Brainscape's Knowledge GenomeTM

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


See full index

Y Pathology! > A/22-25 INFLAMMATION (Tamer) > Flashcards

A/22-25 INFLAMMATION (Tamer) Flashcards

1
Q

Sequence of events in acute inflammation

A

Margination, Rolling, Adhesion –>Transmigration (DIAPEDESIS) –>Chemotaxis --> PMN activation–> Phagocytosis–>Termination

three possible outcomes:

  • 100% Resolution
  • Scar
  • Chronic inflammation
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

give at least 3 stimuli for acute inflammation

A
  • *-INFECTIOUS**
  • *-PHYSICAL**
  • *-CHEMICAL**
  • Tissue Necrosis
  • Foreign Bodies (FBs)
  • Immune „responses” or „complexes
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

what is the purpose of the vascular reactions during acute inflammation ?

A

The purpose of the inflammatory vascular reaction is to deliver the humoral and cellular factors to the site of defence reaction

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

mention the vascular events of inflammation

A

Changes in vascular flow and caliber

Changes in vascular permeability

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

steps of EXTRAVASATION of PMNs

A
  • MARGINATION- (PMN’s go toward wall)
  • ROLLING (tumbling and HEAPING)
  • ADHESION
  • TRANSMIGRATION (DIAPEDESIS)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

mention 2 types of molecules important for adhesion

A

-Selectins (E,P and L) from endothelial cells

-Integrins from many cells (ICAM, VCAM)

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

Transmigration is mediated by

A

CD31

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

upon activation of leukocytes

A

1) Produce Eicosanoids (arachidonic acid derivatives)

  • Prostaglandin/thromboxanes
  • Leukotrienes
  • Lipoxins

2) Undergo DEGRANULATION
3) Secrete CYTOKINES

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

Steps of Phagocytosis

A

• RECOGNITION

• ENGULFMENT

• KILLING
(oxygen dependent and independent mechanisms)

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

give at least 3 general features of chemical mediators

A

1) From plasma or cells
2) Have triggering stimuli
3) Usually have specific targets
4) Can cause a cascade
5) Are short lived

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

Name at least 3 classic chemical mediators

A

–Histamine

  • Serotonine
  • Complement
  • Kinins
  • Clotting factors
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

where is histamine released from ? what is its function ?

A

released from Mast Cells, Basophils

• POWERFUL Vasodilator

  • IgE on mast cell
  • (Vasoactive „amine”)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

where is Serotonin released from ? what is its function?

A

SEROTONIN • (5HT, 5-Hydroxy- Tryptamine)

  • Platelets and EnteroChromaffin Cells release it
  • vasodilatation, but more indirect
  • Evokes N.O. synthetase (a ligase-from argenine)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

give at least 3 general features of the complement system

A
  • >20 components, in circulating plasma
  • Multiple sites of action, but LYSIS is the underlying theme
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

give at least 3 general features of the KININ SYSTEM

A

• BRADYKININ is KEY component,

• from circulating plasma

• ACTIONS
− Increased permeability
− Smooth muscle contraction, NON vascular
− Pain

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

give 3 features of CLOTTING FACTORS

A
  • from circulating plasma
  • Coagulation, i.e., production of fibrin
  • Fibrinolysis
17
Q

mention 3 EICOSANOIDS

(ARACHIDONIC ACID DERIVATIVES)

A

• Part of cell membranes •

1) Prostaglandins (incl. Thromboxanes)
2) Leukotrienes
3) Lipoxins (new)

18
Q

3 functions of PROSTAGLANDINS

(THROMBOXANES INCLUDED)

A
  • Pain
  • Fever
  • Clotting
19
Q

give 3 function of LEUKOTRIENES

A
  • Chemotaxis
  • Vasoconstriction

​ • Increased Permeability

20
Q

give 3 function of LIPOXINS

A
  • INHIBIT chemotaxis
  • Vasodilatation
  • Counteract actions of leukotrienes
21
Q

GIVE 3 FEATURES OF PLATELET-ACTIVATING FACTOR (PAF)

A
  • ITS A Phospholipid
  • From MANY cells, like eicosanoids
  • ACTIVATE PLATELETS, powerfully
22
Q

WHAT ARE CYTOKINES AND CHEMOKINES?

GIVE 2 EXAMPLES OF CYTOKINES

A

• CYTOKINES are PROTEINS produced by LYMPHOCYTES and MACROPHAGES, numerous roles in acute and chronic inflammation -

TNFa, IL-1 by macrophages

• CHEMOKINES are small proteins which are attractants for PMNs (>40)

23
Q

GIVE 2 FEATURES OF NITRIC OXIDE

A
  • Potent vasodilator
  • Produced from the action of nitric oxide synthetase from arginine
24
Q

GIVE AT LEAST 3 EXAMPLES OF PRIMARY LYSOMAL CONSTITUENTS

(A.K.A AZUROPHILIC, or NON-specific )

A
  • Myeloperoxidase
  • Lysozyme (Bact.)
  • Acid Hydrolases
25
Q

GIVE AT LEAST 3 EXAMPLES OF SECONDARY LYSOMAL CONSTITUENTS (Also called SPECIFIC)

A
  • Lactoferrin
  • Lysozyme
  • Alkaline Phosphatase
  • Collagenase
26
Q

NAME 3 FREE RADICALS

HOW DESTRUCTIVE ARE THEY ?

A
  • O2 –(SUPEROXIDE)
  • H2O2 –(PEROXIDE)
  • OH- –(HYDROXYL RADICAL)

VERY VERY DESTRUCTIVE

27
Q

SYSTEMIC EFFECTS OF INFLAMMATION

A

-ACUTE PHASE PROTEINS
bind microbial cell walls and may act as opsonin and fix complement . also bind chromatin aiding in clearing of necrotic cell nuclei

e.g. CRP , fibrinogen , SAA

-LEUKOCYTOSIS - white cells (the leukocyte count) increased above the normal range in the blood .
(15,000-20,000 cells/microliter sometimes >40,000)

especially seen in bacterial infection (neutrophillia) but also in bone tumors as well as leukemia.

  • others :
  • increased TNF (in sepsis) will cause DIC –> thrombosis
  • cytokines injure the liver- Hypoglycemia
  • cytokines induce over production of NO by cardiac myocytes and vascular smc’s –> Heart failure ,Loss of Perfusion Pressure (respectively) –> HEMODYNAMIC SHOCK

All together - heart failure , hypoglycemia , hemodynamic disorders –> SEPTIC SHOCK

28
Q

prolonged production of acute phase proteins may lead to what disorder?

A

secondary amyloidosis in chronic inflammation (especially SAA)

29
Q

elevated serum CRP is used as a marker for what ?

A

A high level of CRP in the blood is a marker of inflammation. for example inflammation of the blood vessels of the heart which can mean increased risk of myocardial infarction .

30
Q

Classification of acute inflammation is based on what ?

A

exudate

31
Q

Name at least 3 types of exudate and give their morphological description home boii

A

assuming that sarah loves big dicks we can use the following mnemonic

“Sarah Fucks Paul Hard & Good”

Serous
seen in mild inflammation, relatively low protein. consistency resembles that of serum, usually seen in diseases like TB.

Common cold,
pleuritis exs
burns
catarrhal inflammation of mucous membranes

Fibrinous

composed of fibrinogen and fibrin. seen in severe injuries difficult to resolve due to blood vessels growing into the exudate filling space that was occupied by fibrin. large amounts of antibiotics for resolution.

exudate may be degraded by FIBRINOLYSIS

Serous membranes:
Pleuritis/pericarditis sicca,
Peritonitis fibrinosa

Mucous memebranes:
Diphtery -PSEUDOMEMBRANE
typhoid fever
dysentery

Purulent
morphology : consists of plasma with active/dead neutrophils, fibrinogen, and necrotic parenchymal cells. found in more severe infections (s.pyogenes) , and is referred to as pus (whitish-yellow)

folliculitis, furuncule, carbuncule
Abscess: circumscibed pus in parenchymal organs Empyema: circumscribed pus in preformed body cavity(e.g. pleura)
Phlegmone: inflammation spreading in tissue spaces

Haemorrhagic

plague
smallpox
anthrax
flu

Gangraenous - failure of inflammation

32
Q

what’s an Ulcer ? where is it common ?

A

local defects on the surface of an organ produced by inflammation.

common sites - stomach , intestines

acute stage - infiltration of pmns+vasodilation

long term - infiltration of lymphocytes ,plasma cells,macrophages +fibroblastic proliferation,scarring

33
Q

what’s chronic inflammation ?

A

is a response of prolonged duration(weeks or months) in which inflammation,tissue injury, and repair coexist, in varying combinations.

“proliferative” rather than “exudative”

34
Q

give at least 3 causes of chronic inflammation

A
  • Persistent infections
  • Hypersensitivity diseases - autoimmune diseases

-Prolonged exposure to toxic agents
(exogenous/endogenous)

  • in neurodegenerative diseases,metabolic syndrome ,type 2 diabetes, certain cancers
  • Foreign bodies
35
Q

name at least 3 cellular players in chronic inflammation

A
  • macrophages- The dominant cells in most chronic inflammatory reactions , derive from monocytes , once monocyte are in the extravscular tissue they become macrophages which have longer half life and higher phagocytic capacity
  • lymphocytes- provides defense against infectious pathogens
  • plasma cells- In immune reactions mediated by IgE and in parasitic infections
  • eosinophils
  • mast cells
36
Q

give at least 3 Morphological Features of chronic inflammation

A
  • Not exsudative
  • Infiltration with mononuclear cells
  • Tissue destruction
  • Attempts of healing
37
Q
A

Y Pathology! (20 decks)

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