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Pathology > 2. inflammation > Flashcards

2. inflammation Flashcards

1
Q

What is the predominant cell type in a pyogenic bacterial infection?

A

Neutrophil

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2
Q

What granulated cells contain receptors for IgE on its cell surface?

A

Mast Cells

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3
Q

B lymphocytes and plasma cells are mediators of chronic inflammation and provide what type of immunity to infectious disease?

A

Antigen-specific

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4
Q

Inflammation of the breast tissue is known as

A

Mastitis

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5
Q

How does mastitis develop?

A

bacteria gain access to the breast tissue (through the ducts, through infiltration of secretions, through fissures in the nipples, or through dermatitis involving the nipple)

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6
Q

How does complement activation induce local edema?

A

Products of complement activation increase permeability of blood vessels

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7
Q

C5a , C3b and C567 are examples of what?

A

Biologically active fragments or complements (C567) generated by complement proteins

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8
Q

What immunologic processes involve complement proteins?

A

Oposonization, cytolysis, and chemotaxis

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9
Q

Name the most potent chemotactic factors for leukocytes at the site of injury

A

Complement Proteins, N-formylated peptides (low molecular weight)/ bacterial and mitochondrial products, Products of arachidonic acid metabolism, and Chemokines

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10
Q

What generates Plasmin?

A

Hageman Factor (clotting factor XII)

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11
Q

What type of enzyme is Plasmin?

A

Fibrinolytic.

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12
Q

What doe Hageman Factor activate?

A

Plasminogen conversion to Plasmin, conversion of prekallikrein to kallikrein, and clot formation through activation of the coagulation system

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13
Q

What is the most significant function of the kinin?

A

Amplifies the inflammatory response by stimulating local tissue cells and inflammatory cells to generate additional mediators, prostenoids,, cytokines, NO , and tachykinins

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14
Q

What is the function fo PMNs (neutrophils)?

A

clear debris and begin the process of wound healing

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15
Q

What is the role of fibroblasts a macrophages at the site of an infarction?

A

they regulate scar tissue formation

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16
Q

What are the 7 vasoactive mediators in the inflammatory response?

A

Histamine, Serotonin, Bradykannin, Anaphylatoxins, Leukotrienes/Prostaglandins, Platelet-Activating factor, NO

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17
Q

How does edema develop during acute inflammation?

A

Increase in the permeability of the endothelial cell barrier.

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18
Q

What response of the arterioles exacerbates fluid leakage?

A

Vasodilation

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19
Q

During inflammation, how doe s the hydrostatic pressure increase in the capillary bed?

A

Vasoconstriction of the postccapillary venules

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20
Q

What is the key source of vasoactive mediators?

A

Hageman Factor (clotting factor XII)

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21
Q

In patients with endotoxic shock, what factor is secreted by monocytes/macrophages when stimulated by Gram - bacteria?

A

Tumor Necrosis Factor A

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22
Q

What do gram negative bacteria secrete to stimulate monoctyes that will act to release TNF-a?

A

Lipopolysaccharide

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23
Q

Differentiate between karyorrexis, karyolysis, and pyknosis.

A

These are all patterns of nuclear changes due to breakdown of DNA and chromatin. Pyknosis: nuclear shrinkage and basophilia, DNA condenses into a solid shrunken mass . This nucleus can unedergo fragmentation so that it becomes karyorrrhexis pattern. Karyolysis is when basophilia of chromatin fade, secondary to Dnase activity.

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24
Q

What physiological change occurs that causes necrosis to occur after periods of ischemia?

A

Decrease in intracellular pH from the build up of lactate in the cytosol from anaerobic glycolysis

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25
Q

An alteration of injured blood vessels which histologically stains with eosin due to the accumulation of plasma proteins is known as what pathological process?

A

Fibrinoid Necrosis.

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26
Q

Contrast transudate vs exudate

A

Transudate (edema fluid with low protein content) and Exudate (edema fluid with high protein content)

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27
Q

A purulent exudate or effusion is characterized by what cellular component?

A

PMNs

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28
Q

A serous exudate or effusion is characterized by the absence of what prominent cellular response. What color is it?

A

Yellow

29
Q

What does a sersoanguineious exudate contain?

A

RBCs . It has a red tinge.

30
Q

What type of reactions are associated with Eosinophilia ?

A

allergic-type reactions and parasitic infestations

31
Q

Skeletal muscle is typically infiltrated by eosinophils when infected by what organism>?

A

Trichinella

32
Q

Muscular Dystrophy patients would show elevations of what molecule in serum?

A

Creatinine Kinase

33
Q

What is Polymositis?

A

An inflammatory myopathy. It along with others are characterized by usually symmetric muscle weakness, initially affecting large muscles of the trunk, neck and limbs. Polymyositis seems to be mediated by CTLs.

34
Q

Children with a deficiency of NADPH oxidase are susceptible to what disease?

A

Recurrent bacterial infections because they can ‘t produce HOCL and are vulnerable to Candida

35
Q

What does Catalase enzyme do?

A

Convert H2O2 to water and molecular oxygen

36
Q

What is Wiskott-Aldrich Syndrome?

A

An X-linked recessive disease characterized by thrombocytopenia, eczema, and vulnerability to recurrent infection. The thymus is initially normal burt there is age-related depletion of T lymphocytes in peripheral blood and lymph nodes, and thus loss of cellular immunity. Patients ars don’t synthesize ABs to polysaccharide antigens and are susceptible to encapsulated, pyogenic bacteria.

37
Q

What is deficient in Hereditary angioedema? What ‘s the consequent of this deficiency?

A

C1 inhibitor, thus, C1 keeps on cleaving C4 and C2 excessively

38
Q

Where is nonpitting edema seen in hereditary angioedema?

A

soft tissues as a result t of chronic complement activation generating vasoactive peptide from C2. Edema can also form in the larynx which is fatal.

39
Q

what enzyme deficiency increases susceptibility to infections with Candida?

A

Myeloperoxidase

40
Q

What do eosoniphils contain to combat parasitic infections like schistosomiasis?

A

Esoinophil major basic protein, leukotrienes, platelet-activating factor, and acid phosphatase

41
Q

What characterizes suppurative inflammation?

A

A purulent exudate accompanied by liquefactive necrosis. It can also be described as PUS.

42
Q

In suppurative inflammation, Abscesses filled with pus are surrounded by what?

A

granulation tissue

43
Q

What are the 3 main cellular components of chronic inflammation?

A

Lymphocytes, Plasma cells, and Macrophages

44
Q

What interactions do na?ve lymphocytes have when a patient has viral myocarditis?

A

The lymphocytes encounter antigen-presenting cells (macrophages and dendritic cells) in the secondary lymphoid organs and are activated to circulate in the vascular system and head to peripheral tissues

45
Q

what happens when vasoactive mediators bind to endothelial cell receptors?

A

Contraction and gap formation. This break leads to the leakage (such as caused by direct injury to endothelial cells) of intravascular fluid into the extravascular space.

46
Q

What terms refer to a fibrinous exudate occurring on a serosal surface?

A

Fibrinous pleuritis or fibrinous pericarditis

47
Q

Exogenous pyrogens stimulate what endogenous pyrigens?

A

Il-1alpha, IL-1beta and TNF-alpha

48
Q

What is the function of IL-1 alpha?

A

It is a protein that stimulates prostaglandin synthesis in the hypothalamic thermoregulatory centers- altering body T.

49
Q

How does aspirin block the fever response?

A

It is an inhibitor of cyclooxygenase and it inhibits PGE2 synthesis in the hypothalamus.

50
Q

What is rigor?

A

profound chills with shivering and piloerection

51
Q

What is leukotriene B4?

A

A chemotactic for neturophils, eosinophils, and monocytes

52
Q

What is the function of Thromboxane A2?

A

TXA2 is platelet synthesized and is also an important stimulus for platelet aggregation. It works alongside ADP to forma primary hemostatic plug, an enlarging platelet aggregate.

53
Q

What enhances phagocytosis?

A

C3b fragment of complement and immunoglobulins

54
Q

What inflammation mediators can cause secondary injury to a the alveolar basement membrane and lung parenchyma for a patient suffering from pneumonia?

A

Lysosomal enzymes

55
Q

what does lysozyme target In degradation?

A

bacterial cell wall of gram + organisms

56
Q

Where is MPO located

A

Neutrophil granules

57
Q

What kind of protein is Entactin?

A

basement membrane protein

58
Q

What is the first response of arterioles to neurogenic and chemical stimuli?

A

transient vasoconstriction. Shortly after, vasodilation occurs allowing blood flow to the inflamed area (AKA Hyperemia)

59
Q

What do Leukotrienes do>?

A

stimulate contraction of smooth muscle and enhance vascular permeability. It is one of other chemical mediators that stimulate mucus production and bronchoconstriction in asthma. Leukotrienes are slow-reacting substances of anaphylaxis

60
Q

How does Histamine effect the vascular wall?

A

They bind to H1 receptors in the vascular wall and they induce endothelial cell contraction, gap formation, and edema

61
Q

What kind of shock occurs from massive Histamine release?

A

Anaphylactic

62
Q

Bradykinin and Hageman factor are derived from where/

A

plasma

63
Q

What does the enzyme cyclooxygenase mediate?

A

the conversion of arachidonic acid to prostaglandins.

64
Q

When is leukopenia encountered?

A

Under conditions of chronic inflammation, especially in malnourished patients or those suffering from a chronic debilitating disease

65
Q

What infections can induce Leukopenia?

A

Typhoid fever, viral and rickettsial infections

66
Q

What is pancytopenia?

A

decreased circulating levels of all formed elements in the blood

67
Q

what are the primary factors responsible for rubor and calor at an injury site?

A

vasodilation of precapillary arterioles and hyperemia

68
Q

How do corticosteroids work? What is the associated side effect?

A

They induce synthesis of an inhibitor of phospholipase A2 and block the release of arachidonic acid from the plasma membranes of inflammatory cells. ; Atrophy of the adrenal glands

69
Q

What are acute phase proteins?

A

proteins synthesized primarily by the liver and are released in the circulation in response to acute inflamm. Challenge. They are mediated by cytokines, IL1 , IL 6 and TNF- alpha. Increased plasma levels of these proteins increase RBC sedimentation rate and thus is used to monitor inflammatory disease activity.

Pathology (30 decks)

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