Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Fellowship Exam > Ch 1 Inflammation > Flashcards

Ch 1 Inflammation Flashcards

1
Q

Leukocyte extravasation (4)

A

1. margination
WBC interacts with endothelial
weak interactions btw glycoprotein adhesion (E,P,L selectins on endothelial) + (integrins on WBC)
2. adherence
WBC to vascular wall high affinity bond
alpha (CD11) + beta (CD18) WBC integrins
**ICAM-1 **adhesions on endothelial
3. diapedesis
WBA migrate inbetween endothelial
via upregulated adhesions molecules on endo (ICAM2)
4. migration
interstitial space along chemical gradient of exogenous or endogenous (chemokines) chemoattractants Il1, TNF substance P

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

stages of acute inflamm (4)

A

1. vasodilation
vasoconstriction: stimulted by vasoactive agents (catecholamines, seratonin, bradykinin and PG from tissue
*vasodilation: *new capillaries, inc blood flow and delivery of mediators and cells
NO, histamine, leukotrines, PG, complement
NA fromsympathetic
2. permeability
increased INTRACELLULAR endothelial gaps mediated by histamine and seratonin
inc INTERCELLULAR gaps > hypoxia, injury, cytokines, mediators (TNF, IL-1)
ODEMA loss of serum protien > decreased intravascular osmotic pressure, increased blood viscosity, and subsequent increases in interstitial osmotic pressure
faciliates delivery of factors to site (ab’s, acute phase protien) and pain + loss of function
3. stasis
[inc] RBC + reduced hydrostatic pressure leads to intravascular stasis
INC contact time btw cells and endothelium
4. extravasation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

what stimulates initial vasoconsriction (4)

A

catecholamines,
seratonin,
bradykinin
PG

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

what stimulates subsequent vasodilation (6)

A

NO,
histamine,
leukotrines,
PG,
complement
NA from sympathetic

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

inflammatory cytokines

A

TNF
IL-1

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Permeability involves (3)

A
  1. increased intracellular gaps (seratonin, histamine)
  2. increased intercellular (hypoxia, innjury, cytokines)

3.ODEMA
loss of serum protein
decreased intravascular osmotic pressure,
increased blood viscosity
increases interstitial osmotic pressure
faciliates delivery of factors to site (ab’s, acute phase protien)

pain + loss of function

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Celullar components of inflam (4)

A

1, neutrophils
local killing and degradation of bacterial macromolecules via phagocytosis and superoxide radicals
PRIMARY azurophil granules > microbial peptides and proteases
SECONDARY granules > metalloproteases
prodices:IL-1a, IL1b, IL 6, TNF a
induce relaese - ROS, inflamm
short lived, replaced by macro 24-48hr
2.macrophages
resdient cells source of pro-inflamm factors (IL1b, IL-6, TNFa), PG + growth factors
attracted by: cytokines, compleement, PDGF, TGFb
phagocytose material, pathogens
secrete coallagenases to resolve matrix
stimulate FiBROBLASTS for wound repair
3. lymphocyte
cell mediated immunity: helper (CD4+) T-cells and the cytotoxic (CD8+) T-cells
T-helper-1 (Th-1) and T-helper-2 (Th-2) cells
interferon (IFN)-γ and IL-12, T-cells differentiate + produce cytokines (IFN-γ and IL-2)
Th-1 > **macrophages, maximizing **the bacterial killing
> (IgG) production by B-cells
Th-2 s > allergic reactions
> IL-4, IL-5, IL-10, and IL-13
* suppression of macrophage, increase IgE
4. mast cell
degranulate dt trauma, complement, microbial or neuropeptides
source: histamine, serotonin, leukotrienes, PG, heparin, and cytokines

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

neutrophils
- job
- granules
- pro-inflamm

A

1, neutrophils
local killing and degradation of bacterial macromolecules via phagocytosis and superoxide radicals
PRIMARY azurophil granules > microbial peptides and proteases
SECONDARY granules > metalloproteases
produces: IL-1a, IL1b, IL 6, TNF a
induce relaese - ROS, inflamm
short lived

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

macrophages
- job
- pro-inflamm + GF
- attarcted by

A

2.macrophages
residient cells, major source of pro-inflamm factors (IL1b, IL-6, TNFa), PG + growth factors
attracted by: cytokines, compleement, PDGF, TGFb
phagocytose material, pathogens
secrete coallagenases to resolve matrix
stimulate FiBROBLASTS for wound repair

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

lymphocytes

types
stimulated by
produce

A

cell mediated immunity: helper (CD4+) T-cells and the cytotoxic (CD8+) T-cells
T-helper-1 (Th-1) and T-helper-2 (Th-2) cells
interferon (IFN)-γ and IL-12, T-cells differentiate + produce cytokines (IFN-γ and IL-2)
Th-1 > macrophages, maximizing the bacterial killing
> (IgG) production by B-cells
Th-2 s > allergic reactions
> IL-4, IL-5, IL-10, and IL-13
* suppression of macrophage, increase IgE

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

mast cells
-produce

A

degranulate dt trauma, complement, microbial or neuropeptides
source: histamine, serotonin, leukotrienes, PG, heparin, and cytokines

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

What are inflammatory stimuli (3)

A
  1. ALarm signals
    Pathogne associated and danger associated molecular patterns (PAMP + DAMPs)
    PAMP: microbial source (foreign)
    DAMP: endogenous i.e. fibrinogen, alert damage
    group B1 mediator in** late sepsis**
    Heat shock protiens
  2. Pattern regcognition receptors
    toll-like receptors
    intiate intracellular signalling > NF- KB, alter genes
  3. neurogenic (tachykinins)
    neuropeptides released by peripheral nueron + WBC dt trauma
    substance P > pain signals + vasodilation (PG, NO) + leukocyte extravasation
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

substance P (3)

A

released by: neurons and leukocytes

pain signals (neurokinin reseptors)

vasodilation + oedema via PGs, NO

WBC chemotaxsis/extravasion

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

inflamm mediators (10)

A
  1. vasoactive amines (histamine)
  2. proinflmmatory cytokines (TNFa, IL1, IL6,
  3. Chemokines (CXC, CC, IL8, MCP, MIP)
  4. anitinflamm (IL-10)
  5. lipid derived (PG, leukotriens, lipoxin)
  6. platetelt activating factor
  7. ROS
  8. NO, HS
  9. acute phase protiens (albumin, CRP, serum amyloid A, complement)
  10. coagulation factors
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

vasoactive amines

A

Histamine rleased by Mast cells
interacts with H1 recepter
vasodliation
attractes eosionphils
peak affect 15-20min

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

pro-inflammatory cytokines (4)

A
  1. TNFa
    activated macrophages
    stimulate pro-infamm cytokines + WBS extravasation
    activate T cells
  2. IL1b
    inactive from > cleaved by caspase
    enhance pro-inflamm (cytokines, NO, PG)
  3. IL-6
    macrophage, T cell, epithelial
    initiate APP
    down regulates pro-inflamm
    = diagnostic marker
  4. Chemokines
    attract WBC
    il-8, monocyte/macrophage chemoarttact protiens
17
Q

aninflamm

A

IL 10
produced by CD4+ Th-2 cells, monocytes, B-cells

decrease pro-inflamm + inhbit NFkB
balance the inflammatory response

18
Q

Eicosanoids (3)

Cell membrane phospholipids&raquo_space;> arachidonic acid via phospholipidase

A

PG
cyclooxygenase pathway, where arachidonic acid metabolism is catalyzed by the enzymes cyclooxygenase (COX)-1 and COX-2
* COX-1 is a **constitutively **expressed > homeostasis
* COX-2 is **induced **by trauma, growth factors, proinflammatory cytokines
recruitment of leukocytes.
induce vasodilation (pain and fever)
leukotriene
* produced in the lipoxygenase pathway
potent chemotactic agent and an activator of neutrophils
* peptidoleukotrienes provoke vasoconstriction, bronchoconstriction, and increased venule permeability
Lipoxin
major antiinflammatory role (attenuate leukotrienes)
* inhibit neutrophil chemotaxis and transmigration

19
Q

Platelet activating factor

A

produced by: enothelial, platelet, WBC

major stimulation of arachidonic acid

subsequently increases eicosanoid production

 direct proinflammatory effects on neutrophils
 causes aggregation and degranulation of platelets

20
Q

ROS

A

Free radicals > destabilize other molecules

ischemia and reperfusion may create ROS

causing peroxidation of membrane phospholipids, which govern cell permeability and the activity of various cellular proteins thus results in oxidative stress and cell damage

induce proinflammatory cytokine (involving NF-κB)

21
Q

NO, HS

A

**Nitric oxide **
synthesized from the amino acid L-arginine by the enzyme nitric oxide synthase
(inducible and constitutively produced)
induced by/induces pro inflamm mediators
produces vasodilation
decreases platelet aggregation and leukocyte adhesion
Sustained release occurs in chronic inflammatory joint disorders

Hydrogen sulfide
produced during cysteine metabolism
H2S > promote inflammation
NSAIDs reduce H2S levels > contributes significantly to (NSAID)-associated gastritis

22
Q

Acute phase protiens (6)

A

albumin
NEGATIVE APP

C-reative protien
Bound to bacteria, C-reactive protein promotes activation of complement
activated macrophages
DIC

Serum amyoid A
* produced in macrophages and endothelial cells
* stimulates proinflammatory cytokines
chemoaatract t cells
decreases PGe2

Complement

coagulation factors

Kininogen
* plasma proteins of the kallikrein-kinin system Factor XII, prekalli-krein, high-molecular-weight kininogen, and low-molecular-weight kininogen
* bradykinin, inter-acts with two membrane receptors, B1 and B2

23
Q

complement

hepatically synthesized proteases that circulate in inactive form.

what are 3 pathways

what are 3 actions

A

activation via 3 pathways:
**Lectin **
interaction lectin proteins with surface carbohydrates on pathogens

**alternative **
contact with foreign microbes

classical pathway
Immune complexes activate

  • all complement pathways merge at the cleavage of C3 to form C3b
    actions
  • Inflammation (recruit/activate WBC) C5a, C3b
  • phagocytosis C3b
  • MAC (C5b binds to C6, C7, C8, and C9 in the terminal complement pathway to form the membrane attack complex
24
Q

coagulation factors

A

factors culminate at the conversion of prothrombin, an acute phase protein, to thrombin, which then mediates the conversion of fibrinogen into fibrin and subsequent clot formation

**proinflammatory effects **through four protease-activated receptors (PARs)

  • In sepsis and inflammatory conditions complicated by DIC, levels of antithrombin III (ATIII), an inhibitor of thrombin and other coagulation factors, are** reduced**
  • activated protein C, limits clotting by inactivating coagulation factors Va and VIIa.
25
Q

what are the outcomes of inflammation (5)

A

resolution
- phagocytosis by macrophages
- pro-to-anti-inflamm

systemic inflammation
- multiple factors > intense inflammatory > imbalance of mediators
SIRS: aberrations in temp, heart rate, blood pressure, respiration, and white blood cell counts.
o Dx sepsis = SIRS is accompanied by a nidus of infection

MODs
progressive dysfunction of two or more organ systems
reperfusion-mediated oxidative injury to the gut epithelium serves as a major source of mediators
o “two-hit” phenomenon

Immunosuppession
overwhelming antiinflammatory response
endotoxin tolerance > celll becomes unresponsive to subsequent stimulation.
recent gene analyses suggest that major “reprogramming

chronic inflamm

26
Q

Chronic inflamm

A

predominantly monocytic infiltrates, angiogenesis, and progressive tissue fibrosis
o inappropriate expression of proinflammatory factors from stromal cells
o** fibroblasts **play a significant role > promotes expression of pro-inflammatory factors such as IL-6 and COX-2 (vicuous cycle)
Leukocyte-derived growth factors > myofibroblasts and ECM production

granulomatous inflamm > macrophages, epitheloid, multinucleated giant cells (suture and glove startch)

Fellowship Exam (135 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions