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Endocrinology USMLE Step 1

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1. are there increased decreased (increased uptake) 13. from where is chief cells in parathyroid gland
or decreased amino parathyroid released?
acids in the exactly what type of
circulation with cells?
increased insulin? 14. from where is prolactin adenohypophysis; increases
2. by what type of neuroendocrine cells; GI released? what effect dopamine synthesis and
cells are carcinoid does it have on the secretion from the
tumors caused by? hypothalamus? hypothalamaus (negative
where are they feedback!) and decreased GnRH
usually located? from hypothalamus
3. even though there is though there is a hyperkalemia due to 15. from where is hypothalamus; inhibition of Gh
hyperkalemia in transcellular shift from acidosis, there somatostatin released? and TSH from adenohypophysis
DKA there is a really is an intracellular depletion what does it result in?
depleted because of the osmotic diuresis 16. from where is TRH hypothalamus; TSH and prolactin
intracellular pulling potassium out (like sodium) released? what does it release from adenohypophysis
potassium. explain. result in?
4. from what aa are tyrosine 17. how can you tell if a decreased uptake
catecholamines patient is suffering from
made? hyperthyroidism due to
5. from what cells is a parafollicular C cells exogenous thyroid ?
medullary thyroid 18. how does a toxic hyperplasia causes gland
carcinoma? multinodular goiter involution
6. from what precursor POMC; ACTH become nontoxic?
is melanotropin 19. how does coma and d/t dehydration from diuresis
made from? what death occur in DKA and acidosis
else does this
precursor make? 20. how does hypercalcemia blocks NaCl reabsorption in the
cause nephrogenic thick ascending limb disrupting
7. from where do the pancreatic buds; in the tail of the diabetes insipidus? counter current exchange and
islets arise from? pancreas causing inability for aquaporin to
and where in the do its thing
pancreas are the
islets most 21. how does obesity because increased adipose
abundant? exacerbate insulin tissue also downregulates insulin
resistance? receptors
8. from where is parafollicular (C) cells of the thyroid;
calcitonin released? oppose action of PTH- decrease bone 22. how does the body decreases aldosterone; causes
what is its function? resorption of calcium (ie cause a respond to the increased even more hyponatremia and
decrease in serum calcium) volume in SIADH? what seizures!; slowly (cerebellar
does this cause? how pontine
9. from where is CRH hypothalamus; ACTH release from should you correct this? myelinosis)
released? what does adenohypophysis
it result in? 23. how do you diagnose a increased serum IGF-1
pituitary tumor of (produced by liver, release
10. from where is hypothalamus; prolactin release somatotrophs? activated by GH), and failure to
dopamine released? inhibition in adenohypophysis; D2 suppress serum GH following
what does it result oral glucose tolerance test
in? in what kind of
receptors? 24. how do you diagnose with water deprivation test, the
diabetes insipidus? and urine doesnt increase in
11. from where is GHRH hypothalamus; Gh release from then how do you osmolality; desmopressin
released? what does adenohypophysis differentiate between the
it result in? two types?
12. from where is GnRH hypothalamus; FSH and LH release 25. how do you differentiate acute (usually S. aureus) will
released? and does acute thyroiditis from have lymphadenoapathy
it result in? subacute?
26. how do you both short stature, but cretin is 36. in 17 alpha hydroxylase XY: pseduohermaphroditism
differentiate a patient increased in weight, pituitary is deficiency, how does an (because no DHT there is female
with cretinism from decreased in weight XY present? XX? external genitalia and because
one with pituitary of MIF presence there is no
dwarfism? internal reprostructures); XX:
27. how do you exogenous wont have increased "sexual infantilism": externally
differentiate between serum c peptide levels phenotypic female with normal
exogenous and internal sex organs but no
endogenous insulin? secondary sexual characteristics

28. How do you nonneoplastic/neoplastic: hot/cold 37. in a adrenal adenoma or atrophies d/t decreased ACTH
differentiate between and multiple nodules/single mass carcinoma, what happens
malignancy of thryoid to the rest of the adrenal
nodules? Give two gland?
ways. 38. in what causes of when there is increased ACTH
29. how do you dexamethasone suppression test cushings do you see (not iatrogenic or Adrenal
differentiate between which is a synthetic ACTH which amennorhea, hirsutism adenoma) and thus increased
the endogenous should result in decreased levels of and acne? androgen:estrogen ratio
causes of cushings? cortisol after a low dose 39. in what form is iodine I-
what should happen taken up from the blood
in a healthy into follicular cells of the
individual? thyroid?
30. how do you in secondary there will be no skin 40. in what form is Vit D Vit D2; Vit D3 (cholecalciferol) ;
distinguish primary hyperpigmentation and no when it is ingested from Vit D (Calcitriol)
from secondary hyperkalemia or met acidosis or plants? when it is
addisons? why? what hypotension because aldosterone is converted from 7
is a secondary form controlled by RAAS not ACTH; dehydrocholesterol in
due to? deficiency in ACTH production the skin? what is the
31. how do you treat a octreotide active form?
pituitary adenoma of 41. in what type of DM is type I, because there is enough
somatotrophs? DKA seen? why not the insulin to prevent ketoacidosis
32. how do you treat either surgical removal of the other type?
hyperaldosteronism? aldosterone secreting tumor or 42. in which congenital 17 alpha hydroxylase def and 11
spironolactone (an aldosterone bilateral adrenal beta hydroxylase deficiency; 21
antagonist that is a potassium hyperplasia do you see hydroxylase def.
sparing diuretic) hypertension?
33. how is T4 converted by 5' iodinase; T3 binds with more hypotension?
to T3? how are they affinity to receptors 43. in which congenital 21 hydroxylase def; 17 alpha
different? bilateral adrenal hydroxylase and 11 beta
34. how is zollinger octreotide, proton pump inhibitors hyperplasia do you see hydroxylase def
ellison syndrome increased renin?
treated? decreased?

35. if vit D cares about because bone has reserve of ca and 44. in which congenital 17 alpha hydroxylase deficiency;
bone health why does phosphate and it is releasing it from bilateral adrenal 21 hydroxylase and 11beta
it activate bone that reserve for bone mineralization hyperplasia do you see hydroxylase deficiencies
resorption? (in other places) male
pseudohermaphrotidism?
female
pseudohermaphrotidism?
45. is insulins effect an anabolic; increased glycogen
overall anabolic or and protein and triglyceride
catabolic effect? give synthesis and storage
examples.
46. of what cells are a chromaffin cells; neural crest 58. T/F all MEN disorders have AR false- AD
pheochromocytoma inheritance
derived from? and 59. T/F all thyroid hormone in the false- only free hormone
where do these cells blood is active (both T3 and T4)
come from?
60. T/F a pituitary adenoma results false- rest of pituitary
47. other than decrease T4 to T3 conversion in the in hyperpituitarism becomes hypopituitary
decreasing periphery
sympathetic 61. T/F beta blockers help FALSE.
activation, what else decrease O2 consumption in
do beta blockers do thyritoxicosis
in thyrotoxicosis? 62. T/F both hashimotos and de true
48. other than hypovitaminosis D, acute pancreatitis Quervains thyroiditis can be
hypoparathyroidism, because FA in fat necrosis bind preceded by hyperthyroid
what are other calcium periods
causes of 63. T/F DM II has an HLA false DM I does
hypocalcemia? association- DR3 and 4
49. other than increased large tongue with deep furrows, big 64. T/F DM II has a weak false- strong
lateral bone hands and feet, deep voice, coarse polygenic genetic
growth,what else facial features, hypertension (sodium predisposition
does acromegaly retention), hyperglycemia, insulin 65. T/F DM II has low beta islet not always
present with? resistance due to hyperglycemia cell number
(increased gluconeogenesis)
66. T/F DM I tends to present true
50. other than increased increased cAMP because decreasing more abruptly while DM II
phosphate in the phosphate reabsorption in the PT manifestations tend to present
urine, what else is results in release of cAMP more chronicly
found in the urine
67. T/F dopamine is tonically true
with PTH?
inhibited by dopamine
51. other than increasing by increasing calcitriol production by
68. T/F follicular thyroid false- that is an adenoma
bone resorption, how increasing 1 alpha hydroxylase and
carcinoma has intact capsule
does PTH result in by increasing calcium reabsorption at
around it
increased calcium? the DCT
69. T/F gastrin secreting tumors not all- also duodenum
52. other than inuslin inability to secrete enough insulin in
are found in the pancreas
resistance, what else response to corresponding glucose
contributes to insulin levels 70. T/F GI carcinoid tumors have not all do- only those that
resistance in DM II? have 5-HT as a marker have metastasized outside
the GI (because liver
53. other than MEN I, Wermers
metabolizes it)
what is it known as
known as? 71. T/F glucocorticoids are used in True
croup and COPD
54. other than renin edema- in primary there is no edema
level, how do you because of escape pathway of 72. T/F glucose is freely filtered true
distinguish between sodium; in secondary there is edema through bowmans capsule
primary and (that is what caused it in the first 73. T/F GnRH uses cAMP false- GHRH (GnRH uses
secondary place! pull of IV volume out) IP3)
hyperaldosteronism?
74. T/F Graves presents with false- nontender
55. other than the kidney stones and stomach ulcers diffuse, symmetrical tender
neoplasias what else (parathyroid and gastrinoma) goiter
does MENI present
75. T/F Hashimotos thyroiditis is false- that is deQuervains
with?
usually preceded by a flulike Subacute thyroiditis
56. other than TRH what estrogen (from OCPs and pregnancy) viral illness and is self limited
else increases
76. T/F hashimotos thyroidits False- enlarged but not
prolactin release?
patients have a enlarged tender
57. T/F ADH V1 receptor False- uses IP3, V2 uses cAMP tender thyroid
uses cAMP
77. T/F hyperreflexia is a sign of true
hypocalcemia
78. T/F hyperthyroidism can false- graves causes this by 98. T/F TBG binds all T3/T4 false- binds MOST- only free
cause exopthalmos activating fibroblasts to in the blood hormone is active
deposit connective tissue 99. T/F tetany is a sign of true
behind eyes hypocalcemia
79. T/F in addisons disease the true 100. T/F the chromaffin cells false- postganglionic and
adrenal medulla is spared of the adrenal cortex ganglionic sympathetic
80. T/F in circulation cortisol is false- bound to are are considered
free corticosteroid binding preganglionic
globulin (CBG) 101. T/F the true
81. T/F Insulin is necessary yes neurohypophysis
always in DM I receives less blood
82. T/F it is more common to see true from the hypophysial
the symptoms of polyuria, portal system than
polydipsea, thirst and weight adenohypophysis
loss in DM I 102. T/F there is insulin false- insulin resistance
83. T/F like the brain, RBCs false only the brain does sensitivity in cushings (acanthosis nigricans!)
depend on glucose and use this, RBCs cant use ketones 103. T/F Thyroid cancer false- euthyroid
ketones during starvation patients usually present
84. T/F maternal thyroid can true! keeps baby euthyroid hypothyroid
cross placenta (brain maturation!) 104. T/F toxic multinodular false
85. T/F most neuroblastomas are false- malignant :( goiter is dependent on
benign TSH activation

86. T/F most thyroid hormone is false! most is in T4 form and 105. T/F TRH uses cAMP false- TSH (TRH uses IP3)
in the T3 form isnt converted to T3 until in 106. T/F you see tetany in false- free ionized Calcium is the
periphery hypoalbunemia same
87. T/f muscle cramps are a sign false; opposite 107. T/F you see tetany in true- free ionized calcium has
of hypercalcemia resp or met alkalosis decreased
88. T/F only T4 is found on TBG false TBG binds both 108. what activates low serum phosphate
89. T/F only vit D2 has to be false- both D3 and D2 have phosphate reabsorption concentrations increase 1 alpha
hydroxylated to 1,25 (OH)2 in to be activated from the intestine how? hydroxylase activity and get
the liver and kidney increased absorption of calcium
and phosphate from the intestine
90. T/F papillary thyroid false
carcinoma has bad prognosis 109. what antithyroid drugs propylthiouracil and methimazole
block peroxidase?
91. T/F peptic ulcers and true
diabetes are sequellae of 110. what are examples of jaw, hands, feet, frontal bossing
cushings lateral bone growth? (enlarged hat size); everything
linear bone growth? (epiphyses have not fused yet)
92. T/F phosphate regulates PTH FALSE.
secretion. 111. what are four causes of pituitary tumor, trauma, surgery,
a central diabetes histiocytosis X
93. T/F PPAR gamma decreases false! increases insipidus?
insulin sensitivity
112. what are four causes of hypomagnesia, DiGeorge
94. T/F prolactin stimulates milk false- oxytocin stimulates hypoparathyroidism? syndrome, autoimmune
release from the breasts the contraction the destruction, accidental surgical
myoepithelial cells, prolactin excision
stimulates milk release
113. what are four causes of lithium, demecyclocine,
95. T/F Reidels thyroiditis is a true nephrogenic diabetes hypercalcemia, hereditary
form of hypothyroidism insipidus?
96. T/F T3 is pure catabolic false- bone growth, CNS 114. what are four symptoms facial flushing, diarrhea, right
maturity (esp fetally!), seen in carcinoid sided heart defects, asthamtic
gluconeogenesis syndrome? wheezing
97. T/F T3 is purely anabolic false- glycogenolysis,
lipolysis
115. what are Kimmelstiel mesangial proliferations in 128. what are the clinical pretibial myxdema and
Wilson Nodules? response to endothelial damage in findings that are opthalmopathy (proptosis and EOM
glomerular basement membranes unique in Graves? swelling) d/t mimicry in fibroblasts
116. what are carrier proteins in the posterior why do they occur? results in connective tissue
neurophysins? pituitary that carry the ADH and deposition
oxytocin hormones in circulation 129. what are the alpha (glucagon), beta (insulin), and
117. what are other causes hypervitaminosis D, granulamotous endocrine pancreas somatostatin; into islets of
of hypercalcemia diseases (especially sarcoidosis), cell types and what langerhans which are collections of
(other than malignancies (paraneoplastic), do they produce? these cells- with beta central (INsulin
hyperparathyroid)? increased bone resorption how are they INside) and alpha cells peripheral
(multiple myeloma or bone mets or organized? and somatostatin cells interspersed
primary bone cancer), thiazides 130. what are the fates of in the adrenal cortex
118. what are secondary when kidney has perception of low androstenedione and androstenedione is turned into
causes of IV volume and renin activated- where do these testosterone and in the periphery
hyperaldosteronism? chronic renal artery stenosis, CHF, changes occur? androstenedione is turned into
what is the renin level? chronic renal failure, cirrhosis, estrone
nephrotic syndrome; high! 131. what are the fates of via 5alpha reductase to DHT; via
119. what are the 4 B's of 1) bone growth 2) brain maturation testosterone in the aromatase to estradiol
T3? 3) b1 4) increased BR periphery?

120. what are the 5 P's of a perspiration, paroxysmal, 132. what are the findings hypertension, truncal obesity, moon
pheo? what else can palpitations, pallor, pain in cushings facies, buffalo hump, hyperglycemia,
you see in a pheo? (headache), pressure (elevated); syndrome? osteoporosis, amennorhea, and
illeus (catecholamines) and anxiety immune suppression, muscle
weakness, orthostatic hypotension
121. what are the acute polyuria, polydipsia, weight loss,
manifestation of polyphagia; DKA (type 1); 133. what are the findings hypokalemia, met alkalosis,
diabetes mellitus? hyperosmolar coma (type II) in hypertension
what is the serious one hyperaldosteronism?
you see more in Type 134. what are the findings fibrotic singular hard goiter
I? how about in Type of Reidels
II? thyroiditis?
122. what are the cardio bradycardia, dyspnea on exertion; 135. what are the four eyes, kidneys, blood vessels, nerves
and resp changes seen chest pain, palpitations, arrythmias body parts that are
in hypo/hyper (a. fib) most affected in
thyroidism? chronic DM?
123. what are the causes of destruction by disease 136. what are the TZDs, bind PPAR gamma a
adrenal atrophy in (autoimmune, milary TH, mets) or glitazones and transcription factor that increase
addisons disease? atrophy; autoimmune destruction thiazolidinediones? insulin sensitivity
what is the mcc? what do they do and
124. what are the lipophillic and insoluble in plasma, how?
characteristics of need to circulate bound to specific 137. what are the immune neutrophilia, eosinophilia,
steroids? what are the binding globulins which increase findings in addisons? lymphocytosis
implications? their solubility 138. what are the immune neutropenia, eosinopenia,
125. what are the clinical protruding umbilicus, protuberant findings in cushings? lymphopenia; increased proteolysis
findings in a cretin? (5 tongue, pale, pot bellied, puffy why muscle
P's) faced, short weakness?
126. what are the clinical galactorrhea, amennorhea, 139. what are the mucor and rhizopus
findings in a infertility, low libido infectious
prolactinoma? complications of
127. what are the clinical hypothyroid, diffuse tender DKA?
findings in thyroidmegaly, jaw pain, increased 140. what are the lab increased free cortisol in urine,
deQuervains ESR, think inflammation! findings in cushings? hypokalemia and metabolic alkalosis
thyroiditis? (cortisol at high concentrations can
act as a mineralicorticoid),
hyperglycemia
141. what are the lab values of Ca, PTH= high, Ca= low, alk 152. what are the signs and kussmaul breathing,
PTH, Alk phos, phosphate in phos= high, phosphate= low symptoms of DKA? what nausea/vomitting, abdominal
secondary parathyroidism? are the lab values pain, psychosis/delirium,
142. what are the lab values of PTH= high, Ca= high, (glucose, acid/base, dehydration, fruity breath odor;
PTH, Ca, Phosphate, alk phos phosphate= low, alk phos= ketone, leukocytes, hyperglycemia, acidosis,
in hyperparathyroidism? what high; cAMP potassium)? decreased bicarb, increased
can you find in the urine? blood ketone levels (more
betahydroxybutyrate),
143. what are the levels of Ca and PTH= really high, Ca= high hyperkalemia
PTH in tertiary
parathyroidism? 153. what are the signs of hyperreflexia, tetany, muscle
hypocalcemia? cramps, tingling, chvostek sign
144. what are the main findings in short stature, short 4th and and trousseau sign
Albrights hereditary 5th digits, hypocalcemia,
osteodystrophy? what are the mental retardation , met 154. what are the symptoms of tetany and muscle weakness
levels of PTH, Ca, and calcification of basal hypokalemia?
phosphate? ganglia; PTH= normal to 155. what are the T3 functions? bone growth (synergism with
high, Ca= low, phosphate= GH), CNS maturation
high (perinatally esp), increases beta
145. what are the main findings in hyperphosphatemia 1 receptors on heart (CO, HR
hypoparathyroidism? (metastatic calcification in and SV all increased),
basal ganglia), increased BMR via increased
hypocalcemia= tetany, Na+/K+ ATPase activity which
Trousseau sign (occlusion increases O2 consumption, RR,
of brachial artery with bp and body temperature and
cuff causes carpal spasm), increased glycogenolysis,
Chvostek sign gluconeogenesis and lipolysis

146. what are the manifestation of increased LDL (due to 156. what are the three enzyme 17 alpha hydroxylase, 21
hyperinsulinemia due to increased triglyceride deficiencies that cause hydroxylase, 11 beta
insulin resistance in the synthesis), decreased HDL, congenital bilateral hydroxylase; 21 hydroxylase
prediabetic metabolic causes hypertension adrenal hyperplasias? deficiency; glucocorticoids;
syndrome? (hints what does it because insulin causes which is the most enlargement of adrenal glands
do to: LDL? HDL? blood sodium retention, CAD common? what product due to an increase in ACTH
pressure and why? your (insulin causes damage to requires all three of these because of low cortisol levels
endothelial cells?) the endothelial cells) enzymes? what is two and hyperpigmentation
common symptoms because MSH (melatonin
147. what are the manifestations of microvascular damage and among all three and what stimulating hormone) is made
nonenzymatic glycosylation macrovascular damage; causes these two from the same precursor as
of large vessels in DM? what retinopathy, glaucoma and symptoms? ACTH is (POMC)
are the complications of these nephropathy; and CAD,
manifestations? peripheral vascular 157. what are the three layers Zona Glomerulosa, Zona
occlusion disease and of the adrenal cortex? (in Fasciculata, Zona Reticularis;
gangrene order from outside to Zona Fasciulata
inside) which is the
148. what are the manifestations of gastric paresis, bladder biggest?
the neuropathy seen in DM? impotence, orthostatic
hypotension 158. what are the three main polyuria, polydipsia, inability to
symptoms of diabetes concentrate urine
149. what are the manifestations of cotton wool spots from insipidus?
the retinopathy in DM ? exudates, hemorrhage,
microaneurysms and vessel 159. what are the three main urine osmolality > serum
proliferation symptoms of SIADH? osmolality; hyponatremia
(dilutional effect from
150. what are the metabolic hypoglycemia hypotonic gain of water);
findings in addisons? excessive water retention
151. what are the radiologic salt and pepper
findings in osteitis fibrosa appearance of bone and
cystica? what is the main subperiosteal bone
symptom? resorption
160. what are the three results of increased fat lipolysis to 174. what autonomic is the adrenal sympathetic; Ach;
no insulin, glucagon excess make increased plasma FFA medulla innervated by? what nicotinic (N); Na+/K
and increased epinephrine and ketoacids, proteinlysis are the NT? what are the ligand gated channels
in DKA? (hint-what does it leads to increase aa and receptors called? what kind of
do to fat? protein? glucose nitrogen in urine, receptors are they?
uptake)? hyperglycemia and osmotic 175. what autonomic receptors use B1, B2, D1, H2, V2
diuresis cAMP as their signalling
161. what are the three tests in fasting serum glucose, pathway?
DM? HbA1C, glucose tolerance 176. what blocks Iodine uptake from anions: perchlorate and
test the blood into follicular cells? pertechnetate
162. what are the two adenohypophysis and 177. what can be found in the plasma increased catecholamine
components of the neurohypophysis; oral of pheo patients? urine? levels; breakdown
pituitary? what are there ectoderm (rathkes pouch) product of
embryological derivatives? and neuroectoderm; norepinephrine: VMA
which makes the majority of adenohypophysis
the pituitary? 178. what can happen to a newborn saltwasting can cause
in 21 hydroxylase deficiency? hypovolemic shock
163. what are the two main nonenzymatic glycosylation
causes of the chronic and osmotic damage 179. what can you find in the urine HMA and VMA
manifestations in diabetes with neuroblastoma?
mellitus? 180. what causes calcitonin increased serum Ca2+
164. what are the two targets of nerves and eyes secretion?
osmotic damage in DM ? 181. what causes the inuslin insulin its self
165. what are the two unique abdominal mass and HTN resistance in diabetes mellitus downregulates its own
features seen in a child with type II? receptors
neuroblastoma? 182. what causes the microvascular diffuse thickening of the
166. what are the urine findings specific gravity is less than damage in DM- more basement membrane-
in diabetes insipidus? 1.006; serum osmolality is specifically what is the response increased type IV
plasma osmolarity? greater than 290 to the nonenzymatic collagen and mesangial
glycosylation of microvessels? deposits (KW nodules)
167. what are the values of Ca, Ca= low, phosphate= high,
phosphate and PTH in PTH= low 183. what causes the osmotic glucose gets turned into
hypoparathyroidism? damage seen in DM? sorbital by aldolase
reductase which is
168. what are three causes of neisseria meningitidis osmotically active and
adrenal hemorrhage? septicemia, DIC, endotoxic causes osmotic damage
shock
184. what causes the tricuspid regurg collagen dep in valves
169. what are three features of a DM, necrolytic erythema, and PS in carcinoid syndrome?
glucagonoma? anemia
185. what causes zollinger ellison gastrinoma either in
170. what are thyroid hormones? iodine containing hormones syndrome? duodenum or pancreas
that control the body's
metabolic rate 186. what cells in the B-FLAT: basophils- FSH,
adenohypohysis are basophils? LH, ACTH, TSH; alpha;
171. what are two causes of hyperphospatemia and all of these cells produce ACTH
metastatic calcification? hypercalcemia; in the CNS hormones with what common
where does it usually (basal ganglia) and eyes subunit? what is the exception?
occur?
187. what cells only have aldolase Schwann cells, lens,
172. what are two main headache and no peripheral reductase? retina and kidneys
symptoms of a pituitary vision; mass effect increases
adenoma? why? ICP and bilateral hemianopia 188. what controls phosphate calcitriol; increasing
d/t pituitary pushing on optic homeostasis? how? absorption from
chiasm intestines and increased
bone resorption
173. what are TZDs used for? used in Type II DM
189. what controls uterine oxytocin
hemorrhage?
190. what decreases TRH? negative feedback by
free T3
191. what do catecholamines do to alpha receptors increase 208. what drugs cause aminoglycosides, alcohol, diuretics;
insulin? insulin decreased Mg2+ diarrhea
192. what does an adrenal cushings syndrome; (and thus
adenoma or carcinoma result nodular adrenal decreased PTH)?
in? what is the gross adrenal hyperplasia; ACTH low; what pathology
look like? what is the ACTH increased cortisol after state cause
level? dexamethasone low and high dose decreased Mg2+?
suppression test response? 209. what effect do dopamine antagonists and estrogens
193. what does bone resorption it means that osteoclasts antipsychotics and stimulate prolactin secretion
mean? and what hormones are releasing calcium and OCPs have on
cause it? phosphate from the bone prolactin
to be resorbed by the secretion?
blood; PTH 210. what effect does met or resp alkalosis causes an
194. what does calcium renal polyuria and renal failure alkalosis have on increased amount of negative charges
stones cause? total and free Ca? on albumin which then takes free
why? ionized Ca to neutralize those
195. what does decreased glucose hyperglycemia, glucosuria charges- total free Ca is normal, but
uptake in DKA result in? and osmotic diuresis which ionized albumin has decreased causing
pulls electrolytes out an increase in PTH
196. what does Ectopic ACTH Cushings syndrome; small 211. what effect does stimulates gastrin release; PUD
cause? what are common cell lung cancer, bronchial calcium have on
releasers of ectopic ACTH? carcinoids; increased the stomach? what
what is the level of ACTH? ACTH; high cortisol haver does
what is the response with both high and low doses hypercalcium
dexamethasone test? of dexamethasone result in because
197. what does excess GH cause in acromegaly; gigantism of this?
an adult? in a child? 212. what effect does maintains blood pressure; upregulates
198. what does excess GH do to sodium retention occur cortisol have on alpha 1 receptors
blood pressure? with both increased GH blood pressure?
and insluin how?
199. what does hypomagnesia hypocalcemia! (via 213. what effect does decreases IL 2 production and
result in? decreased PTH) cortisol have on decreases release of histamine and
200. what does increased lipolysis increased plasma FFA and immune function? serotonin
in DKA result in? ketoacidosis how?

201. what does increased protein increased aa and nitrogen 214. what effect does its antiinflammatory by inhibiting
metabolism in DKA result in? in the urine which pulls out cortisol have on phospholipase A2
how does this add to more water inflammation?
dehydration? how?

202. what does oposclonus myoclonus jerks, chaotic 215. what effect does increases gluconeogenesis, lipolysis
myoclonus, a common eye movements cortisol have on and proteolysis; decreases insulin
paraneoplastic syndrome seen metabolism- concentration
in patients with specifically
neuroblastoma, present with? glucose
metabolism? fat?
203. what does the FSH, LH, prolactin, GH,
protein? insulin?
adenohypophysis secrete? ACTH, TSH, melanotropin
216. what effect does decreases; increases
204. what does vit D deficiency rickets in children and
cortisol have on
cause? osteomalacia in adults
REM? awakeness?
205. what do pheochromocytomas epinephrine,
217. what effect does decreases bone formation by
secrete? norepinephrine, dopamine
cortisol on bone decreasing type I collagen formation
206. what drug can cause SIADH? cyclophosphamide formation? how?
207. what drugs can be used in a dopamine agonists;
prolactinoma? give an bromocriptine
example.
218. what effect does decreases; normal; decreases 229. what effect does decreases its release
hepatic failure somatostatin on TSH?
have on TBG? 230. what effect does both activate and inhibit
free thyroid sympathetic activation insulin secretion; Beta and
hormone? total have on beta cells? through alpha respectively
thyroid what receptors?
hormone?
231. what effect does TNF alpha inhibits its secretion by
219. what effect does because 40% of calcium is bound to have on insulin? how? what inducing the serine kinase of
hypoalbunemia albumin in blood, hypoalbuminemia will is the result on insulin beta receptor rather than the
have on total result in decreased bound albumin (and senstivity? tyrosine; results in increased
and free Ca? thus total Ca) but the same amount of insulin resistance
why? free ionized Calcium so PTH is not
activated- it cause the pathological state 232. what effect do inhibit its secretion by
of normal PTH with low total serum Ca glucocorticoids and inducing threonine
glucagon have on insulin phosphorylation instead of
220. what effect does increased prolactin and thus secretion? how? tyrosine; results in increased
hypothyroidism hypogonadism insulin resistance
have on
prolactin? 233. what else is MEN 2A known sipples syndrome
gonadism? as?

221. what effect does increases, normal, increases 234. what endocrine hormones FLAT CHAMP goes to cAMP:
increased use cAMP as apart of their FSH, LH, ACTH, TSH, CRH,
estrogen signaling pathway? hCG, ADH (V2), MSH, PTH,
(pregnancy) calcitonin, GHRH, glucagon
have on TBG? 235. what enzyme deactivates 24 hydroxylase in kidney;
free thyroid Vit D? what is this new 24,25 (OH)2
hormone? total inactive form?
thyroid 236. what gene is associated ret gene; MEN 2A and MEN
hormone? with which MEN disorders 2B
222. what effect does inhibits glucagon release 237. what happens to all three decreased sex hormones,
insulin have on products of the adrenal decreased cortisol, increased
alpha cells? cortex with 17 alpha aldosterone
223. what effect does increases it by phosphorylating hydroxylase deficiency?
insulin have on phosphofructokinase 2 238. what happens to all three decreased aldosterone,
fructose 2,6 products of the adrenal increased 11-deoxycortisol,
bisphosphate? cortex with deficiency of 11 decreased glucocorticoids,
how? beta hydroxylase? increased sex hormones
224. what effect does increases cellular uptake of potassium 239. what happens to all three decreased aldosterone,
insulin have on products of the adrenal decreased cortisol, increased
potassium? cortex with deficiency of sex hormones
225. what effect does causes Na+ retention 11B hydroxylase?
insulin have on 240. what happens to reflexes relfexes go down and
sodium in the and the GI system in hypo constipation in hypo; reflexes
kidneys? and hyperthyroidism? go up and diarrhea in hyper
226. what effect does hypomagnesia causes 241. what helps you distinguish PTH levels
magnesium have hypoparathyroidism because magnesia is between hypercalcemia
on PTH? why? cAMP cofactor for PTH receptor due to a parathyroid
227. what effect does increases bone resorption by indirectly adenoma or due to a
PTH have on activating osteoclasts through increasing different malignancy?
bones? how production of M-CSF and RANK-L on 242. what HLA is Hashimotos HLA- DR5
exactly? osteoblasts associated with?
228. what effect does decreases serum phosphate and 243. what hormones have a TSH, LH, FSH, hCG; a beta
PTH have on increases urine phosphate by decreases common alpha subunit? unit which determines the
phosphate how? kidney reabsorption at the PT what differentiates them hormones specificity
and how?
244. what increases PTH decreased free serum Ca; 258. what is desmopressin used central diabetes insipidus
secretion? decreases decreased free Mg2+ to treat?
its secretion? 259. what is IGF2? what is it insulin like growth factor 2;
245. what increases the irradiation as a child important for? in what type fetal development;
risk of developing of tumors is it produced in mesenchymal tumors;
papillary carcinoma? and what is the result? hypoglycemia
246. what induces chronic stress 260. what is IGF a receptor for? Growth hormone!
secretion of 261. what is nonenzymatic when hyperglucosemia
corticosteroids? glycosylation? what does it causes glycosylation of aa in
247. what infections are UTIs, external otitis media, candida lead to? endothelial proteins leading
diabetics vulvavaginitis to vessel permeability and
predisposed to? atherogenesis
248. what is 5 HT? serotonin 262. what is osteitis fibrous bone lesions (usually in jaw
249. what is a cause of cretinism cystica? what is the and skull) associated with
hypothyroidism in histology you see for it? hyperparathyroidism; cystic
children? what is the pathogenesis? brown (hemorrhagic)
lesions; osteoporosis due to
250. what is addisons primary chronic adrenal continual bone resorption
disease? what are insufficiency; deficiency of and osteoclast activity
the clinical aldosterone and cortisol causing
symptoms? what is hypotension, salt cravings, 263. what is kidney unresponsiveness to
the most common hyperkalemia, normal anion gap met pseudohypoparathyroidism? PTH (or decreased 1 alpha
cause? what are acidosis, skin hyperpigmentation, what is another name for it? hydroxylase activity);
other causes? fasting hypoglycemia, and what is its mode of Albrights hereditary
lymphocytosis inheritance? osteodystrophy; AD

251. what is a hurthle metaplastic epithelial cell with 264. what is renal bone lesions in secondary
cell? eosinophilic granular cytoplasm osteodystrophy? what is it (or tertiary)
usually due to? hyperparathyroidism due to
252. what is an acute waterhouse friderichsen syndrome; increased levels of
cause of adrenal hemorrhagic infarction d/t parathyroid from
adrenocortical adrenal vessels blockage hypovitaminosis D due to
deficiency? what renal failure
causes the
deficiency? 265. what is T3? T4? DIT + MIT; MIT + MIT

253. what is an example exenatide; increase insulin and 266. what is tertiary autonomous secretion of
of GLP 1 analog? decrease glucagon release hyperparathyroidism? what PTH (even after Ca has been
what is the result? is it usually due to? repleted); usually due to
secondary
254. what is a precipitator stress (pregnancy for ex)
hyperparathryoidism from
of Graves?
chronic renal disease
255. what is a primary aldosterone secreting tumor; conns
267. what is the breakdown HVA, VMA, metanephrine
cause of syndrome; low
produce of dopamine?
hyperaldosteronism?
norepinephrine?
what is it called?
epinephrine?
what is the renin
level? 268. what is the breakdown HVA
product you have find in the
256. what is a toxic its focal areas of hyperfunctioning
urine of a patient with
multinodular goiter? follicle hyperplasia that are TSH
neuroblastoma?
independent d/t a mutation in TSH
receptor 269. what is the cause of death in arrhythmias (a. fib)
thyrotoxicosis?
257. what is a tumor calcitonin; hypocalcemia
marker of medullary 270. what is the cause of endemic endemic goiter!
thyroid carcinoma? cretinism? what is the cause (geographical area with no
what else does it of sporadic cretinism? iodine); defect in T4
cause? formation or development
failure in thyroid formation
271. what is the cause of toxic mutation causes TSH 285. what is the histology hurthle cells, lymphocytic infiltrate
multinodular goiter? what is independent seen in a hashimotos (mononuclear) with germinal
the cause of nontoxic hyperfunctioning follicular patient? centers and fibrosis
goiter? patches; iodine deficiency 286. what is the histology uniform follicles; good
causes TSH dependent seen in follicular
hyperplasia (but not thyroid carcinoma?
hyperthyroid like toxic goiter) what is the prognosis?
272. what is the chvostek sign tapping on the 7th cranial 287. what is the histology follicular hyperplasia turning into
and what is a sign of? nerve causes twitching of seen in Graves? papillary infolding
facial muscles; hypocalcemia
288. what is the histology sheets of parafollicular C cells in
273. what is the clinical use of inflammation, eyes, allergies, seen in medullary an amyloid stroma
glucocorticoids? fetal lung maturation, croup carcinoma?
274. what is the difference GnRH stimulates release of 289. what is the histology granulomatous formation with
between GnRH and GHRH? FSH and LH; GHRH stimulates seen in Subacute multinucleate giant cells
release of GH thyroiditis (de
275. what is the direct precursor 11 deoxycortisol; 11 beta Quervains)?
to the last step in cortisol hydroxylase; mineralcorticoid 290. what is the hyponatremic volume contraction
synthesis and what enzyme hypotension in
is involved in this last step? addisons from?
what type of steroid is the
291. what is the Jod thyrotoxicosis in someone who
precursor?
Basedow was previously iodine def goiter
276. what is the effect of a not only galactorrhea but phenomenon? who become iodine replete
prolactinoma on males? also infertility d/t decreased
GnRH 292. what is the left adrenal left adrenal vein--> left renal vein-
gland vein drainage? -> IVC;
277. what is the embryonal mesoderm right adrenal gland right adrenal vein--> IVC; gonadal
origin of the adrenal vein drainage? to what veins
cortex? veins is this system
278. what is the embryonal neural crest; chromaffin cells similar to?
origin of the adrenal 293. what is the main though decreased aldosterone
medulla? what are the cells clinical presentation there is increased 11deoxcortisol
of the adrenal medulla and why? how does an and results in hypertension,
called? XY present? XX? hypokalemia, metabolic alkalosis;
279. what is the final step in vit D 1 alpha hydroxylase in the XY: precocious puberty; XX:
activation? what three kidney; decreased phosphate, pseudohermaphrotidism
things regulate this last increased PTH, and 294. what is the main hypotension, metabolic acidosis,
step? what downregulates? decreased free calcium; vit D clinical presentation? hyperkalemia, hypoglycemia,
feedback! how does an XY increased renin and volume
280. what is the first step in production of pregnelone present? XX? depletion; XY: precocious
adrenal steroid synthesis? from cholesterol via puberty; XX: virilization (female
what enzyme is involved in desmolase; ACTH and pseudohermaphrotidism)
this step? what activates ketoconazole 295. what is the main hypertension, hypokalemia,
this enzyme? deactivates clinical presentation in metabolic alkalosis, decreased
it? 17 alpha hydroxylase renin, hypoglycemia
281. what is the function of stimulates milk production in deficiency?
prolactin? the best, inhibits ovulation 296. what is the main recurrent ulcers
and spermatogenesis symptom seen in
282. what is the glucose uptake GLUT 1 zollinger ellison
transporter in brain and syndrome?
RBCs? 297. what is the mcc of iatrogenic (exogenous); low;
283. what is the histology in a sheet of chief cells cushings? what levels Cushings SYNDROME
parathyroid adenoma? of ACTH correspond?
284. what is the histology in DM islet leukocytic infiltrate; islet what is it called?
I? DM II? amyloid deposit 298. what is the mcc of parathyroid adenoma
hyperparathyroidism?
299. what is the mcc of Graves' dx 313. what is the overall bone health- provide Ca and
hyperthyroidism? goal of Vit D? what phosphate to ECF for bone
300. what is the mcc of Hashimotos thyroiditis are the two specfic mineralization; increase absorption of
hypothyroidism? functions of vit D? calcium and phosphate (intestine and
kidney) and increase bone resorption
301. what is the mcc of hyperparathyroidism to release Ca and phosphate
nonmalignant hypercalcemia?
314. what is the type II hypersensitivity autoAbs
302. what is the mcc of secondary chronic renal disease, pathogenesis of (activating) to TSH receptor
hyperparathyroidism? what is hypovitaminosis D Graves?
another cause?
315. what is the type II and type IV autoimmune
303. what is the mechanism of block phospholipase A2 so pathogenesis of hypersensitivity disorders (antibodies
glucocoritcoids in that no leukotrienes or hashimotos? to thyroid and as well cytotoxic T cell
inflammation? prostaglandins are formed destruction)
304. what is the most common subacute deQuervains 316. what is the arteriosclerosis; atherosclerosis
cause of painful thyroid? hint: thyroiditis pathology seen in
it is also hypothyroid microvascular
305. what is the most common papilloma carcinoma disease in DM type
endocrine neoplasm and II? macrovascular?
thyroid cancer? 317. what is the PPAR gamma is a nuclear receptor
306. what is the most common prolactinoma peroxisome that is a transcription factor and alters
pituitary adenoma? proliferator gene transcription to iNCREASES
307. what is the most common prolactinoma; acidophils activator receptor insulin sensitivity; TZDs
pituitary adenoma? what kind gamma? what is the
of cells are these? result? what drugs
activate this?
308. what is the most common phechromocytoma
tumor of the adrenal medulla 318. what is the primary viral or immune destruction of beta
in adults? defect in DM I? DM cells; insulin resistance
II?
309. what is the most common phemochromoctyoma;
tumor of the adrenal medulla neuroblastoma 319. what is the alpha and beta chain connected by
in adults? children? proinsulin hormone disulfide bonds and a c peptide
made of? what chain; c peptide gets cut off
310. what is the most common neuroblastoma; post
happens when
tumor of the adrenal medulla ganglionic sympathetic
proinsulin gets cut
in children? of what kind of neurons
into insulin?
cells is this tumor?
320. what is the preganglionic sympathetic fibers;
311. what is the number one cause ectopic (from small cell
regulatory control catecholamines (epi, NE)
of SIADH? what are two other lung cancer for example),
of the adrenal
pathological causes? lung
medulla? what is
disease (TB), CNS
secreted in
disorders/head trauma
response?
312. what is the number one Cushings DISEASE- ACTH
321. what is the ACTH from ant pit (CRH from
endogenous cause of from pituitary adenoma;
regulatory control Hypothalamus); corticosteroids
Cushings? what is the ACTH high; increased cortisol
of the zona
level? what is the with low dose and
fasciculata? and
dexamethasone suppression decreased coritsol after a
what does it
test response? high dose
produce in
response?
322. what is the ACTH (ant pit) and CRH
regulatory control (Hypothalamus); sex androgens
of the zona
reticularis? and
what does it
produce in
response?
323. what is the regulatory renin-angiontensin (Ang II); 338. what is the fluids, insulin, potassium
control of zona Aldosterone treatment for DKA?
glomerulosa? and 339. what is the demeclocycline OR decrease water
what does it produce treatment for intake
in response? SIADH?
324. what is the renin level renin high; normal 340. what is the phenoxybenzamine (irrerversible
in primary Addisons? treatment of a alpha blocker) before surgery;
secondary addisons? pheo? metyrosine
325. what is the result on hirsutism from more free 341. what is the carpopedal spasm; hypocalcemia
females in decreased testosterone trousseau sign and
SHBG (sex hormone what is a sign of?
binding globulin)?
342. what is three orphan annie (ground glass nuclei),
326. what is the result on gynecomastia from lower free histologic features in nuclear membrane grooves gives
males in increase testosterone papillary carcinoma the impression of intranuclear
SHBG (sex hormone thyroid inclusions, and psammoma bodies
binding globulin)?
343. What is stress induced catecholamine surge;
327. what is the rule of 1/3s 1/3 mets, 1/3 multiple, 1/3 present thyrotoxicosis? what hyperthyroid states (like Grave)
in carcinoid with 2nd malignancy is it a serious which cause increased
syndrome? complication of? catecholamine receptors
328. what is the source of follicular cells in the thyroid 344. what is used to glucocorticoids
thyroid hormone? induce fetal lung
329. what is the T3 and decreased; increased maturation?
iodine uptake in 345. what is used to oxytocin by stimulating uterine
someone with stimulate labor? contractions; milke let down
hypo/hyper what else can it
thyroidism? stimulate?
330. what is the therapeutic acute hypercalcemia 346. what is used to treat octreotide
use of calcitonin? acromegaly,
331. what is the three main stones bones and groans: PTH carcinoid,
symptoms seen in causes bone resorption and gastrinoma and
primary lesions, hypercalcemia causes glucagonoma?
hyperparathyroidism? calcific stones, hypercalcemia also 347. what is used to treat GH; turners syndrome
causes constipation GH deficiency? what
332. what is the toxicity of photosensitivity, bone and teeth else can it treat?
demeclocycline? abnormalities, nephrogenic DI 348. what is used to treat demecylcocine; tetracyclines
333. what is the toxicity of nausea, vomitting, pancreatitis SIADH? of what
GLP 1 analogs? drug family is this a
334. what is the toxicity of cushings syndrome; addisons member of?
glucocorticoids? how 349. what kind of anion gap
about if the drug is metabolic acidosis is
stopped after chronic seen in DKA?
use? 350. what marker can be 5-HIAA
335. what is the toxicity of weight gain, edema, found in urine of
TZDs? hepatotoxicity, CV toxicity (CHF carcinoid
precipitated by excess fluid) syndrome?
336. what is the treatment octreotide 351. what nerves are motor, sensory and autonomic (all)
for carcinoid apart of the
syndrome? neuropathy seen in
337. what is the treatment adequate water intake, intranasal DM?
for diabetes insipidus? desmopressin (ADH analogue);
central? nephrogenic? diuretics: HCTZ, indomethacin,
amiloride
352. what oncogene is associated N-myc 367. what specifically is wrong slowed reflex recovery
with rapid neuroblastoma with reflexes in someone
progression? with hypothyroidism?
353. what oncogene is upregulated N myc; a transcription 368. what steroids are produces androstenedione; 17 alpha
in neuroblastoma? what does factor in the zona reticularis? what hydroxylase; 17 ketosteroids
the gene transcribe? enzymes beyond
354. what other cells hormones are gastrin (gastrinoma!), VIP desmolase are required to
secreted from the endocrine (vipoma!) from produce them? what is
pancreas (other than insulin, pancreatic polypeptide excreted in the urine with
glucagon, somatostatin)? (pp) secreting cells production of these?

355. what other complications of cerebral edema, cardiac 369. what stimulatees follicular TSH; TSI (thyroid
DKA are there (think brain, arrythmias, heart failure cells? what else? immunoglobulin in Graves)
heart)? 370. what three neoplasias are parathyroid, medullary
356. what other hormones are epinephrine and GH; associated with MEN 2A? carcinoma of the thyroid,
secreted unopposedly in increase hyperglycemia pheo
diabetes mellitus? what does 371. what three neoplasias are pheo, medullary carcinoma
this do to the hyperglycemia? associated with MEN 2B? of the thyroid, oral/intestinal
357. what pathologic state causes primary ganglioneuromatosis (assoc
high PTH and high Ca? what is hyperparathyroidism; with marfanoid habitus)
the mcc of this? parathyroid adenoma 372. what three neoplasias are parathyroid, pancreas, and
358. what pathologic state causes secondary associated with MEN I? pituitary
low Ca and high PTH? what is hyperparathyroidism; 373. what three steps in the oxidation (I- --> I2),
the most common cause of this? chronic renal failure peroxidase enzyme organification (Iodide added
359. what pathologic state causes PTH independent involved in in thyroid to thyroglobulin), and
low PTH and high Ca? what are hypercalcemia; hormone synthesis? where coupling (of MIT and DIT);
two things that cause this? malignancy induced, do these steps occur? follicular cell, lumen, lumen
excess calcium ingestion 374. what thyroid cancer has a anaplastic, undifferentiated;
360. what pathologic state causes resp/met alkalosis very poor prognosis? what elderly
normal serum Ca but high PTH? is the patient population?

361. what pathologic state results in hypoparathyroidism; 375. what thyroid carcinoma is medullary carcinoma
low PTH and low Ca? what DiGeorge, autoimmune associated with MEN 2A and
causes this state? destruction, surgical MEN 2B
excision, hypomagnesia 376. what two actions does the increasing DCT reabsorption
362. what pathologic state results in hypoalbuminemia PTH have on the kidney? of calcium and increasing 1
normal PTH and low serum Ca? alpha hydroxylase activity

363. what percentage of 10, 10, 10, 10, 10, 10 377. what two drugs can be used levothyroxine and
pheochromocytomas are as thyroxine replacement? triiodothyrine; for
malignant? bilateral? what is the clinical use? hypothyroidism and
extraadrenal? calcify? in kids? toxicity? myxdema; thyrotoxicosis
familial? 378. what two features are seen acid hypersecretion and
364. what percentage of serum Ca++ 40%; free ionized or in the stomach in zollinger increase rugal thickening
is bound to albumin? in what complexed with anion ellison syndrome?
form is the rest? (phosphate) 379. what two neuropeptides do vasopressin (ADH) and
365. what precipitates DKA? what NO insulin and the neurohypophysis oxytocin; in the neurons in
two combining factors does this catecholamine stress secrete? where are these the supraoptic and
result in? (infection) that requires neuropeptides made? paraventricular nuclei
increased insulin where do the cells in the (NEUROpeptides); they are
neurophyophysis come the cell bodies of neurons in
366. what regulates release of ACTH CRH from the from? the hypothalamus (one and
from the adenohypophysis? hypothalamus; increased the same!)
what controls this hormone? cortisol levels decrease
CRH release (and vice 380. what two organs are the eyes and kidneys
versa) target of micro vascular
disease in diabetes
mellitus?
381. what two types of retinopathy and glaucoma 396. what type of steroid is mineralicorticoid;
damage result from aldosterone? 11 mineralicorticoid; androgen;
microvascular damage deoxycortisol? androgen; glucocorticoid
in the eyes due to DM? testosterone and
382. what type of antibodies antimircosomal and estrogen? cortisol?
can be seen in antithyroglobulin 397. what type of symporter is sodium potassium
Hashimotos? used to uptake Iodine?
383. what type of cells make somatotrophs; centrally 398. what type of temperature cold intolerance (decreased
up the majority of the intolerance is seen in BMR and so decreased body
adenohyophysis and hypothyroidism? temp); heat intolerance
where are they located? hyperthyroidism? why? (increased BMR so increased
384. what type of drugs can dopamine agonists; body temp)
cause a shrinkage of bromocriptine and cabergoline 399. what would be the main hypoglycemia
prolactinomas? give two symptom of an
examples. insulinoma?
385. what type of drugs is glucorticoid 400. what would be the main diarrhea, hypotension,
beclamethasone? symptom of a VIPoma? metabolic acidosis,
386. what type of drugs is glucorticoid where would it be hypokalemia
dexamethasone? located?

387. what type of drugs is glucocorticoid 401. what would be the gallbladder stones (inhibition
hydrocortisone? symptoms of a of CCK!), achlorydia (inhibition
prednisone? somatostatinoma? where of gastrin!) steatorrhea and
would it most likely arise constipation; from the
388. what type of drugs is glucocorticoid from? pancreas
triamcinolone?
402. when does GH increase in stress, exercise,
389. what type of episodic hypertension; diastolic normal situations? HYPOGLYCEMIA
hypertension does a hypertension
pheochromocytoma 403. when is prolactin pregnancy and brestfeeding
result in? increased?
neuroblastoma? 404. where are binding liver; estrogen
390. what type of diastolic because calcium in globulins for steroids
hypertension do you see circulation results in increased made? what activates their
in hypercalcemia? why? contraction of smooth muscle production?
arterioles 405. where are glucocorticoids zona fasciculata; 17 alpha
391. what type of diastolic due to water and produced? what enzymes hydroxylase, 21 hydroxylase
hypertension do you see sodium retention; systolic due to beyond desmolase are and 11beta hydroxylase
in hypo/ hyper increased beta 1 receptors required to produced
thyroidism? why? them?

392. what type of episodic and paraoxysmal 406. where are PTH receptors? bone, kidney (PCT and DCT
hypertension is unique in and on 1 alpha hydroxylase)
pheochromocytoma? 407. where else can a all along sympathetic chain
393. what type of myxdema facial and periorbital; pretibial (if neuroblastoma occur
do you see in Graves) other than in the adrenal
hypo/hyper thyroidism? medulla?

394. what type of receptor is a tyrosine kinase receptor that is 408. where is aldosterone in the zona glomerulosa; 21
the insulin receptor? tetrameric (2alpha and 2Beta)- produced? beyond hydroxylase and 11B
with the intracellular 2 Beta part desmolase what enzymes hydroxylase
with tyrosine kinase activity are required to produce
aldosterone?
395. what type of skin do you dry, cool skin and coarse hair in
see in hypo and hyper hypo; moist, warm skin and fine
thyroidism? hair? hair in hyper
409. where is insulin beta cells; ATP from insulin 423. which tissues use B islet cells, small intestine, kidney,
made? and in independent glucose entrance into the GLUT 2 liver
response to what beta cells (GLUT 2) closes K+ channels receptor?
is it released? and results in depolarization which 424. why does because of hydrogen shift into cells
opens Ca+ channels and increased hyperkalemia result and potassium out (to help with
intracellular Ca causes exocytosis of in DKA? acidosis)
insulin
425. why does because lower extracellular calcium
410. where is TG lumen hypocalcemia cause levels depolarizes the membranes
(thyroglobulin) tetany? making them easier to get to AP by
stored? decreasing the threshold poteential
411. which autonomic Alpha 1, M1, M3, H1, V1 and causes contraction
receptors use Gq? 426. why does increased increased BMR via Na+/K+ ATPase
412. which cells dont brain, RBCs, liver, kidney, cornea, T3 increase the
require insulin for intestine (pancreas) body temp
uptake? 427. why does insulin because GH causes gluconeogenesis
413. which cells in the prolactin and Growth hormone resistance occur in and the hyperglycemia causes insulin
adenohypophysis producing cells excess GH? intolerance (same as DM)
are acidophils? 428. why does PTH because PTH is the master of
414. which endocrine ANP, NO (EDRF)- think vasodilators increase calcium calcium- all it wants to do increase
hormones use but decrease free serum calcium and bone
cGMP? phosphate? resorption causes increase of both
415. which endocrine GOAT: GnRH, Oxytocin, ADH (V1 phosphate and calcium and in order
hormones use receptor), TRH to get more free calcium need to get
IP3? rid of phosphate

416. which form of Reidels (due to fibrotic hard mass) 429. why do steroids because protein synthesis from the
hypothyroidism have slow onset of need of gene transcription to make
can present like action? them (their receptors are
cancer? transcription factors that either are in
the cytosol or nucleus)
417. which receptors GH, prolactin and IL2
are receptor 430. why do you see because intermediates in the zona
associated increased sex glomerulosa and fasciculata that
tyrosine kinases hormones in build up can get into reticularis via
(JAK/STAT deficiencies of progesterone intermediates
pathway)? 21hydroxylase and
11B hydroxylase?
418. which receptors insulin, IGF, FGF, PDGF (think growth
are tyrosine factors) 431. why do you see skin because increased ACTH production
kinase receptors? hyperpigmentation (from lack of negative feedback)
in primary results in increased MSH also (both
419. which steroid Vit d, Estrogen, Testosterone, Cortisol, Addisons? where have POMC precursor); on the
receptors are Aldosterone, Progesterone (VET CAP) can you see the buccal mucosa and skin
cytosolic? hyperpigmentation?
420. which steroid T3/T4 432. why is the HR increased B1; increased O2
receptors are increased in T3? consumption
nuclear? RR?
421. which thyroid lymphoma 433. why is their d/t gluconeogenesis and decreased
cancer is hyperglycemia in insulin; decreased collagen synthesis;
associated with cushings? why skin increased androgen: estrogen ratio
hashimotos? changes and
422. which tissues are adipose tissue and skeletal tissue; osteoporosis? why
insulin dependent GLUT 4 amenorrhea,
on getting hirsuitism, acne?
glucose? through
what channel does
the glucose enter?
434. why is there a dilutional hyponatremia seen in DKA? in DKA glucosuria induced osmotic diuresis causes a dilutional
hyponatremia effect that pulls sodium out
435. why is there orthostatic hypotension in cushings? ...
436. Why might a hashimotos patient be hyperthyroid? because initial destruction of follicular cells can cause a release of
thyroid hormone
437. why would nephrotic syndrome and cirrhosis result in because loss of IV protein results in loss of IV osmotic pull and loss of
hyperaldosteronism? volume extravascularly
438. with bone resorption, other than calcium and hydroxyproline
phosphate is released?
439. with what disease states are pheos associated with? VHL, NF 1, MEN 2A and MEN 2B
440. with what is a parathyroid adenoma associated with? MEN I, MEN IIA
441. with what neoplasias is Zollinger Ellison syndrome MEN I
associated?

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