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Pathoma Endo > 15.9 Endocrine Pancreas > Flashcards

15.9 Endocrine Pancreas Flashcards

1
Q

The endocrine pancreas is composed of clusters of cells termed

A

islets of langerhans

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2
Q

insulin is secreted by

A

beta cells

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3
Q

beta cells are located

A

in the center of the islet

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4
Q

major anabolic hormone

A

insulin

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5
Q

insulin upregulates WHAT on adipocytes and skeletal muscle cells

A

GLUT4 (glucose-dependent transporter)

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6
Q

GLUT4 is on what cells?

A

adipocytes and skeletal muscle

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7
Q

insulin –> increased glucose uptake –>

A

increased glycogen synthesis, protein synthesis, and lipogenesis

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8
Q

major catabolic hormone

A

glucagon

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9
Q

glucagon is secreted by

A

alpha cells

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10
Q

in states of fasting, glucagon increases blood glucose via

A

glycogenolysis

lipolysis

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11
Q

insulin deficiency due to autoimmune destruction of beta cells by T cells

A

type 1 DM

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12
Q

histology of type 1 DM

A

inflammation fo islets

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13
Q

Type 1 DM genetic association?

A

HLA-DR3 and HLA-DR4

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14
Q

clinical features of insulin deficiency

A

weight loss, low muscle mass, polyphagia, polyuria, polydipsia;

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15
Q

DM1 labs

A

hyperglycemia glucosuria

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16
Q

dm1 treatment

A

lifelong insulin

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17
Q

why does diabetic ketoacidosis often arise with stress (infection) in dm1?

A

Epinephrine stimulates glucagon secretion –> lipolysis –> FFAs –> ketones

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18
Q

name two ketones

A

beta-hydroxybutryric acid and acetoacetic acid

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19
Q

DKA labs

A

hyperglycemia (> 300)
anion gap metabolic acidosis
hyperkalemia

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20
Q

presentation of DKA

A 
Kussmaul respirations,
dehydration, 
nausea/vomiting,
mental status changes,
fruity smelling breath (due to acetone)
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21
Q

DKA treatment

A
  1. fluids
  2. insulin
  3. electrolytes (potassium)
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22
Q

end-organ insulin resistance leading to a metabolic disorder characterized by hyperglycemia

A

DMT2

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23
Q

what percent of DM is type II?

A

90%

24
Q

what percent of US pop has dmt2?

A

5-10%

25
Q

why is dmt2 associated with obesity?

A

decreased #s of insulin receptors

26
Q

amyloid deposition in the islets

A

histology of dmt2

27
Q

insulin levels early in dmt2?

A

high

28
Q

why does insulin deficiency develop later in dmt2?

A

beta cell exhaustion

29
Q

clinical features of dmt2

A

polyuria, polydipsia, hyperglycemia (often silent though)

30
Q

diagnosis of dmt2

A
  1. random glucose > 200
  2. fasting glucose > 126
  3. glucose tolerance test > 200 after glucose loading
31
Q

dmt2 treatment

A
  1. weight loss (diet and exercise)
  2. sulfonylureas or metformin
  3. exogenous insulin
32
Q

dmt2 –> risk for [emergent complication]

A

hyperosmolar non-ketotic coma

33
Q

hyperosmolar non-ketotic coma mechanism?

A

high glucose (> 500) –> life-threatening diuresis –> hypotension –> coma (nb: no ketones)

34
Q

NEG of large and medium sized vessels leads to

A

atherosclerosis (cvd + peripheral vascular dz)

35
Q

what is the leading cause of death among diabetics?

A

cvd

36
Q

what is the leading cause of non traumatic amputations

A

peripheral vascular dz

37
Q

NEG of small vessels –>

A

hyaline arteriolsclerosis

38
Q

NEG of renal arterioles –>

A

glomerulosclerosis –> small scarred kidneys with a granular surgace

39
Q

preferential hyaline arteriosclerosis of efferent arterioles –>

A

high GFR –> hyper filtration injury (microabuminuria) –> nephrotic syndrome

40
Q

histology of diabetic nephrotic syndrome

A

kimmelstiel-wilson nodules

41
Q

NEF of hemoglobin –>

A

HbA1c

42
Q

what is the leading cause of blindness in the developed world?

A

diabetes

43
Q

what do schwann cells do?

A

myelinate peipheral nervels

44
Q

into what cells does glucose freely enter (causing osmotic damage in diabetes)?

A

schwann cells, pericytes of retinal vessels, lens

45
Q

intracellularly, what converts glucose to sorbitol –> osmotic damage?

A

aldose reductase

46
Q

intracellularly, aldose reductase converts glucose to WHAT, causing osmotic damage

A

sorbitol

47
Q

osmotic damage in diabetes –>

A

peripheral neuropathy, impotence, blinddness, cataracts

48
Q

pancreatic endocrine neoplasms should make you think

A

MEN1

49
Q

MEN1

A

parathryoid hyperplasia
pituitary adenoma
pancreatic endocrine neoplasm

50
Q

episodic hypoglycemia with mental status changes that are relieved by administration of glucose

A

insulinoma

51
Q

how would you diagnose insulinoma

A

decreased serum glucose (<50)

increased insulin + c-peptide

52
Q

what other things could look like insulinoma?

A

exogenous insulin admin (but c-peptide not raised)

sulfonylurea or melitinide abuse

53
Q

treatment-resistnace peptic ulcers; ulcers may be multiple and extend into jejunum

A

Zollinger-Ellison syndrome (gastrinoma)

54
Q

achlorhydria (due to inhibition of gastrin) and cholelithiasis with steatorrhea (inhibitor of cholecystokinin)

A

somatostatinoma

55
Q

watery diarrhea, hypokalemia, achlohydria

A

VIPoma

56
Q

DM, necrolytic erythrema, anemia

A

glucagonoma

Pathoma Endo (7 decks)

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