Unit 3 Part 1 Flashcards
hepatitis
inflm of liver
et of hepatitis
microbes (including virus, bact, fungi, parasite)
drugs
autoimmunity
5 most common viruses in viral hep
Hep A B C D E virus
what are 2 other viruses in viral hep that are more uncommon and have dec threat/concern
hep F G virus
what other viruses may cause viral hep
epstein barr, cytomegalovirus
what is important to remember about viral hep
viruses all have same patho and similar mnfts but have different mode of transmissions, incubation periods, severity
Transmission of Hep a
fecal oral route, person-person, waterbourne, food bourne
incubation of hep a
15-50 days
carrier state/sev of hep a
mild, no carrier state
transmission of hep b
parenterally, sexually, oral-oral, perinatal
incubation period of hep b
28-160 days
what percent of hep b cases are severe
10-15%
carrier state in hep b
possible
what percent of hep c is chronic
80%
transmission of hep c
blood products, infected drug paraphenalia, sex
carrier state of hep c
freq carrier state (chronic) and chronic liver disease
what may follow hep c
Chronic liver disease and cirrhosis, liver CA
incubation period for hep c
15-160 days
2 main mechanisms of viral hep patho
virus causes hepatocyte injury via regular mOa
immune mediated response leading to tissue damage + inflm
what follows both mechanisms of viral hep
damage of livers fx cells -> necrosis
how long may it take for a self limiting case to heal
16 wks
3 phases of mnfts in viral hep
prodormal
clinical
recovery
mnfts of prodormal phase in viral hep
Lethargy, myalgia, anorexia, nausea, vomitting
abdm pain
fever
why does lethary, myalgia, anorexia, N+V occur in the prodormal phase of viral hep
dec liver fx, liver is not metb E or releasing glc
why does abdm pain occur in the prodormal phase of viral hep
rt to inflm, inc liver size -> liver pushes out on its capsule
when does the clinical phase of viral hep b occur
5-10 days post prodormal
what mnfts occur during the clinical phase of viral hep
mnfts get worse
jaundice
pruitis
hepatomegaly
why does jaundice occur during the clinical phase of viral hep
dec number of hepatocytes are available to break down heme -> inc bilirubin levels -> circulation
why does pruitis occur during the clinical phase of viral hep
dt accum of bile salts in the integument
how does hepatomegaly feel in clinical phase of viral hep
inflm, tenderness, pain
when do acute mnfts reside in viral hep
in the recovery phase, may take ~3wks
how do we track recovery from viral hep
using diagnostics
what do we measure when tracking recovery from viral hep
enzyme levels
why are enzyme levels important in recovery from viral hep? what trend should we see if prognosis is good
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).
tx of viral hep (5)
rest liver diet mod no alcohol/hepatotoxic drugs symptomatic relief of pain/prutis post exposure prophylaxis
how do you rest the liver
decrease e req of pt (bed rest, inc sleep_
what diet mods are used to treat viral hep
dec meal size, eat meals with more calories, dec fat
why do we want to decrease fat intake when txing viral hep
bile is used to emulsify fat, inc fat -> inc bile -> inc liver fx
what is post exposure prophylaxis
address factors that may have caused the virus
what post exposure prophylaxis can you use for hep A/B/C
teaching good hygiene, gamma globulin Tx to inc IR
what post exposure prophylaxis can you use for hep A/B
vaccinations
what post exposure prophylaxis can u use for hep c
anti viral drugs
autoimmune hep
severe and chronic form
et of autoimmune hep
idiopathic
complex trait with enviro trigger and HLA gene on chr 6
2 types of autoimmune hep
Type 1
Type 2
what population has increased incidence of type 1 autoimmune hep
women >40yo, normally these pts have other autoimmune issues
what causes damage in type 1 autoimmune hep
abn ab’s
what 2 abn ab’s cause damage in type 1 autoimmmune hep
ANA’s
Anti sm m. Ab’s
ANA
anti nuclear ab, self targets nucleocytes
anti sm. m. ab;s
targetting sm m. in liver, eg vessels and ducts
what population has inc incidence of type 2 autoimmune hep
age 2-14 peds pts, much like RHD
what abs are targetted in type 2 autoimmune hep
microsomes and cytosol
mnfts of autoimmune hep
may be asymptomatic -> liver failure
autoimmune presentations
similar to viral
how to dx autoimmune hep
must exclude other types of hep
test for elevated gamma globulin in blood
what is important to remember in autoimmune hep
self targeting Abs ONLY, no T cells
tx for autoimmune hep
supress pts own IR abs and give new gamma globulins
if drugs dont work - liver transplant?
cirrhosis
end stage liver disease -> liver failure
degeneration of liver tissue -> dec fx capacity
fibrosis - nodular liver
major problems assoc w cirrhosis
dec liver fx
Portal HTN
et of cirrhosis (6)
alcohol abuse (60-70%) hep (mostly c) 10% drugs biliary disease metb disorders idiopathic cryptogene
what metb disorder may be an et of cirrhosis
hemocromatosis - Fe overlaod -> deposition of Fe into tissue surrounding liver -> hepatotoxicity
how much alcohol must be ingested to have alcoholic liver cirrhosis
> 80g/day in men
>40g/day in women
what is the main patho behind cirrhosis
repetitive assault on hepatocytes -> dec regen of hepatocytes until regen doesnt occur
what happens in cirrhosis when hepatocytes are noo longer able to regen
scar tissue forms instead
what does inc scar tissue formation in cirrhosis ->
compression of ducts and vessels
what happens when ducts are compressed by scar tissue (eg cirrhosis)
dec perfusion resulting in venous stasis
what does venous stasis in the liver result in
portal htn rt inc hsp
complication of portal htn
fluid shift out of v -> ascites
what happens if there is bile stasis
gallstones? rt dec bile flow
what happens to metb waste in cirrhosis
dec waste clearance
most common mnfts of cirrhosis
anorexia, wt loss, weakness, hepatomegaly, jaundice
what do we focus on when txing cirrhosis? why?
complications because common mnfts are unspecific
complications of cirrhosis
portal htn ascites varices gi bleed splenomegaly
varices/varix
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
why might a GI bleed occur in cirrhosis
ruptured varix
why is splenomegaly a complication in cirrhosis
rt to engorgement of splenic v. -> fluid shift out of v. -> inc spleen size
tx for cirrhosis
maximize cell regen
tx complications
how do you maximize cell regen in cirrhosis
no alcohol, dec fat intake, rest
portal htn
inc in P in Hps
what is normal hps P
5-10 mmhg
what P indicates portal htn
> 12 mmhg
what is important to remember about HPS
its venous system only
how much of the livers venous blood is the hepatic portal v. responsible for (brings in)
70%
how much blood does the hepatic a. supply the liver with
30%
what percent of hps veins drain the liver
100%
et of portal htn
pre
intra
post hepatic
mostly dt cirrhosis (intra hepatic)
major complication of portal htn
hemorrhaging varix
other complications of portal htn
ascites
portosystemic shunts
spleenomegaly
what is a portosystemic shunt
collateral channels form between hps and assoc veins
why do portosystemic shunts occur
in attempt to displace some of the P out of the hps
why is portosystemic shunts not beneficial
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
why does spleenomegaly occur in portal htn
inc P in hps veins -> engorgement of splenic v. -> inc vol in v. -> inc hsp -> fluid shift into spleen
what is important to remember about spleenomegaly and portal htn
enlargment is not dt hypertrophy and the spleen does not have an inc workload
portosystemic shunting of blood -> dev of collateral channels. what 3 things arise from this?
caput medusae
hemorrhoids
esophageal varices
caput medusae
superficial vessels near umbillicus that becomes engorged dt portosystemic shunt formation. looks like a spiderweb on skin
what 2 things can portosystemic shunting of blood lead to
dev of collateral channels
shunting of ammonia and toxins from GI -> general ciruclation
what can shunting of ammonia and toxins from GI -> general ciruclation result in
hepatic encephalopathy
3 complications of spleenomegaly
anemia, luekopenia, thrombocytopneia
what does ascites follow
cirrhosis, portal htn
how does RS HF lead to ascites
abdm organ distension rt engorgement of vessels in these organs dt inc blood vol -> inc HSP -> fluid shift from organs to body cavity
et of ascites
RS HF
water / na retention and or protein loss dt renal failure
severe changes in HSP and or OP
mnfts of ascites
dyspnea
abdmn distention
dyspnea in ascites
rt inc abdm p dt fluid build up applying its self upwards on to the diaphragm, restricting movement causing difficulty breathing
tx for ascites
small vol: diuretics
large vol: paracentesis + albumin tx
how do diuretics work
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
what does small vol ascites mean
fluid accum
what does large vol ascites mean
fluid accum >5L
why does paracentesis alone not work
removing fluid from cavity results making hsp body cavity
why do you have to do paracentesis with a vol expander eg albumin
vol expander -> inc OP -> keep fluid in vessels while paracentesis occurs (inc OP in vessels pulls fluid in)
Liver failure
cute or chronic
how much fx capacity of liver is lost in failure
> 80%
mortality rate of liver failure
50%
et of liver failure
fulminant hepatitis
toxic liver damage
cirrhosis dt viral hepatitis
which types of et of liver failure are acute
fulminant hep
toxic liver damage
what is important to remember about patho and mnfts of liver failure
hepatiac insuff -> multiorgan failure
what systems does liver failure affect
hematology
metabolism
hepatorenal syndrome
hepatic encephalopathy
how does liver failure impair hemostasis and cause anemia
def in protein synth -> def in clotting factors and fibrinogen + platlet def
what does dec marrow fx rt liver failure ->
thromobcytopneia, luekopneia, erythrocytopneia det dec GF and nutrients to marrow
DIC
dissemiated intravascular coagulation
why does DIC occur in liver failure
dec liver fx -> inadeq clearance of clotting factors -> clotting factors remain thruout vasculature resulting in inc risk for MI and CVA
how does dec liver metb dt LF cause jaundice
inadeq bili processing -> jaundice
why does hypoalbuminemia occur and how does it mnft
rt to dec OP
widespread edema + ascites
hyperammonemia
inc ammonia in circulation
why does hyperammonemia occur
def urea cycle -> inc ammonia dt liver not being able to push eqn to the left to make urea out of excess ammonia
hyperestrogenism
dec estrogen catobolism-> accum of estrogen
how does hyperestrogenism present in women
absence of menses
dec libido
how does hyperestrogenism present in men
atrophy of testes
dec libido
enlargement of breasts
hepatorenal syndrom
idiopathic renal failure
how does LF lead to renal failure
LF -> severe dec in renal perfusion -> inschemia dt dec blood to kidney + dec blood to filter
why is there a dec in blood in LF leading to RF
portal htn results in inc blood vol in HPS and dilated vessels
what 2 conditions occur in RF
oliguria
azotemia
olgiuria
dec renal output
azotemia
build up of nitrogenous waste in blood rt dec sec by kidneys
hepatic ecephalopathy
neuro mnfts rt liver failure
what is happening in hepatic encephalopathy
toxins are not being removed by liver -> inc toxins in circulation dt liver failure + portosystemic shunts -> toxins affect brain
what is the mechanism for hepatic encephalopathy
inc ammonia -> inc glutamate -> alteration of nt’s + change in bloods osmolarity dt inc [glutamate]
early mnfts of hepatic encephalopathy
asterixis
hyperrflexia
asterixis
trembling of hands dt inc nt
late mnfts of hepatic encephalopathy
confusion, death, coma
