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Pathological Processes > Session 2 > Flashcards

Session 2 Flashcards

1
Q

What is acute inflammation?

A

The response of living tissue to injury

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2
Q

What are some characteristics of acute inflammation?

A

Innate
Stereotyped
Immediate/Early
Short Duration (mins, hours, days)

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3
Q

Acute inflammation is controlled by…

A

Chemical mediators

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4
Q

Acute inflammation serves to limit…

A

The tissue damage

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5
Q

Give 5 causes of acute inflammation

A 
Microbial infections 
Hypersensitivity reactions 
Physical agents (e.g. Heat, light, radiation)
Chemicals 
Tissue necrosis
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6
Q

What are 5 clinical features of acute inflammation?

A 
Rubor 
Tumour
Calor 
Dolor
Loss of function
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7
Q

What is rubor?

A

Redness

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8
Q

What is tumour?

A

Swelling

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9
Q

What is calor?

A

Heat

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10
Q

What is dolor?

A

Pain

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11
Q

Acute inflammation involves which 3 changes in tissues?

A

Changes in blood flow
Exudation of fluid into tissues
Infiltration of inflammatory cells

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12
Q

Describe the changes in blood flow seen in acute inflammation with regards to the size of the arterial/capillary lumen

A

Initially vasoconstriction of arterioles

Then vasodilation of arterioles and then capillaries

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13
Q

How long does the initial transient vasoconstriction of arterioles in acute inflammation last for?

A

First few seconds of acute inflammation

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14
Q

Vasodilation of arterioles and capillaries contributes to which symptoms of acute inflammation?

A

Calor

Rubor

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15
Q

How is the permeability of blood vessels affected in acute inflammation? What consequences does this have? What happens to the viscosity of the blood as a result of this?

A

Increased permeability

Exudation of protein rich fluid into tissues and tumour seen

Increased viscosity

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16
Q

Name an immediate early response chemical mediator seen in acute inflammation

A

Histamine

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17
Q

When does histamine begin its action in acute inflammation? Histamine is produced from which cells?

A

Immediately (first 30 mins)

Mast cells, basophils and platelets

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18
Q

Name 3 things that histamine causes…

A

Vascular dilatation
Increase in vascular permeability
Pain

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19
Q

Name some other chemical mediators of acute inflammation?

A

Leukotrienes, bradykinin

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20
Q

Fluid loss from vessels is determined by ___________ law - the balance of __________ and ___________ __________ pressures.

A

Starling’s

Hydrostatic
Colloid Osmotic

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21
Q

What effect will increased hydrostatic pressure in a vessel have on fluid flow to tissues?

What effect will increase colloid osmotic pressure in the interstitial have on fluid flow to tissues?

A

Increased fluid flow out of vessels

Increased fluid flow out of vessels

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22
Q

How does arteriolar dilatation seen in acute inflammation affect hydrostatic pressure in capillaries?

How does increased permeability of vessel walls seen in acute inflammation affect the protein content of the interstitial fluid?

What consequence can both of these factors result in?

A

Increased

Increased protein content (colloid osmotic pressure)

OEDEMA

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23
Q

The fluid in oedema can be either…

A

Transudate

Exudate

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24
Q

What is a transudate? What is an exudate?

Give an example of where each is seen.

A

Fluid in oedema that has the same protein content as plasma
Cardiac failure

Fluid in oedema that has a higher protein content than plasma
Only in inflammation

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25
Q

How does oedema affect lymphatic drainage?

A

Results in increased lymphatic drainage

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26
Q

Give 5 mechanisms by which vessels can become ‘leaky’

A 
Contraction of endothelial cells 
Cytoskeletal reorganisation 
Direct injury - e.g. Sunburn, chemicals
Leukocyte dependent injury 
Increased transcytosis
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27
Q

How does contraction of endothelial cells and cytoskeletal reorganisation result in leaky vessels?

Give an example of a chemical that causes contraction of endothelial cells

Give an example of a chemical that causes cytoskeletal reorganisation

A

Leads to gaps in the walls of vessels

Histamine, leukotrienes

Cytokines IL-1 and TNF

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28
Q

How does leukocyte dependent injury make blood vessels leaky?

A

Leukocyte produce toxic oxygen species and enzymes which damage the vessels

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29
Q

Give an example of a chemical that results in increased transcytosis?

A

VEGF

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30
Q

What is an important protein component of the protein rich exudate seen in acute inflammation?

A

Fibrin

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31
Q

What is the role of fibrin in the protein rich exudate seen in acute inflammation?

Where is this particularly important?

A

Forms a sticky meshwork to localise inflammation

Serosal surfaces - e.g. Pleural cavity, pericardium - so whole cavity isn’t filled with fluid

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32
Q

What is another term for a neutrophil? What is the appearance of these cells under the microscope?

A

Polymorph

Come in multiple shapes with multi-lobed nuclei

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33
Q

What type of blood cell is a neutrophil?

A

White blood cell - type of granulocyte

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34
Q

What is a granulocyte?

A

A WBC with secretory granules in its cytoplasm

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35
Q

What is the main inflammatory cell?

A

Neutrophil

36
Q

How do neutrophils get from within blood vessels to tissues to combat acute inflammation? (4 step process)

A

Margination
Rolling
Adhesion
Emigration

37
Q

Describe the margination process of neutrophils

A

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

38
Q

What happens to neutrophils after their margination around a blood vessel?

A

Rolling - roll along the endothelium, sticking to it intermittently

Adhesion - stick more avidly

Emigration of neutrophils into the tissue through the vessel wall

39
Q

What two things make it possible for the emigration of neutrophils through the blood vessel wall?

A

Relaxation of inter-endothelial junctions

Digestion of the vascular basement membrane

40
Q

How doe neutrophils move once inside the tissues?

A

By chemotaxis

41
Q

What is chemotaxis?

A

Movement along concentration gradients of chemoattractants

42
Q

Give 3 examples of chemotaxins for neutrophils? How do they work?

A

C5a
LTB4
Bacterial peptides

They bind to receptors on the neutrophils, resulting in rearrangement of cytoskeleton, production of pseudopod and movement.

43
Q

What do neutrophils do once in the tissue?

A

Primarily phagocytosis

44
Q

How are microorganisms recognised by neutrophils for phagocytosis?

A

Through the action of opsonins

45
Q

Give an example of an opsonin

A

C3B

Fc (fixed component of antibodies)

46
Q

Internalisation of a microorganism during phagocytosis is a result of what changes in the cell?

A

Changes to the cell cytoskeleton

47
Q

How is a secondary lysosome formed?

A

Fusion of phagosome with lysosome

48
Q

Phagocytosis can take place in neutrophils by which two mechanisms?

A

Oxygen dependent

Oxygen independent

49
Q

How does the oxygen dependent mechanism of phagocytosis in neutrophils work?

A

Produces superoxide and hydrogen peroxide

Produces HOCl*

50
Q

How does the oxygen independent mechanism of phagocytosis in neutrophils work?

A

Enzymes such as lysozyme and hydrolases
Bactericidal permeability increasing protein (BPI)
Cationic proteins

51
Q

What are some chemical mediators of acute inflammation, excluding neutrophils?

A

Proteases
Prostaglandins
Leukotrienes
Cytokines

52
Q

Where are proteases produced?

A

In the liver

53
Q

Prostaglandins and leukotrienes are both metabolites of…

A

Arachidonic acid

54
Q

Which cells produce chemokines/cytokines? Give an example of a cytokine/chemical?

A

WBCs

Interleukins, TNF-a

55
Q

What chemical mediators result in increased blood flow in vessels?

A

Histamine

Prostaglandins

56
Q

Which chemical mediators result in increased vascular permeability?

A

Histamine

Leukotrienes

57
Q

Which chemical mediators are important in neutrophil chemotaxis?

A

C5a, LTB4, bacterial peptides

58
Q

What are some important chemicals for opsonisation?

A

C3B, Fc

59
Q

How does exudation of fluid combat injury? (3)

A

Delivers plasma proteins (e.g. Inflammatory mediators) to area of injury
Dilutes toxins
Increases lymphatic drainage

60
Q

How does increased lymphatic drainage as a result of exudation of fluid combat injury?

A

It delivers microorganisms to phagocytes and antigens to the immune system

61
Q

How does infiltration of cells in acute inflammation combat injury?

A

Removes pathogenic organisms and necrotic debris

62
Q

How does vasodilation in acute inflammation help combat injury?

A

Increases delivery to the area and increases temperature

63
Q

How does pain and loss of function in acute inflammation combat injury?

A

Enforces rest and reduces chance of further traumatic damage

64
Q

What complications can result due to the swelling seen in acute inflammation?

A

Blockage of tubes - e.g. Bile ducts/small intestine

65
Q

What complications can result due to the exudate seen in acute inflammation?

A

Compression - e.g. Cardiac tamponade

66
Q

In what instances of acute inflammation is fluid lost from the body?

A

Burns

67
Q

What are some systemic consequences of acute inflammation?

A 
Fever 
Leukocytosis 
Acute phase response 
Changes in plasma concentration of acute phase proteins 
Shock
68
Q

What causes fever in acute inflammation?

A

Production of endogenous pyrogens e.g. IL-1 and TNF-a

69
Q

Give an example of an endogenous pyrogen?

Which household drug can be given to reduce fever?

A

IL-1, TNF-a, prostaglandins

Aspirin

70
Q

What is leukocytosis?

A

A high WBC level in FBC

71
Q

Bacterial infections are associated particularly with which types of WBC?

Viral infections are more associated with…

A

Neutrophils

Lymphocytes

72
Q

What causes the leukocytosis commonly seen in acute inflammation?

A

IL-1 and TNF-a which produce an accelerated release of WBCs from marrow

73
Q

What are features of the acute phase response?

A

Decreased appetite
Raised pulse rate
Altered sleep patterns

74
Q

Give an example of two acute phase proteins whose concentration changes in acute inflammation?

A

CRP

Fibrinogen

75
Q

What is shock? What causes it?

A

A clinical syndrome of systemic circulatory failure

The spread of microorganisms and toxins in the body

76
Q

What are 4 different outcomes after the development of acute inflammation?

A

Complete resolution
Continued acute inflammations with chronic inflammation
Chronic inflammation and fibrous repair
Death

77
Q

What happens to the exudate in resolution from acute inflammation? What happens to vessel permeability? What happens to fibrin produced? What happens to the neutrophils?

A

Drains into lymphatics

Returns to normal

Degraded by plasmin

Die, break up and carried away or phagocytosed

78
Q

Describe the half-life of mediators of acute inflammation?

A

Short half lives

79
Q

Bacterial meningitis can cause vascular __________ and reduce cerebral ____________

What part of the body does it affect?

A

Thrombosis

Perfusion

Meninges of the brain

80
Q

What is the causative organism for lobar pneumonia? List some symptoms. Can it be resolved?

A

Streptococcus pneumoniae

Worsening fever, dry cough, hypoxaemia, breathlessness

Yes completely if treated

81
Q

Why does the exudate seen in skin blisters appear relatively clear? What can cause skin blisters?

A

Inflammatory cell levels are low

Heat, sunlight, chemicals

82
Q

What are two other terms for an autopsy? Name three types of autopsy.

A

Post-mortem
Necropsy

Medicolegal
Forensic
Consent

83
Q

For which type of autopsies is no consent required?

A

Medicolegal

Forensic

84
Q

Name 4 parts of the body that are common causes of sudden death.

A

Head
Heart
Blood vessels
Lungs

85
Q

What is involved in an autopsy? (3)

A

History
External examination
Internal examination

Pathological Processes (10 decks)

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