tests, 
Biopsy of involved tissue, 
Bronchoscopy, 
Eye exam, 
MRI, CT Scan, PET Scan, Ultrasound
Neurologic Tests, 
Gallium Scan, Urinalysis
questions about environmental exposure
29
Q

Sarcoidosis med mgmt

A
  • Corticosteroids, prednisone, or other immunosuppressants/antinflammatoriesare commonly prescribed for symp control
  • Disease-modifying antirheumatic drugs (DMARDs) such as methotrexate, azathioprine, and leflunomide treat overactive immune systems
  • Monoclonal Antibodies such as infliximab, adalimumab, rituximab, and golimumab to treat overactive immune systems
  • Antibiotics such as minocycline, tetracycline, and doxycycline to treat sarcoidosis on the skin.
  • Antimalarials to treat sarcoidosis of skin, lungs, or nervous system.
  • Colchicine to treat joint pain from sarcoidosis.
  • Pentoxifylline to block TNF-awhich can cause granulomas
  • lung transplant
30
Q

Sarcoidosis Best practice for Physical Therapy Treatment adn pratices

A

take thorough exam while considering baseline for aerobic, balance, ROM, Strength, neuro fxn, respiratoy and vitals with chest exam
- watch fpr progression of dx

31
Q

Gout Definition and Etiology

A

group of dxs related to elevated level of uric acid serum andthe deposition of urate crystals in the joints, soft tissues, and kidneys

  • also known as crystal-induced arthritis
  • 10% cases- increased prodiction of urin acid
  • 90% decrease in renal function (90%) which leads to decr excretion and accumulation
32
Q

Gout Risk fxs, gender and age

A

-Familial history
-Increases in serum urate
-Increasing age
-Decreased renal function.
-Urate overproduction
-Individuals with:Leukemia, Lymphoma, Psoriasis, Hemolytic disorders and tChemotherapy.
-ETOH consumption/abuse
-Obesity
-Fasting medications
-Renal insufficiency
-Hypertension,Hypothyroidism Hyperparathyroidism
-Diet rich in purines(shellfish, trout, organ meats, spinach, beans, asparagus) and Fructose
Men > women
msot common inflammaroty condition in men
over 30 most common

33
Q

Gout clinical presentation

A

4 stages

  • Asymptomatic Hyperuricemia (serum levels more than 7mg/dL)
  • Acute Gouty Arthritis
  • Inter-Critical Gout
  • Chronic Tophaceous Gout

common locations

  • First toe & Fingers
  • Ankle-Knee
  • Wrist/ Elbow
  • Acute pain/onset
  • Erythema
  • Warmth
  • Hypersensitivity
  • Allodynia
34
Q

Gout diagnostic tests

A
  • Arthrocentesis (Invasive) into synovium to check for uric acid crystals
  • “Double Contour Sign” with US
  • blood tests
  • quick response to Rx
35
Q

Gout Best practice for Physical Therapy Treatment

A

Joint ROM(specifically, joints impacted by goutyarthritis)

  • Swelling/circumferential measurements
  • Edema considerations (pitting or not)
  • Strength testing/MMT
  • Focus on pain relif during flare up; tolerated ROM
  • P. flare up focus on strength around joints and deficits

Complex patient MGMT (6 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions