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Pathophysiology II > Week 4 > Flashcards

Week 4 Flashcards

1
Q

hepatic =

A

pertaining to liver

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2
Q

2 surfaces of liver

A

superior/ diaphragmatic
inferior/ visceral

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3
Q

units of liver

A

hepatocytes

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4
Q

oxygenated blood supply into liver

A

proper hepatic artery

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5
Q

deoxygenated blood out

A

portal vein, hepatic vein

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6
Q

what does liver do?

A

removes glucose from bloodstream and stores it as glycogen

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7
Q

what is glycogen?

A

forms of glucose that is stored in liver and muscles

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8
Q

what is bilirubin?

A

pigment excreted into the digestive fluid called BILE

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9
Q

excessive amounts of bilirubin =

A

jaundice/icteric

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10
Q

major ligament that divides left and right lobes

A

falciform

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11
Q

abc produces what inside the macrophage?

A

unconjugated bilirubin (type 1)

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12
Q

is unconjugated bilirubin lipid soluble?

A

yes

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13
Q

where is unconjugated bilirubin found?

A

blood stream, never in urine!

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14
Q

what does liver do with unconjugated bilirubin?

A

combines it with albumin to make conjugate it in the hepatocyte

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15
Q

is conjugated bilirubin water soluble?

A

yes, therefore it goes into urine

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16
Q

how do you make primary bile salts?

A

primary bile acids colic acid and chenodeoxycholic acid, conjugated with glycine and taurine.

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17
Q

what do primary bile salts form?

A

micelles

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18
Q

what is Jaundice?

A

Excessive amounts of bilirubin

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19
Q

if skin seems yellowish, can you assume it is?

A

no, look at eyes.

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20
Q

If sclera of eyes are yellow, is it likely jaundice?

A

yes, but still need to order lab tests

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21
Q

what confirms jaundice in lab tests?

A

Conjugated Bilirubin percentage (CB% = CB:Total Bilirubin (TB)) Ratio

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22
Q

3 levels of jaundice?

A
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23
Q

what is prehepatic jaundice?

A

it means pathology is going on before liver, in the blood

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24
Q

what is hepatic jaundice?

A

pathology happening in the liver (in the process of accepting bilirubin, impairment of intake, or in converting or conjugating bilirubin)

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25
Q

post hepatic jaundice?

A

pathology is after liver, maybe obstructed before or inside of the gall bladder

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26
Q

CB < 20% is what kind of jaundice?

A

unconjugated hyperbilirubin (UCB), pre-hepatic jaundice

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27
Q

who gets CB < 20%

A

newborns, Gilbert syndrom

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28
Q

what is porphyrin?

A

Porphyrin is a group of organic heterocyclic compounds that are comprised of four modified pyrrole subunits connected via methine bridges and form an aromatic macrocyclic structure, which has one or more side chains attached. Many porphyrins are naturally occurring pigments.

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29
Q

CB 20% - 50% jaundice is called?

A

Hepatic Jaundice: Mixed jaundice of UCB and CB

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30
Q

Diagnoses of Hepatic Jaundice?

A

Hepatitis
Hepatocellular carcinoma

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31
Q

what is CB > 50% called?

A

Post-hepatic jaundice, conjugated hyperbilirubinemia

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32
Q

Post-hepatic jaundice diagnoses

A

bile duct obstruction (intra/extrahepatic)

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33
Q

what is viral hepatitis?

A

disease manifestations due to viral infection of hepatocytes

34
Q

what do infection of hepatocytes lead to?

A

apoptosis of hepatocytes

35
Q

what does apoptosis of hepatocytes lead to?

A

necrosis

36
Q

causes of loss of functional hepatocytes?

A

-Elevation of liver enzymes (ALT, AST)
-Hyperbilirubinemia (jaundice)

37
Q

Sx of viral hepatitis?

A

It can be asymptomatic or present with malaise, weakness, nausea, anorexia, jaundice, dark urine

38
Q

Acute Viral Hepatitis defined as?

A

viral hepatitis with signs and symptoms < 6 mo

39
Q

Chronic Viral Hepatitis defined as?

A

viral hepatitis with signs and symptoms > 6 mo

40
Q

How is Hepatitis A transmitted?

A

Fecal-Oral (contaminated food, water, close body contact, rarely blood thru drug use or transfusion)

41
Q

Immune response to HAV

A

ALT spikes in the first two months, immunoglobulin (IgM) anti-HAV mounts after a month and comes down at 5.5 months, and total anti-HAV continues to go up for over a year

42
Q

Cases in US going up or down?

A
43
Q

Acute or recent HAV infection serology

A

Anti-HAV IgM

44
Q

Prior infection or immunization serology

A

Anti-HAV IgG

45
Q

HAV Treatment

A
  • Bed rest
  • If nausea and vomit are pronounced à oral intake substantially decreased à IV 10% Glucose is indicated
  • Diet à palatable meals as tolerated, no overfeeding
  • No strenuous physical exercise, alcohol, hepatotoxic agents
  • Corticosteroids have no benefit in viral hepatitis, including acute liver failure
46
Q

Incubation period of HAV

A

15-50 days
Average: 28 days
Abrupt onset

47
Q

HBV incubation period

A

45-160 days
(old: 50—180)
Insidious onset

48
Q

severity of HAV?

A

Mild

49
Q

Severity of HBV

A

Occasionally severe

50
Q

incubation period of HCV

A

14-180 days
(Old: 20-90)
Insidious onset

51
Q

Severity of HCV

A

Usually subclinical

52
Q

what is Ag

A

Antigen

53
Q

what is Ab

A

Antibody

54
Q

what is Ig?

A

Immunoglobulin

55
Q

What does Hb Ag mean?

A

Hepatitis B antigen

56
Q

what is HBV

A

Hepatitis B virus (enveloped, partially doublestranded DNA virus)

57
Q

what is Hbs Ag?

A

Antigen found on SURFACE of HBV, incubation period, continued presence indicates carrier state (still can transmit to others)

58
Q

What is Anti-Hbs Ag?

A

Antibody to Hbs Ag, incubation, chronic or cured/convalescent stage, or post HBV
vaccination, or history of HBV

59
Q

HbC Ag?

A

Antigen associated with CORE of HBV, rather than the surface

60
Q

Anti-Hbc Ag

A

Antibody to Hbc Ag, positive during window phase, IgM Hbc Ab is an indicator of recent disease, first to appear – initial 1-2 weeks of infection (early stage of infection)

61
Q

Hbe Ag?

A

A second, different antigenic determinant on HBV core, important indicator of transmissibility, EARLY stage presence of HBV

62
Q

Anti-Hbe Ag?

A

Antibody to Hbe Ag, indicates low transmissibility, indicates patient that about to recover from infection (not last long)

63
Q

Delta Agent?

A

Small RNA virus with Hbs Ag envelope, defective virus that replicates only in HBV- infected cells Linda Morse TCM Review – Hepatitis and CNT section. Rarely ordered as a lab test.

64
Q

Most important HBV test?

A

The surface tests. Hbs Ag, anti-Hbc Ab IgM

65
Q
A
66
Q

Tx of HBV?

A

anti-viral agents
Most popular are TAF and TDF, similar to anti-HIV drugs

67
Q

HCV is shifting to what age demographic?

A

from older to younger, namely through injection-drug use

68
Q

efficacy of all-oral, well-tolerated, highly effective Direct Acting Antivirals (DAA’s)

A

95-99%

69
Q

New tools, what does Liver Stiffness by transient elastography do?

A

measure amount of fibrosis

70
Q

why is it important to know fibrosis?

A

Level of severity of disease

71
Q

3 stages of Alcohol Liver Disease

A

Hepatic Steatosis (fatty change)
Alcohol Hepatitis
Alcohol Cirrhosis

72
Q

Hepatic Steatosis early on

A
  • Alcohol is metabolized to
    triacylglycerol
  • Reversible with alcohol abstinence, eating less fat
  • Liver is enlarged and may be tender
73
Q

During fasting for liver cleanup

A

promotes breakdown of stored fats in liver

74
Q

Alcoholic hepatitis 2nd stage

A
  • Acute illness caused by acetaldehyde following binge drinking
  • Some may have no symptoms and others may have RUQ abdominal pain, hepatomegaly, jaundice, malaise, anorexia, or even fulminant liver failure
75
Q

What’s a mallory body?

A

a necrotic hepatocyte with no nucleus and keratin buildup

76
Q

Alcoholic cirrhosis (3rd stage of Alcohol Liver Disease)

A
  • Develops in 15% of alcoholics
  • Typically micronodullar or Laennec cirrhosis
77
Q

Non-alcoholic Fatty Liver Disease

A

NASH (non-alcoholic steatohepatitis -> Cirrhosis from fat buildup.

78
Q

causes of NASH

A

Obesity, hyperinsulinemia, insulin resistance, Type 2 Diabetes

79
Q

Morbidity for NASH?

A

33.2% died or underwent liver transplant

80
Q

Gold Standard for determining severity of NASH

A

Liver biopsy

Pathophysiology II (5 decks)

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