Cramming again b/c it worked :)

When is insulin used/AEs

• Type 1 diabetes: required b/c insulin deficiency

• Type 2 diabetes: required when glucose control is inadequate with other medications or when insulin requirements are high

• Acute severe hyperglycemia and diabetic emergencies

• AEs: hypoglycemia, weight gain, lipohypertrophy/atrophy at injection sites, worsening of diabetic retinopathy with rapid changes in glucose

Rapid-acting insulin

• Lispro

• Aspart

• Glulisine

• Afrezza (fastest, inhaled)

• Used for mealtime/postprandial glucose control (pt needs insulin immediately before a meal)

Short-actin insulin

• Regular insulin (humulin R, novolin R)

• Mealtime coverage, IV for certain emergencies

Intermediate insulin

• NPH (Humulin N or Novolin N)

• Intermediate basal coverage

Long-acting insulin

• Glargine

• Detemir

• Basal insulin coverage

Ultra-long acting insulin

• Degludec

• Glargine U300

• Extended basal coverafe

Sulfonylureas (drugs, MOA, when used, AEs, contraindications)

• Glipizide, Glyburide, Glimepiride, Chlorpropamide (1st gen rarely used)

• Bind to pancreatic beta cells, close potassium channels (depolarizing cell, opening calcium channels and stimulating insulin release)

• T2DM to increase insulin secretion

• AEs: hypoglycemia, weight gain, GI upset, hypersensitivity rxns

• Use caution with renal/hepatic impairment, G6PD deficiency

Meglintinides (drugs, MOA, when used, AEs)

• Repaglinide, nateglinide

• Close potassium channels on pancreatic beta cells, stimulating insulin secretion

• Used when pt needs help controlling post-meal glucose or flexible dosing around meals, rapidly absorbed, peak conc/half life 1 hour, taken before meals (pt has predominantly postprandial hyperglycemia)

• AEs: hypoglycemia (less than sulfonylureas), weight gain, frequent dosing required

Biguanides (drugs, MOA, when used, AEs, contraindications)

• Metformin

• Primary effect= decreases hepatic gluconeogenesis, increases peripheral insulin sensitivity, increases glucose uptake and utilization, decreases intestinal glucose absorption

• Used for T2DM when pt is overweight, does not directly stimulate insulin release (preserves beta cells)

• AEs: GI problems, decreased vitamin B12 absorption (signs: fatigue/anemia), lactic acidosis, NO HYPOGLYCEMIA/WEIGHT GAIN

• Contraindications: eGFR below 30, metabolic acidosis, significant hepatic impairment, excessive alcohol consumption, unstable or acute heart failure

Thiazolidinediones (TZDs) (drugs, MOA, when used, AEs, contraindications)

• Pioglitazone, rosiglitazone

• Activates PPAR gamma nuclear receptors, altering gene expression, improving insulin sensitivity in adipose tissue, liver, and muscle

• Used for T2DM with insulin resistance when pt needs increased sensitivity rather than insulin secretion, preserves beta-cell function

• AEs: weight gain/edema, heart failure, increased fracture risk, hepatic toxicity, macular edema, NO HYPOGLYCEMIA

• Contraindications: heart failure, hepatic impairment, ALT>2.5 x upper limit

GLP-1 receptor (drugs, MOA, when used, AEs, contraindications)

• Exenatide, liraglutide, dulaglutide, semaglutide, lixisenatide, tirzepatide (GIP/GLP-1)

• Increases glucose dependent insulin secretion, decreases glucagon/slows gastric emptying, decreasing appetite

• Used for T2DM with obesity, causes weight loss, low hypoglycemia risk, improves fasting and postprandial glucose

• AEs: GI upset, pancreatitis, acute kidney injury associated with dehydration, medication absorption changes, thyroid C-cell tumors

• Avoid with hx of medullary thyroid carcinoma

DPP-4 inhibitors (drugs, MOA, when used, AEs, contraindications)

• Sitagliptin, saxagliptin, linagliptin, alogliptin

• Inhibit DPP-4, which breaks down incretins such as GLP-1, increases glucose-dependent insulin secretion, decreases glucagon

• Weight-neutral, low hypoglycemia risk, well tolerated, linagliptin does not require renal dose adjustment

• AEs: modest A1c reduction, pancreatitis, heart failure, renal dose adjustments

Alpha-glucosidase inhibitors (drugs, when used, AEs, contraindications)

• Acarbose, miglitol

• Inhibit alpha glucosidase enzymes in intestinal brush border, delaying carbohydrate breakdown and absorption

• Used for pts with elevated postprandial glucose, carbohydrate absorption needs to be slowed

• AEs: GI upset, transaminase elevation

• Contraindications: bowel disorders, renal/hepatic impairment, medication absorption impacts

Amylin/pramlintide (when used, AEs, contraindications)

• Pramlintide= amylin analog, injection

• Mimics amylin, normally co-secreted with insulin by pancreatic beta cells, decreases glucagon, slows gastric emptying, increases satiety

• Used for additional postprandial control in T1 or T2 diabetics

• AEs: nausea and vomiting, hypoglycemia

SGLT-2 inhibitors (drugs, when used, AEs)

• -gliflozins

• Block sodium-glucose cotransporter in the proximal renal tubule increasing urinary glucose excretion

• Used in T2DM with heart failure/chronic kidney disease, cause weight loss, lower blood pressure, low hypoglycemia risk

• AEs: yeast infections, UTIs, dehydration, hypotension, acute kidney injury, diabetic ketoacidosis

Pt presentation correlations just read

Pituitary adenomas

• Lactotroph: produces excess prolactin (MOST COMMON) → amenorrhea and galactorrhea, often microadenoma in premenopausal women

• Somatotroph: produces excess GH → acromegaly in adults, gigantism in children

• Corticotroph: produces excess ACTH → cushing disease

• Gonadotroph: produces excess FSH/LH → no distinct hormone-excess syndrome

Hypopituitarism

• Causes: nonfunctioning pituitary adenoma, ischemic necrosis, sheehan syndrone, empty sella syndrone, and inflammatory lesions, trauma or metastatic tumors

• Presentation: fatigue, weight loss, decreased libido, cold intolerance, anemia, infertility, menstrual irregularities/absent menstruation, loss of hair, failure to lactate

Diabetes insipidus (DI)

• Posterior pituitary disorder

  • Central= insufficient ADH production/release, causes excessive urination/dilute urine

  • Nephrogenic= ADH is present but kidneys are not responding appropriately to it

SIADH

Excess ASH release regardless of serum osmolality

• Causes water retention and dilutional hyponatremia

• Ectopic ADH production from small cell lung carcinomas can cause

Hyperthyroidism

• Findings: weight loss, tachycardia, heat intolerance, muscle weakness

• Primary= low TSH, high T4, secondary= high TSH, high T4

• Grave’s disease= most common cause, includes goiter and eye findings, IgG autoantibodies stimulate TSh receptor

Hypothyroidism

• Findings: weight gain, cold intolerance, lethargy, enlarged tongue

• Primary= high TSH, low T4, secondary= low TSH and T4

• Hashimoto= most common cause, autoantibodies interfere with thyroid function

• Causes cretinism in children

Thyroid tumors

• Follicular adenoma: benign encapsulated painless cold nodule

• Follicular carcinoma: capsular or vascular invasion, spreads to lungs and bones through blood

• Papillary carcinoma: most common thyroid cancer, nuclear grooves, pseudoinclusions, psammoma bodies, lymphatic spread, younger patients, radiation exposure

• Medullary carcinoma: c-cell origin, produces calcitonin, associated with MEN 2A and 2B

• Anaplastic carcinoma: aggressive, rapidly growing neck mass, typically found in older patients

Normal PTH actions

• Increases serum calcium (increases reabsorption in kidney and bone turnover)

• Decreases phosphate reabsorption in the kidney

• Increases vitamin D activation n kidney

Hyperparathyroidism

Primary:

• Inappropriately high PTH relative to serum calcium, most commonly caused by a parathyroid adenoma (can also be hyperplasia or carcinoma)

• Causes renal stones, bone abnormalities, neuromuscular symptoms, and hypercalcemia

• Shows high PTH and high calcium

Secondary:

• Increased PTH due to chronic hypocalcemia, most commonly associated with chronic renal failure or calcium/vitamin D deficiencies

• Kidney-related disturbance in calcium/phosphate/vitamin D drives increased PTH

Hypoparathyroidism/pseudoparathyroidism

• Caused by thyroid/neck sx, congenital absence of parathyroid glands, DiGeorge syndrome, or autoimmune disease

• Low calcium, high phosphate, low PTH

• Tetany, paresthesias, convulsions, laryngospasm, positive chvostek and trousseau signs, cataracts and dental abnormalities may occur

• pseudo: PTH is elevated but body is resistant to effects, high PTH, low calcium, high phosphate, short stature