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Endocrine- MHD > Endocrine Pancreas > Flashcards

Endocrine Pancreas Flashcards

1
Q

What is the #1 cause of new cases of blindness in the US?

A

Diabetes

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2
Q

What is the #1 cause of kidney failure?

A

Diabetes

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3
Q

Random glucose test above what level indicates diabetes?

A

> 200 mg/dL

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4
Q

Fasting glucose levels above what indicates diabetes?

A

> 126 mg/dL

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5
Q

How is an abnormal glucose tolerance test performed?

A

Someone is given a carbohydrate load (75gm glucose dissolved in water) and their blood sugar is tested 2 hours later. If blood glucose >200 mg/dL , they are positive for diabetes

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6
Q

Hbg A1C above what level is considered diabetic?

A

> 6.5%

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7
Q

Which tests for diabetes must be confirmed by a repeat test before a diagnosis can be made?

A

Fasting blood glucose, abnormal glucose tolerance test, and Hbg A1C

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8
Q

What is the pathogenesis of DM type I?

A

Autoimmune destruction of pancreatic beta cells leads to an insulin deficiency

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9
Q

There is linkage of DM type I to which HLA haplotypes?

A

HLA- DR3 and HLA-DR4

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10
Q

What is the mechanism of autoimmune destruction of the pancreatic beta cells?

A

Lack of self-tolerance –> direct attack by T-cells

There is also Th1 cell injury by cytokines, and antibodies directed against islet cell antigens

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11
Q

Name 3 islet cell antigens

A

Insulin
Beta-cell glutamic acid decarboxylase (GAD)
Islet cell autoantigen 512

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12
Q

Why is it important to differentiate type 1 from type II diabetics?

A

Type I MUST be treated with insulin

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13
Q

What causes DM type 2?

A

Insulin resistance

There is also a relative insulin secretion deficiency –> absolute deficiency at later stages

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14
Q

What is the prevalence of type 1 vs type 2 diabetes

A

Type 1: 5-10%

Type 2: 90-95%

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15
Q

Describe the genetic predisposition for DM type II?

A

Not clearly defined

There are known polymorphisms in genes associated with insulin secretion

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16
Q

Name two adipokines responsible for keeping tissues sensitive to insulin

A

Leptin

Adiponectin

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17
Q

What is the affect of obesity on adipokines?

A

Adipokine production is lowered in obese patients

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18
Q

Obesity leads to the increase in FFAs. How do FFAs contribute to the pathogenesis of diabetes?

A

Increase in FFAs overwhelm the intracellular fatty oxidation pathways –> build up of toxic intermediates that attenuate the signaling of the insulin receptor pathway

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19
Q

An increase in what two factors can cause inflammation (in the pathogenesis of diabetes)?

A

Increased FFAs and glucose leads to the secretion of pro-inflammatory cytokines

They act at the major sites of insulin action

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20
Q

What is the protein that is deposited as amyloid in the islets of a diabetic person?

A

Amylin

21
Q

What is the life-threatening state seen in Type I diabetics vs Type II diabetics?

A

Type I: DKA

Type II: Nonketotic hyperosmolar Coma

22
Q

Describe the pathogenesis of Nonketotic hyperosmolar comas

A

Extreme hyperglycemia (>600) –> Serum hyperosmolality and dehydration, –> somnolence, coma, seizure

Old people with decreased thirst mechanisms, poor access to water, in nursing homes etc are at risk

23
Q

What are the three macrovascular diseases that arise as a complication of long term diabetes?

A

MI
Stroke
LE ischemia

24
Q

What are the three microvascular diseases that arise as a complication of long term diabetes?

A

Retinopathy
Nephropathy
Neuropathy

25
Q

What is glycation?

A

Nonenzymatic glycosylation of proteins

Glucose covalently attaches to multiple intra and extracellular proteins. This process of glycation is proportional to the severity of the hyperglycemia

26
Q

What is an advanced glycosylation end product (AGEs)?”

A

Over-time, the labile glycation products undergo complex chemical rearrangements that form stable AGEs.

The formation of AGEs permanently alters the protein structure/function

27
Q

What are Schiff bases?

A

The intermediate labile NEG’d proteins

28
Q

What are the cellular consequences of AGE formation?

A 
Deposition of extracellular matrix
Increased vascular stiffness
Increased vascular permeability
Trapping of LDL and foam cell formation
Endothelial dysfunction
29
Q

What is the more large scale results of AGEs formation/

A

Thickening of basement membranes
Microangiopathy
Large vessel injury –> athersclerosis

30
Q

Describe the glycation of Hb

A

Glucose freely enters RBCs

Glycation of Hb is irreversible

31
Q

How does diabetes lead to the activation of Protein Kinase C?

A

Intracellular hyperglycemia

32
Q

How is VEGF affected by PK C?

A

Increased production of VEGF –> angiogenesis

33
Q

How does activation of PK C affect endothelial NO synthase?

A

Decreased –> increased vasoconstriction

34
Q

How is TGF beta affected by activated PK C?

A

Increased –> increased deposition of extracellular matrix and basement membrane material

35
Q

Protein Kinase C can induce PAI-I. What are the effects?

A

Plasminogen activator inhibitor- 1 reduces fibrinolysis increases the risk of vascular occlusion events

36
Q

Overall, what are the effects of activation of protein kinase C?

A

Changes in retinal and renal blood flow –> retinopathy and nephropathy

Promotes hypertension and atherogenesis

37
Q

What’s the trouble with NADPH and diabetes?

A

Excess glucose is metabolized to sorbitol using NADPH as a cofactor. This can deplete the NADPH levels needed for the regeneration of glutathione (and leads to oxidative damage)

38
Q

Which three tissue types do not require insulin for the uptake of glucose?

A

Nerves
lenses
blood vessels

39
Q

What is the cellular mechanism behind peripheral neuropathy seen in DM?

A

Intracellular oxidative stress (following free flow of glucose into the cells)

40
Q

What is the cause of ocular lens swelling in DM?

A

Increased sorbitol is thought to create an osmotic gradient that leads to swelling

41
Q

Describe preproliferative angiogenesis in the retina

A

Hypoxia –> increased production of VEGF and retinal angiogenesis

These are poorly constructed/leaky and can lead to blood in the retina

42
Q

Describe proliferative retinopathy

A

Retinopathy caused by new vessel formation on the disc, retina and elsewhere –> hemorrhage and vitreous detachment

43
Q

Name two ocular complications of diabetes

A

Cataracts

Glaucoma

44
Q

How can diabetes cause glomerular hyperfiltration?

A

Dilation of the afferents –> hyperfiltration

45
Q

What complication of diabetes is prevented by ranibizumab?

A

Diabetic retinopathy (it is a VEGF inhibitor)

46
Q

What is the risk to the fetus in a mother with preconception diabetes?

A

Low birth weight, congenital malformations

47
Q

What is the risk to a fetus if the mother develops hyperglycemia during pregnancy?

A

High birth weight, obesity, DM later in life

48
Q

Are insulinomas benign or malignant?

A

90% benign

49
Q

How do people with insulinomas present?

A

Signs of hypoglycemia
Glucose <50
high insulin (and high insulin:glucose ratio)

Endocrine- MHD (17 decks)

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