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Immunology > Exam 3 > Flashcards

Exam 3 Flashcards

1
Q

Fungal and viral infections are mediated by what type of immunity

A

Cell mediated

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2
Q
  • Tcell
  • B-cell
  • NKC
    No Abs

What it is lacking is essential for metabolic fxn of TT-cellls and if absent leads to toxin for lymphocytes

SCID

A

Adenosine deaminase deficiency

Converts deoxyadenosine to deoxyinosine which isnt harmful

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3
Q
  • T-cell
    -Bcell
    + NKC

No abs

SCID

Part of VDJ recombo affecting receptor production
Associates with omen syndrome (its partial version)

A

Rag1/2

No BCR/TCR formation

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4
Q
  • TCR
    -BCR
    + NKC

No ABs

No repair of double stranded breaks (such as those created by VDJ recombo) - associates with radiosensitivity

SCID

Increased risk of developing lymphoma

A

Artemis

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5
Q
  • T-cells
  • NKC
    + B-cells

IgM only

SCID

Deficient in signal creation for receptors, cytoplasmic common gamma chain

A

Jak3 Deficiency

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6
Q
  • T-cells
    + B-cells
    + NKC

IgM only

SCID

Lack of ability to stimulate differentiation of lymphoid progenitors into T-cells

A

IL-7R alpha chain deficiency

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7
Q
  • T-cells
    + B-cells
    + NKC

IgM only

SCID

Lack of ability to recieve survival signals

A

CD3 complex deficiency

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8
Q 
T-cell lymphopenia and inability to reject 
Severe opportunistic infections 
Chronic diarrhea 
No memory B-cells 
Symptoms once maternal IgG is depleted 
Thrush/candiditis
Pneumocystis jiroveci 
No IgA for mucosal protection

HSTR and avoid live vaccines

A

SCID - severe combined immunodeficiency disorders

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9
Q

Agammaglobinulemia
Can still eliminate extracellular pathogens and bacteria but intracellular are impacted
Susceptibility to recurrent infections by encapsulated bacteria

A

Selective B-cell immunodeficiencies

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10
Q

-B-cell
+ T-cell
+ NKC

No Abs

B-cell defect

X-linked recessive

Defect in lg chain heavy chain rearrangement with main absence of IgG once child past 6 months

A

Agammaglobinulemia - X-linked BTK kinase deficiency

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11
Q

-T-cell
- NKC
+ B-cell

SCID- only one that is x-linked recessive

IgM only

Cell’s can’t be active to proliferate and used in many cytokines

MOST COMMON SCID

A

Common gamma chain deficiency

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12
Q

+ B-cell, T-cell, NKC

Can induce anaphylaxis due to transfusions

Asymptomatic but can develop autoimunity and allergies

Symptomatic treatment with no vaccine restrictions

A

IgA deficiency

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13
Q

+ B-cell, T-cell, NKC

Mostly normal abs

Defects in several genes with poor responses to polysacharides

Asymptomatic but recurrent viral/bacterial infections of respiratory tract

Symptomatic treatment with no restrictions for vaccines

A

IgG subclass deficiency

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14
Q

+ B-cell, T-cell, NKC

No class switching due ot lack of signal/somatic hypermutation

Loss of CD40L in T-cells, loss of CD40 in B-cells

Abnormal infections with encapsulated bacteria with ineffective protection/opsonization

Symptomatic - no polio

A

Hyper IgM

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15
Q
  • B-cells low
    + T-cells
    + NKC

Infants create class switching later and have no humoral immunity for 3 years

Recurrent respiratory infections with susceptibilty to sinopulmonary infections

Symptomatic no polio

A

Transient hypogammaglobinuremia of infancy

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16
Q

Deficiency in CD3 circulating cells inducing opportunistic infections

Can induce autoimmunity or lymphoid malignancies

A

T-cell immyune deficiencies

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17
Q

+ B-cells
+ T-cellls
- NKC

Abs present

Lack of MHC II and therefore CD4
CD8 is intactt

SCID llike infections (recurrent respiratory, GI, urinary)

A

BLS II - bare lymphocyte syndrome

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18
Q
  • T-cells
    + B-cells
    + NKC

Normal abs

Cardiac malformations with hypothyroidism and hypocalcemia
Frequent URIs

A

DiGeorge Syndrome (obviously thymus too)

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19
Q

+ B-cells
+ T-cells (low CD8 only)
- NKC

Normal abs

Tap 1 defect - transports peptide to ER resulting in inability to load

Recurrent viral infections due to CD8

A

MHC I deficiency

20
Q

Defect in CD8 affecting integrin/sialyl lewis rolling

Phagocytes trap in circulation due to inability to migrate

Recurrent bacterial infections on skin/mucosal membranes
Neutrophilia in blood inducing lack of pus

Delayed detachment of umbilical, slow healing, death in early weeks

Phagocytic immunodeficiency

A

Leukocyte adhesion deficiency

21
Q

X-linked

Deficient NADPH oxidase and failure to generate ROS impairing killing of extracellular pathogens like bacteria/fungi

Formation of granulomas

Susceptibiity to recurrent staph infections

Phagocytic immunodeficiency

A

Chronic granulomatous

22
Q

X-linked hereditary

Inabillity to make NADPH resulting in loss of ROS

Formation of granulomas, ANEMIA DUE TO RBC METAB j

Asymptomatic

Cellular stressed/increased oxygen demand

Phagocytic immunodeficiency

A

Glucose-6-phosphate deficiency

23
Q

deficient in enzyme that catalyzes conversion of hydrogen peroxide to hypthalus acid (bleach) - gives pus green color

Diabetic patient sduring infections and linked to neutrophil killing yeast

Immunohistologica staining of neturophils

Phagocytic immunodeficiency

A

Myeloperoxidase deficiency

24
Q

Abnormal structure of neutrophils with giant granules that don’t contain cathepsin/elastace

Abnormalities in chemotaxis/degranulation/blunted neutrophil rexn

Albinism/recurrent infections due to staph/srept

Splenomegaly/lymphadenopathy

No NKC activity

Phagocytic immunodeficiency

A

Chediak Higashi syndrome - wheelchair bound too

25
Q

Blood levels of proinflammatory cytokines are low due to impaird signaling

Frequent infections by pyogenic bacteria but normal resistance to other common bacteria, fungi, and viruses

Lack of fever

Increased susceptibility to herpes

Phagocytic immunodeficiency

A

TLR deficiency

26
Q

Complement C that if lacking induces deposits in places such as kidneys - susceptibility to RA or SLE

A

C1/C4

27
Q

Complement C that if deficient increases susceptibility to strept/sinopulmonary infections

A

C2

28
Q

Complement deficiency with inability to activate C3 and associates with systemic maningococcal infections

A

Factor D

Fxns to activate factor B by cutting Bb in alternative path

29
Q

Complement deficiency that functions to form Bb/Ba in alternative path and if missing systemic meningococcal infections

A

Factor B

30
Q

Complement deficiency that is the base of kidney disease in hemolytic uremic syndrome via huge deposition of C3 in glomerular BM therefore constantly activating Alternatiive pathway

Functions to dissociate Bb from C3 normally

A

Factor H

31
Q

Factor H/I deficiency

Damaged BM is unable to support complement activation and macular degneration occurs in kidney

factor I prevents continuous activation of classical pathway
Factor H inactivates AP by binding to C3b to displace Bb

A

Hemolytic uremic syndrome

32
Q

C1-inhibitor deficiency
Leads to continuous activation of plasma complement

Body experiences sporadic inflammation in extremities due to overactive kallikrein-kinin systeme

A

Hereditary angioedema

C1-inhibitor inactivates kallikrein (kallikrein cleaves kininogen off to make bradykinin)

Bradykinin induces permeability in vessels

33
Q

Lack of glycosylphosphatidylinisitol anchor in proteins

Lack of CD55 DAF: inhibts C3/C5 by dissociating either C2 or Bb
CD59: inhibits mac formation by blocking C9 polymerization

Protects RBC from susceptibility to complement and therefore if deficient they die

A

Paraxysmal nocturnal hemoglobinuria

34
Q

Subcutaneous administration of a protein ag to immunized individual resulting in formation of complexes and vasculitis

A

Arthus rxn

35
Q

Systemic vasculitis that affects arteries and induces aneurysms
Associates with hep B

A

Polyarteritis nodosa PAN

36
Q

activating of TSH causing hyperthyroidism

Anxiety, irritability, tremor, and heat sensitivity

A

Graves

37
Q

Inability to bind ach

A

Mystheria gravis

38
Q

Type IV collagen destruction

A

Goodpastures

39
Q

Cells associated with increased incidence of pyogenic bacteria

A

B-cell immunodeficiency

40
Q

Defects in _ mediated immunity leads to infection by viruses and intracellular pathogens

A

T-cell (CD4)

41
Q

This deficiency makes patients susceptible to pyogenic infections

A

X-linked hyper IgM syndrome

42
Q

Defect in cell mediated immunity due to bad interaction for T-cel dependent activation of macrophages
Patients are susceptible to opportunistic intracellular microbes like pneumocytis jiroveci

A

Hyper IgM

43
Q

Fungal suggests this type of cell defect

A

T

44
Q

Another missing marker for LAD disease besides CD18 is

A

CD11

45
Q

Recurrent bacterial infections that lead to stuff like otitis emdia and pneumonia are mediated by what cell immunity

A

B-cell immunity

Immunology (2 decks)

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