Endocrine (5%) Flashcards
1
Q
Functions of adrenal cortex hormones
A
- Cortisol – suppresses inflammation, mobilize glucose
- Aldosterone – increases renal absorption of sodium, water reabsorption
- Androgens – secondary sex characteristics
2
Q
Cushing’s Syndrome
A
- Hypercortisolism
- Pathophysiology – ↑ release of ACTH → a ↑ in cortisol production (60-70% caused by pituitary adenomas)
- Symptoms – central obesity, buffalo hump, round face, spontaneous bruising, purple striae, hypertension, hirsutism, hyperpigmentation, poor wound healing
- Labs – hypokalemia, hyperglycemia, hypernatremia
- Diagnostics – dexamethasone suppression test – give 1 mg of dexamethasone at 11 PM, measure serum cortisol at 8 AM
- Treatment – remove source of excess, management consequences (i.e., HTN, hypokalemia, and hyperglycemia)
3
Q
Addison’s Disease (everything except treatment)
A
- Hypocortisolism
- Primary pathophysiology – caused by damage to adrenal cortex → a ↓ in cortisol production
- Secondary pathophysiology – caused by pituitary failure to release ACTH → a ↓ in cortisol production. The sudden withdrawal of systemic corticosteroids → a ↓ in cortisol production from induced corticosteroid suppression
- Symptoms – weakness, fatigue, anorexia, orthostatic hypotension, nausea, vomiting
- Labs – hyponatremia, hyperkalemia, hypoglycemia
- Diagnostics – early AM serum cortisol < 3 is diagnostic
4
Q
Addison’s Disease Treatment
A
- Acute insufficiency – volume resuscitation with NS, dexamethasone 2-4 mg IV q6h + fludrocortisone (Florinef) 50 mcg IV daily prior to ACTH stimulation test, then hydrocortisone 50-100 mg IV q6-8h
- Chronic insufficiency – hydrocortisone 20-30 mg PO daily (2/3 in AM, 1/3 in PM), prednisone 15 mg AM and 10 mg PM, or dexamethasone 4 mg IM prefilled syringes for emergencies
5
Q
Pheochromocytoma
A
- A condition characterized by a rare, benign hormone-producing tumor of adrenal medulla causing excess release of catecholamines
- Symptoms – 5 P’s – pressure (persistent HTN), pain (headache), palpitations (tachycardia), perspiration (profuse sweating with flushing), pallor (secondary to vasoconstriction) – common triad: HTN, headache, and tachycardia
- Labs – increased urinary metanephrines (24-hour urine study), increased urinary VMAs, CT or MRI of adrenals confirms dx
- Treatment – control cardiovascular status with alpha blockers (-osin drugs; prazosin, doxazosin) followed by beta blockers (initial tx; s/s control) until tumor removal (definitive tx); pre-op volume expansion to prevent post-op hypotension
6
Q
Pathophysiology of Insulin
A
- Insulin catalyzes storage of all fuel types – CHOs, fats, and proteins
- Fats are lipid-soluble and can diffuse across cell membranes without the help of insulin but insulin signals for fat storage
- CHOs and proteins are water-soluble and need insulin to activate transport mechanisms in order to cross cell membranes
7
Q
Diagnostic Criteria for DM
A
- Glycosylated hemoglobin A1c – diagnostic of choice, A1C ≥ 6.5% with repeat A1C in asymptomatic patients with glucose of < 200 (if person also has glucose of > 200, no repeat test is necessary)
- Plasma glucose – fasting glucose ≥ 126 on 2 occasions or random glucose of ≥ 200 with symptoms (polyphagia, polyuria, polydipsia, unexplained weight loss)
8
Q
Type 1 DM
A
- Pathophysiology – autoimmune predisposition activated by environmental trigger → destroy beta cells
- Trajectory – relatively short, weeks to months, beta cell destruction results in absolute insulin deficiency
- Symptoms – weight loss, muscle loss, dehydration, acetone breath, mental status change (cells are using fats only as energy)
- Labs – serum ketones, rising BUN/creatinine, hypokalemia, high anion gap (mostly seen with DKA)
- Treatment – insulin replacement that mimics physiologic insulin release (basal + pre-meal short acting)
9
Q
Type 2 DM
A
- Pathophysiology – relative insulin deficiency d/t either distended/distorted peripheral receptors or beta cell dysfunction
- Trajectory – years, distorted insulin receptors result in hyperinsulinemia for about 10 years, beta cell dysfunction gradually decreases insulin production over several years
- Symptoms – subtle, vascular changes d/t chronic hyperglycemia (non-healing rashes, skin insult, hair loss on extremities)
- Labs – chronically, BUN/creatinine can rise as result in renal insult
- Treatment – weight loss in obese patients, oral therapy to sensitize insulin receptors, insulin (basal insulin should be started at time of diagnosis to help preserve beta cell function while the patient is working on weight loss (if obese))
10
Q
When to use insulin in DM treatment
A
- Type 1 – all patients, basal + adjustments for meals via multiple injections or pump
- Type 2 – at time of diagnosis (to achieve initial glycemic control) or when ≥ 2 standard oral agents at optimized doses are not enough to maintain glycemic control
- A1C goal for diabetics = < 7%
11
Q
Oral interventions for DM 2
A
- Biguanide (Metformin) – first-line medication unless contraindicated; insulin sensitizer; does not cause hypoglycemia; can cause renal impairment; can cause lactic acidosis and diarrhea
- Sulfonylurea (Glipizide, Glyburide) – often considered when second medication is needed after Metformin; increases insulin release; can cause hypoglycemia in elderly and those with impaired renal function
12
Q
Types of inulin + onset, peak, and DOA
A
- Short-acting (Lispro [Humalog], Aspart [Novolog]) – onset 10-30 minutes, peaks 1-3 hours, DOA 3-6 hours
- Intermediate-acting (NPH [Humulin N]) – onset 1-2 hours, peaks 6-14 hours, DOA 16-24 hours
- Long-acting (glargine [Lantus], Detemir [Levemir]) – onset 1-2 hours, peak none/minimal, DOA > 24 hours
13
Q
Dawn Phenomenon vs. Somogyi Effect
A
- Dawn phenomenon – blood sugar steadily rises in the morning; treatment is to increase evening dose
- Somogyi effect – a drop in blood sugar overnight/early morning causes rebound hyperglycemia in the morning; treatment is to decrease evening dose
14
Q
DKA (everything but treatment)
A
- Type 1 DM
- Common causes – insulin deficiency, glucocorticoid use, infection, inflammation, ischemia/infarction, intoxication
- Pathophysiology – hyperglycemia secondary to ↑ glucogenesis and ↓ glucose uptake into cells → mobilization and oxidation of fatty acids leading to ketoacidosis
- Symptoms – polyuria, polydipsia, polyphagia, n/v, abdominal pain, Kussmaul’s breathing, mental status changes
15
Q
DKA Treatment
A
- Isotonic fluid replacement (10-14 ml/kg/hr) after 1L bolus
- Regular insulin 10 units followed by IV insulin drip (0.1 unit/kg/hr) until anion gap is normal (normal anion gap = 3-10). If anion gap is high but glucose is < 250, add dextrose to fluids
- Treat precipitating event
