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Pathology > Pathoma 2. Inflammation > Flashcards

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
Q

What opsonizes bacteria for Phagocytosis?

A

IgG and C3b

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26
Q

O2 dependent killing can also be impaired due to another enzyme… whick, and what’s the effect/.

A
  1. MPO

2. Hight risk of Candida inf

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27
Q

WHat is another type of killing that cells do? and what enzyme is major?

A

O2 independent killing

- Lysozyme (from 2ary granules in leukocytes)

28
Q

How does inflammation resolve?

A

N undergo APOPTOSIS in 24h, and Macrophages predominate on 2-3d

29
Q

What are the 4 paths that Macrophages can manage the inflammation into?

A

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
Q

Cite the main differences between CD4+ and CD8+ Tcell activation:

A

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
Q

Once the 2 types of B cells are activated, who do they help and how?

A

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
Q

How does the cytotoxic killing happen?

A
  1. Perforins and granzyme induce apoptosis
    or
  2. Expression of FasL binds Fas on target activating apoptosis thru Caspase
33
Q

How are Bcells activated?

A
  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
Q

What are the 2 subtypes of chronic inflammation?

A

Granulomatous and non-granulomatous

35
Q

What characterises a granulomatous inflammation?

A
  1. Epithelioid hystiocytes
  2. Giant cells
  3. Lymphocyte rim
36
Q

What’s the difference between Non-Caseating Granumloma and Caseating?

A

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
Q

How does a granuloma(cas/or non-cas) form? What are the steps involved ?

A

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
Q

Cite at least 5/8 primary immunodeficiencies

A 
Digeorge Sindrome
SCID
CVID
X-linked Agammaglobulinemia
IgA deficiency
Hyper IgM sme
Wiskott Aldrich Sme
Complement Deficiencies
39
Q

What is Digeorge Sme and how does it manifest?

A

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
Q

Describe SCID Etiology, FP and presentation

A
  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
Q

What happens in X-lnked Agammaglobulinemia?

A

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
Q

DESCRIBE what u know of CVID

A

Low Ig due to Bcell of Tcell defects

43
Q

IgA deficiency

A

increased mucosal inf + Celiac Disease

44
Q

Hyper IgM Sme

A

Mutated CD40 don’t permit 2nd signal to Th2, which would send IL4/5 for Bcell switching.

45
Q

Wiskott Aldrich sme

A

mutation in WASP gene= thrombocytopenia, eczema, recurrent inf

46
Q

Complement deficiencies

A

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
Q

What r the main Automimmune (AI) disorders you remember?

A
  1. SLE
  2. APL
  3. Sjogren
  4. Scleroderma
  5. Mixed connective tissue disease
48
Q

SLE: what type of HSR (hypersensitivity reaction)

A

2 and 3 (cytotoxic and Ab-Ag Complex)

49
Q

What’s the most risky effect of SLE and also, what type of endocarditis does it present?

A
  1. Renal damage: diffuse proliferative GN

2. Libman-Sacks Endocarditis (double sided and not infected=due to Ab-Ag complexes depositoin)

50
Q

What Antibodies Dx SLE?

A
  1. ANA (sensitive)

2. Anti-dsDNA (specific)

51
Q

What Ab is charateristic of drug induced SLE? And what drugs induce SLE?

A

Anti-histone Ab= hydralazine, Procainamide, Isoniazid

52
Q

APL syndrome

A

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
Q

Sjogren Sme (sym, Dx, Main #1 late complication)

A

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
Q

Scleroderma

A 
Activation of fibroblasts and deposition of collagen (fibrosis)
Diffuse=all skin + visceral(mainly esophagus)=Scl70
 or
Localized= CREST
CALCINOSIS
RAYNAUD
ESOPHAGUS
SCLERODACTILY
TELANGIECTASIAS
55
Q

MIXED Connective Tissue Disease

A

Traits of many diseases (SLE, Scleroderma, Polimyositis)

Ab against U1 Ribonucleoprotein

56
Q

Wound Healing!!! What’s the diff btw regeneration and repair?

A

Regeneration replaces damaged tissue with native tissue. Repair replaces it w// a fibrous scar.

57
Q

What are the 3 diff types of tissues?

A
  1. Labile
  2. Stable
  3. Permanent
58
Q

Give examples of each type of tissue

A
  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
Q

Repair occurs when:

A

tissue lacks regenerative capacity(MI=fibrous scar), or has lost stem cells (paper cut=no scar vs. deep cut-scar)

60
Q

What is the initial phase of repair and what does it consist of?

A

GRANULATION

  1. Fibroblasts (deposit type3 collagen)
  2. Capillaries (provide nutrients)
  3. Myofibroplasts (contract wound)
61
Q

How does the scar form?

A
  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
Q

What r the 4 types of collagen and where r they present?

A
  1. bONE
  2. Cartwoolage
  3. BV, Granulation tissue, Embryonic tissue)
  4. Base Membrane
63
Q

Cite some growth factors and what they enhance

A

TGF-b= (syn by macrophages) fibroblast GF+inhibits inflammation.
FGF/VGF=angiogenesis

64
Q

How does 2ary wound healing close the wound?

A

Miofibroblasts

65
Q

What are causes for delayed wound healing?

A
  1. infections
  2. Deficiencies in collagen cycle (lack of Vit.C, Zinc, copper)
  3. Foreign body, ischemia, NIDDM, Malnutrition
66
Q

What are 3 Complications in wound healing?

A
  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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