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MS2 Renal > 9/14- Nephrologist's Approach to Hypertension > Flashcards

9/14- Nephrologist's Approach to Hypertension Flashcards

1
Q

What factors weigh into blood pressure?

A

BP = CO x PVR

Cardiac output

  • Blood volume (Na, mineralocorticoids)
  • Cardiac factors (heart rate, contractility)

Peripheral vascular resistance:

  • Vasoconstricotrs (ang II, catecholamines- a-adrenergic)
  • Vasodilators (prostaglandins, catecholamines- B-adrenergic, potassium)
  • Local factors (adenosine, pH, hypoxia)
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2
Q

How common is essential hypertension?

Among what populations?

  • What may influence it
  • What is it a risk factor for
A
  • 1/3 people have HTN
  • Accounts for > 90% of HTN
  • Older Americans and blacks have increased risk

Influenced by:

  • Genetics (positive FHx)
  • Environment: obesity, fast food diet, high stress, type A
  • Neurohormonal mediators
  • Possibly also metabolic factors like hyperuricemia

Risk factor for:

  • Coronary artery disease (CAD)
  • Congestive heart failure (CHF)
  • Stroke
  • Kidney failure
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3
Q

What organs are affected by essential HTN? Manifestations?

A

Kidney

  • Chronic kidney disease
  • Proteinuria
  • Nephrosclerosis and interstitial fibrosis

CNS damage

  • Stroke

Vascular damage

  • Indicated by retinal exam
  • AV nicking

Heart

  • Cardiac hypertrophy
  • Fibrosis
  • Heart failure
  • Coronary artery disease
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4
Q

How does hypertension cause pathology in the kidneys?

A

Small arteries:

  • Fibrous intimal thickening
  • Reduplication and fragmentation of elastic lamina
  • Medial hyperplasia

Tubules and Interstitium

  • Tubule atrophy
  • Interstitial inflammation and fibrosis

Glomerulus

  • Collapse of capillaries
  • General loss of cells
  • Glomerulosclerosis

Picture is small blood vessel

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5
Q

How does the kidney play a role in essential hypertension?

A

Increased peripheral resistance

  • Renin-angiotensin system
  • Sympathetic nerve system

Sodium retention

  • Primary or secondary
  • Inability to excrete sodium load
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6
Q

What is “salt-sensitive hypertension”?

A

Loss of sensitivity of regulatory process in which sodium loading normally leads to “pressure natriuresis”

  • “Guyton” hypothesis
  • Chronically expanded vascular volume (but may be in upper range of normal)
  • Relative increase in vascular resistance (but may be in upper range of normal)
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7
Q

What are the genetic mechanisms of HTN?

A
  • Multiple genes (angiotensin, adducin…) involved with renal sodium excretion have been implicated (none clearly proven in 1’ HTN)
  • Sodium retention with resultant volume expansion may initiate hypertension
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8
Q

What is resistant HTN (def)?

A

Persistence of HTN despite concurrent use of adequate doses of 3 antihypertensive agents from different classes, including a diuretic

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9
Q

What can cause resistant HTN?

A

Improper BP measurement

Volume overload

  • Excess Na intake
  • Volume retention from kidney disease
  • Inadequate diuretic therapy

Drug-induced or other causes

  • Nonadherence
  • Inadequate doses
  • Inappropriate combos
  • NSAIDs (COX2 inhibitors)
  • Cocaine, amphetamines, illicit drugs…
  • Sympathomimetics

Oral contraceptive hormones

  • Adrenal steroid hormones (anabolic)
  • Cyclosporine and tacrolimus
  • EPO
  • Licorice
  • Selected over-the-counter dietary supplements/meds

Associated conditions

  • Obesity
  • Excess alcohol intake
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10
Q

What is secondary HTN (clues)?

A
  • Onset of severe HTN (BP > 180 systolic or 120 diastolic) after the age of 55 yo
  • Unexplained deterioration of kidney function during antiHTN therapy
  • Esp an acute and sustained elevation in the serum creatinine concentration by > 50% that occurs within 1 wk of instituting therapy with ACEI or ARB
  • Severe HTN in pts with diffuse atherosclerosis (particularly those over 50 yo)
  • Severe HTN in pt with unexplained atrophic kidney or asymmetry in renal sizes > 1.5 cm
  • Severe HTN in pts with recurrent episodes of acute (flash) pulmonary edema or refractory heart failure with impaired renal fucntion
  • A systolic-diastolic abdominal bruit that lateralizes to one side
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11
Q

Screening tests in secondary HTN for:

  • Chronic kidney disease
  • Coarctation of aorta
  • Cushing’s syndrome
  • Drug induced
  • Pheochromocytoma
  • Primary aldosteronism/mineralocorticoid excess
  • Renovascular HTN
  • Sleep apnea
  • Thyroid/parathyroid disease
A

- Chronic kidney disease: estimated GFR

- Coarctation of aorta: CT

- Cushing’s syndrome: Hx; dexamethasone suppression test

- Drug induced: Hx, drug screening

- Pheochromocytoma: 24 hr urinary metanephrine an dnormetanephrine

- Primary aldosteronism/mineralocorticoid excess: 24 hr urinary aldosterone level or specific msmts

- Renovascular HTN: Doppler flow study, MRA

- Sleep apnea: sleep study with O2 sat

- Thyroid/parathyroid disease: TSH, serum PTH

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12
Q

Goldblatt’s hypothesis of acquired kidney injury?

A

Ischemia -> increased renin

  • Increased aldosterone and sodium retention increased blood volume
  • Increased angiotensin II and vasoconstriction increases PVR

Both contribute to HTN

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13
Q

Renal artery stenosis accounts for ___% of causes of HTN

A

Renal artery stenosis accounts for 2-5% of causes of HTN

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14
Q

What is renal artery stenosis?

  • Pathophysiology
  • Prognosis
A

Narrowing of the renal a. causing restriction of renal blood flow that -> HTN

  • Pathophysiology: activation of RAAAS
  • Hemodynamically significant stenosis can lead to renal atrophy and reduction in kidney function
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15
Q

Interrelation among renal artery stenosis, HTN, and chronic renal failure

A
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16
Q

What is the etiology of renal artery stenosis?

A

Atherosclerosis

  • 60-80%
  • Elderly man
  • Affects mainly the proximal third of the main renal artery

Fibromuscular dysplasia

  • 20-40%
  • Young women
  • Involves the distal two thirds and branches of the renal arteries

Neurofibromatosis

Vasculitis

Radiation

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17
Q

Pathophysiology of RVH

A
  • Experimentally, produced by clipping the renal artery; will simulate renal artery stenosis
  • Termed “Goldblatt Hypertension” or model/hypothesis
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18
Q

What was Goldblatt’s Hypothesis on acquired renal injury?

A
  • Primary renal microvascular disease that results in renal ischemia is the cause of hypertension.
  • Renal ischemia leading to oxidative stress, inflammatory cell infiltration and sodium retention is central to the pathogenesis of hypertension

2 kidney, 1 clip model:

  • Increase in aldosterone lead to hypokalemia
  • Usually, need to have at least 70% stenosis prior to the mentioned cascade effect
  • Key point: Pressure natriuresis by the contralateral kidney normalizes blood volume.
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19
Q

What are the phases of RAS?

A
  • Acute phase (I)
  • Transitional phase (II)
  • Chronic phase (III)
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20
Q

What occurs in the acute phase of RAS?

A
  • Renin, angiotensin II, aldosterone increased, sympathetic nervous system stimulated
  • Vascular volume normal because normal kidney excretes sodium and water
  • BP elevated due to vasoconstriction, increased CO
21
Q

What occurs in the transitional phase of RAS?

A
  • System becomes more sensitive to Ang II and SNS
  • Expanded volume / salt and water retention
  • Hypertension is treatable with removal of stenosis
22
Q

What occurs in the chronic phase of RAS?

A
  • Hypertension with normal / slightly increased RAA & SNS
  • Hypertension not treatable after stenosis removal
  • Contralateral kidney gets damaged from persistent high pressures, and volume may increase again
23
Q

What is the 2 kidney, 2 clip model?

A
  • Initial increase in renin with rise in blood pressure
  • No contralateral kidney to perform pressure natriuesis
  • Therefore, volume increases.
  • Increase in volume suppresses renin to near normal levels later on.
  • HTN is volume-dependent.
24
Q

What is the clinical presentation of RAS?

A
  • Onset of HTN under 30 or > 55 yo
  • Severe HTN requiring 3 or more BP medications
  • Development of resistant hypertension in a previously well-controlled patient
  • Flash pulmonary edema
  • Renal failure with ACE inhibitors
  • Abdominal bruit or asymmetry of kidney size
  • Hypertension with renal failure
25
Q

The addition of ACE inhibitors in the presence of _______ (uni/bilateral) RAS will cause ____. Why?

A

The addition of ACE inhibitors in the presence of bilateral RAS will cause kidney failure

  • The efferent arteriole is mostly dependent on angiotensin-II for its vascular tone.
  • Alterations or blockade in angiotensin-II will affect the efferent arteriole the most.
26
Q

How can RAS be diagnosed?

A
  • Angiography** (gold standard)
  • Magnetic resonance angiography (MRA)
  • Spiral CT scan with angiography
  • Doppler ultrasonography
  • Renogram and captopril renogram
  • BOLD MRI
27
Q

How to treat RAS?

  • Medically
  • Surgically
A

Medical therapy

  • Optimal blood pressure control
  • Cessation of smoking
  • Lipid lowering agents with statins
  • Anti-platelet agents
  • RAS Blockade

Surgical therapy

  • Percutaneous transluminal renal angioplasty with stenting
  • Surgical revascularization
28
Q

What is pheochromocytoma?

A

Excessive catecholamine production by tumor from adrenal medulla or sympathetic nerve chain

29
Q

How does pheochromocytoma present?

A

5 Ps:

  • Pressure (HTN) in 90%
  • Pain (headache) in 80%
  • Perspiration in 71%
  • Palpitation in 64%
  • Pallor in 42%
  • (Paroxysms)
30
Q

What is the “rule of 10” in pheochromocytoma?

A

10% extra-adrenal (closer to 15%)

10% occur in children

10% familial (closer to 20%)

10% bilateral or multiple (more if familial)

10% recur (more if extra-adrenal)

10% malignant

10% discovered incidentally

31
Q

How can pheochromocytoma be diagnosed?

A

Biochemical tests

  • Urine studies are more specific (?)
  • Plasma metanephrines are very sensitive; may indicate need for further testing Imaging

- CT abdomen: adrenal pheo, extra-adrenal

- MRI: mores sensitive than CT for extra-adrenal

32
Q

Management for pheochromocytoma?

A
  • Medication with combined alpha and beta adrenergic blockers (phentolamine and propanolol).
  • Surgical resection
33
Q

What is the mechanism behind primary hyperaldosteronism?

A

Excessive secretion of aldosterone by the adrenal cortex due to adenoma or bilateral adrenal cortical hyperplasia

34
Q

How does 1’ hyperaldosteronism present?

A
  • Hypkalemia
  • Metabolic alkalosis
35
Q

Diagnosis of 1’ hyperaldosteronism?

A
  • Document renal K wasting (>20 mEq/24 hr)
  • Plasma aldosterone/renin ratio > 20 is suggestive
  • 24 hr urine aldosterone >14 µg on 250 mEq Na X 3 days
  • Abdominal CT is helpful if adenoma is found
36
Q

Treatment for 1’ hyperaldosteronism?

A
  • Spironolactone or Eplerenone
  • Adrenalectomy*
37
Q

Look at this picture of biosynthesis of aldo & cortisol

A
38
Q

What causes glucocorticoid-remediable aldosteronism (GRA)?

A

Familial hyperaldosteronism type I Genetic defect in chimeric gene

  • ACTH responsive regulatory region of the 11-beta-hydroxylase gene PLUS
  • Structural region of the aldosterone synthase gene
39
Q

Mechanism behind GRA (glucocorticoid-remediable aldosteronism)?

A
  • Hypokalemia and metabolic alkalosis
  • Decreased Plasma renin activity.
  • Increased Aldosterone levels
  • Presence of 18-hydroxycortisol and 18-oxocortisol in urine
40
Q

What is the treatment for GRA (glucocorticoid-remediable aldosteronism)?

A

Low dose glucocorticoids, amiloride, and spironolactone

  • Blocks binding of aldosterone to the mineralocorticoid receptor
41
Q

What is the syndrome of apparent mineralocorticoid excess? Results in?

A
  • Both cortisol and aldosterone are potent activators of renal MCRs.
  • In the kidney, 11β-hydroxysteroid dehydrogenase-2 (11β-HSD-2) converts cortisol to cortisone, which does not activate the renal MCR.
  • 11β-HSD-2 gene mutations lead to elevated levels of cortisol that activates MCR

Results in:

  • Low K
  • Low plasma renin activity
  • Low aldosterone
42
Q

What is treatment of syndrome of apparent mineralocorticoid excess?

A

Spironolactone

  • Blocks binding of both cortisol and aldosterone to the MCR
43
Q

What is Liddle’s Syndrome?

  • Genetics
  • Mechanism
  • Observed
A
  • Mutations in gene coding the beta or gamma subunits of ENaC of the principal cell
  • Results in constitutive expression of ENaC leading to increased rates of Na reabsorption and HTN
  • Early-onset severe HTN, hypokalemia, and metabolic alkalosis
  • Low plasma renin activity and aldosterone
44
Q

What is treatment for Liddle’s syndrome?

A

Amiloride or triamterene

45
Q

What is Gordon’s Syndrome

  • Genetics
  • Mechanism
  • Observed
A

Pseudo hypoaldosteronism type II

  • Genetically-inherited condition
  • Constitutive activation of thiazide-sensitive Na channels in the distal convoluted tubule
  • (Mirror image of Gitelman’s syndrome (inactivation of the thiazide-sensitive Na channels

—- the exact opposite metabolic abnormalities

—- hypokalemia and metabolic alkalosis))

Exhibit:

  • salt-sensitive hypertension
  • hyperkalemia, and
  • non-anion gap metabolic acidosis

in association with a normal GFR

46
Q

Treatment for Gordon’s syndrome?

A

Highly responsive to thiazide diuretics

(- Correctly implying the disease is due to a constitutive activation of thiazide-sensitive Na channels in the distal convoluted tubule)

47
Q

Treatment of HTN

A

BP targets

  • 150/90 in anyone > 60 yo
  • 140/90 for those < 60 yo, with diabetes, or CKD (chronic kidney disease)

Initial drug treatment options for HTN with chronic kidney disease = ACEI or ARB

NEW SPRINT DATA BP

under 120/80 vs. 140/80 showed decreased

  • Heart attack, heart failure, and stroke by 1/3
  • Risk of death by 1/4
48
Q

Initial drug choice of HTN drugs?

A
  • 4 classes for nonblack pts and 2 classes for black
  • Beta blockers no longer recommended for initial therapy b/c they might not protect as well from stroke
49
Q

Summary:

Essential Hypertension : Impaired pressure natriuresis.

Renal Artery Stenosis : If bilateral, renal function worsens with Ace I as it acts on efferent arteriole

Pheochromocytoma: Treat with both Alpha and Beta Blockers.

Hyperaldosteronism: Hypokalemic Metabolic alkalosis, treat with MRB s.

A

(:

MS2 Renal (25 decks)

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