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Endocrinology > Pathology-Nichols > Flashcards

Pathology-Nichols Flashcards

1
Q

What is the essence of diabetes mellitus?

A

hyperglycemia

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2
Q

What does hyperglycemia cause?

A

Excess glucose stick to everything (glycosylation), especially basement membranes

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3
Q

What does excess intracellular glucose go?

A

Goes down sorbitol pathway to fructose, even more potent glycosylator than glucose

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4
Q

Long-Term Complications of Diabetes Mellitus?

ONE

A

1) advanced glycation end products (AGEs), peptides w/glucose irreversibly stuck on them, which strongly cross-link w/collagen, trap albumin in BM and LDL in arterial atheromas, and bind to proinflammatory cell surface receptors (AGE to RAGE)
- causes endothelial generation of injurious ROS such as superoxide, along with pro-coagulant state and a pro-fibrogenic state

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5
Q

Long-Term Complications of Diabetes Mellitus?

TWO

A

2) activation of protein kinase C
- causes production of pro-fibrogenic cytokines (TGF-beta)
- this causes BM thickening & pro-angiogenic cytokines like VEGF (causes neovascularization in retinopathy)

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6
Q

Long-Term Complications of Diabetes Mellitus?

THREE

A

3) disturbance of polyol pathway, with glucose converted to sorbitol (a polylol) by aldose reductase
- fructose, using NADPH as cofactor, diverting it from reducing glutathione, needed to catabolize ROS, causing injury by ROS (oxidative stress)

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7
Q

Type I diabetes mellitus micrograph?

A

-insulitis with T lymphocytes

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8
Q

Type II diabetes micrograph?

A

-amyloidosis of islets

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9
Q

What is the end result of insulitis in Type I diabetes?

A
  • destruction of beta cells

- patients now dependent on exogenous insulin

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10
Q

End result of Type II diabetes?

A
  • insulin resistance, not deficiency

- the amyloidosis of islets renders some patients dependent of exogenous insulin

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11
Q

Common pathway of Type I & II diabetes?

A

sustained hyperglycemia

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12
Q

What does hyperglycemia do?

A
  • impair innate immunity to infection (acquired immunity)
  • upregulates CD11b on neutrophils along with ICAM-1, VCAM-1, & E-selectin on endothelial cells, creating an “adhesive phenotype” impairing neutrophil exodus from blood vessels to sites of infection.
  • causes binding of unactivated C3 complement to Staph. aureus inhibiting activation to functionally active forms (C3b/iC3b) on the bacterial surface, associated with decreased C5a generation & decreased phagocytosis
  • inpairs bacterial killing by oxidative burst, saturates the hexokinase pathway resulting in formation of sorbitol via aldose reductase, high sorbitol decreases NADPH which leads to reduced production of superoxide in phagosomes when & where it is needed for killing bacteria
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13
Q

To much superoxide (& ROS) is a mechanism of?

A

diabetic triopathy

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14
Q

To little superoxide (& ROS) is a mechanism of?

A

diabetic infections

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15
Q

Resistin

A
  • a peptide hormone named for its ability to render cells resistant to insulin
  • produced by monocytes & present at high levels in diabetics
  • inhibits neutrophil chemotaxis & oxidative burst via phosphatidyl-inositol-3-kinase pathways
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16
Q

Activation of neutrophil extracellular trap (NET) formation caused by and causes??

A

Caused by: hyperglycemia

Causes: reduced response to subsequent pathogens normally mediated by IL-6

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17
Q

Malfunction of monocytes and natural killer cells caused by and cause??

A

Caused by: hyperglycemia

Causes: impairs back-up first responders in the innate immune response to infection

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18
Q

Diabetes-impaired neutrophil function leads to more severe infections in?

A

1) Skin
2) Feet (bone, soft tissue)
3) Lungs
4) Urinary tract

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19
Q

Diabetes-impaired neutrophil function leads to more severe infections with?

A

1) Staph. aureus
2) Pseudomonas aeruginosa
3) Candida species
4) Zygomycetes (mucor)
5) many others

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20
Q

Furuncle

A

boil, skin abscess

  • acute necrotizing infection of a hair follicle that breaks through the basement membrane into adjacent subcutaneous fat
  • anything that breaks skin predisposes it (shaving)
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21
Q

Most common cause of furuncles?

A

Staphylococcus aureus

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22
Q

Description of a furuncle?

Treatment?

A
  • painful, tender, fluctuant, central pustule, surrounding erythema and edema
  • draining, spontaneous draining can be aided by warm compressed
  • larger ones need needle draining
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23
Q

Carbuncle?

A
  • coalescence of multiple furuncles creating a subcutaneous complex of abscesses
  • cause systemic symptoms like fever and commonly need incision for drainage
  • more common in diabetics
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24
Q

Pseudomonas aeruginosa in diabetics?

A
  • cause malignant external otitis in diabetics
  • usually involves adjacent mastoid, with osteomyelitis of the ear canal & should be suspected with canal skin necrosis appears
  • pain is disproportionate
  • temp > 102.2 (37C)
  • facial paralysis, vertigo, meningeal signs
  • debridment & antibiotics
25
Q

Mucormycosis

A

(zygomycosis)

  • rhinocerebral form: usually starting in the nose, spreading into paranasal sinuses, orbit, skull base, brain
  • Requires prompt diagnosis, amphotericin and surgery
26
Q

Zygomycetes appearance

A
  • large empty hyphae with rare, random angle branching & collapse
  • look like twisted ribbon
  • biopsy = prompt diagnosis
27
Q

Urinary tract infection

A
  • diabetes predisposes

- can ascent into kidney causing pyelonephritis

28
Q

Pyelonephritis

A

-can combine with ischemia to cause renal papillary necrosis uniquely prevalent in diabetics

29
Q

Foot Ulcers/Gangrene

A

-infection with ischemia and neuropathy

30
Q

Fournier’s gangrene

A

-massive necrosis in perineum

31
Q

Metabolic Syndrome

A

(dyslipidemia syndrome, obesity dyslipidemia syndrome, insulin resistance syndrome, deadly quartet)

1) Diabetes mellitus
2) Hypertension
3) Dyslipidemia
4) Abdominal (male pattern) obesity
* death from heart disease*

32
Q

Metabolic Syndrome Epidemeology

A
  • highest in native Americans
  • Hispanics
  • African Americans
  • European Americans

-increases with age

33
Q

Characteristic Obesity in metabolic syndrome?

A
  • abdominal pattern

- “truncal” “central”

34
Q

Metabolic Syndrome State?

A
  • pro-inflammatory and pro-thrombotic state associated with elevated levels of C-reactive protein, IL-6 and plasminogen activator inhibitor-1
  • use of atypical antipsychotic medications, especially clozapine is associated
35
Q

Major Modifiable risk factors for atherosclerosis

A 
last 4 is metabolic syndrome
Smoking
Hypertension
Obesity
Diabetes
Dyslipidemia
36
Q

Metabolic Syndrome good Diet to help?

A
  • Mediterranean diet (fruits, vegetables, nuts, whole grains, olive oil)
  • DASH - low in sodium
  • foods with a lower glycemic index (whole grains not refined grains)
37
Q

Does metabolic syndrome respond to exercise?

A

yes!

  • practical regular moderate daily minimum of 30 min a day, like brisk walking
  • weight loss, selectively removing abdominal fat (in women)
38
Q

Is the metabolic syndrome really a syndrome?

A
  • maybe not
    1) no unifying pathophysiology has been found
    2) features vary so much there is no consensus definition
    3) the 4 components are only additive factors for heart disease
    4) the diagnosis does not alter treatment
39
Q

Diabetic Neuropathy

A

onset determined by duration and severity of hyperglycemia

1) Peripheral: all eventually get it; 50% subclinical
2) Autonomic: not universal; commonly asymptomatic

40
Q

Diabetic Neuropathy Pathogenesis

A

1) activation of polylol pathway
2) increasing oxidative stress
3) injury to schwann cells
4) demyelination of nerves
5) accumulation of sorbitol & fructose
6) activation of protein kinase C
7) accumulation of advanced glycation end-products (AGEs)

41
Q

Diabetic Neuropathy Earliest Histopathologic Change

A

segmental demyelination

-Luxol Fast Blue stain (myelin blue)

42
Q

Peripheral Neuropathy

A
  • distal symmetric polyneuropathy (length-dependent dying back of axons, primarily sensory)
  • manifested by loss of vibratory sensation and proprioception, then impaired pain, light touch and temperature sensation, ascending from the feet
  • can have pain (early) or weakness
43
Q

Autonomic Neuropathy

A
  • later
  • manifested by resting tachycardia, exercise intolerance, GI dysmotility (especially gastroparesis), impotence, orthostatic hypotension, silent myocaridal ischemia & incarction, increased mortality (30% over 5 years)
44
Q

Diabetes & Aging

A
  • as suggested by the role of AGE in the pathogenesis of diabetic neuropathy, the excess glucose in diabetes sticks to everything-ages faster
  • each year of insulin-dependent diabetes adds a year to the physiologic age
45
Q

Diabetic Retinopathy

A

-a type of microangiopathy

2 forms: background and proliferative

46
Q

Background Diabetic Retinopathy

A

-capillary thickening, microaneurysms, venous dilations, edema, hemorrhages, soft exudates (cotton wool spots = microinfarcts) and hard exudates (precipitates of plasma proteins + lipids)

47
Q

Proliferative Diabetic Retinopathy

A

neovasuclarization and fibrosis

48
Q

3 Types of Diabetic Nephropathy

A

1) Glomerular
2) Papillary
3) Tubulo-interstitial

49
Q

Glomerular Nephropathy: Diffuse Type

A
  • earlier, less severe
  • most common type
  • identical glomerulopathy occurs with hypertension and aging
  • consists of capillary basement membrane thickening and increased mesangial matrix (begins in stalk of glomerular tuft)
50
Q

Glomerular Nephropathy: Nodular Type

A
  • later, usually only after >10 years of diabetes
  • much more characteristic of diabetes, superimposed an diffuse glomerulopathy
  • features Kimmelstiel Wilson nodules and hyaline sclerosis of afferent and efferent arterioles
51
Q

Kimmelstiel Wilson Nodules

A
  • ovoid or spherical, hyaline, sometimes laminated deposits of mucopolysaccharides
  • lipids and fibrillary proteins within mesangium in periphery of glomerular tuft
  • unclear if product of expanded lysed mesangial matrix of massively thickened basement membrane
  • eventually squeeze capillaries shut
52
Q

Exudative Lesions: Fibrin Caps

A
  • crescentic deposits of condensed leaked plasma proteins overlying peripheral capillaries between endothelial cell and basement membrane or between basement membrane and epithelial cell
  • also in non-diabetic*
53
Q

Exudative Lesions: Capsular Drops

A
  • deposits of partly plasma proteins and partly basement membrane in parietal layer of Bowman’s capsule, protruding into urinoferous space
  • NOT in non-diabetic*
54
Q

Renal Failure with Nodular Glomerulosclerosis?

A
  • Kimmelstiel WIlson disease

- renal failure, eventually requiring dialysis

55
Q

Renal Failure with Exudative Lesions?

A

-not correlate with renal failure

56
Q

End Stage Renal

A

-appearance just like hypertensive nephropathy
Gross: diffuse fine granularity of cortical surface
-nephrosclerosis
Microscopic: globally sclerotic glomeruii, dilated tubules resembling thyroid follicles, interstitial fibrosis

57
Q

Most Common Cause of Death Due to Diabetes?

A

atherosclerotic cardiovascular disease (70%)
Second: renal failure (10%)
Third: infection (5%)

58
Q

Long-term complications of diabetes?

A
  • appear 15-20 years after onset of sustained hyperglycemia
  • tight control of blood glucose can delay onset and decrease the severity of microvascular complications, retinopathy, neuropathy, & nephropathy
  • major disadvantages of tight control=hypoglycemia

Endocrinology (15 decks)

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