Hypertension Flashcards
1
Q
What 6 general factors contribute to essential HTN?
A
- Excess NA
- Inc Na intake
- Abnormal Na excretion (4 hypotheses)
- Symp NS
- Reset baroreceptors - new set pt BP
- Stress –> epi which inc NE release
- Faulty NE reuptake
- Dec renal blood flow - inc Na reabsorption
- TPR
- Remodeling of vascular smooth muscle
- May be mediated by RAAS, endothelin-1, transforming growth factor-beta1, insulin like growth factor, hemodynamic shear, dec NO
- Arterial stiffness (hypertrophy, collagen, elastin altered, age)
- Changes in cell membranes
- Remodeling of vascular smooth muscle
- Obesity (inc CO, RAAS, dec NO, inc SNS)
- Low Ca+, Mg+ and K+
- Lead, tobacco, alcohol, caffeine (initially but tolerance develops quickly)
2
Q
11 Causes of Secondary HTN
A
- Renal parenchymal disease - reduced ability to excrete Na and water
- Renovascular HTN - renal artery stenosis –> RAAS
- Adrenal Causes
- Pheochromocytoma - chromaffin cell tumors –> inc BP, tachy, sweating, flushing, tremor
- Primary aldosteronism - adrenal adenoma or adrenal hyperplasia
- Cushing’s - excess cortisol - Coarctation of aorta
- Hypo or hyperthyroidism
- Hyper-parathyroidism
- Sleep apnea
- Meds - erythropoiten, cyclosporine, tacrolimus
- Drugs - cocaine, amphetamines
3
Q
Consequences of HTN (5 main categories)
A
- Cardiac - LVH, coronary heart disease, CHF
- Cerebrovascular - TIAs
- Peripheral - atherosclerosis –> claudication (pain w/ exertion due to transient ischemia)
- Renal - inc renal vascular resistance but maintain GFR (RAAS); RVR gets worse so dec renal perfusion»_space; dec GFR leading to proteinuria; eventually kidney shrinks –> dec RVR now –> progressive dec GFR (nephrosclerosis, glomerulosclerosis) –> ESRD
- Retinal - flame shaped hemorrhages and papilloedema
4
Q
4 Theories for Dec Na Excretion in HTN
A
- 1- altered pressure natriuresis; attain higher baseline so no longer excrete Na in response to same BP
- 2- deficient natriuretic hormone; normally inhibits Na-K ATPase to dec Na reabsorption
- 3- nephron heterogeneity - if some nephrons are ischemic –> renin release despite high BP
- 4- reduced nephron # - fewer nephrons to excrete Na loads
5
Q
Aliskiren
A
- Direct renin inhibitors
- new (2007)
- Side effects = headaches, dizziness, GI
6
Q
Hypertensive Emergency v Hypertensive Urgency
A
- Hypertensive emergency = severe inc BP in presence of end-organ damage - use IV/faster correction
- Hypertensive urgency = severe inc BP w/o end-organ damage - use PO/ correct in 1-24 hrs
7
Q
Scenarios of Hypertensive Emergency (3 systems)
A
- CNS - hypertensive encephalopathy, hemorrhage, thrombotic brain infarction
- Cardiac - acute heart failure, acute coronary insufficiency, aortic dissection, post-vascular surgery
- Renal - rapidly progressing renal fail or rapidly progressing glomerulonephritis
8
Q
Esmolol
A
cardio-selective, short-acting beta blocker; given IV if acute HTN or acute supraventricular rhythm
9
Q
Fenoldapam
A
- DA1 dopamine agonist; dilates renal and mesenteric vascular beds
10
Q
Labetolol
A
- if need both alpha and beta blockade
11
Q
Enalaprilat
A
- pro-drug of enalopril (good if heart fail)
12
Q
Diazoxide
A
- prevents vasoconstriction by opening K+ channels and causes hyperglycemia (use if hypoglycemia)
13
Q
Drug of Choice if Diabetic w/ HTN
A
ACEi (kidney protective)
14
Q
Drugs of Choice if Asthma or COPD
A
Asthma
- NO BETA BLOCKERS
- Can use ACEi - may cause bradykinin cough
- Diuretics can be used but inc risk of hypokalemia (on steroid inhaler- inc K+ excretion)
COPD
- No diuretics in COPD or hypercapnia; diuretic alkalosis would worsen the condition
15
Q
Drugs of Choice in Pregnancy
A
- Present w/ pre-eclempsia, chronic HTN, gestational HTN, PE superimposed on existing HTN
- If asymptomatic PE, treat when 160/105-110 w/ IV infusion of labetolol or hydralazine
- If chronic HTN, use methyldopa or labetolol alone; if resistant add Ca channel blocker
