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How to recognize the different faces of Hypertension. Reena Kuriacose, MD. FACP. March 26,2012. Disclosures. No conflict of interest Not a specialist Statistical data varied. Resistant hypertension. BP above goal in spite of > 3 anti HTN meds All of these in optimal doses

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How to recognize the different faces of hypertension

How to recognize the different faces of Hypertension

Reena Kuriacose, MD. FACP.

March 26,2012


Disclosures
Disclosures

  • No conflict of interest

  • Not a specialist

  • Statistical data varied


Resistant hypertension
Resistant hypertension

  • BP above goal in spite of > 3 anti HTN meds

  • All of these in optimal doses

  • Resistant HTN = Refractory HTN

  • Uncontrolled HTN = Resistant HTN

    Inadequate Rx

    Pseudo resistance


Pseudo resistance
Pseudo resistance

  • Attributed to other factors:

    - Inaccurate measurement

    - Poor adherence to Rx

    - White coat syndrome 20-30%

    (also more in resistant HTN: 37-44%)

  • Suboptimal Rx: Only 18-27% uncontrolled get

    Rx with at least 3 anti HTN meds


Difficult to control htn
Difficult to control HTN

  • Higher baseline

  • Left Ventricular Hypertrophy

  • Older age

  • Obesity- lifestyle and diet

  • AA race

  • Chronic kidney disease

  • Diabetes

  • Medications and herbal supplements


Resistant htn
Resistant HTN

  • Prevalence: Not known- 8.9-16%

  • Pt with ≥ 3 BP meds

    1994: 14% to 2004: 24%

  • 5–20% HTN- specific underlying disorder


I intravascular volume
I. Intravascular volume

  • ↑ Na  ↑ vascular vol  ↑ cardiac output

  • Overtime  ↑ Peripheral resistance

  • Non chloride Na salts have no effect on BP


  • NaCl dependent HTN:

    - Intrinsic renal disease: ↓ capacity to excrete Na

    - ↑ Mineralocorticoid: ↑ tubular Na reabsorption

    - ↑ Neural activity to kidney: ↑ tubular Na

    reabsorption

    ESRD 80% volume dependent and respond to dialysis


Ii autonomic nervous system
II. Autonomic Nervous System

  • Adrenergic receptors:

    α- activated by NE more than epinephrine

    β- activated more by epinephrine than NE

  • α₁ - vasoconstriction,↑ Renal Na reabsorption

  • α₂ - inhibit NE release

  • β₁ - ↑ rate and strength of cardiac contraction

    ↑ CO; ↑ renin release from kidney

  • β₂ - vasodilatation


  • Tachyphylaxis – sustained high levels of

    catecholamines ↓ response

    (orthostatic hypotension in pheo)

  • C/c ↓ catecholamines  temporary

    hypersensitivity to sympathetic stimuli

    (clonidine withdrawal)

  • Sympathetic outflow: ↑ Obesity and OSA


Iii renin angiotensin aldosterone
III. Renin-Angiotensin-Aldosterone

  • Angiotensin II  Vasoconstriction

    Atherosclerosis

  • Aldosterone Na retention


NaCl in distal asc loop of Henle

↓ pr. In afferent renal arteriole

β₁ stimulation of renin secretion

Pharmacological blockade of

a. ACE receptor

b. Angiotensin II receptor

↓K ----------- ↓


Secondary hypertension
Secondary Hypertension

  • Severe or resistant hypertension

  • An acute rise in BP developing in a patient

    with previously stable values

  • Malignant or accelerated hypertension

  • < 30 years in non-obese, -ve FH, no other risk

    factors

  • >50 years


Secondary hypertension1
Secondary Hypertension

Resistant HTN with an identifiable cause:

  • Primary Aldosteronism

  • Renal Artery Stenosis

  • Chronic Kidney Disease

  • OSA

  • Pheochromocytoma

  • Cushing’s Syndrome

  • Aortic Coarctation


Primary aldosteronism
Primary Aldosteronism

  • 10 – 20% of resistant HTN

  • Peak: 30–60 years

  • Unexplained hypokalemia- 37%

    > 50% Normokalemic @ presentation

    Unprovoked hypokalemia : 40-50% primary

    aldosteronism

  • Renal Mag wasting  mild hypomagnesemia


Primary aldosteronism1
Primary Aldosteronism

  • ↑ Aldosterone ↑ Na, ↓ Renin

     ↑ K excretion

  • ↓ K  ↓ Aldosterone synthesis 

    correct K before eval for hyperaldosteronism


Primary aldosteronism2
Primary Aldosteronism

  • Resistant hypertension

  • Spontaneous or thiazide-induced hypokalemia

  • Serum K <3.1 mmol/L

  • Incidentaloma

  • FH of primary hyperaldosteronism


Primary aldosteronism3
Primary Aldosteronism

  • Adrenal adenoma: 60–70%

    Unilateral

    < 3cm

  • Unilateral/ bilateral adrenal hyperplasia

  • Adrenal carcinoma or an ectopic malignancy e.g., ovarian arrhenoblastoma- rare


Primary aldosteronism4
Primary Aldosteronism

  • PAC:PRA ratio (ratio ≥ 20:1)

  • Plasma aldosterone concentration (PAC)

    (>416 pmol/L) (>15 ng/dL))

  • Sensitivity 90% , Specificity 91%

    for aldosterone-producing adenoma

  • Plasma renin activity (PRA) ↓

  • 24 hr urine Na excretion, Creatinine clearance, aldosterone excretion


Primary aldosteronism5
Primary Aldosteronism

  • Medications that alter renin and aldosterone levels:-

    Diuretics (especially spironolactone)- should

    be discontinued 4 weeks before

    ACE inhibitors, ARBs, β -blockers, Clonidine

  • Calcium channel and α-receptor blockers can

    be used


Primary aldosteronism6
Primary Aldosteronism

  • Confirmed by demonstrating : -

    - Failure to suppress plasma aldosterone to

    isotonic saline

    - Failure to suppress aldosterone to

    oral NaCl load/ fludrocortisone/ captopril


Primary aldosteronism7
Primary Aldosteronism

  • High-resolution CT (90%) or MRI scanning

  • Bilateral adrenal venous sampling for plasma

    aldosterone

    (sensitivity 95% and specificity 100%)


Primary aldosteronism8
Primary Aldosteronism

  • Hyperplasia- Aldosterone receptor antagonist

  • Pts not willing for surgery  Medical Rx

    (avoid extensive w/u)


Renal artery stenosis
Renal Artery Stenosis

  • Atherosclerotic disease: 2/3 – older males

    OR

  • Fibromuscular dysplasia: 1/3- younger females

  • Renal artery stenosis:

    1–2% of hypertensive patients

    10-45% of refractory HTN

  • Prevalence 60% in >70 years


Renal artery stenosis1
Renal Artery Stenosis

  • < 20; > 50 years

  • HTN is resistant to ≥ 3 drugs

  • Epigastric / renal artery bruits

  • ↓ Renal perfusion pr → ↑ renin

    (over time secondary renal damage)


Renal artery stenosis2
Renal Artery Stenosis

  • Atherosclerotic disease of the aorta or

    peripheral arteries:

    - 15–25% of patients with symptomatic PVD

    in legs renal artery stenosis

  • Abrupt deterioration in kidney function (30%)

    after administration of ACE inhibitors

  • Episodes of pulmonary edema are associated

    with abrupt surges in BP


Renal artery stenosis3
Renal Artery Stenosis

  • BP meds can effectively control BP in many patients with renovascular HTN

  • Screening is not recommended unless plan is to intervene if a significant stenotic lesion is found:

    * Failure of medical therapy to control BP

    * Intolerance to medical Rx

    * Progressive renal failure

    * Young pt- to avoid life long Rx


Renal artery stenosis4
Renal Artery Stenosis

  • No ideal screening test for renal vascular HTN

  • Magnetic resonance angiography- atherosclerotic

  • Spiral CT with CT angiography

  • Duplex Doppler ultrasonography- operator dependant

  • Renal arteriography, the definitive diagnostic test (suspicion is sufficiently high )

    ----------------------------------------

    * Renal insufficiency limits use of contrasts


OSA

  • OSA seen in 71-85 % of resistant HTN referred

    for sleep study

  • 45% OSA without HTN develop HTN in 4 years

  • Blunted/ No ↓ in nighttime BP

  • >50% OSA  HTN (independent of obesity)


OSA

  • Screen if:

    Obesity + snoring + daytime sleepiness

  • CPAP (> 5.6 hr/night) Decreases both

    systolic and diastolic hypertension


Pheochromocytoma
Pheochromocytoma

  • < 0.1% of all patients with hypertension

  • < 0.3% of Secondary hypertension

  • Incidence: 2-3/ million / yr

    autopsy: 250–1300/ million

  • Episodic HTN(90%) HA (80%)

    Diaphoresis (70%) Palpitation (60%) Anxiety (50%) Tremor (40%)

  • 90% in adrenals; 98% in Abdomen


Pheochromocytoma1
Pheochromocytoma

  • Hyperglycemia 35% • Leukocytosis

  • ↑ RBC • Occa ↑ ESR

  • ↑ Ca

  • PRA may be ↑ ed by catecholamines

  • Meds: Tricyclic antidepressants, Antidopaminergic agents, Metoclopramide, and Naloxone- can pptHTNsive crisis


Pheochromocytoma2
Pheochromocytoma

  • Plasma fractionated free metanephrines

  • Used in high risk pts- FH or personal h/o pheo

  • Sensitivity - 96% ; Specificity - 85%

  • N levels = end of w/u

  • ↑ levels - Physical or emotional stress

    Sleep apnea

    MAO inhibitors,levodopa


Pheochromocytoma3
Pheochromocytoma

  • 24-hour urinary collection for catecholamines and

    metanephrines

    - Sensitivity - 87.5% ; Specificity of 99.7%

    - 2.2 mcg of total metanephrine /mg creatinine

    > 135 mcg total catecholamines /gm creatinine

    - Total u. metanephrine >1300mcg/24hr

  • Lab values varies- Slightly +ve tests not significant

  • 2-3 times above Normal

  • VMA is not required


Pheochromocytoma4
Pheochromocytoma

  • Noncontrast CT - followed by CT with nonionic

    contrast

  • MRI scanning

  • CT/ MRI - sensitivity ~ 90% for adrenal

    pheochromocytoma

  • Less sensitive - recurrent tumors, metastases, and

    extra-adrenal paragangliomas

  • I¹³¹ metaiodobenzyl guanidine if CT/MRI -ve


Cushing s syndrome
Cushing’s syndrome

  • 80% of spontaneous Cushing syndrome HTN

  • ↑ WBC > 11,000/mm3

  • Hyperglycemia

  • Hypokalemic metabolic alkalosis :

    Cortisolrenal mineralocorticoid receptor.


Cushing s syndrome1
Cushing’s syndrome

  • 40% of cases are due to Cushing "disease,“

  • ACTH hypersecretion by the pituitary-benign pituitary adenoma (98% in ant pituitary)

  • 10% nonpituitary ACTH-secreting neoplasms (eg small cell lung Ca) 

    ↑ K & ↑ pigmentation

  • 15% ACTH source that cannot be initially located


Cushing s syndrome2
Cushing’s syndrome

  • 30% of cases- autonomous secretion of cortisol by the adrenals 

    independently of ACTH

  • Benign adrenal adenomas (small) cortisol

  • Adrenocortical carcinomas (large)  cortisol

    + androgens


Cushing s syndrome3
Cushing’s syndrome

  • Tests for diagnosis:

    - 24 hr Urinary free cortisol level

    - 1mg dexamethasone suppression test

    - Evening serum and salivary cortisol level


Cushing s syndrome4
Cushing’s syndrome

  • Urine Cortisol:

    - 24-hour urine collection

    >3-4 times upper limit (>200 µg/24hr)

    3 N urine free cortisol – excludes

  • ↑ Free Urine cortisol: high fluid intake; preg, Carbamazepine and fenofibrate


Cushing s syndrome5
Cushing’s syndrome

  • Dexamethasone suppression test:

    1 mg @11 pm cortisol @ 8 am;

    a cortisol level < 5 mcg/dL or < 2 mcg/dL

  • Phenytoin, Phenobarbital, Primidone, Rifampin, Estrogens (preg / OC) - lack of dexamethasonesuppressibility false +ve

  • 8% of pituitary Cushing disease- also have

    suppression


Cushing s syndrome6
Cushing’s syndrome

  • Midnight serum cortisol level > 7.5 mcg/dL:

    - Same time zone for at least 3 days

    - Fasting for at least 3 hours

    - Indwelling IV line

  • Late-night salivary cortisol test: consistently

    > 0.25 mcg/dL (7.0 nmol/L)


Cushing s syndrome7
Cushing’s syndrome

  • Confirmation:

    - Low dose Dexa suppression test:

    Dexa 0.5mg q6hrX 48hrs

    - Cortisol > 55.2nmol/L (2 µg/dL)  Cushing

    syndrome


Etiology of cushing s
Etiology of Cushing’s

  • To differentiate ACTH dependant vs ACTH

    independent

  • Plasma or serum ACTH:

    < 5pg/mL = adrenal tumor

    > 10-20 pg/mL = pituitary or ectopic ACTH-

    secreting tumors.


Etiology of cushing s1
Etiology of Cushing’s

  • To differentiate Pituitary ACTH vs ectopic ACTH:

    - 8mg Dexamethasone suppression test @ 11pm:

    OR

    - 48-hr Dexamethasone suppression test: 2mg q 6hr X 8 doses

    - Cortisolsuppression <50% of baseline =

    Pituitary ACTH

    - Sensitivity 80%; Specificity 70-80%

    - ↓ of 90% in U free cortisol ~ 100% specific

    for ant pit disease


Cushing s syndrome8
Cushing’s syndrome

  • MRI of the pituitary- pituitary lesion ~ 50%

  • Selective catheterization of the inferior petrosal sinus veins +/- CRH adm

  • CT scan: chest (lungs, thymus) abdomen (pancreas, adrenals)- 60% lesions found

  • 111In-octreotide (OCT, somatostatin receptor scintigraphy) scan: occult tumors

  • Non-ACTH-dependent Cushing syndrome- CT scan of the adrenals


Coarctation of aorta
Coarctation of Aorta

  • 1-8/1000 live births

  • 30 % Subsequent HTN after surgical correction

  • Less severe lesions diagnosed in young

    adulthood


Coarctation of aorta1
Coarctation of Aorta

  • Diminished and delayed femoral pulses

  • Systolic pr gradient b/w R arm and legs / L arm

  • Blowing systolic murmur - posterior L

    interscapular areas

  • Chest x-ray and transesophageal echocardiography


Other causes
Other causes:

  • Renal: Polycystic kidney disease, Renin

    secretorytr, obstructive uropathy

  • Adrenal: 17αhydroxylasedefi, 11βhydroxylase

    dehydrogenasedefi

  • Preeclampsia/ Eclampsia

  • Neuro: psycogenic, polyneuritis, a/c ↑ICP

  • Hyperthyroidism (systolic HTN)

    Hypothyroidism (Mild diastolic HTN)

    ↑ Ca, acromegaly

  • Mendelian forms


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