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REM II > biochem > Flashcards

biochem Flashcards

1
Q

what does anorexigenic mean?

A

makes you want to eat less and be more active

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2
Q

what does orexigenic mean/

A

makes you want to eat more and be less active

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3
Q

what nucleus contains the anorexigenic and orexigenic neurons

A

arcuate nucleus

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4
Q

how does leptin regulate storage of fat?

A

released with excess adipose to signal to decrease wt

it is an adipokine

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5
Q

what pathway does leptin work through?

A

non-receptor tyrosine kinase (JAK/STAT)

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6
Q

what does adiponectin do?

A

downregulates inflammatory response

works opposite leptin

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7
Q

how does increased fat lead to inflammation

A

inc fat -> inc leptin

this leads to dec adiponectin and so less antiinflammatory protection

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8
Q

What are the characteristics of homozygote leptin deficiency?

A

normal birthwt, but obese in childhood
severe hunger w/ being aggressive
tx with recombinant leptin therapy

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9
Q

which hormones are anorexigenic?

A

leptin, insulin, amylin, PYY, CCK

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10
Q

what hormones are orexigenic?

A

ghrelin

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11
Q

what hormone does the pancreas release?

A

insulin

amylin

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12
Q

what hormone does adipose release?

A

leptin

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13
Q

what hormone does the ileum release?

A

PYY (down regulates ghrelin)

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14
Q

what hormone does the stomach release?

A

ghrelin

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15
Q

what hormone does the duodenum release?

A

CCK

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16
Q

what are the actions of ghrelin?

A

released when baroreceptors sense the stomach is relaxing

stim. orexigenic neurons to release GH

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17
Q

When is CCK released?

A

when AA or FA enter the duodenum thereby signaling the release of bile by the gall bladder, amylase by the pancreas and signals satiety

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18
Q

what anorexigenic and orexigenic hormones are released from the hypothalamus?

A

anorexigenic: CART, alpha-MSH
orexigenic: NPY, AgRP

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19
Q

What hormones work on NPY hormone?

A

ghrelin stim
PYY inhib
LEptin and insulin inhib

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20
Q

what hormones work on alpha MSH hormone/

A

insulin and leptin stim

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21
Q

what receptors do alpha MSH bind?

A

MCR3 and 4

22
Q

what receptors do AgRP bind?

A

MCR4 (antagonizes) and Y1R

23
Q

what is the strongest activator of glycolysis

A

F2,6BP

24
Q

what is the regulatory step of glycolysis

A

fructose 6-p to fructose 1,6 bp

regulated by phosphofructokinase-1

25
Q

what does phosphokinase-2 do?

A

convert F6p to F2,6BP

26
Q

what does fructose 2,6 bisphosphatase do

A

removes p from F2,6BP leaving F6p (down regulates gluconeogenesis)

27
Q

what signal lipoprotein lipase? what does it do?

A

insulni

it adds triacylglycerols to adipocytes for storage

28
Q

what signals hormone sensitive lipase? what does it do?

A

glucagon

releases FA from adipocytes which then binds to albumin for transport to muscles

29
Q

how does the FA get into the mitochondria? And what happens to it once it does

A

via acyl carnitine shuttle

once inside the FA is released to form acyl coa then goes to beta oxidation

30
Q

will insulin upregulate or downregulate HMG coa reductase to make cholesterol?

A

upregulate

31
Q

what is the rate limiting step for FA biosynthesis?

A

acetyl coa conversion to malonyl coa

via acetyl coa carboxylase

32
Q

does citrate signal high or low energy?

A

high energy

33
Q

does acetyl coa signal high or low energy

A

high energy

34
Q

how does the body get acetyl coa from mito to cytosol for FA biosynthesis?

A

using citrate shuttle

35
Q

what is the rate limiting step of beta oxidation?

A

when FA shuttled by carnitine acyl transferases

36
Q

What enzyme is used to form ketone bodies from hmg coa

A

hmg coa lyase

37
Q

what enzyme is used to form cholesterol from hmg coa

A

hmg coa reductase

turns it to mevalonate which is need to build cholesterol

38
Q

What is von gierke disease? what tissue is most affected

A

aka glycogen storage dz type 1
glucose 6 phosphatase deficiency
onset in childhood
liver is most affected

39
Q

what are the genetics of von gierke?

A

AR

40
Q

what are the symptoms of von gierke/

A 
fast induced hypoglycemia
seizures
failure to grow
hyperlipidemia
hyperuricemia
41
Q

what is the effect of ribose 5p build up associated with von gierke

A

will drive production of purines leading to gout

42
Q

how does von gierke fasting glucose compare to normal?

A

peaks at meals like normal but plummets in between as they are unable to perform gluconeogenesis or glycogenolysis

43
Q

what is the dietary treatment for von gierke?

A

uncooked corn starch every 1-3 hrs

44
Q

why do von gierke pts have hyperlipidemia?

A

mobilizes lipids to create energy source

45
Q

what is the difference between von gierke type a and type b?

A

type a= inact of g6p

type b= inact of g6p transporter

46
Q

what is pompe disease? genetics?

A

lysosomal acid alpha glycosidase def.
childhood onset
AR, all tissues

47
Q

pathogenesis of pompe dz?

A

glycoen end up in lysosomes where acid alpha glycosidase breaks them down
with def, glycogen builds up in lysosome and is not released

48
Q

what is cori dz? genetics?

A

amylo-1,6 glucosidase def
AR
effects liver heart and muscle

49
Q

what is the pathogenesis of cori?

A

effects glycogen breakdown in cytosol
enzyme amylo-1,6 glucosidase debranches glycogen normally
with def, glycogen use is limited as only the outer portion is able to be broken down

50
Q

what is McArdle? Genetics

A

myophosphorylase def
AR, muscle
childhood/adult onset

51
Q

pathogenesis of McArdle?

A

unable to breakdown muscle glycogen
this leads to lack of muscle endurance
intense exercise can lead to rhabdomyolysis

REM II (11 decks)

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