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Path Pro > Acute Inflammation > Flashcards

Acute Inflammation Flashcards

1
Q

What is inflammation

A

Response of living tissue to injury

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2
Q

Compare the vascular and cellular phase

How is inflammation controlled

A

Cellular: Delivery of neutrophils
Vascular: Blood flow changes, accumulation of exudate

Chemical mediators

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3
Q

Name 5 major causes of acute inflammation

A 
Microbial infections 
Hypersensitivity reactions 
Physical agents (trauma)
Chemicals
Tissue necrosis
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4
Q

Name 5 clinical signs of acute inflammation

A 
Rubour
Tumour
Calor
Dolor 
Loss of Function
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5
Q

How does vascular flow change during acute inflammation

A

Vasoconstriction in first few seconds
Vasodilation in first few minutes
Increased vessel permeability

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6
Q

Regarding fluid movement, what is Starling’s Law?

A

Movement of fluid is controlled by the balance of Hydrostatic Pressure and Oncotic Pressure

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7
Q

How does inflammation cause swelling by altering vascular flow

A
  1. Vasodilation increases hydrostatic pressure
  2. Increased vessel permeability allows plasma proteins to enter interstitium, thus increased interstitial oncotic pressure
  3. Fluid moves out of vessel, into Intersitium
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8
Q

How does fluid leaving vessel affect the contents that remain

A 
Increased viscosity of blood
Reduced flow (Stasis)
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9
Q

Compare Exudate and Transudate

  • Vascular permeability
  • Protein content of fluid
  • When do they occur
A

Exudate:

  • Increased vascular permeability
  • Protein rich fluid
  • In inflammation

Transudate:

  • Unchanged vascular permeability
  • No protein in fluid
  • Heart/ hepatic/ renal failure
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10
Q

State 3 ways vascular permeability can be increased

A
  1. Direct injury (Burns, trauma)
  2. Retraction of endothelial cells
  3. Leukocyte dependent injury (Enzymes/ toxic oxygen species released by inflammatory cells)
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11
Q

How is the vascular phase effective

Give 3 ways

A

More interstitial fluid= Toxins diluted

Exudate delivers proteins such as antibodies and fibrinogen (Mesh limits toxins spread)

Fluid drains to lymph nodes, antigens presented to immune system

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12
Q

How do Neurophils leave vessels in 4 steps

A
  1. Margination (Move towards endothelia)
  2. Rolling (Move along endothelia via weak bonds)
  3. Adhesion (Tight bonds formation)
  4. Diapedesis/ Emigration (Move through endothelia)
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13
Q

Compare the 2 adhesion molecules response for “rolling” and “adhesion” in Neutrophil Emigration

A
  • Selectins on Activated endothelial cells are responsible for Rolling
  • Integrins on Neutrophil surface change from Low to High affinity state, responsible for Adhesion
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14
Q

What is Chemotaxis

How do neutrophils move in this way

A

Movement along an increasing chemical gradient of chemoattractants

Re-arrangement of cytoskeleton

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15
Q

How do Neutrophils recognise pathogens

Give an example

A

Opsonins

Pathogen covered in C3b and Fc opsonins
Neutrophil surface has C3b and Fc receptors

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16
Q

How is the cellular phase effective in 3 ways

A

Removal of pathogens
Removal of necrotic tissue
Release of inflammatory mediators

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17
Q

What are inflammatory mediators

Name 4 ways they originate

A

Chemical messengers that control and co-ordinate inflammatory response

Activated inflammatory cells
Platelets
Endothelial cells
Toxins

18
Q

Name 4 Mediators that cause vasodilation

A

Histamine
Serotonin
Prostaglandins
Nitric Oxide

19
Q

Name 5 mediators that increase vascular permeability

A 
Histamine
Serotonin
Bradykinin
Leukotrienes 
Nitric Oxide
20
Q

Name 4 mediators that stimulate chemotaxis

A

C3a, C5a
IL-1
TNF-Alpha
Leukotrienes

21
Q

Name 3 mediators that cause pain

A

Bradykinin
Histamine
Prostaglandins

22
Q

Name 3 pyrogens (Mediators cause fever)

A

Prostaglandins
IL-1
IL-6

23
Q

Mediators;

Name 2 vasoactive amines
name 1 vasoactive peptides
Name 2 complement proteins

A

Amines: Histamine, Serotonin
Peptides: Bradykinin
Complement: C3a and C5a

24
Q

Mediators;

Name 2 derived from phospholipids
Name 1 Cytokines/ chemokine
Name 1 exogenous mediator

A

Prostaglandins and Leukotrienes
TNF (Tumour Necrosis Factor)
Endotoxins from pathogens

25
Q

What are the 2 types of Complications from Acute Inflammation

Name 4 examples of each

A

Local

  • Obstruction of tubes/ compression of organs
  • Loss of fluid
  • Pain
  • Normal tissue damaged

Systemic

  • Fever
  • Leucocytosis (Increased WBC production)
  • Acute Phase Response (Malaise, Lethargy, Altered sleep) induces rest
  • Septic shock (Huge release of mediators)
26
Q

What are NSAIDs

How do they work?

A

Non-Steroidal Anti Inflammatory drugs

Block mediators that cause fever

27
Q

What are Acute Phase Proteins
Name one that is measured as a marker for inflammation

Name 1 protein made in smaller amounts during Acute Phase Response. Name 2 made in larger amounts

A

Proteins released due to inflammation
C-Reactive Protein

Albumin- made less
Alpha-1 antitrypsin and Fibrinogen- made more

28
Q

Name 4 outcomes of Septic Shock

A

Hypotension
Tachycardia
Multi-organ failure
Death

29
Q

What are the 3 possible outcomes of Acute Inflammation

A
  1. Complete resolution
  2. Fibrosis (Repair with connective tissue)
  3. Chronic inflammation (With repair)
30
Q

When does Acute Inflammation result in Fibrosis

When does it result in Chronic Inflammation

A

Fibrosis- If there is substantial tissue destruction

Chronic- When Acute isn’t enough to combat cause

31
Q

Regarding Complete Resolution,

  1. What happens to Mediators
  2. Vessel diameter and permeabilty
  3. Neutrophils
  4. Exudate
  5. Tissue structure
A
  1. Degraded/ inactivated/ diluted (Short half lives)
  2. Return to normal
  3. Apoptosis and Phagocytosed
  4. Drained via lymphatics
  5. If preserved, undergoes regeneration
32
Q

Name 4 types of Exudate and their appearance

A
  1. Pus/ Abscess- White/ creamy
  2. Haemorrhagic- Bloody
  3. Serous- Clear
  4. Fibrinous- Strands visible
33
Q

What is a Pus/ Abscess exudate

What is a Seroma

A

Accumulation of dead/ dying neutrophils associated with Liquefactive necrosis

Accumulation of serous fluid in a body cavity

34
Q

Hereditary Angio-oedema is an inherited Acute Inflammation Disorder.

What is the biochemical basis
Identify 3 symptoms

A

Deficiency of C1-Esterase inhibitor

Non-itchy cutaneous oedema
Recurrent abdominal pain
Family history of sudden death involving laryngeal involvement

35
Q

Alpha-1 Antitrypsin deficiency is an inherited Acute Inflammation Disorder.

What is the biochemical basis
Identify 2 symptoms

A

Low Alpha-1 Antritrypsin levels

Emphysema (Damaged alveoli)
Hepatocyte damage-> Cirrhosis

36
Q

Chronic Granulomatous Disease is an inherited Acute Inflammation Disorder.

What is the biochemical basis
Identify 3 symptoms

A

Phagocytes can’t make superoxide, so pathogens are Phagocytosed but NOT killed.

Granulomas
Skin/ lymph node abscesses
Many chronic infections in first year of life

37
Q

Describe the process of Appendicitis in 3 steps

What organism causes it

A
  1. Lumen becomes blocked with Faecolith
  2. Accumulation of bacteria + Exudate
  3. Increased pressure-> Perforation

E. coli

38
Q

Describe Pneumonia?

Which 2 organisms cause it

A

Exudate build up in lungs

H. influenazae + Strep pneumoniae

39
Q

Describe Meningitis
What 2 organisms cause it

Identify 3 symptoms
How fatal is it

A

Exudate accumulation in meningeal space
N. mengitidis, E. coli

Headache
Neck stiffness
Photophobia

Rapidly fatal

40
Q

What is Ascending Cholangitis, how is it related to Bile Abscess
What organism causes it

A

Bile duct inflammation caused by bacteria ascending from junction with Duodenum - Can cause a liver abscess

Caused by E. Coli

Path Pro (14 decks)

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