Endocrine (5%)

Question 1

Functions of adrenal cortex hormones

Answer 1

• Cortisol – suppresses inflammation, mobilize glucose
• Aldosterone – increases renal absorption of sodium, water reabsorption
• Androgens – secondary sex characteristics

Question 2

Cushing’s Syndrome

Answer 2

• 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)

Question 3

Addison’s Disease (everything except treatment)

Answer 3

• 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

Question 4

Addison’s Disease Treatment

Answer 4

• 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

Question 5

Pheochromocytoma

Answer 5

• 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

Question 6

Pathophysiology of Insulin

Answer 6

• 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

Question 7

Diagnostic Criteria for DM

Answer 7

• 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)

Question 8

Type 1 DM

Answer 8

• 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)

Question 9

Type 2 DM

Answer 9

• 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))

Question 10

When to use insulin in DM treatment

Answer 10

• 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%

Question 11

Oral interventions for DM 2

Answer 11

• 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

Question 12

Types of inulin + onset, peak, and DOA

Answer 12

• 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

Question 13

Dawn Phenomenon vs. Somogyi Effect

Answer 13

• 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

Question 14

DKA (everything but treatment)

Answer 14

• 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

Question 15

DKA Treatment

Answer 15

• 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

Question 16

HHS (everything but treatment)

Answer 16

• Type 2 DM
• Common causes – insulin deficiency, glucocorticoid use, infection, inflammation, ischemia/infarction, intoxication, dehydration, renal failure
• Pathophysiology – extreme hyperglycemia without ketoacidosis → osmotic DIURESIS and volume depletion with electrolyte disturbances
• Symptoms – dehydration, glucose > 600, increased serum osmolality (thick serum; normal osmo 270-290)

Question 17

HHS Treatment

Answer 17

• Isotonic fluid replacement with NS initially followed by 0.45% NS (estimate 8-10L fluid loss). As you correct the dehydration, the patient tends to correct their own electrolyte imbalances
• Treat electrolyte imbalances. Only replace K while fluid resuscitating because K will continue to drop as you are giving insulin, correct if < 4.0. After fully resuscitated, can correct the others that still need corrected
• Regular insulin 10 units followed by IV insulin drip (0.05-0.1 units/kg/hr)
• Treat precipitating event

Question 18

General principles for hyperglycemic control in acute care setting

Answer 18

• Identify possible reversible causes – diet, dextrose-containing IV fluids, glucocorticoids, post-op
• Treatment goals
• Avoid hypoglycemia (sliding scale alone is not a good method of treatment)
• Avoid extreme hyperglycemia (> 180)
• Insulin therapy is preferred for hyperglycemia in inpatient setting; orals are not recommended d/t risk for hypoglycemia, renal injury, and HF
• Non-ICU and ICU goals are 140-180

Question 19

Estimating total daily dose of insulin for those not on insulin in the acute care setting

Answer 19

o Malnourished, CKD (on dialysis), elderly, liver disease: 0.3 units/kg
o Normal-weight patients, including type 1 DM: 0.4 units/kg
o Overweight: 0.5 units/kg
o Obese, high-dose steroids, or insulin resistance: 0.6 units/kg

Question 20

Estimating total daily dose of insulin for someone who takes insulin in the acute care setting

Answer 20

o Type 1 DM: 0.3-0.5 units/kg

o Type 2 DM: 0.5-0.7 units/kg

Question 21

General insulin dosing

Answer 21

o Basal insulin = 50% TDD
o Prandial insulin (nutritional) = 50% of TDD (divided in 3 daily doses with meals)
o Supplemental insulin (correctional) = (current BG – target BG)/CF; CF = TDD/1700
o If > 2 glucose levels are < 80 in 24 hours, decrease TDD by 20%
o If > 2 glucose levels are > 180 and none are < 80 in 24 hours, increase TDD by 20%

Question 22

Converting IV insulin to SQ insulin

Answer 22

• Establish the 24 hour insulin requirement (TDD of IV insulin)
• Determine the SubQ TDD = 80% of the IV TDD
• Determine the basal subQ dose = 50% of SC TDD
• Determine the prandial subQ dose = 50% of SC TDD (divided into 3 doses with each meal)
• Determine the supplemental dose: (current BG – target BG)/CF; CF = 1700/SC TDD
• Principles of conversion – continue IV insulin until patient is able to eat solid food, continue IV insulin for 2-4 hours after first SC dose is given, and do not switch to only oral agents from IV insulin in type 2 DM

Question 23

Hypoglycemia

Answer 23

 Causes – diabetes (med changes, overdose, infection, diet changes, metabolic change, activity change), meds/drugs, reactive, etc.
 Symptoms – sweating, shaky, tachycardia, dizziness, confusion, blurry vision, mental status change
 Whipple triad – hx of hypoglycemia, low plasma glucose, relief of symptoms on ingesting fast-acting carbs ~ 15 minutes
 Management – non-pharm: avoid fasting, avoid simple carbs, high protein, avoid causative agents; pharm: glucose tabs at onset of symptoms (mainstay), IM glucagon 1mg (may repeat every 20 minutes)

Question 24

SIADH

Answer 24

 Excess ADH production, nephrons conserve excess water
 Commonly caused by head injury or lung cancer
 Labs – WATER OVERLOAD results in serum hyponatremia, serum hypoosmolality and urine hypernatremia, urine hyperosmolality (thin serum, thick urine)
• Normal serum Na 135-145; normal serum osmo 270-290; normal urine Na 10-20; normal urine osmo 300-900
 Symptoms – findings consistent with volume overload and hyponatremia
 Treatment – depends on degree of symptom presentation; free water restriction, loop diuretic with NS, or 3% saline (extreme cases)

Question 25

DI

Answer 25

 Insufficient ADH, nephron cannot conserve water  Central: commonly caused by damage to pituitary or hypothalamus (surgery, tumor, head injury) vs. Nephrogenic: kidneys don’t respond to ADH (genetics, drugs [Lithium])  Labs – FREE WATER DEPLEPTION results in serum hypernatremia, serum hyperosmolality and urine hyponatremia, urine hypoosmolality (thick serum, thin urine) • Normal serum Na 135-145; normal serum osmo 270-290; normal urine Na 10-20; normal urine osmo 300-900  Symptoms – findings consistent with hypernatremia and volume depletion  Treatment – supportive fluid replacement until underlying condition resolves, may replace ADH (DDAVP) in severe cases

Question 26

Hypothyroidism - general signs and symptoms

Answer 26

* Thick, dry skin * Slowed reflexes * Slow thoughts * Small weight gain, largely fluid * Constipation * Menorrhagia (or longer menstrual cycles) * Easily chilled

Question 27

Central vs. primary hypothyroidism

Answer 27

* Primary – problem with thyroid gland itself | * Central – problem with pituitary gland of hypothalamus – hypothalamus not release TRH or pituitary isn’t release TSH

Question 28

Common etiologies of hypothyroidism

Answer 28

* Hashimoto’s thyroiditis (primary) – autoimmune destruction of thyroid (i.e., thyroiditis, iodine deficiency, lithium use, amiodarone use); ↓ T4 and ↑ TSH * Post-radioactive iodine (RAI) treatment (primary) – typically resulting s/p Graves’ disease treatment or thyroid cancer treatment; ↓ T4 and ↑ TSH * Pituitary or hypothalamic dysfunction (central)

Question 29

Hypothyroidism crisis state - myxedema coma

Answer 29

* Symptoms of hypothyroidism x 10 * Typically resulting from infection, major cardiopulmonary disease, or major neurologic illness * Hypothermia, hypotension, hypoventilation, change in mental status, hyponatremia, hypoglycemia * Treatment – 5-8 mc/kg T4 IV initially then 50-100 mcg IV daily until s/s resolve and underlying process fixed

Question 30

Hypothyroidism acute care focused dx and tx

Answer 30

* Diagnosis – ↓ T4 and ↑ TSH * Treatment – levothyroxine (Synthroid) 1.5-1.7 mcg/kg/day (1.0 mcg/kg/day in elderly); need to increase dose in pregnancy (↑ 33% initially then titrate to 50% or greater increase) * Follow up with TSH in 4-6 weeks and titrate to euthyroidism (normal TSH 0.5-5.0)

Question 31

Hyperthyroidism - general signs and symptoms

Answer 31

* Smooth, silky skin * Hyperreflexia * Mind racing * Weight loss (~ 10 pounds) * Frequent, low volume stools * Oligomenorrhea (decreased or no menstrual cycle) * Heat intolerance

Question 32

Common etiologies of hyperthyroidism

Answer 32

* Graves’ disease – autoimmune, multisystem presentation including exophthalmos, tachycardia, proximal muscle weakness, and goiter * Thyroiditis – viral or autoimmune, post-partum, drug-induced, often transient * Toxic adenoma – benign, metabolically active thyroid nodule(s) * TSH-secreting tumor * Medications – amiodarone, interferon, others

Question 33

Hyperthyroidism crisis state - thyroid storm

Answer 33

* Delirium, systolic HTN (wide pulse pressure almost purely systolic; normal pulse pressure 20-40; decreased MAP), hyperthermia * Admit to ICU * Treatment – beta blockade (propranolol 0.5-2g IV q4h), PTU or methimazole 15-25 mg q6h, iodine, consider steroids

Question 34

Hyperthyroidism acute care focused dx and tx

Answer 34

* Diagnosis – ↑ T4 and ↓ TSH * Treatment depends on etiology * Beta blocker therapy (propranolol preferred, initial tx, symptom management!) * Graves’ disease – antithyroid drugs (i.e. methimazole) or radioactive iodine; surgical removal rare * Toxic adenoma pituitary tumor – surgical removal

Question 35

Prolactinoma

Answer 35

 Pituitary tumor that causes release of prolactin  Usually found in infertility workups  Presentation – failure to conceive, irregular menses, chronic headache