liver Flashcards
liver fxn if BG high
glycogenesis: forms glycogen from excess glucose
liver fxn if BG low
glycogenolysis: breaks down glycogen into glucose
beta oxidation
breakdown of fatty acids (liver fxn)
hep A transmission
fecal-oral
hep B transmission
blood, sexual contact (semen, vaginal secretions, saliva)
hep C transmission
blood (transfusions, IVDU, multiple sex partners, piercings, tats, immunocompromised individuals, sharing personal items like razors, occupational exposures)
hep D transmission
percutaneous (increased incidence w IV drug abusers)
hep A & B s/s (+1 A only)
hepatomegaly
liver tenderness
splenomegaly ~15%
A: lymphadenopathy
hep C s/s
longterm consequences s/t inflammation- scarring- hep fibrosis- cirrhosis (30%)- hepatocellular carcinoma (3%)- end stage liver disease
increases Hep C viral load
EtOH lt 50g
hep A fecal excretion
up to 2 wks before clinically apparent illness
hep B onset
more insidious than A, can be abrupt
hep A illness & recovery
acutely ill: 2 - 3 wksfull recovery: ~9 wks
*hep B illness, incubation, recovery
acutely ill 2 - 3 weeks
*incubation 6 wks - 6 mo (avg 12 - 14 wks)
recovery 16 wks
can become chronic
*hep C incubation, illness
*incubation 6 - 7 wksfreq asx for years70% infected develop chronic disease
labs hep A vs B
- WBC WNL
- mild proteinuria
- ↑ bilirubin & alk phos
- ↑ AST & ALT (B gt A)
- bilirubinemia (precedes jaundice)
Hep A specific labs x2
anti-HAV IgM & IgG
- Hep A: IgM
- dx marker
- peaks 1st wk illness
- disappears w/in 3-6 mo
- Hep A: IgG
- indicates prev exposure
- non-infectivity & immunity
- peaks after 1 mo, may persist yrs
*Hep B specific labs x6
HBsAg, HBcAg, HBeAg
anti-HBs
anti-HBc IgM & IgG
*Hep B: first evidence infection / infectivity
HBsAg- persists → clinical illness
- indicates infectivity
- if persists 6+ mo ind chronic Hep B
*Hep B: successful vaccination
anti-HBs
*Hep B: recovery & non-infectivity
anti-HBs appears then disappears
Hep B: anti-HBs
appears after virus clearance
- successful vaccination
- appears/disappears = anti-HBs
Hep B: IgM
- appears shortly after HBsAg
- helps confirm dx in pts who may have cleared HBsAg
- may persist 3 - 6 mo
Hep B: IgG
persists indefinitely whether cured or chronic
Hep B: helps confirm dx in pts who may have cleared HBsAg
IgM anti-HBc
Hep C dx + sens/spec
enzyme immunoassay (EIA) detects ab to JCV- low spec (false +) - mod sens (false -)
Hep C confirmatory dx
HCV-PCR RNA (how much HCV in blood?)
Hep A & B tx
bedrest fluids - PO ADMIT: - cannot maintain hydration - INR gt 1.6 - encephalopathy
when to admit Hep A or B
ADMIT:
- cannot maintain hydration
- INR gt 1.6
- encephalopathy
Hep A specific tx
- handwashing !!
- immune globulin to all close personal contacts
- avoid EtOH, strenuous exercise, hepatotoxic rx (tylenol)
- prevention: inactivated hep A vax
Hep C tx
based on genotype (1-6, 1-3 most common) protocols based on "resp rate" - peginterferon - ribavirin - protease inhibitors - sovaldi
peginterferon
helps healthy cells fight HCV, strengthens immune sys
SE
- flu-like: fatigue, HA, fever, chills, n/v, arthralgias, myalgias
-worsening depression
-mood instability
- ↑ susceptibility to inf
worsening psych seen as SE to which HCV tx?
peginterferon
ribavirin
antiviral (HCV), interferes w RNA metabolism SE - hemolytic anemia - MI - pneumonitis - dyspnea & infiltrates
sofosbuvir (Sovaldi)
HCV polymerase inhibitor
- 12 wk course (varies by genotype)
- may include ribavirin & peginterferon
no chronic form of which Hep?
Hep A
only viral hep that causes fever spikes
Hep A
Hep B vaccination
- initial, 1 & 6 mo
- recombinant-derived
- lasts 15 yrs
- booster if titers lt 10 mIU/mL~90% vax’d dev protective ab to Hep B
single stranded RNA virus + mutates rapidly (difficult to treat)
Hep C
*Hep A: infected markers
anti-HAV
IgM anti-HAV
*Hep A: non-infectivity, immunity
IgG anti-HAV
*Hep B: infected
HBSAg
HBEAg
*Hep B: confirmatory dx
IgM anti-HBC
*Hep B: non-infectivity, immunity
anti-HBSAg
*Hep C specific labs
ab to HCV
HCV RNA assay
chronic hepatitis
B, C, D
- inflammatory response gt 3 to 6 mo
- ↑ ALT & AST
- inflammation of portal sys + lobules (mild, mod, severe)
- fibrosis (mild, mod, severe) or cirrhosis
chronic Hep B s/s
- cirrhosis (40-50% die w/in 5 yrs)
- liver failure
- hepatocellular carcinoma
chronic Hep B tx
interferon (recombinant human interferon alfa-2b) {Intron A} Lamivudine (Epivir) nucleotide analogs: suppress HB DNA for 1 yr
chronic Hep C s/s + risks
- 20% cirrhosis after 20 yrs
- hepatocellular carcinoma
risks: - gt 50g EtOH qd
- acquire HBC @ 40+
- immunosuppressed
chronic Hep C tx
- peginterferon, ribavirin, PI (protocols based on resp rate)
- Sovaldi
chronic Hep D s/s + dx
superimposed on B
- dx: ab to Hep D ag (anti-HDV)
- rapid dev cirrhosis
- ↑↑↑ mortality
alcoholic hepatitis
- REVERSIBLE *
acute or chronic inflammation → necrosis of parenchyma
most common cause of cirrhosis (Hep C #2)
red flag EtOH levels (possible alcoholic hepatitis)
4 oz whiskey15 oz wine4x 12 oz beer (cans)50g/day 10+ years
alcoholic hepatitis: risk factors
- 50g/day 10+ years- female (↓ gastric mucosal EtOH dehydrogenase level)
↑ duration (10-15yrs) + ↑ consumption = ↑ probability AH & cirrhosis
alcoholic hepatitis: s/s
- h/o N/V
- hepatomegaly, splenomegaly
- jaundice, ascites
- abd pain/tenderness
- fever, encephalopathy
alcoholic hepatitis: labs
- CBC: macrocytic anemia, leukocytosis (left shift), thrombocytopenia
- PT ↑ & INR
- AST ↑ gt ALT↑
- ↑ alk phos, bilirubin
- ↓ albumin folic acid deficiency
alcoholic hepatitis: tx
- nutritional support: proteins & CHO to offset catabolism, prev hypogly
- vit supplement (Banana Bag): folic acid, thiamine (B1)
- MUST GIVE GLUCOSE + THIAMINE or → Wernicke-Korsakoff Syndrome *
alkaline phosphatase
protein found in all body tissues, higher in liver, bile ducts, bone.
- Wernicke-Korsakoff Syndrome *
encephalopathy w/ ataxia, confusion, amnesia, confabulation, & impaired learning in alcoholic hepatitis, glucose given without thiamine (B1) can result in this
liver cirrhosis leads to what anemia?
macrocytic anemia
spider nevi s/s of?
cirrhosis
palmar erythema s/s of?
cirrhosis
Dupuytren’s contractures
flexion 4/5 digits indicating cirrhosis
notable late s/s of cirrhosis
pleural effusions, encephalopathy
+ jaundice, ascites, peripheral edema, ecchymotic lesions, asterixis
cirrhosis lab findings
macrocytic anemia
↓ WBC s/t hypersplenism thrombocytopenia
prolonged PT, ↑ INR↑ of AST, alk phos, bilirubin↓ albumin
ascites r/t cirrhosis: pathophys
portal htn: → ↑ hydrostatic pressure (liver enlarged, pushes fluid out of vessels → 3rd spacing)
hypoalbuminemia → ↓oncotic pressure
ascites r/t cirrhosis: tx
restrict Na+ (400-800mg/day)
diuretics: Spironolactone, Furosemide large
-vol paracentesis (4-6L)
TIPS (Transjugular intrahepatic Portosystemic Shunt)
TIPS (Transjugular intrahepatic Portosystemic Shunt)
stent btw branch of hepatic vein & portal vein introduced via IJ
takes blood from liver to IVC
complications of cirrhosis
ascites spontaneous bacterial peritonitis hepatorenal syndrome encephalopathy portal hypertension
spontaneous bacterial peritonitis r/t cirrhosis: risk + s/s + tx
risk: h/o variceal bleeding & PPI uses/s: abd pain, ↑ ascites, fever, progressive encephalopathy
tx: cefotaxime (3rd gen cephalosporin) + IV albumin
hepatorenal syndrome r/t cirrhosis + dx
renal failure s/t ESLD
dx: azotemia, in abs of shock or sig proteinuria, in ESLD where renal fxn doesn’t improve w infusion of 1.5L NS → r/o other causes of renal failure including pre-renal azotemia
hepatorenal syndrome labs
- azotemia
- urine vol lt 500mL/day
- urine Na lt 10mEq/L
- urine osm gt plasma osm
- urine RBC gt 50
- serum Na lt 130mEq/L
hepatorenal syndrome type 1 pathophys
rapid progression - doubling creatinine to gt 2.5mg/dL in 2 wks
hepatorenal syndrome type 2 pathophys
slower progression - more chronic (presents as diuretic-resistant ascites)
presents as diuretic-resistant ascites
type 2 hepatorenal syndrome
is type 1 or 2 hepatorenal syndrome faster?
type 1 progression more rapid
hepatorenal syndrome tx
liver transplantation
encephalopathy r/t liver: pathophys
cerebral edema: poss etiologies inc breakdown of BBB -or- Na+ accumulation s/t inhibition of Na-K ATPase
leads to acute ↑ ICP → ↓ CPP, cerebral blood flow, loss of autoregulation
encephalopathy stages
I - euphoria, depression, mild confusion, slowed mentation, slurred speech, sleep disturbances
II - drowsiness, inappropriate behavior, tremors
III - sleeps but arousable, confused, incoherent speech, abn EEG, tremors
IV - Unarousable, Abn EEG
encephalopathy mgmt
mannitol (hold if serum osm gt 320)↓ ammonia levels:
- lactulose (hold if ileus)
- neomycin (monitor for oto or nephrotoxicity)
portal hypertension r/t cirrhosis
progression of liver failure: pressure back up → ascites & varices (esophageal, gastric, duodenal, rectal)
*pre-disposed to a GI bleed ( coagulopathy + likely to bleed + pressure prob d/t vol back up)
portal hypertension tx
sclerotherapy
TIPS
balloon tamponade
sclerotherapy
tx for portal hypertension: cauterize vessels
fulminant hepatitis + s/s
viral hepatitis → sudden or severe liver disease - massive hepatocellular necrosis s/s (shocky & losing volume) - jaundice - hepatomegaly - ↑ AST & ALT - ↓ H&H - prolonged PT - encephalopathy
fulminant hepatitis tx
SUPPORTIVE
- maintain perfusion (fluids, inotropes)
- vent support
- monitor f&e, maintain normal glucose
- monitor ammonia: tx w lactulose or neomycin
- consider transplantation
Non-Alcoholic Steatohepatitis (NASH)
“silent liver disease”
resembles alcoholic liver dz in individuals who do not drink
NASH clinical findings + dx
↑ ALT & AST
initially pts asx
- liver bx diagnostic
- fatty liver, inflammation, damage to liver cells
NASH dz progression
asx → fatigue, weight loss, weakness
adv disease → liver failure, cirrhosis
NASH tx
initially lifestyle → IBW, balanced diet, avoid unnecessary meds, avoid ETOH, ↑ physical activity
liver failure = only tx is transplantation
