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What are the UK 3 stages of hypertension?

List some causes of hypertension.

1: > or equal to 140/90 (ambulatory BP monitoring if more than or 135/85)

2. > or equal to 160/100 (ABPM if more than or 150/95)

3. > or equal to 180/110


Idiopathic, genetic, environmental, secondary e.g. kidney disese, renal artery stenosis


What are the four main treatments for hypertension? Give drug examples and SEs.

1. Lifestyle/environmental factors e.g. salt decrease. 

Then drugs, 3 classes A,C,D:

A: ACEI : interrupt RAA system, e.g. ramipril, enalapril, SE: cough, K+ retention, angioedema

C: CCBs: block Ca2+ entry to vascular SM and myocardial cells, 2 types:

Dihydropiridine e.g. amylodapine, vasodilation, SE: oedema, flushing Non-dihydropiridine e.g. diltiazem, decease HR, contractility, conduction, SE: SM in gut - constipation

D: diuretics: decrease intravascular volume -> Na+ and H2O loss -> decreased C.O., works in DCT, e.g. thiazide type = first line e.g. indapamide, also loop e.g. furosemide - mainly used in heart failure, works on LoH



Apart from the main 4, list some other agents used to treat hypertension.

Alpha adrenergic blockers (doxazocin, prazocin) vasodilation

Aldosterone blockers (spironolactone)

Beta blockers (metaprolol, bisoprolol, atenolol) vasodilation but bronchospasm SE

Central alpha adrenergic agonists (methyldopa, clonidine)


Define heart failure.

What are the 3 main causes?

C.O. insufficient to deliver necessary blood flow to tissues. Get pulmonary congestion, difficulty breathing and pulmonary oedema.

Mainly ischemic heart disease, also valve defects and dysrhythmias.


How can heart disease lead to heart failure that gradually gets worse?

Heart disease -> heart failure then either:


decrease in renal blood flow -> RAAS -> oedema -> increased preload -> heart failure


decrease in tissue perfusion -> increased sympathetic nerve activity -> vasoconstriction -> increased afterload -> heart failure

So compensatory mechanisms can worsen heart failure.


Define preload and afterload.

What is Sterling's law of the heart?


Preload: end diastolic volume     Afterload: end systole ventricular pressure

Increased venous return = heart beats stronger, stretched myocytes = increased overlap so more shortening per contraction thus stretch ventricles and they'll contract more but this fails in heart failure.


How is heart failure treated? 4 main drugs.

ACEIs, Beta blockers, Diuretics (furosemide, spironolactone). These 3 = heart uses less O2 = decreases risk of dangerous rhythms.

Main goals: decrease preload and afterload, improve stroke vol (and increase C.O), increase tissue perfusion, control fluid intake, decrease salt intake.

Also positive ionotropes increase strength of muscular contractions e.g. digoxin: selectively inhibits monocyte Na+ pump (Na+/K+ ATPase) -> increased intracellular Na+ -> Na+/Ca2+ exchange means increased intracellular Ca2+ -> increased cardiac AP -> decreased HR

Also direct action on conduction at AVN = decreases automacity and slows heart.


What is angina?

Where are the common sites and arteries affected?

What is the main cause of angina

Pain at characteristic workloads from ischaemia of myocardial muscle generally owing to artherosclerotic obstruction (plaque) of coronary BVs.

Site: chest, neck, L.arm. Arteries: L. and R. coronary (myocardial muscle O2 demand > supply, lactic acid -> stim nerve endings = pain!) and circumflex



What are the 3 main treatments for angina?

Nitrates e.g. glyceryl trinitrate, isosorbide mononitrate - vasodilators = reduce preload, vasospasm, and platelet aggregation. SE: headaches, reduced BP

Beta-blockers e.g. bisoprolol, decreases HR and O2 demand, SE: bronchoconstriction

CCBs: decrease SM contractility and O2 demand e.g amilodipine


How are lipids transported?

Excess of which lipoproteins are associated with cardiovascular disease?

List 3 causes.


Packed in lipoproteins.


Diet, environment, genetics


What are the 3 main treatments for lowering cholesterol/lipid? Give examples and SEs.

1. environment/diet alteration

2. statins: inhibit rate limiting step in cholestrol synthesis e.g. simvastatin, atorvastatin, SE: myositis, rhabdomyolysis, interactions with e.g. amylodapine

3. ezetimibe: blocks cholestrol absorption from small intestine, used with statins

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