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Endocrine M2T2 > 13. Pathology of Diabetes > Flashcards

13. Pathology of Diabetes Flashcards

1
Q

Where does gluconeogenesis (GNG) occur in the body?

A

Liver

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2
Q

Pro-insulin is cleaved into which two things?

A

Insulin and C-peptide

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3
Q

How do you tell if someone was given exogenous insulin or if it were endogenous?

A

Exogenous wouldn’t have C peptide levels because it is secreted together with insulin

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4
Q

What are the three lab tests for glucose. Note special characteristic mentioned for each lab test

A

Urine glucose - colorimetric indicators
Finger stick glucose - gives instantaneous glucose levels
Serum glucose - best checked during fasting state

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5
Q

How do we identify glucose in a post-mortem state?

A

Measure in vitreous humor of eye, does degrade though.
Normal values tell you nothing
Very high values tell you patient might have been hyperglycemic

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6
Q

How are glycated proteins formed, and what is an example of one that is used in labs?

A

Glucose attaches to circulating proteins. Initially is reversible; becomes irreversible with long-lasting hyperglycemia

HbA1C = measures glucose levels for past three months

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7
Q

Type 1 diabetes pathogenesis

A

Autoimmune destruction of pancreatic beta cells (they secrete insulin) –> severe lack of insulin
Destruction begins years before symptoms arise at which point 90% of beta cells have been destroyed
CD 4 T cells activate macrophaghes
CD 8 T cells directly kill beta cells

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8
Q

In Type 1 DM, beta cell destruction causes what? Describe it

A

Insulinitis
Autoantibodies against target islet cells, insulin, beta cell antigens i.e. GAD (glutamine acd decarboxylase)
Cytokines IFN, TNF, IL-1 –> apoptosis
See significant infiltration of T lymphocytes

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9
Q

Amyloid depositions are more common in which type of DM? Where do they occur? Congo red stain shows what?

A

Type 2 DM. In and around capillaries and between cells

Green birefringence

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10
Q

Differentiate Type I and Type II DM

A

Type I = autoimmune, insulinitis, marked atrophy and fibrosis, beta cell depletion, and HLA gene linkage
Type 2 = amyloid deposition

Also, Type I usually discovered in younger people; Type 2 is older but now is becoming more prevalent in younger populations as well

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11
Q

Macrovascular disease caused by DM involve which arteries and lead to what?

A

Large and medium sized arteries

Atherosclerosis, MI, strokes, gangrene of lower extremities

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12
Q

Microvascular disease caused by DM involves which structures and lead to what?

A

May effect retina, kidney, peripheral nerves

Numbness in extremities –> foot care is especially important in DM patients

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13
Q

What are the three metabolic pathways that are altered in DM?

A

AGE, activation of PKC pathway (production of DAG), disturbance in polyol pathways

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14
Q

AGE pathway involvement in DM

A

AGE formed from reaction between intracellular glucose and proteins (either intracellular or extracellular)
Results in cross linking –> abnormal matrix-cell or matrix-matrix interactions

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15
Q

Cross-linking AGE to collage type I

A

Decreases elastin and contributes to endothelial cell injury

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16
Q

Cross-linking AGE to collagen type IV

A

Occurs in BM and increases fluid filtration –> fluid leakage

17
Q

AGE cross linked proteins are resistant to _________

A

proteolytic degradation –> increased protein deposition

18
Q

Cross-linking AGE effect on LDL

A

AGE modified matrix components trap LDL –> contribute to atherosclerosis
Diabetic should have less LDL (normal person diet not healthy for diabetic)

19
Q

Cross-linking AGE and albumin interaction

A

Albumin may bind to glycated BM causing thickening of the BM –> microangiopathy

20
Q

Cross-linking AGE has six effects

A
  1. abnormal cell-matrix, matrix-matrix interactions
  2. Collagen type I –> Dec elastin, endothelial injury
  3. Collage type IV –> Bind BM, increase fluid leakage
  4. Resistant to proteolytic degradation
  5. LDL trapped, atherosclerosis
  6. Albumin binds to glycated BM –> thickening of BM –> microangiopathy
21
Q

Effects of circulating plasma proteins modified by AGEs

A

Protein with AGE bind to AGE-R –> generate cytokines, growth factors, and pro-inflammatory molecules
Increased synth of ECM, endo permeability, inc ro-coagulant activity

Narrowed blood vesssels (MI, stroke, gangrene chances)

22
Q

Polyol pathway disturbance in DM

A

Polyol pathway uses NADPH to produce fructos from glucose –> dec glutathione (antioxidant) –> susceptible to ROS damage

23
Q

Microscopic changes in DM

A

Dec in number and size of islets
T cell infiltration (esp in DM1)
Beta cell degranulation (depletion of stored insulin)
Amyloid deposition esp in DM2 in and around blood vessels

24
Q

What is the most common cause of death in DM

A

MI from atherosclerosis

25
Q

T2DM can cause gangrene of lower extremities and hyaline arteriolosclerosis. What is hyaline arteriolsclerosis

A

amorphous hyaline thickening of walls of arterioles -> narrowing of lumen of arterioles

26
Q

Large vessels narrow because of _____, small vessels narrow because of ____

A

large vessels –> atherosclerosis

Sm vessels narrow because of hyaline arteriolosclerosis

27
Q

Diabetic glomerulosclerosis microangiopathy

A

Arterioles injured, resulting in hyalinizing arteriolar sclerosis

Microangiopathy caused by insulin defect and hyperglycemia leading to deposition of collage 4 and fibronectin; AGE; glomerular hypertrophy due to HTN

28
Q

Morphology (microscopic) of diabetic glomerulosclerosis

A 
Cap basement membrane thickening
Diffuse mesangial sclerosis
Kimmelsiel-Wilson nodules
Oval nodules of matrix in glom 
Nodules compress caps
29
Q

Gross features of diabetic glomerulosclerosis

A

Thin cortex
Thick BM
Severe hyaline arteriolosclerosis (hyaline depsoition narrows the vessel lumen)
Diffuse inc in mesangial matrix, cellular nodules

30
Q

Clinical course of Diabetic glomerulosclerosis

A

Initial inc GFR and microalbuminuria
Proteinuria –> nephrotic
Progessive loss of GFR

31
Q

Pyelonphritis

A 
More common in diabetics
Necrotizing papillitis (coagulative necrosis of renal papilla) as a result of pyelo
32
Q

Four kinds of diabetic neuropathy

A

Distal sensory neuropathy - axonal neuropathy, demyelination
Autonomic neuropathy - gastroparesisdifficulty emptyingbladder
Focal or multifocal assymetric neuopathy - vascular insufficiency to peripheral nerves

33
Q

Diabetic retinopathy changes

A

VEGF mediated neovascularization

BM thickening of ciliary body

34
Q

Preproliferative retinopathy

A

BM of retinal BV are thickened (microaneurysms possible)
Macular edema
Retinal microcirculation is hyperpermeable and may also have microoculsion

35
Q

Proliferative retinopathy

A

formation of new vessels from existing vessels
massive hemorrhage can occur
membrane can wrinkle the retina, distorting vision

Endocrine M2T2 (16 decks)

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