Hypertension Flashcards

1
Q

What are the complications of HT?

A

HT itself doesn’t do any damage, it is the complications it causes:

  • Haemorrhage, stroke, cognitive decline, retinopathy, PVD, LVH, CHD, CHF, MI, renal failure etc –> many complications.
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2
Q

Define HT.

A

That BP above which the benefits of treatment outweigh the risks in term of morbidity and mortality.

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3
Q

What is the difference between normotensive and hypertensive BP?

A

Normotensive BP is below 140 mmHg systolic. Hypertensive BP is above 140 mmHg systolic –> 140/90 is hypertension.

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4
Q

Define stage 1 HT.

A

Clinic BP of 140/90, ABPM of 135/85.

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5
Q

Define stage 2 HT.

A

Clinic BP 160/100, ABPM 150/95.

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6
Q

Define severe HT.

A

Clinic systolic BP 180 or over, and diastolic 110 or over –> 180/110.

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7
Q

What are the causes of secondary HT?

A
  • Chronic renal disease: renal artery stenosis, polycystic kidneys
  • Endocrine disease: Cushings, Conns etc
  • Pregnancy: pre-eclampsia
  • Drug-induced: NSAID’s, OCP, corticosteroids
  • Vascular: coarctation of aorta
  • Sleep apnoae
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8
Q

What are the factors that contribute to HT?

A

Smoking (adds 10-20 mmHg), DM, renal disease, male, hyperlipidaemia, previous MI/stroke or LVH.

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9
Q

How is BP controlled?

A

CO, SV, HR and peripheral vascular resistance (TPR).

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10
Q

How does the sympathetic system control BP?

A

Vasoconstruction, reflex tachycardia and increased CO. Sympathetic system increases BP.

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11
Q

What is the renin-angiotensin-aldosterone system stimulated by?

A

Fall in BP, fall in circulating BV or Na+ depletion. Renin released from juxtaglomerular apparatus.

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12
Q

What is the function of the RAAS?

A

Renin converts angiotensin to angiotensin 1. Angiotensin 1 is then converted to angiotensin 2 by ACE.

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13
Q

What are the functions of angiotensin 2?

A

Vasoconstriction, anti-natruiretic and stimulates aldosterone release from adrenal glands. Aldosterone is anti-diuretic and anti-natruiretic.

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14
Q

What are key targets for HT treatment?

A

RAAS and sympathetic system.

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15
Q

What are the 2 main causes of HT?

A

Increased reactivity of resistance vessels and resultant increase in TPR by hereditary causes; or due to kidneys being unable to excrete Na –> Na and fluid are retained, and BP increases.

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16
Q

What other factors contribute to HT?

A

Age

Genetics and FH: closest correlation between siblings

Environment: mental and physical stress

Na intake/diet: BP

Race: African-American popultions are genetically selected to be Na retainers and so have higher BP than Caucasian populations

Weight: obese patients have > BP, 30% of all HT cases are attributable to obesity alone

Birth weight: low birth weight is associated with development of HT in later life

17
Q

What would you do before starting treatment for HT?

A

Assess risk: previous stroke/MI, smoking, DM etc

Assess end organ damage: ECG, echocardiogram, renal function

Screen for treatable causes: renal artery stenosis, Cushings, Conns, sleep apnoea

18
Q

What does using a ‘stepped approach’ mean?

A

Adding medications to current therapy until a target BP is achieved - not continuously changing medication.

19
Q

How should young and elderly people with HT be treated?

A

Young: high renin and ACE inhibitor

Elderly: low renin, Ca channel blocker and Thiazide-type diuretic

20
Q

When should stage 1 HT patients be given treatment?

A

Patients

21
Q

When should stage 2 HT patients be given treatment?

A

ABPM > 150/95 at any age.

22
Q

What is the BP target for > 80 year olds?

A
23
Q

Describe the 4 steps of anti-hypertensive drug treatment.

A

1) Offer with Ca blocker (over 55 or Afro-Caribbean), evidence of heart failure add a thiazide-like diuretic, under 55 do not give ACEI
2) Add thiazide-type diuretic
3) Add CBB, ACEI and diuretic together
4) Consider further diuretic therapy if K+ is 4.5 mmol/L. Over 55? CCB. Under 55? ACEI.

24
Q

Should ACEI be given during pregnancy?

A

No, they can cause malformations and stillbirths if given in the first trimester.

25
Q

Name 2 ACEI’s.

A

Ramipril and perindopril.

Contraindications: renel artery stenosis, renal failure, hyperkalaemia.

ADR’s: cough, first-dose HT, taste disturbance, renal impairment, angioneurotic oedema.

Drug-drug interactions: NSAID’s, K+ supplements.

26
Q

What is the advantage of ARB’s over ACEI?

A

No cough.

27
Q

Describe the actions of CCB’s.

A

Block L-type Ca channels. Anti-hypertensive of choice in women of child-bearing age and over 55’s.

28
Q

Describe the actions of thiazide-like diuretics.

A

Block reabsorption of Na+ and enhance urinary Na+ loss.

29
Q

Which drug is mainly used to treat HT in pregnancy?

A

Methyldopa

30
Q

Describe treatment regimes for over and under 55’s.

A

Over 55: start on CCB, add thiazide-like diuretic, add ACEI, add beta-blocker. CTAB

Under 55: ACEI (child-bearing CCB), thiazide-type diuretic, CCB, B-blocker.

31
Q

What is pre-eclampsia?

A

When BP rises severely from 20 weeks > 140/90 and patient has proteinuria.

32
Q

How are patients wiith hypertensive emergency best treated?

A

Continuous infusion of a short-acting, titratable anti-HT agent.