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Pathology > Tissue response to injury ( 10% ) > Flashcards

Tissue response to injury ( 10% ) Flashcards

1
Q
  1. In acute inflammation, which events occur in the correct chronological order? (Remembered from 2000, 2004 exam.) p50
    (a) transient vasoconstriction, stasis of blood flow, increased permeability, vasodilation
    (b) transient vasoconstriction, increased permeability, vasodilation, stasis of blood flow
    (c) vasodilation, increased permeability, stasis of blood flow, neutrophil accumulation
    (d) neutrophil accumulation, vasodilation, increased permeability, stasis of blood flow
    (e) transient vasoconstriction, vasodilation, stasis of blood flow, endothelial gap formation in venules.
A

(c) vasodilation, increased permeability, stasis of blood flow, neutrophil accumulation

(prior to this all is transient vasoconstriction)

Increased permability -> increased concentration of RBC -> stasis (in conjunction with increased vessel lumen size)

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2
Q

In acute inflammation

  • a. A hallmark is reduced vascular permeability.
  • b. Vasodilation is a late manifestation.
  • c. Extravasation involves movement of leukocytes from interstitial tissue to the vessel lumen.
  • d. Chemotaxis is migration of leukocytes along a chemical gradient
  • e. Selectins have a minor role.
A

d. Chemotaxis is migration of leukocytes along a chemical gradient

  • a. A hallmark is increased vascular permeability.
  • b. Vasodilation is an early manifestation (follows very transietnt vasoconstriction, but begins immediately after injury)
  • c. Extravasation involves movement of leukocytes from the vessel lumen to interstitial tissue
  • e. Selectins have a crucial role in ‘rolling’ (attached to endothelial wall; cf integrins which are on WBC)
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3
Q

In acute inflammation which event occurs first

  • a. Arteriolar dilatation.
  • b. Arteriolar constriction.
  • c. Oedema.
  • d. Leucocyte migration.
  • e. Blood flow stasis.
A
  1. Arteriolar constriction (transient)
  2. Arteriolar dilatation
  3. Oedema
  4. Blood-flow stasis
  5. Leucocyte migration
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4
Q

The first vascular response to injury is

  • a. Slowing of the circulation
  • b. Venular dilation
  • c. Recruitment of vascular beds.
  • d. Capillary engorgement
  • e. Arteriolar vasoconstriction
A

e. Arteriolar vasoconstriction

“Vasodilation is one of the earliest manifestations of acute infl…first involves arterioles dilating and then results in opening of new capillary beds”

  1. Art. vasoconstrict.
  2. Recruitment of vascular beds
  3. Slowing of the circulation
  4. Capillary engorgment
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5
Q

leukocytes move into tissues from the vasculature (extravasation)…

  • a. by the action of actin and myosin
  • b. predominantly as monocytes on the first day post injury.
  • c. in response to C3b.
  • d. in response to the Fc fragment of IgG
  • e. largely in the arterioles.
A

a. by the action of actin and myosin

  • b. predominantly as neutrophils on the first day post injury, monocytes on the 2nd day
  • c. in response to C5a
  • d. Not in response to the Fc fragment of IgG as it is not a chemokine
  • e. largely in the Venules
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6
Q

Regarding leucocyte adhesion and transmigration during acute inflammation:

  • a. There is reduced binding of integrins.
  • b. Transmigration is mediated by E-selectin.
  • c. Leukocyte adhesion deficiency type II is associated with resistance to bacterial infection.
  • d. Leukocyte rolling is reduced.
  • e. There is initial redistribution of pre-formed adhesion molecules to the cell surface
A

e. There is initial redistribution of pre-formed adhesion molecules to the cell surface

  • a. There is increased binding of integrins.
  • b. Transmigration is mediated by PECAM on endoth. and WBC
  • c. Leukocyte adhesion deficiency type II is associated with susceptibility to bacterial infection
  • d. Leukocyte rolling is Increased
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7
Q

In acute inflammation

  • a. Vasoconstriction is the primary event
  • b. Direct injury is due to histamine.
  • c. Vascular leakage occurs mainly by formation of endothelial gaps in arterioles.
  • d. There is outpouring of a transudate due to increased vascular permeability.
  • e. Leukocyte dependent injury occurs mainly in arterioles
A

a. Vasoconstriction is the primary event

Very transient and followed by arteriole dilation, then recruitement of capillary beds

  • b. Direct injury is due to histamine (Histamine increases permeability by endo contraction)
  • c. Vascular leakage occurs mainly by formation of endothelial gaps in Venules
  • d. There is outpouring of an exudate due to increased vascular permeability
  • e. Leukocyte dependent injury occurs mainly in arterioles
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8
Q

. Phagocytosis

  • a. Occurs in 2 steps
  • b. C5a is an opsonin
  • c. IgM is a potent opsonin.
  • d. Bacterial killing occurs by mainly O2 dependent mechanisms
  • e. Doesn’t occur without opsonization.
A

d. Bacterial killing occurs by mainly O2 dependent mechanisms

  • a. Occurs in 3 steps - Recognition, engulfment, intracellular destruction
  • b. C3b is an opsonin
  • c. IgG is a potent opsonin.
  • e. Can occur without opsonisation, it is just slower
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9
Q

Regarding acute inflammation

  • Initial vasoconstriction is the result of histamine and nitric oxide
  • Stasis occurs due to vasodilatation and the larger caliber of vessels
  • Increased permeability leads to protein depleted plasma leaking into the tissue
  • Initial formation of endothelial gaps lasts for only 15-30 minutes
  • Cytokines (IL-1 and TNF) are responsible for the early permeability
A

Initial formation of endothelial gaps lasts for only 15-30 minutes

  • Venule endothelium contraction is the result of histamine, and vasodilation is the result of nitric oxide
  • Stasis occurs due to vasodilatation and the larger caliber of vessels as well as the increasing concentration of RBC due to exudate leaving the vessels -> increased viscosity. All combines to achieve engorgement of vessels with slow moving RBC (aka stasis)
  • Increased permeability leads to protein-rich exudate leaking into the tissue
  • Cytokines (IL-1 and TNF) are responsible for margination of WBC

(as effected by histamine)

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10
Q

Mononuclear phagocytes

  • Are the predominant cells in 3 day old wounds
  • Are common in liver, spleen and pancreas
  • Produce fibroblast growth factor
  • Secrete interferon Y
  • Have a half life of one day
A

Are common in liver, spleen and pancreas

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11
Q

Macrophages are derived from

  • Monocytes
  • T lymphocytes
  • B lymphocytes
A

Monocytes

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12
Q

With regard to the acute inflammatory response, which is the most common mechanism of vascular leakage?

  • a. Endothelial cell contraction
  • b. Junctional retraction
  • c. Direct injury
  • d. Leukocyte-dependent leakage
  • e. Regeneration endothelium
A

a. Endothelial cell contraction

(caused by histamine and occuring primarily in the venules)

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13
Q

In acute inflammation, all of the following are true EXCEPT:

  • a. There is contraction of endothelial cells
  • b. There is a mononuclear infiltrate
  • c. There is induction of adhesion molecules on endothelium
  • d. There is production of arachadonic acid metabolites
  • e. Cytokines induce a systemic acute phase response
A

b. There is a mononuclear infiltrate

(infiltate depends on initiator but is either neutrophil, lymphocyte, or eosinophil)

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14
Q

Cellular events in acute inflammation include all of the following EXCEPT:

  • a. Redistribution of preformed adhesion molecules to the cell surface of leukocytes
  • b. Adhesion and transmigration of leukocytes to endothelium
  • c. Leukocyte activation
  • d. Margination of macrophages to vessel walls
  • e. Extracellular release of lysosomal enzymes and products of arachidonic acid metabolism
A

d. Margination of macrophages to vessel walls

(margination of leucocytes primarily neutrophils)

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15
Q

Vascular changes in acute inflammation include:

  • a. Slowing of the circulation leading to leukocyte margination
  • b. Initial transient vasodilation of arterioles
  • c. Decreased hydrostatic pressure caused by vasodilation
  • d. Leakage of high protein fluid into vessels
  • e. Increased osmotic pressure within vessels
A

a. Slowing of the circulation leading to leukocyte margination

  • b. Initial transient vasoconstriction of arterioles
  • c. Decreased hydrostatic pressure caused by vasodilation (?increased due to RBC accumulation and stasis)
  • d. Leakage of high protein fluid into interstitial space
  • e. Increased osmotic pressure within vessels (?likely reduced due to loss of proteins and cells into the interstium)
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16
Q

Leukocyte extravasation occurs in the following order:

  • a. Activation, rolling, transmigration, adhesion
  • b. Rolling, activation, adhesion, immigration
  • c. Adhesion, rolling, activation, transmigration
  • d. Rolling, activation, adhesion, transmigration
  • e. Transmigration, adhesion, activation, rolling
A

d. Rolling, activation, adhesion, transmigration

(then migration through tissues via chemotaxis)

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17
Q

Regarding acute inflammation:

  • a. Occurs in apoptosis
  • b. Increased vascular permeability resulting in increased colloid osmotic pressure and reduced hydrostatic pressure
  • c. Leukocyte migration through blood vessels is required by binding to selectin and integrin receptors
  • d. Causes venule dilation but not arteriole dilation
  • e. Typically produces transudate
A

c. Leukocyte migration through blood vessels is required by binding to selectin and integrin receptors

  • a. Occurs in necrosis
  • b. Increased vascular permeability resulting in reduced colloid osmotic pressure and increased hydrostatic pressure (due to vasodilation)
  • d. Causes venule dilation AND arteriole dilation
  • e. Typically produces exudate
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18
Q

With regard to the leukocyte extravasation of the acute inflammatory response, which of the following is INCORRECT?

  • a. ELAM-1 is a selectin found on endothelium
  • b. E and P-selectins bind to oligosaccharides found on neutrophils and monocytes
  • c. L-selectin is found on neutrophils, monocytes and lymphocytes
  • d. ICAM-1 belongs to the immunoglobulin family of molecules, and is found on leukocytes.
  • e. VCAM-1 binds to integrins
A

d. ICAM-1 belongs to the immunoglobulin family of molecules, and is found on endothelium

(ICAM on endothelial surface binds Integrins on the WBC, causing firm adhesion)

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19
Q

Regarding chemical mediators of inflammation

  • a. Histamine is derived from plasma.
  • b. C3b is within macrophages
  • c. The kinin system is activated in platelets.
  • d. Nitric oxide is preformed in leukocytes.
  • e. Serotonin is preformed in mast cells.
A

e. Serotonin is preformed in mast cells.

(as per Nick: ‘Listed as correct but unequivocally false. R&C, “major sources are platelets and neuroendocrine cells (not mast cells)”’

(However Wikipedia lists serotonin as a product of mast cell degranulation)

  • a. Histamine is derived from mast cells
  • b. C3b is circulating
  • c. The kinin system is activated in the blood
  • d. Nitric oxide is formed by NO synthase, which is only activated after a 2nd messenger or a cytokineinendothelium and macrophages.
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20
Q

Leukotrienes play a role in all of the following EXCEPT:

  • a. Chemotaxis
  • b. Vasoconstriction
  • c. Platelet aggregation
  • d. Bronchospasm
  • e. Increased permeability
A

c. Platelet aggregation

Leukotrines are produced by mast cells and WBC

Cause leakiness, chemotaxis, WBC adhesion and attraction

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21
Q

. A preformed mediator of inflammation is:

  • a. Prostaglandin
  • b. Histamine
  • c. Leukotriene
  • d. Nitric oxide
  • e. Platelet activating factor
A

b. histamine

Serotonin also pre-formed

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22
Q

Interleukin 1 causes:

  • a. Neutropenia
  • b. Decreased sleep
  • c. Decreased prostaglandin synthesis
  • d. Increased collagen synthesis
  • e. Decreased leukocyte adherence
A

d. Increased collagen synthesis

  • a. Neutropenia
  • b. Decreased sleep
  • c. Decreased prostaglandin synthesis
  • e. Increased leukocyte adherence by increased selectin and integrin expression
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23
Q
  1. The alternative pathway of complement activation can be triggered by:
  • a. IgG antigen-antibody complexes
  • b. Properdin
  • c. Microbial surfaces
  • d. Lysosomal proteases
  • e. C5-9 Membrane attack complex
A

c. Microbial surfaces

IgG antigen-antibody complexes activate classic pathway

C5-9 MAC is an end-product of complement activation system

Lysosomal (or plasmin) proteases can generate C3a and C5a

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24
Q

Which factor ties together activation of the clotting cascade, kinins and the fibrinolytic system?

  • a. Stuart Factor
  • b. Prothrombin
  • c. Plasminogen
  • d. Factor XII
  • e. Kallikrein
A

d. Factor XII

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26
Q

Complement

  • Proteins are usually stored in an active state in lysosomal molecules.
  • Pathway is inhibited by C3 cleavage
  • C3 is the most abundant protein in the complement family
  • Activation by the classical pathway involves microbial surface antigens.
  • Cobra venom activates the lectin pathway.
A

C3 is the most abundant protein in the complement family

  • Proteins are usually circulating in inactive form
  • Pathway is activated by C3 cleavage
  • Activation by the classical pathway involves Antigen-Ig complex
  • Cobra venom activates the alternative pathway.
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27
Q

Regarding mediators of inflammation

  • TNF is a chemokine with chemoattractant properties
  • TNF contributes to cachexia of disease
  • TNF and IL-1 are produced mainly by activated leukocytes.
  • The systemic acute phase response is induced by MIP-1 and RANTES chemokines
  • PAF causes vasodilation when expressed at high levels
A

TNF contributes to cachexia of disease

  • TNF is a cytokine involved in WBC adhesion
  • TNF and IL-1 are produced mainly by activated macrophages
  • The systemic acute phase response is induced by MIP-1 and RANTES chemokines
  • PAF causes vasoconstriction when expressed at high levels (vasodilation at very low levels)
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28
Q

Histamine is involved in acute inflammatory responses and is released from mast cells. Which of the following statements is incorrect?

  • It is found in blood basophils, platelets and mast cells
  • It causes increased permeability of arterioles
  • It may be released by physical trauma
  • It causes constriction of large vessels
  • It acts on the microcirculation via H1 receptors
A

It causes constriction of large vessels

(only one I cannot find mentioned in R&C)

Histamine is released due to cross-linking of IgE expressed on the mast cell surface, physical trauma, or in response to amines such as morphine

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29
Q

Neutrophilia is generally caused by all of the following except

  • Inflammatory disease
  • Bacterial infection
  • Viral infection
  • Corticosteroids
  • Stress
A

Viral infection

(get a lymphophilia)

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30
Q

Regarding chemical mediators of inflammation

  • Histamine is derived from plasma
  • Serotonin is pre-formed in mast cells.
  • Nitric oxide is pre-formed in WBC
  • The kinin system is activated in platelets
  • C3b is within macrophages
A

Serotonin is pre-formed in mast cells.

  • Histamine is released from mast cells*
  • NO is formed by NO synthase, which is only activated after a 2nd messenger or a cytokine*
  • The kinin system is activated in plasma/blood*
  • C3b is circulating*
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31
Q

Regarding chemical mediators of inflammation

  • Histamine exerts pro-inflammatory effects mainly on venules
  • C5a, LTB4, IL-8 are chemotactic
  • Fever and pain are mediated by prostaglandins, IL-1, TNF and kinins
  • Oxygen metabolites are important in host defense
  • All of the above
A

All of the above

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32
Q

Platelet activating factor

  • a. Is produced by platelets
  • b. Induces bronchodilation
  • c. Increases vascular permeability
  • d. Decreases leukocyte adhesion
  • e. Is not produced by mast cells
A

c. Increases vascular permeability

Produced by mast cells, platelets, and WBC

Causes vasodilation, leakiness, chemotaxis, adhesion, pain, fever

33
Q

Chemical mediators of acute inflammation include all except

  • Nitric acid
  • PAF
  • Bradykinin
  • Serotonin
  • Adrenaline
A

Adrenaline

34
Q

In acute inflammation, opsonisation is not enhanced by

  • C3b
  • Lectins
  • Fc fragments of IgG
  • C5b
  • Latex beads
A

C5b

C5b breaks/joins into C6-9 to form Membrane Attack Complexes

35
Q
  1. Which of the following statements regarding prostaglandins is INCORRECT?
  • a. Prostacyclin and thromboxane A2 are synthesized from the same precursor
  • b. Leukocyte adhesion is mediated by thromboxane A2
  • c. Vasodilation is mediated by PGE
  • d. Vasoconstriction is mediated by LTD4
  • e. Chemotaxis is mediated by HETE
A

b. Leukocyte adhesion is mediated by thromboxane A2

TXA-2 constricts bronchial and vascular smooth muscle

It is generated in platelets by COX-1

TXA-2 aids haemostasis by platelet aggregation and vasoconstriction

36
Q
  1. With regard to chemical mediators of inflammation:
  • a. Are solely derived from plasma. Or cells
  • b. Leukotrienes are preformed mediators. Not pre-formed
  • c. Nitric oxide results in vasodilation
  • d. Source of serotonin is leukocytes. Platelets
  • e. Histamine results in vascular leakage
A

c. Nitric oxide results in vasodilation
e. Histamine results in vascular leakage

  • a. Can be derived from plasma OR cells
  • b. Leukotrienes are made de novo when required
  • d. Source of serotonin is platelets and mast cells
37
Q

Regarding chemical mediators of inflammation:

  • a. Histamine exerts its proinflammatory effects mainly on venules
  • b. C5a, LTB4, IL8 are chemotactic
  • c. Fever and pain are mediated by prostaglandins, IL1, TNF and kinins
  • d. Oxygen metabolites are important in host defence
  • e. All of the above
A

e. All of the above

38
Q

Vascular permeability in inflammation is increased by:

  • a. C3b and C3bI
  • b. C3b
  • c. C3a and C5a. via histamine release
  • d. C5-9
  • e. C3bI
A

c. C3a and C5a

(via histamine release)

C3b is involved in opsonisation

C5-9 are involved in Membrane Attack Complexes

39
Q

Pain during an inflammatory process is mediated by

  • NO
  • C3b
  • C5a
  • PAF
  • Bradykinin
A

Bradykinin

and prostaglandins

40
Q

Chemical mediators of inflammation include all except

  • C3a and C5a
  • Bradykinin
  • Histamine
  • Protein C
  • Serotonin
A

Protein C

41
Q

Which is true of chronic inflammation?

  • a. Macrophages have a half life of 5 days. Monocytes = 1 day, macrophages = months - years
  • b. It commonly follows acute inflammation. Can follow acute infl but evidently not commonly
  • c. Frequently resolves. Opposite
  • d. It is characterized by increased vascular permeability and oedema. Mononuclear infiltrate, tissue destruction and healing by connective tissue replacement
  • e. Has the same chemotactic factors as for acute inflammation
A

e. Has the same chemotactic factors as for acute inflammation

  • a. Macrophages have a half life of months-years. Monocytes = 1 day
  • b. It can follow acute inflammation, but not commonly
  • c. Infrequently resolves, is usually persistent
  • d. It is characterized by Mononuclear infiltrate, tissue destruction and healing by connective tissue replacement
42
Q

Chronic inflammation

  • a. Is characterized by prolonged duration and usually results in resolution
  • b. Is associated with structural changes in microvasculature leading to exudation of proteins
  • c. Is characterized by angiogenesis
  • d. Features infiltration by polymorphonuclear cells, mast cells and lymphocytes
  • e. Is usually associated with markedly symptomatic response to persistent infection by certain microorganisms
A

c. Is characterized by angiogenesis

  • a. Is characterized by prolonged duration and usually does not resolve
  • b. Is associated with mononuclear infiltrate, tissue destruction, and healing by connective tissue replacement (fibrosis and angiogenesis)
  • d. Features infiltration by mononuclear cells
  • e. Is usually associated with markedly symptomatic response to persistent infection by certain microorganisms (usually does not cause systemic response)
43
Q

Chronic inflammation

  • Most commonly follows acute inflammation
  • Demonstrates histological features indistinguishable from acute inflammation
  • Is a feature of many autoimmune diseases
  • When resolved will allow return to normal tissue architecture
  • Involves predominately monocytes
A

Is a feature of many autoimmune diseases

(inflammatory prompt is the body itself)

  • Most commonly follows acute inflammation (can but not commonly)
  • Demonstrates histological features indistinguishable from acute inflammation (wrong - mononuclear infiltrate, tissue destruction, healing by connective tissue replacement
  • When resolved will allow return to normal tissue architecture (wrong)
  • Involves predominately macrophages (monocytes activated once in the interstitium)
44
Q

In chronic inflammation the life span of tissue macrophages is closest to:

  • a. 4-8 hours
  • b. 1 day
  • c. 8 days
  • d. 2-4 weeks
  • e. 2 months
A

2 months

Monocytes 1 day

45
Q
  1. The epithelioid cells of follicular granulomas are:
  • a. Reticular
  • b. Fibroblasts
  • c. Modified macrophages
  • d. Plasma cells
  • e. Lymphocytes
A

Modified macrophages

46
Q

Chronic inflammation is characterized by all of the below except

  • Tissue destruction
  • Angiogenesis
  • Infiltration with neutrophils
  • Fibrosis
  • Increased tissue concentration of lymphocytes
A

Infiltration with neutrophils

(correct is infiltation with macrophages)

47
Q

Granulomatous inflammation can be induced by

  • Syphilis
  • Foreign body
  • Cat-scratch disease
  • Silicosis
  • All of the above
A

All of the above

48
Q
  1. Granulomatous inflammatory reactions:
  • a. can be caused by syphilitic infections
  • b. are a type II hypersensitivity reaction
  • c. predominantly contain eosinophils with a modified “epithelial like” appearance
  • d. are surrounded by natural killer cells
  • e. are not associated with inert foreign bodies
A

a. can be caused by syphilitic infections

  • b. are a form of chronic inflammation
  • c. predominantly contain activated macrophages with a modified “epithelial like” appearance (although a ‘collar’ of lymphocytes is described)
  • d. are surrounded by CD4 T cells
  • e. ARE associated with inert foreign bodies
49
Q

Regarding chronic inflammation all of the following are true EXCEPT:

  • a. it can be caused by persistent infections
  • b. it primarily involves tissue destruction
  • c. it may contribute to the formation of atherosclerosis
  • d. it involves mononuclear inflammatory cells
  • e. it can be caused by exposure to toxic agents
A

b. it primarily involves tissue destruction

(primarily involves mononuclear infiltrate but can also involve tissue destruction)

50
Q
  1. In chronic inflammation:
  • a. The most important cells are lymphocytes.
  • b. Mast cells are not involved
  • c. Is always associated with tissue damage
  • d. The most important cells are neutrophils
  • e. Caseous necrosis is only seen in tuberculosis
A

c. Is always associated with tissue damage

  • a. The most important cells are MACROPHAGES
  • b. Mast cells are not involved
  • d. The most important cells are macrophages (and lymphocytes)
  • e. Caseous necrosis is only seen in tuberculosis
51
Q

Granulomatous inflammation

  • a. May sometimes be a component of the acute inflammatory response
  • b. Indicates the presence of tuberculosis
  • c. Consists in part of microscopic aggregates of transformed lymphocytes
  • d. Is always associated with the presence of giant cells
  • e. May result from non-immune mechanisms
A

e. May result from non-immune mechanisms

52
Q
  1. The first vascular response to injury is
  • (a) slowing of the circulation
  • (b) venular dilatation
  • (c) recruitment of the vascular beds
  • (d) capillary enlargement secondary to arteriolar dilation
  • (e) arteriolar vasoconstriction
A

(e) arteriolar vasoconstriction

Then…

  1. capillary enlargement secondary to arteriolar dilation
  2. venular dilatation
  3. slowing of the circulation
53
Q
  1. The first event in acute inflammation is (2000, 2006)
  • (a) arteriolar vasodilation
  • (b) increased permeability
  • (c) diapedesis
  • (d) arteriolar vasoconstriction
  • (e) stasis
A

(d) arteriolar vasoconstriction
2. vasodilation
3. increased permeability
4. increased viscosity
5. stasis
6. .. diapedesis later

54
Q
  1. Leukocytes move into the tissues from the vasculature (extravasation)
  • (a) by the action of actin and myosin
  • (b) predominantly as monocytes on the first day post injury
  • (c) in response to C3b
  • (d) in response to the Fc fragment of IgG
  • (e) largely in the arterioles
A

(a) by the action of actin and myosin

by migration, as integrins (leukocytes) and selectins (endothelial cells) cause adhesis

predominantly as neutrophils on the first day post injury, monocytes on day 2

Chemotaxis occurs in response to endogenous (C5a, IL-8, lipoxygenase pathway) and exogenous (bacterial antigens)

C3b and Fc of IgG are opsonins and cause activation and phagocytosis

Migration occurs largely in the venules

55
Q
  1. Regarding the chemical mediators of inflammation
  • (a) histamine is derived from plasma
  • (b) C3b is within macrophages
  • (c) the kinin system is activated in platelets
  • (d) nitric oxide is preformed in leukocytes
  • (e) Serotonin is preformed in mast cells
A

(e) Serotonin is preformed in mast cells

Histamine is widely distributed in tissues and released from basophils and platelets, in addition to mast cells

C3b is an activated complement fragment, and is present in the plasma

Platelets contain α granules containing fibrinogen, fibronectin, factor V, VIII, PDGF, TGF-β; δ granules contain ATP, ADP, serotonin, histamine, and adrenaline, and do not have a role in the kinin system.

nitric oxide is released on activation of leukocytes, by increases in intracellularcalcium

56
Q
  1. Regarding the complement cascade which of the following statements is true? (2004, 2006)
  • (a) the alternative pathway is stimulated by antigen-antibody interaction
  • (b) C5a is split to C5b.
  • (c) C5a activates the lipooxygenase pathway of arachidonic acid metabolism in neutrophils.
  • (d) C3bBb inhibits the final common pathway
  • (e) Microbial surfaces initiate the classical pathway of the complement cascade.
A

(c) C5a activates the lipooxygenase pathway of arachidonic acid metabolism in neutrophils.

The Classical pathway is initiated by antigen-antibody interaction

The alternative pathway is intiated by microbial surface polysaccharides

C3bBb splits C3 -> C3b

57
Q
  1. Regarding the kinin cascade (2004)
  • (a) Kallikrein feeds back to activate factor XI, and amplifies the clotting cascade
  • (b) activates the complement cascade via the lectin pathway
  • (c) Kallikrein directly cleaves fibrin
  • (d) Bradykinin is formed from kallikrein acting on HMWK
  • (e) Bradykinin amplifies its own production by cleaving prekallikrein to active kallikrein
A

(d) Bradykinin is formed from kallikrein acting on HMWK

Thrombin cleaves fibrinogen to fibrin, plasmin splits fibrin

Kallikrein activates plasminogen to plasmin, which cleaves fibrin

(a) Kallikrein feeds back to activate factor XII, and amplifies the clotting cascade

58
Q
  1. Bradykinin (2006)
  • (a) causes smooth muscle dilatation
  • (b) kallikrein causes prohormone degradation to produce bradykinin
  • (c) in inhibited by Hageman factor
  • (d) ameliorates pain
  • (e) is a potent vasoconstrictor
  • (x) is factor 12
A

(b) kallikrein causes prohormone degradation (of HMWK) to produce bradykinin

Bradykinin causes vascular dilation and non-vascular smooth muscle contraction (ie gut and bronchioles). ACEi lead to increased bradykinin levels, and the cough is a side effect of that.

Causes vasodilation via NO

Is produced by Hageman factor (Factor XII), which activates prekallikrein to kallikrein, which then converts HMWK to bradykinin

59
Q
  1. Which of the following is involved in the initiation of the clotting cascade, complement and kinin systems? (2004)
  • (a) Hageman factor (XII)
  • (b) factor VII
  • (c) antigen-antibody complex
  • (d) Tissue factor
  • (e) Platelet activating factor
A

(a) Hageman factor (XII)

  • [Kinen = activates prekallikrein, kallikrein] activates [fibrynolytic sytstem: plasminogen to plasmin, which can then change C3 to C3a]. [Clotting: XII activates the intrinsic clotting pathway.]*
  • Factor VII activates extrinsic pathway*
  • Antigen-antibody complexes activate alternative pathway of complement*
  • PAF stimulates broncho/vasodilation*
60
Q
  1. Which of the following immune cell is unable to phagocytose
  • (a) neutrophils
  • (b) eosinophils
  • (c) macrophages
  • (d) T-cells
  • (e) monocytes
A

(d) T-cells

61
Q
  1. The most common peripheral circulating lymphocyte is the (2006)
  • (a) B-cell
  • (b) T-cell
  • (c) Macrophage
  • (d) Natural killer cell
  • (e) Polymorphic nucleocyte
A

(b) T-cell (75% in peripheral circulation)

B-cell (25%)

Macrophage, NK cell, PMN are not lymphocytes

62
Q
  1. Macrophages are derived from
  • (a) monocytes
  • (b) T cells
  • (c) B cells
  • (d) Eosinophils
  • (e) Plasma cells
A

Monocytes

Are non-activated and circulating

Monocytes in tissues/the interstitium are macrophages

63
Q
  1. Macrophages may secrete
  • (a) histamine
  • (b) serotonin
  • (c) prostaglandins
  • (d) oxygen free radicals
  • (e) none of the above
A

(c) prostaglandins

‘are produced by mast cells, macrophages, endothelial cells, and many other cell types…’ R&C

  • (a) histamine (mast cells, basophils, platelets)
  • (b) serotonin (platelets)
  • (d) oxygen free radicals (?? WBC in general)
64
Q
  1. Regarding Chronic inflammation, which is correct? (2006)
  • (a) it characterised by hyperaemia, oedema, and leukocyte infiltration
  • (b) monocytes use the same chemotactic pathways as neutrophils
  • (c) it is always preceded by acute inflammation
  • (d) most frequently results in resolution
  • (e) angiogenesis is not a feature
A

(b) monocytes use the same chemotactic pathways as neutrophils

Characterised by mononuclear infiltrate, tissue destruction, and healing by connective tissue replacement

Sometimes preceded by acute inflam.

Does not often resolve

Angiogenesis a prominent feature

65
Q
  1. Regarding chronic inflammation, which is correct?
  • (a) Macrophages have a half-life of 5 days
  • (b) it is always preceded by acute inflammation
  • (c) unlike acute inflammation, lymphocytes do not play a major role
  • (d) prolonged exposure to toxins such as silica causes repeated bouts of acute inflammation, rather than the chronic type
  • (e) attempts at healing are evident
A

(e) attempts at healing are evident

Macrophages have a half life of a several months-years

Not often preceded by acute inflammation

(c) unlike acute inflammation, lymphocytes play a role in cell-mediated reactions, and the production of immunoglobulin. They also stimulate macrophages, and macrophages stimulate them back, propagating chronic inflammation

Prolonged exposure to toxins such as silica causes chronic inflammation

66
Q
  1. Regarding chronic inflammation which of the following is FALSE? p79
  • (a) It is associated with persistent infections
  • (b) It involves attempts at repair, rather than just tissue destruction
  • (c) It may contribute to the formation of atherosclerosis
  • (d) It can be caused by exposure to toxic agents
  • (e) It involves mononuclear inflammatory cells
A

All are true, as per R&C:

‘Chronic inflammation is a response of prolonged duration (weeks or months) in which inflammation, tissue injury, and attempts at repair coexist, in varying combinations.’

Persistent inflammation, hypersensitivity reactions, prolonged exposure to potentially toxic agents (including silica, and endogenous cholesterol leading to atherosclerosis.

Characterised by infiltration with mononuclear cells, tissue destruction, and attempts at healing

67
Q
A
68
Q

Removal of sutures from a wound at 7 days coincides with a wound strength of

  • 1% of unwounded skin strength
  • 10% of unwounded skin strength
  • 50% of unwounded skin strength
  • 75% of unwounded skin strength
  • 100% of unwounded skin strength
A

10% of unwounded skin strength

69
Q

With reference to wound healing

  • Wound regain 70-80% normal strength by 3/12
  • Zinc is essential for the synthesis of collagen.
  • Granulation tissue represents overproduction of collagen.
  • Intercurrent glucocorticoid therapy may assist in the reparative process.
  • At the end of the first week, wound strength is about 25% dependent largely on surgical suturing.
A

Wound regain 70-80% normal strength by 3/12

(which may not improve for life)

  • Zinc is essential for the synthesis of MMPs.
  • Fibrosis represents overproduction of collagen.
  • Intercurrent glucocorticoid therapy will disrupt healing, may lead to fibrosis
  • At the end of the first week, wound strength is about 10%
70
Q

Regarding wound healing

  • Strength at the end of the first week is 50%
  • Myofibroblasts contribute to wound contraction
  • Epithelial closure in healing by primary intention occurs after the 3rd day
  • Macrophages are the 1st cells involved in healing
  • Collagen deposited early in granulation tissue is type I
A

Myofibroblasts contribute to wound contraction

  • Strength at the end of the first week is 10%
  • Epithelial closure in healing by primary intention occurs at about 24-48 hours
  • Neutrophils are the 1st cells involved in healing, within 24 hours. About 72 hours macrophages arrive and begin to lay down granulation tissue such as collagen
  • Collagen deposited early in granulation tissue is not type I (this is found in bone etc. Type 4 found in basement membranes)
71
Q

Wound healing

  • Occurs by secondary intention in surgical wounds
  • Is accelerated by glucocorticoids
  • Achieves maximal wound strength at 2 weeks
  • Does not depend on site or size of wound
  • Occurring by secondary intention involves abundant granulation tissue
A

Occurring by secondary intention involves abundant granulation tissue

  • Occurs by first / primary intention in surgical wounds
  • Is slowed by glucocorticoids
  • Achieves maximal wound strength at 3 months (about 75-80% of normal skin)
  • Does depend on site or size of wound
72
Q

with regard to wound healing

  • macrophage infiltration occurs at 24 hours
  • wound strength is 25% of normal by end of the 1st week
  • type I collagen is replaced by type III collagen
  • neovascularisation is maximal at day 5
  • all of the above
A

neovascularisation is maximal at day 5

  • macrophage infiltration occurs at 72 hours
  • wound strength is 10% of normal by end of the 1st week
  • type I collagen is replaced by type III collagen (wrong - type 1 is in bone and hard tissue, type 3 in hollow organs)
73
Q

concerning the repair of a well opposed clean surgical wound

  • there is an initial inflammatory response
  • 15% of original tissue strength is attained at 1 week
  • granulation tissue does not occur
  • new collagen begins to accumulate after the 1st week
  • dermal appendages destroyed by the incision usually recover.
A

there is an initial inflammatory response

  • 10% of original tissue strength is attained at 1 week
  • granulation tissue does occur, but on a lesser scale than 2’ closure
  • new collagen begins to accumulate after 72 hours (as they are laid down by macrophages)
  • dermal appendages destroyed by the incision never recover (both 1’ and 2’ union)
74
Q

In healing by primary intention

  • There is a large tissue defect
  • The tissue defect cannot be reconstituted
  • It involves excessive granulation tissue
  • An epithelial spur forms on the first day
A

An epithelial spur forms on the first day

75
Q
  1. In healing by primary intention (2006)
  • (a) there is a large tissue defect
  • (b) the tissue defect cannot be reconstituted (is only partially reconstituted)
  • (c) an epithelial spur occurs on the first day
  • (d) there is extensive development of granulation tissue
  • (e) There is a marked degree of wound contraction
A

(c) an epithelial spur occurs on the first day

Technically at 24-48 hours

  1. 0-24 hours, neutrophils appear at the edge of the incision
  2. 24-48 hours epithelial spur
  3. day 3 macrophages replace neutrophils, granulation invasion, vertical collagen, does not bridge cut
  4. day 5 Incision filled with granulation tissue, neovascularisation maximal, oedema disappears at
  5. week 2 proliferation of fibroblasts, regression of vessels, accumulation of collagen 6. week 4 cellular connective tissue. No inflammatory cells. Dermal appendages permanently lost. Months until maximal strength is obtained.
    The main differences between primary and secondary intention healing is:
  • Inflammatory response more intense: More damage, more inflammation
  • Larger amounts of granulation tissue are formed
  • Wound contraction is the most distinguishing feature, with the actions of myofibroblasts
  • (a) there is a large tissue defect (secondary intention)
  • (b) the tissue defect cannot be reconstituted (is only partially reconstituted) (secondary intention)
  • (d) there is extensive development of granulation tissue(secondary intention)
  • (e) There is a marked degree of wound contraction(secondary intention)
76
Q
  1. Following a surgical wound the next thing to happen after clot formation is
  • (a) clot breakdown
  • (b) neutrophil migration to the incision edge
  • (c) an epithelial spur develops
  • (d) contraction of the wound edge
  • (e) macrophage migration
A

(b) neutrophil migration to the incision edge

(within 24 hours)

Epithelial spur develops at 24-48 hours

Macrophage invasion at 72 hours

Contraction of the wound edge occurs in 2’ healing

77
Q
  1. What is the second stage of healing by secondary intention?
  • (a) neutrophils appear at the margins of the clot
  • (b) epithelial cells move from the wound edges (with little proliferation)
  • (c) granulation tissue invasion of the wound space
  • (d) filling of the incisional space with granulation tissue
  • (e) proliferation of fibroblasts
A

(b) epithelial cells move from the wound edges (with little proliferation)

78
Q
A

Pathology (15 decks)

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