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Quiz 4 Flashcards

1
Q

How many Americans have HTN?

A

78M

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2
Q

__ __ medical problem in adults in the industrialized world.

A

1 chronic

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3
Q

___ ___ reason for visits to physicians.

A

Most frequent

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4
Q

__ __ __ __ indications for prescription drug use.

A

One of the leading

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5
Q

Increase of __/__ mmHg __ risk of CVD.

A

20/10 doubles

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6
Q

Over age __, __ is more important risk of CVD than __.

A

over age 50

SBP more important than DBP

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7
Q

Normotensive at age __ have __% lifetime risk of HTN.

A

age 55

90% risk

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8
Q

Most will eventually require __ drugs to achieve BP goal.

A

>/=2

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9
Q

Prevalence v. Control

why?

A
  • black, white, Mexican
  • white, black, Mexican
  • access to care, cost, hesitance for treating asympomatic dz
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10
Q

Natural course of HTN(4)

A
  1. Stroke - htn #1 RF
    • hem and isc
    • greatest effect on morbidity
  2. Coronary Heart Dz
    • angina
    • MI
    • CHF
  3. Retinopathy - infarcts and hemorrhages
  4. Nephropathy - ESRD
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11
Q

4 Primary sources of htn guidelines

A
  1. JNC - Joint National Commitee on Prevention, Detection, Evaluation and Treatment of High Blood Pressure
  2. BHS - British Hypertension Society
  3. ESH/ESC - European Society of Hypertension/European Society of Cardiology
  4. WHO/International Hypertension Society - geared toward developing countries with limited access/range of meds
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12
Q

JNC facts

A
  • first pub 1977
  • current JNC 8, 2014
  • funded by National Heart Lung and Blood Institute NHLBI, a unit of NIH/DHHS
  • written by National High Blood Pressure Education Program coordinating committee
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13
Q

BHS facts

A
  • first pub 1989
  • current version 2011
  • written by BHS working party
  • funded by unrestricted grants from major pharm co’s
    • no reps from drug co
    • not advisory to committee
  • 250 members
    • htn researchers in UK and Ireland
    • MD’s, Nurses, physiologists, other scientists
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14
Q

ESH/ESC facts

A
  • first pub 2003
  • current version 2013
  • written by joint task force from various EU countries
  • Academic societies sim to ACC
    • high presige, less questionable motivation
  • funding sources not disclosed
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15
Q

JNC 8 story

A
  • in 2014, 14 yrs after JNC 7, nothing published
  • NHLBI withdrew support and w/i months JNC 8 was released
  • written by JNC 8 subgroup
  • minority report published disagreeing with elements
  • not sanctioned or endorsed by NHLBI
  • major cardio and other societies came forward in disagreement
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16
Q

AHA/ACC/ASH role.. did/will do

A
  • will author new guidelines promised this year
  • published interim bridge that only applies to CAD
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17
Q

Blood Pressure Classification (JNC 7&8)

A
  • normal <120/<80
  • pre-htn 120-139/80-89
  • stage 1 140-159/90-99
  • stage 2 160/100+
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18
Q

Lifestyle Modifications

A
  • IBW
  • DASH diet
  • Reduce Na
  • Exercise
  • Avoid xs EtOH
  • Stop smoking
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19
Q

Being overweight increases risk for developing htn __ to __ x.

A

2-6x

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20
Q

Factors defining “overweight”

A
  • BMI >=30
  • Waise >=34 women, 39 men
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21
Q

BMI formula

A

kg/m2

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22
Q

Wt loss…

A
  • reduces SBP and DBP, 10lb loss significant
  • augments activity of antihypertensives
  • decreases CHD risks:
    • hyperlipidemia
    • DM
    • CHD
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23
Q

Dietary Na

A
  • studies show assn Na intake and BP
  • blacks and elderly more sens to changes in Na
  • reduce to <2.3g/day in
    • dec BP 6.3/2.2 in older pts
    • inc resp to meds
  • 75% Na is from processed foods
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24
Q

EtOH

A
  • Excess in
    • inc BP, somewhat
    • resistance to drug therapy, moreso
  • Limit to… (half for women and light wt ppl)
    • 1 oz/day
    • 2 oz 100 proof
    • 10 oz wine
    • 24 oz beer
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25
Q

Physical Activity

A
  • improve bp, healht, wt(rf)
  • sedentary = 20-50% inc risk htn
  • Guideline: 30-45 min/day aerobic, most days of week
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26
Q

Potassium

A
  • with K wasting diuretic
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27
Q

Calcium

A
  • RDA 800-1200mg/day
  • inverse relationship between Ca and BP, low Ca inc BP
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28
Q

Magnesium

A
  • No convincing data for supplementation
  • used in hypo K, not BP per se
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29
Q

Dietary fats

A
  • Omega-3 FA’s may dec BP
    • no longterm studies m/m
    • common GI sfx
  • prescribed for hypertrig
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30
Q

Caffeine

A
  • may inc BP short term, but tolerance is rapid
    • intermittant high bp ok, like in exercise
  • no need to restrict
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31
Q

Garlic/onion

A
  • no effect in controlled trials
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32
Q

SBP decreases with lifestyle modification

A
  • wt loss 5-20mmHg (20lb)
  • DASH 8-14mmHg
  • Na reduction 2-8mmHg
  • Exercise 4-9mmHg
  • EtOH moderation 2-4mmHg
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33
Q

Thiazide Diuretic chars

A
  • bad diuretics, diuretic action not sustained
  • best for idiopathic htn
    • JNC 7 drug of choice for essential htn
    • diuretics generally not for htn, but thiazide yes
    • combo for non-idio
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34
Q

Loop Diuretic use in htn when…

A
  • when it results from volume overload (CDK)
35
Q

K sparing diuretic chars

A
  • weak diuretics
  • weak antihypertensive effects
  • used primarily to prevent K wasting from other diuretics
    • side effects offset each other
36
Q

ALD antagonist efficacy

A
  • little long-term data on m/m (indep htn data)
37
Q

Thiazide diuretic agents

A
  • HCTZ
  • chlorthalidone (EU)
  • metolazone
38
Q

Thiazide MOA

A
  • Initial BP reduction through diuresis
  • Chronically dec peripheral vascular resistance
    • move Na and H2O from w/i arteriolar walls
      • effect enhanced by Na restriction
39
Q

Thiazide dosing and usage

A
  • combo rx
  • offsets compensatory Na retention of other rx
  • qd dose in am dec noct diuresis (dim over time)
  • 50mg qd opt/max - 25mg d/t AE’s
40
Q

Thiazide ADR’s

A
  • mild sfx
    • hypo K, Mg
    • hyper lip, gly*
    • ED
  • 25mg not sig less effective than 50, but sfx sig less
41
Q

RAAS pathway

A
  • angiotensinoGEN –renin–> ang I
  • ang I –ACE–> ang II
  • ang II fx:
    • activate SNS
    • vasoconstriction
    • ALD release
      • Na + H2O retention
42
Q

ACEI agents

A

-pril’s

43
Q

ACEI MOA

A
  • blocks ang I to II conversion
    • ang II -
      • potent vasoconstrictor
      • ALD secr - retain fluid
      • stim SNS, norepi
  • blocks degradation of bradykinin (vasodilator)
    • inc natural vasodilator, may make it better than ARB
  • use in HF and CKD - added benefit
44
Q

ACEI specific advantages in? (2)

A
  • HF
  • CKD
45
Q

ACEI warnings

A
  • may inc rate of HF and stroke compared to thiazides
    • maybe, ALLHAT
46
Q

ACEI ADR’s

A
  • hyper K, moreso in HF
  • AKF <1%, stop or dec dose if 35% inc in Cr over baseline
    • early benefit, may worsen CKD eventually
    • this is not a reason not to use, monitor RF
    • overall preserves RFx until it doesn’t
  • angioedema - rare but more in blacks and smokers
  • persistant dry cough in 20%
  • orthostatic hypotension, esp in vol depleted, elderly, or on other vasodilator drugs - uncommon in htn w/o these
  • contraindicated in pregnancy - placental blood flow, teratogen
47
Q

ACEI dosing

A
  • start low and titrate up to desired effect, not specific dose
  • half normal starting dose where risk for hypotension
    • volume depleted
    • HF exacerbation
    • very elderly
    • concurrent vasodilators or diuretics
  • half normal starting dose where risk for severe renal dysfx
    • elderly
    • current CKD
48
Q

ARB agents

A

-sartan

49
Q

ARB MOA and effects

A
  • ang II R agonist
    • RAA system sources
    • tissue sources
  • no effect on bradykinins = no cough
  • otherwise similar to ACEi’s
    • ADR’s
    • not in preg
    • orthostasis
    • angioedema (less than ACEi’s)
50
Q

Direct Renin Inhibitor

agent, moa, effects

A
  • aliskiren (Tekturna)
  • blocks angiotensinogen conversion to ang I by renin
  • otherwise similar to ACEi’s
    • ADR’s
    • not in preg
    • orthostasis
    • angioedema (less than ACEi’s)
  • no advantage over ACEi/ARB’s, still available
51
Q

BB’s

3 types and their agents

A
  1. Cardioselective - no ISA (bisop, nebi, ate, beta, met)
    • atenolol, betaxolol, bisoprolol, metoprolol, nebivolol
  2. Non-selective - no ISA (tim, prop, carv, nad, labe)
    • carvedilol, labetalol, nadolol, propanolol, timolol
  3. Intrinsic Sympathomimetic Activity - not cardiac selective
    • acebutolol, penbutolol, pindolol (acebut, penbut, pind)
52
Q

BB moa

A
  • many physiological effects documented but uncertain what causes BP lowering effect
53
Q

BB: CS v. ISA

A
  • CS: greater affinity for B1R (heart+kidney) than B2R (lungs, liver, panc, arteriolar sm. m.), preferred for htn (non-CS equally B1B2)
    • preffered for htn, narrow range of R’s, less sfx
  • ISA: partial BR agonists = reversible blockade - high conc overcomes blockade and inc HR (CS irreversible)
    • adv in exercise (for recommended wt loss)
    • bad for anx, HF, angina (inc cardio o2 demand)
      • really bad if demand inc during MI
    • not as effective in red CV events as other BB’s
54
Q

BB ADR’s

A

brady, BBB, broncon, rayanaud, rebound

  • brady (lowers d/t loss of adrenergic tone, could BB to brady)
  • dizzy/drowsy - CNS dep in those that cross BBB
  • bronchoconstriction in COPD/asthma - CS only at low dose
    • don’t use either, as dosage increases over time
  • worsens Raynaud’s - vasospasms
  • abrupt d/c may cause rebound htn/hr - taper 1-2wks
    • body producing NE to inc HR, blocked, make more
    • also R upregulation and inc R sens - blocked
    • remove BB - a lot of agonist and oversensitive R’s…
55
Q

CCB’s

2 types and their agents

A
  • dihydropyridine
    • amlodipine, felodipine, isradipine, nicardipine, nifedipine, nisoldipine
  • non-dihydropyridine
    • diltiazem, verapamil
56
Q

CCB moa

A
  • block Ca influx across cell memb = coronary and peripheral vasodilation - potent vasodilators
  • both equally effective in chronic htn
  • all have some neg inotropic effect
  • not first line tx, not as protective as thiazides
57
Q

CCB utility

A
  • 2nd c thz
  • dhp/non = effective
  • neg inotropes
  • no CV event reduction
  • ISH (+thz, esp elderly)
58
Q

dihydro use, sfx, adr

A

ish, tach, orth, diz, flush, ha, p.ed thz

  • very effective for ISH (esp in older pt), often added to thiazide
  • poss reflex tach, have precipitated angina, d/t dropping BP (vasodilatioin)
    • typically w/ short-acting nifedipine - other dihydro’s are SR or have longer duration of action (less “peak effect”)
    • used to squirt or chew nif gel caps, frequent rebound tach
      • inc card o2 demand - MI (htn tx caused MI)
  • orth, diz, flush, h/a, peripheral edema (25mg HCTZ/wk for edema)
59
Q

non-dihydro sfx, adr

A
  • poss cardiac conduction abnormalities
    • caution in brady + AV block
    • no verapamil in HF, brady dec CO
    • mostly at higher doses or in pt’s with pre-existing conduction abnormalities
  • anorexia, nausea, peripheral edema (less than dhp), const (automatically give sl sft)
60
Q

non-dihydro chronotherapeutics

A
  • =time released
  • “timing of dosage form may be important in effacacy of drug”
  • Covera HS and Verelan PM (both verapamil)
    • dose at night = peak conc in early am hours
    • theory: blunting early am bp surge = greater reduction in CV events - no evidence
61
Q

Alpha Blocker agents

A
  • prazosin, terazosin, doxazosin
62
Q

Alpha Blocker moa

A
  • selective a1 R antagonists in peripheral vasculature
    • a1 R stim = vasoconstriction
  • vasodilation and bp lowering
    • note direct vasodilators not good antihypertensives, bp fluxuation, dizzy, ortho – not same level evidence in red m/m (end goal)… so ablockers 2nd line added to other agent
  • trial that showed acei caused hf/stroke showed same inc w/ ablockers
63
Q

Alpha Blocker role in htn

A
  • should only be used in combo w/ other anti-htn agents
64
Q

Alpha Blocker adr’s

A
  • in one major trial inc risk of stroke, HF and CV events
  • first dose effect - massive vasodilation - dizziness, faintness, syncope 1-3h p 1st dose
    • take first few doses HS
    • also occurs w/ dosage change or non-adherence
  • sustained orthostatic hypotension - esp elderly, more prone to orth changes and inc danger in falls, hips, etc
  • CNS effects - lassitude, vivid dreams, dep
  • priapism

*lassitude = a state of physical or mental weariness; lack of energy

65
Q

Central Alpha Agonists

agents, moa, adr

A
  • agents: clonidine, methyldopa
  • moa: (effective…)
    • reduces sympathetic outflow from the vasomotor center in the brain, decreasing hr, co and bp
    • ablockers=periph
    • these are central ags - mimic feedback effect of NE
      • NE released to inc bp/hr, returns to brain to stop further release
  • adrs: (…but at a cost)
    • na/h2o retention, often used with diuretic
    • dep
    • orthostatic hypotension (caution in elderly)
    • anticholinergic effects - sedation, dry mouth, urinary ret
    • profound rebound htn from abrupt cessation
66
Q

DASH diet

A
  • fruit, veg, grain
  • lo/no fat dairy, fish, poultry, beans, nuts, and vegetable oils
  • lo sat fat (meats, dairy, tropical oils)
  • lo suc
67
Q

4 questions answered by guidelines

A
  1. Who do you treat?
  2. When do you treat?
  3. With what do you treat?
  4. To what goal do you treat?
68
Q

JNC 7 principle

A
  • Compelling Indications = reason to choose a class of htn drug because it also treats/prevents…. HF, post-MI, CAD risk, DM, CKD, stroke recurrence …with added benefit of treating BP
69
Q

1st intervention, common to majority of sources..

A

lifestyle mods, then drugs but continue these mods

70
Q

changes from JNC 6 to 7

A
  • fewer categories of htn
  • compelling indications added
71
Q

JNC 7 in a nutshell

A
  • normal, pre, s1, s2 and <130/80 in dm/ckd
  • ci?treat ci
    • :s1 thiazide (or poss ACEi, ARB, BB, CCB, or combo)
    • :s2 thiazide +1
72
Q

JNC 6 strategy not carried forward…

A
  • other guidelines also, treat those at highest risk for comorbidities most aggressively
  • Risk Stratification - A, B, C (notes not specific about ABC criteria)
  • A - lifestyle mods 12 months into s1, or at s2, start 1st rx
  • B - lifestyle mods 6 months into s1, or at s2, start 1st rx
  • C - lifestyle mods, but start 1st rx at high normal (130/85)
    • HF, RF, DM
  • notes ** mult rf’s, consider rx initially as in C
73
Q

ALLHAT design and results

A
  • Anti-htn and Lipid-Lowering tx to prevent HA Trial
  • largest htn trial to date
  • chlorthalidone (thz), lisinopril, amlodipine (CCB), doxazosin (aB)
  • div ppl into these 4 groups - who dies less?
  1. thz more effective wrt bp reduction and htn complications/sfx than other 3
  2. inc risk of hf and stroke with ACEi
74
Q

ALLHAT critique

A

primary outcomes, poor combos, naivety, dm/thz, aust bp study

  • no diff in primary outcomes, i.e. r/t primary hypothesis study was designed to test, only in secondary outcomes
    • not invalidate but low confidence
  • if original drug not effective, add rx in combo
    • better rx combo for thz
    • suboptimal rx combo for ACEi and CCB

…legit conclusion would compare one combo to another, not thz to acei/ccb generalization

  • subjects not naive to htn rx and were high risk
  • authors discounted sig increase in incidence of dm in thz group
  • results contradicted by Australian National BP Study
75
Q

JNC 7 concerns

A
  • 4 ALLHAT authors on JNC 7 executive committee
    • inc advocacy, authors believe in study, or…
  • JNC 7 concerned with selection of 1st rx at dx htn - naive
    • many in ALLHAT had been on long term rx, s2 htn - not naive
    • JNC 7 applied ALLHAT results to disparate pop
76
Q

BHS thresholds

A
  • Risk stratification (like JNC 6) major determinant
    • age, smoker, sbp, total chol:HDL ratio… 10 yr risk for CVD
    • (may be in new US guidelines)
  1. Really high bp straight to tx
  2. Really low reassessed in a few yrs
  3. In the middle 140-159/90-99 (rx by JNC 7/8)
    • target organ damage, CV complication, dm, or 20% 10yr risk — Rx
    • none of these — reassess, no Rx
77
Q

BHS choice of agent for new dx htn

A
  • choose drug based on pathology
  • <55y ACEi/ARB (A)
    • younger white pts htn tends to be d/t elevated RAAS
    • next step - add C or D
  • >55 y or black CCB or Thz Diuretic (C or D)
    • ACEi monotherapy less likely effective - we’ve known for 20 yrs, but not reflected in guidelines
    • next step - block RAAS
78
Q

ESH/ESC 2013

A
  • not so focussed on first drug and inc doses
  • quick to move to combos
    • additive bp effects, not sfx
  • smaller doses of more rx, combo that makes sense, not so focused on first rx like U.S.
79
Q

JNC 8 goal

A
  • # 1 controversy in htn
  • JNC 7 <140/90 goal for most, <130/80 for dm/rf
  • JNC 8 <140/90 inc dm/rf
    • except >60y s dm/rf – <150/90
    • no data to support lower goals
  • In a large cardiology practice pts not considered to have htn by these goals
    • 14.6% hx stroke/TIA
    • 65% had CAD
  • AHA recommends clinicians reject JNC 8, use JNC 7 guideline
80
Q

JNC 8 first drug

A
  • black - D, C or combo
  • white - D, A, C or combo (JNC likes thz even though won’t benefit as much)
  • CKD - A
81
Q

ACC target

A
  • <140/90
  • lower for older, black, hf, dm, ckd
82
Q

ACC rx recommendations

A

compelling indications

  • CAD, MI - BB, ACEi
  • Stroke/TIA - thz, ACEi
  • CKD, HF, DM - ACEi first..
83
Q

New guideline for CAD only

AHA/ACC/ASH

A
  • <130/80 CAD
  • <140/90 everyone else
84
Q

SPRINT

A
  • Sys BP Intervention Trial
  • 9,000 pts >50y
  1. Intensive tx <120
  2. Standard tx <140
  • Excluded stroke, dm, hf, ckd
  • Outcomes observed - MI, ACS, Stroke, HF, CV death
  • Intensive tx group significant reduction in primary outcomes
    • suggests 120 goal for older
  • problems - ortho changes, falls, RF - balancing risk…
    • what about success at reaching 140 goal? now 120?

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