HTN Flashcards
Why should I care about bp and what are the goals for the general population?
Goals is a bp less than 140/90.
I should care because this strongly reduces risks of strokes, LVH, heart failure, coronary artery disease, peripheral artery disease, and renal disease. CV risk DOUBLES with each 20/10 mmHg BP increment. The risk increase is greatest for strokes, though the most common hypertensive disease is probably coronary artery disease. And, most hypertensive patients aren’t meeting their blood pressure goals. Affects 50 million people in the united states.
What is primary HTN?
any hypertension that has no identified cause. This is about 90% of HTN. there is no universally accepted pathophysiologic explanation for primary HTN, but candidates include genetics, cardiac output, sodium intake, renal sodium retention, renin-angiotensin system, stress/sympathetics, peripheral resistance, and vascular endothelial function.
What are some secondary renal parenchymal and endocrine causes of HTN?
Renal parenchymal causes include polycystic kidney disease, chronic interstitial disease, glomerulonephritis.
Endocrine problems that can cause HTN include pheochromocytoma, hyperthyroidism, Cushing’s, primary hyperaldosteronism
What are some secondary vascular or chemical causes of HTN?
vascular: coartcation; renal artery stenosis or fibrous dysplasia. Renal artery stenosis is the leading cause of vascular HTN
Or, chemicals/drugs, including OCPs, decongestants, sympathomimetics, cyclosporine, NSAIDs, antidepressants, corticosteroids, lithium
Describe a framework for understanding HTN pathophysiology
BP = cardiac output X peripheral resistance. In some young hypertensive pts, we see increased cardiac output- but the major finding in established HTN is increased peripheral resistance. This is because of autoregulation: we see peripheral vascular resistance increases in the setting of persistently increased cardiac output.
Salt increases cardiac output by increasing preload.
stress causes sympathetic activation, wich increases contractility and cardiac output. it also causes an excess in the renin-agiotensin system, which increases peripheral resistance vial functional constricution and structural hypertrophy.
genetics usually work on peripheral resistance through both functional constriction and structural hypertrophy.
Obesity and hyperinsulinemia cause structural hypertrophy (aka vascular hyperreactivity) and increased peripheral resistance.
genetic kidney syndromes that cause HTN and relate to the kidney
Liddle syndrome- increased Na reabsorption from mutations in distal Na channels
Gordon’s syndrome: Increased Cl reabsorption- similar to Liddle syndrome.
(others tend to relate to glucocorticoid systems)
potentially, polymorphisms in the angiotensinogen gene (but not other genes in the angiotensin/aldo/renin system) and the adducin gene (cytoskeletal protein) may also play a role in HTN.
How does salt relate to bp and HTN?
Normally, when our bp increases our kidney reduces sodium reabsorption in the proximal tubule and LOH. But, in patients with primary HTN, the pressure-natriuresis curve is reset and the kidney doesn’t excrete Na until they have reached a higher-than-normal blood pressure. So, if BP is reduced by nondiuretic drugs, many of these patients will require a diuretic that helps them excrete sodium- otherwise, their kidneys will retain sodium to return BP to hypertensive levels. The renin-angiotensin system is probably a major factor in resetting these levels, since increased angiotensin reduces renal sodium excretion and impairs pressure-natriuresis. It is important to know that most hypertensive patients have normal or high renin- even though if the physiology were working correctly, we would see lower renin in response to high blood pressure. It may also be related to inherited defects in Na excretion or reduced nephron numbers.
What stimulates renin release? What suppresses it?
stimulated by hypoperfusion and sympathethics; suppressed by Na intake and intravascular volume expansion.
How do the sympathetics affect hypertension?
Sympathetics cause increased cardiac output, direct vasoconstriction, renal sodium retention, and renin release. Excess renin/angiotensin increases sodium retention, which increases preload. We want the sympathetics to work when we are hypotensive, and they are stimulated by the baroreceptors. But, in some pts with HTN, baroreceptor activity is reset with sustained increases in BP such that the higher BP doesn’t suppress baroreceptor activity until a higher level. In other patietns, the baroreceptor becomes less sensitive. These patients usually also have sustained increases in BP, but also display orthostatic HTN because the baroreceptors aren’t really working.
How do you summarize, briefly, the time course of HTN pathophysiology?
In the context of predisposition, BP is initially increased by increased cardiac output and hyperkinetic circulation, either from increased Na, more RAS activity, more sympathetic activity, stress, and vascular reactivity. Later, BP is imatinatined by increased systemic vascular resistance with normal cardiac output, largely due to vascular remodeling from chronically elevated BP.
What is hypertensive nephropathy or benign hyptertensive nephrosclerosis?
This is a progressive renal disease that is associated with chronic hypertension and is diagnosed based on clinical features and, usually, without a renal biopsy. The risk is higher in African Americans.
Clinical features of hypertensive nephropathy
long standing HTN, mild proteinuria (usually less than 1g/day, though higher levels don’t exclude this diagnosis), progressive slow rise in serum creatinine, otherwise unremarkable urinary findings.
Histological features of hypertensive nephropathy
- vascular involvement, usually a hypertrophic response. Se medial hypertrophy and intimal thickening with narrowing of the vascular lumen. Also see deposition of hyaline-like material in damaged vascular walls.
- global sclerosis of the glomerulus that reflects ischemic injury. It is possible to also see focal segmental scelrosis, probably secondary to compensatory hyperfiltration from nephron loss.
- Interstitial fibrosis.
Pathophysiology of hypertensive nephropathy?
d. Pathophysiology: Most of the time, the kidney is able to autoregulate its glomerular pressure in spite of large systemic fluctuations in bp. In hypertensive nephropathy, we are either seing inadequate autoregulation, leading to elevated glomerular capillary pressure and focal glomerulosclerosis. However, most of the time, hypertensive nephropathy is actually caused by excessive autoregulation. In response to hypertension, the afferent arteriole clamps down to prevent hypertension in the glomerulus… but in fact causes glomerular ischemia, leading to global sclerosis and tubular atrophy.
What is malignant hypertension, just definitionally?
this is a pathologic syndrome characterized by severely elevated blood pressure and imminent organ damage. On a fundoscopic exam, you will see hypertensive neuroretinopathy characterized by flame shaped hemorrhages, cotton wool spots, +/- papilloedema.
