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primary vs. secondary hypothyroidism (problem with, labs)
primary- problem with thyroid gland itself (high TSH, low T4)
secondary- problem with pituitary gland (low TSH, low T4)
primary vs. secondary hypothyroidism causes
primary: Hashimoto’s, iatrogenic (thyroidectomy, radioactive iodine, external neck radiation)
secondary: brain/ pituitary (hypothalmic tumors, trauma, surgery)
Hashimotos lab confirmation
incr TSH, positive TPO antibodies
hypothyroidism symptoms
tired, weight gain, always cold, bradycardia
hypothyroidism management
levothyroxine, monitor TSH every 6 weeks
myxedema coma
severe hypothyroid
hypothermia, bradycardia, and altered mental status
hyperthyroidism primary vs. secondary (problem with, labs)
primary- problem with thyroid gland itself (low TSH, high T4)
secondary- problem with pituitary gland (high TSH, high T4)
hyperthyroidism primary vs. secondary causes
primary- Grave’s disease, toxic nodular goiter
secondary- pituitary adenoma
thyrotoxicosis without hyperthyroidism (what is it, causes)
excess thyroid hormones but glands itself aren’t producing them
causes: subacute thyroiditis, silent/ postpartum, amiodarone/ radiation-induced, exogenous hormone ingestion
thyrotoxicosis/hyperthyroidism symptoms (+ cardiac, elderly)
weight loss, incr appetite, feeling hot, jittery (nervous, palpitations), tachycardic, a-fib
*osteoporosis - elderly
Grave’s pathology & classic symptom
TSI (thyroid stimulating immunoglobinin) chronically stimuate TSH receptors
bulging eyes (exophthalmos), pretibial myxedema (orange-peel plaque on shins)
Grave’s dx confirmation
antibodies (TSI, TRAb)
Radioactive Iodine Uptake (RAIU) and Scan (diffuse uptake)
Color-Flow Doppler Ultrasound
thyroid storm symptoms & treatment
fever, tachycardia, CNS dysfunction (confusion)
tx: PTU, beta-blockers
elderly thyroid dysfunction symptoms
atypical- falls, CNS changes
pregnancy & TSH
First Trimester: <2.5 mIU/L.
Second and Third Trimesters: <3.0 mIU/L
may need 30–50% increase in their levothyroxine dose during pregnancy
primary hyperparathyroidism (causes, labs)
issue w/ parathyroid gland itself - parathyroid adenoma, hyperplasia
high PTH, high Ca, low/norm phosphate
primary hyperparathyroidism classic symptoms
"bones, stones, groans, and psychiatric overtones"
bone pain, kidney stones (nephrolithiasis), GI distress, and mood/ cognitive changes
secondary hyperparathyroidism (causes, labs)
CKD, vitamin D deficiency (chronically low Ca state- body tries to overcompensate)
high PTH, low/norm Ca, high phosphate
tertiary hyperparathyroidism (causes/ labs)
excess PTH after a very long-standing period of secondary hyperparathyroidism (end stage renal disease)
high PTH, high Ca, high phosphate
hypoparathyroidism (labs, causes)
low PTH, low Ca, high phosphate
post-surgical (parathyroid glands), autoimmune, genetic (DiGeorge)
chronic hypoparathyroidism symptoms
fatigue, cognitive decline, tingling and numbness, muscle weakness, dry skin
acute hypoparathyroidism symptoms
cramps, tetany, seizures, Chvostek’s & Trousseau’s
(severe drop in Ca)
pseudohypoparathyroidism (PHP)
low Ca, high PTH
end-organ resistance to PTH; short, obesity, mental retardation
primary adrenal insufficiency (cause, labs)
Addison’s disease
low cortisol (in morning), high ACTH —> hyponatremia, hyperkalemia
Addison’s classic symptoms
weight loss, fatigue, orthostatic hypotension, salt craving, GI distress
hyperpigmentation (palms, knuckles, oral mucosa)
secondary adrenal insufficiency (cause, labs)
steroid withdrawal
low cortisol, low/norm ACTH
adrenal crisis
(too low)
hypotension, shock, abdominal pain, fever
adrenal insufficiency/crisis treatment
hydrocortisone (glucocorticoids) + fludrocortisone (mineralcorticoids)
fluids, glucose correction
during rapid Na correction watch for
osmotic demyelination syndrome
Cushing’s syndrome vs. disease
syndrome: chronic cortisol excess
disease: specifically ACTH-producing pituitary adenoma
most common cause: steroid use
Cushing’s symptoms
central obesity, moon face, dorsocervical fat pad (buffalo hump)
easy bruising/ purple striae, thin skin
diagnostic lab to confirm Cushing’s
24hr urine free cortisol
overnight low-dose dexamethasone suppression test
late-night salivary cortisol
DM1
T-cell mediated destruction of pancreatic beta cells
absolute deficiency in insulinD
DM2
insulin resistance, progressive beta-cell dysfunction
gestational diabetes
hyperglycemia usually in 2nd/3rd trimester
placental hormones causing insulin resistance
hyperglycemia symptoms
polyuria, polydipsia (thirst), polyphagia (hunger), weight loss, fatigue
DM1 vs. DM2 presentation differences
DM1- early childhood/ adolescent, significant weight loss
DM2- weigh gaint, acanthosis nigricans and older age onset, often asymptomatic initially.
DKA (diabetic ketoacidosis)
+ketones, anion gap metabolic acidosis
severe dehydration, Kussmaul breathing, fruity breath, altered mental status
DM diagnosis
fasting plasma >126
HbA1c >6.5
random plasma glucose >200
2 hr glucose tolerance test (OGTT) >200
DM chronic complications, routine checking
microvascular- retinopathy, nephropathy, neuropathy
check kidneys (microalbuminuria), feet, retinal exams
macrovascular - stroke, CAD, peripheral artery disease
DM1 diabetes management
insulin replacement, glucose monitoring
DM2 diabetes management
lifestyle- weightloss, exercise
metformin - first-line
GLP1s, SGLT2/ DPP-4 inhibitors, eventually insulin
metabolic syndrome
insulin resistance, hypertension, dyslipedemia, central obsesity, Acanthosis Nigricans
>incr risk of CV disease/diabetes