diagnostics
What are some clinical features suggestive of secondary hypertension?
- new-onset, "sudden" and younger than 25 or older than 65
- not responding to more than 3 anti-hypertensive agents = drug resistant HTN
- bruits, edema
- unexplained hypokalemia (pt not on diuretic)
- initial presentation with severe HTN
1. clinical clue: elevated creatinine
2. clinical clue: snoring, daytime somnolence, obesity
1. chronic kidney disease
2. OSA
How does renal artery stenosis lead to secondary HTN?
renal artery stenosis causes reduced RBF which activates RAAS, which increases angiotensin II and aldosterone
blood volumes increases, peripheral resistance increases leading to secondary HTN
- most commonly affects the renal and carotid arteries
- "string of beads" appearance of vessels
Fibromuscular dysplasia
What are some non-surgical treatments of primary aldosteronism?
- dietary sodium restriction
- intensive medical therapy: spironolactone, amiloride
You suspect primary aldosteronism in your patient, what diagnostic testing are you going to do?
Early AM serum aldosterone and plasma renin activity levels (renin low)
excessive autonomous aldosterone secretion that does not suppress adequately during high levels of dietary Na+ intake
Clinical clue: hypokalemia
primary aldosteronism
How does Cushing's syndrome cause 2ndary HTN?
- excessive glucocorticoid exposure results in increased Na+ and water retention to increase blood volume
- increased expression of angiotensin-II receptors
- increased catecholamine effects on adrenergic receptors
- reduced NO
--> RESULT: Increased systemic vascular resistance
- associated with bicuspid aortic valve
- audible bruits from intercostal collateral arteries on PE
- inferior rib notching on chest radiograph
Name syndrome and anatomical findings
Coarctation of the aorta
- anatomic narrowing of left subclavian artery distal to origin causing outflow obstruction leading to left ventricular overload, hypertrophy and HF
What are 3 lifestyle modifications to recommend to a patient with stage 1 HTN?
Diet: high in fruits, veg, nuts, whole grains; reduce sodium intake
Physical activity: increase
alcohol: limit
You suspect Cushing syndrome, what diagnostic testing do you want to get?
- overnight dexamethasone suppression test
- adrenal CT
clinical clue: continuous abdominal bruits, asymmetric kidney
renovascular disease
How does OSA lead to secondary HTN?
- sympathetic drive increases to stimulate breathing
- increased sympathetic tone increases CO
- increased sympathetic tone increases peripheral resistance
characterized by HTN with Na+ reabsorption and low K+
primary aldosteronism
what are signs/symptoms of end organ damage?
- severe chest pain
- severe headache with confusion and blurred vision
- severe anxiety
- nausea/vomiting
- SOB
- seizures
- unresponsiveness
You suspect congenital adrenal hyperplasia, what are your lab findings regarding blood sugar, sodium, and potassium?
hypoglycemia (hypocortisolism)
hyponatremia
hyperkalemia (hypoaldosteronism)
clue 1. decreased BP LEs or decreased/absent femoral pulses
clue 2. muscle weakness, abdominal striae, easy bruising
1. coarctation of the aorta
2. Cushing syndrome
Name an enzyme deficiency associated with congenital adrenal hyperplasia
11-beta-hydroxylase deficiency
17-alpha-hydroxylase deficiency
leads to increased cortisol, mineralocorticoids, or both
AKA pseudohyperaldosteronism
what's the defect?
Liddle syndrome
- genetic defect causing increased activity of ENaC in distal nephron, which causes kidneys to excrete potassium but retain too much sodium and water: HTN, fluid retention and metabolic alkalosis
hypertensive emergency is characterized by...
- acute or very high BP > 180 systolic or MAP > 135
- signs of end organ damage
you suspect pheochromocytoma, what diagnostic testing?
clinical clue 1: hypercalcemia
clinical clue 2: labile HTN, pallor; sometimes with medullary thyroid cancer (MEN syndrome 2)
1. hyperparathyroidism, granulomatous disease
2. pheochromocytoma
why is estrogen associated with 2nd HTN?
induces hepatic production of angiotensinogen, which converts to angiotensin-II, which causes vasoconstriction; also an indirect effect through aldosterone-mediated sodium and water retention
- rare
- signs/symptoms of sympathetic overdrive due to excess catecholamines being abnormally secreted
pheochromocytoma
what is the drug of choice for treatment of malignant hypertension?
labetalol or nicardipine