B4.041 Hypertension Flashcards
what are some factors that contribute to abnormal lipid values?
high saturated fat and trans fat intake
high simple carb intake
genetic factors
overweight and inadequate exercise
EKG findings consistent with hypertension
LAD, high QRS voltage, left ventricular hypertrophy
interaction between high salt diet and hydrochlorothiazide
increased excretion of potassium
can lead to development of hypokalemia
interaction between caffeine and hydrochlorothiazide
augmented diuretic effect leading to dehydration
discuss the dose dependent effects of hydrochlorothiazide
effects n HTN level off around 12.5 mg
any dose above 12.5 mg furthers K+ excretion effects but doesn’t help HTN anymore
what is the “cornerstone of management” in HTN
therapeutic lifestyle change
categories of BP measurements
normal
elevated
stage 1 HTN
stage 2 HTN
how many measurements do you need to make a diagnosis of HTN?
> 2 readings on >2 occasions
out of office and self monitoring measurements are recommended to confirm diagnosis and for medication titration purposes
old HTN definition
diastolic > 90
systolic > 140
summarize epidemiology of HTN in the US
1 in 3 adults have high BP, only 54% have it under control
1 in 3 have prehypertension
$46 billion in health care costs per year
new HTN definition
diastolic > 80
systolic > 130
what is prehypertension under the new definition
120-129/<80
increased risk of developing HTN and cardiovascular complications, but benefits of treatment undertain
what is malignant HTN
extremely high BP that develops rapidly and causes some type of organ damage
typical BP above 180/120
treated as a medical emergency
risk factors and prevalence of malignant HTN
rare, 1% of people with history of high BP
greater risk if man, black, lower economic status, or poor access to health care
causes of malignant HTN
collagen vascular disease (scleroderma) kidney disease spinal cord injuries adrenal gland tumors use of birth control pills or MAOIs use of illegal drugs, such as cocaine, amphetamines
for an adults 45 years old without HTN, what is the 40 year risk of developing HTN
93%, African American
92% Hispanic
86% white
84% chinese
association between CVD and BP
20 mm Hg higher SBP and 10 mm Hg higher DBP are each associated with a doubling in the risk of death from stroke, heart disease, or other vascular disease
medical diagnoses which have higher risks that are associated with higher SBP and DBP
CVD angina MI heart failure stroke peripheral arterial disease abdominal aortic aneurysm
other CVD risk factors to screen for in adults with HTN
smoking diabetes dyslipidemia excessive weight poor fitness unhealthy diet psychosocial stress sleep apnea
basic testing for primary HTN
fasting blood glucose CBC lipids BMP (electrolytes and creatinine) TSH urinalysis EKG w/ optional echo uric acid urinary albumin to creatinine ratio
cause of HTN
underlying mechanism(s) responsible for the increase in CO, TPR, or both that results in high BP knowing that CO, TPR or both are elevated does not define the cause of HTN
factors which contribute to the development of HTN
aging genetics obesity smoking salt sensitivity high, frequent alcohol consumption high fat diet low fiber diet lifestyle/environmental influences
primary HTN
underlying cause is unknown
likely an interaction of multiple defects in BP regulation w environmental stressors
may be genetic predisposition
more than 95% of cases
secondary HTN
underlying cause is known
5% of cases
2 possibilities of primary HTN causes
- abnormal function of the Na/K ATPase resulting in elevated cytosolic Ca2+ level
- microvascular dysfunction: decreased levels of NO and increased endothelin-1
result of decreased NO or increased endothelin 1
arteriolar constriction
increased TPR
increased MAP
discuss the trends in essential HTN and aging
at younger age, CO contributes most to HTN and decreases as patient ages
at old age, TPR contributes most to HTN and decreases as patients are younger
why does TPR contribute more to HTN as people age
heart and vessels adapt to chronically high pressure
- arterioles hypertrophy which reduced lumen diameter and increase contractile force (progressive increase in TPR over time)
- decreased ventricular compliance due to ventricular hypertrophy, impairs diastolic filling of the heart
examples of conditions causing secondary HTN
renal parenchymal disease renovascular disease pheochromocytoma primary hyperaldosteronism hypothyroidism hyperthyroidism
discuss the pathophys of HTN in renal parenchymal disease
nephron damage leads to impaired renal excretion of sodium and thus water
increased blood volume > increased venous pressure > increased venous return > increased preload > increased SV > increased CO > increased MAP
discuss the pathophys of HTN in renovascular HTN
atherosclerotic plaques in renal arteries > impaired renal blood flow > activation of renin-angiotensin system
what are the effects of increased renin and thus angiotensin II formation?
arteriolar constriction > increased TPR
venous constriction > increased CO
aldosterone secretion > increased blood volume > increased CO
discuss the pathophys of HTN in pheochromocytoma
catecholamine secreting tumor in the adrenal medulla > increased epi and NE in the blood
what are the effects of increased epi and NE in the blood?
arteriolar constriction > increased TPR
venous constriction > increased CO
increased inotropic state> increased CO
increased HR > increased CO
what is primary hyperaldosteronism?
Conn’s syndrome
66% of cases due to enlargement of both adrenal glands
33% of cases due to an adrenal adenoma that produces aldosterone
discuss the different layers of the adrenal glands and their function
outermost > innermost
zona glomerulosa (cortex) - mineralcorticoids - aldosterone
zona fasiculata (cortex) - glucocorticoids - cortisol, corticosterone, cortisone
zona reticularis (cortex) - androgens - dehydroepiandrosterone
adrenal medulla - stress hormones - epi, NE
what are 2 causes of primary hyperaldosteronism and how do treatments differ
adrenal gland tumor- gland is removed
adrenal hyperplasia- aldosterone antagonist given
discuss the pathophys of HTN in primary hyperaldosteornism
increased aldosterone > increased sodium and water reabsorption from kidneys > increased blood volume > increased CO
increased aldosterone> increased potassium excretion > hypokalemia > skeletal muscle weakness
discuss the pathophys of HTN in hypothyroidism
decreased metabolic rate > decreased production of metabolic vasodilators in systemic organs > increased TPR
discuss the pathophys of HTN in hyperthyroidism
increased metabolic rate > increased O2 demand by systemic organs > increased CO
discuss the baroreflex
homeostatic mechanism that helps to maintain BP at nearly constant levels
elevated BP > causes decrease in HR and thus BP
decreased BP > causes HR to increase and restore BP
how does baroreceptor desensitivity occur
cause is unknown
after chronic increases in arterial pressure, baroreceptor sensitivity to changes in arterial pressure is decreased compared to a normotensive person
physiologic dysfunction of the heart in development of HTN
high CO due to abnormal neuronal or hormonal stimulation may contribute to HTN
physiologic dysfunction of blood vessels in development of HTN
- greater than normal sym vasoconstrictor responses
- abnormal reg of vascular tone by local metabolic vasodilators
- ion channel defects in vascular SM
- endothelial dysfunction
- increased circulating levels of vasoconstrictors
physiologic dysfunction of kidney in development of HTN
- impaired renal blood flow
- inappropriate hormone regulation (increased aldosterone release)
- ion channel defects causing sodium retention
- increased renin resulting in higher circulating angiotensin II
physiologic dysfunction of baroreceptor in development of HTN
in a person with HTN, MAP will be maintained at a pressure higher than normal
physiologic dysfunction of adrenal gland in development of HTN
- increased release of aldosterone will raise blood volume and CO
- in pheochromocytoma, excessive NE and epi will increased TPR and CO
heart damage from HTN
workload is increased and oxygen delivery is compromised
ventricular hypertrophy and higher arterial pressure significantly increases myocardial O2 consumption, reduced ventricular compliance, increases filling pressures, and can lead to systolic or diastolic dysfunction and ultimately heart failure
arterial damage from HTN
combined effects of elevated pressure and accelerated atherosclerosis
high pressure may cause endothelial dysfunction
endothelial damage will promote plaque and thrombus formation
physical rupture of an artery (aneurysm) can also occur due to high arterial pressures
lifestyle changes to reduce HTN risk factors
decrease body weight reduced salt intake exercise reduced alcohol consumption and smoking reduce chronic stress biofeedback interventions
first line therapy for stage 1 HTN
thiazide diuretics
CCBs
ACE inhibs or ARBs
therapy for stage 2 HTN
2 first line drugs of different classes
how can improved adherence to therapy be obtained
once daily dosing
combination therapy
preferred diuretic
chlorthalidone
long half life and proven reduction of CVD risk
what should not be used in combo
ACE inhib, ARBs, and direct renin inhib
which drugs increase risk of hyperkalemia in CKD or with supplemental K+ or K+ sparing drugs
ACE inhib and ARBs
which drugs should be discontinued during pregnancy
ACE inhib and ARBs
which drugs cause edema
CCBs and dihydropyrodines
side effects of non-dihydropyridine CCBs
bradycardia and heart block
avoid in HFrEF
when are loop diuretics preferred
in HF and when GFR is < 30
