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Step 1 > Pathology- Inflammation, wound healing > Flashcards

Pathology- Inflammation, wound healing Flashcards

0
Q

Arachidonic acid

A

: mediator of acute inflammation; released from phospholipid membrane by phospholipid A2

  • acted on by either cyclooxygenase = prostaglandins, or
  • 5-lipooxygenase = leukotrienes
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1
Q

Significance of NF-KB

A

NF-KB is a nuclear transcription factor that is activated upon TLR activation by PAMPs
-TLRs are present on APCs and lymphocytes

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2
Q

Which prostaglandins mediate vasodilation and increased vascular permeability?

A

-vasodilation = arteriole; increased vascular permeability = post-capillary venule
: “DIE” PGD2 PGI2 PGE2

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3
Q

What are the functions of PGE2?

A

:vasodilation, vascular permeability, FEVER & PAIN

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4
Q

What are the important leukotrienes? What are the effects?

A

LTC4, LTD4, LTE4- THINK SM CONTRACTION

: vasconstriction, bronchospasm, increased vascular permeability

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5
Q

What are the main mediators of attracting PMNs?

A
  1. LTB4
  2. IL-8
  3. C5a
  4. bacterial products
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6
Q

How are mast cells activated?

A
  1. Cross-linking IgE
  2. complement (C3a, C4a, C5a)
  3. tissue trauma
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7
Q

Function of histamine

A

Vasodilation and increased vascular permeability
Note: delayed response is production of leukotrienes (recall hypersensitivity I) –> this is how the response is maintained

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8
Q

Hageman factor (Factor XII)

A

:inactive pro-inflammatory protein produced in liver; activated when exposed to subendothelial collagen

  • activates coagulation cascade
  • activates complement
  • activates kinin system: kinin cleaves kininogen to bradykinin = vasodilation and increased vascular permeability + pain
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9
Q

Rubor & Calor

A

: d/t vasodilation occurs via SM relaxation of arteriole

- Key mediators: histamine, prostaglandins, leukotrienes

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10
Q

Tumor

A

:swelling; d/t leakage of fluid from postcapillary venules into interstitial space (exudate)
-Key mediator: histamine which causes endothelial cell contraction & tissue damage resulting in endothelial cell disruption

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11
Q

Dolor

A

:pain

-Key mediators: bradykinin and PGE2 –> sensitize sensory nerve endings

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12
Q

Fever

A

pyrogens (LPS from bacteria) cause macrophages to release IL-1, IL-6 and TNF
-IL-1 and TNF increase cyclooxygenase activity (PGE2) in perivascular cells of the hypothalamus which raises the temperature set point

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13
Q

Margination

A
  • vasodilation at the arteriole slows blood flow at the POST-CAPILLARY VENULE
  • cells marginate to the periphery of the vessel
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14
Q

P-selectin

A

:important in rolling, expressed on endothelial cells; released from weibel palade body of endothelial cells, mediated by histamine
-binds sailyl-Lewis X on leukocytes

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15
Q

E-selectin

A

:important in rolling, expressed on endothelial cells; induced by TNF and IL-1
-binds sailyl-Lewis X on leukocytes

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16
Q

What are the cellular adhesion molecules? What induces their expression?

A
  • ICAM-1 (CD54) & VCAM (CD106)

- expressed on the endothelium, induced by TNF and IL-1

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17
Q

What are integrins? Function?

A

:bind to cellular adhesion molecules on the endothelial cell surface to promote tight adhesion

  • CD11/18 integrins, (LFA-1, Mac-1), VLA-4 integrin
  • Integrins are upregulated on leukocytes by C5a and LTB4
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18
Q

What are the steps of leukocyte extravasation?

A
  1. Margination and rolling
  2. Tight binding
  3. Diapedesis (transmigration)
  4. Migration and chemotaxis
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19
Q

What is the respiratory burst?

A

:generation of HOCl within the phagolysosome of the phagocytes
-O2 coverted to superoxide by NADPH oxidase
-Super oxide converted to hydrogen peroxide (H2O2) by superoxide dismutase
H2O2 converted to HOCL (bleach) my myeloperoxidase

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20
Q

Myeloperoxidase deficiency

A

:defective conversion of H2O2 to HOCl

  • patients usually asymptomatic; presentation may be recurrent candida infections
  • NORMAL nitroblue tetrazolium test b/c respiratory burst intact
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21
Q

Acute inflammation

A

:the hallmark of acute inflammation is NEUTROPHILS

  • usually peaks around 24 hrs but can be longer;
  • THE MAIN POINT IS IF PMNs ARE AROUND =ACUTE INFLAMMATION
22
Q

Macrophage roles:

A

:peak around 2-3 days after inflammation begins; they are the “manager”

  1. Resolution and healing: anti-inflammatory cytokines IL-10 and TGF-B
  2. Continue acute inflammation: IL-8 to call in PMNs
  3. Abscess formation: acute inflammation surrounded by fibrosis
  4. Chronic inflammation: macrophages present antigen to CD4 helper cells which secrete cytokines to promote chronic inflammation
23
Q

What cell(s) characterize a granuloma?

A 
Epitheliod histiocytes (macrophages with an abundant pink cytoplasm) 
-Giant cells and a rim of lymphocytes
24
Q

What interactions prompt granuloma formation?

A
  1. Macrophages present via MHCII to CD4 helper cells
  2. Macrophages secrete IL-12 which causes Th1 subtype differentiation
  3. Th1 cells secrete IFN-gamma –> converts macrophages to Epitheliod histiocytes
  4. TNF-a from macrophages maintains granuloma
    Recall: anti-TNF-a drugs cause breakdown of granuloma so always test for latent TB before starting drug
25
Q

What are liable tissues?

A

:posses stem cells that continuously cycle to regenerate the tissue.
Ex: small and large bowel, skin, bone marrow

26
Q

Where are the stem cells in the small and large bowel?

A

mucosal crypts

27
Q

Where are the stem cells of the skin?

A

Basal layer of the dermis

28
Q

What is the hematopoietic stem cell surface marker?

A

CD34

29
Q

What are stable tissues?

A

: comprised of cells that are quiesent (G0) but can reenter the cell cycle to regenerate tissue when necessay
Ex. liver or renal cells

30
Q

What are permanent tissues?

A

:lack significant regenerative capacity

-Heart, skeletal muscle, nerves

31
Q

What is the composition of granulation tissue?

A

Fibroblasts - lay type III collagen
capillaries
myofibroblasts

32
Q

What is the difference between granulation tissue and a scar?

A

type III collagen is replaces with type I collagen

-collagenase removes type III collagen; requires zinc a a cofactor

33
Q

TGF-a

A

epithelial and fibroblast growth factor

34
Q

TGF-B

A

fibroblast growth factor and inhibits inflammation

35
Q

PDGF

A

:platelet derived growth factor; growth factor for endothelium, smooth muscle, and fibroblasts
-secreted by platelets and macrophages

36
Q

VEGF

A

:vascular endothelial growth factor; important in angiogenesis

37
Q

FGF

A

:fibroblast growth factor; important in angiogenesis also mediates skeletal muscle development

38
Q

What are the mediators of wound healing?

A

PDGF, FGF, EGF,TGF-B,TGF-a,VEGF

39
Q

EGF

A

Epidermal growth factor stimulates cell growth via tyrosine kinases

40
Q

Primary intention

A

:form of cutaneous wound healing; wound edges are approximated (eg. suture) –> leads to minimal scar formation

41
Q

Secondary intention

A

:form of cutaneous wound healing; edges are not approximated. Granulation tissue fills the defect & myofibroblasts contract the wound forming a scar

42
Q

Give reasons as to why wound healing would be delayed.

A
  1. Infection –> continued inflammation impairs healing
  2. Vitamin C deficiency: important cofactor in the hydroxylation o proline/lysine procollagen residues
  3. Copper deficiency: cofactor for lysyl oxidase which cross-links lysine and hydroxylysine to form stable collagen
  4. Zinc deficiency: cofactor for collagenase; which replaces type III collagen with type I collagen
43
Q

Hypertrophic Scar

A

:excess production of scar tissue (type I collagen) that is localized to the wound

  • collagen arrangement is parallel
  • infrequently recur following resection
44
Q

Keloid

A

:excess production of scar tissue (type III collagen) that extends beyond the borders of the wound

  • collagen is disorganized
  • frequently recur following resection
  • more common in AA; classically effects earlobes, face and upper extremities
45
Q

Shock

A

Refer to FA pg 222 and shock chart

46
Q

Chromatolysis characteristics:

A

: process involving the neuronal cell body following axonal injury or ischemia
-Changes reflect increase in protein synthesis in an effort to repair the damaged axon:
1. round cellular swelling
2. displacement to the nucleus to the periphery
3. dispersion of nissl substance throughout the cytoplasm
Note: nissl substance = RER

47
Q

Dystrophic calcification

A

Calcium deposition in tissues secondary to necrosis; tends to be localized

  • necrotic tissue acts as a nidus for calcification
  • in the setting of normocalcemia
48
Q

Metastatic calcification

A

widespread calcification in normal tissue secondary to hypercalcemia or high phosphate
- predominately in interstitial tissues of kidney, lungs and gastric mucosa

49
Q

Transudate

A

:transudate is Thin; due to increase in hydrostatic pressure, decrease in oncotic pressure, or Na retention

  • hypocellular
  • protein poor
  • specific gravity <1.012
50
Q

Exudate

A

: due to inflammation/infection or malignancy

  • cellular
  • protein rich
  • specific gravity >1.012
51
Q

ESR

A

:erythrocyte sedimentation rate; products of inflammation coat RBCs and cause aggregation; when aggregated RBCs fall at a faster rate within the test tube

  • Increased ESR: anemia, infection/inflammation, cancer, pregnancy,
  • Decreased ESR: polycythemia, sickle cell, CHF
52
Q

Patient- 5 y/o child presents with sudden lethargy, nausea, vomiting, bloody stool. You suspect the child got into a bottle of prenatal vitamins. Diagnosis?

A

Iron poisoning; iron is extremely corrosive to the GI mucosa; metabolic acidosis is secondary to mitochondrial poisoning

  • most sever in kids< 6 yrs
  • acute:nausea, vomiting, gastric bleeding, lethargy
  • chronic:metabolic acidosis, scarring leading to GI obstruction
53
Q

Autopsy of 75y/o woman shows colon mucosa shows yellow/brown granular pigment in macrophages. What is it?

A

Lipofuscin: wear and tear pigment associated with normal aging

  • formed by oxidation and polymerization of auto-phagocytosed organelles
  • deposits in heart, liver, kidney, eye and many organs

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