Endocrine Flashcards
Hyperthyroidism info
more common in women 8:1. onset 20-40 years old.
Causes: Grave’s disease, toxic adenoma, subacute thyroiditis, TSH secretory pituitary tumor, high dose amiodarone
Hyperthyroid symptoms vs Hypothyroid symptoms
Hyper: nervous, anxious, sweating, fatigue, emotionally labile, fine tremor, hyperreflexia, increased appetite, weight loss, smooth/ warm/ moist skin, fine/thin hair, exophthalmos, lid lag, tachycardia, heat intolerance, increased a.fib
Hypo: extreme weakness, muscle fatigue, arthralgias, cramps, cold intolerance, constipation, weight gain, dry skin, hair loss, brittle nails, puffy eyes, edema of hands and face, bradycardia, slow DTRs,
Hypothyroidism info
primary disease of thyroid gland pituitary deficiency of TSH hypothalamus deficiency of TRH- thyrotropic releasing hormone iodine deficiency Hashimoto's thyroiditis idiopathic causes, damage to gland TX: thyroid supplementation Dx: check TSH
Hyperthyroid diagnosis & management
TSH assay- low
Serum T3, T4, thyroid resin uptake, free thyroxine index: all increased
T4 can be normal, but T3 elevated
thyroid radioactive iodine uptake and scan- high iodine uptake: Grave’s disease. low uptake: subacute thyroiditis.
Management: propranolol- symptomatic relief for subacute thyroiditis
thiourea drugs- for mild cases, small goiters (methimazole or propylthiouracil PTU). Radioactive iodine- destroy goiter. or thyroid surgery, requires thyroid supplementation afterwards
Hypothyroid diagnosis and management
TSH high T4 low or low normal T3 uptake- decreased (not reliable test) hyponatremia, hypoglycemia TX: Synthroid 50-100mcg daily until symptoms stabilize. > 60 years- decrease dosage.
Hyperthyroid crisis
PTU- propylthiouracil 150-250mg q6 hours OR methimazole 15-25 mg q 6 hours with lugol’s solution 10 drops TID, sodium iodide IV push 1gm and propranolol 0.5-2gm IV q 4 hours. or PO ever 6 hours with steroids
steroids: hydrocortisone 50 mg q 6 hours with rapid reduction as situation improves
avoid aspirin- will exacerbate the thyroid storm
Hypothyroid Crisis: Myxedema Coma
protect airway- mechanical ventilation likely needed
fluid replacement,
Synthroid IV 400mcg, then 100mcg every day
support hypotension
slow rewarming with blankets- avoid circulatory collapse
symptomatic care
Cushing’s Syndrome
Too much cortisol: ACTH hypersecretion by pituitary. adrenal tumors, chronic administration of glucocorticoids
Presentation: central obesity, moon face, buffalo hump, acne, purple striae, hirsutism, hypertension, weakness, amenorrhea, impotence, polyuria, polydipsia, diabetes, labile mood, frequent infections
Addison’s Disease
deficient in cortisol, androgens and aldosterone,
CAUSE: autoimmune destruction of adrenal gland. metastatic cancer, bilateral adrenal hemorrhage with anticoagulation therapy. pituitary failure resulting in decreased ACTH
Symptoms: hyperpigmentation in mouth and skin creases- nail beds, nipples, palmar creases, posterior neck
diffuse tanning and freckles, lack of pubic hair, armpit hair,
**orthostasis and hypotension, fever (acute), changes in consciousness (acute)
Cushing’s diagnostics and management
Labs: hyperglycemia, hypernatremia, hypokalemia, glucosuria, leukocytosis, elevated plasma cortisol in the mornings .dexamethasone suppression test to differentiate cause, serum ACTH elevated
TX: discontinue medications that cause (glucocorticoids), TSR of pituitary adenoma, surgical removal of adrenal tumors, manage electrolyte balance
Addison’s disease diagnosis and management
hypoglycemia, hyponatremia, hyperkalemia, elevated ESR, lymphocytosis, low plasma cortisol, cosyntropin simulation test- for Addison’s
TX: glucocorticoid and mineralocorticoid replacement: cortisol, androgen, aldosterone.: hydrocortisone, fludrocortisone (outpatient chronic management)
Inpatient tx: hydrocortisone IV with NS, replace volume with D%NS at 500cc/hour x 4 hours, then taper. vasopressors are ineffective for BP maintenance. treat underlying cause: sepsis.
SIADH vs DI
SIADH: water retention
DI: profound diuresis
SIADH causes and diagnosis
release of ADH independent of osmolality or volume dependent stimulation: due to tumor production of ADH or skull fractures/ head trauma, CNS disorder, chronic lung disease
Symptoms: hyponatremia- causes headache, seizures, coma
decreased DTRs, hypothermia, weight gain, nausea, vomiting, cold intolerance
DI causes and diagnosis
inadequate output of ADH pituitary hormone, or lack of response by kidney to ADH
Centra;: pituitary or hypothalamus- ADH deficiency- idiopathic, damage: surgery or trauma, infection, cancer
Nephrogenic: defect in renal tubule, familial X-linked trait, acquired d/t pyelonephritis, K depletion, sickle cell anemia, chronic hypercalcemia, medications
Psychogenic: refer
Symptoms: polydipsia, polyuria, weight loss, fatigue, AMS, dizziness, fever, tachy, hypotension, dehydration signs
SIADH diagnostic and management
euvolemic hyponatremia, decreased serum osm. increased urine osm. urine sodium? 20. renal cardiac and thyroid function normal.
Tx underlying cause, can restrict fluid intake if sodium low, especially if symptomatic. also hypertonic saline and Lasix if Na< 110. Monitor sodium and potassium losses hourly and replace
DI diagnosis and management
hypernatremia, elevated BUN/ creatinine, increased serum osm, decreased urine osm, decrease urine spec grav due to low concentrated urine.
Do Vasopressin challenge test- measure urine volume, positive result if Central DI, negative in nephrogenic DI.
MRI- look for mass
Treat hypernatremia> 150- D5W- replace 1/2 volume deficit in 12-24 hours- slowly lower- to avoid cerebral edema. when sodium < 150, substitute with 1/2 NS or NS
DDAVP IV or SQ every 12-24 hours for acute situations
Pheochromocytoma: definition and symptoms
sustained hypertension: tumor of adrenal medulla- excess catecholamine release: severe rare disease.
S/s: labile hypertension, diaphoreiss, hyperglycemia, severe headache, tremor tachy, weight loss, postural hypotension
pheochromocytoma: diagnostic and management
TSH normal.
24 hour urine collection: elevated metanephrine and VMA (vanillylmandelic acid) per creatinine ratio.
CT- confirm adrenal tumor
Tx: surgical removal or adrenal tumor
alpha adrenergic meds pre-op to reduce BP: phentolamine, IV. Phenoxybenzamine (PO)
Post-op watch for hypotension (tx with epi, NE), adrenal insufficiency, hemorrhage
Type 1 DM- what testing results common for diagnosis? what genetic predisposition?
human leukocyte antigens- HLA-DR3 or HLA-DR4; antibodies against glutamic acid decarboxylase are found in 80% of patients with Type 1
- Islet cell antibodies found in 90% of patients in the first year of diagnosis.
cause: result of infectious or toxic environmental insult to pancreatic B cells of genetically predisposed persons
DM Type I or II diagnostic criteria
fasting glucose > 126 mg/dl x2 occurrences.
random glucose >200 mg/dl with symptoms (polyuria, polydipsia and weight loss)
OR glucose > 200 within 2 hours of glucose load test or A1C > 6.5
What is the somogyi effect? what is the fix?
** this is considered disproven or rarely occurs. nocturnal hypoglycemia develops stimulating a surge of counter regulatory hormones which raise blood sugar. hypoglycemia at 0300 may rebound with an elevated 0700 glucose. Solution: reduce or omit the bedtime dose of insulin to avoid the hypoglycemia event
What is the Dawn phenomenon? what is the fix?
** this is more commonly accepted. hyperglycemia in morning means bedtime insulin is too low. “The Dawn is rising”. Results when tissue becomes desensitized to insulin nocturnally. blood glucose is progressively elevated throughout the night, resulting in elevated 0700 glucose. Solution: add or increase the bedtime dose. ** need continuous glucose monitoring or frequent monitoring to tell the difference between Dawn effect and Somogyi effect- opposite treatments.
Mechanism of Type 2 DM
tissue insensitivity to insulin. insulin secretory defect; resistance and/or impaired insulin production
Why is DKA not common in DMII?
there is enough circulating insulin to prevent ketoacidosis- but not enough to meet the body’s insulin needs
What are criteria for metabolic syndrome? (5)
Meet any 3 out of the 5 criteria
- Waist circum> 40 inches (Men) and >35 inches (women)
- BP > 130/85 (hypertension)
- Triglycerides > 150
- FBG >100
- HDL <40 men and < 50 in women
What is women specific symptom for DM II presentation?
Vaginitis because of glucosuria.
What is biguanide class of DM drugs?
Metformin- 1st line- old drug, cheap, effective. 250-1000mg BID
many have intolerable GI side effects: cramping, flatus,
mechanism: lower basal and postprandial glucose levels by affecting glucose absorption and hepatic gluconeogenesis
What is black box warning for metformin?
Lactic acidosis (severe muscle pain)- the reduction of LDL may cause lactic acidosis- caution patients against excessive alcohol ingestion. also discontinue 1-2 days before receiving IV iodine contrast
What are GLP-1 agonists? - names, MOA, black box warning
Trulicity- subQ weekly, Victoza (liraglutide) Semaglutide (Ozempic sub Q) semaglutide (tablet)
Mimic endogenous incretin glucagon-like peptide-1; stimulate glucose dependent insulin release, reduce glucagon, slow gastric emptying
Exenatide- has fewer GI side effects- SQ
Liraglutide- once daily
all drugs may cause GI upset
Black box: thyroid cancer
What are the management principles of DKA?
ABCs- protect airway, administer oxygen there can be altered LOC and Kussmaul’s breathing which are threat to airway.
NS fluid bolus. if glucose > 500, use 1/2 NS after first hour as water deficit exceeds sodium loss. when glucose < 250, change to D51/2 NS to prevent hypoglycemia. don’t correct sodium level- will be corrected - dilutional hyponatremia observed.
correct acidosis with bicarb drip, don’t treat initial hyperkalemia- will correct with glucose and insulin restoration.
insulin drip- goal 10% reduction within first hour
hourly urine output monitoring.
What are management principles of HHNK?
airway protection, oxygen.
NS fluid bolus. if glucose > 500, use 1/2 NS after first hour as water deficit exceeds sodium loss. when glucose < 250, change to D51/2 NS to prevent hypoglycemia (same as DKA)
insulin drip goal 10% reduction within first hour
supportive care
What are differences with management of DKA vs. HHNK?
many similarities- airway protection, fluids, insulin.
DKA- management of the acidosis with bicarb and a lot more electrolyte correction/ monitoring: hyponatremia, hyperkalemia.
HHNK- glucose is a lot higher initially so will take longer for the insulin drip to bring down the patient.
