Primary Hyperaldosteronism and Pheochromocytoma Flashcards
describe primary hyperaldosteronism
- autonomous aldosterone secretion
-renin-INDEPENDENT - most common adrenocortical disorder in cats
-middle aged to older cats (median 12.5 years)
-rare in dogs - most commonly due to a unilateral adrenal neoplasm
-65-75% benign
-25-35% malignant - less commonly due to a non-tumorous hyperplasia: bilateral
- increased renal sodium reabsorption, increased intravascular volume expansion, and increased renal hyperfiltration/perfusion
what are the 2 primary functions of aldosterone?
- retain Na+ and therefore water
- excrete K+
what are the physiologic consequences of excess aldosterone
- increased sodium and water retention, increasing peripheral resistance and leading to hypertension
-no hypernatremia in cats because also reabsorbing a shit ton of water too! - hypokalemia
describe clinical signs of hyperaldosteronism
primarily a reflection of hypokalemia and hypertension
hypokalemia signs:
1. hypokalemic polymyopathy:
-generalized weakness
-cervical ventroflexion
-K+ usually <2.5mEq/L
- might also see: ataxia, plantigrade stance, difficulty jumping, progress to flaccid paresis and possible hypoventilation or
- nothing apparent: determined by chronicity, pH, and total body K+
hypertension signs:
1. may be no obvious signs or
2. evidence of target organ damage: ocular, kidney, CNS, cardiac
-most common target organ undergoing hypertensive damage in cats is: ocular (decreased vision, mydriasis, blindness, retinal or vitreous hemorrhage, retinal detachment)
-other target organ damage:
–hypertensive encephalopathy: varied, intermittent, mentation change, ataxia, prostration, central vestibular
–renal injury: AKI or exacerbation of chronic renal disease
–left ventricular hypertrophy
nonspecific clinical signs:
-lethargy
-GI signs
-PU/PD (CKD, or hypokalemia induced nephrogenic DI)
-weight loss
describe UNCOMMON findings of primary hyperaldosteronism in cats
- concurrent diabetes mellitus:
-skin fragility, alopecia
-PU/PD
-due to concurrent cortisol or progesterone secretion from adrenal tumor - hemoabdomen: due to adrenal rupture
- hypoventilation:
-hypokalemic myopathy-induced paresis of ventilation muscles
describe diagnosis of hyperaldosteronism
- compatible clinical findings:
-can be subtle in earlier stages
-hypertension +/- evdence of target organ damage - clin path:
-hypokalemia
-increased urinary fractional excretion of K+ (>4-6% in a hypokalemic animal)
-mild hyperNa+ or high normal Na+
-increased CK
-azotemia
-hypophosphatemia: different from most cases of azotemia! - imaging:
-adrenal mass or enlargement: potential for vascular invasion, hunt for metastatis
-imaging may be normal though: failure to ID a mass does NOT rule out and presence of a mass does NOT confirm! - aldosterone measurement:
-normal to high aldosterone concentration
-normal can be consistent with hyperaldosteronism in the face of hypokalemia! (suggests autonomous secretion of aldosterone)
-not a readily available test though (same for aldosterone:renin and urine aldosterone: creatinine ratio for cats) - suppression tests:
-fludrocortisone suppression: should reduce aldosterone in healthy cats, but poor Sn
-telmisartan suppression test: block angiotensin II receptor and decrease aldosterone secretion in healthy but does not distinguish primary versus secondary
describe surgical treatment for hyperaldosteronism
- surgery is treatment of choice if you can!
-unilateral adrenalectomy, can be curative
-with removal of extension into vena cava
-for non-metastasized tumors - BUT may just have transient hypoaldosteronism after surgery because opposite adrenal atrophy so
-dietary sodium supplementation may help avoid immediately post-op
- +/- fludrocortisone treatment but not generally needed
describe the 3 parts of medical management of hyperaldosteronism
- emergent care
- pre-op stabilization
- long term medical management if not surgical candidate or if metastatic disease
describe treating hypokalemia for hyperaldosteronism patients
- pre-op and post-op PRN
- IV admin of KCl
-IV if mod to severe
-potassium gluconate PO when eating well - may not respond readily to supplementation
-also check for and treat hypomagnesemia if hypoK resistant to resolution
describe treating hypertension and suppressing aldosterone response for hyperaldosteronism patients
hypertension: amlodipine: calcium channel blocker
suppress aldosterone response: spironolactone: aldosterone inhibitor
describe prognosis of hyperaldosteronism
- excellent post surgical
- relapse can occur if malignant though
describe pheochromocytoma
- tumor of chromaffin cells of adrenal medulla that causes overproduction of catecholamines (epi and norepi) that act on alpha and beta receptors
- usually unilateral
+/- invasion of local vasculature - considered malignant if distant metastases
-approx 20% with mets at initial presentation
-some report up to 50% malignant - more in dogs, extremely rare in cats
-median age 10.5 years
-0.01-0.1% of all canine tumors - approx 50% of dogs have other concurrent neoplasia
-often other endocrine tumors
describe history/clinical signs of pheochromocytomas
- can range from mild to collapse and sudden death if tumor ruptures
- catecholamine release, acts on
-alpha receptors
-beta receptors - hormone secretion is episodic and unpredictable but may be more frequent over time
- correlation between tumor size and magnitude of clinical signs
-larger = worse - most common signs:
-cardiac arrhythmias!! (beta-1 receptors): also secondary to myocardial damage, ischemia, and fibrosis from constant catecholamine exposure; common sinus tachycardia, SVT, v-tach, rarely bradycardia, AV. block
-panting/tachypnea (beta-2 receptors)
-anorexia
-vomiting
-collapse
-PU/PD: mechanism unclear, may be primary (USG >1.030 after water deprivation or first morning urine sample
-weight loss
-abdominal pain
-pale MM
-systemic hypertension: via stimulation of alpha receptors but episodic so rarely manifests as signs (epistaxis, retinal hemorrhage/detachment seen)
-neuromuscular: catecholamine-induced arterial vasospasm, CNS hemorrhage, weakness, pacing, disorientation/anxiety, seizures
-other signs of large or invasive tumor: may be silent but potentially ascites, hind limb edema, distension of caudal epigastric veins
-acute tumor rupture: retroperitoneal hemorrhage
describe diagnosis of pheochromocytoma
- compatible clinical signs
- clinpath:
-nothing consistent
+/- anemia (non-regen)
-increased ALT, AST, ALP
-hypercholesteremia in advanced disease
-proteinuria: hypertension-related - ultrasound:
-most commonly used
-contralateral adrenal normal size and shape
-hard to diff. from adrenal cortical tumors
-tumor invasion of local vessels - other:
-FNA: risk of hemorrhage and hypertensive crisis but accurate
-CT/MRI: best to assess vascular invasion, can ID metastases
-nuclear imaging: shows functional adrenomedullary tissue, not widely availabke - biochem eval:
-measure plasma or urine catecholamines and free metanephrines: metanephrine release is not episodic so easier to find!
-but tough sample handling
-urine normetanephrine is easier with a single voided urine sample and has highest Sn
describe treatment of pheochromocytomas
- surgical:
-adrenalectomy is treatment of choice but
-risk of intraop catecholamine surge: malignant arrhythmias, hypertensive crisis, pulmonary edema, cardiac ischemia - pre-op medical management:
-treat hypertension bia phenozybenzamine or prazocin (MOA: alpha-1 blockers)
-treat arrhythmias is needed (atenolol: selective B-1 agonist, start at least 2-3d after alpha-blockers) - other medical:
-toceranib phosphate: tyrosine kinase inhibitor; inhibits tumor angiogenesis
prognosis: not bad
