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Pathoma > Chapter 2: Inflammation, Inflammatory Disorders, and Wound Healing > Flashcards

Chapter 2: Inflammation, Inflammatory Disorders, and Wound Healing Flashcards

1
Q

tissue necrosis is always followed by?

A

acute inflammation – increase in neutrophils

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2
Q

What is the goal of acute inflammation?

A

eliminate pathogen or clear necrotic debris

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3
Q

How do macrophages deal with gram negative bacteria?

A

the CD14 receptor on macrophages recognize LPS on outer membrane of gram negs

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4
Q

Describe pathway of TLR’s

A

Pathogen Associated Molecular Patterns(PAMPs) activate TLR’s on macrophages/lymphocytes causing upregulation of NF-kB which is a nuclear transcription factor that activates immune response genes leading to production of multiple immune mediators

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5
Q

TLR on B-cells importance

A

They cross link enough receptors to NOT need a second signal!

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6
Q

Arachidonic Acid Metabolites

A

Arachidonic Acid released from cell membrane by phospholipase A2 and then acted upon by COX or 5-lipoxygenase creating prostoglandins, prostocyclines, thromboxanes(COX) and leukotrienes(5-lipoxygenase)

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7
Q

Mediates vasodilation and increases vascular permeability

A

PGI2, PGD2, PGE2

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8
Q

mediates pain and fever

A

PGE2

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9
Q

neutrophil chemoattractants

A

LTB4, IL-8, C5a

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10
Q

mediate vasoconstriction, bronchospasm, and increased vascular permeability

A

LTC4, LTD4, LTE4 leukotrienes cause smooth muscle contraction – bronchial muscles, smooth muscle in vessels and pericytes(edema)

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11
Q

Vasodilation occurs at the…

A

arteriole

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12
Q

increased vascular permeability occurs at…

A

venule

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13
Q

Mast cells activated by

A

tissue trauma, complement proteins C3a, C5a or cross linking by IgE

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14
Q

Mast cell immediate response

A

release histamine – vasodilation and increase permeability

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15
Q

Mast cell delayed response

A

release leukotrienes

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16
Q

Complement System

A

Classical Pathway – C1 binds IgG or IgM that’s bound to antigen Alternative pathway – microbial products directly activate Mannose binding lectin pathway - MBL binds to mannose on microorganisms and activates complement

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17
Q

What is important in DIC?

A

Hageman Factor(Factor XII)

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18
Q

Cardinal Signs of inflammation

A

Redness(rubor), warmth(calor) both caused by histamine mediated vasodilation Swelling(tumor) also caused by histamine mediated increase in vascular permeability Pain(dolor) mediated by bradykinin and PGE2 which sensitize nerve endings Fever is caused by the release of IL-1 and TNF which increase cyclooxygenase activity in perivascular cells of the hypothalamus which increases local PGE2 synthesis which raises temperature setpoint

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19
Q

Leukocyte margination occurs through?

A

postcapillary venules! Cells marginate from the center flow to the periphery due to the slow of blood flow from vasodilation

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20
Q

Leukocyte rolling occurs via?

A

selectin speed bumps upregulated in endothelial cells.Histamine causes release of P-selectin from Weibel-Palade bodies. E-selectin is induced by TNF and IL-1. Interaction of P-selectin and E-selectin causes leukocytes to roll along vessel wall

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21
Q

What does selectin on endothelial cells bind on leukocytes (neutrophils, macrophages, etc.)

A

Sialyl Lewis X

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22
Q

Leukocyte adhesion to endothelial cells occur via?

A

upregulation of adhesion molecules, ICAM and VCAM by TNF and IL-1 bind to integrins on leukocytes

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23
Q

What causes upregulation of adhesion molecules?

A

IL-1 and TNF

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24
Q

What causes upregulation of selectins?

A

Histamine for P-selectin from Weibel Palade bodies, TNF and IL-1 for E-selectin

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25
Q

What causes upregulation of integrins on leukocytes?

A

C5a and LTB4, the chemotactic factors!

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26
Q

What is the most common cause of leukocyte adhesion deficiency?

What is the clinical presentation?

A

Defective CD18 subunit.
NOTABLE CLINICAL SIGNS -
– failure of umbilical cord to detach,
– INCREASED circulating neutrophils because they can’t be stored by attaching to vascular walls.(marginated pool).
– Finally, recurrent bacterial infections that LACK pus formation
pus=dead neutrophils sitting in fluid

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27
Q

Opsonins…?

A

IgG and C3b

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28
Q

Chediak-Higashi syndrome

A

impaired phagolysosome formation.
Pathophys: Microtubule polymerization disorder means the “tracks” to get around the cell are broken, as such transport of phagosomes is deficient.

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29
Q

giant granules in leukocytes and defective primary hemostasis, albinism

A

Chediak-Higashi syndrome

abnormal dense granules in golgi apparatus leads to impaired primary hemostasis
giant granules in leukocytes arise from fusion of granules in golgi since they can’t move…

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30
Q

Generation of bleach

A

O2 –> O2- radical –> H2O2 –> HOCl NADPH Oxidase(oxidative burst), Superoxide Dismutase, MPO

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31
Q

NTB dye

A

O2–>O2- radical This reaction is marked, so if NADPH oxidase works, will stain blue

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32
Q

Chronic Granulomatous Disease

What organisms are you susceptible to?

A

poor O2 dependent killing due to NADPH oxidase defect. Particularly vulnerable to catalase positive organisms… Staph. Aureus, Pseudomonas Capacia, Serratia marcescens, Nocardia and Aspergillus. REMEMBER Pseudomonas Capacia

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33
Q

MPO Deficiency

A

defective conversion of H2O2 to HOCl increases risk for candida infections

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34
Q

Leukocyte O2 independent killing.

What does it bind to?

A

Reliant on lysozyme and major basic protein(binds heparin sulfate proteoglycans)

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35
Q

Anti inflammatory cytokines produced by macrophages?

Pro-inflammatory cytokines produced by macrophages?

A

Anti – IL-10 and TGF-ß

Pro – IL-8

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36
Q

Macrophage management of acute inflammation

A

Resolve with IL-10 and TGF-ß
Continue inflammation with neutrophil recruitment using IL-8
Abscess
Chronic inflammation via CD4 lymphocytes

37
Q

Histological description of plasma cells

A

Plasma cells have eccentric nucleus with slight pale pallor next to nucleus. They are not multilobulated like neutrophils

38
Q

T cells have what receptors

A

TCR and CD3 on all T cells

39
Q

CD4+ helper T-cell activation

A

APC presents antigen on MHC II and binds TCR on T-cell

B7 on APC binds T cell CD28 receptor

40
Q

Th1 cytokines

A

IL-2 (T-cell growth factor and CD8+ activator) and IFN-gamma

also, IL-6 (pyrogen, stimulates acute phase proteins)

41
Q

Th2 cytokines

A

IL-4 (facilitates B-cell switch to IgE and IgG)

IL-5 (eosinophil chemotaxis and activation, maturation of B cells to plasma cells and class switch to IgA)

IL-10 (inhibits Th1 phenotype)

42
Q

CD8+ Cytotoxic T-cell activation

how does it initiate apoptosis?

A

Intracellular antigen presented on MHC I
IL-2 from Th1(CD4+) T-cell

CD8 induces apoptosis via perforin and granzyme GRENADES
or
Expression of FasL which binds to Fas receptor on cells inducing apoptosis.

43
Q

B-Cell activation

A

Antigen binding by surface IgM or IgD, results in maturation to IgM or IgD secreting plasma cells. No second signal needed if enough antigen present to activate and cross link Ig’s or antigen activates TLR. Alternate Pathway B-cell presents antigen to Th2 T-cell via MHC II – CD40 receptor on B cell binds CD40L on Th2 as 2nd signal – Th2 secretes IL-4 and IL-5 to mediate isotype switching, hypermutation and plasma cell maturation

44
Q

A granuloma is characteristically defined by

A

epithelioid histiocytes (macrophages with abundant pink cytoplasm) usually surrounded by lymphoctes/giant cells

45
Q

Characteristic of non-caseating granuloma. Common causes?

A

Lacks central necrosis
usually caused by sarcoidosis, reaction to foreign material, beryllium exposure, Crohn’s disease, and cat scratch disease (bartonella hensellae)

46
Q

Characteristic of Caseating granulomas

A

central necrosis characteristic of tuberculosis and fungal infections

47
Q

Steps for Granuloma formation

A
  1. ) Macrophage Processes antigen
  2. ) MHC II on macrophage shows antigen on MHC II to CD4+ cell
  3. ) Macrophage secretes IL-12 differentiating CD4+ to Th1
  4. ) Th1 secretes IFN-gamma converting macrophages to Epithelioid histiocytes and Giant cells
48
Q

DiGeorge Syndrome

A

Failure of 3rd and 4th pouch due to 22q11 microdeletion. remember the MICRODELETION part

Presents with T-cell deficiency (lack of thymus); hypocalcemia (lack of parathyroids); and abnormalities of heart, great vessels, and face

49
Q

lack of thymus, hypocalcemia and abnormalities in heart and great vessels

A

DiGeorge Syndrome (22q11 microdeletion) causes lack of thymus and parathyroids leading to T-cell deficency (recurrent infections) and hypoparathyroidism (low PTF) causing hypocalcemia

50
Q

Bruton’s Agammaglobulinemia or X-linked Agammaglobulinemia

A

Complete lack of immunoglobulin due to disordered B-cell maturation. As such Naive B cells can’t mature into plasma cells and no Ig can ever be secreted. Due to a mutation in a tyrosine Kinase

51
Q

recurrent bacterial, enterovirus (polio,coxsackie), giardia lamblia after 6 months of life

A

Bruton’s agammaglobulinemia. Mother’s Ig’s present first 6 months. Enterovirus due to lack of IgA

52
Q

Severe Combined Immunodeficiency

A

Combined humoral and cell-mediated defection Etiologies via Cytokine receptor defects, ADA(adenosine deaminase deficiency) and MHC Class II deficiency. MHC class II NECESSARY for CD4 to do anything

53
Q

most common selective immunoglobulin deficiency?

a/w?

A

IgA disease

commonly A/W celiac disease and viral gastroenteritis

54
Q

Hyper-IgM Syndrome etiology?

A 
Elevated IgM 
Mutated CD40L(T-cells) or CD40(B-cells) - as such second signal cannot be delivered for required class switching
55
Q

thrombocytopenia, eczema, recurrent infections

A

defective humoral and cellular immunity due to WASP gene. This is X-linked. Called Wiskott-Aldrich Syndrome

Small platelets that do not function properly are removed by the spleen causing the thrombocytopenia

56
Q

C5-C9 deficiencies

A

increased risk for Neisseria infection

57
Q

hereditary angioedema, edema of the skin, periorbital edema and mucosal surfaces

A

C1 inhibitor deficiency

C1 inhibitor is a serine protease inhibitor that is the most important inhibitor of kallikrein in the body.
decreased C1 inhibitor –> increased kallikrein –> increased bradykinin –> increased permeability

58
Q

What’s a method of T-cell inactivation that occurs after mature T-cells leave thymus?

A

Anergy - stimulation without second signal deactivates them

59
Q

Systemic Lupus Erythematosus is what type of hypersensitivity?

A

Type III hypersensitivity, Antibodies against host damage multiple tissues

60
Q

Classic symptom of SLE

A

Renal damage – diffuse proliferative glomerulonephritis

61
Q

Small sterile deposits on both sides of heart valve

A

Libman-sacks endocarditis secondary to SLE. Caused by non-infectious inflammatory response to Ag-Ab caused by Lupus

62
Q

Lupus lab test findings

A

ANA positive, anti-dsDNA(highly specific)

63
Q

anti-histone antibody

Common associations?

A

drug induced lupus, reversible common drugs, hydralazine, procainamide, isoniazid

64
Q

increased PTT time but hypercoaguable?

A

think lupus anticoagulant or anticardiolipin (cardiolipin is present on mitochondrial membrane

65
Q

recurrent pregnancy loss in female with fever and weight loss

A

anti-cardiolipin or lupus anti-coagulant cause frequent thrombosis in arteries and veins ARTERIES AND VEINScausing DVT’s, hepatic vein thrombosis(budd-chiari), placental thrombosis(recurrent pregnancies) and stroke

66
Q

Unilateral enlargement of the parotid gland

A

B-cell lymphoma in marginal zone secondary to Sjogren’s

67
Q

CREST Scleroderma

A 
C - Calcinosis/anti-Centromere antibodies 
R - Raynaud's
E - Esophageal Dysmotility
S - Sclerodactyly
T - Telangiectasias
68
Q

Lots of dental carries and corneal abrasions. What do you test for?

A

ANA and anti-ribonucleoprotein(anti-SS-A/Ro and anti-SS-B/La)

69
Q

Sjogren’s associated with?

A

other autoimmune crap. Mostly rheumatoid arthritis
ALSO
B-cell lymphoma in the MARGINAL zone

70
Q

Serum Ab against U1 ribonucleoprotein

A

mixed connective tissue disease features from SLE, systemic sclerosis and polymyositis

71
Q

Stem cells of lung…

A

type II pneumocyte

72
Q

Stem cell of GI tract

A

mucosal crypts

73
Q

Stem cell of bone marrow are positive for what molecule?

A

CD34+

74
Q

What type of collagen present in keloids?

A

Type III collagen. Also present in blood vessels and embryonic tissue and early wound healing

75
Q

Collagen in early wound healing

A

Type III collagen

76
Q

What cofactor does collagenase require?

A

Zinc

77
Q

TGF-alpha

A

epithelial and fibroblast growth factor

78
Q

TGF-beta

A

important fibroblast growth factor, but also inhibits inflammation

79
Q

platelet derived growth factor

A

growth factor for endothelium, smooth muscle and fibroblasts

80
Q

fibroblast growth factor

A

important for angiogenesis, also mediates skeletal development IMPORTANT FOR ANGIOGENESIS

81
Q

what kind of signaling is wound healing mediated by?

A

paracrine macrophages secrete growth factors that target fibroblasts

82
Q

Necessary factors for wound healing

A

Zinc, Copper and Vitamin C

83
Q

What role does vitamin C play in wound healing

A

it hydroxylates proline residues so that they can cross link each other and form collagen

84
Q

What role does copper play in wound healing?

A

Copper is a cofactor for lysyl oxidase which cross-links lysine and hydroxylysine to form stable collagen

85
Q

What role does zinc play in wound healing?

A

Zinc is a cofactor for collagenase, which replaces type III collagen of granulation tissue with the stronger type I collagen

86
Q

African american recently got an ear piercing. What should you be afraid of?

A

Keloid formation. Characterized by type III collagen

87
Q

What collagen is a hypertrophic scar made out of?

A

Type I.

88
Q

Compare hypertrophic scar with keloid

A

keloid type III collagen hypertrophic scar Type 1 You’ll know a keloid when you see one on the USMLE

89
Q

Treat antiphospholipid syndrome with?

A

lifelong anti-coagulants

Pathoma (7 decks)

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