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Pathology > Lecture 3- Acute Inflammation > Flashcards

Lecture 3- Acute Inflammation Flashcards

1
Q

Inflammation types?

A

Acute and chronic

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2
Q

What is inflammation?

A

Response of living tissue to injury

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3
Q

What does it mean to say acute inflammation is innate and stereotyped?

A

It is the same very time

Adaptive immune system is tailored to toxic insult

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4
Q

What is exudate?

A

Mass of cells and fluid that leaks out of vessel during inflammation

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5
Q

What causes inflammation?

A

Anything that damages body including trauma, hypersensitivity and microbes

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6
Q

What are the 5 clinical signs?

A

Rubor= redness

Tubor= swelling

Dolor= pain

Calor= heat

Loss of function

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7
Q

What changes occur in blood vessels during inflammation?

A

Vascular- changes in blood flow and movement of fluid into tissue

Cellular- movement of inflammatory cells into tissue

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8
Q

How doe

S inflammation change blood flow?

A

Initial transient vasoconstriction

Vasodilation

Permeability increased and oedema

Red cell stasis as blood more viscous in vessels

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9
Q

What changes in vessels and surrounding tissue does inflammation cause?

A

Changes in blood flow

Movement of fluid into tissue

Infiltration of inflammatory cells into tissue

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10
Q

How does movement of fluid into tissues work in inflammation?

A

Governed by Starlings law.

Hydrostatic pressure is greater than oncotic pressure. Vasodilation and increased vessel permeability also help.

Results in oedema and tumor.

Fluid movement out of vessel leads to increased blood viscosity and red cell stasis.

This stasis helps later with tissue infiltration by inflammatory cells

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11
Q

What are the types of interstitial fluid?

A

Exudates and transudate.

Exudate formed in acute inflammation. Protein rich, increased vascular permeability

Transudate occurs in heart failure, liver failure etc where blood pools or lacks proteins etc. Blood pooling increases hydrostatic pressure forcing blood out of vessel. Decreased protein content moves oncotic pressure outside vessel and draws fluid out

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12
Q

How is vascular permeability increased?

A

Histamine causes endothelial contraction and gaps.

Direct injury eg toxic burn

Leukocyte injury

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13
Q

Primary WBC involved in inflammation?

A

Neutrophil

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14
Q

How do neutrophils leave vessel and enter tissue?

A

Increased blood viscosity reduces flow. Neutrophils slow down and line up at the edge of vessel wall known as margination, then roll, then adhere and then undergo emigration through vessel wall.

Chemotaxis leads them to pathogens

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15
Q

What molecules increased in inflammation help neutrophils emigrate into tissues?

A

Selectins on the endothelial surface and integrins on the surface of the neutrophils

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16
Q

How do neutrophils move through the interstitium?

A

Chemotaxis through chemoattractants

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17
Q

How does oedema limit damage?

A

Dilutes toxins

Increases lymphatic drainage and toxin removal. Delivers antigens to lymph nodes for adaptive immune response

Brings plasma proteins to injury site (inflammatory mediators and immunoglobulin)

Brings fibrin which creates mesh (pale yellow stuff indicates healing)

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18
Q

What are immunoglobulin?

A

Antibodies (produced by B lymphocytes)

19
Q

How do inflammatory cells limit damage?

A

Remove necrotic tissue

Destroy pathogens

Release chemical mediators which regulate further inflammation

Stimulate pain which encourages rest and prevents further damage

20
Q

What are chemical mediators?

A

Vast array of chemicals that contribute to inflammatory process. released by endothelial cells, inflammatory cells etc

21
Q

Some chemical mediators at each step?

A

Vasodilation- serotonin, histamine, nitric oxide, prostaglandins which are produced in response to pyrogens

Vascular permeability increase- histamine, bradykinins

Chemotaxis- bacterial peptides

Fever- prostaglandins

Pain- bradykinin, substance P, prostaglandins

22
Q

Why is antihistamine given for allergy?

A

Because it prevents histamine from causing vasodilation and the inflammatory response

23
Q

Local complications of infection?

A

Swelling- blockage of tubes of and ducts eg bile duct

Loss of fluid- burns release exudate

Exudate- compresses organs eg cardiac temponade in pericarditis

Pain and function loss- muscle atrophy

24
Q

Systemic complications of infection?

A

Fever- caused by prostaglandins stimulated by pyrogens which act on hypothalamus

NSAIDs- prevent prostaglandin synthesis eg aspirin and ibuprofen

Leucocytosis- increased lymphocytes and neutrophils

Protein release from inflammatory cells eg CRP used as indicator for infection

Acute phase response eg tiredness, lack of appetite, tachycardia and lack of sleep etc

Septic shock- huge chemical mediator release, systemic vasodilation, tachycardia and hypotension, multi organ failure and death

25
Q

How can you tell if an infection is bacterial or viral?

A

Neutrophils will increase in bacterial infection

Lymphocytes will increase in viral infection

26
Q

What is CRP used for?

A

Protein released by cells during infection. Used as a clinical marker of infection and will be highly elevated in sepsis

27
Q

What is malaise?

A

A general feeling of illness and discomfort with a cause that’s hard to identify

28
Q

How does septic shock lead to death?

A

Huge chemical mediator release- widespread vasodilation- tachycardia and hypotension- multi organ failure- death

29
Q

What is sequelae?

A

Condition or what happens as a consequence of a previous condition or injury

30
Q

What happens with complete resolution?

A

Neutrophils no longer marginate, vascular permeability returns to normal, vessel diameter returns to normal, fibrin mesh degraded, exudate drained away, neutrophils die, mediators degraded and damaged tissue may be able to regenerate if architecture reserved

31
Q

What does citis mean?

A

Acute inflammation

32
Q

What can happen with appendicitis?

A

Lumen is blocked by a cancer or faeces. Appendix is full of bacteria and swells. This reduces blood flow and become ischaemic. Can eventually burst and contents entering the peritoneal cavity can cause peritonitis

33
Q

What is pneumonia?

A

Infection of the lungs.

34
Q

What can cause pneumonia?

A

Streptococcus pneumoniae or haemophilia influenza

35
Q

Symptoms of pneumonia?

A

Coughing, shortness of breath, fever and chest pain

36
Q

Pneumonia risk factors?

A

Smoking, asthma, COPD

37
Q

What causes bacterial meningitis?

A

Neisseria meningitidis mainly

Also caused by E. coli and group B streptococcus

38
Q

What is meningitis?

A

Inflammation of the meninges

39
Q

Why is meningitis so dangerous?

A

Inflamed meninges and exudate along with neutrophils will compress the brain along with the vessels supplying it causing ischemia and death

40
Q

What are the symptoms of meningitis?

A

Fever, neck stiffness, photophobia and an altered mental state

41
Q

What is an abscess?

A

An accumulation of dead and dying neutrophils associated with liquefactive necrosis and can compress structures, nerves and ducts resulting in pain

42
Q

What is distension?

A

Not a condition but just a term used to describe a ballooning effect

43
Q

Serous cavity inflammation example?

A

Exudate pours in

In pericarditis results in pericardial effusion and cardiac tamponade.

Pleural effusion shortness of breath

Abdominal effusion ascites and causes distension of abdomen

Pathology (11 decks)

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