Reading...
Play button
Play button
Use LEFT and RIGHT arrow keys to navigate between flashcards;
Use UP and DOWN arrow keys to flip the card;
H to show hint;
A reads text to speech;
86 Cards in this Set
- Front
- Back
|
Which A/Vs compose the dual blood supply of the LV?
|
hepatic a/v - blood
portal a/v - nutrients |
|
|
T/F LV is the largest solid organ
|
True
beneath 8/9th costals |
|
|
What is the functional unit of the LV
a) nephron b) lobule c) ductule d) none |
lobule
organized around central v. empties into hepatic v -> vena cava |
|
|
the Hepatic V receives blood from _____ and sends it to _____
|
LV
vena cava |
|
|
What is the function of hepatic plates?
a) create bile b) immune function c) supply blood d) all |
LV Cells create bile
|
|
|
What is the function of Kupffer cells?
a) create bile b) immune function c) supply blood d) all |
immune function - type of macrophage
hepatic plates= LV cells- create bile |
|
|
list the components of a lobule
|
hepatic plates
sinusoids endothelial cells kupffer cells centered around Central V bile canaliculi |
|
|
List the basic physiological functions of the LV
|
drug metab
hormone inactivation alcohol metab bile production bilirubin elim protein synth protein catabolism |
|
|
Which of the following does not have an important digestive function
a) bile salts b) cholesterol c) bilirubin d) a,b e) b,c |
cholesterol
bilirubin NO Digestive function |
|
|
Cytochrome P450 has which function
a) chemical modification of drugs b) emulsify fat c) detox d) de-iodination |
chemical modification
|
|
|
T/F
drugs are converted from water soluble to lipid soluble in the LV |
F
lipid soluble -> water soluble |
|
|
Glutathione pathway is important for
a) glucagon deamination b) de-iodination c) proteolysis d) detox |
detox of drugs
|
|
|
LV and hormone related functions include the following except
a) insulin proteolysis b) de-iodination of T4/T3 c) glucagon deamination d) Acetylaldehyde production |
Acetylaldehyde production - alc metab
LV hormone related functions also includes steroid conjugation |
|
|
list the components of bile
|
water (majority)
bile salts bilirubin cholesterol |
|
|
primary component needed to digest fat
a) bile salt b) ADH c) bilirubin d) all |
bile salts- emulsify dietary fat and form micelles- (re-absorbed at ileum)
|
|
|
how much bile is produced
a) 80-200 L/day b) 600-1200 ml/day c) 100-1000 ml/day |
600-1200 ml/day
|
|
|
Where are bile salts recylced
a) ST b) Ileum c) jejunum d) rectum |
ileum- must reabsorp and reuse- otherwise not enough
|
|
|
list causes of Jaundice
|
pre hepatic- xs RBC destruction
hepatic- impaired LV function post hepatic- obstruction of bile duct/canaliculi |
|
|
production of ____ is important to maintain plasma colloid osmotic pressure
|
albumin
higher osmotic prssr prevents edema lo osmotic prssr/ hi hydrostatic pressure -> edema |
|
|
T/F
Damage to LV can cause abnormal bleeding |
True
LV produces proteins necessary for clotting factors test for factors 2, 7, 9, 10- vit k dependent/fat soluble |
|
|
which is not a commonly used LV function test
a) ALT b) GGT c) AST d) Serum Bilirubin |
GGT
|
|
|
protein catabolism includes
____ and ______ |
transamination
deamination |
|
|
product of deamination
a) ketoacids b) ammonia NH3 c) ammonium NH4 d) albumin |
ketoacids, ammonia
-> urea excrete in urine as NH4CL |
|
|
list the causes of acute hepatitis
|
drugs/chemical/toxin
parasite bacteria virus |
|
|
what is the pathogenesis of a viral infection causing acute hepatitis
a) direct cellar invasion b) obstruction of bile duct c) indirect immune response |
direct
indirect |
|
|
Which of the following occurs during the incubation phase
a) Hi ALT b) Rt Flank Pain c) Jaundice d) a,b |
None- NO symptoms during the incubation phase
|
|
|
list the phases of acute jaundice
|
incubation
prodromal/preicterus icteric convalescent |
|
|
which is not a symptom of the preicterus phase
a) distaste for smoking b) hepato-splenomegaly c) HI AST d) GI distress |
hepato-splenomegaly
also: jaundice, severe pruritis, Hi ALT/Bilirubin/AST |
|
|
true statement about icteric phase of acute hepatits
a) occurs 5-10 days following prodromal phase b) all hepatitis progresses to this phase c) includes gradual increase in well-being |
occurs 5-10 days after preicteric phase
|
|
|
an abnormal LV function test first appears during
a) incubation b) icteric phase c) prodromal phase d) convalescent |
prodromal
|
|
|
DNA virus
a) Hep A b) Hep B c) Hep C d) all |
HBV = only DNA form
A,C, D, E = RNA |
|
|
Vaccines are available for which forms of Hepatitis
|
HAV
HBV |
|
|
Which form of hepatitis is not a spread parenterally
a) HAV b) HBV c) HCV d) all are parenteral |
HAV- fecal/oral
|
|
|
Which of the following is not a fulminant type of hepatitis
a) HAV b) HBV c) HCV d) HDV |
HAV
|
|
|
Which types of hepatitis can become chronic persistent hepatitis
a) HAV b) HBV c) HCV d) HDV |
HBV
HCV |
|
|
Which agents can become chronic active
a) HAV b) HBV c) HCV d) HDV |
HBV
HCV |
|
|
What is the criteria for Chronic Persistent Hepatitis
|
elevated AST, ALT for > 6 month
prognosis- benign |
|
|
What is the criteria for Chronic Active Hep
|
elevated AST, ALT > 6 months
prognosis- poor |
|
|
T/F
chronic carriers of Hep can develop into fulminant Hep |
F
Chronic Carriers: HBV, HCV only - asymptomatic only increased risk of hepatoma |
|
|
Which serologic marker for HAV appears during the acute stage
a) IgM anti HAV b) IgG anti HAV c) HAs Ag d) all |
IgM anti HAV
IgG- protective- appears after 1 month of illness and persists |
|
|
Which is the least useful blood marker for HBV?
a) HBsAg b) Anti-HBe c) HBcAg d) Anti HBc |
HBcAg- does not appear in blood
|
|
|
_____is the 1st antibody to appear in the blood for HBV
a) HBsAg b) Anti-HBe c) HBcAg d) Anti HBc |
Anti-HBc
similar to IgM- not protective |
|
|
Serologic marker that signals the onset of resolution of acute HBV
a) HBsAg b) Anti-HBe c) HBeAg d) Anti HBc |
Anti-HBe
done exponentiating |
|
|
Protective marker of HBV
a) HBsAg b) Anti-HBs c) HBeAg d) Anti-HBc |
Anti-HBs- appears after clearance of HBsAg (will appear if vaccinated)
chronic infxn will show little-none AntiHBs and will show primarily HBsAg- therefore still contagious |
|
|
____ serological marker is found for HCV and appears ______ after infection
|
Anti-HCV-
1-2 weeks after exposure IgM - not protective |
|
|
list the causes of Chronic Hep
|
alcohol
drug autoimmune- mostly women virus |
|
|
T/F
Chronic Persistent Hep cannot progress to Chronic Active |
F
may progress- however chronic persistent has minimal LV damage and is asymptomatic |
|
|
Describe the pathology of Cirrhosis
|
Conversion of LV cells to Fibrous/Scar tissue
Obstrxn of blood flow -> portal Hypertension Obstrxn of bile flow -> destruction of LV cells/LV Failure |
|
|
list causes of Cirrhosis
|
alcohol
hepatitis biliary obstruction/congestion cardiac failure metabolic disorder |
|
|
Which of the following is least likely to cause cirrhosis?
a) HAV b) Wilson's Disease c) Hemochromatosis d) all will likely cause |
HAV- self ltd- not chronic hepatitis little damage to LV
|
|
|
Correct statement about postnecrotic cirrhosis
a) autoimmune mechanism b) LV formed by small/large fibrous nodules c) unknown eitiology d) none |
LV formed by small/large fibrous nodules
(post necrotic cirrhosis is related to chronic HBV autoimmune mech = primary biliary cirrhosis |
|
|
scarring of the Small Intrahepatic and LV bile ducts causes enlarged LV and blue/green color
a) postnecrotic cirrhosis b) primary biliary cirrhosis c) primary sclerosing cholangitis d) all |
primary biliary cirrhosis - usually autoimmune
postnecrotic cirrhosis = HBV- LV becomes fibrous tissue primary sclerosing = fibrosis of intra and extra hepatic bile ducts causing cholestasis and LV destruction |
|
|
inflammation of intrahepatic and extrahepatic bile ducts
a) postnecrotic cirrhosis b) primary biliary cirrhosis c) primary sclerosing cholangitis d) all |
primary sclerosing cholangitis -> cholestasis and destruction of LV tissue
|
|
|
_____ causes damage to the LV due to alcohol
|
acetylaldehyde
|
|
|
list the toxic effects on acetylaldehyde on the LV
|
impedes Mitochondrial e- transport syst to decrease ATP
impairs detox of free radicals impairs protein synth promo collagen synth and fibrosis |
|
|
incorrect statement about LV damage to to alcohol
a) increases mitoch oxidation of fatty acids b) damage is reversible c) may cause portal hypertension d) steatosis may present without symptoms |
DECREASES mitochondrial oxidation of fatty acids
|
|
|
list manifestations of Cirrhosis
|
weightloss (maybe masked by ascites)
weakness anorexia dull/aching flank pain/fullness hepatomegaly jaundice portal hypertension LV failure bleeding |
|
|
Bleeding disorder due to LV failure may cause all of the following except
a) gynecomastia b) increased NH3 in blood c) indigestion d) lo albumin |
all
also causes feminizing patter of pubic hair in males due to testicular atrophy |
|
|
Portal hypertension is defined as sustained portal vein pressure above
a) 10 mmHg b) 12 mmHg c) 14 mmHg d) none |
12 mmHg
|
|
|
portal hypertension due to chronic hepatitis is classifies as
a) prehepatic b) intrahepatic c) posthepatic d) none |
intrahepatic
|
|
|
Portal hypertension due to Ht Failure is classified as
a) prehepatic b) intrahepatic c) posthepatic d) none |
posthepatic
pre- below the LV- tumors/lymph nodes/etc intra- anything causing chronic Hepatitis |
|
|
Portal hypertension due to a tumor would be classified as
a) prehepatic b) intrahepatic c) posthepatic d) none |
pre-hepatic
|
|
|
T/F
Portal Hypertension will cause portosystemic shunt |
T
causes: hemmrhoid caput medusae esophageal varices splenomegaly ascites |
|
|
caput medusae is a common pathology of
a) LV Cancer b) Cholecystitis c) HBV d) Portal Hypertension |
Portal Hypertension
also: hemmrhoid esophageal varices splenomegaly ascites |
|
|
List predisposing factors of LV cancer
|
chronic HBV
cirrhosis (hepatocarcinoma only - not cholangiocarcinoma) aflatoxin- moldy peanuts |
|
|
T/F
Cirrhosis can cause cholangiocarcinoma |
F
hepatocarcinoma |
|
|
Which blood test can screens for LV cancer
a) ALT b) AST c) Alpha foeto protein d) alkaline phosphotase |
alpha foete protein +
|
|
|
T/F
LV cancer has a good prognosis |
False
|
|
|
list the components of Bile
|
bile salts
cholesterol bilirubin lecithin fatty acids water electrolytes |
|
|
list the 4 F Factors that may contribute to the formation of Cholethiasis
|
40
female fertile fatty |
|
|
_____ are needed to help dissolve cholesterol. proper ratio prevents stones
|
Bile salts
|
|
|
a patient had part of their ileum removed. they are more likely to experience
a) chronic hepatitis b) cholelythiasis c) pancreatitis d) all |
cholelythiasis
removed ileum -> impaired hepato-enteric cycle of bile- bc biles salts cannot be recycles |
|
|
cholesterol gall stones are likely due to
a) genetic disorder b) hemolytic disorder c) impaired hepato-enteric cycle d) cholecystitis |
all (esp genetic) EXCEPT
hemolytic disorder-> pigment stone |
|
|
List predisposing factors of Gall Stones
|
abnormal concentration of bile salts/lecithin/cholesterol
stasis recurrent cholecystitis 4Fs Clofibrate Cholest Drug impaired hepato-enteric cycle genetic (cholesterol) hemolytic disorder (pigment stone) |
|
|
T/F
birth control may put women at risk for gall stones |
T
estrogen -> stasis |
|
|
Possible complication of cholelythiasis except
a) cholecystitis b) peritonitis c) cirrhosis d) all |
cirrhosis
|
|
|
Which is not a manifestation of Gall stones
a) LUQ pain b) increase transaminase c) back pain d) fever |
LUQ pain
manifestations: RUQ pain, colickly pain radiating pain to R shoulder/scapula/back N/V jaundice, fever increase WBC/Bilirubin/transaminase |
|
|
Cholecystitis may cause serum tests to present with the following except:
a) Hi WBC b) Hi Bilirubin c) Hi Transaminase d) HI Alpha- Foeto Protein |
alpha- phoeto protein = cancer
|
|
|
as an exocrine gland the pancreas secretes _____
|
water
bicarb protease amylase lipase |
|
|
Which is not a cause of acute pancreatitis
a) GB Stones b) Viral Infection c) alcohol d) calcification of pancreatic duct |
calcification of pancreatic duct causes chronic calcifying pancreatitis
acute pancreatitis also caused by: hyperlipemia LUQ trauma Thiazide, Steroid |
|
|
pathology of acute pancreatitis
|
inflammation ->
leaking of pancreatic enzymes into pancreas and nearby tissue -> necrosis, auto-digestion, hemorrhage |
|
|
correct statement about acute pancreatitis
a) insidious onset b) Jaundice c) pain aggravated by supine position d) activation of symp nervous syst |
pain aggravated by supine
activation of symp- tachycardia, cool/clammy skin, fever (insidious onset, jaudine = chronic) |
|
|
With acute pancreatitis blood test will show
a) increase amylase b) increase WBC c) Increase Blood Sugar d) all |
ALL
amylase WBC- inflammation/infxn Increase BS- not producing insulin w pancreas damaged |
|
|
Chronic obstructive pancreatitis is caused by______
|
obstruction of ODDI sphincter- chronic obstructive
calcified protein plugs in pancreatic duct- chronic calcifying |
|
|
complication of chronic pancreatitis
|
failure of endo and exocrine functions
|
|
|
list risk factors for pancreatic cancer
|
smoking
hi fat/meat diet diabetes chronic pancreatitis |
