HTN Lecture Flashcards
Resistant HTN?
PT fails to achieve BP goal despite use of 3 meds (ideally 1 is diuretic)
Isolated HTN?
SBP > 140 AND DBP > 90 (widening pulse pressure)
Indicative of arterial stiffness and increased CV risk
Large determinants of SBP? DBP?
CO largely determines SBP (SV, HR, venous capacitance)
Total peripheral resistance largely determines DBP
MAP?
2/3DBP + 1/3SBP
Cardiac output affected by?
Blood volume (Na, mineralcorticoids, ANP) Cardiac factors (HR, contractility)
Total peripheral resistance (TPR) affected by?
Humoral (Constristrictors: (CATLE) catecholamine, angiotensin 2, thromboxane, leukotrienes, endothelin; Dilators: (PKN) prostaglandins, kinins, NO)
Neural ( alpha, beta adrenergic)
Local factors (ionic/pH/hyhpoxia)
Inhibit Na, Cl reabsorption in the DCT ( = Na, Cl, water elimination)
Over time, volume normalizes but decrease in peripheral reistsance keeps BP lower
Thiazide/thiazide like diuretics
Best tolerated med for HTN
Not effective for pts w/ poor KF *****(CrCl < 30 ml/min or SCr > 2.5 mg/dL)
Thiazide (hydrochorothiazide)/thiazide like diuretics
Non-thiazides?
Metolazone (**use for when KF < 30)
Indapamide
Chlorothalidone
MIC the “thigh guy”
Thiazides most effective when combined with?
ACEI or ARB
Inhibit conversion of angiotensin 1 to angiotensin 2, causing?
ACEI
Reduces:
vascular smooth muscle constriction
aldosterone synthesis/release
Na reabsorption (thus increasing excretion)
HR
ADH release
ACEI also increases availability of?
Bradykinin, which is a vasodilator
ACE itself is responsible for breakdown of bradykinin
BUT bradykinin is involved in production of prostacyclin/NO (a humoral dilator)
Despite bradykinin’s vasodilator effects, it also has some negative effects…?
angioedema/dry cough (adverse effects of ACEI)
ACEI reduced efficacy in what pop?
African-Americans (however, effective when combined with CCBs/diuretics)
Those with renal insufficiency
Considerations/Adverse events for ACEI?
taste disturbances
hyperkalemia
increase in BUN (up to 20% acceptable)
Renal artery stenosis
SHOULD MONITOR K, SCr, BUN @ baseline, 2 weeks
Mixing ACEI w/ what can increase rsk of arrythmias/deaht?
K-sparing diuretics/K supps
Increase in SK levels -> arrhythmias
Drug induced acute injury death?
RENAL TRIFECTA
Diuretics (concentrate blood urine)
ACEI/ARB (dilates afferent arteriole)
NSAIDS (inhibits prostaglandins/bradykinins -> constriction of afferent renal arteriole)
ACEI end in?
Only IV only ACEI?
-pril
Enalaprilat
ARBs act on what receptor?
Antagonize angiotensin2 at the AT1 receptor (which predominates in the vasculature) thus prevents vasoconstriction
Allows blocks aldosterone secretio (reducing salt/water retention)
ARBs/ACEIs are similar, except?
ARBs are generally more expensive (which is why they’re reserved for those who can’t tolerate ACEIs)
However, ARBs don’t significantly affect bradykinin (no cough/angioedema
Considerations/Adverse events for ARBs?
hyperkalemia
increase in SCr/BUN (up to 20% acceptable)
Renal artery stenosis
Caution w/ K-sparing diuretics/K supps (Increase in SK levels -> arrhythmias)
ARBs end in?
-sartan
Both ACEIs/ARBs?
Cat D (pregnancy)
Renal stenosis
Directly inhibits renin (thus reducing Angiotensin 1,2 and aldosterone)
Aliskiren
(not routinely combined w/ ACEI/ARBs)
ADE: diarrhea, cough/angioedema, hyperkalemia, incraesed BUN/SCr
Hypersensitivity to sulfonamide