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USMLE pathologgy > acute inflammation > Flashcards

acute inflammation Flashcards

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USMLE® Step 1 flashcards
1
Q

What characterizes acute inflammation?

A

The presence of edema and neutrophils in tissue

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2
Q

What are the two primary triggers for acute inflammation?

A

Infection (to eliminate pathogens) and tissue necrosis (to clear necrotic debris).

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3
Q

What type of immune response is acute inflammation?

A

It is an immediate response with limited specificity, part of innate immunity.

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4
Q

What are Toll-like receptors (TLRs) and where are they found?

A

TLRs are present on innate immune cells (e.g., macrophages, dendritic cells) and are activated by pathogen-associated molecular patterns (PAMPs

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5
Q

What does CD14 recognize?

A

CD14 (a co-receptor for TLR4)recognizes lipopolysaccharide (a PAMP) on the outer membrane of gram-negative bacteria

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6
Q

What is the result of TLR activation?

A

Upregulation of NF-κB, a transcription factor that activates immune response genes and produces immune mediators.

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7
Q

How do TLRs contribute to chronic inflammation?

A

TLRs are also present on adaptive immune cells (e.g., lymphocytes), where they mediate chronic inflammation.

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8
Q

What releases arachidonic acid (AA) from the phospholipid membrane?

A

Phospholipase A2 releases AA.

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9
Q

What are the two pathways that act on arachidonic acid, and what do they produce?

A

1.Cyclooxygenase produces prostaglandins (PGs).

  1. 5-lipoxygenase produces leukotrienes (LTs).
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10
Q

What do prostaglandins PGI2, PGD2, and PGE2 mediate?

A

Vasodilation and increased vascular permeability.

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11
Q

What additional functions does PGE2 mediate?

A

PGE2 also mediates pain and fever.

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12
Q

What does leukotriene LTB4 do?

A

LTB4 attracts and activates neutrophils.

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13
Q

What do leukotrienes LTC4, LTD4, and LTE4 mediate?

A

Vasoconstriction, bronchospasm, and increased vascular permeability (slow-reacting substances of anaphylaxis).

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14
Q

Where are mast cells commonly found?

A

Mast cells are widely distributed throughout connective tissue.

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15
Q

What are the three main ways mast cells can be activated?

A

1.Tissue trauma.
2.Complement proteins C3a and C5a.
3.Cross-linking of cell-surface IgE by antigen.

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16
Q

What is the immediate response of mast cell activation?

A

Release of preformed histamine granules, which mediate vasodilation of arterioles and increased vascular permeability

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17
Q

What is the delayed response of mast cell activation?

A

Production of arachidonic acid metabolites, particularly leukotrienes.

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18
Q

What is the role of complement proteins in inflammation?

A

Complement proteins are proinflammatory serum proteins that “complement” inflammation by enhancing immune responses.

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19
Q

What are the three pathways of complement activation?

A

1.Classical pathway: C1 binds IgG or IgM bound to antigen.

2.Alternative pathway: Microbial products directly activate complement.

3.Mannose-binding lectin (MBL) pathway: MBL binds to mannose on microorganisms to activate complement.

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20
Q

What are the key functions of complement components?

A

C3a and C5a (anaphylatoxins): Trigger mast cell degranulation, causing histamine-mediated vasodilation and increased vascular permeability.

C5a: Chemotactic for neutrophils.

C3b: Acts as an opsonin for phagocytosis.
MAC (Membrane Attack Complex): Lyses microbes by creating a hole in the cell membrane.

21
Q

What is the Hageman factor (Factor XII), and how is it activated?

A

Hageman factor is an inactive proinflammatory protein produced in the liver. It is activated upon exposure to subendothelial or tissue collagen

22
Q

What systems are activated by the Hageman factor?

A

Coagulation and fibrinolytic systems
Complement system
Kinin system associated with bradykinin

23
Q

What is the role of bradykinin in inflammation?

A

Bradykinin mediates vasodilation, increased vascular permeability (similar to histamine), and pain.

24
Q

What causes redness (rubor) and warmth (calor) during inflammation?

A

Redness and warmth are due to vasodilation, which increases blood flow. Key mediators are histamine, prostaglandins, and bradykinin.

25
Q

How does swelling occur in inflammation and what are the key mediators ?

A

Swelling is caused by fluid leakage from postcapillary venules into the interstitial space (exudate). Key mediators are:

Histamine: Causes endothelial cell contraction.
Tissue damage: Leads to endothelial cell disruption

26
Q

What mediates pain during inflammation?

A

Bradykinin and PGE2 sensitize sensory nerve endings, causing pain.

27
Q

What triggers fever during inflammation?

A

Pyrogens (e.g., bacterial LPS) cause macrophages to release IL-1 and TNF, increasing cyclooxygenase activity in hypothalamic perivascular cells. This leads to increased PGE2 and a higher temperature set point.

28
Q

What causes margination of neutrophils during inflammation?

A

Vasodilation slows blood flow in postcapillary venules, allowing neutrophils to marginate from the center to the periphery.

29
Q

How do neutrophils roll along the vessel wall?

A

Selectins (“speed bumps”) on endothelial cells bind sialyl Lewis X on leukocytes:

P-selectin: Released from Weibel-Palade bodies, mediated by histamine.
E-selectin: Induced by TNF and IL-1.

30
Q

What mediates firm adhesion of neutrophils to the vessel wall?

A

Cellular adhesion molecules (ICAM and VCAM) on the endothelium (upregulated by TNF and IL-1) bind integrins on leukocytes (upregulated by C5a and LTB4).

31
Q

What are the clinical features of leukocyte adhesion deficiency?

A

Delayed separation of the umbilical cord.

Increased circulating neutrophils.

Recurrent bacterial infections without pus formation.

32
Q

How do neutrophils transmigrate and move toward the site of inflammation?

A

Neutrophils transmigrate across postcapillary venules and are attracted by:

Chemical attractants: Bacterial products, IL-8, C5a, and LTB4

33
Q

What enhances phagocytosis by neutrophils?

A

Opsonins such as IgG and C3b enhance phagocytosis.

34
Q

What is Chediak-Higashi syndrome?

A

An autosomal recessive protein trafficking defect impairing phagolysosome formation. Clinical features include:

Increased risk of pyogenic infections.
Neutropenia.
Giant granules in leukocytes.
Defective primary hemostasis.
Albinism.
Peripheral neuropathy.

35
Q

What is the most effective mechanism for destroying phagocytosed material?

A

O2-dependent killing via the oxidative burst, generating HOCl (bleach) in phagolysosomes:

NADPH oxidase: Converts O2 to O2ꜙ.
Superoxide dismutase (SOD): Converts O2ꜙ to H2O2.
Myeloperoxidase (MPO): Converts H2O2 to HOCl.

36
Q

What causes CGD, and what is its inheritance pattern?

A

CGD is due to a defect in NADPH oxidase and can be inherited as X-linked or autosomal recessive.

37
Q

What are the clinical features of CGD?

A

Recurrent infections and granuloma formation.
may preseent with fever and sevral abscess formation

Infections by catalase-positive organisms such as:
Staphylococcus aureus
Pseudomonas cepacia
Serratia marcescens
Nocardia
Aspergillus

38
Q

How is CGD diagnosed?

A

Using the Nitroblue Tetrazolium (NBT) test:
DHR floow ccytometry shows absence of fluoroscene

Normal: Dye turns blue (functional NADPH oxidase).

CGD: Dye remains colorless (defective NADPH oxidase).

39
Q

What is the defect in MPO deficiency?

A

Defective conversion of H2O2 to HOCl due to myeloperoxidase (MPO) deficiency.

40
Q

What are the clinical features of MPO deficiency?

A

1.Increased risk for Candida infections.
2..Most patients are asymptomatic.

41
Q

How does the NBT test appear in MPO deficiency?

A

Normal, because the respiratory burst (O2 to H2O2) is intact

42
Q

What mechanism is used in O2-independent killing?

A

Enzymes in secondary granules, such as:

Lysozyme in macrophages.
Major basic protein in eosinophils.

43
Q

What happens to neutrophils after resolving the inflammatory stimulus?

A

Neutrophils undergo apoptosis and disappear within 24 hours.

44
Q

When do macrophages predominate in inflammation, and how do they arrive?

A

Macrophages predominate 2-3 days after inflammation begins. They arrive via margination, rolling, adhesion, and transmigration.

45
Q

What mechanisms do macrophages use to destroy phagocytosed material?

A

Phagocytosis (augmented by opsonins).
O2-independent killing via enzymes in secondary granules (e.g., lysozyme).

46
Q

What are the four possible outcomes of the inflammatory process managed by macrophages?

A

Resolution and Healing: Anti-inflammatory cytokines (IL-10, TGF-β).
Continued Acute Inflammation: IL-8 recruits additional neutrophils.
Abscess Formation: Acute inflammation surrounded by fibrosis mediated by macrophages.
Chronic Inflammation: Macrophages present antigens to CD4+ helper T cells, promoting chronic inflammation.

47
Q

what are the innate immune cells ?

A

macrophages and dendritic cells

48
Q

what are the mediators of acute inflammation ?

A

toll like receptors
arachidonic acid
mast cells
complement
hageman factor

49
Q

which complement activate mast cell degranulation ?

A

C3a and C5a

USMLE pathologgy (8 decks)

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