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Endocrine / Reproduction > Week 1 - Endocrine > Flashcards

Week 1 - Endocrine Flashcards

1
Q

Group 1 Hormones

A

steroids, thyroid
lipophilic, transported bound to proteins
long plasma half life
intracellular receptors (thyroid=nuclear, steroid=cytoplasmic) - act on transcription/translation

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2
Q

Group 2 Hormones

A

Peptides, proteins, glycoproteins, catecholamines
hydrophilic, transported freely
short half-life
plasma-bound receptors
mediators: cAMP, cGMP, Ca, metabolites, kinases

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3
Q

Origin of pituitary components

A 
hypophyseal diverticulum (Rathke's pouch)
anterior wall= pars distalis
superior extension= pars tuberalis
posterior wall= pars intermedia
Infundibulum= stalk + pars nervosa
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4
Q

Origin of thyroid components

A 
thyroid diverticulum (endoderm)= thyroid follicular cells
Neural crest= parafollicular cells
Dorsal wing of pharyngeal arch 3,4 (endoderm)= parathyroid principal cells
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5
Q

Primary germ layer origin of glands

A 
pituitary= ectoderm
thyroid/parathyroid= endoderm
adrenal= mesoderm
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6
Q

Hyperprolactinemia

A

Causes:
-prolactinoma (most common)
-drugs (metoclopramide, risperidone, D2 antagonists)
-infundibular stalk compression (from larger pituitary mass)
-pregnancy, lactation, stress, sleep
Sx: women have menstrual abn, galactorrhea, men have ED and hypogonad
Tx: dopamine agonists (cabergoline, bromocriptine), very effective

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7
Q

Acromegaly

A

excess growth hormone (GH)
GH stimulated by GHRH, inhibited by somatostatin and IGF-1(feedback from liver)
Sx: skull and extremity growth, thick skin, etc
Dx: serum IGF-1, or oral glucose tolerance test
Tx: surgery, radiation, octreotide, lanreotide, pegvisomant

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8
Q

Things pituitary releases

A 
Anterior:
ACTH- glucocorticoids (stim by CRH)
TSH- T3,T4 (stim by TRH)
GH- IGF-1 (stim by GHRH, inhi by somatostatin,IGF-1)
Prolactin- (inhib by dopamine)
Gonadotropins- FSH and LH (stim by GnRH)
Posterior: vasopressin(ADH), oxytocin
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9
Q

Growth hormone deficiency

A

Sx: in neonate= hypoglycemia,, in child= fat, microphallus, delayed puberty, short
Tx: rGH, check IGF-1 to dose

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10
Q

PTH feedback loop

A

low Ca - PTH secretion -

  • kidney: Ca reabsorption, convert 25 to 1,25 vitD
  • Intestine: Ca absorption
  • Bone: Ca resorption (and P)
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11
Q

Calcium sensing receptor (CaSR)

A

expressed in parathyroid and kidney
loss of fxn= familial hypocalciuric hypercalcemia (FHH)
gain of fxn= autosomal dominant hypocalcemia (ADH)

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12
Q

Primary hyperparathyroidism

A

hypercalcemia (PTH dep)
usually sporadic, single tumor
MEN (multiple endocrine neoplasias)
Familial isolated hyperparathyroidism
Familial hypocalciuric hypercalcemia (FHH)
ectopic PTH (rare)
Sx: hyperparaosteitis, brown tumor (bone), thinning of bone cortex

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13
Q

Familial hypocalciuric hypercalcemia (FHH)

A 
CaSR loss of fxn (usually, not always)
autosomal dom
asymptomatic, lifelong
PTH not suppressed
use 24hr urine Ca and creatinine to rule out
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14
Q

PTH independent hypercalcemia

A 
PTH is low
malignancy
calcitriol-mediated (granulomatous, sarcoid)
-excess vitD
hyperthyroidism (inc bone resorbtion)
immobilization
milk
--PTHrP
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15
Q

Tx of hypercalcemia

A

fluids, loop diuretics (furosemide)

bisphosphonates (inhibit osteoclasts)

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16
Q

Hypocalcemia lab findings ddx

A

primary hypoparathyroid: PO4 up/n, PTH down/n, vitD n
Pseudohyperparathyroid (PTH resistant): PO4 up/n, PTH up, vitD n
Mg depletion: PO4 n, PTH down/n, vitD n
secondary hyperparathyroid: PO4 down/n, PTH up, vitD down

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17
Q

Hypoparathyroidism

A

hypocalcemia, PO4 up
either genetic or autoimmune or infiltrative
Sx:basal ganglia calcification, hypocalcemic tetany (hand contraction)

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18
Q

Pseudohyperparathyroidism

A

PTH resistance
GNAS mutation
Albright’s Hereditary Osteodystrophy= short, round face, short 4th metacarpals, ossifications

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19
Q

Hypocalcemia flow chart

A

PTH down or nl= probable hypoparathyroidism, r/o Mg def
PTH up with high phos= PTH resistance, renal insuff
PTH up with low/n phos= vitD def, occult malabsorption ,, measure 25vitD and 24hr urine Ca and creatinine, check for celiac ds, check BMD

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20
Q

FGF23

A

-made by osteocytes
Intestine: decreased Ca and PO4 absorbtion by decreased 1,25vitD production
Kidney: increased PO4 excretion
Bone: decreased mineralization due to hypophos and low 1,25vitD
Excess= hypophosphatemia, rickets, osteomalacia
Decreased= hyperphosphatemia, tumoral calcinosis

21
Q

Pituitary adenomas

A

women more than men, 30-60yo
prolactinoma most common, non-secreting second-most
well-circumscribed, one cell type, destruction of normal reticulin pattern

22
Q

Sheehan’s syndrome

A

postpartum pituitary necrosis
bc gland enlarges during pregnancy, more susceptible to ischemia
obstetrical hemorrhage or shock can make it worse
results in hypopituitarism

23
Q

Rathke cleft cyst

A

may be asymptomatic
columnar/cuboidal cells with cilia
thin-walled cyst under pituitary

24
Q

Craniopharyngioma

A

kids: adamantinomatous (palisading squamous epithelium with keratin)
adults: papillary (no keratin)
Sx: optic chiasm probs, hypopituitary

25
Bone disease in hyperparathyroidism
osteitis fibrosa cystica= osteoclasts, thin cortex, fibrosis of marrow Brown tumor= osteoclasts, giant cells, hemorrhage, like giant cell tumor
26
Parathyroid adenoma
solitary nodule in single gland sheets of chief cells, decreased stromal fat rim of normal parathyroid at edge Parathyroid carcinoma= super rare, fibrous adhesions
27
Renin angiotensin aldosterone system
decrease blood pressure- kidney makes renin- renin activates angiotensinogen to AngI- ACE converts to AngII- causes vasoconstriction and adrenals to make aldosterone- Aldo causes renal water and Na retention and K and H secretion- increased blood pressure
28
Renin system drugs
Renin inhibitors: aliskiren ACE inhibitors: -pril Angiotensin receptor blockers (ARBs): -sartan Mineralocorticoid (aldo) receptor antagonists: spironolactone, eplerenone
29
Primary hyperaldosteronism
hypertension, hypokalemia high plasma aldo, low plasma renin activity (ratio high) also secreting adrenocortical adenoma bilateral hyperplasia of zona glomerulosa Tx: adrenalectomy
30
Secondary hyperaldosteronism
renal ischemia decreased intravascular volume Na wasting disorders
31
Apparent mineralocorticoid excess
11BHSD2 deficiency | that protein converts cortisol to cortisone in the kidney, so if it isn't there then cortisol can act like aldosterone
32
Liddle's Syndrome
mutation in amiloride sensitive ENaC | Tx: amiloride, triamterene (K-sparking diuretics)
33
Pheochromocytoma
tumor of chromaffin cells (neuroendocrine) of adrenal medulla secrete both epi and norepi can be metastatic or benign "zellballen" cell balls, abundant cytoplasm, granular, basophilic Paragangliomas: extra-adrenal tumor secrete mostly norepi Sx: tachycardia, HTN, sweating, headaches, etc (Paroxysmal events) Dx: 24hr urine catecholamines and plasma metanephrines Tx: begin alpha block, then beta-block, hydration, surgery
34
Cortisol-Cortisone shuttle
cortisol is active, cortisone is not 11B-HSD2 in kidney converts cortisol to cortisone 11B-HSD1 in liver converts it back to cortisol
35
Adrenal Insufficiency (low cortisol)
Sx: fatigue, anorexia, weight loss, increased skin pigmentation, salt craving(primary) Hyponatremia,, (hyperkalemia in primary) Causes: critical illness (TB), pituitary injury(secondary), withdrawl from corticosteroids, narcotics, mifepristone, malignancy, hemorrhage Drugs that cause it: ketoconazole, metyrapone, mitotane, etomidate Genetic: congenital adrenal hyperplasia (170HP), Adrenoleukodystrophy (accumulate long chain fatty acids) Tests: ACTH (Cosyntropin) cortisol response, or juct check them both in the AM Most common= autoimmune adrenalitis (Addison's) Tx: glucocorticoid and mineralocorticoid(fludrocortisone) replacement for primary,, just gluco for secondary Primary= high ACTH, high renin, low aldo Secondary= low/n ACTH, norm renin, norm aldo
36
Cushing's Syndrome
ACTH-dependent hyperaldosteronism ACTH-secreting tumor (in pituitary or ectopic) Sx: weight gain, hump, osteoporosis, inc BP, hypogonad, androgen excess, easy bruise Tests: late-night salivary cortisol, overnight DST, 24hr urine cortisol If ACTH is low, then get adrenal CT for primary tumor If ACTH is high/n, get MRI of pituitary and petrosal sinus sample to determine where the tumor is Tx: surgery, remove tumor,, Pasireotide= somatostatin agonist, Metyrapone= 11B hydroxylase inhibitor, Mifepristone= glucocorticoid inhibitor
37
Structure of adrenal glands
``` Cortex: -zona glomerulosa= mineralocorticoids -zona fasciculata= glucocorticoids -zona reticularis= estrogen and androgen Medulla: chromaffine cells= catecholamines ```
38
Adrenocortical hyperplasia
bilateral thickenening of adrenal cortex mostly faciculata cells= clear cells= make glucocorticoids can be diffuse or multi-nodular
39
Adrenocortical Adenoma
yellow, encapsulated can be functional or non-functional (most non) mostly faciculata cells
40
Adrenocortical carcinoma
rare, large, invasive necrosis and hemorrhage lymph node metastasis can be well or poorly differentiated
41
SIADH
common hyponatremia due to excess H2O retention causes: lung ds, brain ds, drugs, misc low Na, hypotonic serum, euvolemic, high urine osmolarity and Na Dx: exclusion, R/O hypothyroid and adrenal insuff Tx: fluid restrict, IV salt, AVP receptor antagonists (conivaptan and talvaptan), loop diuretics, Demeclocycline Be sure to slowly correct the serum Na to avoid bad brain stuff
42
Diabetes Insipidus (DI)
``` Deficient ADH (thus polyuria, hypernatremia) central(neurogenic): autoimmune, trauma, tumors, infiltrative of pituitary/hypopthalamus Nephrogenic: x-linked recessive, hypokalemia, hypercalcemia, renal ds, drugs, lithium high Na, euvolemic, variable urine Na polyuria, low urine osmolality, abnormal water restriction test Tx: central= DDAVP/desmopressin,, nephrogenic= low salt diet, thiazide diuretic, NSAIDs ```
43
Congenital hypothyroidism
more common in girls, hispanics mostly from dysgenesis, some from dyshormonogenesis, iodine def is rare here occasionally from central hypothyroid (MPHD) or transient Sx: asymptomatic at birth, then lethargy, macroglossia, large fontanels, jaundice, etc,, brain damage less common after age 3 Newborn screening often just measures TSH, can miss central hypothyroid Tx: levothyroxine
44
Chronic Lymphocytic Thyroiditis (Hashimoto's)
autoimmune, own lymphocytes against thyroglobulin, thyroid peroxidase, or TSH receptor cytokines and inflammation destroys the gland diffuse enlargement, lymphocytic inflammation, germinal centers, Hurthle cell change
45
Hypothyroidism
Most common= Hashimoto's causes: infiltrative, infxn, dysgenesis, iodine def, iodine excess(Wolff-Chaikoff), drugs, lithium viral=painful, self-limited fibrous=hard and fixed, painless Secondary: tumors, trauma, drugs, dopamine Sx: fatigue, weight gain, constipation, hypothermia, periorbital puffiness, bradycardia Dx: serum TSH Tx: levothyroxine
46
Graves Disease
hyperthyroidism due to autoimmune which stimulates thyroid via TSI thyroid stimulating immunoglobulin increased rad-I uptake uniform and bilateral -irregular follicles, scalloped colloid
47
Hyperthyroidism (Thyrotoxicosis)
Sx: nervousness, palpitations, weight loss, heat intolerance, tremor, sweating, proptosis, tachycardia Proptosis: eyeball extrusion due to antibody cross-react with muscles behind eye pretibial myxedema: thickeneing of the skin, mucopolysaccharide deposition -Graves -Solitary toxic nodule -Toxic multinodular goiter Tx: Methimazole (blocks oxidation of iodine in thyroid), propylthiouracil (for pregnant), Iodide (pre-surgery), I-131 (thyroid destruction) -Thyroid I uptake is low in destructive thyroiditis (give b-blocker)
48
Follicular adenoma (of thyroid)
benign, various appearances most non-functional, but some can produce thyrotoxicosis do NOT progress to carcinoma have fibrous capsule, smaller follicles
49
Thyroid carcinoma
uncommon, more women risk: ionizing radiation Papillary: most common, BRAF mutation, younger age, lymphatic spread, good prognosis, nuclear features are key Follicular: RAS mutation, older age, vascular spread, worse prognosis, invasion Medullary: RET mutation, neuroendocrine parafollicular C-cells, secrete calcitonin, MEN-2, amyloid stroma Anaplastic: p53 mutation, super bad, undifferentiated, distant metastasis, variable, pleomorphic

Endocrine / Reproduction (7 decks)

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