Secondary Hypertension

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Slide 1: 

Secondary Hypertension Dr .RABIE Z. AL-ANSI Sanaa yemen

Case 1 : 

Case 1 30 y female pt complains episodic : abrupt headaches suddenly stopped after 30 min with palpatations, diaphoresis & BP was 220/120 No famly hx ,no medications ,examination is normal , BP=140/100 ,routine lab normal. What is appropriate next step in the evaluation of this pt ?

Hypertension : 

Hypertension Essential Hypertension Systemic hypertension of unknown cause 90-95% Secondary Hypertension Hypertension that results from an underlying, identifiable, often correctable cause 5-10%

Classification : 

Classification

Goals for Evaluation (JNC-VI) : 

Goals for Evaluation (JNC-VI) Detection and Confirmation of Hypertension Detection of Target Organ Disease Identification of Other Risk Factors for Cardiovascular Diseases Detection of Secondary Hypertension

Assessment of hypertension : 

Assessment of hypertension Clinic assessment Medical history Physical examination Routine laboratory tests Optional tests Finds secondary causes: potential for cure Detects end organ damage: intensive treatment Allows calculation of cardiovascular risk scores

Drugs that Raises Blood Pressure : 

Drugs that Raises Blood Pressure Immunosuppressive agents Cyclosporine, tacrolimus, corticosteroid NSAID Ibuprofen, naproxen, piroxicam COX-2 inhibitors Celecoxib, rofecoxib, valdecoxib Estrogens Weight-loss agents Sibutramine, phentermine, ephedrine Minerocorticosteroids Fludrocortisone Antiparkinsonian Bromocriptine Monoamine oxidase inhibitors Phenelzine Anabolic steroids Testosterone Sympathomimetics Pseudoephedrine Stimulants Nicotine, amphetamines

The physician should suspect a secondary cause whenhypertension has the following characteristics: : 

The physician should suspect a secondary cause whenhypertension has the following characteristics: Poor response to therapy (resistant) Worsening of control in previously stable hypertensive patients Stage 3 hypertension (SBP>180 or DBP>110) Onset younger than age 20 or older than age 50 Significant hypertensive target organ damage Lack of family history of hypertension Findings on history, physical examination, or laboratory testing suggesting a secondary hypertension

Screening history : 

Screening history Family hx,renal ds. Past hx: drugs ,renal, endocrinal ds, Flank pain ,hematuria ,periorbital swelling Snoring, daytime somnolence, obesity Weight gain, fatigue, weakness, hirsutism, amenorrhea, purple striae, truncal obesity Triad ;headaches, diaphoresis, palpitations, Fatigue, cold intolerance, hair loss, muscle weakness, menorrhagia Heat intolerance, weight loss, palpitations,exophthalmos tremor, Headache,Cold feet, claudication,exercise induced pain

Screening physical examination : 

Screening physical examination Face,eye,brow,cushing,flushing,moon,hirsutism,plethoric, periorbital odema, Orofacial neuromas Striae, acne, thin skin, bruises, hyperpigmentation, café-au-lait spots Body built ,obesity ,,underwt Measurement truncal obesity Pulse delayed femoral pulse Abdominal Abdominal/flank masses, striae Hand sweating ,dry thick,tremor,cold hot Myopathy Murmurs front/back chest

Slide 14: 

Café-Au-Lait Spot Multiple endocrine neoplasia type lib: mucosal neuromas

Slide 15: 

Findings That Suggest Secondary Hypertension

Slide 16: 

Findings That Suggest Secondary Hypertension

Slide 17: 

Findings That Suggest Secondary Hypertension

Detection of Target Organ Disease : 

Detection of Target Organ Disease Heart Brain Kidney Eye

Slide 20: 

Papilloedema: swollen, hyperaemic disc with blurred margins

Diagnosis: ABCDE : 

Diagnosis: ABCDE A:, Apnea, Aldosteronism B: Bruits, Bad Kidney C: Catecholamines, Coarctation, Cushing’s Syndrome D: Drugs, Diet E: Erythropoietin, Endocrine Disorders

Routine tests : 

Routine tests Urinalysis (blood, protein, infection) Full blood count U&E & glucose Lipid profile (random cholesterol, triglycerides and HDL cholesterol) 12-lead electrocardiogram Chest X-ray

Chest X-ray: may find…. : 

Chest X-ray: may find…. ….rib notching of coarctation Also useful for heart size? Need to do echo Assessment of LVF, concomitant pathology

Optional tests : 

Optional tests Microalbuminuria 24-hour protein excretion 24-hour urinary catecholamines Serum calcium Serum uric acid Fasting glucose Glycated haemoglobin TSH PTH Plasma renin activity/ urinary sodium 24-hour BP report Echocardiography Ultrasonography renal tract Measurement of ankle/arm index Carotid doppler neck CT head

Renal causes : 

Renal causes Renal parenchymal Glomerulonephritis; Pyelonephritis ; Nephrocalcinosis ; Neoplasms ; Glomerulosclerosis ; Nephritis: interstitial, hereditary, or radiation Renal trauma Renin-secreting renal tumors Obstructive uropathies and hydronephrosis Renovascular Renal arterial lesions; occlusions; stenosis; aneurysms; thrombosis; vasculitis Connective tissue or autoimmune: renal vasculitis or glomerulitis (polyarteritis, SLE) Coarctation of the aorta (gives renal ischaemia)

Renal Parenchymal Disease : 

Renal Parenchymal Disease Common cause of secondary HTN (2-5%) HTN is both cause and consequence of renal disease Multifactorial cause for HTN including disturbances in Na/water balance, depletion or antagonism of vasodepressors/ prostaglandins, pressor effects on TPR Renal disease from multiple etiol, treat underlying disease, dialysis/ transplant if necessary

Renovascular HTN : 

Renovascular HTN Incidence 1-30% Etiology Atherosclerosis 75-90% Fibromuscular dysplasia 10-25% Other Aortic/renal dissection Takayasu’s arteritis Thrombotic/cholesterol emboli CVD Post transplantation stenosis Post radiation

Renovascular HTN - Pathophysiology : 

Renovascular HTN - Pathophysiology Decrease in renal perfusion pressure activates RAAS, renin release converts angiotensinogen? Ang I; ACE converts Ang I? Ang II Ang II causes vasoconstriction (among other effects) which causes HTN and enhances adrenal release of aldosterone; leads to sodium and fluid retention Contralateral kidney (if unilateral RAS) responds with diuresis/ Na, H2O excretion which can return plasma volume to normal with sustained HTN, plasma renin activity decreases (limited usefulness for dx Bilateral RAS or solitary kidney RAS leads to rapid volume expansion and ultimate decline in renin secretion

Renovascular HTN - Clinical : 

Renovascular HTN - Clinical History onset HTN age <30 or >55 Sudden onset uncontrolled HTN in previously well controlled pt Accelerated/malignant HTN Intermittent pulm edema with nl LV fxn PE/Lab Epigastric bruit, particulary systolic/diastolic Azotemia induced by ACEI Unilateral small kidney

Renovascular HTN - diagnosis : 

Renovascular HTN - diagnosis Physical findings (bruit) Duplex U/S Captopril renography Magnetic Resonance Angiography Renal Angiography

RAS screening/diagnostics : 

RAS screening/diagnostics

Renal causes : 

Renal causes Microaneurysms Polyarteritis Nodosa Polycystic Kidneys End stage Kidneys US or angiography

Renovascular causes : 

Renovascular causes Renal artery stenosis Fibromuscular dysplasia US (less sensitive) or angiography (definitive)

Fibromuscular dysplasia : 

Fibromuscular dysplasia 10-25% of all RAS Young female, age 15-40 Medial disease 90%, often involves distal RA ~ 30% progressively worsen but total occlusion is rare Treatment – PTRA Successful in 82-100% of patients Restenosis in 5-11% “Cure” of HTN in ~60%

Atherosclerotic RAS : 

Atherosclerotic RAS 75-90% of RAS Usually men, age>55, other atherosclerotic dz Progression of stenosis 51% @ 5years, 3-16% to occlusion, with renal atrophy noted in 21% of RAS lesions >60% ESRD in 11% ( higher risk if >60%, baseline renal insufficiency, SBP>160) Treatment PTRA success 60-80% with restenosis 10-47% Stent success 94-100% with restenosis 11-23% (1yr) “Cure” of RV HTN <30%

Slide 37: 

Fibromuscular Dysplasia, before and after PTRA Atherosclerotic RAS before and after stent Safian & Textor. NEJM 344:6;

Renovascular HTN – Medical Rx : 

Renovascular HTN – Medical Rx Aggressive risk fx modification (lipid, tobacco, etc) ACEI/ARB safe in unilateral RAS if careful titration and close monitoring; contraindicated in bilat RAS or solitary kidney RAS

Primary Aldosteronism : 

Primary Aldosteronism Prevalence .5- 2.0% (5-12% in referral centers) Etiology Adrenal adenoma Other: bilat adrenal hyperplasia, glucocorticoid suppressible hyperaldo, adrenal carcinoma Clinical: May be asymptomatic; headache, muscle cramps, polyuria Retinopathy, edema uncommon Hypokalemia (K normal in 40%), metabolic alkalosis, high-nl Na

Primary Aldosteronism- Dx : 

Primary Aldosteronism- Dx Aldosterone / Plasma Renin Activity ratio Early am after ambulation ~10-15 min Ratio >20-25 with PRA <1 and Aldo >15 should prompt further testing, endo referral Confirmatory/physiologic testing Withold BP meds 2wks High serum aldo after IV saline (1.25L x 2hr) load followed by low PRA after salt restricted diet (40mg/d) or diuretic (lasix up to 120mg) serum aldo <8.5 ng/dL after IV saline rules out primary aldosteronism Imaging – CT, scintography

Primary Aldosteronism - Treatment : 

Primary Aldosteronism - Treatment Surgical removal of adrenal tumor, can be done laparoscopically Pretreatment for 3-4 wks with spironolactone minimizes postoperative hypoaldosteronism and restores K to normal levels, response of BP to spiro treatment is predictor of surgical outcome

Aldosteronoma : 

Aldosteronoma

Obstructive Sleep Apnea : 

Obstructive Sleep Apnea Published reports estimate incidence of 30-80% of pt with essential HTN have OSA and 50% pt with OSA have HTN1 Prospective studies show link between OSA (apneic-hyponeic index) and development of HTN independent of other risk fx2 Clinical Daytime somnolescence, am headaches, snoring or witnessed apneic episodes Dx – Sleep studies Rx – wt loss, CPAP, surgical (UPPP)

Pheochromocytoma : 

Pheochromocytoma Rare cause of HTN (.1-1.0%) Tumor containing chromaffin cells which secrete catecholamines Young-middle age with female predominance Clinical Intermittent HTN, palpitations, sweating, anxiety “spells” May be provoked by triggers such as tyramine-containing foods (beer,cheese,wine), pain, trauma, drugs (clonidine, TCA, opiates)

Pheochromocytoma - Screen : 

Pheochromocytoma - Screen Best detected during or immediately after episodes Lenders, et al. JAMA 2002 Mar 20;287(11):1427-34

Pheochromocytoma - Diagnosis : 

Pheochromocytoma - Diagnosis Imaging for localization of tumor Akpunonu, et al. Dis Month.October 1996, p688

Pheochromocytoma - treatment : 

Pheochromocytoma - treatment Surgical removal of tumor Anesthesia- avoid benzo, barbiturates or demerol which can trigger catechol release Complications include ligation of renal artery, post op hypoglycemia, hemorrhage and volume loss Mort 2%, 5 yr survival 95% with <10% recurrence Caution with BB – can cause unopposed alpha stimulation/pheo crisis BP control with alpha blockers (phentolamine, phenoxybenzamine, and prazosin)

Cushing’s syndrome/ hypercortisolism : 

Cushing’s syndrome/ hypercortisolism Rare cause of secondary HTN (.1-.6%) Etiology: pituitary microadenoma, iatrogenic (steroid use), ectopic ACTH, adrenal adenoma Clinical Sudden weight gain,truncal obesity, moon facies, abdominal striae, DM/glucose intolerance, HTN,prox muscle weakness, skin atrophy, hirsutism/acne

Cushings syndrome : 

Cushings syndrome

Cushings syndrome - dx : 

Cushings syndrome - dx Screen: 24 Hr Urine free cortisol >90ug/day is 100% sens and 98% spec false + in Polycystic Ovarian Syndrome, depression Confirm Low dose dexamethasone suppression test 1mg dexameth. midnight, measure am plasma cortisol (>100nmol is +) Other tests include dexa/CRH suppresion test Imaging CT/MRI head (pit) chest (ectopic ACTH tumor)

Cushings syndrome - Rx : 

Cushings syndrome - Rx Cushings dz/ pit adenoma Transphenoidal resection Pituitary irradiation Bromocriptine, octreotide Adrenal tumors - adrenalectomy Removal of ACTH tumor

Coarctation of Aorta : 

Coarctation of Aorta Congenital defect, male>female Clinical Differential systolic BP arms vs legs (=DBP) May have differential BP in arms if defect is prox to L subclavian art Diminished/absent femoral art pulse Often asymptomatic Assoc with Turners, bicuspid AV If uncorrected 67% will develop LV failure by age 40 and 75% will die by age 50 Surgical Rx, long term survival better if corrected early

Coarctation of Aorta : 

Coarctation of Aorta Brickner, et al. NEJM 2000;342:256-263

Slide 54: 

Coarctation of the Aorta with Dissection

Hyperthyroidism : 

Hyperthyroidism 33% of thyrotoxic pt develop HTN Usually obvious signs of thyrotoxicosis Dx: TSH, Free T4/3, thyroid RAIU Rx: radioactive ablation, propanolol

Hypothyroidism : 

Hypothyroidism 25% hypothyroid pt develop HTN Mechanism mediated by local control, as basal metabolism falls so does accumulation of local metabolites; relative vasoconstriction ensues

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