Brainscape's Knowledge GenomeTM

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


See full index

Summer Patho > Hepatic Pathophysiology > Flashcards

Hepatic Pathophysiology Flashcards

1
Q

what effects does hepatic dysfunction have on the digestive system?

A 
impaired metabolism (carbs, cholesterol, bile salts)
esophageal varices
GI bleeding
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

what effects does hepatic dysfunction have on the cardiovascular system

A

portal hypertension = RHF
ascites = reduced cardiac function and cardiomyopathy
blood pressure disorders (hypotension)

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

what effects does hepatic dysfunction cause on the respiratory system?

A

ascites = diaphragm pressure causing alveolar dysfunction

portal hypertension = porto-pulmonary hypertension = aspiration risk

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

what effects does hepatic dysfunction cause for hematology?

A

anemia - d/t GI bleed, hypersplenism, hemolysis
malnutrition
disorders of coag and homeostasis - d/t decreased protein production in liver

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

what effects does hepatic dysfunction cause on the adrenal system?

A

pre-renal azotemia (elevated urea and nitrogen in blood)
severe electrolyte disorder
- hyponatremia: parallels ascites formation and triggers encephalopathy
- hypokalemia: common in setting of cirrhosis
- acid-base disturbances: range from classic resp alkalosis to high anion gap met acidosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

what effects does hepatic dysfunction have on the central nervous system?

A

hepatic encephalopathy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

cholelithiasis - definition, etiology, and risk factors

A

definition: hardened deposits of digestive fluid that form in your gallbladder (stones)
etiology: cholesterol over-secretion, excess bilirubin, gallbladder hypomotility
risk factors: obesity, hyperlipidemia, diabetes, pregnancy, family history, female

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

cholelithiasis signs and symptoms

A

RUQ pain - or referred pain to shoulder
N/V
indigestion

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

acute cholecystitis

A

occurs when a gallstone obstructs the cystic duct causing gallbladder to become distended and inflamed

patients will present with fever, RUQ pain, tenderness over gallbladder

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

management of cholelithiasis

A

initial - fluids, abx, pain
stabilized? take them for lap chole
septic shock? percutaneous chole

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

cholecystectomy anesthetic considerations

A

risk of opioid-induced sphinter of Oddi spasm

- treat this with glucagon, narcan, or nitrate

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

choledocholithaisis - definition and S&S

A

definition: complication of cholelithiasis in which a gallstone obstructs the common bile duct impeding the flow of bile from the liver to the duodenum

S&S: biliary colic (N/V/Cramp RUQ intermittent) and cholangitis (fever, rigors, jaundice)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

management of choledocholithaisis

A

surgical or endoscopic removal of the obstruction

  • preop ERCP to ID stone
  • followed by endoscopic sphincterotomy to remove obstruction
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

hyperbilirubinemia definition and types

A

build up of bilirubin in blood

  • conjugated (direct): follows biliary obstruction
  • unconjugated (indirect): imbalance between synthesis and catabolism of bilirubin
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

conjugated/direct hyperbilirubinemia

A 
remember this type is more related to biliary obstruction 
****obstructive jaundice***
intrehepatic cholestasis
hepatocellular injury
congenital infections
benign post-op jaundice
dubin-johnson
biliary atresia
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

unconjugated/indirect hyperbilirubinemia

A 
remember this type is more to do with synthesis/catabolism
***hemolytic anemia***
physiologic jaundice of the newborn
jaundice of prematurity
hgb disorder (sickle cell, thalassemia)
hereditary defects in conjugation
red blood cell enzyme disorders
drug inducted sepsis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Obstructive Jaundice

A

form of conjugated/direct hyperbilirubinemia
most commonly d/t obstruction of common bile duct
damage to hepatocytes = hepatitis
conjugated bili is unable to pass from liver to intestines
- enters the blood (likely through rupture of bile canaliculi
- direct emptying of bile into lymph system

MOST BILI IN PLASMA IS CONJUGATED

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

hemolytic jaundice

A

type of unconjugated/indirect hyperbilirubinemia
increased production of RBCs = increased production of bilirubin by macrophages = increased unconjugated bilirubin in blood
liver cannot conjugate all of the bilirubin so you get a primary risk in unconjugated bilirubin and a secondary rise in conjugated bilirubin
****excretory function of liver is not the problem - its the overproduction of bili
- there is in an increased urobilinogen production and excretion rate

** most bilirubin in plasma is unconjugated

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

Gilbert Syndrome

A
  • benign autosomal dominant inherited disorder that results in unconjugated hyperbilirubinemia
  • etiology = decreased activity of the uridine diphosphoclucuronate glucuronyltransferase
  • S&S = jaundice, fatigue, or abdominal discomfort that is precipitated by dehydration, exercise, fasting, or stress
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

Crigler-Najarr

A

one of the most severe forms of inherited unconjucated hyperbilirubinemia - autosomal recessive - diagnosed by lab (high serum concentration of unconjucgated bilirubin)

no or very little expression of the enzyme UGT1A1

severe jaundice, fever, and vomiting - can result in severe brain damage if left untreated

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

treatment for crigler-najjar

A

daily exchange transfusion
12 hours/day phototherapy
heme oxygenase inhibitors
oral calcium phosphate is often used to bind bili in the gut

curative - liver transplant before the onset of brain damage

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

benign postop intrahepatic cholestasis

A

definition - postop jaundice in which there is no hepatic inflammation or cell necrosis
etiology - multifactorial and associated with hypotension, significant blood loss, multiple transfusions or hypoxemia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

S&S of benign postoperative intrahepatic cholestasis

A

bilirubin and alk phos levels can increase two-to-fourfold within the first 7-10 days postop

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

hepatitis

A

inflammation of the liver

mostly do not have symptoms - clinical manifestations depend on severity of the inflammatory reaction and amount of cellular necrosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

symptoms of chronic viral hepatisis

A

fever, fatigue, loss of appetite, N&V, abd pain, dark urine, light-color stools, joint pain, jaundice

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

Hep B Virus

A

can cause both acute and chronic disease
transmitted by exposure to infected blood, semen, and other body fluids
high risk of death from cirrhosis and liver cancer

Vaccine offers 98-100% protection

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

Hep C Virus

A

most common viral hepatitis leading to liver transplantation in the US
antiviral medications can cure > 95% of persons affected

no effective vaccine

28
Q

Hep A Virus

A

lacks chronic stage and contributes only to acute infection
present in feces of infected persons
transmission - consumption of water food that is contaminated

29
Q

hep D virus

A

does not produce hepatitis by itself

  • occurs as a coinfection with acute HBV or as a super infection with chronic HBV
  • Hep B vaccines provide protection from Hep D
30
Q

hep E virus

A

rarely results in chronic liver disease

transmitted through consumption of contaminated water/food

31
Q

autoimmune hepatitis

A

inflammatory disease of the liver characterized by autoantibodies and hypergammaglobulinemia
S&S - can present with minimal/no symptoms, as an acute disease, or chronic disease
diagnosed by exclusion

32
Q

management of autoimmune hepatitis

A

prednisone alone or in combo with azathioprine
refractory disease therapy - immunosuppression with mycophenolate, cyclosprine A, or tacro
failed therapy = liver transplant

33
Q

covid 19 liver injury

A

etiology - unknown, but the theory is viral-induced injury, cytokine storm, sepsis, drug-induced injury

diagnosis - abnormal liver chemistries with elevated aminotransferases

treatment - ICU, vent support, CRRT, maintain hemodynamics and treat MODS

34
Q

alcohol-associated liver disease definition and diagnosis

A

a spectrum of liver injury resulting from alcohol use, ranging from hepatic steatosis to more advanced forms including alcoholic hepatitis, alcohol-associated cirrhosis, and acute AH presenting as acute-on-chronic liver failure

diagnoses with alcohol-specific biomarkers such as ethyl glucuronide and ethyl sulfate, which are detected in the urine, blood, and hair can be used to narrow the diagnosis

35
Q

signs and symptoms of ETOH liver disease

A

none with early ALD or with compensated cirrhosis
patient may present with clinical manifestations of alcohol abuse such as malnutrition, muscle wasting, or parotid gland hypertrophy
evidence of jaundice, ascites, hepatosplenomegaly, or pedal edema

36
Q

management of ETOH liver disease

A

abstain from alcohol and manage liver failure

liver transplant is the cure

37
Q

nonETOH fatty liver disease

A

excessive fat accumulation in the liver without any clear cause, associated with obesity, insulin resistance, type 2 DM, and metabolic syndrome

38
Q

signs and symptoms of NASH

A

hallmark feature is hepatic steatosis which occurs when there is more than 5% of fat in hepatocytes

progression will happen in these fatty hepatocytes are exposed to insults or stress which can then cause NASH

diagnosed via liver biopsy

39
Q

drug-induced liver injury

A

liver injury resulting from direct toxicity of an administered drug or from an immune-mediated mechanism
signs and symptoms are the same as all the other ones plus some systemic hypersensitivity (rash, fever, eosinophilia)

diagnosed by exclusion and knowledge of med list

management - cessation of the inciting drug, supportive care, and evaluation for liver transplantation

40
Q

inborn errors of metabolism

A

a group of rare genetic or inherited disorders resulting from an enzyme defect that affects the breakdown or storage of carbs, fats, and proteins

inherited as autosomal recessive, can rarely be autosomal dominant or x-linked

the diseases are wilson, AAT, hemochromatosis

41
Q

Wilson Disease

A

hepatolenticular degradation characterized by impaired copper metabolism, excess copper levels lead to increased oxidative stress in the cells of the liver, basal ganglia of the brain, and the cornea

autosomal recessive

managed by copper chelation therapy
oral zinc can also be used to stimulate binding of copper in the gut, preventing absorption and transport of copper to the liver

42
Q

S&S&diagnosis of wilson disease

A

asymptomatic or present with fulminant hepatic failure, alone with neuro or psych manifestations

other findings = hemolytic anemia, thrombocytopenia, renal failure, cardiomyopathy, hyperpigmentation

43
Q

alpha 1 antitrypsin (AAT) deficiency

A

a genetic disorder that results in defective production or AAT protein which is a protein that protects the liver and lungs from neutrophil elastase

autosomal dominant

diagnoses with elevated transaminase levels and may present with signs of liver dysfunction - confirmed with AAT phenotyping

44
Q

AAT signs and symptoms and management

A

transplant

early onset panlobular emphysema and symptoms of COPD

45
Q

hemochromatosis

A

disorder assoc with excess iron in the body that can lead to MODS

autosomal recessive

presents with cirrhosis, heart failure, diabetes, adrenal insufficiency, or polyarthropathy
fatigue and malaise

management - phlebotomy, iron chelating drugs, liver transplant

46
Q

diagnosis of hemochromatosis

A

serum transferrin, transferrin saturation, ferritin levels
genetic testing for the HFE mutation or other common mutations will confirm the diagnosis
echo and MRI can be used to ID cardiomyopathy and assess liver
biopsy can be used to quantify iron in liver and assess liver damage

47
Q

primary biliary cholangitis

A

autoimmune disorder that leads to progressive destruction of intrhepatic bile ducts in addition to periportal inflammation and cholestasis

trigger - environmental like cigarettes and hair dye

48
Q

primary sclerosing cholangitis

A

chronic inflammatory autoimmune disease affecting the bile ducts (primarily the large ducts)

S&S - fibrosis of biliary tree leading to cirrhosis and ESLD
40yo male

49
Q

cardiogenic ischemic hepatitis

A

insufficient perfusion of liver secondary to cardiogenic shock (caused by hypotension)

50
Q

congestive hepatopathy

A

passive hepatic congestion caused by elevated right sided heart pressures = perisinusoidal edema and impairment of the diffusion of oxygen and nutrients to hepatocytes

51
Q

portal hypertension

A

high BP in splanchnic venous system d/t high vasc resistance in portal vein from fibrosis and regenerative nodules within the liver

diagnosed via hepatic venous pressure gradient measurement

treat with intrahepatic portosystemic shunt

52
Q

prehepatic portal hypertension

A

increased blood flow or obstruction within portal vein or splenic vein

  • thrombosis
  • compression
  • splenomegaly, AVM, fistula
53
Q

intrahepatic portal hypertension

A

pre-sinusoidal - early primary biliary cholangitis, chronic active hepatitis
sinusoidal - cirrhosis, hepatitis, cytotoxicity
post-sinusoidal - sinusoidal obstruction, veno-occlusive disease

54
Q

post hepatic portal hypertension

A

heart - right heart fail, constrictive pericard
hepatic vein - budd chiari syndrome
IVC - stenosis, thrombosis, tumor invasion

55
Q

hepatic venous pressure gradient

A

1-5: normal
>10: clinical significant portal hypertension
>12: variceal rupture

56
Q

ascites

A

accumulation of fluid in peritoneal cavity causing abdominal swelling usually caused by cirrhosis

extensive liver fibrosis blocks blood flow from portal vein, blood backs up causing portal hypertension, fluid leaks out of portal vein into abdomen

diagnosed by paracentesis

57
Q

management of ascites

A

mild - low salt diet, diuretics, albumin replacement, avoid NSAIDs and alcohol
more severe ceases - paracentesis
refractory cases - TIPS, transplant

58
Q

varices

A

enlarged veins in lining of esophagus caused by portal hypertension
diagnosed by endoscopy
asymptomatic until varices begin to bleed - hematemsis black, tarry stools

59
Q

management of varices

A

prevent further liver damage
prevent varices from bleeding - nonselective beat blockers or variceal ligation
control bleeding if it occurs - volume resuscitation - endoscopy for ligation - TIPS for refractory bleeding

60
Q

variceal bleeding

A

high mortality: 40-70% for cirrhotic patient and 5-10% for non-cirrhotic
30% of initial bleeding episodes are fatal

treatment - TIPS, shunt, balloon tamponade, banding, sclerosant injection, pharm

61
Q

hepatic encephalopathy

A

brain injury d/t accumulation of ammonia
can be triggered by infection, electrolyte, metabolic disturbance, or meds (benzos and antipsychotics)
s&S = confusion, poor concentration, stupor, coma, asterixis, rigidity, hyperreflexia
diagnosed with serum ammonia levels

62
Q

management of hep enceph

A

treat underlying cause

lactulose - decrease absorption of ammonia
rifaximin- kills bowel flora that produce ammonia

63
Q

hepatorenal syndrome

A

development of renal failure in patient with advanced chronic liver disease - significant circulatory dysfunction secondary to locally acting vasodilators such as NO and prostaglandins

S&S are increased serum creat, normal urine sediment, minimal proteinuria, decreased urine sodium, oliguria

diagnosis is presence of cirrhosis and acute renal failure and exclusion of other causes of renal failure

managed by midodrine, octriotide, and albumin, hemodialysis, TIPS, liver transplant

64
Q

hepatopulmonary syndrome

A

hypoxemia due to dilated intrapulm vasc in the presence of liver disease or portal hypertension

platypnea - SOB that worsens in upright position and improves when lying supine

diagnosed via detection of an intrapulmonary right to left shunt by bubble study

manage with liver transplant

65
Q

portopulmonary hypertension

A

pulmonary arterial hypertension in the setting of portal hypertension with or without liver disease

etiology - systemic vasodilation with local pulm production of vasoconstrictors

S&S - dyspnea, weakness, systolic murmur, JVD, edema, ascites, hypoxemia, increased A-a gradient

mPAP > 25 at rest, screen with TEE and diagnosis with heart cath

Summer Patho (10 decks)

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