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Immunology Flashcards

1
Q

What does delayed separation of the umbilical cord suggest?

A

LAD (leukocyte adhesion deficiency)

Defect in integrins normally expressed on leukocytes (CD18)

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2
Q

Chediak Higashi Syndrome

A

Defect in microtubules prevents neutrophil phagosome-lysosome fusion

Inc risk of pyogenic infections, neutropenia, giant granules in leukocytes, defective primary hemostasis, partial albinism (melanocytes can’t pass pigment to keratinocytes), peripheral neuropathy, nystagmus

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3
Q

DiGeorge syndrome

A

Maldevelopment of the 3rd and 4th pharyngeal pouches
Thymic and parathyroid hypoplasia, abnormalal facies, and cardiac defects
T cell deficiency = immunosuppression

CATCH 22
Cardiac defects
Abnormal facies
Thymic dysplasia
Cleft palate
Hypocalcemia
Deletion in chromosome 22
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4
Q 
Chronic Granulomatous Disease
Cause?
Susceptible to?
Test?
Treatment?
A

Neutrophils have a defect in NADPH oxidase and can’t kill catalase positive organisms
Most common: pseudomonas and staph aureus and aspergillus

Test: nitroblue tetrazolium dye test or Dihydrorhodamine flow cytometry test

Treatment: IFN gamma

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5
Q

Nitroblue tetrazolium dye test

A

Used to evaluate for chronic granulomatous disease
Turns blue if NADPH oxidase works
Stays clear if NADPH oxidase is defective

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6
Q

HLA B27

A 
PAIR: 
Psoriatic arthritis
Ankylosing spondylitis
Inflammatory bowel disease
Reactive arthritis
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7
Q

HLA DR4

A

Rheumatoid Arthritis

4 walls in a “rheum”

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8
Q

Hyper IgE syndrome

A

Deficiency of Th17 cells - impaired recruitment of neurotrophils and decreased IgG production and decreased IFN-gamma

FATED
course Facies
staph Abscesses
retained primary Teeth
inc igE
Dermatologic problems (eczema)
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9
Q

Foscarnet

A

Anti-viral (pyrophosphate analog)
Inhibits DNA polymerase in herpes virus and reverse transcription in HIV.

*Does not require intracellular activation by viral OR cellular kinases

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10
Q

Enteracept

A

TNFa inhibitor that impairs cell-mediated immunity. Before starting this medication, important to screen for latent TB to prevent reactivation

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11
Q

Mechanism of fever

A
  1. Macrophages release IL1 and TNF in response to a pyrogen (ex. LPS on bacteria)
  2. Inc COX activity in hypothalamus
  3. Inc production of PGE2
  4. Inc body temp (fever)
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12
Q

What are the anaphylatoxins in the complement cascade?

A

C3a and C5a

Trigger mast cell degranulation resulting in vasodilation and increased vascular permeability

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13
Q

What is the mechanism of the mast cell DELAYED response?

A

Production of arachidonic acid metabolites

Especially leukotrienes that cause increased bronchial tone/bronchospasm

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14
Q

What in the arachidonic acid pathway leads to increased chemotaxis of neutrophils?

A

LTB4

“Neutrophils arrive B4 others”

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15
Q

Where does vasodilation in inflammation occur?

A

Arterioles

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16
Q

Which prostaglandin mediates fever?

A

PGE2 (FEEEver)

Also mediates pain

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17
Q

Which prostaglandins mediate pain?

A

PGE2 and bradykinin

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18
Q

Where does vascular permeability occur during inflammation?

A

Post capillary venules

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19
Q

What causes inc susceptibility to recurrent Neisseria infections?

A

MAC complex (C5-C9) deficiency

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20
Q

Pathogenesis of granuloma formation (cells and products involved)

A

TH1 cells release IFN gamma –> activates macrophages

Macrophages release TNF alpha –> induces and maintains granuloma formation

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21
Q

Considerations when starting a patient on TNFa inhibitors (Enteracept)

A

Test for latent TB – lack of TNF alpha can lead to granuloma breakdown and leads to systemic disease

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22
Q

Hypercalcemia and granulomas

A

Granulomas produce calcitriol (1,25 OH2 vitamin D3) which causes an increase in calcium levels

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23
Q

c-ANCA
p-ANCA

(Anti-neutrophil cytoplasmic antibodies)

A

c-ANCA: target antigen is proteinase 3

p-ANCA: target antigen is MPO

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24
Q

Child is being evaluated for an eczematous skin rash. His past medical hx is significant for several bouts of severe respiratory infections. Initial evaluation reveals increased bleeding time. His CBC shows a WBC count of 9,000 and a platelet count of 40,000. His platelets are small and deformed on blood smear. What is the most likely diagnosis?

A

Wiskott Aldrich syndrome: X linked, combined B and T cell immunodeficiency.

WATER
Wiskott
Aldrich
Thrombocytopenia
Eczema
Recurrent infections
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25
Q

What protein deficiency can cause SCID? (Most common cause is X linked)

A

Adenosine deaminase deficiency – adenosine accumulation is toxic to lymphocytes and leads to widespread death of T and B lymphocytes

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26
Q

Part of the lymph node

A

Follicle: B cells

Paraxcortex: T cells

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27
Q

Parts of the thymus and role in T cell maturation

A

Cortex: immature T cells
- Positive Selection: T cells expressing TCR’s capable of binding self-MHC on cortical epithelial cells survive

Medulla: mature T cells
- Negative Selection: T cells expressing TCR’s with high affinity for self-antigens undergo apoptosis

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28
Q

What cells are responsible for the destruction of cells with decreased or absent MHC class I proteins on their surfaces

A

NK cells

29
Q

Function of CD40 on B cells

A

promotes class switching of immunoglobulins. If there is no CD40, then the cells can only produce IgM (complement fixation)

30
Q

Hyper-IgM syndrome

A

Due to defective CD40L on Th cells → Leads to severe pyogenic infections early in life; opportunistic infection with Pneumocystis, Cryptosporidum, and CMV

31
Q

What causes immunodeficiency in ataxia telangiectasia? What is the genetic mutation in this disorder?

A

IgA deficiency

DNA break repair

32
Q

Hypersensitivity type: Serum sickness

A

3

33
Q

Hypersensitivity type: Goodpasture syndrome

A

2

34
Q

Hypersensitivity type: multiple sclerosis

A

4

35
Q

Hypersensitivity type: autoimmune hemolytic anemia

A

2

36
Q

Hypersensitivity type: rhinitis

A

1

37
Q

Hypersensitivity type: eczema

A

1

38
Q

Hypersensitivity type: polyarteritis nodosa

A

3

39
Q

Hypersensitivity type: contact dermatitis

A

4

40
Q

Hypersensitivity type: myasthenia gravis

A

2

41
Q

In what transplants do you see GVHD?

A

Bone marrow and liver transplants

42
Q

Mechanism of apoptosis

A

Bcl2 in the cytoplasm is inactivated, cytochrome c can exit the mitochondria and enter the cytoplasm where it activates caspases that initiate apoptosis

o Caspases are proteolytic enzymes that destroy cell components. They contain cysteine and are able to cleave aspartic acid residues (cysteine-aspartic-acid-proteases)

43
Q

Stem cell locations (skin, bowel, and bone marrow and lung):

A

skin – basal layer
bowel – mucosal crypts
bone marrow – hematopoietic stem cells
lung – type 2 pneumocytes

44
Q

What do macrophages secrete to recruit more neutrophils?

A

IL-8

“clean up on aisle 8”

45
Q

Interferon alpha and beta in viral infections

A

A part of innate host defense gainst DNA and RNA viruses

Cause transcription of antiviral enzymes capable of halting protein synthesis

46
Q

Which cytokines are anti-inflammatory?

A

IL-10 and TGF-B

47
Q

What attracts neutrophils?

A

Il-8 (macrophages)
C5a (complement cascade)
LTB4 (lipooxygenase pathway)

48
Q

C1 esterase inhibitor deficiency

A

causes hereditary angioedema due to unregulated activation of kallikrein (Inc bradykinin)

**ACE inhibitors are contraindicated because will lead to accumulation of even more bradykinin

49
Q

C3 deficiency:

A

inc risk of severe, recurrent pyogenic sinus and respiratory tract infections

50
Q

C5-C9 deficiencies:

A

terminal complement deficiency increases susceptibility to recurrent Neisseria bacteremia due to inability to form MAC complex

51
Q

Which complement is involved in neutrophil chemotaxis?

A

C5a

52
Q

What stimulates class switching to IgE?

A

IL-4

53
Q

What stimulates eosinophils?

A

IL-5

54
Q

What stimulates class switching to IgA?

A

IL-5

55
Q

What cytokines cause fever?

A

IL-1

IL-6

56
Q

B cell deficiencies vs T cell deficiencies

A

B cell deficiencies tend to produce recurrent bacterial infections, whereas T cell deficiencies produce more fungal and viral infections

57
Q

Calcineurin inhibitors

A

Cyclosporine and Tacrolimus

block T cell activation by preventing IL-2 transcription

58
Q

Sirolimus

A

block T cell activation and B cell differentiation by preventing response to IL-2 – mTOR inhibitor

59
Q

Daclizumab and Basiliximab

A

monoclonal antibodies that block IL-2 receptor

60
Q

Mycophenolate:

A

reversibly inhibits IMP dehydrogenase, preventing purine synthesis of B and T cells

61
Q

Role of Fas

A

The Fas receptor acts to initiate the extrinsic pathway of apoptosis.

Mutations involving the Fas receptor or Fas ligand can prevent apoptosis of autoreactive lymphocytes, thereby increasing the risk of autoimmune disorders such as SLE

62
Q

What is released from mast cells during anaphylaxis

A

Histamine and tryptase

63
Q

Which part of the complement cascade is deposited on antigen and acts as opsonin for phagocytosis? Which immunoglobulin has the same function?

A

C3b

IgG

64
Q

Dihydrorhodamine flow cytometry test

A

Used for diagnosis of chronic granulomatous disease – will show absence of green fluorescence that is characteristic of normal neutrophils

65
Q

What are people with ileal resection at risk of?

A

Patients with an ileal resection are at greater risk of infection due to loss of peyers patches (normally in the ileum) and dec ability to differentiate B cells to secrete IgA in response to gut pathogens

Also vitamin B12 deficiency as that is where is is absorbed

66
Q

Killed vs Live vaccines induce which part(s) of the immune response?

A

Killed – humoral response only

Live – humoral and cell mediated immune responses

67
Q

What enzymes can eliminate free radicals?

A

Superoxide dismutase
Glutathione peroxidase
Catalase

68
Q

What increases ESR?

A

IL-6, IL-1 and TNF alpha induce the release of acute phase reactants –> release of fibrinogen causes an inc in ESR

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