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1st Year Med > Vascular Physiology > Flashcards

Vascular Physiology Flashcards

1
Q

where in the CV system does BP decrease?

A

from LV to RV (systemic)
from RV to LV (pulmonary)

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2
Q

what is the equation for mean arterial pressure?

A

diastolic BP + 1/3 pulse pressure (difference between systolic and diastolic)

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3
Q

how can BP be reduced medically?

A

modifying TPR

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4
Q

define BP

A

circulation of fluid contained within a space of definite volume

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5
Q

how do arterioles regulate blood flow?

A

intrinsic - local conditions surrounding blood vessels
extrinsic - nervous system input

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6
Q

what is the sympathetic regulation of blood vessels?

A

nerve terminals release neurotransmitters acting on vascular smooth muscle to induce vasoconstriction or vasodilation

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7
Q

name 3 signalling molecules responsible for vasoconstriction

A

norepinephrine
ATP
neuropeptide Y

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8
Q

name 2 signalling molecules responsible for vasodilation

A

vasoactive intestinal peptide (VIP)
nitric oxide

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9
Q

name the factors that alter vascular resistance

A

vascular viscosity
blood vessel length (increased length = increased resistance)
blood vessel radius

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10
Q

what increases after vasodilation in arterioles?

A

capillary pressure

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11
Q

what are some of the local controls of arterioles?

A

changes in O2, CO2, cellular metabolites dilate arterioles (active hyperaemia)

blocking blood flow induces reactive hyperaemia

flow autoregulation: flow through vessels releases molecules regulating blood vessel diameter

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12
Q

what is blood flow determined by?

A

pressure gradient (high -> low)

TPR

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13
Q

what are the controlled variables in the central control of BP?

A

CO
TPR
local controls
capillary fluid shift

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14
Q

what happens in the brain during BP control? (increase)

A

baroreceptor input to nucleus tractus solitarius (NTS) at a2 receptors
vagal nucleus activated producing ACl reducing CO
bulbar circulatory centres inhibited reducing noradrenaline, dilating blood vessels

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15
Q

what happens in the brain during BP control? (decrease)

A

baroreceptor input goes to NTS at b1 receptors
vagal nucleus inhibited reducing ACl production increasing HR
bulbar circulatory centres activated producing noradrenaline constricting veins increasing force/flow

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16
Q

what are the risk factors for hypertension?

A

age
obesity
salt-heavy diet
sedentary lifestyle

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17
Q

explain the structural changes occuring in vessels with hypertension

A

loss of elasticity
arteriole - arteriolosclerosis
artery - arteriosclerosis
endothelial lining damage
collagen deposition and calcification
vessel layer overstretching

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18
Q

what are the causes of secondary hypertension?

A

renal hypertension
pheochromocytoma

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19
Q

what can chronic hypertension lead to?

A

atherosclerosis
stroke
MI
heart/renal failure
retinopathy

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20
Q

give some examples of beta adrenoreceptor blockers and explain the mechanism

A

propranolol (b1/b2), atenolol (b1)
competitive reversible antagonists
lower BP by blocking sympathetic tone on heart and reducing renin released from kidney
also lowers HR, SV and CO

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21
Q

what are the side effects of beta adrenoreceptor blockers?

A

exacerbates asthma (b2 block)
intolerance buildup
hypoglycaemia
vivid dreams

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22
Q

give some examples of alpha adrenoreceptor blockers and explain their mechanism

A

phentolamine (a1/a2), doxazosin/prazosin (a1)
competitive reversible antagonists lowering BP and PR by decreasing sympathetic tone in arterioles (a1)

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23
Q

what are the side effects of alpha adrenoreceptor blockers?

A

postural hypotension (loss of sympathetic venoconstriction)
reflex tachycardia (via baroreceptors)

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24
Q

give some examples of ACE (angiotensin converting enzyme) inhibitors and explain their mechanism

A

capropril/enalapril (-pril suffix)

inhibits renin-angiotensin-aldosterone system (RAAS) which converts angiotensin I into active angiotensin II

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25
Q

explain the actions of angiotensin II

A

raises BP (vasoconstriction)
reduces blood volume through aldosterone release (reduced renal reabsorption of Na and water)

26
Q

what are the side effects of ACE inhibitors?

A

sudden fall in BP on first dose
persistent irritating cough (reduced bradykinin breakdown)

27
Q

what are the subtypes of angiotensin receptors and what medication can target one of them?

A

AT1 and AT2
AT1 mediates vasoconstriction and aldosterone release from AT2

AT1 blockers - losartan/candesartan
(side effects better than ACE inhibitors)

28
Q

name an example of a diuretic and explain their mechanism

A

bendroflumethiazide (a thiazide)

lowers BP by reducing blood volume (reducing renal reabsorption of Na and water)
small vasodilator action reduces PR

29
Q

what is the side effect of diuretics?

A

reduced K+ plasma concentration

30
Q

what are the 3 types of Ca channel blockers? give an example of each

A

dihydropyrodines (amlodipine)
phenylalkylamines (verapamil)
benzothiazepines (diltiazem)

31
Q

how do L-type voltage operated Ca channels work?

A

open on membrane depolarisation allowing Ca entry into cardiac and vascular smooth muscle
blocked by Ca channel blockers

32
Q

explain the mechanisms of Ca channel blockers

A

reduces BP by blocking Ca entry into vascular smooth muscle (induces vasodilation and reduces PR)
reduces CO by blocking Ca entry into cardiac muscle (lowers HR)

33
Q

what conditions must be met for Ca channel blockers to work?

A

must have allosteric modulators bound to allosteric site to reduce probability of channel opening at a given voltage

34
Q

what are the side effects of Ca channel blockers?

A

headache (cerebral vasodilation)
constipation (relaxed GI smooth muscle)
heart block (low Ca reduces contractility of heart)
cardiac failure

35
Q

what kind of input does the vasomotor nerve provide and what does it do?

A

sympathetic input

vasoconstricts blood vessels

36
Q

what is atherosclerosis?

A

the hardening of blood vessels involving plaque formation due to endothelial disruption

37
Q

what are the general risk factors for vascular endothelial damage?

A

smoking
high shear stress
infection
diabetes

38
Q

explain the formation of FOAM cells in atherosclerotic plaques

A

damage to vascular endothelium causes LDLs to diapedeses into cell where they oxidise
this promotes monocyte receptors on t-intima surface
monocytes enter and become macrophages
LDL + macrophage = FOAM cell

39
Q

what is the action of FOAM cells acting on the tunica media?

A

FOAM cells release IGF promoting SM cells from t-media to enter t-intima

SM cells produce collagen in the t-intima

40
Q

what occurs in atherosclerotic plaques to cause inflammation?

A

FOAM cells release chemokines to recuit more monocytes

when FOAM cells die, their lipid debris recruits lymphocyes and pro-inflammatory factors

T cells adhere to monocytes and produce inferferon gamma to promote inflammation

41
Q

what occurs in unstable fibrous plaques?

A

fibrous cap thins due to oxidant and stress and eventually ruptures

thrombus forms which can cause intraplaque haemorrhage, vessel occlusion or MI

42
Q

what is cholestorol essential for?

A

cell membrane incorporation
maintaining membrane fluidity and permeability
steroid and fat-soluble vitamin production

43
Q

what is the role of the liver in terms of cholestorol?

A

monitors cholestorol levels and regulates them through synthesis, absorption and bile secretion
(drugs to treat hyperlipidaemia target this process)

44
Q

what is cholestorol carried around the bloodstream in?

A

lipoproteins

45
Q

what is contained in a lipoprotein?

A

lipids - cholestorol, triglycerides, phospholipids
apoproteins - unique metabolic functions (one or more per protein)

46
Q

name the 5 different lipoproteins?

A

chylomicrons
VLDL
IDL
LDL
HDL

47
Q

what is the function of chylomicrons?

A

carries triglycerides from intestines to liver/muscle/adipose

48
Q

what is the function of VLDL’s?

A

carry newly synthesised triglycerides from liver to adipose

49
Q

what is the function of LDL’s?

A

cholestorol resevoir
taken up via LDL receptors by endocytosis

50
Q

what is the function of HDLs?

A

absorb cholestorol released by dying cells
reverse transport - return cholestorol to liver

51
Q

explain the exogenous pathway of cholestorol

A

intestine -> chylomicron -> if liproprotein lipase present: adipose, if not: chylomicron remnant -> remnant receptor on liver -> liver

52
Q

explain the endogenous pathway of cholestorol transport

A

liver -> VLDL -> capillary -> if LDL: adipose, if not: IDL -> liver -> hepatic lipase turns IDL into LDL -> peripheral tissue

53
Q

what occurs in the liver and capillaries in hypercholestorolaemia?

A

lowered LDL receptors in liver means more VLDL enters capillaries, resulting in higher IDL than LDL in tissues

54
Q

what are the signs of familial hypercholestorolaemia?

A

xanthomas (fatty cholestorol deposits in skin)
xanthelasmas (fatty deposits in eyelids)
arcus senilis (white ring around cornea)

55
Q

what are the common causes of hypercholestorolaemia?

A

high circulating cholestorol and triglycerides (primary)

diabetes, alcoholism, hypothyroidism, liver disease, drugs, diet (secondary)

56
Q

give examples of statins and explain their mechanism of action

A

simvastatin/pravastatin/rosuvastatin

competitive inhibitors of rate limiting step in cholestorol biosynthesis
decreases cholestorol levels and stimulates LDL receptor up-regulation
(most effective at night)

57
Q

what is the main difference between selective and non-selective alpha adrenoreceptor antagonists?

A

selective - no effect on HR or CO

58
Q

explain the main characteristics of lipids and name the main types

A

soluble in organic solvents and insoluble in water

cholestorol, triglycerides, phospholipids

59
Q

name 3 things cholestorol produces or is a precursor for

A

vitamin D
bile acids
steroid hormones

60
Q

describe the structire of lipoproteins

A

spherical shaped
centre core of hydrophobic lipids (triglycerides)
surface layer of polar components (phospholipids/proteins)

61
Q

what are apolipoproteins

A

amphiphilic compounds with a hydrophobic region interacting with a lipid core to provide structure, and a hydrophilic region acting with aqueous environment

62
Q

what is the function of apolipoproteins?

A

form lipoproteins by acting as ligands for lipoprotein receptors
activators/inhibitors of enzymes in lipoprotein metabolism

1st Year Med (52 decks)

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