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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
cholesterol role in: - cell membrane - cell signalling
- helps maintain fluidity and structure | - forms lipid rafts between receptors and secondary messengers
26
what is cholesterol a precursor for (3)
bile/bile acids, vit D and fat-soluble hormones
27
what type of storage are triglycerides
high conc. energy store
28
role if triglycerides in cell membrane
similar to cholesterol, structure and fluidity
29
what carries lipids around the body
lipoproteins
30
what is the triglyceride composition of lipoproteins leaving the liver and what happens as they travel around the body
TG rich, progressively lose TGs as they circulate and become more dense
31
what enzymes snips off triglycerides in the endothelium of blood vessels
lipoprotein lipase
32
role of HDL
carries TG from tissues to liver
33
earliest changes of atherosclerosis in blood vessels
- increased endothelium permeability to lipoproteins and plasma consituents - upregulation of WBCs and endothelium adhesion molecules - WBC migration
34
what mediates atheroscleorsis formation
oxidised LDL
35
earliest visible signs of atherosclerosis | later joined by what
fatty streaks, SM cells
36
describe the process of atherosclerosis formation
- SM cell migration - T-cell activation - foam cell formation - platelet aggregation and adherence
37
what are foam cells
macrophages laden with lipids
38
when is a fibrous cap formed
when the fatty streaks progress to intermediate and advanced lesions
39
what do fibrotic caps do and what do they form as a result of
cap off the lesion in a healing/fibrous response to injury
40
what do fibrous caps cover
WBCs, lipids, debris
41
what forms a necrotic core in a fibrous caps
debris
42
why do necrotic cores form in fibrous caps
result of apoptosis, necrosis, increased proteolytic activit and lipid accumulation
43
how do atherosclerotic lesions expand at the edges
continues WBC adhesion and entry
44
how do thrombus form and where does this usually occur
- rupture or ulceration of fibrotic plaques | - sites of fibrous cap thinning
45
how do fibrotic caps thin
result of continues influx and activation of macrophages that release proteolytic enzymes degrading the matrix
46
what do labs measure in terms of cholesterol and why
- cholesterol, total cholesterol, HDL, total HDL, triglycerides - estimate CV risks
47
what is the lipid hypothesis
decreased cholesterol and saturated fats, decreases atherosclerosis and risk of CV disease
48
case-control study
two groups with a different outcome identified and compared on a basis of a suspected casual factors
49
cohort study
follow a group of people over time with reference to disease risk factors
50
systematic review
lit review focused on a research question - high quality evidence
51
meta-analysis
stat technique for combining results of different studies
52
randomised clinical trial
experiment where trial pateints are randomly assigned treatment under study
53
statin MoA
inhibit cholesterol formation from acetate in the liver
54
how do lipoproteins become acetate
via liver LDL receptors
55
whilst lowering cholesterol what else do statins do
inibit processes involving cholesterol and inflammation i.e. SM migration, T cell activation
56
what happens to atherosclerotic plaques as a result of statins
- dont form as much | - existing ones become more stable

Principles (65 decks)

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