HTN Flashcards

1
Q

Definition

A

Stage 1- 140/90. Treat high risk, DM, end organ damage.

Stage 2- 160/100. Treat all.

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2
Q

Aetiology

A

85% essential
Isolated systolic HTN- atherosclerosis.
Malignant/ accelerated phase HTN- rapid rise causes vascular damage, common in young and black.
Secondary eg renal disease, endocrine (aldosteronism, phaeochromocytoma, cushings, hyperPTH), coarctation, pregnancy, drugs (steroids, OCP, NSAIDs).
Conn’s aldosterone secreting adenoma= HTN and hypoK.
Cushings- excess cortisol secretion.
Phaeochromocytoma- adrenal medulla tumour secretes catecholamines.

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3
Q

symptoms

A

Usually asymtpomatic

Sometimes headache, blurred vision, nosebleed, SOB.

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4
Q

Management

A

Lifestyle

Drugs eg thiazides, BB, Ca antagonist, ACEi, ARB, sm relaxant, renin inhibitors.

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5
Q

Complications

A
Cardiovascular disease eg cerebrovascular events, IHD, HF.
Kidney failure.
Retina
Aorta
AF
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6
Q

Diagnosis

A

Opportunistic screening in high risk
Ambulatory 24 hour BP or hom BP monitoring
S1- over 140/90 in clinic, over 135/85 in home or ambulatory.
S2- over 160/100 in clinic, 150/95 others.
Severe- over 180/110.
Assess end organ damage and CVS RFs and secondary causes eg bm, cholesterol, ECG, urine analysis, UE, Ca.
Special tests- renal US, urinary cortisol, renin, aldosterone.
Drug and social hx.

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7
Q

Differentials

A
Steroid use
Sympathomimetic drugs
Acute vasculitis
Serotonin syndrome
Phaeochromocytoma- adrenaline secreting tumour of adrenal gland
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8
Q

Under 55 years drug steps

A
  • ACEi or ARB 1st line
  • then add CCB OR thiazide diuretic
  • then add BOTH the above
  • then add further diuretic OR alpha blocker OR BB
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9
Q

Over 55 or black any age

A
  • CCB or thiazide 1st line
  • then CCB OR thiazide
  • then ACEi+ CCB OR ACEi+ thiazide.
  • then all three
  • then add further diuretic OR alpha blocker OR BB
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10
Q

Happy drug combinations

A

Diuretic + ACEi

Diuretic + BB

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11
Q

ACEi eg ramipril

A
1st line antiHTN
AE- dry cough, renal fail, hyperK
Caution- renal impairment, PVD
Contra indications- pregnancy, rebovascular HTN
Monitor renal function
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12
Q

Dihydropriridine CCB eg amlodipine

A

Bind alpha su of L channel
1st line antiHTN
Ok if concurrent angina
AE- SNS effects eg tachyc, flushing, sweat, headache.
Ankle swell, oedema, gingivial hyperplasia.

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13
Q

Phenylalkylamine CCB eg verapamil

A

Use if not tolerate DHP
AE- constipation, bradyc
DDI- DONT use with BB= severe bradyc.

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14
Q

BB eg atenolol

A

Beta 1 antagonist and decrease renin release.
Not used alone for HTN
Ok if concurrent angina, chronic HF, past MI, AF.
AE- reduced concentration, bradyc, raynauds, decrease glucose tolerance. Risk acute HF.
Caution if PVD and DM.
Contra indictated if asthma, COPD, HB.

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15
Q

ARBs eg losartan

A

ACEi substitute if bad cough
Use in HTN with LVH
AE- hyperK, renal fail, angioedema rare.
Caution in renal impairment
Contraindicated in pregnancy and renovascular HTN

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16
Q

Centrally acting eg methyldopa, clonidine, moxonidine

A

Alpha 2 agonists decrease SNS outflow
Less used for HTN
Alpha methyl dopa can be antiHTN in pregnancy, but BB 1st line.
AE- tired, depression.

17
Q

Direct renin inhibition eg aliskirin

A

Binds renin pocket and prevents angiotensinogen cleavage.
Alternative to ACEi and ARB.
NOT use with ACEi
Caution if risk hyperK, Na and volume depleted, HF, renal impairment.
Contra indicated in pregnancy.
DDI with furosemide.

18
Q

Loop eg furosemide

A

Block NCCK in thick ascending limb
Less used in HTN
AE- hypovolaemia, high uric acid, glucose intolerance, high LDL, hypoK. Ototoxicity and myalgia.
DDI- with amongolycoside= oto and nephrotoxicity.

19
Q

Thiazide eg bendroflumethazide

A

Block NaCl in DT
Widely used in HTN due to vasodilation.
AE- high risk hypoK, high uric acid, glucose intolerance, high LDL, erectile dysfunction.
NOT work in renal failure.
DDI- thiazide or loop + digoxin= hypoK= increase digoxin effect
Thiazide+ BB= hyperglycaemia, hyperlipidaemia, hyperuricaemia.
Thiazide or loop+ steroid= more hypoK
Thiazide +carbamazepine= more hypoNa

20
Q

Aldosterone antagonist eg spironolactone

A

Best for HTN due to primary hyperaldosteronism eg Conns
Add on in HTN if not controlled by ACEi+CCB+thiazide.
AE- hyperK, androgenic x reactivity, painful gynaecomastia.

21
Q

Signs

A

End organ damage- retinopathy, LVH, proteinuria.
For secondary- renal disease, coarctation (radiofemoral delay, weak femoral pulse), renal bruits, palpable kidneys, cushings, phaeochromocytoma (headache, palpitation, sweating), hyperaldosteronism (weakness, polyuria), apnoea (snoring, day time somnolence, morning confusion).

22
Q

K

A

More K IN due to-
Insulin, aldosterone, catacholamine (all 3 by stimulating Na/K ATPase), high ECF K, alkalosis.
More K OUT-
Exercise, lysis, high ECF osmolarity, low ECF K, acidosis of ECF.

23
Q

Explanation

A
  • blood pressure refers to the amount of pressure that blood puts on blood vessels walls as it is pumped. High blood pressure usually occurs with no obvious cause. But it can be due to other things like kidney problems, hormone problems, preganancy and one drugs.
  • over time the high pressure can damage the blood vessels putting you at risk of heart, eye and kidney problems.
  • lifestyle changes like stopping smoking, reducing alcohol, eating healthily and exercising regularly will help to reduce the pressure and lower the risk of some of the complications i mentioned.
  • drug treatment can also help. So drugs that reduce the volume of blood mean that there is less blood there to make that pressure against the walls. Also drugs to dilate blood vessels and reduce force of the heart.