hypertension evaluation 2

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HYPERTENSION Evaluation of Hypertension - 2 Mohammad Ilyas, M.D. Assistant Clinical Professor University of Florida / Health Sciences Center Jacksonville, Florida USA 1

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Page 1: Hypertension   evaluation 2

HYPERTENSION

Evaluation of Hypertension - 2

Mohammad Ilyas, M.D.

Assistant Clinical Professor

University of Florida / Health Sciences Center

Jacksonville, Florida USA 1

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Outline

1. Definition, Regulation and Pathophysiology

2. Measurement of Blood Pressure, Staging of Hypertension and Ambulatory Blood Pressure Monitoring

3. Evaluation of Primary Versus Secondary

4. Sequel of Hypertension and Hypertension Emergencies

5. Management of Hypertension (Non-Pharmacology versus Drug Therapy)

6. The Relation Between Hypertension: Obesity, Drugs, Stress and Sleep Disorders.

7. Hypertension in Renal diseases and Pregnancies

8. Pediatric, Neonatal and Genetic Hypertension

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Types of Hypertension

• Primary HTN:

• >95% cases of HTN in adult

• Cause Unknown.

• Multiple risk factors: including age,

family history, genetics, race,

environment etc…

• Secondary HTN:

• < 5% HTN in adult are secondary

• Secondary to other potentially

rectifiable causes.

• Often overlooked & under screen

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Secondary HTN

Overview

• Testing for secondary HTN can be expensive and requires high

index of clinical suspicion.

• General principles:

• New onset HTN if <30 or >50 years of age

• HTN refractory to medical Rx (>3-4 meds)

• Specific clinical/lab features typical for dz :

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Causes of Secondary HTN

• Common

1. Intrinsic renal disease

2. Renovascular disease

3. Mineralocorticoid excess

4. Sleep Breathing disorder

• Uncommon

1. Pheochromocytoma

2. Glucocorticoid excess

3. Coarctation of Aorta

4. Hyper/hypothyroidism

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1. 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, vasodepressors/ prostaglandins imbalance

• Renal disease from multiple etiologies.

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2. Renovascular HTN

•Incidence 1-3%

•Etiology

•Atherosclerosis 75-90% (elder)

•Fibromuscular dysplasia 10-25%

(younger)

•Other

•Aortic/renal dissection

•Takayasu’s arteritis

•Thrombotic/cholesterol emboli

•CVD

•Post transplantation stenosis

•Post radiation

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Renovascular HTN – History

• History

• Onset HTN age <30 or >55

• Negative FH of HTN

• Sudden onset uncontrolled HTN in previously well controlled patient

• Accelerated/malignant HTN

• Intermittent pulmonary edema with normal LV function

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Renovascular HTN - Clinical

• Clinical exam. /Lab. findings

• Epigastric bruit, particularly systolic/diastolic

• Advanced fundal changes, grade III/IV retinopathy

• Azotemia induced by ACEI, ARBs or diuretics

• Paradoxical worsening of HTN with diuretics

• Secondary aldosteronism : ↑ plasma renin & ↓ s. Na & K

• Unilateral small kidney, difference >1.5cm, on sonography 9

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Renovascular HTN – Diagnostic studies

• Physical findings (bruit)

• Duplex U/S

• Captopril renography

• Magnetic Resonance Angiography

• Renal Angiography

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Fibromuscular dysplasia Atherosclerotic RAS

• Fibromuscular dysplasia

• 10-25% of all RAS

• Young female, age 15-40

• Medial disease 90%, often

involves distal RA

• Atherosclerotic RAS

• 75-90% of RAS

• Usually men, age >55,

• Other atherosclerotic

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RAS screening/diagnostics

Sens Spec Limitation

Bruit 39-65% 90-99% Insensitive, severe stenosis may be silent

Duplex U/S 90-95% 60-90%

Operator dependent, 10-20%

Captopril

Renography 83-91% 87-93%

Accuracy reduced in pt with renal insufficiency,

lacks anatomical info; good predictor of BP

response

MRA 88-95% 95% False positive artifact resp, peristalsis, tortuous

vessels; cost

Angiography Gold std Gold std Invasive, nephrotoxicity, little value in

predicting BP response

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Fibromuscular Dysplasia, before and after PTRA Atherosclerotic RAS before and after stent

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3. Primary Aldosteronism

• Primary Aldosteronism, previously felt to be an unlikely cause of secondary

HTP, now is more commonly observed depending on the severity of HTP :

• 8% Stage 2

• 13% of Stage 3 and

• 20% of those with resistant hypertension.

(10th Annual SMA-ASH Carolinas Georgia Chapter Meeting, 2006)

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Primary Aldosteronism

• Prevalence 0.5- 2.0% (5-12% in referral centers)

• Etiology

• Adrenal adenoma

• Bilateral adrenal hyperplasia, glucocorticoid suppressible hyperaldo, adrenal carcinoma

• Clinical:

• May be asymptomatic.

• Headache, weakness, paralysis, polyuria

• Retinopathy, edema uncommon

• Hypokalemia (K normal in 40%), metabolic alkalosis, high-normal Na

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Screening for Hyper aldosteronism

• Spontaneous hypokalemia (<3.5 mmol/L).

• Profound diuretic-induced hypokalemia (<3.0 mmol/L).

• Hypertension refractory to treatment with 3 or more drugs.

• Incidental adrenal adenomas.

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4. Pheochromocytoma

• Catecholamine-producing neuroendocrine tumor that arises from

chromaffin cells

• Adrenal Medulla : 80-85% pheochromocytomas

• Extra-adrenal paragangliomas

• Often in head and neck (glomus jugulare) and rarely produce catecholamines.

• Some can be dopamine producing.

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Epidemiology

• Incidence: 1 in 100,000 each year

• Prevalence among pts with HTP

• In adults – 0.1-0.6%

• In children – 1%

• Traditional rule of 10

• 10% bilateral, 10% familial, 10% extra-adrenal, and 10% malignant.

• Recent reports found 12-24% of sporadic pheochromocytoma with germline mutation.

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Clinical Presentation

• Paroxysmal attacks of Headache, palpitations, and sweating.

• Adults more often have paroxysmal hypertension (50%).

• Children have sustained hypertension (70-90%).

• 20% of children will be normotensive at diagnosis.

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Pheochromocytoma – Testing

• Best detected during or immediately after episodes

TEST Sensitivity Specificity

Plasma free metanephrine

>0.66nmol/L

99% 89%

24hr urine metanephrine

(>3.7nmol/d)

77% (95%) 93% (96%)

24 urine VMA 64% 95%

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Lenders, et al. JAMA 2002 Mar 20;287(11):1427-34

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Pheochromocytoma - Diagnosis

• Imaging for localization of tumor

TEST Sens Spec PPV NPV

MIBG scintigraphy

(metaiodobenzylguanidine)

78% 100% 100% 87%

CT Scan 98% 70% 69% 98%

MRI 100% 67% 83% 100%

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Akpunonu, et al. Dis Month.October 1996, p688

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5. Cushing’s syndrome

(Hypercortisolism)

• Rare cause of secondary HTN

(0.1- 0.6%)

• Etiology

• Pituitary micro adenoma,

• Iatrogenic (steroid use),

• Ectopic ACTH,

• Adrenal adenoma

• Clinical

• Sudden weight gain, truncal obesity,

moon faces, abdominal striae,

DM/glucose intolerance, HTN, prox

muscle weakness, skin atrophy,

hirsutism /acne

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Cushings syndrome

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Cushings syndrome - diagnosis

• 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 suppression test

• Imaging

• CT/MRI head (pit) chest (ectopic ACTH tumor)

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6. Coarctation of Aorta

• Congenital defect, male>female

• Clinical

• Differential systolic BP arms v/s legs (=DBP)

• May have differential BP in arms if defect is prox to L subclavian art

• Diminished/absent femoral art pulse

• Often asymptomatic

• Echo-Doppler, CT angiography, aortography.

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7. Hyperthyroidism

• 33% of thyrotoxic pt develop HTN

• Usually obvious signs of thyrotoxicosis

• Dx: TSH, Free T4/T3, thyroid

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8. Hypothyroidism

• 25% hypothyroid patient develop HTN

• Mechanism mediated by local control, as basal metabolism falls so

does accumulation of local metabolites; relative vasoconstriction

ensues

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Summary

• Screening for 2ry HTN can be expensive and requires clinical suspicion and knowledge of limitations of different tests

• General principles:

• New onset HTN if <30 or >50 years of age

• HTN refractory to medical Rx (>3-4 meds)

• Specific clinical/lab features typical for dz :

• Hypokalemia in the absence of diuretic therapy may indicate a state of mineralocorticoid excess

• Excess aldosterone production (Conn’s)

• Excess glucocorticoid production (Cushing’s)

• Excess T3 & T4 (hyperthyroidism)

• Epigastric bruits, differential BP in arms, episodic HTN/flushing/palp.

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Page 33: Hypertension   evaluation 2

Time for quiz !!

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Quiz 1. TRUE or FALSE

1. Renal Parenchymal diseases are the common cause of primary HTN.

2. Hypertension is both cause and consequence of renal parenchymal disease.

3. Renal Parenchymal HTN is only due to disturbances in Na/water balance.

4. Renal Vascular disease usualy cause resistive HTN

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Quiz 1. TRUE or FALSE

1. Renal Parenchymal diseases are the common cause of primary HTN. FALSE

2. Hypertension is both cause and consequence of renal parenchymal disease. TRUE

3. Renal Parenchymal HTN is only due to disturbances in Na/water balance. FALSE

4. Renal Vascular disease usualy cause resistive HTN. TRUE

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Quiz 2. All of the following studies are helpful in

diagnosis of Renovascular HTN - EXCEPT

A. Urine pH

B. Doppler renal U/S

C. Captopril renography

D. Magnetic Resonance Angiography

E. Renal Angiography

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Quiz 2. All of the following studies are helpful in

diagnosis of Renovascular HTN – EXCEPT?

A. Urine pH

B. Doppler renal U/S

C. Captopril renography

D. Magnetic Resonance Angiography

E. Renal Angiography

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Quiz 3. Which of the following statement is not true

about Primary Aldosteronism?

A. May be asymptomatic.

B. Can cause headache, weakness, paralysis, and polyuria.

C. Retinopathy, edema are common finding.

D. Can cause hypokalemia, metabolic alkalosis and high-normal Na.

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Quiz 3. Which of the following statement is not true

about Primary Aldosteronism?

A. May be asymptomatic.

B. Can cause headache, weakness, paralysis, and polyuria.

C. Retinopathy, edema are common finding.

D. Can cause hypokalemia, metabolic alkalosis and high-normal Na.

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Quiz 4. Which of the following in NOT true about

Pheochromocytoma?

A. Clinical presentation includes paroxysmal attacks of headache,

palpitations, and sweating.

B. Adults more often have paroxysmal hypertension.

C. Children have sustained hypertension.

D. Majority of children could be normotensive at diagnosis.

E. MIBG scintigraphy (metaiodobenzylguanidine) is diagnostic study

for Pheochromocytoma

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Quiz 4. Which of the following in NOT true about

Pheochromocytoma?

A. Clinical presentation includes paroxysmal attacks of headache,

palpitations, and sweating.

B. Adults more often have paroxysmal hypertension.

C. Children have sustained hypertension.

D. Majority of children could be normotensive at diagnosis.

E. MIBG scintigraphy (metaiodobenzylguanidine) is diagnostic study

for Pheochromocytoma

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Quiz 5. Which of the following statement is FALSE

about Coarctation of Aorta?

A. Mostly present as Congenital defect

B. More common in male than female

C. BP in lower extremity is lower than upper extremity

D. Often symptomatic

E. Echo-Doppler, CT angiography, aortography.

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Quiz 5. Which of the following statement is FALSE

about Coarctation of Aorta?

A. Mostly present as Congenital defect

B. More common in male than female

C. BP in lower extremity is lower than upper extremity

D. Often symptomatic

E. Echo-Doppler, CT angiography, aortography.

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Mohammad Ilyas MD, FAAP 44