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Pathology > 7 immune system > Flashcards

7 immune system Flashcards

1
Q

Hypersensitivity reaction definition

A

Altered immunologic reactivity to antigen –> pathologic immune response after re-exposure

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2
Q

Allergy definiition

A 
Immunological hypersensitivty 
 exogenous antigens (allergen)
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3
Q

How many types of hypersensitivty reactions are there

A

4

type I through IV

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4
Q

Type I HR

A

Allergic reaction, IgE mediated, immediate response
Most common form of allergic reaction
Ranges from mild to severe (anaphylaxis)

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5
Q

Type II HR

A

Tissue specific, cytotoxic, antibody mediated

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6
Q

Type III HR

A

Immune complex

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7
Q

Type IV HR

A

Cell mediated, delayed hypersensitivty

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8
Q

3 phases of type I HR

A

Sensitization of Mast and basophils
Initial-phase response
Late-phase response

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9
Q

Phase 1 of type I HR (sensitization of mast and basophils)

A

Exposure to allergen
Type 2 helper t-cells release cytokines in response followed by 2 important events
-B-Cell differentiation into plasma cells, IgE production (primary response)
-Eosinophil recruitment (secondary response)
Mast cells in tissue and basophils in bloodstream are then sensitized via addition of IgE to their cell membranes

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10
Q

Primary (initial) phase response Type I HR

A

Allergen binds to IgE causing degranulation of mast cells and basophils, which release pre-formed chemical mediators (histamine, acetylcholine, adenosine, chemotactic factors, kinins)
Response in 5-30 minutes, lasting 60 minutes
Vasodilation, increased cap perm, inflammation and smooth muscle contraction

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11
Q

Late-phase response in type I HR

A

Arachidonic Acid pathway, 2-8 hours later lasting several days
Mast cell/basophil cell membrane phospholipids breakdown into arachidonic acid which synthesizes leukotrienes and prostaglandins
Cytokines are released which cause influx/recruitment of eosinophils and leukocytes

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12
Q

Clinical manifestations of HR

A

Nausea/vomiting/GI cramps
Conjunctivitis, rhinitis, asthma, uticaria (white fluid filled blisters surrounded by erthema) hives
E.g asthma, hay fever, dermatitis (eczema) and anaphylaxis

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13
Q

Anaphylatic

A

Rapid and severe (within minutes of re-exposure)
Can be general or systemic
Hemodynamic compromise is key, due to presence within blood stream
Also major risk of upper/lower airway compromise

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14
Q

Type II HR reaction

A

Cytotoxic - tissue specific reactions
Characterized by destruction of a target cell
May be endogenous, or exogenous etiology
Through actions of IgG and IgM

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15
Q

Type II HR IgG and IgM

A

Tissue specific antigens cause
Cell destruction
Tissue inflammation
Cell dysfunction

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16
Q

Cell destruction by IgG and IgM in type II HR

A

Antigens targeted by IgG and IgM and are destroyed either by complement system or leukocytes
E.G transfusion reactions, rheumatic fever, RH incompatibility, certain drug reactions and transplant rejection

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17
Q

Tissue inflammation in type II HR by IgG and IgM

A

Antibodies in extracellular tissue (basement membrane or matrix) are deposited, leading to a complement mediated inflammation
Seen in renal disease and transplant rejection related to organ vasculature

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18
Q

Cell dysfunction in type II HR and IgG and IgM

A

Antibody mediated change in function of a given cell rather than destruction
E.g graves disease is TSH receptor binding causing overproduction of thyroixine leading to hyperthyroidism
Also Myasthenia gravis is destruction of ACH receptors at neuromusclular endplates

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19
Q

Type III HR

A

Immune complex mediated (IgG and IgM again)
Complexes ar formed in circulation, deposited later in vessel walls and extravascular tissue which cause compliment activation and neutrophils

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20
Q

Examples of type III HR

A

Arthus (localized inflammatory and tissue necrosis)
Immune complex lodged in vessels causing vasculitis
SLE
Polyarthitis nodosa

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21
Q

Type IV HR

A

Cell mediated destruction (not antibody mediated)
Carried out by sensitized t lymphocytes
Response to microorganisms, chemical antigens, self, transplants
Antigen presented by APC to helper t-lymphocytes (sensitized by helper T)
Direct or delayed

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22
Q

Direct cell mediated cytotoxicity (type IV HR)

A

Primary helper T cells directs T lymphocytes (CD8) to directly kill cells that express certain surface antigens
E.g viral hepatitis, destruction of hepatocytes is caused by cytotoxic t-lymphocytes rather than virus
poison ivy
transplant rejection

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23
Q

Delayed-type HR disorders (type IV)

A

Pre-sensitazaion of helper T lymphos (CD4) release cytokines upon re exposure leading to a delayed response by a number of inflamm cells causing cell damage

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24
Q

Examples of delayed type HR disorders

A

TB test, contact dermatitis (metal and latex) hypersensitivty pneumonitis and transplant rejection

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25
Q

*Type I name

A

IgE bound to mast cells release histamine and others

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26
Q

*Type I mechanism

A

IgE

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27
Q

*Type I examples

A

Seasonal allergic rhinitis, anaphylatic reactions

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28
Q

*Type II name

A

Cyotoxic/tissue specific reaction,

IgG and IgM bind to antigens of cells

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29
Q

*Type II mechanism

A

IgG and IgM

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30
Q

*Type II examples

A

Hemolytic anemia
Myasethenia Gravis
Transplant rejection

31
Q

*Type III name

A

Immune complex mediated - deposited in tissues

32
Q

*Type III mechanism

A

IgG and IgM

33
Q

*Type III examples

A

Systemic lupus erythematous, polyarthris nodosa

34
Q

*Type IV name

A

Cell mediated/ delayed reaction

35
Q

*Type IV mechanism

A

T-lymphocytes

36
Q

*Type IV examples

A

Contact sensitivty to poison ivy, metals, TB test, transplant rejection

37
Q

Autoimmune disease overview

A

Represent a group of disorders when the body cannot identify self vs non self
MHC part of it, but there are other proteins/glycoproteins on our cells that are also recognized as self-antigens

38
Q

Etiology of autoimmune

A 
Largely unknown but there is a genetic predispositon and
environvmental factors (triggering event interacts to precipitate the altered immune state) can be caused by infections, hormones, toxins
39
Q

Breakdown of t-cell anergy in autoimmune

A

Anergy is a state of unresponsiveness to antigens when t-cells encounter our self antigens
MS and RA (or infection, tissue necrosis, inflammation) can cause certain tissue to release chemicals to cause breakdown of t-cell anergy

40
Q

Hidden antigens autoimmune

A

Self-antigens are hidden and exposed later, then perceived as foreign

41
Q

Molecular mimicry autoimmune

A

Microbe share an immunological epitope with the host. Body produces immune response to microbe’s epitope (acute glomeruloneephritis and RF)

42
Q

Neoantigens autoimmune

A

Haptens bind to our tissue and create hapten adduct. Environmental chemicals or drug metabolites form these

43
Q

Forbidden clone autoimmune

A

During normal T and B cell proliferation in the thymus the lymphocytes react to MHCs and are deleted. Sometimes they survive

44
Q

Superantigens autoimmune

A

Infectious toxins that have ability to disrupt normal immune response process and create inappropriate activation of CD4 helper Ts which target our self antigens (food poisoning and chron’s)

45
Q

Examples of systemic autoimmune disorders

A

RA, RF, SLE

46
Q

Autoimmune of parietal cells (stomach)

A

pernicious anemia

47
Q

Organ specific autoimmune

A 
Hashimotos
Graves
IDDM
Myasthenia Gravis
Chron's and ulcerative colitis
48
Q

SLE

A 
Type III HR
Chronic inflammatory disease
Marked by remission/exacerbations
Mutifactorial etiology (family)
Mostly women between 20-40
UV light may trigger it
49
Q

Patho of SLE

A

Large number of circulating antibodies against DNA, platelets, RBCs and nucleic acids
Immune complexes deposited in CT anywhere, activating complement and causing inflammation and necrosis
Vasculitis in many organs

50
Q

Areas of SLE

A

Kidneys (lupus nephritis) lungs heart brain skin GI

Diagnosis based on minimum 4 areas

51
Q

Clinical manifestations of SLE

A 
Most common 
Arthalgia
Fever
Malaise
Facial erythema (butterfly rash)
52
Q

Other forms of lupus

A

Discoid (cutaneous) does not affect internal organs

Drug induced - symptoms disappear 6 months after stopping drug (or sooner)

53
Q

Transfusion reaction is a

A

Type II HR

54
Q

Immunogoblins in transfusion reactions

A

IgM (ABO)
IgG (Rh)
Person with antigen A have type A blood

55
Q

ABO reactions (IgM)

A

Causes RBC agglutination and hemolysis

56
Q

S&S of transfusion reactions

A 
Heat along venous infusion site
Flushed face
headache
uticaria
fever and chills
lower back pain
chest pain
abdo cramps N/V
Tachycardia, hypotension, SOB
Renal deficits
57
Q

Rh incompatibility

A

Antigen present is Rh+
If Rh- pt receives Rh+ blood THEN the body will build up antibodies
Second transfusion with Rh+ blood is given
Hemolysis and severe reaction will occur

58
Q

Pregnancy and Rh

A

Mother is Rh- and fetus is Rh+ creates incompatibility. First pregnancy is okay, but when placenta tears mom is exposed to Rh+ antibodies
Subsequent pregnancies Rh antibodies cross to fetus

59
Q

Complications and treatment of pregnancy Rh incompatibility

A

Hemolysis, anemia, low Hb, high bilirubin, jaundice
Heart failure and death
Tx is Rh immunoglobuin to mother after first delivery which prevents sensitization

60
Q

You have AIDS

A

HIV is causative agent
Aids is active stage
Can take 6-14 months to develop antibodies which can be detected
HIV positive for months to years before full blown AIDS

61
Q

High risk for aids

A

Unprotected sex regardless of orientation
IV drug users
Hemophiliacs

62
Q

So you have AIDS and you want to know the pathophysiology

A

Retrovirus (genetic info in form of RNA rather than DNA)
Binds to host cells surface and inserts RNA which is converted to DNA into hosts material
CD4 on surface of t-helper acts as receptor. Virus kills t-helper and the immune system is compromised

63
Q

Phase one of AIDS

A

Phase 1 is initial infection and development of antibodies

Self limiting and flu-like S&S

64
Q

Phase two of AIDS

A

Latent period, virus is hiding. Virus has mutated or crippled specific immunity against it
Usually asymptomatic, may have lymphadenopathy

65
Q

Phase three of AIDS

A

Low CD4+ levels.

All the bad stuff happens

66
Q

Generalized manifestations of AIDS

A

Lymphadenopathy, fatigue/weakness, headache, GI effects (severe diarrhea, vomting, ulcers), severe weight loss
Neuro (AIDS dementia) from infection of brain cells
Secondary infectioons (herpes, candida, pneumocystis carinii)

67
Q

Treatment for AIDS

A

Treatment with antiviral drug azidothymidine (AZT)

68
Q

Organ transplant overview

A

Cells, tissue or organs all referred to as grafts
Self = autologous
Identical Twin = syngeneic
Related = allogenic (genetically different)
Unrelated = allogenic
Immunosupprsents are used (Cyclosporine, AZT, prednisone)

69
Q

MHC

A

Major histocompatibility complex AKA HLA human leukocyte antigen
Group of genes found on chromosome 6. Closer the antigen match the less rejection

70
Q

Pathogenesis of tissue rejection

A

Cell mediated rejection usually
T-cells type IV HR can be direct or delayed
May be humoral medaited type 2/3 HR

71
Q

Hyperacute clinical manifestations of tissue rejection

A

Antibody mediated, occurs in minutes
Previous tranfusions, transplants or pregnancy lead to development of target antibodies that attack donor tissue.
Usually type II or III HR
Often in vascular areas

72
Q

Acute clinical manifestations of tissue rejection

A

T cell mediated in days to months

Direct or delayed lysis and inflammation of tissue

73
Q

Chronic clinical manifestations of tissue rejection

A

Idiopathic
Months to years
Fibrotic changes in tissue

Pathology (24 decks)

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