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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
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2
Q

give at least 3 stimuli for acute inflammation

A
  • *-INFECTIOUS**
  • *-PHYSICAL**
  • *-CHEMICAL**
  • Tissue Necrosis
  • Foreign Bodies (FBs)
  • Immune „responses” or „complexes
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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

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4
Q

mention the vascular events of inflammation

A

Changes in vascular flow and caliber

Changes in vascular permeability

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5
Q

steps of EXTRAVASATION of PMNs

A
  • MARGINATION- (PMN’s go toward wall)
  • ROLLING (tumbling and HEAPING)
  • ADHESION
  • TRANSMIGRATION (DIAPEDESIS)
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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)

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7
Q

Transmigration is mediated by

A

CD31

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8
Q

upon activation of leukocytes

A

1) Produce Eicosanoids (arachidonic acid derivatives)

  • Prostaglandin/thromboxanes
  • Leukotrienes
  • Lipoxins

2) Undergo DEGRANULATION
3) Secrete CYTOKINES

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9
Q

Steps of Phagocytosis

A

• RECOGNITION

• ENGULFMENT

• KILLING
(oxygen dependent and independent mechanisms)

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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

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11
Q

Name at least 3 classic chemical mediators

A

–Histamine

  • Serotonine
  • Complement
  • Kinins
  • Clotting factors
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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”)
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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)
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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
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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

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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
GIVE AT LEAST 3 EXAMPLES OF **SECONDARY LYSOMAL CONSTITUENTS** (Also called SPECIFIC)
* Lactoferrin * Lysozyme * Alkaline Phosphatase * Collagenase
26
NAME 3 FREE RADICALS HOW DESTRUCTIVE ARE THEY ?
* O2 –(SUPEROXIDE) * H2O2 –(PEROXIDE) * OH- –(HYDROXYL RADICAL) **VERY VERY DESTRUCTIVE**
27
SYSTEMIC EFFECTS OF INFLAMMATION
-**FEVER** - in response to substances called *pyrogens* ------------------------------------------------------------------------------ -**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
prolonged production of acute phase proteins may lead to what disorder?
secondary amyloidosis in chronic inflammation (especially SAA)
29
elevated serum CRP is used as a marker for what ?
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
Classification of acute inflammation is based on what ?
exudate
31
Name at least 3 types of exudate and give their morphological description home boii
assuming that sarah loves big dicks we can use the following mnemonic **"S**arah **F**ucks **P**aul **H**ard & **G**ood" **S**erous 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 **F**ibrinous 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 **P**urulent 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 **H**aemorrhagic plague smallpox anthrax flu **G**angraenous - failure of inflammation
32
what's an Ulcer ? where is it common ?
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
what's chronic inflammation ?
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
give at least 3 causes of chronic inflammation
- 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
name at least 3 cellular players in chronic inflammation
- **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
give at least 3 Morphological Features of chronic inflammation
- **Not exsudative** - Infiltration with **mononuclear cells** - Tissue **destruction** - Attempts of **healing**
37

Y Pathology! (20 decks)

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