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40 Cards in this Set
- Front
- Back
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what are the values for hypertension
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140/90
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what is hypertension a risk factor for?
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IHD, vascular, stroke, ARTERIOSCLEROSIS
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what is the difference between 1ry and 2ry hypertensin
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1ry - familial or occurs alone - mix of genetics and environment
2ry - renal stenosis, endocrine, phaecytochroma |
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does smoking affect blood pressure
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NO
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inital hypertension control - lifestyle
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cholesterol, obestiy, inactivity, alcohol and salt intake
DIABETES - big CVS risk factor more serious need better control |
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between what values is hypertensive treatment based on the individuals cvs risk
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140-159/ 90-99 unless diabetic
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what is the standard treatment for under 55 (not afro)
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ace inhibitors
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what is standard treatment for over 55
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ca channel blocker and diuretic
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what happens to both under 55 and over 55 eventually
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combination of the alternative therapy added to original
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why should beta blockers be avoided in asthmastics
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trigger bronchospasma
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what is the method of action of a thiazide
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vasodilator and naturetics
acts on distal tubule - reduces Na reabsopriton lowers blood volume and thus TPR |
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what are the ADRs of thiazides
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gout, hypokalaemia, impaired glucose tolerance, inc cholesterol, activates RAAS
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how are beta blockers used to reduce blood pressure
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reduce myocardial contractility, HR and CO
inhibits renin release - overal reduction in TPR eventually |
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what are the side effects of BB
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cold extremities, impaired exercise tolerance, bronchospasm, precipitates acute heart fialuire, impaired glucose tolerance, bradycardia
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what is the simple overall action of ace inhibitors
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lowers ang 2, vasodilatation and naturesis
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what are the main ADRS od ace inhibitors
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hypotension, impaired renal function esp if stenosed, hyperkalaemia, dry cough,
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which group of pateints are ACE in hibitor not as effective in
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afro carribeans
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what are angiontensin receptor blockers
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block ang 1 receptors - inhibit vasoconstriction and aldosterone action - effec ang 2
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adrs of ang receptor blockers
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renal failure, hyperkalaemia
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ca channel blockers - which sub unit do they binds and what is their action on arteries (no action on veins0
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vasodilates peripheral coronary and pulmonary artiers
l type calcium channel blocker |
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what are the 3 main classes of ca blockers - dihydropyridenes, benzothiazepenes, phenylalkyamines
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DHD - vasodilate, short acting tachcardia, sns activation - adrs
BTP - prolongs refractory period, vasodilates, redcued preload - brady cardia Palkys - verapamil = depress SA node and slows AV node, prolong refracrtory, vasodilation adrs - constipation and bradycardia |
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what are the results of alpha blockers
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vasodilation, redcued peripheral resistance,
ADRS - postural hypotension, dizziness, headache, fatigue, oedema |
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renin inhibitors - block renin and angiotensinogen cleavage but why do they not work long term
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renin levels increase to overcome this
elimination is more faeces over renal contra i - hyperkalaemia, sodium, volume depletion, Hf, renal impairement, stenosis |
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what can aortic dissection present with?
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tearing pain that radiates to the back
but also st eleveation - DO NOT GIVE THROMBOLYTICS |
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where is plasminogen synthesised?
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liver
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what does tissue plasmina activator do?
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converts plasminogen to plasmin
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what other plasminogen activators are there
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urokinase type
plasminogen bound to fibrin converts fibrin into degradation products |
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what does streptokinase do
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activates endogenous plasminogen - releases plasmin
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what bacterias is SPK formed from
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beta haemolytic streptococci - complete hameolysis
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what are the issues with SPK
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allergies, cannot use twice, hypotension, short half life requies long infusion times
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why is recombinant tpa superior
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can be give more than once as it is not immunogenic
still a short hlaf life of minutes |
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what is co daministered with tpa to prevent thrombi and platelet activation
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heparin
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when would you use thombolytics
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mi, pe , major thrombi
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why is it dangerous to use thrombolytics in stroke paitents
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cerebral haemorrhage - time window of benefit
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what happens to thrombi as they age
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more difficult to lyse
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coronary occlusion and venous thrombo emboli have a wondow of 12 horus to treat - how long is there in ischaemic stroke `
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less than three
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what is the main ADR of thrombolyses
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haemorrhae - esp if female, old, hypertensive
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what are contraindications of thormbolytics
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bleeding sites, neoplasms of cns, aortic dissection , heady injury recently, recent surgery/trauma, stroke, hypertension, coagulation defects
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what are less serious adrs
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peptic ulcer, tia, warfarin, pregnancy, refractory
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what is an antidote to thrombolytcs
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transexaemic acid - lysine analogue, binds to lysine on plasminogen and prevetns bidnging to fibrin and streptokinase
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