endocrine Flashcards
thyroid hormone fxn
T4 = 90%, T3 = 10% of production, also calcitoninaffects almost all body tissuesmaintains metab stability by regulating O2 reqs & metabprotein synthesis & catabolism (if x hormone)temp regimpacts CHO metab: enhances epi to stim glycogenolysis & gluconeogenesisaffects lipid metabolism (accelerates degradation of LDL)↑s AV node depol to ↑ HR↑s resp drive, mental alertness, GI motility
when hypothalamus releases TRH x2
in resp to ↓ circulating T3 & T4cerebral cortex resp to ↓ body T or cold
TRH & TSH impact
- TRH: anterior pituitary → release TSH * TSH stimulates thyroid to release T3 & T4
thyroid hormones: secreted most vs active hormone
T4 secreted 90%unbound T3 is most active (90% from T4 deiodination)
hormone ↑ in primary hypothyroidism
TSH
hormone ↓ in primary hyperthyroidism
aka Graves DiseaseTSH
hormone ↑ in primary hyperthyroidism
FT4 (false if on heparin)T4
hormone ↓ in primary hypothyroidism
FT4T4
palpable thyroid nodules: mgmt
1. thyroid fxn tests (TSH, FT4, thyroid antibodies)#2. imaging – US (assess if more than 1 nodule, if it is a cyst or solid)#3. Fine Needle Aspiration bx
thinning of outer third of eyebrows sign of
hypothyroidism
primary vs secondary hypothyroidism
primary: gland dysfxnsecondary: pituitary or hypothalamus dysfxn (normal or ↓TSH)
most common cause of hypothyroidism
Hashimoto’s (autoimmune)- evidence of ab to thyroid ags
Hashimoto’s Thyroiditis
transient hyperthyroidism w/ an ↑in antibodies fol↓ed by hypothyroidism
Graves Disease
autoimmune disease w enlarged thyroid goiterthyroid eye disease (opthalmoptosis)↓TSH↑ T4 or Ft4↑ antithyroglobulin ab, alk phos, thyroid radioactive iodine uptake)hypercalcemia
hypothyroidism tx
Levothyroxine (Synthroid, Levoxyl)
Graves Disease tx
- inderal (Propranolol)- thiourea drugs: PTU, methimazole (Tapazole)- radioactive I- surgery
thiourea drugs
block synthesis of T3 & T4PTU, methimazole (Tapazole)call NP: fever, infection, agranulocytosis (abs neut count lt 500)
hypothyroidism: monitor & goal
TSH (barometer vs T4 for dx)maintenance dosage levothyroxine 100 - 200 ug/d
if thyroid replacement too rapid
↑HR, dyspnea, orthopnea, angina, palpitations, nervousness, insomnia
thyroid crises + s/s
myxedema or thyroid stormAMS, altered thermal reg, precipitating event/illness
- myxedema *
Severe HYPOTHYROIDISM- ↓ thyroid fxn + subsequent ↓T3 & T4 → alteration F/E - ↑ capillary permeability, fluid retention- non-pitting edema hands/feet- 50-80% mortality rate d/t hypercapnia & hypoventilation
- myxedema presenting s/s *
- resp depression, hypotension *stupor, coma, hypothermia
thyroid storm
Extreme form of HYPERTHYROIDISMMay be brought on by stressful illness or trauma, radioactive iodine, or thyroid surgery↑ mortality rate
- thyroid storm s/s *
- CV collapse *↑ feverSevere agitationConfusionResp distress if thyroid enlargedVomiting & Diarrhea
thyroid storm tx
Inderal (monitor carefully: HF)Thiourea Drugs (PTU, Tapazole)HydrocortisoneSodium Iodine (radioactive I) - 1 hr after Thiourea- goal: destroy thyroid parenchyma
adrenal layers - what secretes what?
outer: aldosteroneinner: cortisol
cortisol
major glucocorticoid, counters insulin → inhibits insulin secretion, ↑ hepatic gluconeogenesis
- ↑ skin pigmentation cardinal sign of *
Addison’s disease
Addison’s dx
Cosynthropin Stimulation Test → give ACTH (corticotropin) & check serum cortisol levels in 30 & 60 minutes,eval for plasmas cortisol rise, in Addison’s level ↓
Cosynthropin Stimulation Test
Addison’s dx test
Addison’s tx
replacement tx: mineralocorticoidsglucocorticoids- hydrocortisone- prednisone (alternate)- fludrocortisone
fludrocortisone
for insufficient salt retention during Addison’s, stimulates renal tubules to reabsorb Na/excrete K
adrenal crisis
acute adrenal insufficiencyresult of insufficient cortisol either from insufficient intake or ↑d need
- adrenal crisis s/s *
- hypotension s/t ↓ vascular tone (shock-like state), hyperpigmentation *HA, confusion, coma, n/v/d, abd pain, fever, dehydration
addison’s + infections
must be tx immediately & vigorously: ↑ hydrocortisone - w major stresses, surgery, trauma, ↑ dose, MediAlert bracelet!
adrenal crisis mgmt
hydrocortisone IV STAT3L bolus NS or D5NS over 2-3 hrtx precipitating factors & hypoglycemiaone resolved, determine degree of insufficiency - cosynthropin stimulation test
Cushing’s Sydrome causes x3
exces intake glucocorticoids (Prednisone)if spontaneous (rare):- excess ACTH by pituitary (70%)- lung cancer (SCLC = ectopic source, 15%)- adrenal tumor (15%)
Cushing’s tests x3
screening: 1mg dexamethasone (Decadron) @ 2300 + check serum cortisol @ 080024 hr urine test (cortisol & creatinine; cort/cr gt 95mcg = hypercort)suppression test (further testing)- give decadron, collect urine day 2- urine free cortisol gt 20 = Cushing’s
- the key to Cushing’s mgmt *
DETERMINE CAUSE/SOURCE- ACTH normal or ↓: ot pituitary- ACTH ↑ = Cushing’s
Cushing’s tx
treat the causetransphenoidal resection if pituitary tumor +/- radunilateral adrenalectomy + hydrocort replacement tx until remaining gland recovers
ADH
works in tubules: ↑ H2O reabsorptionreleased: serum Na ↑(hyperosmolar) or hypovolemiaunder influence of neural input (CNS) & baroreceptors in the chest
diabetes insipidus causes
familialpituitary or hypothalamus damagenephrogenic DI (inability of kidney to respond to vasopressin)
- DI dx *
- 24 hour urine ** vasopressin challenge: desmopressin (IN) = measure UOP & intake *clinical s/sMRI: pituitary tumor
DI tx
desmopressin (IN, PO, IV)mild: adeq fluid intake
SIADH s/s
- euvolemic & not osmolality dependent- hyponatremia- serum osm lt 280 mOsm/kg + inappropriate ↑ urine osm gt 900mOsm/kg- no cardiac, liver, lung dz- urine Na gt 20mEq/L- no edema or HTN bc ↑ H2O evenly distributed
SIADH causes
CNS structural (basilar skull fx) or metabolic disorderSCLC (ectopic source)drug induced: antidepressants (amitriptyline), carbamazepine, haloperidol, chlorproamide
SIADH tx
drug induced? dcmild-mod H2O intox? restrict fluid 800-1000 mL/daysevere hypoNa + neuro changes: 250 - 500 mL 3% NaCl over 2-4 hr and Lasix- avoid rapid correction d/t risk of demyelination of pons!
somogyi phenomenon + mgmt
morning REBOUND hyperglycemia & ketouria responding to NOCTURAL HYPOGLYCEMIA (stims counter-reg hormones)monitor: 3AM glucoses (expect ↓)tx: ↓ insulin qH 10% or + ↑ CHO @ qHS
dawn phenomenon + mgmt
AM fasting hyperglycemia, no sx nocturnal hypoglycemia Normal or ↑BG @ qHS blood glucose checkd/t circadian rhythm & release of growth hormone → ↑ BG btw 5 & 8AMtx: ↑qHS insulin 2-3 units
non-ketotic hyperglycemic hyperosmolar coma: serum osm 310 manifestation
lethargy & confusion
non-ketotic hyperglycemic hyperosmolar coma: serum osm 320 - 330 manifestation
coma
non-ketotic hyperglycemic hyperosmolar coma: dx
hyperglycemia 600+serum osm 310+pH 7.3+HCO3 15+anion gap lt 14
non-ketotic hyperglycemic hyperosmolar coma
partial/relative insulin insufficiency triggering gluconeogenesis but NOT ACIDOSIS= profound volume depletion (6-10 L) resulting in RENAL INSUFFIENCY = ↓ glucose excretion & contrib to ↑BGpoorly recognized until profound volume depletion
- cornerstone of non-ketotic hyperglycemic hyperosmolar coma therapy *
- FLUID REPLACEMENT! *- hypotn: NS 1-2L first hr- normotn: 0.45% NS 4-6L in 1st 8 hrs- glucose @~250 = D5W or D1/2NSgoals- glucose: 250-300 (↓ risk cerebral edema)- UOP 50cc +monitor for HF esp elderly
critically ill: target glucose
140 - 180monitor q 30 w 2 hr IV infusions
non-critically ill: target glucose
fasting lt 140random checks lt 180preferred insulin: scheduled SQ + basal, nutritional, correction components
basal insulin requirement
0.01 u/kg/hr