Session 3 Flashcards
Map equation?
Impact of angiotensin 2?
Co x TPR
Vasoconstriction
ADH release so water absorption in collecting duct
Aldosterone from adrenal cortex causing tubular NA CL absorption thus h20 retention in kidney. And k excretion
Increase sympathetic
Where is ACE found?
Through what receptors does angiotensin 1/2 have its effect?
Luminal surface of capillary endothelium predominantly in lungs
AT1 and AT2
Effects of ACEi?
Relevance of bradykinin?
Complications of ACEi’s
Inhibits circulating and tissue ACE
Ace breaks down this vasodilator so inhibitor furthers vasodilation
Hypotension,dry cough, hyperkalaemia as low alsodsterone reduces k excretion. Renal failure especially if renal artery stenosis as efferent constriction is vital.
When should ACEi not be used?
Renal artery stenosis,AKI, pregnancy, breastfeeding
Why might you use angiotensin receptor antagonists/AT1 receptor blockers instead of ACEi?
Names of angiotensin blockers?
No effect on bradykinin therefore no dry cough/angioedema
Candesartan
Losartan
What do CCB’s target?
Where do they act?
Where are these VOCC/LTCC’s located?
When are CCB’s the primary option?
Calcium initiated Sm contraction in hypertension
On alpha subunit of VOCC
Cardiac myocytes and vascular smooth muscle cells
Antihypertensive in low renin patients
Three calcium channel blockers?
Dihydropyradines-peripheral vasculature, first line hypertension
Non dihydropyradines-phenylalkamines-negative inotropy as depresses as node and slows AV node conduction
Non dihydropyradines-benzothiazapines-do middle of both
2 main of dihydropyradine class and role?
Complications?
Amlopidine
Nimodipine-cerebral vasculature-sub arachnoid
Ankle swelling,flushing,palpitations
Example and use of phenylalkamines?
Why elderly black African treated with CCB not ACEi to start with?
How are type 2 diabetic patients with hypertension first treated?
If first line treatment don’t work what you do?
Verapamil, anti arythramtic prolonging ap, negative chronograph and inotropic effects.
Naturally have low renin levels so no point targeting that system is system ain’t working
ACEi/ARB,s
Series of steps eventually using all ACEi, arb’s, CCB, thiazides
Benefits of ACEi on diabetic hypertension?
Not only aids hypertension by reducing peripheral vascular difference but also prevents glomerular nephropathy as dilates efferent arteriole reducing intraglomerular pressure.
Options in resistant hypertension?
What do b blockers do?
Side effects of b blockers?
Spironolactone-aldosterone receptor antagonists but do not use in hyperkalaemia. If too high k then a/b blockers.
In pregnancy labetalol reduces sympathetic outflow (b)
Block NA thus lower sympathetic tone and reduce myocardial contraction thus lower CO
Bronchospaam, heart block, impotence
What do a adrenoreceptor antagonists do?
Complications?
Average CO?
Symptoms of heart failure?
Decrease sympathetic tone lowering PVR
Dizzy,syncope,headache
5L/min
Dysponea, exercise intolerance and fatigue
Ejection fraction?
Normal?
If low?
If not but still HF?
Blood pumped out/blood total in ventricle
> 50
Contractility/systolic problem
Diastolic/filling problem
Treatment of heart failure with reduced ejection fraction?
Causes of this heart failure?
Why BB’s treat heart failure?
Furosemide as diuretic, bisprolol as BB, lisinopril as ACEi,
Narrowed artery or valve issue.
Slow heart rate and allow ventricle to fill with blood
Why NSAIDS increase k?
Prostaglandins dilate afferent arteriole, NSAIDs inhibit this, so lower GFR, so less k excretion
