Acute Inflammation Flashcards

1
Q

Cardinal Signs of Inflammation

A
Rubor
Calor
Tumour
Dolor
Loss of Function
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2
Q

Causes of Acute Inflammation

A
Micro-organism
Mechanical
Chemical
Physical
Necrosis
Hypersensitivity
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3
Q

In microcirculation capillary beds are fed by ______ by ______ and ______ by _______

A

oxygen and arterioles

drained and venules

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4
Q

Starling forces

A

Control fluid flow across the membrane - Hydrostatic and oncotic pressure

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5
Q

Hydrostatic pressure

A

Increases filtration of fluid out of capillaries

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6
Q

Oncotic Pressure

A

Pulls fluid into capillaries and prevents it from leaking

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7
Q

Poiseuille’s Law

A

Flow is proportional to radius to the power of four

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8
Q

Pathogenesis of Acute inflammation

A

Changes is vessel radius flow
Changes in permeability
Movement of neutrophils from vessel to extravascular space

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9
Q

TRIPLE RESPONSE

A
  1. Red- Vasodilation of capillaries and venules
  2. Flare- Arteriolar dilation
  3. Wheal- increased permeability and exudation
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10
Q

Consequences of increased permeability

A

Imbalance of Starling forces
Exudation = oedema
Fluid loss = increase in viscosity
Decrease in blood flow = decreased in blood pressure

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11
Q

Neutrophil flow in inflammation

A

Margination –> pavementing –> emigration –> extravascular tissue

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12
Q

Diapedesis

A

Passage of blood cells through the intact wall of capillaries during inflammation

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13
Q

Benefits of acute inflammation

A

Non specific response
Neutrophils destroy organism
Plasma protein localises process

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14
Q

Outcomes of acute inflammation

A

Resolution
Organisation
Chronic Inflammation
Suppuration (pus)

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15
Q

Inflammation of Peritoneal Cavity

A

Peritonitis

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16
Q

Inflammation of Meninges

A

Meningitis

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17
Q

Inflammation of Appendix

A

Appendicitis

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18
Q

Inflammation of Pleural Cavity

A

Pluerisy

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19
Q

Functions of Neutrophils (8)

A
Recognise foreign antigens
Chemotaxis
Adhere to organism
Release granules with oxidants and enzymes
Release granule contents
Phagocyte and destroy
Produces pus
Extend inflammation to other tissues
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20
Q

Plasma proteins

A

Fibrinogen

Immunoglobulin

21
Q

Fibrinogen Function

A

coagulation factor that forms fibrin and clots exudate

22
Q

Immunoglobulin Function

A

Humoral response

23
Q

Mediators of Acute Inflammation (cells)

A
Histamine
Serotonin
Prostaglandin
Thromboxane
Nitric Oxide
Oxygen free radicals
24
Q

Mediators of Acute Inflammation (endothelial cell surface membranes)

A

ICAM-1- helps neutrophil stick

25
Mediators in plasma
Fibrinolysis Kinin Complement cascade
26
Preformed is mast cells besides vessels and released in result of local injury and IgE mediated reaction
Histamine
27
Preformed in platelets and released when platelets degranulate during coagulation and causes vasoconstriction
Serotonin
28
Produced from arachidonic acid via cyclo-oxygenase pathway and increases the effect of histamine
Prostaglandin
29
Promotes platelet aggregation and vasoconstriction
Thromboxane A2
30
Nitric Oxide
Smooth muscle relaxation Anti-platelet Leukocyte recruitment
31
Released by neutrophils in phagocytosis, amplify other mediators
Oxygen free radicals
32
Fibronolysis
Breaks down fibrin and prevents blood clots
33
Kinin system
Bradykinin (pain)
34
Complement cascade
inflammation-immune system
35
Molecules inside cells-signalling
PAMP | Danger associated molecular pattern
36
Intracellular pathways
NF-kB MAPK JAK-STAT
37
Collective effect of mediators
``` Vasodilation Increased permeability Neutrophi adhesion Chemotaxis Itch and pain ```
38
Immediate systemic effects
Pyrexia (pyrogens from WBC) Fell unwell Neutrophilia
39
Longer term effects
Lymphadenopathy Weight loss Anaemia
40
Outcomes of acute inflammation
Granulation Healing and repair Fibrosis and formation of scar
41
Granulation tissue
universal patch forms new capillaries (angiogenesis), fibroblasts, collagen and macrophages
42
Cardiac output
amount of blood pumped by heart in a minute
43
Stroke volume
amount of blood pumped by the left ventricle
44
___ = SV X HR
cardiac output =
45
_____ = CO X systemic vascular resistance
blood pressure =
46
Pathogenesis of Septic Shock
mediators lead to vasodilation and and loss of systemic vascular resistance. Results in catecholamine release, increase in HR to compensate
47
What happens when compensation of increased HR fails to restore SVR
low BP Reduced perfusion of tissues Tissue hypoxia- cell death
48
Causes vasoconstriction
Serotonin