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Unit 9 > Physiology of Inflammation > Flashcards

Physiology of Inflammation Flashcards

1
Q

5 cardinal signs of inflammation

A
  • calor (heat)
  • rubor (redness)
  • tumor (swelling)
  • dolor (pain)
  • functio laesa (loss of function)
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2
Q

3 phases of inflammation

A

1) Initiation

  • stimulus occurrence and its recognition
  • local production of inflammation mediators

2) Patent inflammation processes

  • local dilation of capillaries increase blood flow
  • micro vascular structural changes and escape plasma proteins from the blood stream

3) Resolution

  • removal of stimulus
  • inhibitory feedbacks and counter- balanced cellular and humoral responses
  • repair, wound healing, if adaptive- memory development
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3
Q

Causes of inflammation

A
  • infections or microbial specific exotoxins, endotoxins and pathological mechanisms
  • tissue injury/ death
  • hypersensitivity
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4
Q

Examples of inflammatory diseases

A
  • Gout
  • IBS
  • rheumatoid arthritis
  • autoimmune diseases
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5
Q

Morphological patterns of inflammation

A
  • Serous
  • fibrinous
  • haemorrhagic
  • suppurative
  • necrotising
  • ulcers
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6
Q

2 classifications of inflammation

A
  • Acute
  • Chronic
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7
Q

Features of acute inflammation

A
  • fast onset
  • prominent signs
  • mild outcomes
  • self limited
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8
Q

Features of chronic inflammation

A
  • slow onset
  • less prominent signs
  • severe outcomes
  • progressive disease
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9
Q

Examples of acute phase proteins

A
  • ↑ CRP
  • Fibrinogen
  • Haptoglobin
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10
Q

What happens in stimulus occurrence?

A

Infection
- virus
- bacteria
- fungi
- eukaryotic parasites

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11
Q

What happens in stimulus recognition?

A

Humoral factors
- complement system
- antibodies
- other proteins

Innate cell recognition
- PRRs (Toll-like receptors)
- complement and antibody responses

Adaptive immuno-recognition
- specific responses

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12
Q

What does PAMPS stand for?

A

Pathogen associated molecular patterns

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13
Q

What does DAMPs stand for?

A

Damage associated molecular patterns

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14
Q

What does SAMPS stand for?

A

Self/suppression associated molecular patterns

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15
Q

Feature of the initial local mediator release

A

Autocrine and paracrine cellular responses:

  • mediated by diverse cell types and vast ranger of different receptors
  • release of other mediators by surrounding cells, local and systemic responses
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16
Q

Mediators of inflammation and examples

A
  • Amines (histamine)
  • Lipids (prostaglandins, Leukotrienes
    platelet-activating factor)
  • Peptides (bradykinin)
  • Proteins (cytokines)
  • Chemokines
  • Enzymes
17
Q

How does vasodilation occur?

A

Mainly due to histamine and NO

  • released by mast cells and macrophages
  • also promoted by PAF, bradykinin PGE1 and 2
18
Q

What causes swelling?

A
  • micro vascular leakage occurs in post capillary venules
  • mainly due to histamine
    endothelial cells retraction and rearrangement of tights-junctions forming gaps between them and allows fluid exudation
  • loss of protein leads to oedema
19
Q

Where is histamine released from?

What do histamines do? (2)

A
  • Mast Cells
  • dilate blood vessels
  • ↑ micro vascular permeability
20
Q

What is the function of Histamine H1 receptors?

A

G protein couple receptor

  • ↑ Ca2+
  • smooth muscle contraction
  • ↑ capillary permeability
  • vasodilation
  • sensory nerve endings pain and itching

IMPORTANT- for asthma and allergies

21
Q

Lipids as mediators of inflammation (4)

A

1) stored in phospholipid molecule

2) enzyme phospholipase A2 breaks down phospholipids

3) IFN-y, IFN-a, b-FGF receptor - phosphorylation and CA2+ influx

4) Phospholipid broken down into Arachidonic acid and Lyso-glyceryl-phosphorylcholine (Platelet activating factor)

22
Q

How is platelet activating factor produced?

A

Produced mainly by platelets, mast cells, neutrophils, macrophages, endothelial cells:
1. Phospholipids
2. Lyso-glyceryl-phosphorycholine
3. Platelet activating factor
4. PAF-receptors

23
Q

What does platelet activating factor do? (8)

A
  • Strong vasodilation
  • ↑ vascular permeability
  • bronchoconstriction
  • platelet aggregation and degranulation
  • leukocyte chemotaxis, extravasation
  • promote neutrophil oxidative burst
  • ↑ production of eicosanoids by inducing Cox2 transcription
  • ↑ transcription of IL-6, MMPs and iNOS
24
Q

Eicosanoids precursors

A

Arachidonic acid (20 carbon lipid)

EPA = Eicosapentaenoic acid (omega-3 fatty acid)

DHA = Docosahexaenoic acid ( 22 carbon omega 3 fatty acid)

25
Q

What can eicosapentaenoic acid (EPA) form?

What can docosahexaenoic acid (DHA) form?

A
  • Resolvins
  • Resolvins
  • Protectins
  • Maresins
26
Q

What do eicosanoids effects depend on? (3)

A
  • half life
  • type of receptors they interact with
  • each cell type has a different set of eicosanoids synthetic enzymes, receptors and responses - so competent to produce and release a variety of molecules
27
Q

NSAIDS as cyclooxygenase inhibitors

A
  • Inhibit Cox1 and Cox2
  • so block synthesis of PGs and TXs

arachidonic acid → (Cox +O2) → PGH2 → PGE2 etc.

28
Q

Function of PGE2 (4)

A

Gastric protection
↑ mucus secretion
↑ bicarbonate
↑ mucosal blood flow

(Cox1 inhibition causes peptic ulcers and GI bleeding)

29
Q

Adverse effects due to Cox1 inhibition (3)

What should you prescribe?

A

↑ gastric acid secretion

↓ gastric/ duodenal mucus/ HCO3- secretion

↑ risk of GI ulceration

  • prescribe PPI for gastro- protection or using co-formulation (e.g.naproxen + esomeprazole)
30
Q

Eicosanoids Leukotriene example

A

LTB4
- made by neutrophils & erythrocytes
- G-coupled receptors
- pro-inflammatory
- neutrophil chemotaxis
- activation of transmigration

31
Q

Eicosanoids lipoxins example

A

LXA4

  • produced by neutrophils
  • G couple receptor
  • modulation of LKs and cytokine action
  • control resolution of inflammation by stopping neutrophil chemotaxis, adhesion and transmigration
  • inhibit NK functions
32
Q

Glucocorticoids mechanism of action

A

1) Bind to cytoplasmic GR receptors (normally inactive and associated with HSPs)

2) Upon binding, HSP dissociate and activated receptors dimerise

3) Dimer of activated receptors translocate to nucleus

4) In nucleus, dimers bind to DNA-motifs called glucocorticoid response elements (GRE)

5) Gene transcription modified

33
Q

Effects of glucocorticoids

A
  • inhibit transcription of pro-inflammation genes
  • Cox2, IL-2, TNF-a, IL-1, IL-4, adhesion molecules
  • induce expression of anti-inflammatory genes
  • lipocortins (annexin 1) IL-10, IL-1ra

annexin 1 interferes with phospholipase A2: inhibit leukocyte activities and activating lipoxin A4 receptor

34
Q

Adenosine functions

A

MACROPHAGES (A2A, A2B, A3):
- ↓ TNFa, IL-6, IL-22
- ↑ IL-10

DENDRITIC CELLS:
- A1/A3: regulation of chemotaxis & maturation
- A2A: ↓ pro-inflammatory cytokine release
- A2B: ↑ Th17 mediated response
- A2B:↑ TNF-a, IFN-y, IL-6/8, TGF-b, VEGF, Cox2

MAST CELLS:
- A2B: regulation of degranulation
- A1/A3: ↑ chemotaxis and phagocytosis

NEUTROPHILS (A2A):
- ↓ neutrophil adhesion
- ↓ phagocytosis
- ↓ IL-8 and ROS

LYMPHOCYTES (A2A):
- ↓ IL-4 / IFN-y
- ↑ NF-kB in T regs
- maintenance T/B cells ratio in germinal centres

35
Q

Major mediators of inflammation:

Enzymes (complement system) (5)

A
  • Ig-Ag, microbial surface, polysaccharide

C3a = inc vascular permeability

C5a = inc vascular permeability, chemotaxis

C3b = opsonisation

C3b-C9 (MAC) = cell lysis

36
Q

Major mediators of inflammation:

Enzymes (coagulation fibrinolytic cascades) (3)

A

Adhesion of thrombin → fibroblast proliferation

Fibrinopeptides factor Xa → vascular permeability and leukocyte exudation

Plasmin → C3a

37
Q

Major mediators of inflammation:

Enzymes (kinin system)

A

Hageman factor → ( tissue injury) → bradykinin → pain, vasodilation, increased permeability

(- Hageman factor converts Prekallikrein to kallikrein
- Kallikrein converts Kininogens to Bradykinin)

38
Q

Features of phosphorylesterases (PDEs)

A

PDEs:
- enzyme superfamily
- control cAMP and cGMP catabolism

They have different:
- subcellular distribution
- enzymatic activity
- kinetic properties
- substrate specifity
- cell type-specific
- cell responses

39
Q

Mediators of inflammation:

Features of Cytokines (10) and Chemokines (1)

A
  • promote differentiation, proliferation and activation of leukocyte
  • promote leukocyte adherence to endothelium (IL-1, TNFa)
  • promote leukocyte production in bone marrow (IL-3)
  • promote B-lymphocyte class switching (IL-4, INFa)
  • activate local tissue destruction 9 (IL-1b, IL-17)
  • regulate chemokine production (IL-17)
  • induce of acute phase protein production at liver (IL-6)
  • induces haemoatopoietic GF (IL-17)
  • induce vascular changes (IL-1,IL-17, IL-6)
  • kinase-linked receptors
  • chemokines attract leukocytes (CXCL)

Unit 9 (6 decks)

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