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Pathology > Diabetes Path > Flashcards

Diabetes Path Flashcards

1
Q

Essence of DM is?

A

Hyperglycemia

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2
Q

What can increased extracellular glucose turn into? Why is it bad?

A

Fructose, even more potent of a glycosylator than glucose

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3
Q

3 Major mechanisms of DM long term complications

A
  1. Formation of AGEs
  2. Activatior of protein kinase C
  3. Disturbance of polyol pathway
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4
Q

What are AGEs? What do they do?

A

AGEs are peptides with glucose irreversibly boud

They strongly crosslink collagen, trap albumin in BM and LDL in arteries

Also bind to RAGE on pro-inflammatory cells to make ROS and pro caogulative state

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5
Q

What does protein kinase C do?

A

Causes production of pro-fibrinogneic cytokines like TGF-B –> BM thickening and pro-angiogensis (neovascularization in retinopathy)

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6
Q

What happens when DM causes disturbance of polyol pathway

A

Glucose gets converted to sorbtiol by aldose reductase, then to fructose (using NADPH)

That NADPH can’t be used to reduce glutathionine which would catabolize ROS

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7
Q

Type I DM histopath of pancrease? Type II?

A

Type I: Insulitis with T lymphocytes

Type II: Amyloidosis of islets

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8
Q

What is seen here?

A

Type 1 DM:

Insulitis w/ T lymphocytes

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9
Q

What is seen here?

A

Type II DM:

Amyloidosis of islets

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10
Q

What is the end result of insulits in DM I? What is the end results of insulin resistance in type II?

A

Type 1: Destruction of the beta cells

Type II: Amyloidosis of islet

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11
Q

How does hyperglycemia impair innate immunity? Pathophys (4 mechanisms)?

A

Impaired neutrophil function by:

1) Adhesive factors upregulated (CD11b, I-CAM1), neutrophil exodues from blood vessels impair
2) Unactivated C3 binds S. aureus (won’t work)
3) Oxidative burst impaired: sorbitol takes away needed NADPH when being formed
4) Constituitive activation of NET formation (reduced IL-6 response)

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12
Q

What dos too much superoxide cause in DM? What does too little cause?

A

Too much: Major mechanism of diabetic triopathy

Too little: Mechanism of diabetic infections

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13
Q

What is resistin

A

Peptide hormone that renders cells resistant to insulin (inhibits neutrophil chemotaxis and oxidatve burts via pIP3 kindase pathways)

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14
Q

Where does DM lead to infections more often (4 in order of appearance)

A
  1. Skin
  2. Feet
  3. Lungs
  4. Urinary tract
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15
Q

What bugs infect pt’s w/ DM more commonly (4 in order)

A
  1. S aureus
  2. Pseudomonas aeruginosa
  3. Canida species
  4. Zygomycetes (Mucor, etc)
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16
Q

What is a faruncle? most common cause?

A

Acute, necrotizing infection of a hair follicle that breaks through DM into adjacent sub-q fat.

S. aureus is most common cause

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17
Q

What can Pseudomonas aeruginosa cause in DM? When should it be suspected?

A

Malignant otitis externa, usually involving adjacent mastoid with osteomyelitis in ear canal

Should be suspected w/ skin necrosis, very bad pain, fever, and facial paralysis

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18
Q

What is seen here? how do you treat?

A

Mucormycosis

Treat with Amphotericin and surgery

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19
Q

What is seen here? Features?

A

Large empty hyphae with rare, random angle branching and collapse (twisted ribbon)

Zygomycetes

20
Q

What is seen here? How does it occur in Diabetics

A

Renal papillary necrosis

Pyelonephritis + Ischemia in DM

21
Q

How can infection lead to gangrene in diabetics

A

Infection combines with ischemia and neuropathy

22
Q

4 thigns involved in metabolic syndrome

A

DM, HTN, Dyslipidemia, Abdominal obesity

23
Q

Who gets metabolic syndrome

A
  1. Native Americans
  2. Hispanics
  3. African Americans
  4. Whites

Odds increase with age

24
Q

What levels are elevated in metabolic syndrome? what meds can lead to it? best treatment?

A

C-reactive protein, IL-6, and plasminogen activator inhibitor-1

Antipsycotic medications (Clozapine)

Best treatment is diect and exercise

25
Q

Two major forms of diabetic neuropathy in patients

A
  1. Peripheral: all will eventually get but 50% subclinical
  2. Autonomic: not universal and common asymptomatic
26
Q

Pathogenesis of diabetic neuropathy

A

Polylol pathway gets activated, which leads to increased oxidative stress and injury to schwann cells –> Nerves get demyelinated

Sorbitol and fructose builds up, activates protein kinase C and AGEs build up

27
Q

What is seen here?

A

Segmental demyelination

Earliest histopathologic change in diabetic neuropathy

28
Q

What is seen in peripheral neuropathy

A

distal symmetric polyneuropathy manifested first by loss of vibratory sensation and proprioception

29
Q

What is seen in autonomic neuropathy

A

Resting tachycardia

Exercise intolerance

GI dysmotility

Silent myocadial ischemia

Increased mortality (30% over 5 years)

30
Q

2 forms of diabetic retinopathy

A

Background and Proliferative

31
Q

What is background diabetic retinopathy

A

Capillary thickening, microaneurysms, venous dilations,edma

Soft exudates (cotton wool spots = microinfarcts)

Hard exudates (precipitates of plasma proteins and lipids)

32
Q

3 majors types of diabetic nephropathy

A

Glomerular

Papillary

Tubulointerstitial

33
Q

Most common type of diabetic nephropathy

A

Diffuse diabetic glomerular nephropathy

Capillary basement mebrane thickening and increased mesangial matrix

34
Q

What is seen here?

A

Diffuse diabetic glomerular nephropathy

(mesangial thickening in purple)

35
Q

Two main features of nodular type diabetic nephropathy

A

Kimmelstiel Wilson nodules and hyaline sclerosis of afferent and efferent arterioles

*KW nodules eventuall squeeze capillaries shut

36
Q

What is seen here?

A

Hyaline sclerosis of arteriole and small nodular lesions

(Nodular type)

37
Q

What is seen here?

A

Large nodule KW lesion and small capsular drop (arrow)

38
Q

2 types of exudative lesions seen in diabetic glomeruloar nephropathy? What do they correlate with?

A

Capsular drops and Fibrin caps

Do not correlate with renal failure (nodular lesions do)

39
Q

Three most comon causes of death due to diabetes

A

CV disease (70%)

Renal failure (10%)

Infection (5%)

40
Q

When do long term complications of DM occur? What helps prevent? What is a shortfall of that?

A

15-20 years after onset of sustained hyperglycemia.

Tight glucose control can help but that can lead to episodes of hypoglycemia

41
Q

What is seen here?

A

S. aureus sub-q abscess showing aggregates of bacteria coated with protein and neutrophils

42
Q

how does DM accelerate atherosclerosis

A

Trapping LDL in arterial tunica intima

43
Q

With rhinocerebral zygomycosis, what might the only facial finding be? what do you need to do?

A

Edema

You need to look inside the mouth

44
Q

A 30 year old female with DM has adbominal pain, bloating, fullness, and nausea. What is this due to? What is it?

A

Glucose metabolized to sorbitol

Diabetic gastroparesis: failure of gastric empyting due to autonomic neuropathy

45
Q

First step of diabetic neuropathy pathogenesis

A

Activation of polylol pathway metabolizing glucose to sorbitol by aldose reductase

Pathology (10 decks)

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