Hypertension (Linus) Flashcards
What are the postulated causes of primary (essential) hypertension?
1) Sodium intake
2) Alcohol
3) Excess calories (obesity)
4) Stress
5) Sedentary lifestyle
6) Smoking
7) Low K or Ca intake (controversial)
What are the causes of secondary HTN?
Renal–> Renal HTN, parenchymal disease
Others–> Cushings, pheochromocytoma, primary hyperaldosteronism, coarctation of the aorta, sleep apnea, drug induced, thyroid/parathyroid
What is the theory as to how increased CO and impaired natriuresis might lead to a sustained increase in TPR even when CO has returned to a lower level? Please describe in your own words.
The thought seems to be that increased pressure causes increased Na excretion. The correlate is that the kidney adjusts to the higher pressure in order not to lose Na. When CO drops and the pressure is reduced to normal, the capillary beds/arterioles have thickened and adjusted the TPR such that the perfusion is kept constant. For some reason this persists once the CO returns to baseline. Guyton termed this “autoregulation.” Essentially, HTN becomes necessary to sustain the sodium balance. However, treatment with a thiazide diuretic is postulated to correct this problem via the same mechanism in the opposite direction. (This topic is not explained to my satisfaction in the lecture notes)
What three factors stimulate renin release?
1) Activation of renal sympathetic nerves
2) Stimulation of renal baroreceptors by reduced EABV
3) Activation of the macula densa chemoreceptor by decreased delivery of NaCl to the distal tubule
What is the pathophysiology behind systemic increase in BP when one renal artery is partially occluded?
Renal baroreceptors sense low EABV–> increase absorption in the proximal tubule–> decreased sodium return to the macula densa–> release of renin–> increased levels of ATII–> Increased blood pressure/perfusion pressure on the contralateral kidney–> decreased proximal tubule Na absorption–> increased Na absorption–> net normal Na excretion and ECF volume.
** Increased BP will presumably damage the contralateral kidney over time
What is the definition of a hypertensive crisis?
The point at which acute management of high BP plays a decisive role in the outcome. This is relative to baseline (eg in pregnancy and otherwise healthy people).
What is the basis for diagnosis of a malignant hypertension?
Fundoscopic examination which reveals hypertensive neuroretinopathy (HNR). This is further defined as the presence of striate hemorrhages and cotton-wool spots with or without papilledema.
** The clinical importance is that HNR signifies the presence of a systemic hypertensive vasculopathy with fibrinoid necrosis and obliterative arteriopathy (failure of autoregulation). If left untreated, it will lead to end-stage renal disease and death within 1 year.
Prevalence of HTN in US?
50-60 million.
Starting at 115/75, cardiovascular disease risk doubles with each increment of ____.
20/10 increase.
Which is worse for you, high systolic or diastolic BP?
systolic
What is Guyton’s hypothesis for generation of HTN?
Blames the kidney. Primary defect in renal Na excretion–> increase in plasma volume–> increase in CO–> autoregulatory increase in TPR–> increase in BP (and afterload mediated normalization of CO)
What is the Cellular hypothesis for HTN?
Blames the myocyte. Inhibition of the Na/K transporter–> increased intracellular Na–> decrease in Na/Ca exchange–>increase in cell Ca–> increase in cell contraction and TPR as a result of increased intracellular Ca–> increase in BP
Stage I HTN treat with _____. Stage II treat with ___.
Thiazide.
Thiazide + “something else”
What is the biggest difference between diltiazem/verapamil and DHP?
Diltiazem/verapamil decrease cardiac contractility, so can be used in arrythmias (commonly afib).
Dihydropyridines do not affect contractility.
What are indications for use of non-dihydropyridines (diltiazem/verapamil)?
HTN
atrial fibrillation rate control
migraine prophylaxis
Angina
**These are assx with more drug/drug interactions
