Acute Endo Flashcards
Endocrine Organs
-Hypothalamus
-Pineal
-Pituitary Gland
-Thymus gland
-Thyroid gland
-Parathyroid gland
-Adrenal gland
-Ovaries
-Testes
Pituitary Gland (hormones of the anterior lobes)
-Adrenocorticotropic hormone (ACTH)
-Follicle stimulating hormone (FSH) & Luteinizing hormone (LH)
-Growth hormone (GH)
-Prolactin (PRL)
-Thyroid stimulating hormone (TSH)
-Oxytocin
-Antidiuretic Hormone (ADH)/Vasopressin
Adrenocorticotropic hormone (ACTH)
Regulates cortisol production from the adrenal gland
Follicle stimulating hormone (FSH) & Luteinizing hormone (LH)
-Regulates estrogen/progesterone production from the ovaries, ovulation during LH surge
-Regulates testosterone production, spermatogenesis from the testes
Growth hormone (GH)
Stimulates linear growth in children
Affects many other tissues – bone, muscle, fat, etc.
Prolactin (PRL)
Responsible for milk production during lactation
Thyroid stimulating hormone (TSH)
Regulates secretion of thyroid hormones (T4, T3) from the thyroid gland
Antidiuretic hormone (ADH)/vasopressin
Regulates retention of water in the body at the level of the kidney
Oxytocin
-Causes contractions during the 2nd and 3rd stages of labor
-Acts on the mammary glands during lactation
Pituitary Feedback Loops
-both ACTH and cortisol levels should be normal.
-Primary: dysfunction of the endocrine gland itself
-Secondary: dysfunction of the pituitary gland
Thyroid Gland
-Controls the burning of energy that directs the body’s metabolism
-Thermogenic regulation
-Thyroid hormones
TSH
T4
T3
Parathyroid Gland
-Four small glands on the posterior aspect of the thyroid gland
-Secrete parathyroid hormone (PTH), cause serum calcium levels to rise
*Osteoclast stimulation
*Increased renal resorption of calcium
*Increased GI absorption of calcium
Pancreas
-Exocrine function-produce enzymes to assist with the digestion of food
-Endocrine function – regulate blood glucose
-Islet of Langerhans
Alpha cells: Glucagon (to increase BG)
Beta cells: Insulin (to decrease BG)
Delta cells: Somatostatin (reduce acid secretion)
Adrenal Glands
-Two glands that sit directly above the kidneys
-Adrenal cortex
-Adrenal medulla
Adrenal Cortex: Adrenal Gland
-Zona glomerulosa-mineralocorticoids (aldosterone)
-Zona fasciculata -glucocorticoids (cortisol)
-Zona reticularis -androgens
Adrenal Medulla: Adrenal Gland
-Catecholamines
Cortisol
-Released by the adrenal gland in the adrenal cortex-zona fasciculata
-Glucocorticoid
-Glycogenolysis (breaks down glycogen to glucose and byproduct), resulting in gluconeogenesis
-Anti-stress and anti-inflammatory
-Stress raises levels
-ACTH from the pituitary controls the production of cortisol
Aldosterone
-Adrenal Cortex hormone-Zona glomerulosa-mineralocorticoids
-RAAS system
-Increased renal absorption of sodium-water retension
Androgens
-Adrenal cortex hormone-Zona reticularis
-Small amounts secreted
-Sex characteristics
Adrenal Insufficiency
-Deficient in cortisol
-Primary adrenal insufficiency/Addison’s Disease
-Secondary Adrenal insufficiency
Primary Adrenal Insufficiency: Addison’s Disease
-Destruction of the adrenal glands deficiency of glucocorticoids and mineralocorticoids
-Most common cause in the US: Autoimmune (80%)
-Most common worldwide: TB
-Bilateral adrenal disease (adrenal hemorrhage, cancer, trauma, etc.)
-Hyperpigmentation, Salt cravings
Secondary Adrenal Insufficiency
-Pituitary dysfunction deficiency of glucocorticoids ONLY
-Most often caused by withdrawal of exogenous steroids
-Others: pituitary issues, opioids, etc.
**much more common
S/S of Adrenal Insufficiency
Chronic (nonspecific)
-Fatigue, n/v, dizzy, weakness, weight loss, joint pain, diarrhea, amenorrhea, hypoglycemia
Acute
-Usually with unrecognized AI and concomitant illness, Addisonian crisis, dehydration, hotn, acute abdomen, AMS, eosinophilia, hyponatremia, hypokalemia, unexplained fever
Adrenal Insufficiency Testing
-ACTH
-Cortisol (Avoid checking cortisol in patients on > 5 mg equivalent of prednisone – should be low)
-Primary AI: Na/K, Renin
Cortosyn stimulation test
-Primary AI-No response to synthetic ACTH.
-Secondary AI: inadequate response, but may be normal
Adrenal Insufficiency Treatment
-Glucocorticoid replacement
——-1st line: Hydrocortisone 15-25 mg/day divided 2-3x/day, largest dose in morning (mimics endogenous cortisol), short 1/2 life
——-Prednisone 4-5mg daily as an alternate
Mineralocorticoid replacement
——-Primary adrenal insufficiency only
——-Fludrocortisone 0.05-0.2 mg daily
Adrenal Insufficiency Stress Dosing
-Double/triple PO dose of glucocorticoid only x 3 days during illness
-IM steroid to have at home for emergencies (IM dex 4 mg, solu-medrol 40 mg, solu-cortef 100 mg)
*Unsure they have AI by suspicious—stress dose
—Don’t check cortisol after administering hydrocortisone (will be high) or after high dose dex/methylpred (will be low)
Adrenal Disorder: Addisonian Crisis
-Don’t delay treatment if suspected
-2-3 liters of NS IVF or D5 NS if hypoglycemic
-High dose steroids (Hydrocortisone 100mg IV bolus or dexamethasone 4 mg IV bolus, then hydrocortisone 50 mg IV q6-8h–taper doses over 1-3 days)
-Frequent vitals and lytes monitoring
-Treat underlying issues
-Mineralocorticoid replacement is not needed
Adrenal Disorder: Cushing Syndrome
-Syndrome of excess cortisol
-MOST COMMON cause: glucocorticoid administration (exogenous)
–Endogenous (rare)-ACTH-dependent or indepenent-tumor
* too much ACTH or too much cortisoL
Cushing Syndrome s/s
Weight gain (abdomen), extremity wasting, buffalo hump, straie on abdomen, muscle weakness, easy bruising, thinning skin, supraclavicular fullness, acne, hirsutism, osteopenia/osteoperosis, worsening DM, HTN, hypogonadism, emotional liablity
Cushing’s Syndrome Workup
-Difficult, multiple tests
-24-hour urine for cortisol
-AM/PM cortisol
-ACTH
-Dexamethasone suppression test
-IPSS
-MRI head, CT abdomen… etc.
Cushing Syndrome Tx
Look for underlying cause & treat it
Treat comorbidities!
HTN
DM
Osteoporosis
Florid Cushing’s – Mifepristone, ketoconazole?
Pheochromocytoma
Catecholamine producing adrenal tumor
Pituitary Disorders: SIADH
-(Syndrome of Inappropriate Antidiuretic Hormone) is a common cause of hyponatremia
-results when ADH secretion is not suppressed by plasma sodium concentrations below osmotic threshold (excessive secretion of ADH)
-Classified as a euvolemic, hypo-osmolar hyponatremia (urine osmolality > serum osmolality)
SIADH Etiology
-Tumor-Lung cancer, GI tract cancers, lymphoma, thymic
-CNS-brain tumors, head trauma, meningitis, encephalitis, abscess, SAH, SDH
-Meds: DDAVP, SSRIs, TCAs, NSAIDs, colchicine, thiazide diuretics, carbamazepine, cyclophosphamide, tramadol, opiates
-Pulmonary-TB, pneumonias, COPD
-MS, GB, HIV
SIADH Symptoms
-Speed of hyponatremia determines severity
-Severe
Coma, seizures, brain herniation, cerebral edema
-Others: HAs, gait disturbances, anorexia, fatigue, cognitive abnormalities
Criteria for Dx of SIADH
-Decreased plasma osmolality (< 280)
-Inappropriate urine concentration (urine osmolality > 100)
-Clinical euvolemia
-Elevated urinary sodium excretion (> 40 mmol/L)
-Rule out hypothyroidism, adrenal insufficiency, diuretic use, impaired cardiac or renal function
SIADH Tx
Chronic
-May not need treatment if sodium > 130
-Treat underlying conditions
-Fluid restriction of < 800-1000 mL/day
-Oral salt/high solute intake
-Possibly use oral urea, demeocycline, vasopressin receptor antagonists
Acute
-IV hypertonic saline 3%, bolus or infusion
-Don’t correct Na too quickly-4-6 mEq/L increase in plasma Na over several hrs
Pituitary Disorders: Diabetes Insipidus
No secretion of or no response to ADH
-Central/hypothalamic (more common): head trauma/surgery, inherited, tumors, sarcoidosis, metastases, granulomatous disease
-Nephrogenic: kidneys do not respond to ADH
S/S of DI
Polyuria (> 4-5 L/day)
Polydipsia (2-20 L of fluid/day)
Inability to concentrate urine
DI Workup
-Hypernatremia with high serum osmolality
-Low urine osmolality
-Water deprivation test (outpatient)
-Desmopressin challenge
-Head MRI
DI Tx
-Underlying cause if possible
-Desmopressin (nasal spray, tablets, IV) is first line for central DI
-Caution – don’t over treat!
? IV steroids
-Drink to thirst
-Nephrogenic: Diuretic (HCTZ, amiloride), NSAID (indomethacin)
Pituitary Disorder: Acromegaly
Syndrome of growth hormone excess after fusion of the epiphyses
Thyroid Disorders: Hyperthyroidsim
-Syndrome of excess thyroid hormone
-Hypersecretion of T4 and T3
-Low TSH (Hypopituitarism patients always have low TSH – check T4)
Hyperthyroidism Etiology
-Graves’ disease (most common)
-Toxic adenoma
-Plummer’s disease (toxic multinodular goiter)
-Thyroiditis
Graves Disease
is autoimmune – antibodies causing hypersecretion of thyroid hormone.
-Smoking makes this worse
Hyperthyroidism S/S
-Hyperactivity
Irritability or nervousness
Palpitations, Fatigue
Weight loss despite normal appetite, Diarrhea or more frequent bowel movements
Polyuria, Heat intolerance
Menstrual dysfunction
Eye symptoms
-Tachy, afib, enlarged thyroid gland, tremors, thinning of hair & skin, hyperreflexia, exophthalmos, pretibial myxedema, mucsle weakness, warm/dray skin
Workup for Hyperthyroidism
-TSH
-Free T4
-Total T3
-Thyroid autoantibodies (Graves’): TrAB, TSI
-Imaging
Ultrasound highly vascular, diffuse, enlarged gland
Hyperthyroidism Tx
-Ablation of thyroid tissue w/RAI
-Surgery
-Anti-thyroid medications
Methimazole: start 10-30 mg/day
PTU: start 150-400 mg/day (3 divided doses/day)
-Can use beta blockers (propranolol) to prevent arrhythmia and thyroid storm
Subacute Thyroiditis
-Also known as painful thyroiditis or de Quervain’s thyroiditis
-Typically occurs after common cold/viral infections, and usually only ONCE
Treatment
-NSAIDs +/- analgesics
-Glucocorticoids as second line (pred 40-60 mg daily for several weeks and taper based upon response)
Drug Induced Thyroiditis: Amioderone
-Contains a large amount of iodine
-Long half time (~100 days)
-Often masked as the beta blocking activity of amiodarone minimizes symptoms
-Arrhythmias
-Exacerbated IHD or HF
-Weight loss
-Restlessness
-Fever
AIT
Type 1 methimazole 30-40 mg daily
Type 2 prednisone 40-60 mg daily
D/c on slow taper, outpatient follow-up
Thyroid Storm
-Emergency!!
-Deadly hypermetabolic state
-Causes: trauma, major stress, infection, thyroid surgery, uncontrolled DM, antithyroid drug OD, pregnancy, abrupt withdrawal of antithyroid medications
Thyroid Storm S/S
Think of the s/sx of hyperthyroidism x 10
Fever
Flushing
Excessive diaphoresis
Seizure
Arrhythmias/tachycardia
Hyperglycemia
Jaundice
Diarrhea
Vomiting
Thyroid Storm Tx
-Antithyroid meds: PTU, Methimazole
-Propranolol
-Glucocorticoids
-Thyroid inhibitors: Iodine, SSKI, Lugols solution
-Decrease stimuli
-Antipyretics
-Possible bile acid sequestrants
-DON’T GIVE ASA-interferes with binding T4
-Thionamide blocks new hormone synthesis
Hypothyroidism
-Elevated TSH, low T4
-Hashimoto’s (autoimmune) most common cause
-Subclinical hypothyroidism
Elevated TSH, normal T4
Often seen in setting of recent illness
Recheck 4-6 weeks
–Levothyroxine tx
Hypothyroidism S/S
Fatigue
Dry skin
Cold intolerance
Constipation
Weight gain
Hair loss/alopecia
Bradycardia
Carpal tunnel-like symptoms
Hyporeflexia
Myxedema Coma
-Severe hypothyroidism
-Emergency
-Most common in elderly & women
-Hallmark s/s: decreased LOC and hypothermia
Myxedema Coma: s/s
Hotn, Bradycardia
Hyponatremia, Hypoglycemia
Hypoventilation
Puffiness of hands and face
Thickened nose, Swollen lips
Enlarged tongue
Causes of Myxedema Coma
-Long term non-compliance with meds
-MI
-Opioids
-Infection
-Cold temperature exposure
-Check TSH, T4, Cortisol
Myxedema Coma Tx
-Supportive care
-T4 & T3 combos-IV as slow bolus
-T4 (200-400 mcg IV flw by daily 50-100 mcg IV until POs)
-T3: 5-20 mcg IV flw by 2.5-10 mcg q8h)
-Glucocorticoids until AI has been excluded
Sick Euthyroid Syndrome/Acquired Transient Central Hypothyroidism
-Don’t check thyroid function in ICU unless there is STRONG suspicion of thyroid dysfunction
-Generally advised against treatment with thyroid hormone if no history of underlying thyroid disorder
-Recommend checking outpatient 1-2 weeks post-hospitalization
Parathyroid/Calcium Disorder: Hyperparathyroidism
-Common: W>M
-Most common cause of hypercalcemia in ambulatory setting
-Causes:
Primary-85% due to benign parathyroid adenoma (most often one)
Secondary-CKD (most common), vitamin D def
Tertiary-Advanced-prolonged CKD causing parathyroid hyperplasia
Other causes of hypercalcemia
-PTHrP production by tumors, neoplasms, sarcoidosis, TB, Vit D toxicity, thiazides, vit A, aluminum toxicity, Pagets, hypophosphatemia
Hyperparathyroidism S/S
Most asymptomatic
-Classical
Bones, stones, groans, moans”
General/neuromuscular
Bones
Renal Nephrolithiasis
Neuropsychiatric
Gastrointestinal
CVD
Hyperparathyroidism Workup
-Elevated Ca fund on routine screening-fasting? Repeat
-High Ca
-Low phos
-24 hr urine Ca + creatnine
-Vit D low
-Albumin-40-45% of Ca is bound to albumin
Hyperparathyroidism Tx
-Mild asymptomatic-observe
-Parathyroidectomy
-Severe HyperCa-albumin corrected Ca–Ionized Ca
-IV hydration: Isotonic
-Calcitonin
-Add bisphonates
-HD
Parathyroid/Calcium Disorder: Hypoparathyroidism
-Low PTH causing hypocalcemia and hyperphos
-Uncommon-from parathyroidectomy and/or thyroidectomy
-Other causes: PGA type 1, heavy metal toxicity, DiGeorge syndrome
Hypoparathyroidism S/S & Dx
-Tetany: Chvostek’s sign, Trousseau sign
-Low PTH, Ca
-High Phos
-albumin
-Check vit D
-Mag may be low
-EKG prolonged QT, T wave abnormalities
Hypoparathyroidism Tx
-Correct hypoCa-
-Ca gluconate in severe cases
-Treat other abnormal lytes
Osteoporosis
-Disorder of low bone mass, microarchitecural disruption, and skeletal fragility
-Dexa Scan
-Smoking cessation, limit alcohol, fall prevention, weight bearing exercises
-Vit D and Ca
-Bisphosphantes-1st line
-2nd line: Antiresorptive/RANKL inhibitor, estrogen
Dexa Scan
-Tscore:
-1.0 to -2.4 osteopenia
-2.5 or less osteoporosis
Z-score: age-matched comparison
Z score < -2.0. Diagnosis of low bone density for age (< 50)
Use FRAX calculator
