adrenal cortex: aldosterone Flashcards
diseases of adrenal cortex
-primary hyperaldosteronism
-PH
-conn’s disease
mineralocorticoids
-In individuals with normal salt intake, the average daily secretion of aldosterone ranges between 0.1 and 0.7 mol (50 and 250 g).
-During a single passage through the liver, >75% of circulating aldosterone is normally inactivated by conjugation with glucuronic acid.
regulation of aldosterone
-Normal regulation of aldosterone secretion is mediated to varying degrees by:
-Renin (kidney)
-Serum potassium and sodium levels
-Intravascular volume status
-Adrenocorticotropic hormone (ACTH)
-hypotension -> renin -> angiotensin -> reabsorb Na and therefore water -> excrete K
-H excreted and HCO3- reabsorbed
causes of mineralocorticoid excess
-primary aldosteronism:
-SINGLE adrenal (conns) adenoma- mutations, adrenal adenomas -> INDEPENDENT OF RENIN
-bilateral (micronodular) adrenal hyperplasia- mostly micronodular and rarely macronodular
-bilateral macronodular adrenal hyperplasia/idiopathic adrenal hyperplasia (IAH)
-glucocorticoid- remediable hyperaldosteronism (dexamethasone-suppressible hyperaldosteronism)- ACTH driven aldosterone production (NOT PRIMARY)
-other: (RARE)
-cushings
-glucocorticoid resistance
-adrenocortical carcinoma
-congenital adrenal hyperplasia
pathophysiology: primary aldosteronism
-Primary aldosteronism
-renin-independent, inappropriately high and non-suppressible aldosterone secretion and is associated with adverse cardiovascular disorders -> Autonomous aldosterone production
-PA should be suspected with early-onset hypertension or stroke before age 50 years
-secondary HTN
Conn syndrome
-Primary Hyperaldosteronism [PH]
-Increased aldosterone secretion
-Suppressed plasma renin activity (PRA)
-Elevated plasma and urine aldosterone levels.
-Results in:
-Hypertension (severe or drug resistant)
-Hypokalemia -> may cause polyuria, polydipsia, muscle weakness
-high prevalence in AA
-women > men
-low renin and high aldosterone
hyperaldosteronism presentation: HTN and K
-Hypertension:
-resistant
-Sustained systolic BP > 150 mm Hg or diastolic > 100 mm Hg over 3 measurements on 3 diff days
-Systolic BP > 140 mm Hg or diastolic > 90 mmHg AND resistant to 3-drug therapy
-Features of hypokalemia
-Fatigue
-Muscle weakness, cramping
-Headaches
-Paresthesia in severe cases due to metabolic alkalosis
-Polyuria and polydipsia
-Palpitations
-Constipation
-Absence of significant edema (due to aldosterone escape) -> DIFF FROM CHF (swelling and hypotension)
hyperaldosteronism who to suspect
-Patients with refractory hypertension (HTN)
-Patients with spontaneous or unprovoked hypokalemia, especially if the patient is also hypertensive
-Patients who develop severe and/or persistent hypokalemia in the setting of low to moderate doses of potassium-wasting diuretics
-Patients with variants:
-HTN, strokes, and other significant cardiovascular events are described in young persons with this syndrome.
other causes of increase renin
-renal artery stenosis
-obstruction to renal artery
-blood pressure can be normal -> kidney is just getting less flow
-renin and aldosterone is high
hyperaldosteronism : screening and dx
-Considerable diagnostic challenge
-Can often be cured with the proper surgical intervention (1ry)
-Diagnosis:
-initial screening
-confirmation of the diagnosis
-determining specific subtype of PH
(1) sustained hypertension above 150/100 mm Hg on 3 diff days;
(2) HTN resistant to 3 conventional antihypertensive drugs, including a diuretic;
(3) controlled BP requiring 4 or more antihypertensive drugs;
(4) hypokalemia, particularly when unrelated to diuretics;
(5) personal or family hx of early-onset HTN or CVA at age 40 or younger;
(6) first-degree relative with primary aldosteronism
(7) presence of an adrenal mass;
(8) low renin
hyperaldosteronism testing
-Potassium - low K
-HCO3 - high
-Aldosterone to renin ratio (ARR)
-Oral sodium loading test
-Saline infusion test
-Adrenal CT
-Adrenal venous sampling
-primary aldosteronism - low renin high aldosterone
-secondary aldosteronism- high renin and aldosterone
hyperaldosteronism management
-Clinically, the distinction between the 2 major causes of PH is vital because the treatment of choice for each is different.
-Unilateral aldosteronomas, CA - Surgery
-Bilateral disease –medical therapy:
-Control BP/ electrolytes
-Normalization of serum aldosterone levels -> Spironolactone
hyperaldosteronism : complications
-Related chronic hypertension
-Myocardial infarction
-CVA
-Congestive heart failure
-And those related to the specific therapy:
-Drug reactions
-Surgical complications
