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Endocrine II DF > Endocrine Pancreas Guerin > Flashcards

Endocrine Pancreas Guerin Flashcards

1
Q

how can the islets of langerhans cells be differentiated

A

ultrastucturally and by their hormone content

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2
Q

what do PP cells do

A

pancreatic polpeptide stimulates the secretion of gastric and intestinal enzymes
-inhibits intestinal motility

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3
Q

rare cell types in islets of langerhans

A

D1 cells: VIP
enterochromaffin cells: serotonin
-tumor of these can cause carcinoid syndrome

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4
Q

what does VIP do

A

induces glycogenolysis and hyperglycemia

stimulates GI fluid secretion and causes secretory diarrhea

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5
Q

what is fasting plasma glucose levels usually detemined by

A

hepatic glucose output

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6
Q

insulin action on adipose tissue

A

increase glucose uptake
increase lipogeneisis
decrease lipolysis

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7
Q

insulin action on liver

A

decreased clugoneogenesis
increased glycogen synthesis
increased lipogenesis

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8
Q

insulin action on striated muslce

A

increase glucose uptake
increase glycogen syn
increase protein syn

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9
Q

mitogenic effects of insulin

A

initiation of DNA synthesis in certain cells and stimulation of their growth and differentiation

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10
Q

what pathway intracellulary is responible for GLUT4 transport to the PM

A

PI3K/ATK

and CBL

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11
Q

In the US diabetes is the leading cause of what

A

ESRD
adult onset blindness
non traumatic LE amputations

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12
Q

populations at greatest risk for diabetes

A

NAH

native americans, africans, hispanics

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13
Q

diagnosis of diabtes with fasting glucose of

A

126 or greater

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14
Q

diagnosis of diabetes: random plasma glucose

A

200 or greater (in pts with clasic hyperglycemis signs)

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15
Q

diagnosis of diabetes: 2 hour plasma glucose at ___ or greater during an oral glucose tolerance test with load dose of __

A

200 mg/dL

75 gm

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16
Q

diagnosis of diabetes: HbA1C level at

A

6.5% or above

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17
Q

which of the diagnosis of diabetes does not need confirmation test on separate visit

A

random blood glucose test in pt with classic hyperglycemic signs

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18
Q

what can lead to transient hyperglycemia

A

acute stress

infections, trauma, burns

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19
Q

impaired glucose tolerance (prediabetes)

fasting plasma glucose ___

2 hour plasma glucose with 75 gm OGTT ____

HbA1C level ___

will they develop overt diabetes?

increased risk for what?

A

100-125 mg/dL

140-199 mg/dL

5.7-6.4%

1/4 will over 5 years

increased risk for cardiovascular complications

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20
Q

genetic susceptibility in DM1

main ones

A

HLA gene cluster on chrom 6p21

  • 90-95% of caucasians with HLA-DR3 or DR4
  • DR3 or DR4 plus DQ8 has highest risk
    • DQA11301-DQB10302 alleles
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21
Q

genetic susceptibility in DM1 other genes

A 
wasinsulin
polymorphism in CTLA4 and PTPN22
VNTR in promoter region of insulin gene
gene for immune regulators (AIRE)
   -cause autoimmune polyendocrinopathy syndrome, type 1
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22
Q

environmental factors for diabetes type 1

A

possible viral infection but unknown which one

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23
Q

autoantigen target in B cell destruction for DM1

A

insulin
GAD (glutamic acid decarboxylase)
islet cell autoantigen 512

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24
Q

how much of islet B cell needs to be loss before get hyperglycemia and ketosis

A

90%, long period btwn initiation of autoimmune process and appearance of diseas

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25
Q

inadequate insulin secretion (b cell dysfunction) in DM2

A

initially there is insulin hypersecretion to overcome resistance

  • from a combo of excess FFA (lipotox)
  • chronic hyperglycemia (glucotox)
  • abnormal incretin effect
  • amyloid deposition within islets, and genetics
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26
Q

insulin resistance in liver

A

failure to inhibit gluconeogenesis (endogenous glucose production)

contributes to high fasting blood glucose levels

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27
Q

insulin reseistance in fat

A

failure to inhibit activation of HSL–> excess TG breakdown and excess circulating FFA

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28
Q

which adipokines decrease blood glucose by increasing insulin sensitivity and how are they effected in obesity

A

leptin and adiponectin

adiponectin levels are reduced in obseity and contribute to insulin resistance

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29
Q

PEP C and gluconeogensisis in central obesity

A

central obesity increases lipolysis of adipose tissue = excess FFA, which has DAG intermediate, which canc stop insulin signaling
-insulin usually stops gluconeogensis by blocking PEP carboxykinase, so without insulin PEPC ramps up gluconeogeneisis

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30
Q

central obesity and inflammation

A

proinflammatory cytokines are secreted in response to excess nutrients like FFAs and glucose =
insulin resitance and b cell dysfunction
-excess FFas within macrophages and b cells can activate inflammasome = more proinflamm cytokines = insulin resitance

31
Q

several mechanism for b cell dysfunction in overt diabetes in type 2

A

excess FFA compromise b cell function and attenuate insulin release (lipotox)

impact of chronic hyperglycemia (glucotox)

abnormal incretin effect = reduced GIP and GLP-1 that normally causes insulin release

amyloid deposition wihtin islets, in people with long standing DM2 in 90% of pts

32
Q

monogenic forms of diabetes, genetic defect in b cell function

A

no b cell loss
b cell mass and or insulin production effecte4d
was called MODY bc like DM2 but earlier onset
gene mutation is in glucokinase, this is the RLS for oxidative glucose metabolism which in turn is coupled to insulin secretion within islet b cells
-can also have defect in genes for ATP/K+ channel

33
Q

monogenic forms of diabetes, genetic defects that impair tissue response to insulin

2 types
-symptoms associated with each

A

insulin receptor mutations

  • acanthosis nigricans
  • women have polycysitic ovaries and elevated androgen levels

-lipoatrophic diabetes
:hyperglycemia with loss of adipose tissue in subcut fat
:also have hyperTGemia, acanthosis nigricans, and fat deposition in liver

34
Q

pregestational diabetes and pregnancy increased risk for

A

stillbirth

congenital malformations

35
Q

gestational diabetes
what is it
how to fix
what can develop

A

women develops impaired glucose tolerance and diabetes for first time during pregnancy

  • typically resolves after delivery
  • majority develop overt diabetes in next 10-20 yrs
36
Q

poorly controlled diabetes later in pregnancy can cause

A

large for gestational age newborn

child at increased risk of developing obesity and diabetes later in life

37
Q

classic triad in DM1
if severe get
also see

A

polyuria, polydipsia, polyphagia
when severe enough you get diabetic ketoacidosis too
-also see weight loss and muscle weakness

38
Q

DM type 2 can present with

A

fatigue, dizziness, or blurred vision

39
Q

diabetic ketoacidosis is typically triggered by

A

failure to take insulin (most common)
other stressors: infections, illness, trauma, drugs (epinephrine, blocks insulin action and stimulates glucagon secretion)

40
Q

glucose level for diabetic ketoacidosis

A

250-600 mg/dL

41
Q

how are ketone bodies formed

A

decreased insulin = increased HSL–>increased FFA–>in liver FA esteried to fatty acyl coA–>in liver mitochond oxidize this to produce acetoacetic acid and b-hydroxybutyric acid

42
Q

clinical manifestations of diabeti ketoacidosis

A 
fatigue
nausea and vomiting
ab pain
fruity odor
deep, labored breathing (kussmaul breathing)
-can get CNS depression and coma
43
Q

why is ketoacidosis less common in DM 2

A

bc of higher portal vein insulin levels that prevent unrestricted hepatic fatty acid oxidation and keeps formation of ketone bodies in check

44
Q

what is this called when
severe dehydration from sustained osmotic diuresis
-in pts who don’t drink enough water to compensate for urinary loss
-what pts?
when usually seek medical attention?
hyperglycemia at what?

A

hyperosmolar hyperosmotic syndrome in type 2 DM

older pts and disabled pts by stroke or infection

seek attention when

  • severe dehydration
  • impaired mental status

hyperglycemia 600-1200 mg/dL

45
Q

signs and symptoms of hypoglycemia

A

dizziness, confusion, sweating, palpitations, tachycardia

46
Q

chronic complication of diabetes

-diabetic macrovascular disease

A

large and medium sized muscular arteries

  • accelerated atherosclerosis (hallmark)
    • increased risk of MI, stroke, LE ischemia
  • HTN and dyslipidemia in type 2 DM
  • diabetics have increased PAI-1 = procoag = formation of atherosclerotic plaques
47
Q

chronic complications of diabetes

microvascular disease

A

small vessels

retina, kidneys, and peripheral nerves

48
Q

diabetic microangiopathy

A

diffuse thickening of basement memrbanes

  • capillaries are more leaky than normal to plasma proteins
  • seen in skin, muscle, retina, renal glomeruli and medulla
  • leads to diabetic nephropathy, retinopathy, and some neuropathy
49
Q

diabetic neprhopathy first sign

  • marker for what
  • may develop
A

microalbuminuria over 30 mg/day but less than 300 mg/day

  • also marker for greatly increased CV mobidity and mortality
  • 80% of type 1 and 20-40% of type 2 over 10-15 yrs will develop overt nephropathy with macroalbuminuria and HTN
50
Q

3 lesions in diabetic neprhopathy

A

glomerular lesions
-capillary BM thickening, diffuse mesangial sclerosis, and nodular glomerulosclerosis

renal vascular lesions, principally arteriolosclerosis

pyelonephritis, including necrotzing papillitis

51
Q

capillary basement membrane thickening

  • what % of pts
  • seen how
  • when begins
  • what else occurs
A

in virtually all diabetic nephropathy, only seen by electron microscopy

begins 2 years after onset of type 1

also have thickening of tubular basement membranes

52
Q

diffuse mesangial sclerosis

  • depositions are positive for what
  • progression of disese
A

PAS positive

as progresses, becomes nodular

53
Q

nodular glomerulosclerosis

  • name of disease
  • where
  • progression?
A

kimmelstiel-wilson disease

nodules of matrix (PAS positive) in periphery of glomerulus

progression: nodules enlarge and obliterate glomerular tuft

54
Q

arterioles in and tubes in diabetic nephropathy

A

hyalinosis of both afferent and efferent glomerular hilar arterioles

glomerular and arteriolar lesions –> ischemia–>tubular atrophy and intersitital fibrosis

55
Q

diabetic neuropathy

distribution
types

A

glove and stocking pattern (LE first)
sensory and motor

autonomic neuropathy: bowel, bladder, ED

mononeuopathy: sudden footdrop, wristdrop, or isolated cranial nerve palsies

56
Q

diabetic retinopathy

other eye manifestations

A

from neovascularization from hypoxia induced overexpression of VEGF in the retina

glaucoma and cataracts

57
Q

diabetics have increased susceptibility to infections of the

A

skin, TB, pneumonia, and pyelonephritis

58
Q

criteria for malignancy in pancreatic neuroendocrine tumors

A

can’t predict behavior based on microscopic appearance bc bland

criteria is metastases, vascular invasion, local infiltration

59
Q

90% of insulin producing tumors are benign or malignant?

A

benign

60
Q

60-90% of non insulin functioning and nonfunctioning NETs are what

A

malignant

61
Q

genetic alterations in sporadic pancreatic NETs

A 
MEN1
LOF: PTEN and TSC2
inactivating mutations in 
-ATRX
-DAXX
62
Q

most common clinical syndromes in PanNETs

A

hyperinsulinism
hypergastrinemia
MEN

63
Q

classic clinical picture of insulinoma

A

hypoglycemic episodes if blood gluose under 50 mg/dL

64
Q

morphology of insulinoma

A

small (less than 2 cm diameter)
look like giant islets
deposition of amyloid

65
Q

hyperinsulinism not from insulinoma

A

focal or diffuse hyperplasia of islets (use to be called nesidioblastosis)

  • maternal diabetes
  • beckwith-wiedemann syndrome
  • rare mutations in B cell K+ channel protein or sulfonylurea receptor
  • mor common in neonates and infants from congenital malformation
66
Q

other causes of hypoglycemia

A

abnormal insulin sensitivity
diffuse liver disease
inherited glycogenoses
ectopic production of insulin by retroperitoneal fibromas and fibrosarcomas

-induced by self injection of insulin

67
Q 
zollinger-ellison syndrome
oversecretion of what
location
metastases?
syndrome involved 
histology
A 
hypersecrtion of gastrin
in duodenum or pancreas
>50% are locally invasive or have already metastasized at time of diagnosis
-25% arise as part of MEN?
-histologically bland
68
Q

multifocal gastrinoma vs sporadic

A

MEN-1 syndrome is multifocal

sporadic is single

69
Q

if you have unusual location of ulcer in the jejunum think what

A

zollinger-ellison syndrome

70
Q

clinical course of ZE

metastases?

A

peptic ulcers in duodenum and stomach
50% have diarrhea
pts with hepatic metastases–>eventual liver failure within 10 yrs

71
Q

treatment of ZE

A

PPI

total resection

72
Q

other rare pancreatic endocrine neoplasms

  • mild diabetes, skin rash (necrolytic migratory erythema) and anemia
  • in perimenopausal and postmenopausal women mostly
A

SAM is an a-cell tumor bc he is menospausal

73
Q

other rare PanNETs

-diabetes mellitus, cholelithiasis, steatorrhea, hypochlorhydria

A

D-cell tumor (somatostatinomas)

-D High school class

74
Q

watery diarrhea, hypokalemia, achlorhydria

syndrome?

A

VIPoma

WDHA syndrome

Endocrine II DF (7 decks)

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