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Endocrine Flashcards

1
Q

thyroid axis

A

thyrotropin-releasing hormone TRH (hypothalamus) –>
TSH (pituitary) –> T3/T4 (thyroid)

  • Neg Feedback: if thyroid hormone levels become too high, they inhibit secretion of both TRH (hypothal) and TSH (pituitary)
  • Pos Feedback: low blood levels of T3/T4 are sensed by hypothalamus –> inc TRH –> inc release of TSH
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2
Q

adrenal axis

A

corticotropin-releasing hormone CRH (hypothalamus) –>
adrenocorticotropic hormone ACTH (pituitary) –>
cortisol (adrenal gland)

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3
Q

sex hormones axis

A

gonadotropin-releasing hormone GRH (hypothalamus) –>

FSH + LH (pituitary) –> estrogen, progesterone + some testosterone (ovaries) + testosterone (testes)

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4
Q

tertiary disorder

A

HYPOTHALAMUS IS THE PROBLEM

-LABS IN SAME DIRECTION

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5
Q

secondary disorder

A

PITUITARY IS THE PROBLEM
-LABS IN SAME DIRECTION

  • pituitary adenoma:
  • inc TSH + inc T4/T3
  • inc ACTH + inc cortisol

-hypopituitarism - low pituitary hormones and low target organ hormones (both low)

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6
Q

primary disorders

A

TARGET ORGAN IS THE PROBLEM
-LABS IN OPPOSITE DIRECTIONS

  • thyroid:
  • graves, toxic goiters, toxic adenoma: inc T4/T3, dec TSH
  • hashimoto’s, thyroiditis: dec T4/T3, inc TSH
  • adrenal:
  • addison’s: dec cortisol + inc ACTH
  • adrenal adenoma: inc cortisol + dec ACTH
  • ovaries:
  • menopause: dec estrogen + inc FSH/LH
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7
Q

thyroid function tests

A

TSH - BEST THYROID FX SCREENING TEST

Free T4 - FREE THYROXINE, ordered when TSH abnormal to determine hyper/hypo

  • elevated TSH, low FT4 = PRIMARY HYPO
  • elevated TSH, normal FT4 = SUBCLINICAL HYPO
  • elevated TSH, high FT4 = TSH MEDIATED HYPER (2/3ry)
  • low TSH, low FT4 = 2ry/3ry HYPO (RARE)
  • low TSH, normal FT4 = SUBCLINICAL HYPER
  • low TSH, high FT4 = PRIMARY HYPER, THYROTOXICOSIS

Thyroid AB
-ANTI-THYROID PEROXIDASE AB, ANTI-THYROGLOBULIN AB –> DX HASHIMOTO’S OR AUTOIMMUNE

-THYROID STIMULATING AB –> GRAVE’S DZ

Free T3 - serum triiodothyronine
-useful to dx hyperthyroidism when TSH is low and T4 normal

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8
Q

thyroid - radioactive iodine test (RAIU)

A

diffuse uptake –> grave’s dz or TSH-secreting pituitary adenoma

decreased uptake –> thyroiditis (hashimotos, postpartum, dequervain)

hot nodule –> toxic adenoma

multiple nodules –> toxic multinodular goiter

cold nodule –> r/o malignancy

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9
Q

subclinical hypothyroidism

A

inc TSH, normal T4/T3

-tx- LEVOTHYROXINE IF SX (pt devo hyperlipidemia, hypothyroid sx, TSH >20)

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10
Q

HYPOthyroid

A

-sx- weight gain, cold intolerance, dry skin, hair loss (outer eyebrow), goiter, nonpitting edema, fatigue, memory loss, dec DTR, constipation, bradycardia, menorrhagia, hypoglycemia

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11
Q

HYPERthyroid

A

-sx- weight loss, inc app, heat intolerance, warm, moist, skin, easy bruising, hyperactive, anxiety, tremors, diarrhea, tachy, palpitations, high output heart failure, scant periods, hyperglycemia

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12
Q

cretinism

A

CONGENITAL HYPOTHYROIDISM due to maternal hypothyroidism or infant hypopituitarism

  • sx- macroglossia, hoarse cry, coarse facial features, umbilical hernia, weight gain
  • mental devo abnormalities if not corrected

-tx- LEVOTHYROXINE

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13
Q

euthyroid sick syndrome

A

abnormal thyroid hormone levels w/ normal thyroid function seen w/ NONTHYROIDAL ILLNESS (surgery, malignancies, sepsis, heart dz)

  • DEC FREE T3/T4, DEC TSH (T3 abnormally low)
  • INCREASED REVERSE T3
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14
Q

thyroid storm (thyrotoxicosis crisis)

A

POTENTIALLY FATAL COMPLICATION OF UNTREATED THYROTOXICOSIS USUALLY AFTER A PRECIPITATING EVENT (surgery, trauma, infx, illness, pregnancy)
-RARE (1-2% w/ hyperthyroid, high mortality 75%)

  • sx- HYPERMETABOLIC STATE: PALPITATIONS, TACHY, A-FIB, HIGH FEVER, N/V, PSYCHOSIS, TREMORS
  • dx- INC FREE T3/T4, DEC TSH (may be undetectable)

Treatment is:

1) beta blocker (propranolol)
2) thionamide (propylthiouracil or methimazole)
3) iodine solution
4) glucocorticoids (supportive - inhibits peripheral conversion of t4 to t3 and impairs thyroid hormone production)
- AVOID ASPIRIN (causes increased T3/T4)

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15
Q

myxedema crisis

A

EXTREME FORM OF HYPOTHYROIDISM
-MC IN ELDERLY WOMEN W/ LONG STANDING HYPOTHYROIDISM IN WINTER

  • patient will have acute precipitating factor (infx, CVA, CHF, sedative/narcotics) AND undiagnosed HYPO, noncompliance w/ HYPO meds
  • patient will show severe signs of HYPO: BRADYCARDIA, obtunded, hypothermia, hypoventilation, HYPOGLYCEMIA, HYPONATREMIA, HYPOTN

-labs will look like HYPO –> inc TSH, dec T4/T3

  • tx- IV LEVOTHYROXINE (give even w/ high suspicion)
  • ICU ADMIT, treat underlying, PASSIVE WARMING
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16
Q

grave’s disease

A

AUTOIMMUNE - MC CAUSE HYPERTHYROID
-TSH receptor AB cause inc thyroid hormones + thyroid growth (worse w/ stress like illness, pregnancy)

-patient will be female, with enlarged thyroid, clinical hyperthyroid sx, THYROID BRUITS, EXOPHTHALMOS/PROPTOSIS, PRETIBIAL MYXEDEMA (nonpitting, edematous pink to brown plaques/nodules shin)

-labs will show + THYROID-STIM IMMUNOGLOBULINS AB,
maybe thyroid peroxidase and anti-TG-AB
-inc T3/T4, dec TSH
-RAIU: DIFFUSE UPTAKE

  • MC therapy: RADIOACTIVE IODINE + HORMONE REPLACE
  • METHIMAZOLE OR PROPYTHIOURACIL (PTU)
  • BB for symptoms
  • Thyroidectomy if radioactive iodine c/i (pregnancy)

*PTU PREFERRED IN PREGNANCY, ESP 1ST TRIMESTER

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17
Q

toxic multinodular goiter (plummer’s disease)

OR toxic adenoma (one nodule)

A

autonomous functioning nodules
toxic adenoma - one autonomous functioning nodule

  • patient will be ELDERLY, with clinical hyperthyroidism, diffusely enlarged thyroid, NO SKIN/EYE CHANGES, +/- palpable nodules
  • COMPRESSIVE SX: DYSPNEA, DYSPHAGIA, STRIDOR, HOARSENESS
  • labs will show inc T3/T4, dec TSH
  • RAIU: PATCHY AREAS OF INC AND DEC UPTAKE or HOT NODULE (in TA)
  • TX RADIOACTIVE IODINE
  • surgery if compressive symptoms
  • METHIMAZOLE OR PROPYTHIOURACIL (PTU)
  • BB for symptoms
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18
Q

TSH secreting pituitary adenoma

A

autonomous TSH secretion

-patient will have clinical HYPERthyroidism, diffusely enlarged thyroid, BITEMPORAL HEMIANOPSIA, mental disturbances

  • labs: INC T3/T4 AND TSH (SAME DIRECTION)
  • RAIU: DIFFUSE UPTAKE
  • MRI shows adenoma

-TRANSPHENOIDAL SURGERY TO REMOVE ADENOMA

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19
Q

hashimoto’s thyroiditis

A

autoimmune (chronic lymphocytic)

-patient will have clinical HYPO, painless, enlarged thyroid

  • labs: +THYROID AB: THYROGLUBULIN AB, ANTIMICROSOMIAL & THYROID PEROXIDASE AB
  • DEC T3/T4, INC TSH

-LEVOTHYROXINE

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20
Q

silent thyroiditis OR postpartum thyroiditis

A

autoimmune (+/- temporary)

-patient will have painless, enlarged thyroid
THYROTOXICOSIS –> HYPOTHYROID (depends on when they present)

  • labs: +THYROID AB
  • TFTs: hyper or hypo (depends on when present)
  • RAIU: decreased uptake
  • 80% return to euthyroid state w/in 12-18 mo w/out treatment
  • ASPIRIN
  • NO ANTI-THYROID MEDS
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21
Q

de Quervain’s throiditis (granulomatous)

A

MC POST-VIRAL or inflam rx

-patient will have PAINFUL, TENDER NECK/THYROID, CLINICAL HYPERTHYROID (thyrotoxicosis –> hypothyroid) present at w/ Hyper sx bc of neck pain

  • labs: INC ESR, NO THYROID AB
  • TFTs: USUALLY HYPER
  • decreased uptake RAIU
  • most return to euthyroid state w/in 12-18 mo w/out treatment
  • ASPIRIN
  • NO ANTI-THYROID MEDS
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22
Q

med induced thyroiditis

A

AMIODARONE (contains iodine)
LITHIUM
ALPHA INTERFERON

thyrotoxicosis –> hypothyroid
-often returns to euthyroid when med stopped

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23
Q

acute thyroiditis (suppurative)

A

MC STAPH AUREUS

  • patient will have PAINFUL, FLUCTUANT THYROID, appear ill, FEBRILE
  • labs: inc WBC, left shift
  • abx; I+D if abscess
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24
Q

Riedel’s thyroiditis

A

FIBROUS thyroid

FIRM, HARD, “WOODY” NODULE, may devo HYPO

+/- surgery

25
Q

MC cause of hypothyroidism

A

in US: hashimoto’s

in world: iodine deficiency

26
Q

thyroid nodules

A

RF: extremes of age, history of head/neck irradiation

  • 90% in women are benign (papillary ca mc women)
  • most found in children or men are malignant
  • sx- most asymptomatic, +/- compressive symptoms
  • if functional (rare) –> +/- thyrotoxiciosis
  • exam: benign nodules vary (smooth, firm, irregular, discrete, painless) MALIGNANT: RAPID GROWTH, FIXED, NO MOVEMENT W/ SWALLOW
  • most patients euthyroid
  • dx- FINE NEEDLE ASPIRATION W/ BX BEST TO EVAL
  • Radioactive Iodine Uptake Scan (if FNA +/-) –> COLD NODULES ARE HIGHLY SUSPICIOUS FOR MALIG
  • ultrasound
  • tx- SURGERY IF CANCER SUSPECTED (or indeterminate FNA w/ cold scan) –> total vs partial thyroidectomy
  • OBSERVATION OF NODULES Q6-12MO W/ US

-FOLLICULAR ADENOMA MC TYPE OF THYROID NODE

27
Q

thyroid cancer

A
  • about 5% nodules malignant
  • INC SUSPICION IN PT <20, COLD NODULE ON RAIU
  • most patients are euthyroid
  • PAPILLARY + FOLLICULAR ARE WELL DIFFERENTIATED (BETTER PROGNOSIS), ANAPLASTIC POORLY DIFF (WORSE PROGNOSIS)
  • PAPILLARY - 80% MC TYPE
  • MC AFTER RADIATION EXPOSURE, YOUNG FEMALES
  • LEAST AGGRESSIVE; CERVICAL METS COMMON, DISTANT METS UNCOMMON
  • HIGH CURE RATE
  • tx- surgery: total vs partial (w/ radioiodine therapy +/- thyroid suppression)
  • FOLLICULAR - 10%
  • inc w/ iodine deficiency; mc 40-60yo
  • more aggressive but slow-growing
  • DISTANT METS COMMON (LOCAL LESS COMMON)
  • HIGH CURE RATE
  • tx- surgery: total vs partial (w/ radioiodine therapy +/- thyroid suppression)
  • MEDULLARY 10%
  • MC W/ MEN2 (NOT ASSOC W/ RADIATION)
  • MORE AGGRESSIVE - ARISES FROM PARAFOLLICULAR CELLS - SECRETE CALCITONIN
  • local cervical lymph node involved early, distant mets occur late
  • poorer prognosis - don’t take up iodine
  • tx-TOTAL THYROIDECTOMY + NECK DISSECTION (LYMPH NODES AND FATTY TISSUE)
  • CALCITONIN LEVELS USED TO MONITOR
  • ANAPLASTIC <5%
  • may occur years after radiation exposure
  • MC MALES >65
  • MOST AGGRESSIVE - RAPID GROWTH +/- COMPRESS
  • MAY INVADE TRACHEA, local + distant mets
  • POOR PROGNOSIS (most don’t live 1 yr after dx)
  • MOST NOT AMENABLE TO SURGICAL RESECTION –> radiation, chemo, +/- PALLIATIVE TRACHEOSTOMY
28
Q

calcium

A
  • vit D required for intestinal Ca absorption
  • Ca range maintained by 3 hormones:
  • HYPOCALCEMIA stimulates INC PTH + INC CALCITRIOL (VIT D) secretion –> increases blood Ca via inc GI/kidney Ca absorption and inc bone Ca resorption (via osteoclasts)
  • PTH also inhibits phosphate reabsorption

-HYPERCALCEMIA stimulates INC CALCITONIN SECRETION –> DECREASES BLOOD CA (dec Ca absorption in GI/kidney and inc bone mineralization (osteoblasts)

29
Q

hyperparathyroidism

A

Primary:

  • MC - EXCESS PTH PRODUCTION
  • PARATHYROID ADENOMA MC CAUSE - 80%
  • PARATHYROID HYPERPLASIA/ENLARGE - 15-20%
  • occurs in 20% of patients taking LITHIUM, MEN1 + 2a
  • sx- STONES, BONES, ABDOMINAL GROANS, PSYCHIC MOANS + DEC DTR
  • dx- HYPERCA + INC PTH + DEC PHOS
  • INC 24h URINE CALCIUM EXCRETION, inc Vit D
  • osteopenia on bone scan, imaging to detect adenoma
  • tx- PARATHYROIDECTOMY (subtotal/3/5 gland) or total w/ autotransplantation of parathyroid tissue in forearm

Secondary:

  • INC PTH DUE TO HYPOCA OR VIT D DEFICIENCY (parathyroid tries to compensate by inc PTH)
  • CHRONIC KIDNEY FAILURE (MC CAUSE 2RY)
  • severe Ca or Vit D deficiency
  • tx- vit D / Ca supplementation

Tertiary:

  • prolonged PTH stimulation after 2ry hypoparathyroidism
  • -> autonomous PTH production; can be seen post-transplant too
30
Q

hypoparathyroidism

A

RARE –> either low PTH or insensitivity to its action
-MC CAUSE SURGICAL (ACCIDENTAL DAMAGE/REMOVAL) OR AUTOIMMUNE DESTRUCTION, radiation tx, hypomagnesemia (req to produce PTH), cong

  • sx- HYPOCALCEMIA –> carpopedal spasms, TROUSSEAU’S + CHVOSTEK’S SIGNS, INC DTR
  • dx- HYPOCALCEMIA, DEC PTH, INC PHOS
  • tx- CA SUPPLEMENT + VIT D (IV calcium gluconate if severe)
31
Q

HYPOcalcemia

A

hypoCa w/ dec PTH –> HYPOPARATHYROID MC

hypoCa w/ inc PTH –> CHRONIC RENAL DZ, LIVER DZ

  • VIT D DEFICIENCY
  • HYPOMAGNESEMIA, inc phosphate, hypoalbuminemia
  • high citrate states (blood transfusions), acute pancreatitis, rhabdo
  • meds: PPIs
  • sx-
  • hypoCa decreases excitation threshold for heart, nerves, muscle –> LESS STIM NEEDED FOR ACTIVATION/CONTRACTION
  • NEURO: cramping, bronchospasm, syncope, seizures, FINGER/CIRCUMORAL PARESTHESIAS
  • TETANY: CHVOSTEK’S, TROUSSEAUS SIGN, INC DTR
  • CARDIO: CHF, arrhythmias
  • skin: dry, psoriasis
  • GI: D, abd pain
  • skeletal: abn dentition, osteomalacia, osteodystrophy

-labs: DEC IONIZED CA + total serum Ca (<8.5)
+/- inc phosphate, dec magnesium
-check PTH, BUN, Cr

-ECG - PROLONGED QT INTERVAL

-tx- SEVERE: IV CALCIUM GLUCONATE or cal carbonate
-mild: PO CA + VIT D, K + Mg repletion may be needed
-CORRECTED CA IN PT W/ LOW SERUM ALBUMIN:
[0.8 X (normal albumin (4.4) - pt’s albumin)] - serum Ca

32
Q

HYPERcalcemia

A

-90% of cases due to primary hyperparathyroidism or malignancy

PTH-mediated:
-PRIMARY HYPERPARATHYROIDSM MC CAUSE OVERALL: INC CA, INC PTH, DEC PHOSPHATE

PTH-independent:

  • MALIGNANCY (SECRETES INC PTH-RELATED PROTEIN), DEC PTH
  • Vit D excess, Vit A excess, THIAZIDES, LITHIUM
  • hyperCa increases excitation threshold for heart, nerves, muscles –> STRONGER STIM NEEDED FOR ACTIVATE/CONTRACT
  • MOST PT ASYMPTOMATIC +/- arrhythmias
  • STONES: KIDNEY STONES, POLYURIA
  • BONES: PAINFUL BONES, FRX (INC REMODELING)
  • ABD GROANS: ILEUS, CONSTIPATION
  • PSYCHIC MOANS: weakness, fatigue, AMS, dec DTR, depression or psychosis, blurred vision
  • labs: INC IONIZED CA (most accurate), inc total serum Ca (>10), PTH-related protein, 1,25 Vit D levels, 24 urinary Ca
  • ECG: SHORTENED QT INTERVAL (prolonged PR interval, QRS widening)
  • tx- SEVERE: IV SALINE –> FUROSEMIDE 1ST LINE (loops enhance renal excretion), AVOID HCTZ (INC CA)
  • CALCITONIN, BIPHOSPONATES, STEROIDS
  • mild: no tx needed, tx underlying cause
33
Q

osteoporosis

A

LOSS OF BONE DENSITY –> due to inc absorption or decreased formation
-LOSS OF BOTH MINERAL AND MATRIX

  • PRIMARY: I - POSTMENOPAUSAL + SENILE
  • RF: cauc, asian, thin, smoking, steroids, kidney dz, ETOH, low Ca or vit D diets, inactivity
  • SECONDARY: due to CHRONIC DZ OR MEDS
  • hypogonadism, PROLONGED HIGH DOSE CORTICO USE, Cushing’s syndrome, thyrotoxicosis, hyperparathyroidism, DM, liver disease, low estrogen, malignancy, immobilization, heparin, anticonvulsants
  • sx- usually asymptomatic - 1st sx may be frx, back pain
  • PATHOLOGIC FRX: MC VERTEBRAL, HIP, DISTAL RADIUS
  • postmeno: mostly trabecular bone loss –> inc vertebral compression + wrist fractures
  • senile: travecular and cortical bone loss –> hip/pelvic
  • SPINE COMPRESSION: MC UPPER LUMBAR AND THORACIC; LOSS Of VERTEBRAL HEIGHT
  • dx- DEXA - best to show extent of demineralization
  • OSTEOPOROSIS: T SCORE < -2.5
  • OSTEOPENIA: T SCORE < -1.0-2.5
  • labs: serum Ca, phos, PTH + ALP usually normal, dec vit D
  • xray: shows demineralization; mostly axial skeleton
  • tx-BISPHOSPHONATES 1ST LINE
  • VIT D ASSOC WITH SLOWER PROGRESSION +/- Ca
  • SELECTIVE ESTROGEN RECEPTOR MODULATOR: RALOXIFENE (reduce progress, protect vs breast ca, not inc risk of endo cancer)
  • ESTROGEN - also helps w/ sx menopause; inc risk endo + breast ca, CAD, stroke, venous thromboembolism
34
Q

osteogenesis imperfecta

A

genetic mutation for type 1 collagen (necessary for bone integrity) - assoc w/ severe osteoporosis, spontaneous frx in childhood, BLUE-TINTED SCLERAE + PRE-SENILE DEAFNESS

35
Q

renal osteodystrophy

A 
bone disorders (OSTEITIS FIBROSIS CYSTICA + OSTEOMALACIA) assoc w/ CKD
-failing kidneys don't eliminate phosphate properly + poorly synthesize vit D --> HYPOCALCEMIA --> INC PTH --> OSTEOIDS (DEC MINERALIZATION)

-sx- BONE + PROXIMAL MUSCLE PAIN (IN CONTEXT OF UREMIA) +/- pathological fractures, chondrocalcinosis

  • dx- 2ry HYPERPARATHYROIDISM
  • labs: dec Ca, inc phos, inc PTH
  • inc PO4 (not able to excrete it), hypoCa (due to dec vit D production by kidney) = inc PTH
  • xray: OSTEITIS FIBROSIS CYSTICA = PERIOSTEAL EROSIONS, BONY CYSTS “SALT + PEPPER APPEARANCE ON SKULL” - due to osteoclast activity (stim by inc PTH)
  • CYSTIC BROWN “TUMORS” on bx (not actual tumors)
  • tx- PHOSPHATE BINDERS: CALCIUM CARBONATE, CALCIUM ACETATE, SEVELAMER goal < 5.5
  • active Vit D = calcitriol + calcium
36
Q

osteomalacia + rickets

A

VIT D DEFICIENCY –> dec Ca AND phosphate –> DEMINERALIZATION –> SOFT BONES
-dec of mineralization only (osteoporosis is mineral + matrix proportionally)

  • sx-
  • RICKETS (CHILDREN): DELAYED FONTANEL CLOSURE, GROWTH RETARD, DELAYED DENTITION, COSTAL CARTILAGE ENLARGE, BOWING LONG BONES
  • OSTEOMALACIA (ADULTS): BONE PAIN, MUSCLE WEAKNESS, BOWING OF LONG BONES
  • dx- DEC VIT D, DEC CALCIUM AND PHOSPHATE, INC ALK PHOS
  • xray: LOOSER LINES (ZONES): transverse “pseudo fracture” lines

-tx- VITAMIN D (ERGOCALCIFEROL) 1ST LINE

37
Q

adrenal zones

A

GFR for layers, ACE for hormones they produce

  • Zona Glomerulosa –> Aldosterone (outer layer cortex)
  • Zona Fasciculata –> Cortisol (middle layer cortex)
  • Zona Reticularis –> Estrogens/Androgens (inner layer cortex)
38
Q

Primary chronic adrenocortical insufficiency / Addison’s Disease

A

ADRENAL GLAND DESTRUCTION (LACK OF CORTISOL AND ALDOSTERONE)

  • AUTOIMMUNE: MC CAUSE INDUSTRIALIZED COUNTRIES –> CAUSES ADRENAL ATROPHY
  • INFECTION: MC CAUSE WORLDWIDE (TB, HIV) –> CAUSES ADRENAL CALCIFICATION
  • vascular: thrombosis or hemorrhage in adrenal gland
  • metastatic dz
  • medications: KETOCONAZOLE, RIFAMPIN, PHENYTOIN
  • sx-
  • HYPERPIGMENTATION (inc ACTH stimulation of melanocyte-stim hormones))
  • Dec Aldosterone: ORTHOSTATIC HYPOTENSION, HYPONATREMIA, HYPERKALEMIA, NON-GAP META ACIDOSIS, HYPOGLYCEMIA
  • Dec Sex Hormones in Women: loss of libido, amenorrhea, loss of axillary + pubic hair
  • dx-
  • screen w/ am cortisol??
  • SCREEN FOR ADRENAL INSUFFICIENCY: HIGH DOSE ACTH (COSYNTROPIN) STIM TEST (blood or urine cortisol measured before and after IM injection ACTH)
  • normal –> rise in blood/urine cortisol levels after ACTH
  • ADRENAL INSUFFICIENT –> LITTLE/NO INC IN CORTISOL
  • CRH STIMULATION TEST: differentiates btw causes of adrenal insufficiency
  • PRIMARY/ADDISON (ADRENAL) –> INC ACTH BUT LOW CORTISOL (opposite)
  • secondary (pituitary) –> low ACTH and cortisol

-tx- HYDROCORTISONE 1ST LINE + FLUDROCORTISONE
(hormone replace = synth glucocorticoid and synth mineralocorticoid)
-replace TT for women (adrenals only place it comes from, men have testes)

39
Q

secondary chronic adrenocortical insufficiency

A

Secondary: PITUITARY FAILURE OF ACTH SECRETION
( = lack of cortisol)
-EXOGENOUS STEROID USE MC CAUSE esp w/ abrupt cessation

  • sx- usually have normal mineralocorticoids (aldosterone) fx
  • weakness/muscle ache, myalgias, fatigue, WL, anorexia, N/V/D, abd pain, HA, sweat, abnormal periods, mild hypoNa, HYPOTENSION
  • dx-
  • SCREEN FOR ADRENAL INSUFFICIENCY: HIGH DOSE ACTH (COSYNTROPIN) STIM TEST (blood or urine cortisol measured before and after IM injection ACTH)
  • normal –> rise in blood/urine cortisol levels after ACTH
  • ADRENAL INSUFFICIENT –> LITTLE/NO INC IN CORTISOL
  • CRH STIMULATION TEST: differentiates btw causes of adrenal insufficiency
  • PRIMARY/ADDISON (ADRENAL) –> INC ACTH BUT LOW CORTISOL (opposite)
  • secondary (pituitary) –> low ACTH and cortisol

-tx- HYDROCORTISONE 1ST LINE (synthetic glucocorticoid = cortisol)

40
Q

glucocorticoid vs mineralocorticoid

A 
glucocorticoid = cortisol 
(synthetic = hyrdorcortisone, prednisone, dexamethasone)
mineralocorticoid = aldosterone
(synthetic = fludrocortisone)
41
Q

chronic adrenal insufficiency considerations (stress/surgery)

A
  • must be treated w/ IV glucocorticoids + IV isotonic fluids before and after surgical procedures (mimics body’s natural response)
  • during illness/surgery/high fever, oral dosing needs to be adjusted to recreate the normal adrenal gland response to stress (ex. triple normal dose)
  • should carry medical alert tag and injectable form of cortisol for emergencies
42
Q

adrenal (addisonian) crisis

A

-sudden worsening of adrenal insufficiency due to “stressful” event (normal response is 3x inc cortisol)

  • ABRUPT W/DRAWL OF GLUCOCORTIOIDS MC (in pt not gradually tapered off steroids)
  • previously undiagnosed pt w/ Addison’s dz, exacerbation of known Addison’s dz w/ no increase in glucocortico, bilateral adrenal infarction (hemorrhage)
  • sx- SHOCK –> HYPOTENSION, HYPOVOLEMIC
  • ab pain, N/V, fever, weakness, lethargy, coma

-dx- labs: BMP (HYPONATREMIA, HYPERKALEMIA, HYPOGLYCEMIA), cortisol levels, ACTH, CBC

  • tx-
  • FLUIDS (NRML SALINE FOR HYPOTN), D5-NS IF HYPOGLYCEMIC
  • IV HYDROCORTISONE (if Addison’s), dexamethasone if undiagnosed
  • reverse electrolyte disorders
  • FLUDROCORTISONE (synthetic mineralocorticoid)
43
Q

cushing’s syndrome

A

cushing’s SYNDROME = SIGNS/SX RELATED TO CORTISOL EXCESS
cushing’s DISEASE = CUSHING’S SYNDROME CAUSED SPECIFICALLY BY PITUITARY INC ACTH SECRETION

  • exogenous: IATROGENIC –> LONG TERM TX (MC CAUSE)
  • endogenous: CUSHING’S DZ (BENIGN PITUITARY ADENOMA OR HYPERPLASIA –> SECRETES ACTH)
  • ECTOPIC ACTH (secretes ACTH - small cell lung cancer)
  • ADRENAL TUMOR - cortisol-secreting adrenal adenoma
  • sx- 2ry to excess cortisol + glucocorticoids
  • CENTRAL (TRUNK) OBESITY, MOON FACIES, BUFFALO HUMP, SUPRACLAVICULAR FAT PADS
  • WASTING OF EXTREMITIES, PROXIMAL MUSCLE WEAKNESS, SKIN ATROPHY, STRIAE, inc infx, hyperpigmentation
  • HTN, WEIGHT GAIN, HYPOKALEMIA, ACANTHOSIS NIG
  • depression, mania, psychosis
  • ANDROGEN EXCESS: hirsutism, oily skin, acne, inc libido, amenorrhea

-dx-
-SCREEN:
-LOW-DOSE DEXAMETHASONE SUPPRESSION: nrml response is cortical suppression;
NO SUPPRESS = CUSHING’S SYNDROME
-24 HOUR URINE FREE CORTISOL
-SALIVARY CORTISOL (usually at night)

  • DIFFERENTIATING:
  • HIGH-DOSE DEXAMETHASONE SUPPRESS –>
  • SUPPRESSION = CUSHING’S DZ
  • NO SUPPRESSION = ADRENAL OR ECTOPIC ACTH-producing TUMOR

ACTH LEVELS:

  • DECREASED ACTH –> ADRENAL TUMORS (produce high levels of cortisol, suppressing ACTH levels via HPA axis)
  • NORMAL/INCREASED ACTH –> CUSHINGS DZ OR ECTOPIC ACTH-PRODUCING TUMOR (secrete ACTH independent of HPA axis)

-tx-
-Cushing’s Dz (pituitary) –> TRANSPHENOIDAL SX (alt radiation)
-Ectopic ACTH-secreting or adrenal tumors –> SURGERY
(KETOCONAZOLE in inoperable pt, dec cortisol product)
-Iatrogenic steroid therapy –> GRADUAL STEROID TAPER

44
Q

hyperaldosteronism

A

Primary: RENIN-INDEPENDENT

  • idiopathic or bilateral adrenal hyperplasia, MC, women
  • CONN’S SYNDROME: ADRENAL ALDOSTERONOMA

Secondary: DUE TO INCREASED RENIN

  • INC RENIN –> 2ry INC IN ALDOSTERONE VIA RAAS
  • MC DUE TO RENAL ARTERY STENOSIS or dec renal perfusion (CHF, hypovolemia, nephrotic syndrome)
  • sx-
  • HYPOKALEMIA: muscle weakness, polyuria, fatigue, dec DTR, hypoMg
  • HYPERTENSION: HA, flushing, NOT EDAMATOUS
  • dx-
  • labs: HYPOKALEMIA W/ METABOLIC ACIDOSIS (due to dumping K and H in exchange for Na)
  • Screen: ALDOSTERONE:RENIN RATIO
  • Definitive: Saline Infusion Test
  • CT/MRI - look for adrenal or extra-adrenal mass
  • tx-
  • Conn’s Syndrome: EXCISION + SPIRONOLACTONE (blocks aldosterone)
  • Hyperplasia: SPIRONOLACTONE, ACEI, correct electros
  • Secondary (renovascular htn): ANGIOPLASTY DEFINITIVE, ACEI
45
Q

pheochromocytoma

A

CATECHOLAMINE-SECRETING ADRENAL TUMOR –> SECRETES NOREPI AND EPI AUTONOMOUSLY AND INTERMITTENTLY

  • triggers: sx, exercise, pregnancy, meds
  • 90% benign
  • sx- HYPERTENSION!!!
  • “PHE” - PALPITATIONS, HEADACHES, EXCESSIVE SWEAT
  • dx- INC 24h URINARY CATECHOLAMINES
  • MRI/CT to visualize adrenal tumor
  • labs: hyperglycemia, hypoK
  • tx- COMPLETE ADRENALECTOMY
  • PREOP a-BLOCKADE: PHEnoxybenzamine or PHEntolamine x7-14d –> followed by BB to control HTN
  • DON’T INITIATE THERAPY W/ BETA-BLOCKADE to prevent unopposed a-constriction during catecholamine released triggered by surgery or spontaneously (life threatening HTN)

*cocaine mimics same effect, same tx

46
Q

anterior hypopituitarism

A
  • pituitary destruction or deficient stim from hypothalamus, tumor, bleeding into pituitary, infarxtion
  • deficient in GROWTH HORMONE, TSH, GONADATROPIN (FSH/LH/GnRH), ACTH
  • tx- hormone replacement
47
Q

anterior pituitary tumors

A

most benign MICROadenomas that are: FUNCTIONAL, NON-FUNCTIONAL, COMPRESSIVE (may cause mass effect on optic chiasm –> bitemporal hemianopsia)

  • PROLACTINOMAS: MC TYPE
  • women: oligomenorrhea, amenorrhea, galactorrhea, infertile
  • men: impotence, dec libido, hypogonadism, infertility
  • tx- CABERGOLINE or BROMOCRIPTINE 1ST LINE (dopa agonists inhibit prolactin) - NOT SX
  • SOMATOTROPINOMA: secretes growth hormone
  • ACROMEGALY IN ADULTS, GIGANTISM IN CHILDREN
  • DM AND GLUCOSE INTOLERANCE
  • dx- INSULIN-LIKE GROWTH FACTOR (SCREEN); confirm w/ ORAL GLUC SUPPRESSION TEST (inc GH levels)
  • ADRENOCORTICOTROPINOMAS: secrete ACTH
  • CUSHING’S DZ + HYPERPIGMENTATION
  • TSH-SECRETING ADENOMAS
  • THYROTOXICOSIS (T3/T4 + TSH all increased)
  • dx- MRI - look for SELLAR LESIONS/PIT TUMORS
  • endocrine studies
  • tx- TRANSSPHENOIDAL SURGERY TX OF CHOICE for removal of ACTIVE or compressive tumors (EXCEPT PROLACTINOMAS)
  • acromegaly: TSS + BROMOCRIPTINE; OCTREOTIDE (somatostatin analogue that inhibits GH secretion)
  • prolactinoma: CABERGOLINE or BROMOCRIPTINE 1ST LINE (dopa agonists inhibit prolactin) - NOT SX
48
Q

hyperprolactinemia

A

PROLACTINOMAS MC CAUSE, hypothyroid, acromegaly, cirrhosis, renal failure

  • DOPAMINE ANTAGONISTS (bc dopa inhibits prolactin) - metoclopramide, promethazine, prochlorperazine, SSRIs, TCAs, cimetidine, estrogen)
  • pregnancy, stress, exercise
  • increased prolactin inhibits gonadotropinRH –> dec FSH/LH
  • women: oligomenorrhea, amenorrhea, galactorrhea, infertile
  • men: impotence, dec libido, hypogonadism, infertility

-dx- TSH, BUN/Cr, LFTs, B-hCG, prolactin, +/-MRI

  • tx- stop offending drugs
  • CABERGOLINE or BROMOCRIPTINE 1ST LINE (dopa agonists inhibit prolactin)
  • surgical tx in select pt
49
Q

gynecomastia

A

increased effective estrogen (inc production or dec degradation) or decreased androgens

  • Infants: due to high maternal estrogen
  • Puberty: esp 10-14y (lasts about 6mo-2y)
  • Older men: due to decreased androgen production
  • idopathic, cirrhosis, testicular tumors, hyperthyroid, CKD, klinefelter syndrome, alcoholism
  • meds: spironolactone, ketoconazole, cimetidine, 5-alpha reductase inhibitors, digoxin, GnRH agonists (leuprolide)

-dx- clinical, check TT levels

  • tx- stop offending meds, observe if early (most regress spontaneously), ideal tx should be in first 6 mo (after 12 mo, tissue may start fibrosis)
  • meds: TAMOXIFEN (estrogen modulator), aromatase inhibitors, androgens in hypogonadism
  • surgical if all else fails
50
Q

diabeties mellitus - complications

A

Type 1: autoimmune beta cell destruction; onset <30y

Type 2: insulin resistance + relative impairment of insulin secretion –> due to genetic + enviro factors, esp WG + dec physical activity MC >40y
-RF: family hx, 1ry relative, Hispanic, AA, pacific island, HTN, HLD, delivery of baby >9lbs, syndrome X, atherosclerosis, obesity, stroke

NEUROPATHY:

  • Sensorimotor: paresthesia, dec proprioception “STOCKING GLOVE” PATTERN, pain, dec DTR
  • Autonomic: ORTHOSTATIC HYPO, N/V/D/C, incontinence
  • CN3 palsy: but pupil size remains normal

RETINOPATHY: painless deterioration of sm retinal vessels

  • dx- fundoscopy, angiography
  • Nonproliferative (background) - microaneurysms –> hard exudates form lipoproteins, dot or flame hem from blood
  • Proliferative: neovascularization
  • Maculopathy: macular edema, blurred vision, central loss

NEPHROPATHY: kidney deterioration leading to microalbuminuria (fist sign)

  • dx- ALBUMINURIA, anemia, acidosis
  • kidney bx - KIMMELSTIEL WILSON (nodular glom-scler)
  • tx- ACE

MACROVASCULAR
-artherosclerosis –> coronary artery dz, periph vascular dz, stroke

*inc risk infections bc of vascular insufficiency + immunosuppression from hyperglycemia

HYPOGLYCEMIA

  • Autonomic sx: sweating, tremors, palp, nervous, tachy
  • CNS sx: HA, lightness, confusion, slurred speech, dizzy
  • mild <60 –> 10-15g fast-acting carb, recheck 15 min
  • severe/unconscious <40 –> IV bolus of D50 or inject glucagon SQ
51
Q

diabetes mellitus - diagnosis

A

FASTING PLASMA GLUCOSE: fasting at least 8 hours on 2 occasions - GOLD STANDARD

  • impaired tolerance: 110-125
  • DM: >126

2-Hour GTT - (3Hr GTT gold standard in gestational)

  • impaired tolerance: >140-199
  • DM: >200

Hemoglobin A1C

  • impaired tolerance: 5.7-6.4%
  • DM: >6.5%

Random Plasma: in pt w/ classic DM sx or complications
-DM: >200

SCREENING:
ADA: all adults >45 every 3 years OR any adult w/ BMI >25 and 1 additional risk factor
USPSTF: any 40-70yo that is overweight or obese (q 3y)

52
Q

diabetes mellitus - management

A
  • diet, exercise + lifestyle change should be tried 1st in type II –> oral antihyperglycemic agents
  • Diet: 50-60% Carbs, 15-20% Protein, 10% Unsat Fats
  • Insulin preferred for gestational DM
  • A1C goal: <7.0 (check q3 mo if not controlled, q6 mo if controlled)
  • pre-meal BG goal: 80-130
  • post-meal BG goal: <180
  • Lipids: LDL <100, HDL >40, TG <150
  • Neuropathy: gabapentin, foot care, +/- TCAs
  • Retinopathy: DM control, laser photocoag, bevacizumab (proliferative), yearly eye screen
  • Nephropathy: DM control, ACEI if microalbumin, HTN control, yearly BUN/Cr checks
  • Type I –> most need 0.5-1.0 units/kg each day (divide between long-acting and meals)
53
Q

DKA

A

INSULIN DEFICIENCY + counterregulatory hormonal excess in DM as RESPONSE TO STRESSFUL TRIGGERS:
-INFECTION MC, INFARCTION, NONCOMPLIANCE W/ INSULIN, dose change, undiagnosed

  • cortisol stress hormone –> inc glucose + patients can’t meet demand of inc insulin requirements
  • YOUNGER PT W/ TYPE 1 DM

insulin deficiency –> hyperglycemia, dehydration, ketonemia (high anion gap meta acidosis), potassium deficit

-sx- HYPERGLYCEMIA, ABD PAIN, KETOTIC BREATH, KUSSMAUL’S RESPIRATIONS, weak, fatigue, confusion, tachy, hypoTN, decreased turgor

-dx-
PLASMA GLUCOSE: >250
Arterial pH: <7.3 mild --> <7.0 severe
Serum Bicarb: 15-18 mild --> <10 severe
Ketones: POSITIVE
Serum Osmolarity: varies

-tx-
initial: ABC, mental status, vitals, vol status, screen for precipitating event
-IV FLUIDS CRITICAL 1ST STEP –> ISOTONIC 0.9% NS UNTIL HYPOTN RESOLVES –> 0.45% NS –> D5 0.45 NS to prevent hypoglycemia from insulin tx
-when the blood glucose is < 200 mg/dL, treatment involves adding dextrose to the intravenous fluids
-INSULIN (REG) - lower serum gluc –> dec gluconeogenesis, recuced ketone production
-POTASSIUM: despite serum K levels, pt is always total body K deficient (correction of DKA will cause hypokalemia) If serum K high, wait til normal and then replete
+bicarb if severe acidosis

54
Q

hyperosmolar hyperglycemia (HHS)

A

INSULIN DEFICIENCY + counterregulatory hormonal excess in DM as RESPONSE TO STRESSFUL TRIGGERS:
-INFECTION MC, INFARCTION, NONCOMPLIANCE W/ INSULIN, dose change, undiagnosed

  • cortisol stress hormone –> inc glucose + patients can’t meet demand of inc insulin requirements
  • OLDER PT W/ TYPE 2 DM (higher mortality)

usually some illness leading to reduced fluid intake (mc infx) –> dehydration, increased osmolarity, hyperglycemia, potassium deficit, absence of severe ketosis (type 2 typically make enough insulin to prevent ketogenesis)

-sx- HYPerGLYCEMIA, MENTAL STATUS CHANGE, fever, weak, fatigue, confusion, tachy, hypoTN, decreased turgor

-dx-
PLASMA GLUCOSE: >600
Arterial pH: >7.3 
Serum Bicarb: >15
Ketones: Small
Serum Osmolarity: >320

-tx-
initial: ABC, mental status, vitals, vol status, screen for precipitating event
-IV FLUIDS CRITICAL 1ST STEP –> ISOTONIC 0.9% NS UNTIL HYPOTN RESOLVES –> 0.45% NS –> D5 0.45 NS to prevent hypoglycemia from insulin tx
-INSULIN (REG) - lower serum gluc –> dec gluconeogenesis, reduced ketone production
-POTASSIUM: despite serum K levels, pt is always total body K deficient (correction of DKA will cause hypokalemia) If serum K high, wait til normal and then replete
+bicarb if severe acidosis

55
Q

multiple endocrine neoplasia I (MEN 1)

A

Rare inherited disorder of 1+ overactive endocrine gland tumors (3 P’s) - most tumors are benign (esp <30yo)
PARATHYROID (90%), PANCREAS (60%), PITUITARY (55%)

  • sx-
  • HYPERPARATHYROIDISM - MC
  • PANCREATIC TUMORS - 2nd MC - highest malig pot’l
  • Gastrinomas (zes) –> multiple peptic ulcers
  • Insulinomas –> WHIPPLE’S TRIAD: fasting/exertional hypoglycemia, low bg during attach, relieved w/ glucose (inappropriate insulin w/ fasting) –> sx removal
  • Glucagonomas –> NECROLYTIC MIGRATORY ERYTHEMA, TYPE 2 DM –> sx removal
  • VIPomas (vasoactive intestinal peptide tumors) . –> watery diarrhea, hypoK, achlorhydria, dehyrdration
  • Somatostatinomas –> steatorrhea, cholelithiasis, type 2 DM
  • PITUITARY ADENOMAS
  • Prolactinomas MC
  • Somatotropinomas –> acromegaly (excessive GH)
  • Corticotropinomas –> cushing’s disease (excess ACTH)
  • Screening for MEN 1:
  • genetic testing –> DEFECT IN MENIN GENE
  • PTH + CA (hyperparathyroid often 1st sign)
  • GASTRIN (mc pancreas manifestation)
  • PROLACTIN (mc pituitary tumor)
56
Q

multiple endocrine neoplasia 2 (MEN 2)

A

Rare autosomal dominant (RET proto oncogene) disorder of multiple endocrine gland tumors

-MEN 2a (90%): MEDULLARY THYROID CARCINOMA, PHEOCHROMOCYTOMA, HYPERPARATHYROIDISM

  • MEN 2b (5%): medullary thyroid carcinoma, pheochromocytoma, NEUROMAS, MARFANOID
  • assoc w/ presence of mucosal neuromas, and have a more aggressive form of thyroid cancer (presents in infancy)

-FAMILIAL MTC: MEDULLARY THYROID CARCINOMA

  • sx-
  • Medullary Thyroid Carcinoma: usually first feature
  • cells SECRETE CALCITONIN
  • palpable neck mass, compressive sx –> TOTAL THYROIDECTOMY (prophylactically in 1st 6mo for MEN2b)
  • Pheochromocytoma: usually appears btw 10-30yo
  • adrenal medullary tumor w/intermittent secretion of catecholamines (epi/norepi) –> palp, HA, sweating
  • dx- 24h urine catecholamines, adrenal CT or MRI
  • tx- complete adrenalectomy
  • Hyperparathyroidism (only MEN 2a!) - not usually presenting feature as in MEN1; screen MEN2a yearly
  • hypercalcemia “stones, bones, abd groans, psych moans”
  • tx- parathyroidectomy (3.5 or 4 w/ transplantation)

SEEN IN 2B ONLY:

  • Neuromas: mucosal of the lips, tongue, eyelids, conjunctiva, nasal/laryngeal mucosa
  • Marfan-Like Body: high arched palate, pectus excavatum, scoliosis

Screening:

  • genetic testing for RET PROTO-ONCOGENE
  • routine labs: CALCITONIN, EPINEPHRINE, PTH/CALCIUM
57
Q

metabolic syndrome (syndrome x, insulin resistance syndrome)

A

syndrome of multiple metabolic abnormalities that inc risk for complications like DM and CVD

-pathophysiology: INSULIN RESISTANCE –> free fatty acids released, causes an increase in trigs and glucose production an reduction of insulin sensitivity –> insulin resistance and hyperinsulinemia (high levels of insulin cause sodium resabsorption leading to HTN)

  • dx - at least 3 of the following:
  • dec HDL: <40 men, <50 women
  • inc BP: >135 systolic or >85 diastolic (or meds for BP)
  • inc fasting trigs: >150 (or meds for trigs)
  • inc fasting blood sugar: >100 (or drug tx)
  • inc abdominal obesity: waist circ >40” men, >35” women
  • tx-
  • lifestyle
  • weight loss:
  • PHENTERMINE (3 mo only), PHENTERMINE/TOPIRAMATE (no restriction on duration)
  • LORCASERIN - selective serotoninagonist induces satiety
  • ORLISTAT - inhibits fat absorption
  • bariatric sx
  • LDL: statins, Exetimibe, bile acid sequestrants
  • Trigs: FIBRATES, nicotinic acid, omega3
  • HDL: NICOTINIC ACID, statins, fibrates, bile acid seq
  • BP: diet, exercise, ACE/ARBs
  • Insulin resistance: metformin
58
Q

growth hormone deficiency

A 
Most common cause: pituitary tumor
↓ Muscle mass
↓ Bone density
↑ Lipids
↓ Memory
dx: ↓ IGF-1
59
Q

diabetes insipidus

A

Patient will be complaining of polyuria and polydipsia
Labs will show increase in plasma osmolality and a decrease urine osmolality
Central DI: Most commonly caused by a decrease in ADH production
Diagnosis is made by vasopressin challenge test: > 50% increase in urine osmolality and decrease urine volume
Treatment is intranasal DDAVP
Nephrogenic DI: Patient with a history of taking lithium
Most commonly caused by renal unresponsiveness to ADH
Diagnosis is made by water deprivation test: no change in urine osmolality
Treatment is HCTZ, amiloride, indomethacin

Concepts / Lists (16 decks)

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