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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
Q

Bone disease in hyperparathyroidism

A

osteitis fibrosa cystica= osteoclasts, thin cortex, fibrosis of marrow
Brown tumor= osteoclasts, giant cells, hemorrhage, like giant cell tumor

26
Q

Parathyroid adenoma

A

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
Q

Renin angiotensin aldosterone system

A

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
Q

Renin system drugs

A

Renin inhibitors: aliskiren
ACE inhibitors: -pril
Angiotensin receptor blockers (ARBs): -sartan
Mineralocorticoid (aldo) receptor antagonists: spironolactone, eplerenone

29
Q

Primary hyperaldosteronism

A

hypertension, hypokalemia
high plasma aldo, low plasma renin activity (ratio high)
also secreting adrenocortical adenoma
bilateral hyperplasia of zona glomerulosa
Tx: adrenalectomy

30
Q

Secondary hyperaldosteronism

A

renal ischemia
decreased intravascular volume
Na wasting disorders

31
Q

Apparent mineralocorticoid excess

A

11BHSD2 deficiency

that protein converts cortisol to cortisone in the kidney, so if it isn’t there then cortisol can act like aldosterone

32
Q

Liddle’s Syndrome

A

mutation in amiloride sensitive ENaC

Tx: amiloride, triamterene (K-sparking diuretics)

33
Q

Pheochromocytoma

A

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
Q

Cortisol-Cortisone shuttle

A

cortisol is active, cortisone is not
11B-HSD2 in kidney converts cortisol to cortisone
11B-HSD1 in liver converts it back to cortisol

35
Q

Adrenal Insufficiency (low cortisol)

A

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
Q

Cushing’s Syndrome

A

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
Q

Structure of adrenal glands

A 
Cortex: 
-zona glomerulosa= mineralocorticoids
-zona fasciculata= glucocorticoids
-zona reticularis= estrogen and androgen
Medulla: chromaffine cells= catecholamines
38
Q

Adrenocortical hyperplasia

A

bilateral thickenening of adrenal cortex
mostly faciculata cells= clear cells= make glucocorticoids
can be diffuse or multi-nodular

39
Q

Adrenocortical Adenoma

A

yellow, encapsulated
can be functional or non-functional (most non)
mostly faciculata cells

40
Q

Adrenocortical carcinoma

A

rare, large, invasive
necrosis and hemorrhage
lymph node metastasis
can be well or poorly differentiated

41
Q

SIADH

A

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
Q

Diabetes Insipidus (DI)

A 
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
Q

Congenital hypothyroidism

A

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
Q

Chronic Lymphocytic Thyroiditis (Hashimoto’s)

A

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
Q

Hypothyroidism

A

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
Q

Graves Disease

A

hyperthyroidism due to autoimmune which stimulates thyroid via TSI thyroid stimulating immunoglobulin
increased rad-I uptake uniform and bilateral
-irregular follicles, scalloped colloid

47
Q

Hyperthyroidism (Thyrotoxicosis)

A

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
Q

Follicular adenoma (of thyroid)

A

benign, various appearances
most non-functional, but some can produce thyrotoxicosis
do NOT progress to carcinoma
have fibrous capsule, smaller follicles

49
Q

Thyroid carcinoma

A

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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