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Competency > Hypertension > Flashcards

Hypertension Flashcards

1
Q

What is the BP for Grade 1 HTN? (diagnosed with HTN)?

A

140-159/90-99 mmHg

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2
Q

What is the BP for Grade 2 HTN and above? (diagnosed with HTN)?

A

≥ 160/100 mmHg

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3
Q

What is the BP for high-normal BP?

A

≥ 130-139/85-89 mmHg

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4
Q

At what BP should action be taken?

A

≥ 130/85 mmHg

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5
Q

How to calculate pt’s 10 year CV risk if no risk factors for CVD?

A

Singapore-modified Framingham Risk Score (SG-FRS-2023)

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6
Q

What is the benefit of lowering SBP by 5 mmHg?

A

Lowers risk of major CV events by 10%

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7
Q

What is the benefit of lowering SBP by 10 mmHg and DBP by 5 mmHg?

A

Lowers risk of heart disease, stroke, coronary heart disease, CV mortality and all-cause mortality

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8
Q

What is considered high to very high CV risk and what is the target BP?

A

Pts with CVD, CKD, DM or HMOD (hypertension-mediated organ damage) OR risk score >20%

< 130/80 mmHg

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9
Q

What is considered low to intermediate CV risk and what is the target BP?

A

Pts with no risk factors OR risk score ≤ 20%

< 140/90 mmHg (can go lower as tolerated)

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10
Q

Which group of patients should have target BP of < 150/90 mmHg (less stringent)?

A
  • older age (>80y)
  • frail
  • orthostatic hypotension
  • limited life expectancy
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11
Q

Should the target BP be < 120/70 mmHg? Why?

A

No, evidence of benefit beyond this threshold is inconsistent & potential for increased risk of SE can lead to tx discontinuation

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12
Q

What are some lifestyle interventions of elevated BP?

A
  • DASH diet (fruits, veg, low-fat dairy products, reduce saturated & total fat)
  • reduce Na intake
  • alcohol consumption moderation
  • increased physical activity
  • weight reduction if overweight/obese
  • smoking cessation
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13
Q

What is hypertension-mediated organ damage (HMOD)? Examples?

A

Structural / functional changes in arteries or end organs (e.g. heart, brain, eyes, kidneys, blood vessels)

E.g. left ventricular hypertrophy, albuminuria, hypertensive retinopathy

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14
Q

When to start pharmacotherapy for pts with elevated BP?

A
  • high-normal BP with high to very high CV risk (presence of relevant conditions or risk score >20%) esp if not controlled after 3-6m
  • grade 1 HTN with low to intermediate CV risk (risk score ≤20%) esp if risk score 10-20% or BP not controlled after 3-6m
  • grade 1 HTN with high to very high CV risk (presence of relevant conditions or risk score >20%)
  • grade 2 HTN and above with any CV risk
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15
Q

What are the 1st lines for HTN?

A
  • ACEi
  • ARB
  • DHP-CCB
  • thiazide/thiazide-like diuretics
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16
Q

Why are thiazide/thiazide-like diuretics considered alternative 1st lines?

A

Due to SE
- hyperglycaemia
- hyperuricemia
- increased urination
- electrolyte derangements (hypoK, hypoNa, hyperCa)
- hypotension, dizzy
- photosensitivity

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17
Q

What are some meds that can cause HTN (secondary)?

A

NSAIDs, steroids, decongestants, diet pills, COC, stimulants

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18
Q

What is considered major CV events?

A
  • fatal / non-fatal stroke
  • fatal / non-fatal MI or IHD
  • HF causing death or hospital adm
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19
Q

How does dry cough happen when using ACEi?

A

ACEi inhibits breakdown of bradykinin -> causes dry cough

20
Q

What triggers juxtaglomerular (JGA) cells to release renin?

A
  • reduced pressure -> smooth muscle cells less stretched -> sensed by JGA cells
  • reduced pressure -> sensed by vasomotor centre -> activate SNS -> activate JGA cells via renal nerves
  • reduced pressure -> less fluid filtration & reabsorption -> sensed by macula densa cells -> signal to JGA cells via paracrine communication
21
Q

Where are juxtaglomerular cells found?

A

In juxtaglomerular apparatus located next to glomerulus, all in the nephron

22
Q

What is the MOA of renin?

A

Cleave angiotensinogen into angiotensin-1 (partially active)

23
Q

How is angiotensin-II formed?

A

Angiotensinogen cleaved by renin to angiotensin-I, which is cleaved by ACE into angiotensin-II

24
Q

What does angiotensin II act on to maintain BP?

A
  • arterioles -> vasoconstrict -> increase BP
  • CV control center in medulla oblongata -> increase CV response -> increase BP
  • hypothalamus -> increase thirst & increase ADH -> increase water intake & reduce water excretion -> increase vol, maintain osmolarity -> increase BP
  • adrenal cortex -> increase aldosterone -> increase Na reabsorption by kidneys -> increase vol, maintain osmolarity -> increase BP
25
Q

DHP-CCB main SE?

A
  • hypotension
  • flushing
  • HA
  • peripheral edema
  • reflex tachycardia
26
Q

ACEi/ARB main SE?

A
  • bradykinin: dry cough, angioedema
  • hypotension, dizzy
  • increased K levels
  • AKI
27
Q

When to monitor __ for ACEi/ARB and diuretics?

A

Kidney function: serum K
Before and after initiation, after dose increase (2-4w), Q1y when stable

28
Q

When can BB be used as 1st line monotherapy?

A
  • stable IHD
  • HF
  • AF
29
Q

Classification of BB?

A
  • cardioselective (atenolol, bisoprolol, metoprolol, nebivolol)
  • non-cardioselective (propranolol, carvedilol)
30
Q

Which BBs are preferred for pts with respiratory diseases?

A

Cardioselective BBs

31
Q

Who can low dose dual therapy be initiated for?

A
  • SBP/DBP ≥20/10 mmHg above target
  • Grade 2 or higher
  • comorbidities (e.g. DM, CKD) requiring more intensive tx
32
Q

What combi of antiHTN to avoid and why?

A
  • ACEi + ARB: increased risk of hyperK, AKI, lower BP (similar MOA)
  • BB + non-DHP CCB: increased risk of bradycardia +/ AV block
  • BB + diuretic: increased risk of T2DM
33
Q

Recommended combi for low-dose dual therapy initiation?

A
  • ACEi/ARB + DHP-CCB
  • ACEi/ARB + thiazide-like diuretic
34
Q

What is resistant HTN?

A

Uncontrolled BP even tho pt is taking ≥3 optimally-tolerated antiHTN (including diuretic)

35
Q

When to follow up on pts with HTN?

A

At least Q6m

36
Q

When to give more frequent follow-ups for HTN?

A
  • increased risk of HTN-related complications (≥160/100 mmHg, CKD, DM, HMOD or high CV risk)
  • med change (dose adj, switch med, add new med)
  • if response to tx is not as expected
37
Q

Which antiHTN is CI in pregnancy?

38
Q

Some SE of BB?

A
  • hypotension, dizzy
  • bradycardia
  • AV nodal block
  • fatigue
  • depression
  • bronchospasm esp non-cardioselective
  • sexual dysfunction
  • mask hypoglycaemic sx
  • acute decompensated HF
39
Q

Non-DHP CCB SE?

A
  • edema
  • bradycardia
  • constipation (verapamil)
  • HA (verapamil)
  • hepatotoxicity
  • acute decompensated HF (due to -ve inotropic effect)
40
Q

What is white-coat HTN?

A

Office BP ≥130/80 mmHg after 3m trial of lifestyle modification but daytime ABPM (ambulatory BP monitoring) or HBPM (home BP monitoring) BP <130/80 mmHg

41
Q

What is masked HTN?

A

Office BP 120-129/<80 mmHg after 3m trial of lifestyle modification but daytime ABPM (ambulatory BP monitoring) or HBPM (home BP monitoring) ≥130/80 mmHg

42
Q

Which antiHTN is preferable for pts with HTN and albuminuria?

43
Q

Which antiHTN is preferable for pts with stroke/TIA?

A

ACEi/ARB, thiazide diuretics

44
Q

Which antiHTN is preferable for pts with coronary heart disease?

A

BB + ACEi/ARB

45
Q

Which antiHTNs are preferred for pregnancy?

A

Labetalol, nifedipine LA, methyldopa

Competency (30 decks)

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