Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Transition to Clinical Medicine > Immune disorders > Flashcards

Immune disorders Flashcards

1
Q

Immune Reactions

A

Immune system has numerous functions including
Prevention/defense from infection
Inactivation and clearance of foreign substances

Immune reactions can cause host tissue injury
Hypersensitivity reactions cause release of inflammatory mediators that lead to tissue damage and eventually can lead to scarring (repair)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Hypersensitivity Reactions

A

Type I – Immediate (anaphylactic)
Mediated by TH2 cell cytokines
Via IL-4 action on B cells get class switching to IgE
Via IL-5 get development and activation of eosinophils

Type II – Antibody-mediated
Secreted ***IgG and IgM antibodies participate directly in injury to cells

Type III – Immune complex mediated
IgG and IgM antibodies bind antigens and the antigen-antibody complexes deposit in tissues and induce inflammation

Type IV – Cell mediated
Sensitized T-lymphocytes (TH1, TH17 cells and CTLs)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

hypersensitivity and granuloma

A

Type IV hypersensitivity

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Type I Hypersensitivity Disorders

A

Anaphylaxis
Hypotension secondary to vasodilation that may lead to shock
Laryngeal edema that may lead to airway obstruction
Inflammation and tissue destruction leading to scarring

Asthma
Reversible bronchoconstriction
Mucous hyperplasia
Inflammation and tissue destruction leading to scarring

Urticaria
Dermal angioedema with wheals
Itching

Food allergies
Increased intestinal peristalsis
Inflammation and tissue destruction leading to scarring

Allergic rhinitis and sinusitis
Mucous hyperplasia
Inflammation and tissue destruction leading to scarring

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Type I Immediate Hypersensitivity

A

Immediate phase: *** 5 to 30 minutes post exposure
for about an hour

Dilated leaky vessels –> edema
Contraction of smooth muscle
Increased mucus production

Late phase: **2 to 24 hours later and may lasts days

Inflammation with eosinophilia–> tissue injury

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

petechiae and echymoses, what do you start to think?

A

platelets and/or von Willebrandt’s

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

granulomas associated with?

A

Type IV- cell mediated hypersensitivity (activated T lymphocytes)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Type II hypersensitivity

A

Type II- antibody mediated. IgG or IgM binding

good pasture syndrome

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Mechanisms of type I hypersensitivity

A

Early - TH2 activation  IgE class switch in B cells  IgE  release of mediators from mast cells

Later - TH2, epithelial and mast cells secrete IL-5 and eotaxin → eosinophils → enzyme (major basic protein and cationic protein) release → tissue destruction

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

signs/ symptoms of anaphylaxis

A 
lightheadedness
SOB, stridor
skin-- hives, itchiness, flushing
Heart-- fast or slow, low blood pressure
swelling of lips, tongue and/or throat
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Mast cell secretagogues

A

IgE (via Fc receptors), Anaphylatoxins C5a, C4a and C3a –> Mast cell –> Eosinophil chemotactic factor

among many other things

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Urticaria

A

dermal hyperpermeability & wheals

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

angioedema

A

edema of dermis, mucosae and deeper tissues

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

hereditary angioedema

A

autosomal dominant C1 inhibitor deficiency

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

asthma

A

reversible airway obstruction

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

autoimmunity

A

reactions against an individual’s own tissues and cells

types 2,3, and/or 4

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Placental transfer in autoimmune disorders

A

Maternal igG antibodies

thyroid hormone receptor –> graves
RBCs–> hemolytic anemia
platelets–> thrombocytopenia
acetylcholine receptor–> myasthenia gravis
Ro & La–> Cutaneous lupus & heart block

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

HLA alleles and the diseases

A 
Rheumatoid arthritis- DR4
Type 1 diabetes DR3/DR4
Ankylosing spondylitis- B27
Postgonococcal arthritis-- B27
Autoimmune hepatitis- DR3
Primary Sjogren syndrome- DR3
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

Non-HLA genes associated with autoimmune diseases

A

PTPN22– protein tyrosine phosphatase
May affect signaling in lymphocytes
may alter activation of self-reactive T cells

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

Types II/III Antibody Mediated Hypersensitivity

A

Antibody-dependent complement-mediated cytotoxicity (Type II)
Classical complement cascade activation leads to lysis of cells
Direct lysis via membrane attack complex (C5b - C9), punches holes in cell
Mechanism normally used for killing Neisseria spp. bacteria
Antibody-dependent cell-mediated cytotoxicity (Type II)
Binding of antibody leads to activation of macrophages, neutrophils, eosinophils, natural killer cells, etc. that lead to cell injury and death
Mechanism normally used for killing other microorganisms, etc
Antibody-dependent cellular dysfunction (Type II)
Antibody binding causes abnormal cellular function (e.g. Graves disease)
No normal use for this mechanism
Antigen-antibody complex mediated attack on host tissues (Type III)
Antigen-antibodies complexes deposit or are initiated in tissue
Complement is activated (C5a attracts infl. Cells, C3a and C5a cause local vasodilation, etc.)
No normal use for this mechanism

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

Mechanisms of Antibody-mediated Injury

A

Antibody-dependent complement-mediated cytotoxicity
e.g. ABO incompatibility

Antibody-dependent cell-mediated cytotoxicity
e.g. killing virally infected cell

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

Autoimmune hemolytic anemia - mechanism

A

opsonization and phagocytosis of red cells

direct hemolysis via complement with ABO mismatch

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

Immunologic Thrombocytopenic Purpura

A

Spleen: normal size, congested sinusoids, prominent germinal centers, occasional megakaryocytes
Marrow: increased megakaryocytes
Peripheral blood: megathrombocytes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

Goodpasture Syndrome

A

Diagnose = linear fluorescence

Antigen hidden in type collagen IV—exposed by smoking, solvents etc.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

antigen and manifestation: SLE

A

lupus
nuclear antigens
nephritis, skin lesions, arthritis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

antigen and manifestation: poststreptococcal glomerulonephritis

A

streptococcal cell wall antigen

nephritis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

antigen and manifestation: polyarteritis nodosa

A

Hep B virus antigens (some cases)

Systemic vasculitis

pulmonary arteries are NOT involved

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

antigen and manifestation: Reactive arthritis

A

Bacterial antigens

acute arthritis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

antigen and manifestation: serum sickness

A

foreign serum protein

arthritis, vasculitis, nephritis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

antigen and manifestation: arthus reaction

A

injected foreign proteins

cutaneous vasculitis

31
Q

acute proliferative glomerulonephritis

A

can be post infectious (strepto, staphylo, virus)

Immune complexes formed in circulation or on membrane, c3 deposited before others

32
Q

Rheumatoid arthritis

A

citrullinated self proteins?

chronic arthritis

33
Q

MS

A

antigens to myelin basic protein

myelin destruction by activated macrophages

demyelination in CNS

34
Q

Type 1 diabetes mellitus

A

antigens of pancreatic islet beta cells

destruction of islet cells by CTLs

insulitis, destruction of beta cells

35
Q

inflammatory bowel disease

A

chronic intestinal inflammation

Th1 and Th17 cytokines

36
Q

psoriasis

A

plaques in the skin

Th17 cytokines

37
Q

contact sensitivity

A

environmental antigens, poison ivy, etc.

skin rash and blisters

Th1/ Th17? cytokines

38
Q

Guillain Barre Syndrome

A

Often begins after an infection or vaccination
Ascending paralysis (also some sensory loss)
2-5 % mortality
20% disability
Increased CSF protein
Viral or bacterial disease or vaccination  T cell mediated peripheral nerve demyelination
Segmental demyelination of peripheral nerves
Axons damaged when severe
Chronic inflammation—most intense in spinal and cranial nerve roots

39
Q

Rheumatic fever

A

molecular mimicry

40
Q

Acute Rheumatic Fever

A

Pericarditis
Myocarditis; Aschoff bodies, Anitschkow cells

Endocarditis

41
Q

CREST syndrome associated with

A

centromeric (coarse speckled) staining

42
Q

SLE, Drug-induced lupus associated with

A

Homogenous staining

histone antigens

43
Q

Fine speckled staining associated with

A

non specific

44
Q

systemic sclerosis antigens

A

DNA topoisomerase I

45
Q

autoimmune myosiis antigens

A

histidyl-tRNA synthetase

46
Q

Sjogren syndrome antigens

A

RNP

47
Q

SLE antigens

A

pretty much everything

48
Q

how many criteria make SLE?

A

4 or more of the 11

photosensitivity, hemolytic anemia, anti-dna antibody, antiphospholipid antibodies, false-positive for syphilis, e.g.

49
Q

prevalence of stuff in SLE

A 
hematalogic 100
arthritis 80-90
skin 85
renal 50-70
raynaud 15-40
50
Q

SLE features

A

butterfly rash, fever, joint pain
LE bodies or hematoxylin bodies
cells that engulf these bodies are called LE cells

In situ immune complex formation antigens probably the most important

anti-phospholipid syndrome
thrombotic microangiopathy
recurrent miscarriages

Nuclear antigens: nucleosomes- DNA and histones
anti double stranded DNA

Smith antigen
Ro/SS-A, La/ SS-B

Kidneys (75% of patients have renal involvement)
Increased serum creatinine
RBCs and RBC casts in the urine

51
Q

Sjogren syndrome

A

Mikulicz syndrome - lacrimal and salivary gland enlargement from any cause
Sicca syndrome
Keratoconjunctivitis sicca  dry eyes with blurred vision, thick secretions in conjunctival sac
Xerostomia  dry buccal mucosa, difficulty swallowing, buccal fissures
Dry nasal mucosa

SS-A (Ro) and SS-B (La)
Lip biopsy
Schirmer test

52
Q

Systemic Sclerosis

A 
polyarthralgia
tight skin on hands and face
telangiectasias
difficulty swallowing
morphea
CD4+ lymphocytes stimulate fibroblasts and collagen formation

Anti-Scl-70- against nuclear topoisomerase
anti-centromere
90% anti-centromere in CREST

GI tract- esophagus most common
kidneys- intimal proliferation and thickening of arteries –> ischemia

53
Q

CREST

A 
calcinosis
raynaud phenomenon
esophagal dysmotility
sclerodactyly
telangiectasias

ANTI-Centromere antibody

54
Q

Dermatomyositis

A

heliotropic rash
often associated with occult tumors
anti-Jo-1

55
Q

Polymyositis

A

Autoimmune disease involving skeletal muscle without skin involvement

56
Q

Mixed connective tissue disease

A

Ill-defined autoimmune disease with overlapping features

57
Q

Transplantation

A

Mechanisms of rejection
T Cell related
Cytotoxic T lymphoctes–> parenchymal & endothelial cell injury
CD4+–> delayed hypersensitivity reactions
CD4+–> activation of macrophages
Antibody Mediated

Types of Rejection
Hyperacute -preformed antidonor antibodies are present 
Acute cellular -(direct pathway) T cells of recipient recognize allogeneic (donor) MHC molecules on the donor’s APCs
Acute humoral - (indirect pathway) exposure to the class I and class II HLA antigens of the donor graft may evoke antibodies and attack graft vessels (vasculitis)
Chronic - (indirect pathway) recipient T cells recognize MHC antigens of the graft donor after they are presented by the recipient's own APCs and induce direct cell mediated inflammatory damage or production of circulating antibodies that cause vascular injury in graft
58
Q

HIV phases

A

acute- similar to flu for a few weeks about 3-6 weeks post infection
middle chronic: asymptomatic for years, prolonged by HAART
AIDS fever, weight loss, diarrhea, generalized generalized lymphadenopathy, multiple opportunistic infections, neurologic disease, and secondary neoplasms or

59
Q

transplant phases

A

0-3 days hyperacute
4 days to 6 months- acute
more than 6 months- chronic rejection

60
Q

bone marrow transplant rejection

A

graft vs host diseases

61
Q

Bruton

A

x linked agammaglobulinemia

males after 6 months
bruton tyrosine kinase mutation
decreased B cells
no plasma cells
no intestinal IgA (giardia infections)
No Igs for opsonization of organizms (encapsulated bacteria)
62
Q

DiGeorge

A

Thymic Hypoplasia
22q11
abnormal 3rd & 4th pharyngeal pouches
Thymus, parathyroids, some of the clear cells of the thyroid, and ultimobranchial body defects
Hypoparathyroidism with hypocalcemia can lead to tetany
Cardiac outlet defects
Facial abnormalities
Viral, fungal and protozoal infections

T-cell deficiency

63
Q

Hyper IgM

A

Inability of helper T cells to induce IgG, IgA, and IgE formation

64
Q

Common Variable Immunodeficiency

A

Absent plasma cells (maturation blockage)
No immunoglobulins
Normal numbers of other B cells

65
Q

Isolated IgA deficiency

A

Low levels of secretory and serum IgA

Anaphylactic transfusion reactions to IgA in donor plasma
Immune disorders such as SLE and RA

66
Q

complement deficiencies

A

C1 inhibitor = hereditary angioedema induced by stress or trauma
Episodes of edema affecting skin and mucosal surfaces
Life-threatening asphyxia
Nausea, vomiting, and diarrhea
Rx - C1 inhibitor concentrates

C5, 6, 7, 8, or 9 (attack complex)
Recurrent neisserial (gonococcal and meningococcal) infections
67
Q

Wiskott-Aldrich Syndrome

A

WASP (Wiskott-Aldrich syndrome protein) gene mutation
Thrombocytopenia, eczema & recurrent infections
Petechiae or purpura, hematemesis or melena, epistaxis
Recurrent infections, ending in early death

68
Q

HIV immunity

A

1% of white Americans inherit two defective copies of the CCR5 gene and are resistant to infection

69
Q

CDC AIDS-defining conditions

A 
cervical cancer, invasive
encephalopathy
kaposi sarcoma
lymphoma: burkitt, immunoblastic, primary of brain
wasting syndrome
70
Q

Major abnormalities of immune function in AIDS

A

selective loss of CD4+ helper T cell subset

susceptibility to opportunistic infections
susceptibility to neoplasms
hypergammaglobulinemia and circulating immune complexes

71
Q

aids-related malignancy

A

B cell lymphoma

72
Q

Amyloidosis

A

cross beta pleated sheet conformation
congo red stain
apple green birefringence

73
Q

Classification of amyloidosis

A

primary- monoclonal plasma cell proliferations (immunoglobulin light chains, chiefly delta)
secondary- chronic inflammatory conditions (SAA)
chronic renal failure (beta two microglobulin)
alzheimer (APP)
type 2 diabetes (islet amyloid peptide)

systemic senile amyloidosis– transthyretin
medullary carcinoma of thyroid- calcitonin

Transition to Clinical Medicine (6 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions