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competency 10/11 > cardio: HTN > Flashcards

cardio: HTN Flashcards

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1
Q

pathophysiology of HTN

A
  • defects in renal sodium hemostasis
  • functional vasoconstriction
  • defects in vascular smooth muscle and structure
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2
Q

secondary causes of HTN

A

CKD, cushing’s syndrome, thyroid disease, NSAIDs, aspirin, decongestants, excessive consumption of licorice, st. john’s wort, bb or centrally acting a-agonists when abruptly discontinued

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3
Q

recommending BP monitor cuff sizes: adult

A

width 37-50% of limb’s length (length: width ratio, 2:1), inflatable bladder must cover 75-100% of the arm’s circumference

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4
Q

recommending BP monitor cuff sizes: obese

A

consider using wrist meters place at level of heart
- below heart - overreads
- above heart - underreads

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5
Q

recommending BP monitor cuff sizes: paediatrics

A

right arm BP, unless coarctation of aorta (aka imbalance of BP on L and R side)

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6
Q

grade 1 HTN

A

140-159/90-99

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7
Q

grade 2 HTN

A

160-179/100-109

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8
Q

grade 3 HTN

A

> = 180/ >= 110

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9
Q

unless c/i, advise patients to reduce weight to a BMI below

A

23kg/m2, and to a waist circumference below 90cm in men and below 80cm in women (for Asians)

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10
Q

advise pt to restrict salt intake to ___g per day

A

5-6

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11
Q

moderate alcohol consumption to no more than

A

2 standard drinks per day for men, and to no more than 1 standard drink per day for women

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12
Q

drug treatment should not be delayed without reason beyond ____________ if indicated

A

3-6months

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13
Q

advise pt to do at least ____ minutes of moderate dynamic exercise ____ days/week

A

30 mins, 5-7 days

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14
Q

any physical exercise above the basal level up to ____mins/week, confers incremental cv and metabolic benefits including BP reduction

A

150

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15
Q

bp lowering effects are likely similar btw classes, but

A

disease outcomes mismatch degree of bp reduction

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15
Q

which antihypertensive drug class have evidence of reducing risk of ESRD?

A

ACEi/ARB - most effective agents to reduce albuminuria, delay progression of diabetic and non-diabetic CKD

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15
Q

should we combine ACEi and ARB?

A

nope, no added benefit and excess of renal adr

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16
Q

when are ACEi/ARBs compellingly indicated?

A

post MI, HFrEF, albuminuria and CKD, HTN in DM

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17
Q

Antihypertensive class choice in pregnancy?

A

Labetalol, methyldopa, nifedipine, or vasodilators
- do not use ACEi (teratogenic in 2nd and 3rd trimester), ARB or direct renin inhibitors

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18
Q

BP target for most pt

A

120-130/70-80

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19
Q

initiation of antihypertensive drug therapy with 2 first-line agent of different classes, either as separate agents or in a fixed-dose combi, is recommended in adults with

A

stage 2 hypertension (BP>160/100mmHg) and an average BP >20/10mmHg above their BP target

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20
Q

what might help w DHP CCB a/w LL edema?

A

tolerance w time and combine w RASi (decr vasoconstriction) with CCBs (decr vascular SM tone)

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21
Q

avoid non-DHP in

A

HFrEF

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22
Q

caution use of non-DHP in

A

high-grade SA and AV block, bradycardia <60bpm, concomitant use of BB

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23
loop diuretics site of action
thick ascending limb
24
thiazides site of action
distal convoluted tubule
25
K-sparing diuretics
aldosterone antagonist, mineralocorticoid antagonist
26
thiazide-like diuretics eg
indapamide
27
thiazide-like diuretics vs thiazides
thiazide-like diuretics have: - better BP lowering effect, longer duration of action - more RCT evidence in reducing CV events and mortality
28
thiazides/thiazides-like diuretics: reduced effectiveness when eGFR<____ml/min
45 - thiazides probably ineffective when eGFR<30, may req loop diuretics for intended diuresis
29
ADR of thiazide/thiazide-like diuretics
electrolyte dysregulation: hypoK/Na, enhanced Ca reabsorption dysmetabolic effects: insulin resistance, new-onset DM (do not use with BB, may be attenuated by K-sparing diuretic), hyperTG/LFL, hyperuricemia
30
Which BB can be used with diuretics?
Nebivolol
31
ADRs of BBs
- associated with new onset DM (do not use with diuretics, except nebivolol) - sexual dysfunction (less with nebivolol) - severe claudication: muscle pain triggered by activity
32
Compelling indications for use of BB
Angina, heart rate control, a
33
thirdline agents used for
resistant hyperTN: full dose of 3 drugs and BP still not controlled
34
compelling indications: HF
BB + ACEi/ARB or ARNI -> aldosterone antagonist -> diuretics DO NOT use non-dhp ccb, but can use amlodipine or felodipine
35
compelling indications: angina pectoris
BB -> ACEi/ARB or DHP CCB (reduce LVH)
36
compelling indications: post MI
BB -> ACEi or ARB
37
compelling indications: AF prevention
BB, ACEi or ARB (may prevent recurrence)
38
compelling indications: AF ventricular rate control
BB
39
compelling indications: DM
ACEi or ARB -> DHP CCB: slows progression of carotid atherosclerosis -> diuretic or BB
40
compelling indications: DM with albuminuria (moderately or severely increased albuminuria)
ACEi or ARB DO NOT use any combi of ACEi with ARB
41
compelling indications: recurrent stroke prevention
thiazide-like diuretic + ACEi
42
compelling indications: gout
DO NOT use diuretics
43
compelling indications: bilateral renal stenosis
DO NOT use ACEi/ARB
44
compelling indications: ESRD
DO NOT use ACE/iARB/aldosterone antagonist (worsens renal function and hyperK)
45
compelling indications: heart block
DO NOT use BB, non-DHP CCB
46
compelling indications: peripheral artery disease
ACEi or DHP CCB
47
compelling indications: aortic aneursym
BB
48
compelling indications: isolated SBP
diuretic, or DHP CCB
49
BP goal for 65-80yo
stepwise <150mmHg, then <140mmHg if tolerated and achievable, ideally <130mmHg
50
perindopril +/- indapamide
reduces intracranial bleeding by 46%, in pt w or without AF on antithrombotic
51
isolated systolic hyperTN
wide pulse pressure (SBP-DBP>80mmHg) + SBP>140mmHg and DBP<90mmHg - function of aging and arteriolar stiffness - when treating ISH, may lead to orthostatic hypoTN - start low, go slow, watch to avoid OH
52
preferred antihypertensives in older adult
CCB, diuretics
53
oral contraceptives can cause
incr BP, proportionate with duration fo use
54
orthostatic hypoTN
supine-to-standing BP decr by >20mmHg SBP or >10mmHg DBP, within 3 mins of standing - possible etiologies: age-related, severe volume depletion, baroreflex dysfunction, autonomic insufficency eg diabetes, certain antihypertensives - postural unsteadiness, dizziness, fainting, may be a/w falls and fractures - educate pt to rise slowly
55
hypertensive emergency
severe HTN (grade 3>180/110mmHg) a/w acute HMOD - often life threatening and requires immediate but careful intervention to lower BP (usually iv) - complaints: HA, visual disturbances, chest pain, dyspnea, dizzines sand other neurological deficits - rarely: somnolence, lethargy, tonic clonic seizures, and corticol blindess may precede a loss of consciousness
56
hypertensive urgency
severe HTN but no evidence of acute HMOD, does not require admission to hospital
57
adrenaline moa
a1 (vasodilatation of arteries and increased vascular permeability leading to loss of intravascular fluid and subsequent hypotension/vasopressor), b1 (increased myocardial force of contraction (positive inotrope) and heart rate (positive chronotrope)), b2 (bronchial smooth muscle relaxation that helps to relieve bronchospasm) stimulation
58
ACEi is particularly useful in treating
- chronic renal failure: diminish proteinuria and stabilise kidney function (even in the absence of decreased BL), particularly useful in slowing progress of diabetic nephropathy - HF and post MI: slowing remodeling effects
59
CCBs bind more effectively to _____ and ____ channels
open and inactivated - binding of the drug reduces freq of opening in response to depolarisation and decreases transmembrane calcium current vs neuronal cells possess L-type calcium channels but less sensi to these drugs as the channels spend less time in open and unactivated state
60
DHPs vs non-DHPs
DHPs are more selective as vasodilators (relax vascular SM, leading to vasodilation) and have less cardiac effects
61
why are skeletal muscles not depressed by CCBs?
they use intracellular pools of calcium
62
CCBs: lowering BP
DHP = diltiazem = verapamil
63
CCBs: vasodilator
DHP>diltiazem>verapamil
64
CCBs: cardiac depressant
verapamil>diltiazem>DHP
65
a1 adrenoceptor antagonist MOA
block vasoconstriction, esp. visceral blood flow (dilate both resistance and capacitance vessels) - retention of salt and water increased when administered without diuretics, hence more effective when used with diuretic or bb
66
toxicities of a1 blockers
dizziness, palpitations, headache, lassitude
67

competency 10/11 (31 decks)

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