Secondary hypertension

1. Secondary hypertension

2. Patients with essential (idiopathic or primary) hypertension undergo a relatively limited work-up because extensive laboratory testing is of limited utility. • It is not cost effective to perform a complete evaluation in every hypertensive patient.

3. 4 major clinical clues that suggest secondary HTN • Severe or refractory hypertension. • An acute rise in blood pressure over a previously stable value. • Proven age of onset before puberty or above the age of 50 to 55 years; an accurate history is important in the latter setting because hypertension may be first noted above age 50 but the patient may not have had a previous blood pressure measurement for many years. • Age less than 30 years in non-obese, non-black patients with a confirmed negative family history of hypertension.

4. 55 year old man is brought into the ED by his wife for acute and severe shortness of breath. • His history is notable for DM2 and HTN for which he has been on HCTZ and enalapril for the last 10 years; two weeks ago, his PCP doubled his enalapril dose because of a clinic BP of 150/100. • On exam in the ED, his BP is 180/110, his O2 sat is 95% on 5L, his lungs have rales 2/3 up each side, and there is a systolic-diastolic abdominal bruit on the left side. • Labs show an elevation in his serum creatinine from baseline 1.1 to 1.8

5. RENOVASCULAR DISEASE

6. History and physical • Malignant hypertension: patients with severe hypertension and signs of end-organ damage such as acute renal failure, retinal hemorrhages or papilledema, heart failure, or neurologic disturbance • An acute elevation in the plasma creatinine concentration that occurs shortly after the institution of therapy with an angiotensin converting enzyme (ACE) inhibitor or angiotensin II receptor blocker (ARB) [AII preferentially increases efferent arteriole constriction and resistance]

7. History and physical • Moderate to severe hypertension in a patient with an unexplained atrophic kidney or asymmetry in renal sizes of >1.5 cm. A unilateral small kidney (9 cm) has a 75 percent correlation with the presence of large vessel occlusive disease • Moderate to severe hypertension in patients with diffuse atherosclerosis (eg. CAD, PVD), particularly those over age 50 • Moderate to severe hypertension in patients with recurrent episodes of acute (flash) pulmonary edema or otherwise unexplained heart failure

8. Work-up • Renal arteriography (gold standard) • MRA (UNC’s gold standard?) • CTA • Duplex Doppler USG • Captopril renogram (a marker of GFR such as DTPA will show ACE-I induced decline in GFR in the stenotic kidney, and accompanying increase in GFR in non-stenotic kidney) • Captopril renin assays (measure rise of renin ~1 hour after captopril load)

9. Treatment • Stents • Studies show the effect is to decrease number of meds not make patient normotensive

10. 24 year old African-American male is a new ACC patient. He wants to know why his legs are getting swollen; also, in the morning, he has swollen eyelids. • On exam, his BP is 150/95 and he has 3+ pitting edema to the knees.

11. PRIMARY RENAL DISEASE

12. History and physical • Depends on cause of intrinsic renal disease

13. Work-up • Chem 10, CBC • U/A, urine sediment • Biopsy

14. Treatment

15. 67 year old woman is a new ACC patient – before seeing her, you do a CIS chart biopsy. You see that she has recently seen a psychiatrist at UNC for “nerves;” reading this note, you see under Axis III the words “no known past medical history.” • In the psychiatrist’s assessment, however, you see that he set this appointment up to rule out “organic” causes for her psychiatric condition. • She is somewhat anxious appearing and complains of severe “pounding” headaches, two to three times a week episodes of “breaking out in sweats,” palpitations, and nausea. • Her BP in clinic is 150/100. She says, “That must be a mistake, because at the psychiatrist’s office they checked me and I was much lower than that.” On exam, she is diaphoretic and her heart rate is tachycardic but regular.

16. PHEOCHROMOCYTOMA

17. History and physical • Paroxysmal elevations in BP • Classic triad of headaches (usually pounding), palpitations, and diaphoresis • Less common are anxiety, nausea, abdominal pain, heat intolerance, tremors, and weight loss • Family history of MEN type 2, von-Hippel Landau, NF type 1, or “idiopathic” pheochromocytomas • Incidentally discovered adrenal mass

18. Work-up • Short answer is measure fractionated metanephrines and catecholamines in a 24-hour urine collection (sensitivity = 98%, specificity = 98%; n.b. you should also measure a 24-hour urine creatinine to verify an adequate collection) • Some use fractionated plasma free metanephrines as a first-line test for pheochromocytoma; the predictive value of a negative test is extremely high, and normal fractionated plasma metanephrines excludes pheochromocytoma except in patients with early preclinical disease; a plasma test is also attractive because of simplicity; however, the test has a very poor specificity and will give a high number of false positives • Long answer is……

20. Treatment • Endocrinologist • Surgeon

21. A bit harder • A 20 year old man is a new ACC patient. He says that over the last 3 months he’s felt “horrible” and, when you ask him to be more specific, he says, “I just feel weak.” • On exam, his BP is 158/98 but otherwise is unremarkable, including no focal weakness or deficits. • He asks you if it’s alright if he eats something – he’s hungry, apparently. You say sure and watch as he takes a banana out of his knapsack. He bites into his banana and asks, “So, what do you think is wrong with me?” • Stalling, you say, “So, do you like bananas?” He replies, “Can’t get enough of ‘em, doc.”

22. HYPERALDOSTERONISM (PRIMARY ALDOSTERONISM)

23. History and physical • Elevated BP may be the only “symptom” but hypokalemia can lead to poor quality of life (the banana munchers support group)

24. Work-up • Serum and urine K as hyperaldosteronism leads to urinary potassium wasting (>50% of patients will be eukalemic on blood work) • Might as well get a transtubular K gradient, and might as well make those serum and urine K levels 24 hour collections

25. Work-up • Plasma aldosterone concentration (PAC), plasma renin concentration (PRC), and ratio of PAC to PRC (n.b. PRC will be low in primary hyperaldosteronism but high in secondary hyperaldosteronism, as in renovascular disease) • CT or MRI to look for adrenal carcinomas, adenomas, or ectopic adrenal ademonas

26. Treatment • Depends on etiology, but in general it’s surgery vs. aldosterone receptor blockers

27. This patient has a BP 155/90

28. CUSHING’S SYNDROME

29. History and physical • Cushingoid facies • Central obesity • Proximal muscle weakness • Ecchymoses • Striae • May be on steroids for some other reason

30. Work-up • 24 hour urinary cortisol excretion provides the most direct and reliable practical index of cortisol secretion and should be your screening test • If positive, send to endocrine for possible dexamethasone suppression test, late evening serum or salivary cortisol, etc….. • Will probably need imaging to rule out malignancy

31. Treatment • Endocrinologist +/- surgeon

32. 23 year old previously healthy 2nd year medical student is a new ACC patient. • In her ICM course last week, she and her classmates practiced taking BPs on each other. Her three classmates all got BP recordings on her in the 130s/80s. She asks, “Isn’t that a bit high for someone like me?” as she twirls around to display her athletic physique. • She doesn’t drink or smoke; she started on birth control pills one month ago and also takes an occasional multivitamin. • On exam, she is thin and well-appearing in a jogging suit. Her BP in clinic is 134/86.

33. OCPs

34. History and physical • New elevation in BP temporally related to OCP use

35. Work-up • Thorough history and physical to rule out other causes of secondary hypertension

36. Treatment • Change classes of OCP to lower estrogen-containing regimen • No smoking!

37. 55 year old ACC patient who has had HTN since his mid-30s. He is presently on HCTZ and amlodipine. • On exam, his BP is 148/92 and his BMI is 38 • Trying to measure his neck circumference, you run out of measuring tape • His wife asks you, “Can you do something about his snoring? He sounds like he’s about to choke sometimes.” • Last week he fell asleep at the wheel and killed three pedestrians

38. OBSTRUCTIVE SLEEP APNEA

39. History and physical • Obesity • Snoring • Daytime somnolence and fatigue • Large, thick neck (if possible, measure circumference) • Parallel history from bedmate about apneic episodes

40. Work-up • Sleep study • At UNC, this must be ordered by a neurologist or pulmonologist

41. Treatment • CPAP or BiPAP

42. Other causes of secondary hypertension to consider • Coarctation of the aorta • Delayed femoral pulses and low or unobtainable BP in legs • Hypothyroidism • Classic hypothyroid symptoms with elevated TSH • Primary hyperparathyroidism • Hypercalcemia (+/- symptoms of hyper-Ca++)

43. 4 major clinical clues that suggest secondary HTN • Severe or refractory hypertension. • An acute rise in blood pressure over a previously stable value. • Proven age of onset before puberty or above the age of 50 to 55 years; an accurate history is important in the latter setting because hypertension may be first noted above age 50 but the patient may not have had a previous blood pressure measurement for many years. • Age less than 30 years in non-obese, non-black patients with a confirmed negative family history of hypertension.