Week 2 Flashcards Preview

Endocrine > Week 2 > Flashcards

Flashcards in Week 2 Deck (109)
Loading flashcards...
1
Q

diabetes and CVD risk

A
  • risk of mortality: diabetes without prior MI ~ non-diabetes with prior MI
  • diabetes + prior MI –> much higher risk
2
Q

mediators of diabetes –> atherosclerosis

A

hyperglycemia, hyperinsulinemia, endothelial dysfuction, hypercoagulability, obesity, lipid profile

3
Q

macrovascular complications of diabetes

A

CVD

4
Q

Tx to reduce risk of CV complications in diabetes

A
  • for type 1: intensive glycemic control (A1C 7.0%) in early stages of disease is preventative over long term (even if control worsens after). improves microvascular Sx in short term
  • for type 2: same!

BUT tight control in patients with long-standing diabetes is not necessarily beneficial

5
Q

Screening in diabetes

A

PLAGUE-F:

  • Pressure (bp < 100)
  • Aspirin (Secondary prevention, 10-year risk >10%)
  • Glycemia (A1C < 7%)
  • Urine (Microalbumin, Creatinine annually)
  • Eyes (dilated eye exam annually)
  • Feet (Annual foot exam, neuropathy screening)
6
Q

first-line Tx for T2DM

A

lifestyle + metformin

7
Q

sites of action for glucose-lowering drugs

A
  • liver (glucose output)
  • skeletal muscle (glucose uptake)
  • Gut (glucose absorption and incretin secretion)
  • pancreas (insulin/glucagon secretion)
8
Q

advantageous characteristics for T2DM drugs

A
  • weight neutral or weight loss
  • no hypoglycemia
  • freq of administration
  • PO vs injectable
9
Q

disadvantageous characteristics for T2DM drugs

A
  • weight gain (reversal of osmotic diuresis, reversal of starvation/normalization of glucose, fluid retention)
  • hypoglycemia
  • frequency
  • injectable vs PO
10
Q

metformin (biguanide). Action, mechanism, effect, weight, metabolism, adverse effects, hypoglycemia, contraindications, efficacy

A
  • reduces hepatic gluconeogenesis and lipid synth, sensitizes liver and muscle to insulin
  • activation/phosphorylation of AMPK
  • improves pre-meal glucose with modest effect on post-prandial glucose
  • weight neutral/weight loss
  • not metabolized. renally excreted
  • anorexia, nausea, dirrhea, lactic acidosis (must ramp dose slowly)
  • no hypoglycemia
  • contra: prone to acidosis, hypoxic states, renal failure, MI, T1DM
  • lowers A1C by as much as 2% (higher start point –> bigger effect)
11
Q

sulfonylureas Action, mechanism, effect, weight, metabolism, adverse effects, hypoglycemia, contraindications, efficacy

A
  • stimulates pancreatic insulin secretion 12-24 hrs
  • binds to sulfonyl R in beta cells resulting in depolarization via ATP-dependent K+ channels
  • mostly effects pre-meal glucose
  • hepatic metabolism, excreted by kidney. active metabolites. caution in renal impairment
  • contra: T1DM, DKA, sulfa allergy
  • adverse: hypoglycemia, weight gain, hunger
  • A1C reduction up to 1.5% Higher start point–> bigger effect
12
Q

meglitinides/glinides. Action, mechanism, onset, effect, weight, metabolism, adverse effects, hypoglycemia, contraindications, efficacy

A
  • Stimulates pancreatic insulin secretion for 3-4 hrs
  • Binds Sul 1 R on beta cells, depolarization via ATP-dependent K+ cahnnels
  • Fast onset
  • Adverse: hypoglycemia 2-4 hrs after a meal, weight gain, patient adherence (take with every meal
  • metabolism: hepatic P450, GI excretion
  • contra: T1DM, liver failure, DKA, sulfa allergy
  • lowers A1c ~0.4%
13
Q

Thiazolidinediones (PPAR-gamma agonists) Action, mechanism, effect, weight, metabolism, adverse effects, hypoglycemia, contraindications, efficacy, controversy

A
  • decreases peripheral insulin resistance in muscle, liver, adipose
  • binds to nuclear PPAR-gamma, increasing GLUT4 expression
  • PO 1-2x daily
  • lowers pre-meal and post-meal glucose
  • adverse: weight gain due to improved glycemic control and intravascular colume expansion. hepatocellular injury
  • contra: active liver disease, heart failure, renal insufficiency. Reduces TGs but increases LDL/HDL
  • no hypoglycemia
  • lowers A1c up to 1.8%
  • controversy: link to bladder cancer. Risk of CVD (?)
14
Q

alpha-glucosidase inhibitors Action, mechanism, effect, weight, metabolism, adverse effects, hypoglycemia, contraindications, efficacy

A
  • competitively inhibit oligosaccharide breakdown enzymes in small intestine brush border
  • Delay gut carbo absorption, increases GLP-1
  • post-prandial glucose only
  • pills taken with meals
  • side-effects: flatulance, bloating
  • no hypoglycemia
  • contra: GI disorders esp IBD
  • not metabolized; renally excreted
  • lowers A1c ~0.4%
15
Q

exenatide/liraglutide. Action, mechanism, effect, weight, metabolism, adverse effects, hypoglycemia, contraindications, efficacy

A
  • GLP-1 R agonists
  • potent glucose-dependent insulin secretion, slows gastric emptying
  • peptides –> sub-cut admin 2x day
  • adverse: nausea, bloating
  • no hypoglycemia (effect declines as glucose level declines)
  • contra: gastroparesis
  • increases satiety –> weight loss
  • A1C ~1% but some people lose a lot
16
Q

incretin system

A
  • secreted by gut in response to food.
  • Increases I/G ratio, slows gut motility, induces satiety
  • inactivated by DPP-4 in 1-7 minutes
17
Q

gliptins. Action, mechanism, effect, weight, metabolism, adverse effects, hypoglycemia, contraindications, efficacy

A
  • increase duration of action of GLP-1
  • inhibit DPP-4
  • immediate effect, mostly on post-meal glucose
  • not metabolized, excreted renally
  • PO once daily
  • contra: no
  • adverse: GI
  • no hypglycemia and weight neutral
  • reduces A1c ~1%
18
Q

Canagliflozin (sodium-glucose transport inhibitor). Action, mechanism, effect, weight, metabolism, adverse effects, hypoglycemia, contraindications, efficacy

A
  • inhibits SGLT2, decreases glucose reabsorption
  • hepatic metabolism
  • contra: severe renal impairment, ESRD, dialysis
  • adverse: vulvovaginal candidiasis/mycotic infection, UTIs, polyuria
  • lowers A1c ~1% and weight loss ~2.2%
19
Q

insulin mechanism and effect

A

binds to insulin and IGF-1 Rs resulting in phosphorylation/2nd messenger cascade and GLUT translocation
Anabolic: TG synth/storage in adipose, glycogen and protein synth in muscle, glycogen synth and reduced glucose output in liver.

20
Q

metabolism of insulin

A

endogenous: 60% degraded in first-pass of liver. remaining 40% degraded in kidneys
Exogenous: 60% kidney, 40% liver

21
Q

indications for insulin Tx

A
  • T1DM
  • inadequately controlled T2DM
  • temporary use: hospitalization, pregnancy, renal disease, initial control in severe T2DM
22
Q

bolus insulin

A
  • used for coverage of food intake or correction of hyperglycemia.
  • Short acting: regular
  • Rapid acting: aspart, lispro, glulisine
23
Q

aspart/lispro

A
  • AA substitution decreases formation of hexamer. monamers exert action much faster.
  • faster absorption, higher peak concentration, shorter duration than regular insulin
24
Q

basal insulin

A
  • maintain euglycemia in the fasting state
  • intermediate: NPH (1-2x daily)
  • long acting: glargine, detemir
25
Q

glargine

A

long-acting insulin. packaged at acidic pH. forms crystals once injected –> slow release

26
Q

Detemir

A

long-acting insulin modified so it binds albumin, released slowly

27
Q

split/mixed insulin regimen

A

combination of lispro/NPH injected once in the morning and once in the evening
requires regimented eating and can result in peaks/valleys

28
Q

lispro pump regimen

A

pump delivers basal level, injections for meals

29
Q

basal-bolus regimen

A

lispro injected for meals, glargine injected at night for basal levels

30
Q

disadvantages of insulin pump

A

requires carb counting and frequent blood glucose checking. can go into DKA quickly if don’t monitor blood glucose

31
Q

factors determining insulin dose

A

provider: weight, blood glucose, insulin sensitivity
patient: carb intake (ideally ratio), blood glucose, physical activity

32
Q

complications of insulin

A

hypoglycemia, lipatrophy/lipohypertrophy locally, allergy (rare), resistance

33
Q

ileus

A

cessation of GI motility due to non-mechanical causes (can be due to electrolyte imbalance i.e. from DKA)

34
Q

Kussmaul’s breathing

A

rapid, shallow breathing (i.e. to breathe off acetone in DKA)

35
Q

main tissues utilizing glucose

A

brain, muscle, red and white cells, renal medulla.

brain can adapt to ketones

36
Q

sources of glucose

A

ingestion, glycogenolysis (liver) 24-36hrs fast (12 hrs in children). Gluconeogenesis (liver)

37
Q

hormonal control of fasting systems

A

fasting systems: glycogenolysis, gluconeogenesis, lipolysis, ketogenesis
insulin: inhibits all
glucagon: stimulates gylcogenolysis, gluconeogenesis
Epinephrine: stimulates gylcogenolysis, lipolysis, ketogenesis
Cortison: stimulates gluconeogenesis
Growth hormone: stimulates lipolysis

38
Q

normal glucose range

A

60-100 mg/dL

39
Q

glucose range for Sx, activation of glucose counterregulatory hormones, diagnostic threshold, therapeutic threshold

A

activation of hormones: 65-70 mg/dL
Sx: 50-55
Cognitive dysfuction: 45-50
Diagnostic: 70

40
Q

Diagnosis of hypoglycemia

A

whipple’s triad

  • Sx of hypoglycemia
  • measured low glucose at time of Sx
  • correction with food or glucose
41
Q

neurogenic Sx of hypoglycemia

A

perception of physiological changes cause by CNS-mediated sympathetic discharge (adrenergic and cholinergic
Previous episodes of hypogylcemia may blunt, especially adrenergic response (HAAF)

42
Q

neuroglycopenic Sx of hypoglycemia

A

brain dysfunction (dizziness, fatigue, blurred vision, headache…death)

43
Q

post-prandial hypoglycemia

A

rare “reactive” hypoglycemia

  • Late Dumping Syndrome (hyperinsulinemic hypoglycemia). occurs in ppl w/ abdominal surgery
  • Early diabetes (dysregulation of insulin)
  • idiopathic
  • congenital metabolic disorders (galactosemia, hereditary fructose intolerance)
44
Q

Fasting hypoglycemia mechanisms

A
  • insulin-mediated (insulinoma, congenital hyperinsulinism, exogenous insulin)
  • failure of counter-regulation
  • congenital metabolic defects
45
Q

insulin-induced hypoglycemia labs

A
increased glucose utilization
-hyperinsulinemia, high C-peptide
hypo FFAs
hypo ketones
glycemic response to glucagon
46
Q

insulinoma

A

usually benign, solitary, but can have multiple ectopic
increased pro-insulin/insulin ratio.
can be small: must localize and resect!

47
Q

congenital hyperinsulinemia

A

dysregulation of beta-cell secretion. defects change ATP level regulation (ATP is trigger for membrane depol)
eg dominant GOF for glucokinase or Glutamate dehydrogenase
mutations to ATP-dep K channel (most severe)

48
Q

Tx congenital hyperinsulinemia

A

diazoxide: stimulates ATP-dependent K channels
somatostatin: inhibits Ca++ release in beta cells
octreotide: multiple effects, including K-ATP channel activation
for focal: surgical

49
Q

immune-mediated hypoglycemia

A

can have activating antibodies or antibodies to insulin itself

50
Q

hypoglycemia in GH/cortisol deficiency

A
shortened fasting (impairment of gluconeogenesis, lipolysis), midline defect or microphallus, ketotic hypoglycemia (can mimic hyperinsulinism)
Tx: replace hormones.
51
Q

G6Pase deficiency (problem, Sx, labs, Tx, complications)

A

can’t release glucose from liver.
Sx: failure to thrive, hepatomegaly
Labs: hyperlacticacidemia, hyperTGs, hyperuricemia, lack of glycemic response to glucagon
Tx: frequent CHO
Late complications: liver tumors, nephropathy

52
Q

F16Pase deficiency

A

gluconeogenic defect
Sx: attacks of acidemia, hyperuricemia
triggers: fasting or fructose
Tx: limit fasting, no fructose/sucrose

53
Q

GSD type 3 (defect, clinical, labs, Tx, complications)

A

defect in glycogenolysis (debranching enzyme)
clinical: failure to thrive, hepatomegaly, muscle weaksness
Labs: hyperketonemia, inc LFT
Tx: frequent low CHO feed
Late complications: cardiomypoathy, mypoathy

54
Q

Tfs in pituitary development

A

Prop-1, Plt-1

Deficiency –> hypopituitaryism for some/all hormones

55
Q

Ant pituitary hormone

A
  • Glycoproteins: (TSH, LH, FSH)–share alpha subunit, different beta-subunit
  • ACTH (from large molecule POMC)
  • GH/PRL (structural homology and affinity for PRLR)
56
Q

ant pituitary cell types

A

somatotrope (GH), thyrotrope (TSH), lactotrope (PRL), gonadotrope (LH/FSH), Corticotrope (ACTH)

57
Q

ACTH (synthesis, function, stimuli, inhibitors, rhythm)

A
  • POMC cleaved to form ACTH and melanotropin
  • induces secretion of cortisol, stimulates lipolysis, and increases skin pigmentation.
  • stimuli: CRH, Stress, hypoglycemia, anxiety, depression
  • inhibitor: cortisol
  • diurnal: peaks in morning
58
Q

GH axis

A

hypothal: GHRH (+) and somatostatin (-)
GHRH: episodic release, stimulated by hypoglycemia, dietary protein, exercise
somatotropes: GH –> liver
liver: IGF1 –| pit, hypothal
somatostatin: inhibitory, extra-pituitary receptors (GIT), pharm application

59
Q

GH ( release, regulation, lab)

A

pulsatile release, regulated by age, sex, nutrition, sleep, stress, exercise. stimulates post-natal grown via IGF-1.
lab: measure IGF1–integrated measure of GH’s effects

60
Q

PRL axis

A
  • normally suppressed by DA from hypothal
  • neural stimulus (e.g. suckling) acts on hypothal
  • “PRFs” induce PRL secretion.
  • PRL acts on mammary gland
  • PRL feeds back on hypothal (-) and suppresses gonadotropins via GnRH

stimulators: breast stimulation, stress, estrogen, sleep, DA antagonists, TRH
Inhibitors: DA and DA agonists

61
Q

H-P-G axis

A

hypothal: GnRH
GnRH: FSH/LH
estrogens/ testosterone/progesterone feedback on hypothal and pituitary

62
Q

GnRH

A

pulsatility and pulse freq are critical

greater freq and amplitude of pulses in puberty

63
Q

H-P-T axis

A

hypothal: TRH –> TSH/PRL
Pit: TSH
TSH: T4–>T3
T3 feeds back on pituitary. When intracellular T3 reaches certain level, TRH-Rs are removed from membrane

64
Q

MCAD deficiency

A
  • Hypoketotic hypoglycemia
  • Mimics Reye’s
  • Newborn screening
  • Tx: limit fasting
65
Q

Iatrogenic Hypoglycemia

A
  • Sulfonylureas
  • Salicylate OD (esp children)
  • Beta blockers (blocks adrenergic warning cells, hypoketotic hypoglycemia pattern– impaired lipolysis)
  • exogenous insulin (high insulin, low C peptide)
  • Pentamide (for pneum carnii)
66
Q

Alcohol induced hypoglycemia

A

Oxidation of EtOH –> NADH –| gluconeogenesis

  • occurs in absence of glyocgen (starvation)
  • can be lethal in children
67
Q

non-islet cell tumor hypoglycemia (types, mechanism of hypoglycemia)

A
  • Mesenchymal, epithelial, leukemia/lymphoma
  • Poor nutrition w/ advanced malignancy, tumor consumption of glucose, reduced hepatic gluconeogenesis (metastatic disease involving liver)
68
Q

Critical sample in hypoglycemia

A

Must be done at time of hypoglycemia

  • counter regulation: insulin/C-peptide, GH, cortisol
  • metabolites (ketones, FFAs, etc)
  • tox and drug screen
69
Q

Diagnostic tree hypoglycemia

A

Acidmia: high lactate (gluconeogenic eg EtOH) vs high ketones (glycogenolysis, defect of counter-regulation)

No acidemia: Low ketones/high FFA –> FAO defects vs low ketones/low FFA –> hyperinsulinemic

70
Q

General DDx hypoglycemia

A
  • counter-regulation
  • glycogenolysis
  • gluconeogenesis
  • ketogenesis
71
Q

glycogen metabolism in muscle vs liver

A

muscle glycogen is available only for muscle

72
Q

leptin system

A

secreted by adipose, binds to Mc4R in brain

73
Q

effect of fat location on risk

A

central/visceral obesity much worse than peripheral: Diabetes, NAFLD, sleep apnea, CVD, Cancer
sarcopenia in thighs –> no bueno!

74
Q

Management of obesity

A

Lifestyle (10k steps)
Diet (reduce calories)
Exercise (if possible)
Treat related illnesses

75
Q

Rx in obesity

A

not a lot of good drugs. Sympathetic side-effects

Olistat (Alli) inhibits pancreatic lipase (–> steatorrhea)

76
Q

Bariatric surgery

A
  • Adjustable gastric banding
  • Vertical Sleeve Gastrectomy
  • Roux-en-Y (most invasive, greatest reduction in weight, decreases weight and fat, sleep apnea, risk of cancer. long-term can have deficiencies, dumping syndrome (Vagal overload after big meals), recurrent severe hypoglycemia)
77
Q

anabolic pathways for muscle

A

follistatin, IGF-1, androgens

interest in these to counteract cachexia in cancer

78
Q

Tx cachexia

A

controlled refeeding
Diagnose and Tx underlying disease (anorexia, cancer)
Anabolic Rx: megesterol, THC

79
Q

common features in endocrine tissues

A

ductless (vs exocrine), vascular, organization (blocks, cords, plates), epithelial (except in gonads–mesenchymal and post pet/adrenal medulla–neural), polyhedral, numerous organelles

  • specialized secretory cells
  • proximity to blood vessels (fenestrated endothelium)
  • individual endocrine cells (enteroendocrine, juxtaglomerular)
80
Q

histologic cell types in ant pituitary

A

acidophils (somatotropes, lactotropes)
basophils (corticotropes, gonadotropes, thyrotropes)
Chromophobes (unknown function)

81
Q

histology of post pit

A
unmyelinated nerve axons and pituicytes (supportive cells), with capillaries
Herring bodies (granules at axon terminals storing hormones)
82
Q

histology/function of thyroid

A
  • characteristic follicle with large lumen surrounded by simple cuboidal epithelium
  • Extracellular thyroglobulin called colloid accumulates in the follicles (UNIQUE TO THYROID)
  • Follicular cells use thyroglobulin to produce T3/T4
  • parafollicular cells (C cells) produce calcitonin
83
Q

parathyroid glands hist/function

A
  • usually 4
  • regulate calcium
  • lobules of cells with fine capillary network
  • fat cells common (inc with age)
  • principle (chief cells) secrete PTH
  • oxyphil cells–larger and pink (unknown function, lots of mitochondria)
84
Q

Adrenal hist and function

A

cortex (90% weight): cords of steroid-secreting cells, sperated by sinusoids

  • Z Glomerulosa (Mineralcorticoids)
  • Z Fasciculata (Glucocorticoids)–clear foamy cells
  • Z Reticularis (Gonadocorticoids)

medulla (neuralectoderm origin): innervated by symp nerve fibers.
-chromaffin arranged in groups or cords clustered around capillaries and venules (“post synaptic w/o axons)
Large dense core vesicles: norepinephrine
Small less dense core vesicles: epinephrine

85
Q

pheochromocytoma

A

often benign tumor of adrenal medulla (makes NE or E)

86
Q

pancreas (hist/function)

A
acini: exocrine
islets (more numerous in tail--1-2% overall): endocrine
-A cells: glucagon (periphery of islets)
-B cells: insulin
-D cells: somatostatin
-minor types
87
Q

severe hypoglycemia in T1DM (causes, complications)

A

insulin OD. with greater # of episodes, Sx go down, so can be unaware
-QT prolongation –> sudden cardiac death

88
Q

Strategies for transplantation in T1DM

A
  • pancreas with kidney
  • pancreas after kidney
  • experimental: islets with/after kidney

-pancreas with kidney is most successful because come from same donor so will be rejected at the same rate…serum creatinine is much more sensitive marker of function and rejection than is hypoglycemia)

89
Q

good indicators for pancreas transplant

A
  • recipient <50

- donor not obese

90
Q

islet cell transplant

A
  • infused directly into portal vein, engraft on liver
  • OK for preventing hypoglycemia (fasting)
  • lower function with glucose challenge (need insulin)
  • newer protocols improve efficiency
  • can reverse HAAF
91
Q

pituitary adenomas

A
  • any kind of ant pit cell

- protein hormones tend to be efficient in secretion and cause recognizable clinical Sx more often

92
Q

somatotroph adenoma (signs, latency, Dx, consequences, Tx)

A
  • acromegaly: nose, jaw, fingers, lips swell
  • latency to diagnosis ~10 yrs
  • Dx: measure IGF-1, failure to suppress GH on oral glucose load
  • arthritis, colon cancer, CVD, neuropathy, sleep apnea, mortality
  • Tx: surgical, pharm (DA agonists, somatostatin analogs, GH antagonists), radiation
93
Q

lactotroph ademona (Sx, Tx)

A

-Premenopausal: amenorrhea/oligomenorrhea, sometimes galactorrhea
postmenopausal: neurological
Men: decreased libido, fertility, potency
-Tx: DA agonist–> tumor regression

94
Q

DDx high PRL

A
  • physiologic: pregnancy, nursing, exercise, stress

- pathologic: adenoma, DA antagonists, catecholamine inhibitors, estrogens, opiates H2 antagonists

95
Q

thyrotroph adenoma (Sx, Tx)

A

-usually inefficient–hyperthyroidism uncommon

Tx: somatostatin analog (inhibits TSH)

96
Q

Gonadotroph adenomas (Sx,

A

-usually very inefficient–neuro Sx most common, hormonal abnormality (premature puberty, ovarian hyperstim) uncommon

97
Q

Hypercortisolism (Chushingoid) causes

A

-bilateral hyperplasia 80% (pit ACTH, ectopic ACTH (e.g. lung cancer), primary hyperplasia, idopathic/iatrogenic)
-Adenoma 10%
-Carcinoma 10%
In CHILDREN:
-carcinomas much more common (50%), adenoma more common, hyperplasia 35%

98
Q

adrenocortical carcinoma (gross characteristics, Sx, prognosis, syndromes

A

gross: large size, necrosis, hemorrhage, invasion
micro: cellular pleomorphism, capsular invasion, vascular invasion, metastases, mitosis
Sx: (don’t necessarily have to do with hormone secretion) weigh gain/loss, fever, anorexia, hormone secretion (commonly cortisol but could be anything)
Prognosis: poor
Syndromes: (Li-Fraumeni syndrom (p53), Beckman-Wiedemann, Familial adenomatous polypsis coli, multiple endocrine neoplasia type I)

99
Q

Definitive criteria for malignancy of adrenocortex

A
  • distant metastasis

- local invasion

100
Q

hyperaldosteronism causes

A
  • adenoma (65%)
  • bilateral hyperplasia (35%)
  • carcinoma (v rare)
101
Q

hypofunction (Addison’s) of adrenal cortex causes

A
  • autoimmune destruction
  • replacement (TB, fungi, amyloid, tumor)
  • need 90% of both cortices destroyed for Sx
102
Q

hyperfunction of medulla causes

A
  • neoplasm (pheochromocytoma)
  • hyperplasia
  • neuroblastoma (rare)
103
Q

pheochromocytoma clinical triad

A

paroxysmal HTN
headaches
diapheresis

104
Q

characteristic of familial-syndrome pheochromocytoma

A

multi-centered!

105
Q

criteria for malignant pheochromocytoma

A

most reliable is presence of metastases.
PASS score is pretty predictive (>4)
NOT necrosis, mitoses, vasc invasion

106
Q

MEN syndromes

A

genetically defined, familial syndromes with multiple endocrine organ involvement. signs and symptoms vary. Also have lesions in non-endocrine systems

107
Q

MEN 1

A

3 Ps:
hyperplasia and neoplasia of pituitary, parathyroid, pancreatic
-prognosis related to lesions of pancreas (can develop into malignancies
-mutation in MENIN – multiple sites

108
Q

MEN 2A/2B

A

MEN2A: Neoplasia/hyperplasia of Thyroid C cells, Adrenal medulla, parathyroids (15-25%)

  • Men2B: same lesions, no parathyroid + neural tissue of oral/GI systems and eye abnormalities. 50% familial, 50% sporadic
  • mutations in ret
109
Q

causes of hypercortisolism by age

A

Adults: hyperplasia (80%) > adenoma (10%)/carcinoma (10%)
Children: carcinoma (50%) > hyperplasia (35%) > adenoma (14%)