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Pathological Processes > 2. Acute Inflammation > Flashcards

2. Acute Inflammation Flashcards

1
Q

What are the causes of acute inflammation?

A
  • Foreign bodies
  • Immune reactions
  • Infections
  • Trauma
  • Physical and chemical agents (e.g burns, irradiation)
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2
Q

What are the clinical signs of acute inflammation?

A 
Rubor = redness
Calor = heat
Tumour = swelling
Dolor = pain
Loss of function
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3
Q

Name the 3 main tissue changes that occur during acute inflammation.

A
  1. Changes in blood flow
  2. Formation of exudate
  3. Neutrophil emigration
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4
Q

What is the first arteriole change that occurs in acute inflammation?

A

Transient vasoconstriction

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5
Q

What clinical sign does vasodilation of the arterioles cause?

A

Heat and redness due to increased blood flow

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6
Q

What chemical mediators are involved in vasodilation?

A

Histamin
Serotonin
Prostaglandins

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7
Q

What is the purpose of arteriole vasodilation in acute inflammation?

A

Vasodilation of arterioles increases the flow and pressure in the capillaries, increasing the delivery of fluid and proteins to the area of damage.

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8
Q

What changes occur to the vessels following vasodilation?

A

Increased permability

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9
Q

What is the reason for increased permeability of the capillaries?

A

Protein-rich plasma (exudate) can leak through the endothelial gaps into the tissue. Delivery of important proteins - fibrin

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10
Q

Which chemical mediators are involved in causing vascular permeability?

A

Histamine
Leukotrienes

Others: Serotonin,Bradykinin, C3a,C4a,C5a

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11
Q

How does vascular stasis arise following increased permeability?

A

The concentration of cells (haematocrit) in the blood increases and fluid leaves the vessel, increased viscosity. Blood slows = vascular stasis.

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12
Q

Histamine is stored in granules in which cells?

A

Mast cells

B

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13
Q

Explain the change in Starling’s forces which occur during acute inflammation. What is the net result?

A
  1. The semi-permeable membrane becomes leaky
  2. Increased capillary hydrostatic pressure due to arteriole vasodilation
  3. Increased colloid osmotic pressure of interstitium

Net flow of fluid out of the vessel and into tissue spaces.

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14
Q

How does exudate help to combat the tissue injury?

A

Delivers plasma proteins to area of injury Immunoglobulins
Inflammatory mediators
Fibrinogen
Dilutes toxins
Increases lymphatic drainage
Delivers micro-organisms to phagocytes and antigens to immune system

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15
Q

Name 3 defensive proteins which are in exudate.

A
  1. Opsonins
  2. Complement
  3. Antibodies
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16
Q

What is the function of opsonins?

A

Coat foreign material and make them easier to phagocytose

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17
Q

What is the difference between exudate and transudate?

A

Exudate is protein rich and only occurs during inflammation.

Transudate is protein-poor and occurs under normal membrane permeability in conditions such as heart failure.

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18
Q

What is the primary type of leucocyte involved in acute inflammation?

A

Neutrophils

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19
Q

Why are neutrophils often referred to as polymorphs?

A

Multi-lobed nuclei

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20
Q

Where are neutrophils usually found, what is the significance of this?

A

Blood and bone marrow

If they are found in the tissue then indicates invasion by pathogen or tissue injury.

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21
Q

What are the 4 stages involved in the infiltration of neutrophils into tissues?

A
  1. Margination
  2. Rolling
  3. Adhesion
  4. Emigration
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22
Q

What is margination?

A

Stasis of blood flow causes neutrophils to line up at the edge of blood vessels along the endothelium.

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23
Q

What is chemotaxis?

A

Chemotaxis is the directional movement towards a chemical attractant (chemotaxin)

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24
Q

Give some example of chemotaxins.

A
  1. Clotted blood
  2. C5a
  3. Bacterial peptides - LPS from the outer membrane of gram negative bacteria.
  4. Substances released from leucocytes - LTB4
25
Q

What is neutrophil activation?

A

When chemotaxin binds to surface receptors, causing changes which “activate” the neutrophil and make it stickier.

26
Q

Explain the process of margination, rolling, adhesion and emigration.

A
  1. Margination - stasis causes neutrophils to line up at the edge of blood vessels
  2. Neutrophils roll along the endothelium, sticking intermittently.
  3. They then stick = adhesion
  4. Emigrate through vessel wall
27
Q

What is diapedesis?

A

The movement of leukocytes through the endothelial wall of capillaries.

28
Q

How do neutrophils pass through vessel walls?

A
  1. Relaxation of inter-endoethlial cell junctions

2. Digestion of basement membrane - collagenase

29
Q

Name 2 examples of opsonins.

A

igG antibody

C3b

30
Q

What are the 2 killing mechanisms of phagocytes?

A
  1. Oxygen- dependent killing

2. Oxygen- independent killing

31
Q

What is O2 dependent killing?

A

Uses oxygen derived free radicals (H2O2, superoxide and hydroxyl) which are released into the phagosome. This mechanism of killing is called the oxygen burst or respiratory burst.

32
Q

What is O2 independent killing?

A

Using enzymes, e.g., proteases, phospholipases, nucleases and lysozyme.

33
Q

How can phagocytosis result in damage to the host tissue?

A

Activated neutrophils may release toxic metabolites and enzymes causing damage to the host tissue

34
Q

How does infiltration of immune cells help to combat injury?

A

Removes pathogenic organisms, necrotic debris

35
Q

How does vasodilation help to combat injury?

A

Increases delivery, increases temperature

36
Q

Why does pain and loss of function help to combat injury?

A

Enforces rest, reduces chance of further traumatic damage

37
Q

What are some local complications of acute inflammation?

A
  • Swelling can cause blockage of tubes e.g bile duct, intestine
  • Exudate can cause compression e.g cardiac tamponade
  • Damage to normal tissue by substances produced by neutrophils and released during the process of phagocytosis.
  • Loss of fluid
  • Pain and loss of function
38
Q

How can local inflammation lead to systemic complications?

A

Although produced locally, inflammatory mediators can enter the blood stream in significant amounts and have systemic effects.

39
Q

What are the 4 main systemic effects of acute inflammation?

A
  1. Fever
  2. Leucocytosis (Increased leucocytes)
  3. Acute phase response
  4. Shock
40
Q

What causes fever?

A

Endogenous pyrogens produced: IL-1 and TNFa

These cytokines cause an increase in synthesis of prostaglandin E2 within the anterior hypothalamus.

41
Q

What causes leukocytosis?

A
  • IL-1 and TNFa produce an accelerated release from marrow
    –Macrophages and T cells produce colony- stimulating factors which stimulate the bone marrow to produce more neutrophils.
42
Q

What are the clinical signs of acute phase response ?

A

Decreased appetite, raised pulse rate, altered sleep patterns and changes in plasma concentrations of acute phase proteins.

43
Q

Give examples of acute phase proteins.

A 
- CRP
– a1 antitrypsin
– Haptoglobin
– Fibrinogen
– Serum amyloid A protein
44
Q

What is shock and how can it occur?

A

If bacterial products or inflammatory mediators enter systemic circulation, inflammation can occur throughout the body. This results in shock.
Shock is a dramatic drop in blood pressure due to widespread vasodilatation and increase in vascular permeability with resultant fluid exudation. It is often fatal.

45
Q

What 4 things might happen after acute inflammation?

A
  1. Complete resolution
  2. Continued acute inflammation with chronic inflammation = abscess
  3. Chronic inflammation with fibrous repair
  4. Death
46
Q

Name some clinical examples of acute inflammation.

A 
bacterial meningitis
lobar pneumonia
ascending cholangitis
liver abscess
acute appendicitis
47
Q

When may it not be possible for a tissue to return to normal?

A

If tissue architecture is destroyed, cannot regenerate and fibrous scar tissue will replace.

48
Q

How is resolution achieved?

A
  1. Mediators have short half lives
  2. Vascular permeability returns
  3. No more neutrophil margination
  4. Exudate absorbed into vessels or lymph
  5. Fibrin degraded
  6. Neutrophils apoptose and phagocytosed.
49
Q

How are chemical mediators regulated during resolution?

A
  • short half life
  • may be inactivated by degradation
  • inhibitors can bind
  • may be unstable
  • diluted in exudate
50
Q

Which type of necrosis occurs in the centre of an abscess?

A

Liquefactive necrosis

51
Q

Name some examples of disorders of acute inflammation.

A
  • Hereditary angio-oedema (‘angioneurotic oedema’)
    • Alpha-1 antitrypsin deficiency.
  • chronic granulomatous disease
52
Q

When would a coroners autopsy be required?

A
  • Deceased unknown
  • Deceased not seen by a doctor within 14 days of death
  • Attending doctor not able to give cause of death
  • Obviously unnatural death (murder, accident, suicide)
  • Death related to occupational disease or accident
  • Death related to medical treatment or procedure
53
Q

What is chronic granulomatous disease?

A

Genetic deficiency in one of components of NADPH oxidase responsible for generating superoxide.

Engulfment of bacteria does not result in activation of oxygen-dependent killing mechanisms.

54
Q

What is alpha 1 - antitrypsin?

A

a protease inhibitor which deactivates enzymes released from neutrophils at the site of inflammation.

55
Q

How can alpha 1-antitrypsin deficiency lead to emphysema and liver disease?

A

α1-antitrypsin is correctly folded, cannot be packaged so accumulates in ER.
The systemic deficiency of the enzyme means that proteases within the lung can act unchecked and lung tissue is broken down.
Liver disease: accumulated abnormal protein causes hepatocyte damage and cirrhosis.

56
Q

What is hereditary angio-oedema?

A

Deficiency in C1 esterase inhibitor

57
Q

What are the symptoms and signs of heriditary angio-oedema?

A
  • attacks of non itchy cutaneous angio-oedema
  • recurrent abdominal pain - intestinal oedema
  • family history of sudden death
58
Q

What is hereditary angio-oedema?

A

Deficiency in C1 esterase inhibitor

59
Q

What are the symptoms and signs of heriditary angio-oedema?

A
  • attacks of non itchy cutaneous angio-oedema
  • recurrent abdominal pain - intestinal oedema
  • family history of sudden death

Pathological Processes (12 decks)

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