Chapter 24- Endocrine Pancreas Flashcards Preview

Robbins Pathology- Endocrine (Chapter 24) > Chapter 24- Endocrine Pancreas > Flashcards

Flashcards in Chapter 24- Endocrine Pancreas Deck (60)
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1

What is the process of insulin release

1) GLUT2 take glucose into the cells
2) Glucose generates ATP
3) ATP inhibits the membrane potassium channels
4) Depolarization results in calcium influx
5) Calcium influx causes insulin release

2

What are the locations that Islets of Langerhans are located

Neck and tail of pancreas

3

What is the effect of insulin on the adipose tissue

Increased glucose uptake
Increased Lipogenesis

4

What is the effect of insulin on striated muscle

Increased glucose uptake
Increased glycogen synthesis
Increases protein synthesis

5

What is the effect of insulin on the liver

Increased glycogen synthesis
Increased lipgenesis
Decreased gluconeogensis

6

What is the serum marker that is indicative for endogenous insulin

C peptide, as it is only created which insulin is cleaved into its activated form.

*Can be used to differentiate synthetic and endogenous insulin

7

What causes the release of incretins

Oral glucose

8

What are the incretins

-Glucagon like peptide-1 (GLP-1)
-Glucose dependant insulin releasing polypeptide (GIP)

9

What is the mechanism of action for incretins

Stimulate insulin release and inhibit glucagon release, resulting in a lower blood sugar level

10

What is the role of dipeptidyl peptdidase 4 (DDP-4) on incretin levels

Inactivate incretins, so the blood glucose level will rise

11

What is the significance of DDP on potential diabetes treatment

By blocking DDP4, there will be less incretin breakdown. As a result, there will be more blood glucose uptake and a reduction in the serum blood levels

12

What is the major gene linking to T1D

MHC class 2 on chromosome 6p21

13

How much of the pancreas must be destroyed to see T1D symptoms

>90%

14

What are the major risk factors for T2D

-First degree relatives, so there is a familial aspect
-Obesity

15

What is are the characteristics of maturity onset diabetes of the young (MODY)

T2D like, but in the young:
-Increased blood insulin
-No Autoantibodies
-NOnketotic

16

What is the genetic link to MODY

Mutations resulting in the loss of function in glucokinase

17

When is the time to scan for gestation DM

-At the time of initial visit
-Second visit, at 24 to 28 weeks gestation.

18

What is the triad for diabetes

-Polyphagia (eating more)
-Polyuria (peeing more)
-Polydipsia (drinking more)

19

How is T2D usually identified on screening in children

-Fatigue or vision changes
-Increased thirst and urination
-Extreme hunger
-Weight loss
-Irritability of behavior changes
-Fruity smelling breath

20

What is the HLA typing for T1 or T2D

HLA DQ/DR on chromosome 6

21

What is a large deciding factor on T1 or T2DM

Presence of autobodies

22

How does the level of antibodies in T1D different between races

-Present in >90% of Caucasian children
-Present in < 50% of African American and Hispanic children

23

Diabetic ketoacidosios is more commonly seen in which form of diabetes

Type 1

24

What is the triad of diabetic ketoacidosis

-Hyperglycemia
-Ketonemia
-Metabolic acidosis

25

What are the common causes of diabetic ketoacidosis

-Noncompliance*** most common
-Precursor infections such as pneumonia and UTI

26

How to test for ketones

IN the urine

27

What are the usual clinical presenting signs from DKA

-Nausea/Vomiting
-Tachycardia
-Kussmaul respiration’s

28

What is Hyperglycemic hyperosmotic syndrome (HHS)

Acute hyperglycemic crisis in T2DM

29

What are the presenting features for HHS that differentiation for DKA

-Hyperglycemia (>600)
-Severe dehydration
-Hyperosmolaloty (can cause coma)
-Impaired renal function
-NO KETONESSS******

30

What is the most common cause of death in diabetics

Myocardial infarction