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ENRP - Exam 2 > Endocrine Pancreas/DM > Flashcards

Endocrine Pancreas/DM Flashcards

1
Q

Where are a majority of the Pancreatic Endocrine Islets of Langerhans?

A

Neck

Tail

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2
Q

Alpha cells release?

A

Glucagon

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3
Q

Beta cells release?

A

Insulin

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4
Q

Delta cells release?

A

Somatostatin

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5
Q

PP cells release?

A

Pancreatic Polypeptide

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6
Q

D1 cells release?

A

VIP

vasoactive intestinal polypeptide

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7
Q

If there is low glucose, describe what occurs?

A
  • Alpha cells release Glucagon to the liver

- Liver breaks down glycogen to release Glucose

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8
Q

If there is high glucose, describe what occurs?

A
  • Beta cells release Insulin

- Liver and Peripheral tissues uptake the glucose which lowers blood levels

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9
Q

Describe how insulin is released from beta cells in response to glucose elevation

A
  • Glucose enters beta cell through GLUT-2
  • Glucose is metabolized to form ATP
  • ATP blocks channel that allows K+ out of the cell so it accumulates
  • Cell Depolarization
  • Calcium enters the cell
  • Insulin leaves the cell
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10
Q

Describe how insulin is released from the beta cell in response to glucose elevation

A
  • Glucose enters beta cell through GLUT-2
  • Glucose is metabolized to form ATP
  • ATP blocks channel that allows K+ out of the cell so it accumulates
  • Cell Depolarization
  • Calcium enters the cell
  • Insulin leaves the cell
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11
Q

How is insulin formed?

A

Proinsulin is cleaved into:

  1. Insulin
  2. C-peptide
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12
Q

What is C-peptide used for?

A

Marker of ENDOGENOUS insulin

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13
Q

Insulin lowers blood sugar, but what are its main effects on peripheral tissues?

A
  • Increase glucose uptake into cells for energy
  • Protein/Glycogen synthesis
  • Lipogenesis
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14
Q

Oral glucose causes the release of?

A

Incretins

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15
Q

What are 2 Incretins and what causes them to be released/activated?

A

GLP-1
GIP
– Oral glucose causes their activation/release

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16
Q

What is the job of Incretins? (GLP-1, GIP)

A

Stimulate insulin release and (-) Glucagon release

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17
Q

What can (-) the release of Incretins?

A

DPP-4

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18
Q

If DPP-4 (-) the release of Incretins, what then occurs?

A

(-) release of insulin and (+) release of glucagon => glucose elevation
– INCRETINS DO THE OPPOSITE

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19
Q

Diabetes Mellitus is impaired glucose homeostasis. What in general, is it due to?

A

Defective Insulin secretion

Defective Insulin effect (resistance)

20
Q

What are the levels of A1C, FPG, OGTT and RPG tests that diagnose Diabetes?

A

A1C: > 6.5%
FPG: > 126
OGTT and RPG: > 200

21
Q

What causes Type 1 DM?

A

Autoimmune disease due to failure of T Lymphocyte self tolerance
–> T cells attack antigens on Beta cells!

22
Q

Once over ____ of beta cells are destroyed with Type 1 DM, there will be symptoms.

A

> 90%

23
Q

When does Type 1 DM usually onset and what genetic link does it have?

A 
Onset: childhood/adolescence
Genetic link: MHC class II genes (HLA-DR/DQ on chr. 6)
24
Q

What marker will be (+) with Type 1 DM?

A

Islet Autoantibodies

25
Q

What will be seen on histo with Type 1 DM? (3)

A

Insulitis:

  • T cells and Macrophages infiltrate
  • Low level of beta cells
  • Islet Atrophy
26
Q

If you have Insulitis, with t cells and macrophages infiltrating the pancreas and islet atrophy, what type of DM do you have?

A

Type 1

27
Q

Describe the stages of Type 1 DM

A

Stage 1 = autoantibodies are formed
Stage 2 = Beta cells are being attacked, there is dysglycemia present
Stage 3 = SYMPTOMS

28
Q

What is the triad of symptoms seen in a child with Type 1 DM?

A

Polyphagia but thin
Polydipsia
Polyuria

29
Q

What is the triad of symptoms seen in a child with Type 1 DM?

A

Polyphagia but thin because glucose cannot enter cells
Polydipsia
Polyuria

30
Q

What causes Type 2 DM? (2)

A

Insulin resistance in peripheral tissues

Beta cell Dysfunction

31
Q

When does Type 2 DM usually onset and what is a major risk factor?

A

Onset: adulthood
Risk: OBESITY

32
Q

What will be seen on histo with Type 2 DM?

A

Amyloid

– mild decrease in beta cells too

33
Q

How does obesity lead to the pathogenesis of Type 2 DM?

A
  • Elevated Adipokines, FFA and inflammation

- These molecules disrupt signals that enable insulin uptake and cause beta cell dysfunction/damage

34
Q

Once Adipokines, FFA, and inflammation disrupt signals that enable insulin uptake to occur, insulin resistance occurs. Describe what occurs with the beta cells

A

First: Compensate by secreting more insulin
Later: beta cells fail completely and stop secreting insulin

35
Q

Type 2 DM will manifest symptoms when what occurs?

A

Beta cell Dysfunction/Failure

36
Q

What are some general symptoms of Type 2 DM?

A

Fatigue

Vision changes

37
Q

MODY

A

Mature onset of Diabetes in the Young

38
Q

What is MODY?

A

Resembles Type 2 DM but occurs in the YOUTH

39
Q

What usually causes MODY?

A

Loss of function mutations in Glucokinase that is responsible for creating ATP from glucose in beta cells

40
Q

3 signs of MODY?

A
  • Increased blood insulin
  • NO autoantibodies
  • NO ketones
41
Q

3 signs of MODY?

A
  • Increased blood insulin
  • NO autoantibodies
  • NO ketones
42
Q

What is mom at risk for with Gestational DM?

A

C-section

43
Q

What are 3 things that a baby is at risk for with Gestational DM?

A
  • Neonatal Hypoglycemia
  • Congenital malformations
  • Macrosomia
44
Q

If a neonate has hypoglycemia, what did the mother likely have and what is the baby at risk for?

A
  • Mother had Gestational DM

- -> SEIZURE

45
Q

If you see amyloid deposition in the islets, what type of DM should you think it is?

A

Type 2

ENRP - Exam 2 (21 decks)

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