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ENRP Exam II > Endocrine Pancreas Path Singh > Flashcards

Endocrine Pancreas Path Singh Flashcards

1
Q

What regulates glucose homeostasis?

A
  • hepatic release of glucose
  • tissue utilization of glucose
  • hm control of glu by insulin and glucagon
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2
Q

What is a marker of endogenous insulin? what is the significance of this?

A

C peptide, it allows you to tell the difference between insulin administered vs made by self

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3
Q

What is type 1 diabetes? When do symptoms occur?

A
  • Autoimmune disease due to failure of T cell self tolerance
  • Immune mediated destruction of islet cells → once 90% of islet cells are destroyed you begin to get sx
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4
Q

What causes type 2 DM?

A

Insulin resistance + Beta cell dysfunction

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5
Q

Why is obesity a risk for T2DM?

A
  • excess adipose results in free fatty acids, inflammation, and adipokines accumulating
    • adipokines and ffa disrupt paths that enable insulin uptake
    • inflammation causes direct damage to beta cells and can also disrupt cell uptake of insulin
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6
Q

What is MODY? Cause?

A
  • maturity onset diabetes of the young
  • Resembles T2DM clincally but happens in the young, blood insulin may be high normal or low
  • NO autoantibodies
  • nonketotic
  • Most often caused by mutations resulting in los of function of glucokinase
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7
Q

Risks to the fetus if mom has gestational diabetes?

A
  • neonatal hypoglycemia → seizure → brain damage
  • macrosomia
  • congenital malformation
  • still birth
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8
Q

Classic triad of T1DM?

A
  • polyphagia
  • polyuria
  • polydipsia
  • severe → DKA
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9
Q

How do you differentiate T1DM and T2DM?

A
  • autoantibodies
    • 90% white kids have
    • <50% west african descent and Latinx populations have, so it is difficult to tell 1 from 2
  • HLA typing
    • HLA DR/DQ on chr 6
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10
Q

DKA triad?

A
  • hyperglycemia
  • ketonemia
  • metabolic acidosis
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11
Q

How does epinephrine impact glucose?

A

Body can’t use glucose so it accumulates in the blood

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12
Q

How does a stressful situation (infections) induce DKA in a diabetic patient?

A
  • With high epinephrine the body isn’t able to utilize glucose
  • Glucagon gets released promoting gluconeogenesis
  • Insulin deficiency promotes FFA generating ketones
  • as glucose and ketones accumulate in blood kidneys begin to dump that → osmotic diuresis
  • leading to shock and dehydration which causes more epinephrine to be released repeating the cycle
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13
Q

How do you test for DKA?

A

Accumulation of ketones in the urine

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14
Q

What is Hyperglycemic Hyperosmotic syndrome? What are the symptoms?

A
  • acute hyperglycemic crisis in T2DM resulting from a prolonged insulin deficiency
    • increased gluconeogenesis
    • decreased glucose uptake in peripheral tissue
  • Glucose >600
  • severe dehydration
  • Hyperosmolality → coma
  • Impaired renal fxn
  • NO ketones
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15
Q

Compare DKA and HHS.

  • anion gap acidosis
  • osmolality
  • hyperglycemia
  • ketonemia
A
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16
Q

what is Hemoglobin A1C, what is the use, and target?

A
  • glycosylated form of hemoglobin that takes a month to form
  • it measures long term diabetic control
  • target is <6.5-7.0
17
Q

What are the risks assoc. with chronic hyperglycemia?

A
  • stroke
  • MI (most common COD)
  • lower extremity gangrene (100x higher risk)
18
Q

Advanced glycatedd end products?

A
  • breakdown product of glucose
  • modify and crosslink proteins (makes it abnormal) as they accumulate and they can act on receptors in endothelial cells to create cellular dysfunction and damage
19
Q

What is the leading cause of ESRD in the US?

A

Diabetic nephropathy

20
Q

What are the three primary pathologic conditions seen in diabetic nephropathy?

A
  • Glomerular sclerosis:
    • thickening of basement membrane
    • disruption of protein cross links that make membrane effective filter → leak large molecules into urine
  • Renal vascular lesions:
    • arteriolosclerosis
  • Pyleonephritis
21
Q

What are the pathologic changes seen in diabetic nephropathy?

A
  • Nodular mesangial matrix accumulation in glomeruli called Kimmelstiel Wilson disease
  • Also grossly see diffuse nephrosclerisis due to the underlying microscopic changes
22
Q

How do you test for diabetic nephropathy

A

Urine albumin Creatinine ratio testing is the gold standard (UACR)

23
Q

Describe neovasculariztion seen with diabetic retinopathy?

A
  • Hypoxia leads to VEGF overexpression →
  • Hemorrhage →
  • Blindness
24
Q

Besides diabetic retinopathy what are other occular complications of diabetes?

A

Cataracts and glacuoma

25
Q

Commonalities between Pancreatic neuroendocrine tumors?

A
  • solid yellow tan
  • predilection for neck and tail
  • well differentiated neuroendocrine tumors
  • secretory granules
26
Q

Describe an insulinoma

  • involved cell
  • metastasis
  • clinical presentation
  • gross/histo
A
  • Beta cells
  • 10% mets
  • hypoglycemia
  • small tumors less than 2cm produces symptomatic hypoglycemia
  • amyloid is common on histo
27
Q

Gasstrinoma presentation and triad?

A
  • Islet cell tumor
  • Gastric acid hypersecretion
  • Peptic ulceration
    • DO NOT respond to therapy
28
Q

Somatostatinoma presentation?

A
  • Diabetes, cholelithiasis, steatorrhea
  • silences beta cells leading to reduced insulin
  • reduces gallbladder motility
  • reduces exocrine pancreatic secretions
  • metastatic at time of diagnosis usually because these are so hard to diagnose
29
Q

Glucagonoma presentation?

A
  • mild diabetes
  • characteristic rash → necrolytic migratiory erythema groin and LE
  • 4 D’s:
    • Diabetes, Dermatitis, Depression, DVT
30
Q

VIPoma?

A
  • Vasoactive intestinal peptide secreted by D1 cells
  • WDHA syndrome:
    • watery diarrhea
    • hypokalemia
    • achlorhydria
  • some patients have flushing
    • consider carcinoid syndrome in ddx

ENRP Exam II (9 decks)

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