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PAtho > Unit 3 Part 1 > Flashcards

Unit 3 Part 1 Flashcards

1
Q

hepatitis

A

inflm of liver

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2
Q

et of hepatitis

A

microbes (including virus, bact, fungi, parasite)
drugs
autoimmunity

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3
Q

5 most common viruses in viral hep

A

Hep A B C D E virus

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4
Q

what are 2 other viruses in viral hep that are more uncommon and have dec threat/concern

A

hep F G virus

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5
Q

what other viruses may cause viral hep

A

epstein barr, cytomegalovirus

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6
Q

what is important to remember about viral hep

A

viruses all have same patho and similar mnfts but have different mode of transmissions, incubation periods, severity

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7
Q

Transmission of Hep a

A

fecal oral route, person-person, waterbourne, food bourne

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8
Q

incubation of hep a

A

15-50 days

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9
Q

carrier state/sev of hep a

A

mild, no carrier state

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10
Q

transmission of hep b

A

parenterally, sexually, oral-oral, perinatal

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11
Q

incubation period of hep b

A

28-160 days

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12
Q

what percent of hep b cases are severe

A

10-15%

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13
Q

carrier state in hep b

A

possible

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14
Q

what percent of hep c is chronic

A

80%

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15
Q

transmission of hep c

A

blood products, infected drug paraphenalia, sex

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16
Q

carrier state of hep c

A

freq carrier state (chronic) and chronic liver disease

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17
Q

what may follow hep c

A

Chronic liver disease and cirrhosis, liver CA

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18
Q

incubation period for hep c

A

15-160 days

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19
Q

2 main mechanisms of viral hep patho

A

virus causes hepatocyte injury via regular mOa

immune mediated response leading to tissue damage + inflm

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20
Q

what follows both mechanisms of viral hep

A

damage of livers fx cells -> necrosis

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21
Q

how long may it take for a self limiting case to heal

A

16 wks

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22
Q

3 phases of mnfts in viral hep

A

prodormal
clinical
recovery

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23
Q

mnfts of prodormal phase in viral hep

A

Lethargy, myalgia, anorexia, nausea, vomitting
abdm pain
fever

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24
Q

why does lethary, myalgia, anorexia, N+V occur in the prodormal phase of viral hep

A

dec liver fx, liver is not metb E or releasing glc

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25
Q

why does abdm pain occur in the prodormal phase of viral hep

A

rt to inflm, inc liver size -> liver pushes out on its capsule

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26
Q

when does the clinical phase of viral hep b occur

A

5-10 days post prodormal

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27
Q

what mnfts occur during the clinical phase of viral hep

A

mnfts get worse
jaundice
pruitis
hepatomegaly

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28
Q

why does jaundice occur during the clinical phase of viral hep

A

dec number of hepatocytes are available to break down heme -> inc bilirubin levels -> circulation

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29
Q

why does pruitis occur during the clinical phase of viral hep

A

dt accum of bile salts in the integument

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30
Q

how does hepatomegaly feel in clinical phase of viral hep

A

inflm, tenderness, pain

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31
Q

when do acute mnfts reside in viral hep

A

in the recovery phase, may take ~3wks

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32
Q

how do we track recovery from viral hep

A

using diagnostics

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33
Q

what do we measure when tracking recovery from viral hep

A

enzyme levels

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34
Q

why are enzyme levels important in recovery from viral hep? what trend should we see if prognosis is good

A

decreasing levels, because decreasing ez levels = normalizing liver fx. inc ez means there is still cell lysis and necrotic cells are releasing their content (thus inc ez level).

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35
Q

tx of viral hep (5)

A 
rest liver
diet mod
no alcohol/hepatotoxic drugs
symptomatic relief of pain/prutis
post exposure prophylaxis
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36
Q

how do you rest the liver

A

decrease e req of pt (bed rest, inc sleep_

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37
Q

what diet mods are used to treat viral hep

A

dec meal size, eat meals with more calories, dec fat

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38
Q

why do we want to decrease fat intake when txing viral hep

A

bile is used to emulsify fat, inc fat -> inc bile -> inc liver fx

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39
Q

what is post exposure prophylaxis

A

address factors that may have caused the virus

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40
Q

what post exposure prophylaxis can you use for hep A/B/C

A

teaching good hygiene, gamma globulin Tx to inc IR

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41
Q

what post exposure prophylaxis can you use for hep A/B

A

vaccinations

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42
Q

what post exposure prophylaxis can u use for hep c

A

anti viral drugs

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43
Q

autoimmune hep

A

severe and chronic form

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44
Q

et of autoimmune hep

A

idiopathic

complex trait with enviro trigger and HLA gene on chr 6

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45
Q

2 types of autoimmune hep

A

Type 1

Type 2

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46
Q

what population has increased incidence of type 1 autoimmune hep

A

women >40yo, normally these pts have other autoimmune issues

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47
Q

what causes damage in type 1 autoimmune hep

A

abn ab’s

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48
Q

what 2 abn ab’s cause damage in type 1 autoimmmune hep

A

ANA’s

Anti sm m. Ab’s

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49
Q

ANA

A

anti nuclear ab, self targets nucleocytes

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50
Q

anti sm. m. ab;s

A

targetting sm m. in liver, eg vessels and ducts

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51
Q

what population has inc incidence of type 2 autoimmune hep

A

age 2-14 peds pts, much like RHD

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52
Q

what abs are targetted in type 2 autoimmune hep

A

microsomes and cytosol

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53
Q

mnfts of autoimmune hep

A

may be asymptomatic -> liver failure
autoimmune presentations
similar to viral

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54
Q

how to dx autoimmune hep

A

must exclude other types of hep

test for elevated gamma globulin in blood

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55
Q

what is important to remember in autoimmune hep

A

self targeting Abs ONLY, no T cells

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56
Q

tx for autoimmune hep

A

supress pts own IR abs and give new gamma globulins

if drugs dont work - liver transplant?

57
Q

cirrhosis

A

end stage liver disease -> liver failure
degeneration of liver tissue -> dec fx capacity
fibrosis - nodular liver

58
Q

major problems assoc w cirrhosis

A

dec liver fx

Portal HTN

59
Q

et of cirrhosis (6)

A 
alcohol abuse (60-70%)
hep (mostly c) 10%
drugs
biliary disease
metb disorders
idiopathic cryptogene
60
Q

what metb disorder may be an et of cirrhosis

A

hemocromatosis - Fe overlaod -> deposition of Fe into tissue surrounding liver -> hepatotoxicity

61
Q

how much alcohol must be ingested to have alcoholic liver cirrhosis

A

> 80g/day in men

>40g/day in women

62
Q

what is the main patho behind cirrhosis

A

repetitive assault on hepatocytes -> dec regen of hepatocytes until regen doesnt occur

63
Q

what happens in cirrhosis when hepatocytes are noo longer able to regen

A

scar tissue forms instead

64
Q

what does inc scar tissue formation in cirrhosis ->

A

compression of ducts and vessels

65
Q

what happens when ducts are compressed by scar tissue (eg cirrhosis)

A

dec perfusion resulting in venous stasis

66
Q

what does venous stasis in the liver result in

A

portal htn rt inc hsp

67
Q

complication of portal htn

A

fluid shift out of v -> ascites

68
Q

what happens if there is bile stasis

A

gallstones? rt dec bile flow

69
Q

what happens to metb waste in cirrhosis

A

dec waste clearance

70
Q

most common mnfts of cirrhosis

A

anorexia, wt loss, weakness, hepatomegaly, jaundice

71
Q

what do we focus on when txing cirrhosis? why?

A

complications because common mnfts are unspecific

72
Q

complications of cirrhosis

A 
portal htn
ascites
varices
gi bleed
splenomegaly
73
Q

varices/varix

A

dilation of a v. assoc with hps, not in portal system! blood moves to these veins causing inc P in these assoc veins and dilate them

74
Q

why might a GI bleed occur in cirrhosis

A

ruptured varix

75
Q

why is splenomegaly a complication in cirrhosis

A

rt to engorgement of splenic v. -> fluid shift out of v. -> inc spleen size

76
Q

tx for cirrhosis

A

maximize cell regen

tx complications

77
Q

how do you maximize cell regen in cirrhosis

A

no alcohol, dec fat intake, rest

78
Q

portal htn

A

inc in P in Hps

79
Q

what is normal hps P

A

5-10 mmhg

80
Q

what P indicates portal htn

A

> 12 mmhg

81
Q

what is important to remember about HPS

A

its venous system only

82
Q

how much of the livers venous blood is the hepatic portal v. responsible for (brings in)

A

70%

83
Q

how much blood does the hepatic a. supply the liver with

A

30%

84
Q

what percent of hps veins drain the liver

A

100%

85
Q

et of portal htn

A

pre
intra
post hepatic
mostly dt cirrhosis (intra hepatic)

86
Q

major complication of portal htn

A

hemorrhaging varix

87
Q

other complications of portal htn

A

ascites
portosystemic shunts
spleenomegaly

88
Q

what is a portosystemic shunt

A

collateral channels form between hps and assoc veins

89
Q

why do portosystemic shunts occur

A

in attempt to displace some of the P out of the hps

90
Q

why is portosystemic shunts not beneficial

A

it passes the inc P onto other veins, making the problem bigger and it allows blood to bypass liver -> inc of unfiltered blood in circulation

91
Q

why does spleenomegaly occur in portal htn

A

inc P in hps veins -> engorgement of splenic v. -> inc vol in v. -> inc hsp -> fluid shift into spleen

92
Q

what is important to remember about spleenomegaly and portal htn

A

enlargment is not dt hypertrophy and the spleen does not have an inc workload

93
Q

portosystemic shunting of blood -> dev of collateral channels. what 3 things arise from this?

A

caput medusae
hemorrhoids
esophageal varices

94
Q

caput medusae

A

superficial vessels near umbillicus that becomes engorged dt portosystemic shunt formation. looks like a spiderweb on skin

95
Q

what 2 things can portosystemic shunting of blood lead to

A

dev of collateral channels

shunting of ammonia and toxins from GI -> general ciruclation

96
Q

what can shunting of ammonia and toxins from GI -> general ciruclation result in

A

hepatic encephalopathy

97
Q

3 complications of spleenomegaly

A

anemia, luekopenia, thrombocytopneia

98
Q

what does ascites follow

A

cirrhosis, portal htn

99
Q

how does RS HF lead to ascites

A

abdm organ distension rt engorgement of vessels in these organs dt inc blood vol -> inc HSP -> fluid shift from organs to body cavity

100
Q

et of ascites

A

RS HF
water / na retention and or protein loss dt renal failure
severe changes in HSP and or OP

101
Q

mnfts of ascites

A

dyspnea

abdmn distention

102
Q

dyspnea in ascites

A

rt inc abdm p dt fluid build up applying its self upwards on to the diaphragm, restricting movement causing difficulty breathing

103
Q

tx for ascites

A

small vol: diuretics

large vol: paracentesis + albumin tx

104
Q

how do diuretics work

A

remove fluid from vasculature -> dec blood vol -> dec HSP -> this means hsp in body cavity> then hsp in vessels, causing fluid to shift into vessles

105
Q

what does small vol ascites mean

A

fluid accum

106
Q

what does large vol ascites mean

A

fluid accum >5L

107
Q

why does paracentesis alone not work

A

removing fluid from cavity results making hsp body cavity

108
Q

why do you have to do paracentesis with a vol expander eg albumin

A

vol expander -> inc OP -> keep fluid in vessels while paracentesis occurs (inc OP in vessels pulls fluid in)

109
Q

Liver failure

A

cute or chronic

110
Q

how much fx capacity of liver is lost in failure

A

> 80%

111
Q

mortality rate of liver failure

A

50%

112
Q

et of liver failure

A

fulminant hepatitis
toxic liver damage
cirrhosis dt viral hepatitis

113
Q

which types of et of liver failure are acute

A

fulminant hep

toxic liver damage

114
Q

what is important to remember about patho and mnfts of liver failure

A

hepatiac insuff -> multiorgan failure

115
Q

what systems does liver failure affect

A

hematology
metabolism
hepatorenal syndrome
hepatic encephalopathy

116
Q

how does liver failure impair hemostasis and cause anemia

A

def in protein synth -> def in clotting factors and fibrinogen + platlet def

117
Q

what does dec marrow fx rt liver failure ->

A

thromobcytopneia, luekopneia, erythrocytopneia det dec GF and nutrients to marrow

118
Q

DIC

A

dissemiated intravascular coagulation

119
Q

why does DIC occur in liver failure

A

dec liver fx -> inadeq clearance of clotting factors -> clotting factors remain thruout vasculature resulting in inc risk for MI and CVA

120
Q

how does dec liver metb dt LF cause jaundice

A

inadeq bili processing -> jaundice

121
Q

why does hypoalbuminemia occur and how does it mnft

A

rt to dec OP

widespread edema + ascites

122
Q

hyperammonemia

A

inc ammonia in circulation

123
Q

why does hyperammonemia occur

A

def urea cycle -> inc ammonia dt liver not being able to push eqn to the left to make urea out of excess ammonia

124
Q

hyperestrogenism

A

dec estrogen catobolism-> accum of estrogen

125
Q

how does hyperestrogenism present in women

A

absence of menses

dec libido

126
Q

how does hyperestrogenism present in men

A

atrophy of testes
dec libido
enlargement of breasts

127
Q

hepatorenal syndrom

A

idiopathic renal failure

128
Q

how does LF lead to renal failure

A

LF -> severe dec in renal perfusion -> inschemia dt dec blood to kidney + dec blood to filter

129
Q

why is there a dec in blood in LF leading to RF

A

portal htn results in inc blood vol in HPS and dilated vessels

130
Q

what 2 conditions occur in RF

A

oliguria

azotemia

131
Q

olgiuria

A

dec renal output

132
Q

azotemia

A

build up of nitrogenous waste in blood rt dec sec by kidneys

133
Q

hepatic ecephalopathy

A

neuro mnfts rt liver failure

134
Q

what is happening in hepatic encephalopathy

A

toxins are not being removed by liver -> inc toxins in circulation dt liver failure + portosystemic shunts -> toxins affect brain

135
Q

what is the mechanism for hepatic encephalopathy

A

inc ammonia -> inc glutamate -> alteration of nt’s + change in bloods osmolarity dt inc [glutamate]

136
Q

early mnfts of hepatic encephalopathy

A

asterixis

hyperrflexia

137
Q

asterixis

A

trembling of hands dt inc nt

138
Q

late mnfts of hepatic encephalopathy

A

confusion, death, coma

PAtho (31 decks)

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