HTN Flashcards
what is secondary HTN
caused by renal disease, sleep apnea, or adrenal disease
what is primary or essential HTN
what most people have
cause is unknown but attributed to risk factors
which systems have increased activity in HTN
sympathetic nervous system
Renin-angiotensin-aldosterone system
Describe how the RAAS system increases blood pressure
low blood pressure signals the liver to release angiotensinogen and renin which converts to angiotensin I. ACE then converts this to Angiotensin II which causes aldosterone secretion and vasoconstriction. aldosterone prompts increase Na and water reabsorption increasing blood volume.
how does an ACE inhibitor affect blood pressure
it prevents ACE from inactivating bradykinin (which causes vasodilation) and prevents the conversion of angiotensin I to angiotensin II
how does the sympathetic nervous system cause increased blood pressure
low blood pressure signals the brain to release Norepi which causes vasoconstriction by activating the alpha-1 receptors as well as increased HR and contractility by activating the beta 1 receptors
What do DHP CCBs affect?
SVR (systemic ventricular resistance)
what do non-dhp ccbs affect
contractility and heart rate
Normal blood pressure
<120/<80
top or bottom number: systolic
top
top or bottom number diastoli
bottom
HTN values
> /= 130/ >/= 80
what should sodium intake be reduced to for HTN management?
<1500mg/daily
when to start drug treatment
stage 2 HTN (>140/>90)
or
stage 1 HTN + ASCVD risk >/=10% or clinical CVD
First-line agents: non-black patients
thiazide, CCB, ACE inhibitor, ARB
First-line agents: black patient
thiazide or CCB
First-line agents: CKD (all races)
ACEi or ARB
First-line agents: diabetes with albuminuria
acei or arb
First-line agents: stage 2 HTN with readings >150/90
start 2 first-line agents
which first line agents should not be used in combo
acei and arbs
can you add a second agent before the first one is titrated to max?
Yes! actually works better and can prevent side effects
which htn drugs have a boxed warning for fetal toxicity when used in pregnancy
acei, arbs, and aliskiren
what is recommened in patients with a high risk of preclampsia
low dose aspirin daily after first trimester
when to treat chronic htn in a pregnant patient
if >/= 160/105
First-line agents: pregnant patient
labetalol and nifedipine ER
MOA thiazide diuretics
inhibit sodium reabsorption in the distal convoluted tubules, increasing excretion of sodium, cl, water, and K
thiazides CI
sulfonamide allergy