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Pathoma 2. Inflammation Flashcards

1
Q

Acute Inflammation is basically characterised by:

A
  1. Edema

2. Neutrophils

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2
Q

Acute Inflammation arises in response to :

A
  1. INfection

2. Tissue Necrosis

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3
Q

What are TLRs (toll like rcp), what activates them? And who do they activate in the sequence?

A

TLR are present on outer mb of innate immunity cells (like macrophages/dendritic cells), and they correspond to the CD# (CD14, CD40, etc!!) they’re activated by PAMPs (pathogen assoc. molecular pattern), which could be the Antigen (LPS of GNeg. bacterias or anything that identifies a pathogen), the TLR+PAMP combo=activates immune response/mediators (eg. CD14+LPS=upregulation of NF-kappaB)

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4
Q

INFLAM MEDIATORS:

PGI2, D2, E2 are released thru the cycloxygenase cycle and favor inflammation by:

A
  1. Increasing VD of arterioles

2. Increasing Vascular Permeability (VP) of venules

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5
Q

HY PGE2 has a special function:

A

Also mediates FEVER and PAIN

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6
Q

Leukotrienes LTC4, D4, E4 are released thru the 5-Lipoxygenase cycle and favor inflammation by:

A
  1. VC
  2. Bronchospasm
  3. Increasing Vascular Permeability
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7
Q

LTB4 has a special function:

A

Attracts and activates Neutrophils

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8
Q

HY What are the 4 key molecules that bring in N?

A

LTB4
C5A
IL8
Bct products

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9
Q

HY: Mast cells are activated by:

A
  1. tissue Trauma
  2. Complement ptns C3a, C5a
  3. Cross-linking of all surface IgE by Ag
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10
Q

What si the immediate response of Mast cells

A
  1. Histamine Granules

2. VD+VP

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11
Q

What is the delayed response of Mast Cells?

A

Synthesis of Arachidonic Acid metabolites: especially Leukotrienes (these are iMP bc they MAINTAIN ht einflam response. it is the delayed…

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12
Q

Describe what some of the key products of Complement activation do:

  1. C3a+C5a
  2. C5a
  3. C3b
  4. MAC
A
  1. Triggers Mast cell activation
  2. Call Neutrophils
  3. Opsonin for Phagocytosis
  4. lyses microbes and makes holes in their membranes
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13
Q

Hageman Factor is produced in whick organ and has IMP roll in which disease?

A

LIVER. IMP roll in DIC. (it activates coagulation, fibrinolytic system+Kinin System

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14
Q

What does the Kinin System do?

A

It cleaves HMWK+Bradykinin, which mediates VD+VP+ (Pain, like PGE2)

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15
Q

Cardinal signs of Inflammation:

A
  1. Redness(rubor)+ Warmth (Calor)= due to VD. key mediator=HISTAMINE
  2. Swelling (tumor)= Due to VP. key mediators= Histamine/Tissue Damage
  3. Pain (dolor)= Bradykinin+PGE2 sensitise sensory nerve endings
  4. Fever: Pyrogens cause Macrophages to release IL-1+TNF
    COX activity is increased in perivascular cells of hypothalamus (PGE2 raises temp set point=creating fever)
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16
Q

Acute inflammation has 3 general phases

A
  1. Fluid
  2. Neutrophils
  3. Macrophages
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17
Q

What are the 7 steps of the Neutrophil phase?

A
  1. Margination
  2. Rolling
  3. Adhesion
  4. Transmigration and Chemotaxis
  5. Phagocytosis
  6. Destruction of Phagocytosed Material
  7. Resolution
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18
Q

Weibel-Palade Bodies are mediated by Histamine and release 2 factors:

A
  1. P-Selectin (for N rolling)

2. VWF for coagulation

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19
Q

So what up-regulates P Selectins for N rolling?

A

Weibel palade bodies

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20
Q

What 2 components are needed for N adhesion and what up-regulates them?

A

Cell adhesion Molecules: TNF and IL-1 upregulates (same as fever mediators)
Integrins: C5a/LTB4 upregulates

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21
Q

What is leukocyte adhesion deficiency and how does it manifest?

A

Ar defect in Integrins.

  1. Delayed separation of umbilical cord
  2. high rate of circulating neutrophils
  3. recurrent bct inf that lack pus
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22
Q

What 4 molecules attract N thru chemostasis?

A
  1. LTB4, C5a, IL-8, Bct products
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23
Q

What is the disease in which phagolysosomes can’t be formed? and how does it present?

A

Chediak-Higashi sme. (bc of microtubular defect

  • High risk of pyogenic infection
  • Neutropenia (no cytokinesis in cell division)
  • Giant granules in leukocytes (golgi can’t send out)
  • Peripheral Neuropathy
  • Albinism
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24
Q

How is the phagocytosed material destroyed in the cell and what results from a defect in this process?

A

O2 dependent killing

Disease called: Chronic Granulomatous Disease
o2_NADPH oxidase—O2-__SOD–H2O2__MPO—HOCl
*Defect in NADPH oxidase enzyme stops the cycle progression (but many bct can still offer H2O2 to produce bleach. EXCEPT Catalase+ ones (IMP=think of CGD in Pseodomonas cepacia infection!

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25
What opsonizes bacteria for Phagocytosis?
IgG and C3b
26
O2 dependent killing can also be impaired due to another enzyme... whick, and what's the effect/.
1. MPO | 2. Hight risk of Candida inf
27
WHat is another type of killing that cells do? and what enzyme is major?
O2 independent killing | - Lysozyme (from 2ary granules in leukocytes)
28
How does inflammation resolve?
N undergo APOPTOSIS in 24h, and Macrophages predominate on 2-3d
29
What are the 4 paths that Macrophages can manage the inflammation into?
HY 1. Resolution+Healing (IL-10 +TGF-Beta) HY 2. continued acute inflam (IL-8) 3. Abscess 4. Chronic Inflammation=they ingest Ag and express it on mb so Helper T cells can come!
30
Cite the main differences between CD4+ and CD8+ Tcell activation:
For CD4+: EC Ag are phagocytosed and presented to them via MHC-II, 2nd signal is thru B7 binds on CD28 rcp on CD4 cells. CD8: IC Ag is processed and presented on MHC-1, 2nd signal is thry IL-2 from Th1 CD4+cells
31
Once the 2 types of B cells are activated, who do they help and how?
CD4 Helper 1 helps CD8+ they IL-2 and Macrophages thru IFN-gamma ``` CD4 Helper 2 helps B-cells thru IL-4, 5, 10 IL4-class switching to IgG and IgE IL5 switching to IgA and maturation of Plasma cells Il10 inhibits TH1 phenotype, to stop activating macrophages and shut down inflammation. ```
32
How does the cytotoxic killing happen?
1. Perforins and granzyme induce apoptosis or 2. Expression of FasL binds Fas on target activating apoptosis thru Caspase
33
How are Bcells activated?
1. When Ag binds to surface IgM/IgD Bcell turns into Plasma cell 2. B cell presents Ag to Th2 CD4+ thru MHC-II and 2nd signal which is CD40 rcp binds CD40L on Tcell. Helper 2 then secretes IL4, 5 which activates switch for IgG, E.
34
What are the 2 subtypes of chronic inflammation?
Granulomatous and non-granulomatous
35
What characterises a granulomatous inflammation?
1. Epithelioid hystiocytes 2. Giant cells 3. Lymphocyte rim
36
What's the difference between Non-Caseating Granumloma and Caseating?
Non-caseating presents: organised/nucleated tissue=NO CENTRAL NECROSIS. Et: usually reaction to foreign material (eg. breast implant) Also Sarcoidosis, Bryllium exposure, Crohn and Cat scratch disease. Caseating: unorganised/unnucleated= necrotic debris Et: TB/fungal inf To Dx TB granuloma=AFB stain Fungal granuloma=silver(GMS stain)
37
How does a granuloma(cas/or non-cas) form? What are the steps involved ?
It's the Interaction btw Macrophage+TH1 CD4+ 1. . Macrophage presents Ag to CD4+ 2. Macrophage dumps IL-12 which transforms cell into Th1 3. Th1 Secrete IFNgamma which converts Macrophages into Epithelioid Hisiocytes +giant cells
38
Cite at least 5/8 primary immunodeficiencies
``` Digeorge Sindrome SCID CVID X-linked Agammaglobulinemia IgA deficiency Hyper IgM sme Wiskott Aldrich Sme Complement Deficiencies ```
39
What is Digeorge Sme and how does it manifest?
Failure of the 3-4 pharyngeal pouches due to 22q11 microdeletion: Presents: T-cell deficiency bc of lack of Thymus Hypocalcemia (lack of parathyroids)
40
Describe SCID Etiology, FP and presentation
1. ADA deficiency 2. Defective Cell mediated + Humoral Immunity 3. Susceptible to all infections (viral/fungal=bc of lack of T-cells) /(bct/Protozoal bc of lack of Bcell) 4. TTM: sterile isolation/ Stem cell transplant AVOID LIVE VACCINES!
41
What happens in X-lnked Agammaglobulinemia?
Mutated BTK (Bruton's Tyrosine Kinase)= B-cells don't mature=no plasma cells=no Igs!!! ``` After 6mo (when breastfeeding is over), all infections start showing up in a recurrent way! AVOID LIVE VACCINES! ```
42
DESCRIBE what u know of CVID
Low Ig due to Bcell of Tcell defects
43
IgA deficiency
increased mucosal inf + Celiac Disease
44
Hyper IgM Sme
Mutated CD40 don't permit 2nd signal to Th2, which would send IL4/5 for Bcell switching.
45
Wiskott Aldrich sme
mutation in WASP gene= thrombocytopenia, eczema, recurrent inf
46
Complement deficiencies
C5-9 =risk of Neiserria inf C1 inhibitor deficiency= Hereditary Angioedema-periorbital and mucosal. (bc there's no inhibitor to stop the complement from generating inflammation.)
47
What r the main Automimmune (AI) disorders you remember?
1. SLE 2. APL 3. Sjogren 4. Scleroderma 5. Mixed connective tissue disease
48
SLE: what type of HSR (hypersensitivity reaction)
2 and 3 (cytotoxic and Ab-Ag Complex)
49
What's the most risky effect of SLE and also, what type of endocarditis does it present?
1. Renal damage: diffuse proliferative GN | 2. Libman-Sacks Endocarditis (double sided and not infected=due to Ab-Ag complexes depositoin)
50
What Antibodies Dx SLE?
1. ANA (sensitive) | 2. Anti-dsDNA (specific)
51
What Ab is charateristic of drug induced SLE? And what drugs induce SLE?
Anti-histone Ab= hydralazine, Procainamide, Isoniazid
52
APL syndrome
Auto-Ab against proteins bound to phospholipids. 2 most commom: 1. Anticardiolipin= false+ Syphilis test 2. Lupus Anticoagulant Ab=false + PTT lab. (Ab inhibits the lupus anticoagulant=Thombosis of all types! requires lifelong anticoagulation
53
Sjogren Sme (sym, Dx, Main #1 late complication)
Dry mouth, dental carries in women. Dx=ANA+AntiSS-A/B (they target ribonucleoproteins) RISK FOR BCELL LYMPHOMA=vignette=bilateral inflam of Parotids followed by LATE unilateral enlargement of parotid=HY
54
Scleroderma
``` Activation of fibroblasts and deposition of collagen (fibrosis) Diffuse=all skin + visceral(mainly esophagus)=Scl70 or Localized= CREST CALCINOSIS RAYNAUD ESOPHAGUS SCLERODACTILY TELANGIECTASIAS ```
55
MIXED Connective Tissue Disease
Traits of many diseases (SLE, Scleroderma, Polimyositis) | Ab against U1 Ribonucleoprotein
56
Wound Healing!!! What's the diff btw regeneration and repair?
Regeneration replaces damaged tissue with native tissue. Repair replaces it w// a fibrous scar.
57
What are the 3 diff types of tissues?
1. Labile 2. Stable 3. Permanent
58
Give examples of each type of tissue
1. Labile= Skin, GI tract, Bone Marrow (CD34+ Marker), Lung (type 2 pneumocytes) 2. Stable (quiescent)= Liver, Kidney (takes long to recover after ATN-may need dialysis) 3. Permanent=myocardium, skeletal muscle, neurons
59
Repair occurs when:
tissue lacks regenerative capacity(MI=fibrous scar), or has lost stem cells (paper cut=no scar vs. deep cut-scar)
60
What is the initial phase of repair and what does it consist of?
GRANULATION 1. Fibroblasts (deposit type3 collagen) 2. Capillaries (provide nutrients) 3. Myofibroplasts (contract wound)
61
How does the scar form?
1. Collagenase removes Type 3 collagen(which had come for granulation tissue) using Zinc as cofactor 2. Type 3 collagen is replaced with Collagen type 1.
62
What r the 4 types of collagen and where r they present?
1. bONE 2. Cartwoolage 3. BV, Granulation tissue, Embryonic tissue) 4. Base Membrane
63
Cite some growth factors and what they enhance
TGF-b= (syn by macrophages) fibroblast GF+inhibits inflammation. FGF/VGF=angiogenesis
64
How does 2ary wound healing close the wound?
Miofibroblasts
65
What are causes for delayed wound healing?
1. infections 2. Deficiencies in collagen cycle (lack of Vit.C, Zinc, copper) 3. Foreign body, ischemia, NIDDM, Malnutrition
66
What are 3 Complications in wound healing?
1. Dehiscence=abdominal scar reopens 2. Hypertrophic scar (doesn't outgrow the wound site=excessive type 1 Collagen. 3. Keloid= outgrows wound site=excess type3 collagen. (af.americans. Ear lobes, face, upper extremities)

Pathology (5 decks)

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