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GRAND ROUNDS

GRAND ROUNDS. Gina Galindo, MD Northeast Family Medicine Residency Program March 12, 2014. CASE. 69yo female with h/o severe bitemporal headache, nausea and vomiting for 3 days. Sudden onset No h/o CAD, HTN Past medical Hx : MM s/p BMST & chemo Orthostatic hypotension - chemo.

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GRAND ROUNDS

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  1. GRAND ROUNDS Gina Galindo, MD Northeast Family Medicine Residency Program March 12, 2014

  2. CASE 69yo female with h/o severe bitemporal headache, nausea and vomiting for 3 days. Sudden onset No h/o CAD, HTN Past medical Hx: MM s/p BMST & chemo Orthostatic hypotension - chemo

  3. Physical Examination: Vitals: BP 238/102 HR: 68x’ RR: 20x’ Gen: acutely ill, uncomfortable. HEART: RRR, no M/R/G, nl S1/S2 LUNGS:CTAB ABDOMEN/EXTR: soft, NT/ND, BS present, no bruits. NEURO: AxOx3, photophobia Labs: BUN:10 Creatinine:0.6 Na:138 K:2.6 CT head: no acute abnormalities

  4. -US Renal & Arterial Doppler: Elevated peak systolic velocity in the mid right renal artery with suggestion of parvustardus wave form suspicious for moderate to severe right renal artery arterial stenosis. Probable mild left renal artery stenosis. -Bilateral renal angiography: Successful balloon dilatation of probable fibromusculardysplasia, right renal artery without obvious complication.

  5. SECONDARY HYPERTENSION • Type of HTN with underlying and potentially correctable cause. • 5-10% of HTN cases are thought to result from 2y causes. • Secondary etiology may be suggested by symptoms, examination findings or laboratory abnormalities.

  6. Indications for further investigation: • Resistant HTN (defined by the JNC 7 as blood pressure that is above the patient's goal despite the use of 3 or more antihypertensive agents from different classes at optimal doses, one of which should ideally be a diuretic) • Worsening of control in previously stable hypertensive patient. • Stage 3 HTN • Early onset of HTN <20yo, or older >50yo • Findings on exam (sings and symptoms)

  7. General Approach to the patient: • Confirm appropriate measure of BP’s • Diet • Drugs

  8. COMMON CAUSES OF 2y HTN BY AGE Children and Adolescent (birth – 18years of age) Renal Parenchymal Disease: • Glomerular and interstitial diseases, congenital abnormalities, reflux nephropathy. • Sometime not apparent until young adulthood. • Initial evaluation: BUN, Creatinine, UA, Renal US.

  9. Coarctation of the aorta: • 2nd most common cause • 2-5 times more common in boys • Usually diagnosed around 5 years of age with the onset of HTN or murmur. • Classic findings: HTN upper extremities, diminished or delay in femoral pulses and low or unobtainable arterial BP in the lower extremities.

  10. Classic findings: HTN upper extremities, diminished or delay in femoral pulses and low or unobtainable arterial BP in the lower extremities. • Initial testing : EKG, Chest x ray and confirmation with Echo/MRI

  11. Young adults (19-39 years of age) Renal Artery Stenosis caused by Fibromuscular dysplasia: • 10% of the cases. • Unknown etiology • Predominantly young women. • Bilateral arterial involvement 60-70%

  12. Suspected if hypertension occurs in patients younger than 35 years of age or if transient ischemic attacks, stroke, aneurysm, or dissection occurs in young patients • Diagnostic test: Angiography (gold standard)/MRI with gadolinium/CTA (patients with normal renal function) / Renal Doppler (high sensitivities). * MRI and CTA equally accurate in visualizing stenosis.

  13. Labs: creatinine rarely elevated • Treatment: percutaneous transluminal renal angioplasty

  14. Thyroid Dysfunction: • Thyroid hormones affect cardiac output • Hypothyroidism * Major CV changes: decrease in cardiac output and contractility, ↓HR, ↑Peripheral vascular resistance. *Symptoms and signs: exertional dyspnea and exercise intolerance, bradycardia, HTN, cardiac dysfunction, edema (non pitting), pericardial effusions. *Diagnosis: TSH *Treatment: thyroid hormone (levothyroxine)

  15. Hyperthyroidism: *Major CV changes: ↑HR, ↑cardiac contractility, ↑cardiac output, ↑diastolic relaxation, ↓systemic vascular resistance. *Signs and Symptoms: tachycardia (rest/sleep), palpitations, systolic HTN, DOE & angina. *Diagnosis: TSH *Treatment: Radioactive iodine or anti-thyroid drug. Beta blockers (propranolol, atenolol)

  16. Middle-Aged Adults: (40-64 years of age) Aldosteronism: overproduction of aldosterone independent from its usual regulator, the renin-angiotensin system. • Most common causes: *Unilateral aldosterone producing adenoma (approx. 50%) *Bilateral Idiopathic hyperaldosteronism. • 3-15% prevalence in patients with HTN.

  17. Pathogenesis: ↑aldosterone→ disruption of normal renin angiotensin system Na+ retention→ Volexpansion→HTN ↑K excretion→Hypokalemia ↑H ion excretion→Metabolic alkalosis Supression of plasma renin • Clinical Features: -HTN often resistant to treatment -Hypokalemia (inconsistent finding)→Muscle weakness, fatigue, constipation, irregular HR with arrhythmias

  18. Diagnosis: -Best initial test is Aldosterone/Renin ratio, most sensitive test. -Levels should be measured in the am at least 2 hrs after waking. -Aldosterone/Renin ratio >20 -40 ng/dL and aldosterone level > 15 ng/dL→Refer endocrinologist for confirmatory tests (oral salt loading test, saline suppression test, fludrocortisone suppression test). -Imaging: CT→ unilateral macroadenomas >1cm.

  19. OSA: • Repetitive episodes of apnea or reduced inspiratory airflow due to upper airway obstruction during sleep. • Intermittent hypoxia with arousal response • Cause of 2y HTN particularly in 40-59 year olds. • Standard diagnostic test: polysomnography but also the nighttime pulsoxymeter can be used to diagnose mod to severe OSA.

  20. Pheochromocytoma: • Responsible for approximately 0.5% of cases of 2y HTN. • Age 30-60 years of age. • Not part of the initial evaluation for 2y HTN unless specific symptoms are suggestive • Clinical findings paroxismal elevations BP Triad: Headache, Palpitations Sweating. • Dx: plasma free metanephrines or 24 hr urine

  21. Cushing Syndrome: • Signs and symptoms associated with long term exposure to inappropriately high levels of Cortisol. • The most common causes: *Exogenous→(iatrogenic) steroids - glucocorticoid drugs are #1 * Endogenous→ Cushing Disease/ Adrenal Adenoma / Ectopic ACTH(paraneoplasic tumor)

  22. Sings and Symptoms HTN Increase weight Hyperglicemia Moon fascies Buffalo hump Truncal obesity • Diagnosis: Suggested by body changes/HTN/ Hyperglicemia.

  23. 24 urine free cortisol Low dose dexamethasone supression Late night salivary cortisol test.

  24. Older Adults: (65 years and older) Renal Artery Stenosis caused by atherosclerosis: • >90% or RAS are athero- sclerotic in nature. • Higher risk in older patients smokers, PAD • Bilateral RAS should be suspected in patients with h/o “flash” or episodic pulmonary edema

  25. Clinical Clues: *Onset severe HTN >55yo *Unexplained deterioration of kidney function during antihypertensive tt x (Sustained elevation in the serum Creatinine by more than 50% within 1 week of ACEI or ARB) * Severe HTN with an unexplained kidney atrophy or asymmetry in renal sizes >1,5cm. • Radiologic testing: Doppler renal US, CTA, MRA. • Treatment: medical ttx/ PCTA/Vascular Revascularization.

  26. SUMMARY

  27. Literature • Diagnosing Secondary Hypertension EDWARD ONUSKO, M.D., Clinton Memorial Hospital, Wilmington, Ohio Am Fam Physician. 2003 Jan 1;67(1):67-74. • Diagnosis of Secondary Hypertension: An Age-Based Approach ANTHONY J. VIERA, MD, MPH, and DANA M. NEUTZE, MD, PhD University of North Carolina at Chapel Hill School of Medicine, Chapel Hill, North CarolinaAmFam Physician. 2010 Dec 15;82(12):1471-1478. • Evaluation of Secondary Hypertension E. Eugene Baillie, MD JAMA. 1977;238(23):2494. doi:10.1001/jama.1977.03280240040007. • http://hyper.ahajournals.org. • Up to date • DynaMed

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