Hyperaldosteronism Flashcards

1
Q

aldosterone responsible for ECV homeostasis via:

A

> K+, H+
resorption Na, Cl
DCT, CD
increase Na = > extracellular fluid

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2
Q

aldosterone is released in response to:

A

macula dense senses decreased renal perfusion (< Cl)
(decrease extracellular blood volume)

JG - release renin - renin cleaves angiotensinogen to AT1
ATI-ATII via ACE
ATII = vasoconstricts, ADH, aldosterone

.:. ATII acting on zona glomerulosa

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3
Q

K controls aldosterone secretion via.:

A

direct effect on the adrenal zona glomerulosa (increasing secretion?)

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4
Q

PHA primary hyperaldosteronism causes:

why metabolic alkalosis in PHA?:

A
  1. systemic hypertension
  2. > urinary loss of K = profound hypokalemia
  3. metabolic alkalosis

1- K shifts extracellularly, H+ shifts intracellularly
2- increased urinary loss of hydrogen ions

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5
Q

typical presentation:

A

geriatric cats (although can be younger)
weak from hypoK
hypertensive TOD (11/30 study detached retinas)
+/- PU/PD, diarrhea, weight loss

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6
Q

Classic biochemical abnormalities:
Na normal or only mildly increased why?:

Urinary fractional excretion of K:

A

mod-severe hypokalemia
increased water resorption that accompanies

greatly increased because of the effects of aldosterone

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7
Q

How does PHA worsen CKD:

Proteinuria:

adrenal tumors - what do you expect of renin

A

leads to hyaline arteriolar sclerosis
glomerular sclerosis
tubular atrophy
interstitial fibrosis

greater magnitude than that seen with CKD

low or absent because of negative feedback inhibition
but in some cases renin escapes from suppression

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8
Q

Hyperaldosteronism is implicated in metabolic syndrome:

A

characterized by insulin resistance, impaired beta-cell function, excessive proinflammatory proteins, and a prothrombotic tendency

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9
Q

cause:

A

adrenal adenomas or carcinomas - most common

unilateral carcinoma, adenomas sometimes bilateral few reports of bilateral adrenal hyperplasia.

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10
Q

MEN1

A

MEN is a well-recognized group of autosomal dominant syndromes in which single human patients develop multiple tumors originating in endocrine organs. The MEN I syndrome usually involves the pancreas, parathyroid glands, and pituitary gland

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11
Q

dx:

diagnostic hallmark of PHA

A

suspected in cats with hypokalemia and hypertension (often refractory) another cause cannot be identified

Increased aldosterone concentration is the

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12
Q

Conn’s disease in humans and frequ. of hypoK:

A

Currently, hypokalemia is rarely seen in human PHA or found only late in the disease course

Similarly, some cats with PHA do not display hypokalemia on initial presentation.

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13
Q

why must serum aldosterone be interpreted in light of serum K levels:

A

K is a major stimulus for aldosterone secretion
K is a potent suppressor of aldosterone secretion

aldosterone concentration is in the high-normal range, but

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14
Q

urinary aldosterone:creatinine ratio (UACR) advantages:

renin levels - less readily available but will be:

A

aldosterone over time

low

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15
Q

dx further imaging:

ddx for cat adrenal mass:

A

US, CT, MRI

Adrenal masses in the cat are often incidental findings known as:
incidentalomas
hypercortisolism (cortisol-secreting)
pheochromocytomas

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16
Q

Tx. sx for unilateral

MST

A

curative for both adenomas and carcinomas

many years

17
Q

Tx w medical management:

PHA is being recognized more frequently in cats. Usual hallmarks of the disease include hypokalemia and systemic hypertension. Ultrasound frequently detects an abnormality in the affected adrenal gland. Diagnosis is based on increased plasma or serum aldosterone concentrations, particularly in the face of hypokalemia and low renin activity (when measurement is available). Cats with PHA have good prognoses with surgical excision of tumor-bearing adrenal glands. Medical management can stabilize patients for many months.PHA should be considered a differential for cats with hypertension of unknown cause or that is refractory to treatment

A

spironolactone therapy
potassium supplementation
antihypertensive drugs

Reported survival times for cats treated medically often range from many months to years