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Endo > DM Complications (Nichols) > Flashcards

DM Complications (Nichols) Flashcards

1
Q

Glycosylation favors what structures

A

basmement membranes

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2
Q

What does the sorbitol pathway do? Significance with DM (2 things)?

A

Sorbitol pathway converts glc → sorbitol → fructose

  1. it is inc in DM and fructose, the product is a more potent glycosylator than glc
  2. mediated by aldose reductase, using NADPH
    NADPH is needed by glutathione to catabolize/breakdown ROS → more ROS is around → oxidative stress
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3
Q

What are the 3 major mechanisms for long-term complications of DM?

A
  1. formation of AGEs
  2. activation of PKC
  3. ↑sorbitol pathway
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4
Q

3 major effects of ↑AGEs that contribute to long term complications of DM

A
  1. trap LDL in arterial artheromas
  2. bind cell surface receptors (RAGE) → ROS
  3. causes things to age faster: each year of insulin-dept DM adds 1 year to the persons physiologic age
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5
Q

How does activation of PKC contribute to long term complications of DM

A

pro-fibrinogenic and angiogenic cytokines released:

  • TGF-beta → BM thickening
  • VEGF → neovascularization in retinopathy
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6
Q

insulitis with T lymphocytes (in islets

A

T1DM

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7
Q

_______ increases susceptibly to infections

A

hyperglycemia

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8
Q

Ways that hyperglycemia inc susceptibly to infections (2(.5) reasons)?

A

Microbes “RAN –> away from C3(PO)”
Ros, Adhesion Molecules, Nets –> C3

  1. Upregulates CD11b on neutrophils and ICAM-1, VCAM-1, and E-selectin on endothelial cells → neutrophils cannot get to site of infection
  2. impairs phagocyte killing by oxidative burst bc hexokinase pathway is saturated so more glc enters sorbitol pathway → Decreased NADPH → decreased production of superoxide in phagosomes
  3. constitutive NET formation → decreased response to subsequent pathogens
  4. is specific to S. aureus?? causes binding of UN-activated C3 to S. aureus → C3 cannot become activated (form C3b/iC3b) on bacterial surface → decreased phagocytosis
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9
Q

Destruction of beta cells by lymphocytes → insulin DEFICIENT

A

T1DM

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10
Q

too much superoxide is mech of …

A

diabetic triopathy

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11
Q

too little superoxide is a mech of …

A

diabetic infections

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12
Q

peptide hormone made in monocytes that

(1) renders cells resistant to insulin
(2) inhibits neutrophil chemotaxis
(3) decreases oxidative burst via phosphatidyl-inostiol-3-kinase pathway

A

resistin

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13
Q

amyloidosis of islets

A

T2DM

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14
Q

normally mediated by IL-6

A

constitutive NET formation

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15
Q

Where in the body are infections in DM most likely?

A 
DM pts get --> Sick w/the FLU
Skin
Feet
Lungs
Urinary tract
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16
Q

What does resistin do?

A

(1) renders cells resistant to insulin
(2) inhibits neutrophil chemotaxis
(3) decreases oxidative burst via phosphatidyl-inostiol-3-kinase pathway

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17
Q

Insulin RESISTANCE is characteristic

A

T2DM

**but the amyloidosis renders them somewhat deficient too

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18
Q

What are the most likely organisms for diabetic pts to be infected with?

A

Sick Patients Cause Messes

S. aureus
Pseudomonas aeruginosa
Candida
Zygomycetes/Mucormycosis

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19
Q

skin abscess from acute necrotizing infection of hair follicle

A

furuncle

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20
Q

how deep is a furuncle?

A

down to subcut

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21
Q

most common but to cause furuncles

A

S. aureus

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22
Q

Treatment of furuncle

A

Drained!! warm compress to aid spontaneous drainage or use a needle

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23
Q

coalescence of multiple furuncles that creates a subcut complex of abscesses

A

Carbuncle

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24
Q

other than their size and #of follicles involved, what diff a carbuncle from a furuncle

A

carbuncles can cause systemic symptoms like fever

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25
Q
  • Facial paralysis, vertigo
  • Pain is disproportionate
  • Temp >102.2/39
A

malignant external otitis

+ other signs, like necrosis of skin in ear canal or meningeal signs

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26
Q

What is infected in malignant external otitis?

A

Osteomyelitis of ear canal (and often adjacent mastoid)

necrosis of skin in ear canal

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27
Q

What bug commonly causes malignant external otitis?

A

Pseudomonas aeruginosa

28
Q

Need incision for drainage malignant external otitis

A

carbuncle

29
Q

Large empty hyphae that looks like a twisted ribbon on microscope

A

Murcomycosis/zygomycosis

30
Q

has rhinocerebral form

A

Murcomycosis/zygomycosis

31
Q

Common consequence of UTI that is untreated in diabetic pt

A

UTI → pyelonephritis + ischemia related to diabetes → renal papillary necrosis

32
Q

pattern of progression for rhinocerebral of Murcomycosis/zygomycosis

A

starts in the nose → paranasal sinuses → orbit → skull base → brain

33
Q

necrosis of skin in ear canal = you should suspect

A

malignant external otitis

34
Q

Why are foot ulcerations and gangrene more common in diabetic pts?

A

infection + ischemia + neuropathy

35
Q

Fournier’s gangrene

A

massive necrosis in perinuem

36
Q

Metabolic syndrome =

A

DM + HTN + Dyslipidemia + Abdominal obesity

37
Q

Metabolic syndrome “speeds pts toward death from ______”

A

heart disease

38
Q

Rank races in order of highest to lowest prevalence of metabolic syndrome

A

Native Americans > Hispanics > African Americans > European Americans

39
Q

Pts with metabolic syndrome are in a _______ states. Evident by what labs?

A

pro-thrombotic and pro-inflammatory

elevated CRP, IL-6, and PAI-1

40
Q

Metabolic syndrome is assc with the use of what drugs?

A

clozapine and atypical anti-phycotics

41
Q

5 major risk factors for artherlosclerosis

A

SHODDY: smoking, HTN, obesity, DM, dyslipidemia

42
Q

T or F: metabolic syndrome responde to diet and exercise

A

T:

  • Mediterranean, DASH diet, diet of foods with a lower glycemic index
  • Exercise might be most beneficial when it removes abdominal fat
43
Q

What determines the onset of diabetic neuropathy

A

duration and severity of hyperglycemia

44
Q

What are the 2 forms of diabetic neuropathy

A

peripheral and autonomic

45
Q

Pathogenesis of diabetic neuropathy

A

hyperglycemia …
→ increased sorbitol pathway → inc oxidative stress → injury to schwann cells → DEMYELINATION
→ accumulation of sorbitol and fructose → activation of PKC → Nerve damage
→ accumulation of AGEs → nerve damage

46
Q

earliest histo change seen with diabetic neuropathy

A

segmental demyelination

47
Q

Peripherial diabetic neuropathy presents as
(proximal, distal)
(symmetric, asymmetric)
(mono, poly neuropathy)

A

distal, symmetric, poly

48
Q

Describe the presentation of diabetic neuropathy

A

ascends from feet
can have pain (early) or weakness
PRIMARILY SENSORY LOSS
-vibratory sensation, proprioception, impaired pain, temp, and touch perception

49
Q

Describe the presentation of autonomic neuropathy

A
  • Resting tachycardia, exercise intolerance
  • GI dysmotility (constipation or diarrhea)
  • Impotence
  • Orthostatic hypotension

OH, Tits Get Increased (but he cant get hard if he has autonomic neuropathy)

50
Q

Type of microangiopathy

A

diabetic retinopathy

51
Q

2 forms of diabetic retinopathy and how are they distinct/defining characteristic

A

background: cotton wool spots from micro infarcts, also see edema, hemorrhages, microaneurysms, and capillary thickening
proliferative: neovascularization and fibrosis

52
Q

2 types of diabetic glomerulopathy

A

diffuse = global (early and less severe)

nodular (later and severe)

53
Q

3 patterns of diabetic nephropathy

A

glomerular
papillary
tubulo-interstitial

54
Q

Identical to the glomerulopathy seen with HTN and aging

A

diffuse diabetic glomerulopathy

55
Q

Eventually requires dialysis

A

nodular diabetic glomerulopathy

56
Q

What are Kinnelstiel Wilson nodules? Where are they deposited?

A

Oval/spherical depostis of mucopolysaccharides, lipids, and fibrillary proteins within the MESANGIUM

57
Q

What are the 2 types of exudative lesions? how are they differentated?

A

both made of plasma protiens!!!!

fibrin caps: crescentric deposits between epithelial cell and BM

capsular drops: round deposits in the parietal layer of Bowman’s capsule

58
Q

crescentric deposits of condensed leaked plasma proteins

A

fibrin caps

59
Q

Oval/spherical depostis of mucopolysaccharides, lipids, and fibrillary proteins within the MESANGIUM

A

Kinnelstiel Wilson nodules

60
Q

diffuse fine granularity of cortical surface

A

end stage diabetic nephropathy

= HTN nephropathy

61
Q

Capillary BM thickening and increased mesangial matrix

A

diffuse diabetic glomerulopathy

62
Q

deposits of plasma protein and BM (in the parietal layer of Bowman’s capsule)

A

capsular drops

63
Q

does the presence of fibrin caps and capsular drops correlate to the development of renal failur

A

no

64
Q

globally sclerotic glomeruli

A

end stage diabetic nephropathy

65
Q

ranks the most common cause of death in DM pts

A

atherosclerosis > renal failure > infection

66
Q

when do the long-term consequences of DM appear?

A

15-20 yrs after onset of sustained hyperglycemia

67
Q

What can delay the onset and decrease the severity of these complications?

A

tight control of blood glc

Endo (28 decks)

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