ACUTE INFLAMMATION- Vascular events

ACUTE INFLAMMATION- Vascular events

Q. 1

All are `celsus’ signs of inflammation except

 A

Pain

 B

Swelling

 C

Cyanosis

 D

Redness

Q. 1

All are `celsus’ signs of inflammation except

 A

Pain

 B

Swelling

 C

Cyanosis

 D

Redness

Ans. C

Explanation:

Ans. is ‘c’ i.e., Cyanosis

Inflammation

  • “Inflammation is a series of molecular and cellular responses to eliminate foreign agents or damaged (necrotic) cells and to promote repair of damaged tissues”.
  • Inflammation is fundamentally a protective response, the purpose of which is to destroy the damaging agent, initiate repair processes and return the damaged tissue to useful function.
  • In the absence of inflammation, wounds and infection will never heal and progressive destruction of the tissues would compromise the survival of organisms.
  • However, inflammation and repair may be potentially harmful, i.e., inflammation can damage healthy host tissues also e.g., in RA, interstitial lung fibrosis, atherosclerosis.
  • Inflammation is divided into acute and chronic patterns : ‑

1. Acute inflammation

0 Rapid in onset

  • Of relatively short duration.
  • Main characteristics are the exudation of fluid & plasma proteins (edema) and the emigration of neutrophils.
  • Cardinal signs of inflammation are characteristic of acute inflammation.
  • Celsus’ four cardinal signs of inflammation are –

i)

Rubor

—>

Redness (due to vasodilatation of small blood vessels)

ii)

Tumor

 

Swelling (due to exudation of fluid)

iii)

Color

—>

Heat (due to increased blood flow i.e., hypermia which is caused by vasodilatation).

iv)

Dolor

—>

Pain (Due to stretching of tissue from edema and also from chemical mediators,

bradykinin)

  • A fifth clinical sign was added later by Virchow

v) Functio laesa —> Loss of function

2. Chronic inflammation

  • Slow in onset
  • Of longer duration
  • Characterized by presence of lymphocytes & macrophages the proliferation of blood vessels, fibrosis and tissue necrosis.
  • Signs of acute inflammation (i.e., Cardinal signs of inflammation) are not present.

Q. 2

In acute inflammation due to the contraction of endothelial cell cytoskeleton, which of the following results –

 A

Delayed transient increase in permeability

 B

Early transient increase in permeability

 C

Delayed permanent increase in permeability

 D

Early permanent increase in permeability

Q. 2

In acute inflammation due to the contraction of endothelial cell cytoskeleton, which of the following results –

 A

Delayed transient increase in permeability

 B

Early transient increase in permeability

 C

Delayed permanent increase in permeability

 D

Early permanent increase in permeability

Ans. B

Explanation:

Ans. is ‘b’ i.e., Early transient increase in permeability

Increased vascular permeability

o The hallmark of acute inflammation is increased vascular permeability

The following mechanisms have ben proposed for increased permeability.

i) Formation of endothelial gaps in venules (immediate transient response)

  • This is the most common mechanism of vascular leakage and is caused due to the mediators such as histamine, bradykinin, leukotrienes, neuropeptide sustance
  • Classically this type of leakage affects venules, leaving capillaries and arterioles unaffected.
  • The precise reason for this restriction to venules is uncertain, it may be because there is greater density of receptors for mediators in venular endothelium.
  • Binding of mediators such as histamine to their receptors on endothelial cells activate intracellular signaling pathways that lead to phosphorylation of contractile and cytoskeletal proteins such as myosin.
  • These proteins contract leading to contraction of endothelial cells and separation of intercellularjunction.
  • Thus the gaps in the vascular endothelium are largely intercellular or close to the intercellular junctions.
  • This type of leakage occurs rapidly after exposure to the mediator and is usually reversible and short lived (15-30 minutes), it is thus known as immediate transient response.
  • Cytokines such as interleukin-1 (IL-1), tumour necrosis factor (TNF) and interferon y also increase vascular permeability by inducing a structural reorganization of the cytoskeleton such that the endothelial cells retract from one another.
  • In contrast to the histamine effect, the cytokine induced response is somewhat delayed (4-6 hrs) and long lived (24 hrs or more).

Direct endothelial injury resulting in endothelial cell necrosis and detachment (immediate sustained response)

  • This effect is usually encountered in necrotizing injuries and is due to direct damage to the endothelium by injurious stimulus e.g severe burns or lytic infections.
  • The reaction is known as immediate sustained response because the leakage starts immediately after the injury and is sustained at high levels for several hours until the damaged vessels are thrombosed or repaired. o All levels of microcirculation are affected including venules, capillaries and arterioles.

iii) Delayed prolonged leakage

  • This is curious but relatively common type of increased permeability that begins after a delay of 2-12 hours, lasts for several hours or even days and involves venules as well as capillaries.
  • This type of leakage is caused by mild to moderate thermal injury, X-ray radiation or ultraviolet radiation and certain bacterial toxins.
  • It is caused either by direct effect of injurious agent or by cytokine mediated endothelial retraction.

iv) Leucocyte mediated endothelial injury

  • Leucocytes adhere to endothelium relatively early in inflammation.
  • These leucocytes may be activated releasing toxic oxygen species and proteolytic enzymes which then cause endothelial injury or detachment.
  • This type of leakage affects venules (mostly); pulmonary & glomerular capillaries.

v) Increased transcytosis across the endothelial cytoplasm

  • Transcytosis occurs across channels consisting of clusters of interconnected uncoated vesicles and vacuoles called the vesiculovacuolar organelle, many of which are located close to intercellular junctions.
  • It usually occurs in venules.

vi) Leakage from new blood vessels

  • During repair formation of new vessels occur (angiogenesis)
  • New vessel sprouts, remain leaky until the endothelial cells mature.

Q. 3

Rubor in inflammation is due to –

 A

Dilation of arterioles

 B

Increased vascular permeability

 C

Increased viscocity of blood

 D

Edema

Q. 3

Rubor in inflammation is due to –

 A

Dilation of arterioles

 B

Increased vascular permeability

 C

Increased viscocity of blood

 D

Edema

Ans. A

Explanation:

Ans. is ‘a’ i.e., Dilation of arterioles

Quiz In Between


Q. 4

The 4 classical features of inflammation are described by –

 A

Celsus

 B

Hippocrates

 C

Aristotle

 D

Galen

Q. 4

The 4 classical features of inflammation are described by –

 A

Celsus

 B

Hippocrates

 C

Aristotle

 D

Galen

Ans. A

Explanation:

Ans. is ‘a’ i.e., Celsus


Q. 5

First change seen in acute inflammation is:

September 2009

 A

Increased permeability

 B

Vasodilation

 C

Neutrophil migration

 D

Vasoconstriction

Q. 5

First change seen in acute inflammation is:

September 2009

 A

Increased permeability

 B

Vasodilation

 C

Neutrophil migration

 D

Vasoconstriction

Ans. D

Explanation:

Ans. D: Vasoconstriction

Cardinal signs:

  • Rubor (redness) due to dilatation of arterioles
  • Calor (heat)
  • Dolor (pain) due to pressure on nerve endings by edema fluid and chemical mediator bradykinine
  • Tumor (swelling) due to edema.
  • Functio laesa (loss of function) due to inhibition of movement by pain and tissue necrosis.

Q. 6

Increased vascular permeability in acute inflammation is due to ‑

 A

Histamine

 B

IL 2

 C

TGF beta

 D

FGF

Q. 6

Increased vascular permeability in acute inflammation is due to ‑

 A

Histamine

 B

IL 2

 C

TGF beta

 D

FGF

Ans. A

Explanation:

Ans. is ‘a’ i.e., Histamine

Quiz In Between


Q. 7

The role of bradykinin in process of inflammation is

 A

Vasoconstriction

 B

Bronchodilation

 C

Pain

 D

Increased vascular permeability

Q. 7

The role of bradykinin in process of inflammation is

 A

Vasoconstriction

 B

Bronchodilation

 C

Pain

 D

Increased vascular permeability

Ans. D

Explanation:

Ans. d. Increased vascular permeability

  • The role of bradykinin in process of inflammation is to increase vascular permeability.
  • “Bradykinin increases vascular permeability and causes contraction of smooth muscle, dilation of blood vessels, and pain when injected into the skin.”- Robbins 8/e p65

Kinins

  • Kinins are vasoactive peptides derived from plasma proteins, called kininogens, by the action of specific proteases called kallikreins.
  • The kinin and coagulation systems are also intimately connected.
  • The active form of factor XII, factor XIIa, converts plasma prekallikrein into an active proteolytic form, the enzyme kallikrein, which cleaves a plasma glycoprotein precursor, high-molecular-weight kininogen, to produce bradykinin
  • Bradykinin increases vascular permeability and causes contraction of smooth muscle, dilation of blood vessels, and pain when injected into the skinQ.
  • These effects are similar to those of histamine.
  • The action of bradykinin is short-lived, because it is quickly inactivated by an enzyme called kininase.
  • Any remaining kinin is inactivated during passage of plasma through the lung by angiotensin-converting enzyme.
  • Kallikrein itself is a potent activator of Hageman factor, allowing for autocatalytic amplification of the initial stimulus.
  • Kallikrein has chemotactic activity, and it also directly converts CS to the chemoattractant product C5aQ.

Q. 8

Sequence of events in acute inflammation ‑

 A

Vasodilatation  → Stasis  → Transient vasoconstriction  → Increased permeability

 B

Transient vasoconstriction → Stasis  → Vasodilatation → Increased permeability

 C

Transient vasoconstriction → Vasodilatation  → Stasis  → Increased permeability

 D

Transient vasoconstriction  →Vasodilatation  → Increased permeability  → Stasis

Q. 8

Sequence of events in acute inflammation ‑

 A

Vasodilatation  → Stasis  → Transient vasoconstriction  → Increased permeability

 B

Transient vasoconstriction → Stasis  → Vasodilatation → Increased permeability

 C

Transient vasoconstriction → Vasodilatation  → Stasis  → Increased permeability

 D

Transient vasoconstriction  →Vasodilatation  → Increased permeability  → Stasis

Ans. D

Explanation:

Ans. is ‘d’ i.e., Transient vasoconstriction  → Vasodilatation → Increased permeability  → Stasis 


Q. 9

Increased permeability in acute inflammation is due to all except ‑

 A

Cell contraction

 B

Endothelial injury

 C

Lytic enzymes

 D

Cytokines

Q. 9

Increased permeability in acute inflammation is due to all except ‑

 A

Cell contraction

 B

Endothelial injury

 C

Lytic enzymes

 D

Cytokines

Ans. C

Explanation:

Ans. is ‘c’ i.e., Lytic enzymes 


Q. 10

Increased permeability in acute inflammation is due to

 A

Histamine

 B

IL-2

 C

TGF-(3

 D

FGF

Q. 10

Increased permeability in acute inflammation is due to

 A

Histamine

 B

IL-2

 C

TGF-(3

 D

FGF

Ans. A

Explanation:

Ans. is ‘a’ i.e., Histamine 

  • Formation of endothelial gaps in venules, i.e. immediate transient response is the most common mechanism causing increased vascular permeability in acute inflammation.
  • Mediators involved in this mechanism are :-
  • Immediate (more important) : Histamine, bradykinin, leukotrienes, neuropeptide substance P.
  • Somewhat delayed: IL-1, TNF, IFN-y

Quiz In Between



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