Hyperaldosteronism Flashcards
aldosterone responsible for ECV homeostasis via:
> K+, H+
resorption Na, Cl
DCT, CD
increase Na = > extracellular fluid
aldosterone is released in response to:
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
K controls aldosterone secretion via.:
direct effect on the adrenal zona glomerulosa (increasing secretion?)
PHA primary hyperaldosteronism causes:
why metabolic alkalosis in PHA?:
- systemic hypertension
- > urinary loss of K = profound hypokalemia
- metabolic alkalosis
1- K shifts extracellularly, H+ shifts intracellularly
2- increased urinary loss of hydrogen ions
typical presentation:
geriatric cats (although can be younger)
weak from hypoK
hypertensive TOD (11/30 study detached retinas)
+/- PU/PD, diarrhea, weight loss
Classic biochemical abnormalities:
Na normal or only mildly increased why?:
Urinary fractional excretion of K:
mod-severe hypokalemia
increased water resorption that accompanies
greatly increased because of the effects of aldosterone
How does PHA worsen CKD:
Proteinuria:
adrenal tumors - what do you expect of renin
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
Hyperaldosteronism is implicated in metabolic syndrome:
characterized by insulin resistance, impaired beta-cell function, excessive proinflammatory proteins, and a prothrombotic tendency
cause:
adrenal adenomas or carcinomas - most common
unilateral carcinoma, adenomas sometimes bilateral few reports of bilateral adrenal hyperplasia.
MEN1
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
dx:
diagnostic hallmark of PHA
suspected in cats with hypokalemia and hypertension (often refractory) another cause cannot be identified
Increased aldosterone concentration is the
Conn’s disease in humans and frequ. of hypoK:
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.
why must serum aldosterone be interpreted in light of serum K levels:
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
urinary aldosterone:creatinine ratio (UACR) advantages:
renin levels - less readily available but will be:
aldosterone over time
low
dx further imaging:
ddx for cat adrenal mass:
US, CT, MRI
Adrenal masses in the cat are often incidental findings known as:
incidentalomas
hypercortisolism (cortisol-secreting)
pheochromocytomas