Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Patho 2 > Chap 18- Liver and Gallbladder > Flashcards

Chap 18- Liver and Gallbladder Flashcards

1
Q

what is the functional unit of the liver

A

lobule

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

liver circulation

A
  • portal vein supplies 70%

- hepatic artery supplies 30%

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

how does hepatic BF change with aging?

A

significantly declines

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

result of hepatic ischemia/ hypoxia

A
  • temporary protection of hepatocytes
  • cellular acidosis protects against hepatocyte death
  • adenosine is a hepatoprotector against liver damage by CCl4/ ethanol
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

major functions of liver

A
  • detoxification
  • metabolism of CHO, fats, proteins
  • form coagulation factors
  • form bile
  • filter/ store blood
  • store vitamins and Fe
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

kupffer cells

A
  • macrophages found in liver
  • located in sinusoids
  • removes 99% of bacteria from gut that flows to liver
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

glycogenesis

A

excess glucose after meal is converted to glycogen

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

glycogenolysis

A

decreased glucose between meals stimulates breakdown of glycogen

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

gluconeogenesis

A

exhaustion of glycogen reserves stimulates glucose production from AA and sugars

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

liver protein metabolism

A
  • deamination of AA
  • removal of ammonia by making urea
  • formation of plasma proteins
  • synthesis of nonessential AA
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

where does ammonia come from?

A

bacterial degradation of amines, AA, purines, and urea in gut

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

liver fat metabolism

A
  • conversion of CHO and proteins to fat
  • beta oxidation of fatty acids
  • synthesis of lipoproteins
  • cholesterol
  • phospholipids
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

what coagulation factors does the liver make

A
  • prothrombin
  • VII
  • IX
  • X
  • requires vitamin K to do so
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

effect of abnormal liver function on coagulation factors

A
  • abnormal synthesis
  • dysfunctional coagulation factors
  • increased consumption
  • platelet disorders
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

bilirubin

A
  • formed from breakdown of heme

- heme found in hemoglobin, myoglobin, cytochromes, catalase, peroxidase

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

what is the role of heme oxygenase

A

convert heme to unconjugated bilirubin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

where is heme oxygenase found

A
  • spleen

- kupffer cells

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

what is the role of bilirubin conjugation?

A
  • unconjugated bilirubin is poorly soluble in water and toxic
  • conjugation allows for elimination
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

how does bilirubin conjugation occur

A

through glucuronic acid conjugation in liver

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

urobilinogen

A
  • produced in intestines by bacterial breakdown of bilirubin
  • partially absorbed in bowel
  • mainly excreted in urine
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

when is urinary urobilinogen excretion increased?

A
  • excessive bilirubin production
  • inefficient hepatic clearance of urobilinogen
  • excessive exposure of bilirubin to intestinal bacteria
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

when is urinary urobilinogen excretion reduced?

A
  • biliary obstruction

- severe cholestasis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

causes of elevated serum bilirubin

A
  • overproduction
  • impaired uptake, conjugation, or excretion
  • backward leak from damaged hepatocytes or bile ducts
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

beneficial effects of bilirubin

A
  • antioxidant
  • protective against CV disease and cancer
  • heme oxygenase reduces replication of Hep C virus
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

ways to protect against bilirubin toxicity

A
  • binding to plasma albumin
  • rapid uptake
  • conjugation
  • clearance
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

jaundice

A
  • yellowish tint of body tissues
  • classified as either hemolytic or obstructive
  • occurs when bilirubin concentrations are 3 times normal
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

hemolytic jaundice

A
  • due to increased destruction of RBC

- rapid release of bilirubin into blood

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

obstructive jaundice

A
  • obstruction of bile ducts or damage to liver cells

- results in inability to excrete bilirubin into GIT

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

biochemical markers of liver injury

A
  • serum aminotransferases (ALT* and AST)
  • bilirubin and bile acids
  • alkaline phosphatase
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

liver function markers

A
  • albumin

- prothrombin time

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

tests to detect injury to hepatocytes

A
  • serum aminotransferases (ALT* and AST)

- released when hepatocyte gets injured

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

tests for livers capacity to transport organic anions and metabolize drugs

A
  • bilirubin and bile acids
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

tests for the livers biosynthetic capacity

A
  • serum albumin

- prothrombin time

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

what enzyme reflects cholestasis

A

alkaline phosphatase

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

hepatic lymphatic vascular system

A
  • 50% of lymph formed in liver
  • fenestrations in sinusoidal endothelial cells leak fluid and proteins into space of disse
  • lymph flows through space of disse
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

what is the result of increased sinusoidal pressure?

A
  • increases lymph production

- fluid accumulates in abdominal cavity -> ascites

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

what signals hepatocytes to enter mitosis

A
  • macrophages
  • hepatic stellate cells
  • liver sinusoidal endothelial cells
  • hepatic stellate cells are not active in healthy liver
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

acute liver failure

A
  • occurs suddenly
  • also see encephalopathy and elevated prothrombin time
  • no cirrhosis or preexisting liver disease
  • duration of <26 weeks
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
39
Q

what are the main cause of acute liver failure?

A
  • viral

- drug induced- APAP

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
40
Q

clinical manifestations of acute liver failure

A
  • liver test abnormalities*
  • hepatic encephalopathy*
  • prolonged prothrombin/INR*
  • jaundice
  • hepatomegaly
  • r upper quadrant tenderness
  • coagulopathy
  • increased portal HTN
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
41
Q

hepatic encephalopathy

A
  • impaired brain function

- reversible

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
42
Q

pathogenesis of hepatic encephalopathy

A
  • hyperammonemia
  • oxidative stress
  • oxindole
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
43
Q

hyperammonemia

A
  • increases brain uptake of AA -> altered synthesis of DA, NE, and serotonin
  • increases intracellular osmolarity in astrocytes
  • alters neural electric activity
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
44
Q

oxindole

A
  • tryptophan metabolite
  • formed by gut bacteria
  • causes sedation, muscle weakness, hypotension, coma
45
Q

how does APAP cause liver injury?

A
  • converted to NAPQI which is cytotoxic

- NAPQI binds to proteins and DNA to form adducts

46
Q

acute alcohol ingestion and APAP

A
  • protective to liver

- alcohol competes with APA for CYP enzymes -> decreased NAPQI produced

47
Q

chronic alcohol ingestion and APAP

A
  • increases CYP activity two fold

- reduces glutathione levels

48
Q

what are the three possible fates of APAP metabolism?

A
  • produce free NAPQI via CYP
  • renal excretion
  • conjugation of NAPQI urinary excretion
49
Q

cirrhosis

A
  • late stage progressive hepatic fibrosis
  • distortion of hepatic architecture
  • irreversible
  • requires liver transplant
  • associated with chronic liver failure
50
Q

etiology of chronic liver failure and cirrhosis

A
  • chronic viral hepatitis (B and C)
  • alcoholic liver disease
  • hemochromatosis
  • nonalcoholic fatty liver disease
51
Q

what is the main source of hepatic fibrosis

A

stellate cells that become activated

52
Q

portal HTN

A
  • resistance to portal BF
  • often develops in cirrhosis
  • develop structural and dynamic changes
53
Q

structural changes with portal HTN

A
  • fibrosis
  • angiogenesis
  • vascular occlusion
54
Q

dynamic changes with portal HTN

A
  • increased production of vasoconstrictors

- reduced release of endothelial vasodilators

55
Q

main clinical consequences of portal HTN

A
  • ascites
  • congestive splenomegaly
  • hepatic encephalopathy
56
Q

ascites

A
  • accumulation of excess fluid in peritoneal cavity
  • most often caused by cirrhosis
  • portal HTN causes changes in splanchnic circulation
57
Q

liver alcohol metabolism

A
  • generates acetaldehyde in liver via alcohol dehydrogenase (ADH)
  • acetaldehyde metabolized to acetate via ALDH
  • acetaldehyde can produce liver injury
58
Q

gastric alcohol metabolism

A
  • stomach has ADH activity

- h pylori and gastritis can reduce activity of gastric ADH

59
Q

alcoholic steatosis

A
  • reduced oxidation of hepatic fatty acids
  • increased lipogenesis
  • chronic consumption of alcohol increases expression of genes like fatty acid synthase
60
Q

alcoholic steatohepatitis

A
  • cytokine release and inflammation
  • antigenic adduction formation- acetaldehyde and hydroxyethyl radicals
  • immunologic
61
Q

types of alcoholic liver disease

A
  • alcoholic steatosis

- alcoholic steatohepatitis

62
Q

where are iron stores normally found

A
  • Hb in circulating RBC
  • iron containing proteins other than Hb
  • iron bound to transferrin in plasma
  • storage iron as ferritin or hemosiderin
63
Q

causes of iron overload

A
  • increased intake- blood transfusion

- increased absorption- hereditary hemochromatosis and chronic liver disease

64
Q

what is the main clinical consequence of iron overload?

A
  • organ damage
  • when taken into organs it creates hydrogen peroxide
  • OH is a ROS -> damage, inflammation, fibrosis
65
Q

transferrin

A

protein in the blood that transfers iron throughout body

66
Q

what happens when iron burden increases?

A
  • tranferrin becomes saturated
  • iron binds to other molecules - non-transferrin bound iron
  • NTBI taken up in liver, heart, endocrine organs
67
Q

cause of hereditary hemochromatosis

A

mutation in HFE gene

68
Q

what is the clinical outcome of hemochromatosis

A
  • increased absorption of iron from intestine

- fibrosis and cirrhosis due to iron

69
Q

mechanism of liver injury in hereditary hemochromatosis

A
  • lipid peroxidation due to increased ROS
  • interaction of ROS with DNA
  • activation of stellate cells
70
Q

hemochromatosis pathogenesis

A
  • hepcidin activity is reduced
  • have unchecked iron-export by ferroportin in macrophages
  • excess iron -> accumulation in tissues and organ damage
71
Q

hepatitis A virus

A
  • self limited
  • does NOT become chronic infection
  • can prevent with vaccine, immune globulin, proper hygiene
  • complete recovery within 6 mo in most pts
72
Q

how is HAV spread?

A
  • contaminated water and food
  • shed in stool
  • consumption of raw or steamed shellfish
73
Q

pathogenesis of HAV

A
  • replication occurs in hepatocyte
  • damage mediated by CD8+ and NK cells
  • interferon-gamma promotes clearance of infected hepatocytes
74
Q

what is the incubation period for HAV

A
  • 28 days

- contagious during incubation pd and 1 week after jaundice appears

75
Q

symptoms of HAV

A
  • N/V
  • anorexia
  • fever
  • malaise
  • abdominal pain
  • jaundice
  • scleral icterus
  • hepatomegaly
76
Q

Hep B virus

A
  • global problem
  • clinical manifestations vary from either acute or chronic
  • outcome depends on age, level of HBV replication, immune status
77
Q

how is HBV spread?

A
  • blood
  • semen
  • other bodily fluids
  • child birth
  • needle sharing
78
Q

pathogenesis of HBV

A
  • CD8 mediated
  • HBV mutations can affect severity of liver disease
  • development of chronic infection
79
Q

acute hepatitis clinical manifestations

A
  • subclinical or anicteric hepatitis

- more severe in pts with co-infection or underlying liver disease

80
Q

phases of chronic HBV infection

A
  • immune tolerance
  • immune clearance- HBeAg pos
  • inactive carrier
  • reactivation- HBeAg neg
81
Q

hepatitis C virus

A
  • majority of infected are not clinically ill
  • no vaccine
  • persistent infection and chronic hepatitis are hallmarks
82
Q

how is HCV spread?

A
  • blood borne

- mostly through sharing needles

83
Q

pathogenesis of HCV

A
  • acute spread through hepatic a, viral replication and INF increase
  • chronic hep c
  • liver cirrhosis
  • hepatocellular carcinoma
84
Q

HCV associated carcinogenesis

A
  • combo of indirect host mediated and direct HCV mediated mechanisms
  • persistant inflammation -> ROS damage
  • impaired DNA repair
  • repeated cycles of destruction and fibrosis -> cancer field
85
Q

nonalcoholic fatty liver disease

A
  • spectrum of disorders
  • nonalcoholic fatty liver (NAFL)
  • nonalcoholic steatohepatitis (NASH)
86
Q

effect of visceral adipose and intrahepatic fatty acids

A
  • induce gluconeogenesis
  • increase production of FFA
  • insulin resistance
87
Q

progression of NAFLD

A
  • simple steatosis -> steatohepatitis -> fibrosis

- simple steatosis is low risk for significant fibrosis

88
Q

pathogenesis of inflammation in NAFLD

A
  • free cholesterol -> liver injury
  • kupffer cells secrete pro-inflammatory mediators
  • stellate cells increase liver fibrogenesis
  • hepatocytes induce lipid peroxidation and lipotoxicty
  • mitochondrial dysfuntion
89
Q

insulin resistance and hepatic steatosis

A
  • increased FFA released from adipose
  • accumulation in liver
  • decreased glucose uptake
  • net result=increase glucose production and decreased uptake
  • hyperglycemia and hyperinsulinemia -> lipogenesis
90
Q

clinical features of NAFLD/ NASH

A
  • simple steatosis generally asymptomatic
  • clinical presentation related to insulin resistance or diabetes
  • AST and ALT elevated
  • CVD is frequent cause of death
91
Q

bile

A
  • liver secretes 1L/day
  • fat emulsification and absorption
  • medium for excretion of bilirubin and cholestrol
92
Q

bile salts

A
  • amphipathic
  • emulsification of lipids
  • transport of lipids
93
Q

cholelithiasis classifications

A
  • pure cholesterol stones
  • pigmented- mainly bilirubin
  • mixed- varying cholesterol, bilirubin, calcium carbonate, calcium phosphate
94
Q

major risk factors of cholelithiasis

A
  • age and sex- age >40 and female
  • environmental factors- estrogen
  • acquired disorders
  • hereditary factors- ABC transporters
95
Q

conditions that contribute to formation of cholesterol gallstones

A
  • suppression of bile with cholesterol
  • hypomotility of gallbladder
  • defective conversion of cholesterol to bile acids
  • hypersecretion of mucus in gallbladder
96
Q

pathogenesis of pigmented stones

A
  • elevated unconjugated bilirubin in bile from bacterial contamination
  • e coli increases likelihood of stone formation
97
Q

clinical features of cholelithiasis

A
  • most are asymptomatic
  • most common sx- biliary colic
  • pain in RUQ or epigastrium, can radiate to shoulder
  • inflammation
98
Q

cholecystitis

A
  • inflammation of gallbladder

- either acute, acalculous, or chronic

99
Q

acute calculous cholecystitis

A
  • chemical irritation and inflammation of gallbladder obstructed by stones
  • mucus layer is disrupted
  • prostaglandins released in wall
100
Q

acute acalculous cholecystitis

A
  • d/t ischemia

- inflammation and edema of wall, gallbladder stasis and accumulation of biliary sludge causes obstruction

101
Q

chronic cholecystitis

A
  • associated with presence of gallstones
  • result of mechanical irritation or recurrent attacks of cholecystitis
  • results in fibrosis and thickening of gallbladder
102
Q

carcinoma of gallbladder

A
  • uncommon
  • highly fatal
  • most are dx at advanced stage
103
Q

risk factors for carcinoma of gallbladder

A
  • pt demographics- age, female
  • gallbladder abnormalities
  • pt exposure i.e. smoking
  • infections- salmonella and h pylori
  • common thread= chronic inflammation
104
Q

pathogenesis of gallbladder carcinoma

A
  • cholelithiasis

- mutations in KRAS and p53

105
Q

cholestatic disease

A
  • decrease in bile flow

- due to hepatocellular impairment of bile formation or obstruction of bile flow

106
Q

clinical presentation of cholestatic disease

A
  • jaundice
  • scleral icterus
  • pruritis
107
Q

pathogenesis of pruritis in cholestasis

A
  • retention of bile salts
  • release of endogenous opioids
  • lysophosphatidic acid and autotaxin
108
Q

risk factors for hepatocellular carcinoma

A
  • cirrhosis
  • HBV
  • HCV
  • hereditary hemochromatosis

Patho 2 (15 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions