Endocrine Flashcards

Question 1

Q

Thyroid development

derived from
connections to tongue and what it turns into
thyroglossal duct cyst: sxs
thyroid follicular and parafollicular cells derived from

Answer

A

primitive pharynx
thyroglossal duct -> normally disappears but can persist as pyramidal lobe
anterior midline neck mass that moves w/ swallowing
endoderm

Question 2

Q

Adrenal Cortex

derived from
glomerulosa: primary reg, hormone produced, hormone class
fasiculata
reticularis

Answer

A

mesoderm
Angiotensin II, Aldosterone, mineralcorticoids
ACTH, cortisol, glucocorticoids
ACTH, DHEA, androgens

Question 3

Q

Adrenal Medulla

- dervied from

Answer

A

neural crest

Question 4

Q

Ant pit

secretes
derived from
basophila

Answer

A

FSH, LH, ACTH, TSH, prolactin, GH,
oral ectoderm
FSH, LH, ACTH, TSH

Question 5

Q

Post pit

secretes
created
transported
derived

Answer

A

vasopressin and oxytocin
hypothalamus
post pit via neurophysins
neuroectoderm

Question 6

Q

Endocrine Pancreas

alpha cell
beta cell
delta cell
arise from

Answer

A

glucagon
insulin
somatostatin
pancreatic buds

Question 7

Q

Insulin

synthesis: 1st product, 2nd product, final product
function: binds, next steps
anabolic effects: muscle, adipose, glycogen, triglyceride, Na, proteins, K and AA, glucagon, lipolysis
insulin dependent glucose transporters: location
organs with non insulin dependent glucose transporters: BRICK LIPS
regulation
insulin binding pathway
insulin release pathway

Answer

A

preproinsulin -> cleavage of presignal -> proinsulin -> cleavage of proinsulin -> exocytosis of insulin and C peptide
binds insulin receptor -> induce glucose uptake -> gene transcription
increase glucose in muscle and adipose, glycogen synthesis and storage, triglyceride synthesis, Na retention, protein synthesis, cellular uptake of K and AA; decreased glucagon release, and lipolysis
GLUT 4: adipose and muscles
Brain, RBC, Intestine, Cornea, Kidney, Liver, Iselt cells, Placenta, Spermatocyte
controlled by glucose concentration in blood, increase in glucose causes increase in insulin
insuling binds receptor -> PIP 3 activated -> glut 4 to membrane -> glucose into cell
glucose binds glut2 -> ATP/ADP ratio increased -> K channels close -> voltage gated Ca channel open -> increase in intracellular Ca -> exocytosis of insulin

Question 8

Q

Glucagon

made by
function
regulation

Answer

A

alpha cells of pancrea
glycogenolysis, gluconeogenesis, lipolysis, ketogenesis -> elevates blood sugar to maintain homeostasis
secreted in response to hypoglycemia

Question 9

Q

Hypothalamic - Ant Pit Hormones

ADH: function,
CRH: function
Dopamine: function
GHRH: function
GnRH
MSH
Oxytocin
Prolactin
Somatostatin
TRH

Answer

A

ADH: increase in water permeability to DCT and collecting guct -> increase water reabsorption
CRH: Increase ACTH and beta endorphin
Dop: decrease in prolactin
GHRH: increase GH
GnRH: increase FSH, LH
MSH: increase melanogenesis by melanocytes
Oxy: causes uterine contraction during labor, responsible for milk letdown reflex
Prolactin: decrease in GnRH
Somato: decrease in GH, TSH
TRH: Increase in TSH, prolactin

Question 10

Q

Prolactin

source
function: breast milk, fertility
reg: inhibition,

Answer

A

ant pit
stimulates milk production, inhibits ovulation and spermatogenesis by inhibiting GnRH synthesis and release
inhibited by dopamine; prolactin inhibits own secretion by increasing dopamin synthesis

Question 11

Q

Growth Hormone

other name
production
function
regulation: released in response to, inhibited by
excess secretion of GH causes -> TX

Answer

A

somatotropin
ant pit
linear growth and muscle mass
pulsatile, released in response to growth hormone releasing hormone, which is increased during exercise, deep sleep, puberty, hypoglycemia; inhibited by glucose and somatostatin
acromegaly of gigantism; TX w/ somatostatin analogs

Question 12

Q

Appetite Reg

Ghrelin: function; produced by; sleep deprivation/ prader willi causes; location of effect
Leptin: function; produced by; mutation causes; sleep deprivation or starvation causes
Endocannabinoids: location; function; exogenous

Answer

A

stimulates hunger and GH release; produced by stomach; sleep deprivation or prader willi causes increased ghrelin production; lateral area of hypothalamus
satiety hormone; produced by adipose tissue; congenital obesity; decrease in leptin production
act at cannabinoid receptor in hypothalamus to increase appetite; reason why exogenous cannabinoid causes the munchies

Question 13

Q

Anti-diuretic Hormone

other name
production
function
regulation
central diabetes insipidus vs nephrogenic

Answer

A

vasopressin
hypothalamus and stored and secreted in post pit
reg serum osmolality and blood pressure via reg of aquaporin channel insertion in principal cells
plasma osmolality/ hypovolemia
ADH decreased vs ADH normal

Question 14

Q

Cortisol

source
function: increases, decreases
regulation

Answer

A

adrenal zona fasiculata
increase appetite, DP, insulin resistance, gluconeogenesis/lypolysis/proteolysis; decreases fibroblast activity, inflammatory and immune responses, bone formation
CRH stimulates ACTH release causes cortisol

Question 15

Q

Ca homeostasis

forms
increased pH
decreased pH

Answer

A

ionized, hound to albumin, bound to anions
albumin binds more Ca -> decrease free Ca -> increase PTH
albumin binds less Ca -> increase in free Ca -> decrease PTH

Question 16

Q

PTH

source
function
reg: increases PTH; decreases PTH

Answer

A

chief cells of parathyroid
increase bone resorption of Ca and PO4, kidney reabsorption of Ca in DCT, and D3 production; decrease reabsorption of PO4 in PCT
decreased serum Ca, high PO4, low serum MG; very low MG

Question 17

Q

Calcitonin

source
function
reg

Answer

A

parafollicular cells of thyroid
decrease bone resorption of Ca
increase serum Ca -> calcitonin secretion

Question 18

Q

Thyroid Hormones

source
secreted form vs activated form
function- 6 B’s
reg
TBG: what is it, function, increased by, decreased by

Answer

A

follicles of thyroid
T4 vs T3
Brain maturation, bone growth, beta adrenergic effects, increase basal met rate, increase blood sugar, breaks down lipids
TRH -> TSH -> T4 -> T3 -> w/ neg feeback from T3/T4
thyroxine binding gobulin; binds T3 and T4 making it inactive in blood -> will increase w/ estrogen, heaptic failure, steroid use, nephrotic syndrome

Question 19

Q

Signaling Pathways of endocrine hormones

cAMP: pathway; FLAT ChAMP CGGH
cGMP: BAD GraMPa
IP3: GOAT HAG
Intracellular receptor: PEE CAT TV
Tyrosine Kinase: Get Found In the MAP
Non TK: PIGGlET

Answer

A

G-alpha-s -> AC -> cAMP -> PKA; FSH, LH, ACTH, TSH, CRH, hCG, ADH, MSH, PTH, calcitonin, GHRH, glucagon, histamine
BNP, ANP, NO
GnRH, Oxytocin, ADH, TRH, histamine, angiotensin II, Gastrin
Progesterone, estrogen, tetosterone, cortisol, aldosterone, T3/T4, Vit D
Insulin, IGF-1, PDGF
Prolactin, Immunomodulators, GH,G-CSF, Erythropoeitin, Thrombopoeitin

Question 20

Q

Adrenal Steroid Synthesis

aldosterone
glucocorticoids: 2 pathways; inhibited by
androgens
estrogen

Answer

A

chol -> pregnenolone -> progesterone + 21- hydroxylase -> 11-deoxycorticosterone + 11 beta hydroxylase -> corticosterone -> aldosterone
chol -> pregnenolone -> 17 hydroxy pregnenolone -> 17 hydroxy progesterone -> 11 deoxy cortisol -> cortisol –OR– Chol -> pregnenolone -> progeterone -> 17 hydroxy progesterone -> de oxy cortisol -> cortisol; metyrapone
chol -> pregnenolone -> 17 hydroxy pregnenolone -> DHEA -> androstenidione -> testosterone -> DHT –OR – chol -> pregnenolone -> progesterone -> 17 hydroxy pregnenolone -> androstenidion -> testosterone
aromatase, from androstenidione or testosterone

Question 21

Q

Androgen Enzyme Deficiencies

17 alpha hydroxylase: amount of mineral corticoids, amount of cortisol, amount of sex hormone, BP, [K], labs, presentation
21 hydroxylase: amount of mineral corticoids, amount of cortisol, amount of sex hormone, BP, [K], labs, presentation
11 beta hydroxylase: amount of mineral corticoids, amount of cortisol, amount of sex hormone, BP, [K], labs, presentation

Answer

A

used to make 17 hydroxy pregnenolone and progesterone -> will result in lots of mineral corticoids, low cortisol and androgens , high BP, low K; XY: ambiguous genitalia w/ undescended testes and XX lacks seconday sex development
low mineral corticoids, low cortisol, high sex, low, BP, high K, high renin and 17-hydroxy progesterone; salt wastin or precocious puberty w/ virilization in women
low aldosterone but high deoxycorticosterone, low cortisol, high sex, high BP (deoxycoritco), decreased K, decreased renin, virilization in women

Question 22

Q

Cushing syndrome

etiology
causes (3 ish)
findings
DX
Exogenous glucocorticoids or adrenal tumor
Ectopic ACTH
Cushing DX

Answer

A

increased cortisol
exogenous corticosteroids, adrenal adenoma/ hyperplasia/ carcinoma; ACTH secreting pit adenoma
hypertension, weight gain, moon face, buffalo hump, skin changes, hirsutism, amenorrhea
increased free cortisol on 24 hr UA, increased late night salivary cortisol, no suppression w/ low dose dexamethasone
suppressed ACTH test
elevated ACTH w/ no suppression on dexamethasone test and no increase in ACTH and cortisol w/ CRH
elevated ACTH w/ adequate suppression on dexamethason test and an increase in ACTH and cortisol on CRH stim test

Question 23

Q

Nelson Syndrome

what is it
sequalae
sxs
tx

Answer

A

removal of cortisol feedback after bilateral adrenalectomy for refractory cushing dx
enlargement of existing ACTH secreting pit adenoma
hyperpigmentation, headache, bitemporal hemianopia
pit radiation or resection

Question 24

Q

Adrenal insufficiency

what is it
sxs
tx

Answer

A

inability of adrenal gland to generate enough glucocorticoids +/- mineralcorticoids
weakness, fatigue, orthostatic hypotension,
glucocorticoid and mineralcorticoid replacement

Question 25

Q

Primary Adrenal Insufficiency

what is it// caused by
acute
addisons dx
waterhouse- friedrichsen: what is it

Answer

A

deficiency of aldosterone and cortisol production because of loss of gland function
hypotension, hypekalemia, metabolic acidosis, skin/mucosal hyperpigmentation
sudden, presents w/ shock in acute adrenal crisis
caused by adrenal atrophy/destruction by DX (Autoimmune or TB)
acute primary adrenal insuff bc of adrenal hemmorrhage associated w/ septicemia, DIC and endotoxin shock from N meningitidis

Question 26

Q

Secondary Adrenal insufficiency

caused by
sxs

Answer

A

decreased in pit ACTH production

- no hyperpigmentation and no hyperkalemia bc aldosterone is intact

Question 27

Q

Tertiary Adrenal insufficiency

caused by
adlosterone

Answer

A

chronic use of exogenous steroids w/ abrupt withdrawal

- aldosterone unaffected so K and htn should be fine

Question 28

Q

Hyperaldosteronism

what is it
sxs
primary: caused by; aldosterone vs renin levels; main sxs
secondary:

Answer

A

increased secretion of aldosterone from adrenal gland
hypertension, decreased K, met alkalosis
caused by adrenal adenoma or bilateral adrenal hyperplasia; increase in aldosterone with decrease in renin; treatment resistant HTN w/o edema
pts w/ renovasc HTN, juxtaglomerular tumors and edema

Question 29

Q

Neuroendocrine tumors

what is it
GI, Pancreas, lungs, thyroid, adrenals

Answer

A

heterogenous groups of neoplasms originating frm neuroendocrine cells
GI tract (gastrinoma) , pancreas (insulinoma), lungs (small cell), thyroid (medullary carcinoma), adrenals (pheochromocytoma)

Question 30

Q

Neuroblastoma

what is it
derived from / location
sxs

Answer

A

most common tumor of adrenal medulla in children
neural crest cells, anywhere along sympathetic chain
abdominal distention and firm irregular mass that can cross midline, normotensive, opsoclonus-myoclonus syndrome (dancing eyes and feet)

Question 31

Q

Carcinoid Syndrome

what is it
sxs
markers
tx
mets

Answer

A

syndrome caused by neuroendocrine tumors secreting hormones such as serotonin, histamine, leukotriene
recurrent diarrhea (serotonin on GI), cutaneous flushing (histamine dilating vessels), athmatic wheezing (serotonin causing broncho constriction) , right sided valvular heart dx (serotonin increasing fibrin deposition in heart)
chromogranin A and synaptophysin
surgical resection and somatostatin analog for sxs control (somatostatin binds to tumor and prevents release of hormones)
liver

Question 32

Q

Pheochromocytoma

etiology
symptoms
findings
tx

Answer

A

most common tumor of adrenal medulla in ADULTS
chrommafin cells (come from neural crest cells)
NF1, VHL, RET, MEN 2A and 2B
epi, nor epi, dopamine -> HTN or EPO -> polycythemia; in spells
increase in catecholamines and metabolites in urine
Irreversible alpha antagonist (phenoxybenzamine) and beta blocker before resection

Question 33

Q

Insulinoma

what is it
whipple triad
labs
tx

Answer

A

tumor of pancreatic beta cell -> over production of insulin -> hypoglycemia
low blood glucose, sxs of hypoglycemia, and resolution of sxs after glucose normalization
low glucose and high c peptide
surgical resection

Question 34

Q

Glucagonoma

what is it
sxs (5 D’s)
tx

Answer

A

tumor of pancreatic alpha cell -> over production of glucagon
dermatitis, diabetes, DVT, declining weight, depression
octreotide, surgery

Question 35

Q

Somatostatinoma

what is it
sequalae
sxs

Answer

A

tumor or pancreatic delta cells -> overproduction of somatostatin
decrease in secretion of glucagon, insulin, gastrin
diabetes, glucose intolerance, gallstones, steatorrhea
surgical resection, somatostatin analogs

Question 36

Q

Zollinger Ellison Syndrome

what is it
sequelae
sxs
secretin stimulation test

Answer

A

gastrin secreting tumor of pancreas or duodenum
acid hyper secretion causes recurrent ulcers in duodenum and jejunum
abdominal pain and diarrhea
gastrin levels remain elevated after secretin administration

Question 37

Q

VIPoma

what is it
location
syndrome
sxs

Answer

A

rare neuroendocrine tumor that secretes vasoactive peptide
pancreas
MEN 1
Watery diarrhea, hypokalemia, achloryhydia

Question 38

Q

Hypothyroidism vs Hyperthyroidism

metabolic findings
skin/ hair findings
ocular findings
GI findings
MS
Reproductive
Neuro
CV
Labs

Answer

A

O: cold intolerance, sweating, weight gain– ER: heat intolerance, sweating, weight loss
O: dry/cool skin w/ brittle hair and diffuse allopecia, brittle nails, puffy face; ER: warm/moist skin, fine hair, pretibial myxedema
O: peri-orbital edema; ER: exophthalmos and lid lag
O: constipation; ER: diarrhea
O: myopathy, carpal tunnel; ER: thyrotoxic myopathy w/ increased risk of fracture
O: abnrml uterine bleeding and decreased libido; ER: abnrml uterine bleedin, gynecomastia
O: lethargy, fatigue, weakness, depression; ER: restless, anxious, insomnia
O: bradycardia, dyspnea on exertion; ER: tachcardia, palpations, arrythmias
high TSH, low T3 and 4; low TSH, high T3 and 4

Question 39

Q

Hyperthyroidism Causes

Graves Dx: epi, pathogenesis, triggers, HLA, histo
Toxic multi nodular goiter: what is it, labs, prognosis
Thyroid storm: what is it, triggers, labs, tx 4 ps
Jod-Basedow phenomenon: what is it

Answer

A

most common cause; Thyroid stimulating Ig stimulates TSH receptors, dermal fibroblasts, orbital fibroblasts; stress, HLA 3 and 8, tall crowded follicular epi cells w/ scalloped colloid
focal patch of hyperfunctioning follicular cells w/ colloid working independently of TSH; increase release T3/4, non malignant
complication when hyperthyroidism is untreated and significantly worsens w trigger, infection/ trauma/ surgery; agitation/ delirium/ fever/ diarrhea/ arrythmia; increase lfts; propanolol, propylthiouracil, prednisolone, potassium iodide
Ionine induced hyperthyroidism, pt with iodine deficieny and autonomous thyroid tissue is given iodine

Question 40

Q

Hypothyroidism Causes

Hashimotos Thyroiditis: epi, pathogenesis, HLA’s, histo, increased risk of, sxs
Post partum thyroiditis: what is it, sxs; tx; sxs; histo
Congenital Hypothyroidism: what is it; caused by; sxs (6 Ps)
Subacute Granulomatous thyroiditis: caused by; course; sxs; histo
Riedel: what is it; mimics; thyroid feels
Other causes

Answer

A

most common cause of hypothryoidism; AI w/ anti-thyroid peroxidase and thithyroglobulin; HLA-DR3 and DR5; increase risk of non hodgkins lymphoma; huerthle cells; enlarged, non tender thyroid
self limited thyroiditis; transient hyperthyroidism, hypothyroidism, or both; euthyroid following resolution; thyroid is painless and normal size; lymph infiltrate w/ occasional germinal centers
severe fetal hypothyroidism bc of maternal anti-bodies; Pot bellied, Pale, Puffy face, protruding umbilicus, protuberat tongue, poor brain development
self limited dx following flu like illness; can start as hyperthyroid and followed by hypothyroid; granulomatous inflammation; increased ESR, jaw pain, very tender thyroid
thyroid replaced by fibrous tissue w/ inflamm infiltrate which can extend to local strx (trachea and esophagus); mimics anaplastic carcinoma; fixed, rockhard, painless goiter
iodine deficiency

Question 41

Q

Radiation induced damage to thyroid gland

- what is it

Answer

A

exposure to radiation can increase risk of hypothyroidism

- potassium iodide will saturate thyroid gland with stable iodine

Question 42

Q

Thyroid adenoma

what is it
hot vs cold
histo

Answer

A

benign solitary growth of thyroid
most are cold and do not cause hyperthyroidism and others are hot
follicular, absence of capsular or vascular invasion

Question 43

Q

Papillary Carcinoma

epi
prognosis
histo
mutation

Answer

A

most common
excellent
empty appearing nuclei w/ central clearing, psammoma odies, nuclear grooves
RET/ PTC rearrangements and CRAF mutations

Question 44

Q

Follicular Carcinoma

prognosis
invades
histo
spread
mutations

Answer

A

good
thyroid capsule and vasculature
uniform follicles
blood
RAS and PAX8 - PPAR translocation

Question 45

Q

Medullary Carcinoma

cells type
secretes
histo
associated w

Answer

A

parafollicular cells
calcitonin
sheets of amyloid stroma
MEN 2A and B

Question 46

Q

Undiff anaplastic carcinoma

epi
sxs
prognosis
mutation

Answer

A

older pts
enlarging neck mass -> compressive sxs
very poor
TP53

Question 47

Q

Hypo-parathyroidism

caused by
sxs
Chvosteck sign
Trosseau sign
pseudo 1A: genetics, pathogenesis, sxs, inherited from
pseudo-pseudo: what is it, inherited from

Answer

A

injury to parathyroid glands or their blood supply
hypocalcemia, tetany, hyperphosphatemia
tapping of facial n causing contraction of facial muscles
occlusion of brachial a w/ BP cuff causing carpal spasm
auto dom, inactive Gs protein causing kidney and bone resistance to PTH; hypocalcemia despite high PTH; shortened 4th and 5th digits, short, obese, developmental delay, inherited from mother and caused by imprinting
auto dom, features of albright hereditary osteodystrophy (above findings) w/o PTH resistance and normal Ca levels; inherited from father but normal maternal allele maintain response to PTH

Question 48

Q

Hyperparathyroidism

primary: caused by; labs; sxs
secondary: caused by, labs
tertiary: caused by, labs

Answer

A

due to parathyroid adenoma or hyperplasia; hyper Ca, calciuria, hypophosphatemia, high PTH; asymptomatic
secondary hyperplasia due to decrease in Ca absorption and/or increase in PO4 in CKD; hypo Ca w/ hyper PO4]
Refractory hyperparathyroidism from CKD, high PTH and Ca

Question 49

Q

Familial hypocalciuric hypercalcemia

what is it
sequalae
labs

Answer

A

defective G coupled Ca sensing receptors in multiple tissues, specifically parathyroid and kidneys
higher than normal Ca levels required to suppress PTH
Excessive renal reabsorption causing hypercalcemia w/ normal PTH levels

Question 50

Q

Hypopituitarism

what is it
non secreting pituitary adenoma: what is it
sheehan syndrome: what is it; pathogenesis; sxs
empty sella syndrome: what is it; cause; associated with
pit apoplexy: what is it; associated with; sxs
TX

Answer

A

undersecretion of pit hormone
cancer in the pituitary gland that renders it unable to do its job
ischemic infarct of pituitary following postpartum bleeding -> pituitary increases in size during pregnancy because of increase in hormones and since it is normally fed through a plexus it is already low in blood flow so when postpartum bleeding occurs it is one of first areas to become ischemic; failure to lactate, absent mensturation, cold intolerance
atrophy or compression of pituitary; idiopathic; idiopathic intracranial hypertension
sudden hemorrhage of pit; existing pit adenoma; sudden onset severe headache, visual impairment, diplopia
hormone replacement therapy

Question 51

Q

Acromegaly

what is it
caused by
sxs: tongue, voice, hands/feet, face, sweat
DX
tx

Answer

A

excess GH in adults
pit adenoma
large tongue, deep voice, large hands and feet, coarsening of facial features w/ age, frontal bossing, diaphoresis
increased serum IGF-1 and failure to suppress GH w/ oral glucose tolerance test; pit mass seen on MRI
pit adenoma resection and octreotide

Question 52

Q

Laron Syndrome

genetic
caused by
labs
sxs

Answer

A

AR
defective GH receptors -> decreased linear growth,
high GH, low IGF1
short stature, small head circumference, saddle nose and prominent forehead, small genitals

Question 53

Q

Syndrome of inappropriate ADH

what is it
causes
labs
pathogenesis of labs
tx

Answer

A

ADH being secreted when its not supposed to be
ectopic ADH, CNS disorder, pulm dx, drugs (cyclophosphamide)
hyponatremia with continued urinary excretion of Na and urine osmolality > serum osmolality
increase in water causes decrease in ADH and increase ANP -> increases Na excretion
cerebral edema and seizures
fluid restriction, salt tablets, IV hypertonic saline, diuretics, ADH antagonist; must be corrected slowly to avoid osmotic demyelination syndrome

Question 54

Q

Diabetes Insipidus

what is it
central: what is it, causes
nephrogenic: what is it, causes
labs
water deprivation test: central vs nephrogenic
TX: central, nephrogenic

Answer

A

inability to concentrate urine caused by problems with ADH
central: unable to produce ADH; pit tumor, AI, trauma, surgery
nephrogenic: ADH unable to bind on CT of kidney; hereditary, secondary to hyper Ca, hypo K, lithium
urine gravity and urine osmolality are low, serum osmolality is high
C: > 50% increase in urine osmolality after ADH analog given; N: minimal change in urine osmolality
C: Desmopressin and hydration; HCTZ, indomethacin, hydration, salt restriction

Question 55

Q

Diabetes mellitus

sxs
small vessel complications
large vessel complications
dx

Answer

A

polydipsia, polyuria, polyphagia, weight loss, DKA (I)
diffuse thickening of basement membrane -> retinopathy, glaucoma, nephropathy
atherosclerosis, CAD, peripheral vascular occlusive dx -> gangrene and high incidence of MI
HgbA1C greter than 6.5, fasting glucose over 126, 2 hr oral glucose tolerance over 200

Question 56

Q

Type I vs Type II DM

primary defect
insulin in tx
age
obesity
genetic
glucose intolerance
insulin sensitivity
ketoacidosis
beta cell number in islets
serum insulin levels
histo

Answer

A

primary cause - 1: AI destruction of beta cells; 2: increased resistance to insulin w/ progressive pancreatic beta cell failure
insulin tx - 1: always; 2: sometime
age - 1: < 30 yrs, 2: > 40 yrs
obesity - 1: no; 2: yes
genetic - 1: relatively weak; 2: relatively strong
gluc intol - 1: severe, 2: mild to moderate
insulin sen - 1: high, 2: low
DKA - 1: common, 2: rare
B cell - 1: low, 2: variable
serum - 1: low, 2: variable
hist - 1: islet leukocyte infiltration, 2: Islet amyloid deposits

Question 57

Q

DKA

caused by
occurs in
sxs
labs
sequlae of labs
complications
TX

Answer

A

excess fat break down causing increase in ketoacids made
type I DM
Delirium/ psychosis, kussmaul respirations, abd pain, dehydration, fruity breath
hyperglycemia, high H, low HCO3, high ketones in blood and urine
K starts being switched out for H intracellularly to help with acidosis -> increase in K levels causes increase in excretion of K -> causes decreased overall K levels
cardiac arrythmias, heart failure
IV fluids, IV insulin, and K+, glucose to prevent hypoglycemia

Question 58

Q

Hyperosmolar hyperglycemic state

what is it
epi
pathogenesis
sxs
w/o tx
labs
tx

Answer

A

state of profound hyperglycemia induced dehydration and high serum osmolality
elderly Type 2 DM, unable to drink much
hyperglycemia -> excessive osmotic diuresis -> dehydration
thirst, polyuria, lethargy, focal neuro deficits
coma/death
hyperglycemia and high serum osmolality w/o acidosis
aggressive IV fluids and insulin therapy

Question 59

Q

MEN 1

organs involved
mutation

Answer

A

pituitary (prolactin or GH), pancreas (zollinger-ellison syndrome, insulinoma, VIPoma), parathyroid adenoma
MEN1 (menin on chrom 11)

Question 60

Q

MEN 2A

- organs involved

Answer

A

parathyroid hyperplasia, medullary thyroid (parafollicular C cells -> secrete calcitonin), pheochromocytoma (catecholamines)
mutation in RET

Question 61

Q

MEN 2B

organs involved
associated w
mutation

Answer

A

thyroid, pheochromocytoma, mucousal neuroma
marfanoid habitus
RET gene

Question 62

Q

Diabetic Injectables

Insulin preparation: MOA (liver, muscle, fat); side effect
Amylin Analog: MOA
GLP-1 analog: MOA

Answer

A

bind insulin receptor -> liver and muscle stores glucose, fat stores TG; hypoglycemia, lipodystrophy, hypersensitivity
decrease glucagon release, decrease gastric emptying, increase satiety; hypoglycemia
decrease glucagon release, decrease gastric emptying, increase glucose dependent insulin release; nausea, vomiting, pancreatitis, weight loss

Question 63

Q

Insulin preparation

rapid acting: name and peak
short acting: name and peak
intermediate acting: name and peak
long acting: name and peak

Answer

A

Lispro, aspart, glulisine; 1 hr peak
regular; 2-3 hr peak
NPH: 4-10 hr peak
detemir, glargine; no real peak

Question 64

Q

Diabetic oral drugs

biguanides
sulfonylureas
meglitinides
DPP4 inhibitors
glitazone
Na- gluc cotransporter inhibitor
alpha glucosidase inhibitors

Answer

A

inhibit hepatic gluconeogenesis and action of glucagon
close K channel in pancreatic beta cell membrane -> cell depolarizes -> insulin release via increase in Ca influx; 1 - chlorpropamide, tolbutamide; 2 - glimepiride, glipizide, glyburide
same as sulfonylureas; nateglinide, repaglinide
inhibit DPP-4 enzyme that deactivates GLP-1 -> decrease glucagon release and gastric emptying while increasing glucose dependent insulin release; linagliptin, saxagliptin, sitagliptin
activate PPAR - gamma -> increase insulin sensitivity and levels of adiponectin -> regulates glucose metabolism and fatty acid storage; pioglitazone, rosiglitazone
block reabsorption of glucose in PCT; canagliflozin, dapagliflozin, empagliflozin
inhibit intestinal brush border alpha glucosidases -> delayed carb hydrolysis and glucose absorption -> decreased postprandial hyperglycemia; acarbose, miglitol

Answer 65

A

block thyroid peroxidase -> inhibit oxidation of iodide -> inhibit thyroid hormone synthesis
hyperthyroidism
propylthiouracil and then methimazole

Answer 66

A

thyroid hormone replacement
hypothyroid, myxedema
can be abused for weight loss

Answer 67

A

block activation of ADH at V2 receptor; SIADH; conivaptan, tolvaptan
Central DI
GH deficiency, turners syndrome
labor induction
acromegaly

Answer 68

A

ADH antagonist
SIADH
Nephrogenic DI

Answer 69

A

synthetic analog of aldosterone w/ little glucocoticoid effects
mineralcorticoid replacement in primary adrenal insuff

Answer 70

A

sensitizes Ca sensing receptor in parathyroid gland to circulating Ca -> decrease PTH
secondary hyperparathyroidism in CKD, hyper CA in primary hyperparaythyroidism

Answer 71

A

nonabsorbable phosphate binder that prevents phosphate absoprtion from the GI tract
hyperphosphatemia in CKD