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Immuno and Sero > IS Lec Final - Diseases > Flashcards

IS Lec Final - Diseases Flashcards

1
Q

3 Disorders of Neutrophils

A

Noninfectious Neutrophil-Mediated Inflammatory Disease
Abnormal Neutrophil Function
Congenital Neutrophil Abnormalities

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2
Q

2 Types of Noninfectious Neutrophil-Mediated Inflammatory Disease

A

inappropriate phagocytosis
inappropriate activation of phagocytosis

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3
Q

prolonged activation of NADPH oxidase

A

inappropriate phagocytosis

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4
Q

phagocytes attempt to engulf particles that are too large, releasing oxygen radicals and granule contents onto the particle, but these escape into the surrounding tissues, generating tissue damage.

A

inappropriate phagocytosis

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5
Q

Ex: in response to dust inhalation and smoking (e.g., nicotine) and in persistent infections such as cystic fibrosis

A

inappropriate phagocytosis

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6
Q

Autoimmune diseases such as Grave’s disease, rheumatoid arthritis, multiple sclerosis

A

inappropriate activation of phagocytosis

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7
Q

4 types of Abnormal Neutrophil Function

A

Quantitative or qualitative defects of neutrophils
Impaired leukocyte mobility
Defective locomotion or leukocyte immobility
Defect in the cellular response to chemotaxis

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8
Q

high rate of infection

A

Quantitative or qualitative defects of neutrophils

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9
Q

Quantitative or qualitative defects of neutrophils examples

A

recurrent systemic bacterial infections (e.g., pneumonia), disseminated cutaneous pyogenic
lesions, and other types of life-threatening bacterial and fungal infections

too low (neutropenia) or too high (neutrophilia) both translates to high infection rate

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10
Q

defects in the granules and neutrophils

A

Impaired leukocyte mobility

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11
Q

Impaired leukocyte mobility ex

A

rheumatoid arthritis, cirrhosis, CGD

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12
Q

total immobility, prone to recurrent bacterial infections

A

Defective locomotion or leukocyte immobility

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13
Q

Defective locomotion or leukocyte immobility ex

A

Lazy leukocyte syndrome, patients in steroids

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14
Q

recurrent bacterial infection

A

Defect in the cellular response to chemotaxis

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15
Q

Defect in the cellular response to chemotaxis ex

A

Chediak Higashi anomaly, sepsis, Job’s syndrome (hyperimmunoglobulinemia E)

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16
Q
  • qualitative disorder of neutrophils
  • Autosomal recessive
  • Abnormal granulation of platelets and neutrophils
  • impaired chemotaxis and delayed killing of ingested bacteria
    occurs during childhood
A

Chédiak-Higashi syndrome (anomaly)

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17
Q

group of disorders of oxidative metabolism affecting the cascade of events required for H2O2 production by phagocytes

A

Chronic granulomatous disease (CGD)

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18
Q

mutation in CYBB – required for microbicidal ROS production by neutrophils and monocytes

A

Chronic granulomatous disease (CGD)

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19
Q

Results to life- threatening infections and granulomatous complications

A

Chronic granulomatous disease (CGD)

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20
Q
  • deficiency of CR3 on phagocytic cells presents as a leukocyte adhesion deficiency
A

Complement receptor 3 (CR3) deficiency

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21
Q

marked abnormalities of adherence-related functions

A

Complement receptor 3 (CR3) deficiency

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22
Q

Leukocyte adhesion deficiency type 1 (LAD- 1) - deficiency of CD18

LAD-2 - absence of sialyl–Lewis X (CD15s) blood group antigen

A

Complement receptor 3 (CR3) deficiency

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23
Q

innately present on the body and needed for leukocyte adhesion, adhesion is impaired, translates to LAD 1 and 2

A

Complement receptor 3 (CR3) deficiency

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24
Q

patient’s phagocytes manifest a mild to moderate defect in bacterial killing and a marked defect infungal killing in vitro

A

Myeloperoxidase deficiency

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25
Q

azurophilic granules are present but MPO are absent, MPO causes greenish coloration in pus, infancy to childhood, manifested by delayed separation in umbilical cord, sipon bacterial (greenish to yellowish) viral (watery & colorless, no medication, dengue has no antibiotics)

A

Myeloperoxidase deficiency

26
Q

an iron- containing heme protein responsible for the peroxidase activity characteristic of azurophilic granules

A

Myeloperoxidase

27
Q

azurophilic granules are also called ____

A

non specific bc they are found in all granulocytes

28
Q

caused by a failure to synthesize specific granules and some contents of other granules during differentiation of neutrophils in the bone marrow.

A

Specific granule deficiency

29
Q

Results to recurrent, severe bacterial infections of the skin and deep tissues, with a depressed inflammatory response

A

Specific granule deficiency

30
Q

5 Primary and Secondary Abnormalities of Monocyte-Macrophage Function

A

Defect in phagocyte killing
Defective monocyte cytotoxicity
Defective release of macrophage-activating Factors
Depressed migration
Impaired phagocytosis

31
Q

Defect in phagocyte killing examples

A

Chronic granulomatous disease, corticosteroid therapy, newborn infants, viral infections;
liver, lungs, spleen, lymph nodes

32
Q

Defective monocyte cytotoxicity examples

A

Cancer, Wiskott-Aldrich Syndrome, TIE (thrombocytopenia, immunodeficiency, eczema)

33
Q

Defective release of macrophage-activating Factors examples

A

Acquired Immunodeficiency Syndrome (AIDS), Intracellular infections (lepromatous leprosy, tuberculosis, visceral leishmaniasis)

34
Q

In AIDS, what is dominant?

A

CD8 (cytotoxic cells) becomes more dominant than CD4 (t-helper cells)

35
Q

Depressed migration examples

A

AIDS, burns, diabetes, immunosuppressive therapy, newborn infants

36
Q

what is the state of blood in diabetes?

A

blood is viscous in diabetes and membranes are thickened which results to plug formation, impaired migration of phagocytes

37
Q

Impaired phagocytosis examples

A

Congenital deficiency of CD11-CD18, monocytic leukemia, systemic lupus, erythematosus

38
Q

Qualitative Monocyte-Macrophage Disorders aka ___

A

lipid storage disorders

39
Q

systemic enzymatic defect permits the accumulation of cell debris normally cleared
by macrophages

A

lipid storage diseases

40
Q

resistance to infection can be impaired, at least partially, because of a defect in macrophage function

A

lipid storage diseases

41
Q

they store lipid products, which need to be degraded by certain enzymes

when they lack specific enzymes needed for lipid metabolism, it will accumulate

A

monocytes and macrophages

42
Q

Deficiency of β-glucocerebrosidase, the enzyme that normally splits glucose from its parent sphingolipid, glucosylceramide

A

Gaucher’s Disease

43
Q

Accumulation of cerebroside in histiocytes

A

Gaucher’s Disease

44
Q

Cells are large, with one to three eccentric nuclei and a characteristically wrinkled cytoplasm

A

Gaucher’s Disease

45
Q

Found in the bone marrow, spleen, and other organs of the mononuclear phagocyte system

A

Gaucher’s Disease

46
Q

Production of erythrocytes and leukocytes decreases as these abnormal cells infiltrate the bone marrow

A

Gaucher’s Disease

47
Q

Recessive deficiency of the enzyme
sphingomyelinase

A

Niemman Pick Disease

48
Q

Accumulation of sphingomyelin in the
mononuclear phagocytes

A

Niemman Pick Disease

49
Q

The characteristic cell is similar in appearance to Gaucher’s cell, although the cytoplasm of the cell is foamy

A

Niemman Pick Disease

50
Q

lack of enzyme means that majority of the waste material remains in the lysosome

A

Gaucher’s Disease

51
Q

Disease States Involving Leukocyte Integrins

A

Leukocyte adhesion deficiency (LAD)

52
Q

what do you call the adhesive molecules?

A

integrins

53
Q

leads to recurrent and often fatal bacterial and fungal infections

A

Leukocyte adhesion deficiency (LAD)

54
Q

5 features of Leukocyte adhesion deficiency (LAD)

A
  • Delayed separation of umbilical cord
  • Gingivitis
  • Recurrent and persistent bacterial or fungal skin infections
  • Impaired wound healing
  • Lack of pus formation
55
Q

can affect people of all racial groups

A

LAD-1

56
Q

a deficiency of the β2-integrin subunit (CD18)

A

LAD-1

57
Q

The phenotypes are severe, moderate, and novel or variant

A

LAD-1

58
Q

affects people from the Middle East and Brazil

A

LAD-2

59
Q

failure to convert guanosine diphosphate (GDP) mannose to fructose

A

LAD-2

60
Q

no deficiency, just failure of conversion

A

LAD-2

Immuno and Sero (4 decks)

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