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1st Year Med > Vascular Physiology > Flashcards

Vascular Physiology Flashcards

(62 cards)

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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
explain the actions of angiotensin II
raises BP (vasoconstriction) reduces blood volume through aldosterone release (reduced renal reabsorption of Na and water)
26
what are the side effects of ACE inhibitors?
sudden fall in BP on first dose persistent irritating cough (reduced bradykinin breakdown)
27
what are the subtypes of angiotensin receptors and what medication can target one of them?
AT1 and AT2 AT1 mediates vasoconstriction and aldosterone release from AT2 AT1 blockers - losartan/candesartan (side effects better than ACE inhibitors)
28
name an example of a diuretic and explain their mechanism
bendroflumethiazide (a thiazide) lowers BP by reducing blood volume (reducing renal reabsorption of Na and water) small vasodilator action reduces PR
29
what is the side effect of diuretics?
reduced K+ plasma concentration
30
what are the 3 types of Ca channel blockers? give an example of each
dihydropyrodines (amlodipine) phenylalkylamines (verapamil) benzothiazepines (diltiazem)
31
how do L-type voltage operated Ca channels work?
open on membrane depolarisation allowing Ca entry into cardiac and vascular smooth muscle blocked by Ca channel blockers
32
explain the mechanisms of Ca channel blockers
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
what conditions must be met for Ca channel blockers to work?
must have allosteric modulators bound to allosteric site to reduce probability of channel opening at a given voltage
34
what are the side effects of Ca channel blockers?
headache (cerebral vasodilation) constipation (relaxed GI smooth muscle) heart block (low Ca reduces contractility of heart) cardiac failure
35
what kind of input does the vasomotor nerve provide and what does it do?
sympathetic input vasoconstricts blood vessels
36
what is atherosclerosis?
the hardening of blood vessels involving plaque formation due to endothelial disruption
37
what are the general risk factors for vascular endothelial damage?
smoking high shear stress infection diabetes
38
explain the formation of FOAM cells in atherosclerotic plaques
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
what is the action of FOAM cells acting on the tunica media?
FOAM cells release IGF promoting SM cells from t-media to enter t-intima SM cells produce collagen in the t-intima
40
what occurs in atherosclerotic plaques to cause inflammation?
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
what occurs in unstable fibrous plaques?
fibrous cap thins due to oxidant and stress and eventually ruptures thrombus forms which can cause intraplaque haemorrhage, vessel occlusion or MI
42
what is cholestorol essential for?
cell membrane incorporation maintaining membrane fluidity and permeability steroid and fat-soluble vitamin production
43
what is the role of the liver in terms of cholestorol?
monitors cholestorol levels and regulates them through synthesis, absorption and bile secretion (drugs to treat hyperlipidaemia target this process)
44
what is cholestorol carried around the bloodstream in?
lipoproteins
45
what is contained in a lipoprotein?
lipids - cholestorol, triglycerides, phospholipids apoproteins - unique metabolic functions (one or more per protein)
46
name the 5 different lipoproteins?
chylomicrons VLDL IDL LDL HDL
47
what is the function of chylomicrons?
carries triglycerides from intestines to liver/muscle/adipose
48
what is the function of VLDL's?
carry newly synthesised triglycerides from liver to adipose
49
what is the function of LDL's?
cholestorol resevoir taken up via LDL receptors by endocytosis
50
what is the function of HDLs?
absorb cholestorol released by dying cells reverse transport - return cholestorol to liver
51
explain the exogenous pathway of cholestorol
intestine -> chylomicron -> if liproprotein lipase present: adipose, if not: chylomicron remnant -> remnant receptor on liver -> liver
52
explain the endogenous pathway of cholestorol transport
liver -> VLDL -> capillary -> if LDL: adipose, if not: IDL -> liver -> hepatic lipase turns IDL into LDL -> peripheral tissue
53
what occurs in the liver and capillaries in hypercholestorolaemia?
lowered LDL receptors in liver means more VLDL enters capillaries, resulting in higher IDL than LDL in tissues
54
what are the signs of familial hypercholestorolaemia?
xanthomas (fatty cholestorol deposits in skin) xanthelasmas (fatty deposits in eyelids) arcus senilis (white ring around cornea)
55
what are the common causes of hypercholestorolaemia?
high circulating cholestorol and triglycerides (primary) diabetes, alcoholism, hypothyroidism, liver disease, drugs, diet (secondary)
56
give examples of statins and explain their mechanism of action
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
what is the main difference between selective and non-selective alpha adrenoreceptor antagonists?
selective - no effect on HR or CO
58
explain the main characteristics of lipids and name the main types
soluble in organic solvents and insoluble in water cholestorol, triglycerides, phospholipids
59
name 3 things cholestorol produces or is a precursor for
vitamin D bile acids steroid hormones
60
describe the structire of lipoproteins
spherical shaped centre core of hydrophobic lipids (triglycerides) surface layer of polar components (phospholipids/proteins)
61
what are apolipoproteins
amphiphilic compounds with a hydrophobic region interacting with a lipid core to provide structure, and a hydrophilic region acting with aqueous environment
62
what is the function of apolipoproteins?
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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