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Principles > Biochemistry: Application 1+2 > Flashcards

Biochemistry: Application 1+2 Flashcards

1
Q

what does insulin signal and pathways does it switch on

A

fed state and metabolic pathways involved in using or laying down ingested fuels

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2
Q

what does insulin stop (5)

A
  • proteolysis
  • glucogenesis
  • glycgenolysis
  • lipolysis
  • ketogenesis
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3
Q

what does insulin start (5)

A
  • glucose uptake in muscle and adipose tissue
  • glycolysis
  • glycogen synthesis
  • protein synthesis
  • ion uptake
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4
Q

what pathways does insulin switch off

A

those involved in mobilising fuel stores

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5
Q

describe the consequences of decreased cellular glucose uptake in an insulin-deficient/resistant patient

A

leads to hyperglycaemia (glucose not used) -> glycosuria -> osmotic diuresis (lots of peeing lots of glucose) -> dehydration -> hypotension and shock

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6
Q

describe the consequences of increased lipolysis in an insulin-deficient/resistant patient

A

this is an attempt to source glucose leading to

increased ketones in blood -> acidosis -> vomiting -> dehydration -> hypotension and shock

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7
Q

what is the result of hypotension and shock from insulin deficiency/resistance

A

anti-insulin factors are released exacerbating the cycle

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8
Q

anti-insulin factors

A
  • cortisol
  • growth hormone
  • AVP
  • catecholamine
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9
Q

what is the main reason for insuline resistance and why

A
  • obesity

- too much fuel is stored as fat so the body becomes resistant to laying down more

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10
Q

role of hormone sensitive lipase in lipolysis and when this occurs

A
  • releases free fatty acids and glycerol

- when energy is needed

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11
Q

where are ketone bodies formed

A

liver mitochondria

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12
Q

what happens to the bicarbonate equilibrium when there is excess ketones in the blood

A

a R shift due to excess H+ being mopped up by H2CO3

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13
Q

why is the bicarbonate equilibrium never reached in a right shift

A

CO2 is blown off and therefore backwards reaction cant occur

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14
Q

what is acidotic breathing

A

deep breathing

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15
Q

can dipsticks detect ketones in urine

A

no

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16
Q

what are the fates of glucose on the liver

A
  • glycogen stores

- triglyceride stores

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17
Q

when are glycogen and triglyceride stores used

A

when quick energy is needed - sprinting

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18
Q

what other sources can glucose be made from

A
  • amino acids
  • glycerol
  • lactate
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19
Q

what is glycogenolysis

A

breakdown of glycogen to form glucose

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20
Q

what is gluconeogenesis

A

synthesis of glucose from alternate sources

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21
Q

what IC enzymes appear in plasma due to normal cell turnover (MSK and Liver)

A
  • MSK - CK and AST

- liver - ALT, AST. ALK Phos, Gamma GT

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22
Q

what what IC enzymes appear in plasma due to tissue damage (blood, bone, heart, pancreas)

A
  • blood - AST and LDH
  • heart - AST, CK, troponin, LDH
  • bone - ALK Phos
  • pancreas - amylase, lipase
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23
Q

what IC enzymes are good diagnostic indicators

heart, blood, bone, pancreas, MSK, liver

A
  • heart - troponin
  • blood - LDH and AST
  • bone - ALK Phos
  • pancreas - amylase
  • liver - ALK Phos, ALT, Gamma GT
  • MSK - CK
24
Q

how is lactate recycled to glucose when body is stuck for energy and where

A

lactate -> pyruvate -> glucose (+6-P)

- liver

25
Q

cholesterol role in:

  • cell membrane
  • cell signalling
A
  • helps maintain fluidity and structure

- forms lipid rafts between receptors and secondary messengers

26
Q

what is cholesterol a precursor for (3)

A

bile/bile acids, vit D and fat-soluble hormones

27
Q

what type of storage are triglycerides

A

high conc. energy store

28
Q

role if triglycerides in cell membrane

A

similar to cholesterol, structure and fluidity

29
Q

what carries lipids around the body

A

lipoproteins

30
Q

what is the triglyceride composition of lipoproteins leaving the liver and what happens as they travel around the body

A

TG rich, progressively lose TGs as they circulate and become more dense

31
Q

what enzymes snips off triglycerides in the endothelium of blood vessels

A

lipoprotein lipase

32
Q

role of HDL

A

carries TG from tissues to liver

33
Q

earliest changes of atherosclerosis in blood vessels

A
  • increased endothelium permeability to lipoproteins and plasma consituents
  • upregulation of WBCs and endothelium adhesion molecules
  • WBC migration
34
Q

what mediates atheroscleorsis formation

A

oxidised LDL

35
Q

earliest visible signs of atherosclerosis

later joined by what

A

fatty streaks, SM cells

36
Q

describe the process of atherosclerosis formation

A
  • SM cell migration
  • T-cell activation
  • foam cell formation
  • platelet aggregation and adherence
37
Q

what are foam cells

A

macrophages laden with lipids

38
Q

when is a fibrous cap formed

A

when the fatty streaks progress to intermediate and advanced lesions

39
Q

what do fibrotic caps do and what do they form as a result of

A

cap off the lesion in a healing/fibrous response to injury

40
Q

what do fibrous caps cover

A

WBCs, lipids, debris

41
Q

what forms a necrotic core in a fibrous caps

A

debris

42
Q

why do necrotic cores form in fibrous caps

A

result of apoptosis, necrosis, increased proteolytic activit and lipid accumulation

43
Q

how do atherosclerotic lesions expand at the edges

A

continues WBC adhesion and entry

44
Q

how do thrombus form and where does this usually occur

A
  • rupture or ulceration of fibrotic plaques

- sites of fibrous cap thinning

45
Q

how do fibrotic caps thin

A

result of continues influx and activation of macrophages that release proteolytic enzymes degrading the matrix

46
Q

what do labs measure in terms of cholesterol and why

A
  • cholesterol, total cholesterol, HDL, total HDL, triglycerides
  • estimate CV risks
47
Q

what is the lipid hypothesis

A

decreased cholesterol and saturated fats, decreases atherosclerosis and risk of CV disease

48
Q

case-control study

A

two groups with a different outcome identified and compared on a basis of a suspected casual factors

49
Q

cohort study

A

follow a group of people over time with reference to disease risk factors

50
Q

systematic review

A

lit review focused on a research question - high quality evidence

51
Q

meta-analysis

A

stat technique for combining results of different studies

52
Q

randomised clinical trial

A

experiment where trial pateints are randomly assigned treatment under study

53
Q

statin MoA

A

inhibit cholesterol formation from acetate in the liver

54
Q

how do lipoproteins become acetate

A

via liver LDL receptors

55
Q

whilst lowering cholesterol what else do statins do

A

inibit processes involving cholesterol and inflammation i.e. SM migration, T cell activation

56
Q

what happens to atherosclerotic plaques as a result of statins

A
  • dont form as much

- existing ones become more stable

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