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Patho II Test 1 > Liver Diseases > Flashcards

Liver Diseases Flashcards

1
Q

The Liver as a Digestive Organ

A

Biles salt secretion for fat digestion
Processing and storage of fats, carbohydrates, and proteins absorbed by the intestines
Processing and storage of vitamins and minerals

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2
Q

The Liver as an Endocrine Organ

A

Metabolism of glucocorticoids, mineralocorticoids, and sex hormones
Regulation of carbohydrate, fat, and protein metabolism

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3
Q

The Liver as a Hematolotgic Organ

A

Temporary storage of blood
Removal of bilirubin from the bloodstream
Hematopoiesis in certain disease states
Synthesis of blood clotting factors

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4
Q

The Liver as an Excretory Organ

A

Excretion of bile pigment
Excretion of cholesterol via bile
Synthesis of urea
Detoxification of drugs and other foreign substances

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5
Q

How much of the liver can be destroyed before life is threatened?

A

80%

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6
Q

Hepatocellular Failure

A

Typical manifestations: jaundice, muscle wasting, ascites, excessive bleeding, deficiencies of important blood proteins and vitamins, glucose imbalance, and impaired hormone production.

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7
Q

Jaundice

A

green-yellow staining of tissues by bilirubin, impaired bilirubin metabolism and one of the most characteristic signs of liver disease
divided into prehepatic, hepatic, and posthepatic/cholestatic

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8
Q

Prehepatic Jaundice

A

most common causes are hemolysis and ineffective erythropoiesis. The resorption of large hematomas in patients with mild liver disease is a frequent and harmless cause of mild jaundice attributable to UNCONJUGATED hyperbilirubinemia

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9
Q

Hepatic Jaundice

A

in neonate, immature UDPGT levels may result in jaundice. Various genetic disorders of UDPGT synthesis are characterized by high levels of UNCONJUGATED bilirubin in the blood
Viral hepatitis, alcoholic liver disease, autoimmune hepatitis, often result in jaundice because dysfunction within the liver cells results in elevate levels of conjugated bilirubin

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10
Q

Mutant UDPGT enzymes

A

can produce the common and benign Gilbert syndrome, low levels of UNCONJUGATED bilirubin may be increased by fasting or illness
viral gastroenteritis

Crigler-Najjar type I and II syndromes with severe neonatal unconjugated hyperbilirubinemia

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11
Q

Mutant UDPGT enzymes

A

can produce the common and benign Gilbert syndrome, low levels of UNCONJUGATED bilirubin may be increased by fasting or illness
viral gastroenteritis

Crigler-Najjar type I and II syndromes with severe neonatal unconjugated hyperbilirubinemia

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12
Q

posthepatic jaundice

A

level of canalicular bilirubin transport, rare inherited Dubin-Johnson and Rotor syndromes cause conjugated hyperbilirubinemia. both conditions have excellent prognosis
Benign cholestasis of pregnancy from high sex hormone levels in certain women (characterized by jaundice and itching)

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13
Q

A significant elevation in the levels of trranasminases out of proportion to the other live enzymes indicates

A

primarily hepatocellular disorder such as hepatitis

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14
Q

AST levels markedly higher than ALT

A

alcoholic and other toxic hepatitdes

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15
Q

ALT markedly elevated in related to AST

A

viral hepatitis

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16
Q

elevation of ALP indicates

A

intrahepatic cholestasis
generally caused by infiltrative process or drug reaction

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17
Q

Portal Hyptetension

A

a condition resulting from impaired blood flow through the liver as a result of increased resistance from fibrosis and degeneration of liver tissue.
Venous drainage of much of the GI tract is congested
anorexia, varices

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18
Q

Gastroesophageal Varices Etiology

A

results from portal hypertension; results from cirrhosis caused by chronic alcoholism or viral hepatitis
In tropical countries, schistosoma species of liver fluke is major cause

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19
Q

Gastroesophageal Varices pathogenesis

A

venous pathways dilate, common collateral pathways include spontaneous deep and usually asymptomatic portosystemic shunts such as splenorenal shunts; dilated veins in the small intestine, colon, and rectum are common too
can rupture which results in massive GI bleeding, life-threatening

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20
Q

Gastroesophageal Varices Clinical Features

A

Varices will affect more than half of cirrhotic patients
diagnosis made endoscopically, CT scans, upper GI barium examinations

21
Q

initial symptoms and signs of gastroesophageal varices

A

hematemesis, melena, bright red rectal bleeding, profound anemia, signs of shock
Two distinct phases, one coincident with and shortly after the bleeding, the other a period of 6-8 weeks after initial bleed, greatest occur of rebleed in first 72 hours

22
Q

Gastroesophageal Varices Treatment

A

perform fluid resuscitation, correcting coagulopathy, stop further bleeding
EGD
Endoscopic sclerosis
endoscopic ligation of esophageal varices
TIPS
liver transplantation

23
Q

Hepatic Encephalopathy

A

complex neuropsychiatric syndrome characterized by symptoms ranging from mild confusion to lethargy to stupor and coma

24
Q

Hepatic Encephalopathy Pathogenesis

A

“liver flap”
fulminant hepatic failure, severe chronic liver disease, live function severely depressed, blood is shunted
arterial ammonia level correlates positively with the level of encephalopathy

25
Q

Hepatic Encephalopathy Clinical Manifestations

A

hypokalemia, hyponatremia, alkalosis, hypoxia, hypercarbia, infection, use of sedatives, GI hemorrhage, protein meal gorging, renal failure, constipation
graded 1-4

26
Q

Hepatic Encephalopathy Grade 1

A

confusion, subtle behavioral changes, no flap

27
Q

Hepatic encephalopathy Grade 2

A

drowsy, clear behavioral changes, flap present

28
Q

Hepatic encephalopathy Grade 3

A

stuporous but can follow commands, marked confusion, slurred speech, flap present

29
Q

Hepatic Encephalopathy Grade 4

A

Coma, no flap

30
Q

Hepatic encephalopathy treatment

A

thiamine, ammonia levels drop protein can be reintroduced, antibiotics, laxatives

31
Q

Cerebral Edema Pathogenesis

A

swelling of the brain, both vascular and toxic mechanisms have been implicated as etiologic factors, major COD with acute hepatic failure
increased intracranial pressure, decreased blood perfusion

32
Q

Cerebral Edema Clinical Manifestations

A

systolic hypertension, irregular respirations, bradycardia, Cushing triad, deepening coma, extensor rigidity, pupillary dilation, respiratory arrest

33
Q

Cerebral Edema Treatment

A

intravenous infusion of hypertonic saline and mannitol, semi-Fowler position, barbiturate induced coma, liver transplant

34
Q

Ascites

A

accumulation of fluid in the peritoneal cavity
abdominal paracentesis should be performed, fluid studies
dietary sodium should be restricted, bed rest, diuretics,

35
Q

Spontaneous Bacterial Peritonitis

A

variety of defects in host defense predisposing to infection in the peritoneal cavity, specifically with low protein concentration
mild abdominal discomfort, acute renal failure, abdominal paracentesis
antimicrobial therapy, antibiotics

36
Q

Hepatorenal Syndrome

A

dire complication of patients with liver failure
rising serum creatinine levels and oliguria
intrarenal blood flow is seriously disturbed,
liver transplant

37
Q

hepatitis

A

inflammation of the liver parenchyma

38
Q

Hepatitis A (HAV)

A

RNA fecal-oral route
asymptomatic in children or mildly symptomatic in children
adults develop non specific GI, jaundice
IgG (long term), IgM (acute)
active immunization

39
Q

Hepatitis B (HBV)

A

double stranded DNA, highly prevalent (5% of world population)
infected blood/needles, sexual contact, perinatal infection in developing countries, healthcare care settings, tattooting etc

40
Q

Hepatitis C (HCV)

A

single stranded RNA, intravenous blood/drug transfer, a

41
Q

Hepatitis D (HDV)

A

incomplete viral organism that requires HBV for replication
parenteral routes, or sexual contact, blood contact

42
Q

Hepatitis E (HEV)

A

RNA virus spread via fecal-oral route

43
Q

Chronic Hepatits

A

lasts 6 months or longer
toxic, autoimmune, or metabolic

44
Q

chronic persistent hepatitis (triaditis or transaminitis)

A

low- grade liver inflammation
asymptomatic, mild non-specific symptoms , no drug treatment is indicated

45
Q

chronic active hepatitis (piecemeal necrosis)

A

progressive, destructive

46
Q

Cirrhosis

A

irreversible end stage of hepatic injuries,
CAH, steatohepatitis, metal storage disease, alcoholic liver disease, toxic hepatitis

47
Q

Biliary Cirrhosis

A

obliteration of bile ductules, PBC, often associated with lupus

48
Q

Biliary Flukes

A

immigrants/forgein travelers, treatment with anti-parasitic agents

49
Q

Primary Sclerosing Cholangitis

A

recurrent episodes of cholangitis with progressive biliary scarring and obstruction

Patho II Test 1 (2 decks)

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