Path 2- alcoholic/NAFLD/Metabolic Flashcards

1
Q

Alcoholic Liver Disease

alcohol leading cause of? (liver)

3 forms of liver injury by alcohol? cirrhosis in what fraction?

Morph 1- begin in zone?

hepatic steatosis (aka)- amount alcohol for fatty droplets?begins as then?color? feel? reversible?

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2
Q

Alcholic Liver disease Morph 2

Alcoholic (aka) hepatitis charcterized by? 3

h- is? M- what is it? what structure? specificlaly? specific? can b eseen in? N- where? particularly what cells?

alcholic steatofibrosis- cells? sclerosis begins where? accumulates? pattern of hepato? type of cirrhosis?

later on? reversible?

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3
Q

Alcoholic Liver Disease path

amount/duration- mild,reversible? sig risk for severe? really bad? how often cirrhosis?

gender? why? perm? CD? what cells? increased?

Ethnic/genetics- race? genetic component? cant oxidize?

Comorbid conditions- 3 syndergize with alcohol

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4
Q

Alcholic Liver Disease

exposure to alcohol causes? 5 hepatocelluar4 steatosis results from? 3?

toxin that casues? induces? lipid? ROS via? alcohol impairs metab of?

inflammatory moecules? 4 vaso? stellate?

chronic? featuring? (symptoms) 4

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5
Q

Alcholic Liver Disease clin

Hepatic steatosis organ problem? blood level rise? hepatitis appear when?

nonspecific symptoms? 5 levels of? 4

AST vs ALT? ratio?

alcoholic hepatitis clear if? how quickly?

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6
Q

Alcholic Steatosis clin 2

alcoholic cirrhosis sim to? lab findings? blood? detected? causes of death? 5

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7
Q
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8
Q

NAFLD aka?

what is it? wehre? in what population? most common cause of? detected clinically?

Steatohepatitis resergved for?

histo- looks like?

increasing rates due to? can lead to what diseases?3 this is different to other ways this happens how?

race? 2

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9
Q

NAFLD path

two hit model?

hepatitic steatosis arise from? 3 ex?

insulin resistance what is wrong with adipose? leads to production of? 2 which do what?

formation of what histo? how?

other cells?

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10
Q

NAFLD Morph

path steatosis involves how much of hepatocytes? type of fat accumulating? whats not present?

NASH? similar to? differ how? 2

steatofibrosis?

cryptogenic cirrhosis is?

pediatric differs how? 3

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11
Q

NAFLD clin

simple steatosis signs? imaging shows? most reliable diagnostic? must be excluded?

AST and ALT? in who? symptoms?cause of death in this group?

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12
Q
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13
Q

Hemochromatosis

caused by? most goes where? if inherited called? secondary if caused by?

normal amount?

fully developed cases exhibit? (triad) 3 m,d,a

how quick does it present? women?

gender?

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14
Q

Hemochromatosis path

get iron out of body how? so control how? in hemochrom?

liver injury mechanisms 3 reverisble?

main regulator of iron absorption? encoded by? transcription increased by? decreased?

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15
Q

Hemochromatosis path

three other proteins? h,t,h

adult form almost always caused by mutation of? chromosome? HLA? most common mutatioin on that gene? next most common?

C is most common in what population?

adult or juvenile milder? which cause severe juvenile?

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16
Q

Hemochromatosis- morph

characterized by? 3 H where? C, p where? stain with?

inflammation present? color? septa? liver parenchyma color?gold standard? now use more often?

pacreas color? present? heart? skin? color?

pseduogout? testes?

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17
Q

Hemochromatosis- clin

principal minfestations of classic hemochrom? 6

tetrad? death from? 3 treatment improve cancer risk? treatment via?

Neonatal- manifested by? inherited? related to? biopsy? treatment?

secondary- associated with?

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18
Q

Wilson disease

inheritance? mutation of? results in? what tissues?

cipper binds to what in liver? excess coppper transported where? normal total body copper?

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19
Q

Wilsons disease path

mutation in? location? chromosome? encodes for? majority have what?

deficiency prevents what from happening? decrease in? toxic liver injury via? 3

trigger a sudden illness via?

in urine?

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20
Q

Wilson disease morph

orgen gets fucked most? fatty change? inflammation? stain? copper also accumulates in? most helpful for diagnosis? genetic testing?

toxic injury location?

in the eye?

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21
Q

Wilsons disease clin

age? initial presentation? neuro? confused with?anemia?

biochem diagnosis increase in? decrease? what is most specific? treatment?

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22
Q

a1 Antitrypsin deficiency

inheritance? what is wrong? marked by? major fucntion of protein? leads to what problem? in the liver problem due to? chromosome?

most common genotype? most common mutation is? if both? expression of alleles are?

age of presentation? which makes this what?

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23
Q

a1 antitrypsin

path- most variants? problem occurs where? what mutant polypeptide? accumulates where? problem?

morph- on histo? stain what positive?

clin- can be seen neonatal? adolescence presenting symptoms? 3 silent until often? cacner? if pulm then?

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