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Immune System > 1.1 Hypersensitivity Reactions > Flashcards

1.1 Hypersensitivity Reactions Flashcards

1
Q

What is the main cause of immunodeficiency?

A

Malnutrition

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2
Q

What group suffers the most from immunodeficiency?

A

Over 60yrs / elderly

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3
Q

Give examples of organ specific hypersensitivity reactions?

A

Goodpastures syndrome
Haemolytic anaemia
Myasthenia gravis

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4
Q

Give examples of non-organ specific hypersensitivity reactions?

A

SLE

RA

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5
Q

What is hypersensitivity?

A

the antigen- specific immune responses that are either inappropriate or excessive and result in harm to host

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6
Q

What are the 2 effects that can occur in hypersensitivity affecting organs?

A

Change in function

Damage to tissue

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7
Q

What exogenous antigens can trigger a hypersensitivity reaction?

A

Non infectious substances (innocuous) - peanuts
Infectious microbes
Drugs (Penicillin)

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8
Q

What intrinsic antigens can trigger a hypersensitivity reaction?

A 
Infectious microbes (mimicry) - strep throat 
Self antigens (auto-immunity)
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9
Q

Why is hypersensitivity to intrinsic antigens difficult to treat?

A

Infectious microbes - some mimick

Self antigens - wdeyguhefrjrhddrjyyj

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10
Q

What are the 4 types of hypersensitivity reaction?

A
  1. Type I – Immediate - Allergy- ~5mins
  2. Type II- Antibody mediated -5-12h
  3. Type III- Immune complex mediated – 3-8h
  4. Type IV- Cell medicated- Delayed 24-72h
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11
Q

What are the 2 phases of hypersensitivity reactions?

A

Sensitisation Phase– initial exposure to the antigen Effector Phase – re exposure to the antigen

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12
Q

What occurs in a type 1 hypersensitivity reaction?

A

Inappropriate response to benign allergens, which can be external (allergy) or internal (autoimmune reaction). Immediate antibody mediate reaction.
Abnormal T helper 2 cell response to allergens. Secretes IL-4, IL-5 and IL-13 that cause B cell differentiation into plasma cells and IgE production

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13
Q

Describe the mechanism of sensitisation?

A

Antigens picked up by antigens presenting cells
Are processed and presented on the cell cell surface
APC carries allergen to near by lymph tissue (lymph node)
Allergen presented to TH2 cells
TH2 cells activate the B cells to become plasma cells via IL-21
IL-4 stimulates the B cells to class switch to an IgE immunoglobulin
Plasma cells are now IgE secreting plasma cells that are primed against a specific allergen
Heavy chain of the IgE will bind to FC receptors on mast cells and basophils and waits there.

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14
Q

What occurs in the effector phase of type 1 hypersensitivity reactions?

A

On subsequent exposure the allergen the bound IgE on mast cells and basophils will recognise the allergen and bind to it
On mast cells the allergen cross links the IgE, activating these cells to degranulation and release histamines
This increases vascular permeability and vasodilation. Extravasation of neutrophils and acute inflammatory cells.

In late phase, hours after exposure, other mediators (leucotrienes, prostaglandins, ECF.A) are synthesised after the cells degranulate.

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15
Q

What is anaphylaxis?

A

The most severe form of type 1 hypersensitivity reaction. Life threatening.

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16
Q

What are the symptoms of anaphylaxis?

A 
Feeling of impending doom
Hypotension
Oedema of the lips and neck
Severe bronchoconstriction
Tachycardia
Anaphylactic shock 
Cardiovascular collapse 
Generalised urticaria 
Angioedema
Breathing problems
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17
Q

What is atopy?

A

Immediate hypersensitivity reaction with an environmental trigger and a strong familial predisposition

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18
Q

What is the treatment for type 1 hypersensitivity reactions?

A 
Allergen desensitisation 
Anti IgE antibody 
Antihistamine
Leucotriene receptor antagonists 
Corticosteroid
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19
Q

What is a hypersensitivity type 2?

A

Antibody binds with cell surface antigen to activate compliment resulting in cell and organ damage

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20
Q

Give examples of hypersensitivity type 2 reactions

A 
Haemolytic transfusion reactions
Haemolytic disease of newborn
Myasthenia gravis
Grave’s disease
Autoimmune haemolytic anaemia 
Goodpastures syndrome
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21
Q

What are the treatment options for type 2 hypersensitivity reactions?

A

Cell tissue damage:
-Anti inflammatory drugs - prednisolone. Usually given with steroid sparing agent to reduce dosage.
-Plasmapheresis - removing antibodies and replacing the plasma
-Splenectomy - limits clearance of opsonised platelet and RBCs
-Intravenous immunoglobulin - blocks Fc receptor of macrophages and phagocytic cells
Physiological change
- correct metabolism
- replacement therapy

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22
Q

What is a type 3 hypersensitivity reaction?

A

Soluble antibody antigen complex forms causing an immune complex to be deposited resulting in damage and disease development

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23
Q

What are common sites of damage in type 3 hypersensitivity reactions?

A

Joints
Skin
Small vessels
Kidney

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24
Q

Give some examples of type 3 hypersensitivity reactions

A

Rheumatoid arthritis
Glomerulonephritis
Systemic lupus erythematosus

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25
Q

What is a type 4 hypersensitivity reaction?

A

Driven b lymphocytes and macrophages, TH1 T cells

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26
Q

Give some responses that occur in type 4 hypersensitivity reactions to exogenous antigens

A

Contact
Tuberculin
Granulomatous

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27
Q

Give some responses that occur in type 4 hypersensitivity reactions to endogenous antigens

A

Insulin dependent diabetes mellitus
Hashimoto’s thyroiditis
Rheumatoid arthritis

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28
Q

What are the treatment options for type 3 and type 4 hypersensitivity reactions?

A

Anti-inflammatory drugs

Monoclonal antibodies

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29
Q

What is urticaria?

A

Raised rash due to oedema of the epidermis caused by mast call activation

30
Q

What is angioedema?

A

Raised swellings due to mast cells activation in the deep dermis

31
Q

How is anaphylaxis treated?

A

Adrenaline

32
Q

What distinguishes the different blood groups

A

Presence or absence of carbohydrate antigens on the RBC surface.
Type A blood has the “A” antigen, type B blood has “B” antigen, type AB has both antigens, and individuals with type O blood have neither of these antigens.

33
Q

Why does mismatch of the ABO system rarely cause haemolytic disease of the newborn?

A

Naturally occurring anti- A/B antibodies are usually IgM, which do not cross the placenta.

34
Q

What is haemolytic disease of the new born?

A

When the fetus has Rhesus +ve blood group and the carrying mother is Rhesus -ve. As the d antigen is highly immunogenic, if the mother is exposed to small amounts of d-positive RBCs, she produces anti-D IgG antibodies. If the mother becomes pregnant in the future with another Rhesus +ve baby, these IgG antibodies can cross the placenta and opsonise foetal RBCs. These are then cleared from the circulation by the liver and spleen macrophages.

35
Q

How might a baby with haemolytic disease of the newborn present?

A

Profound anaemia = fatigue, not feeding

Jaundice = yellow skin and sclera

36
Q

What are the main complications of increased bilirubin levels for the baby?

A

Seizures and brain damage if it affects the CNS

37
Q

What blood tests could be performed during pregnancy to confirm destruction of RBCs?

A

Amniocentesis - look for increased bilirubin in the amniotic fluid
Blood test from the umbilical vein - would show decreased level of haematocrit

38
Q

What is the therapeutic benefit of RhoGam in Rhesus negative women?

A

RhoGam is anti-d immunoglobulin. Prevents the sensitisation of maternal immune system against the d antigen. Prevents anti-d IgG antibodies being produced and therefore no haemolytic disease of the newborn in future pregnancies

39
Q

What is the indirect Coombs test?

A

Tests for RBC antibodies in serum samples
An antibody screen that is performed by mixing a patient’s serum with reagent red cells with known antigens. If the patient has serum antibodies directed against any of the red cell antigens, the specimen will agglutinate (clump) after antiglobulin is added.

40
Q

What is the direct Coombs test?

A

patient’s RBCs are mixed directly with antiglobulin. Patients with delayed hemolytic transfusion reactions or with autoimmune hemolytic anemias have red cells coated with antibodies that agglutinate, yielding a positive reaction.

41
Q

What is febrile nonhaemolytic transfusion reactions?

A

most common acute transfusion events.
The patient often experiences chills, rigors, and a temperature increase of 1°C or more during or after the transfusion.
This reaction is due to pyrogenic cytokines (IL-6 or TNF) that are stimulated in the recipient by leukocytes in the transfused product or that have already been produced in the transfusion product during storage. Most patients are pretreated with an antipyretic (e.g., acetaminophen) to avoid this reaction.

42
Q

What is a haemolytic transfusion reaction?

A

Occurs most commonly when ABO incompatible blood is transfused.
The most common cause is human error in matching identification of the patient and appropriate blood product! Antibodies in the patient’s serum react with antigens on the transfused cells and complement-mediated intravascular hemolysis occurs.
Along with fever, patients may have chills, chest pain, hypotension, and diffuse bleeding. Renal failure, shock, and DIC can follow. Death occurs in 10 to 40% of cases.

43
Q

Why can haemolytic transfusion reactions be delayed?

A

If the person who is receiving the incorrect blood has been previously sensitised during a previous transfusion but has undetectable antibodies on pretransfusion testing.
Several days to weeks after the second transfusion, the patient produces more antibodies, which coat the surface of the transfused cells. Presenting symptoms are fever, anemia, and jaundice due to extravascular hemolysis as the antibody-coated RBCs are removed in the spleen. A direct Coombs test is often positive

44
Q

Why are antihistamines often given before transfusing blood?

A

To prevent an allergic transfusion reaction.

45
Q

Why might babies develop hyperbilirubinaemia?

A

After delivery of baby with Haemolytic Disease of the Newborn (HDN), bilirubin present in the neonate’s blood is no longer cleared via the placenta, leading to the accumulation of bilirubin in the baby’s bloodstream (called hyperbilirubinemia) and other tissues/fluids resulting in JAUNDICE.

46
Q

What is the main complication of increased bilirubin levels for the baby?

A

If levels continue to rise, bilirubin may enter the brain to cause kernicterus, a potentially fatal condition that leaves permanent neurological damage in the babies that survive.

47
Q

Which serology tests are used to diagnose myasthenia gravis?

A

Blood test to check for anti-acetylcholine receptor (AChR) and anti-muscle-specific tyrosine kinase (MuSK) antibodies.

48
Q

What is the basic pathophysiology of myasthenia gravis?

A

Anti-acetyl choline receptor antibody blocks the receptor. This stops the K+ channel from opening and therefore the membrane does not become depolarised. Less APs fire.

49
Q

Newborn infants from mothers with myasthenia gravis exhibit symptoms of myasthenia gravis at birth. Describe the immune mechanism responsible for the disease in the infant and explain why the disease eventually disappears.

A

IgG autoantibodies from the mother transfer to the fetus across the placenta. This trigger the fetus to have similar symptoms to the mother. Symptoms disappear after 6 on this when the maternal autoantibodies are degraded or removed.

50
Q

How would you treat a patient with myansthenia gravis? What side effects are associated with this treatment?

A

Pyridostigmine - They prolong the action of acetylcholine by inhibiting the action of the enzyme acetylcholinesterase.

Overstimulation of PS autonomic nervous system due to higher levels of ACh:
Sweating ( sympathetic nervous system but uses AcH)
Over salivation
Increased need to urinate
Increased GI motility
Increased rear production

51
Q

Explain how plasmapheresis can be used for the treatment of a life- threatening myasthenic crisis.

A

Plasma of the patient containing the autoantibodies is separated from the blood and removed. Adds in a substitution fluid. As the acetyl choline receptor antibodies have been removed, this rapidly relieves symptoms.
Filters out primary antibodies,good for short term symptom relief

52
Q

What is neuromuscular transmission?

A

Process whereby an action potential in a motoneuron produces an action potential in the muscle fibers that it innervates.

53
Q

What are the steps in neuromuscular transmission? 8.

A

1) An action potential is propagated down the motoneuron until the presynaptic terminal is depolarized.
2) Depolarization of the presynaptic terminal causes voltage-gated Ca2+ channels to open, and Ca2+ flows into the nerve terminal.
3) Uptake of Ca2+ into the nerve terminal causes exocytosis of stored acetylcholine (ACh) into the synaptic cleft.
4) ACh diffuses across the synaptic cleft to the muscle end plate, where it binds to nicotinic ACh receptors (AChRs).
5) The nicotinic AChR is also an ion channel for Na+ and K+. When ACh binds to the receptor, the channel opens.
6) Opening of the channel causes both Na+ and K+ to flow down their respective electrochemical gradients. As a result, depolarization occurs.
7) This depolarization, called the end plate potential, spreads to the neighboring regions of the muscle fiber.
8) The muscle fibers are depolarized to threshold and fire action potentials.

54
Q

What is the function of acetyl cholinesterase?

A

Ach is degraded by acetylcholinesterase, an enzyme that is also present on the muscle end plate. This degradative step, whose byproducts are choline and acetate, terminates the action of ACh on the muscle fiber. Choline is taken up into the motoneuron terminal and recycled into the synthesis of more ACh.

55
Q

What is pyridostigmine?

A

Pyridostigmine is an acetylcholinesterase inhibitor that binds to acetylcholinesterase and thereby reduces binding and degradation of ACh at the muscle end plate. In the treatment of myasthenia gravis, pyridostigmine prevents the degradation of ACh, increasing its synaptic concentration and prolonging its action.

56
Q

What things does the immune system protect us from?

A

Non- self = external pathogens
Infection
Altered self = cancers

57
Q

How is the immune system associated with disease?

A

Immunodeficiency
Autoimmune conditions
Allergies / hypersensitivities

58
Q

What is the typical presentation of myasthenia gravis?

A

Muscle weakness

Ocular weakness - eyelid drooping

59
Q

What is the typical presentation of Graves’ disease?

A

Exothalmus due to inflammation of the tissue around the eye

60
Q

What exogenous antigens can cause hypersensitivity?

A

Non infectious substances (innocuous)
Infectious microbes
Drugs (Penicillin)

61
Q

What intrinsic antigens can cause hypersensitivity?

A 
Infectious microbes (mimicry)
Self antigens (auto-immunity)
62
Q

Give an example of hypersensitivity to intrinsic antigens due to mimicry by infectious microbes?

A

Rheumatic fever - causing heart valve damage as heart valve protein is similar to streptococcus pyogenes.

63
Q

How do different hypersensitivity reactions differ in their driving factors?

A

Type 1 = antibody driven. IgE
Type 2 = antibody driven IgM or IgG. Antigen is membrane bound
Type 3 = antibody driven IgM or IgG. Soluble antigen
Type 4 = cell mediated, involves lymphocytes (TH1) and macrophages . No antibodies involved.

64
Q

What is the sensitisation phase?

A

First encounter with the antigen. Activation of APCs and memory effector cells. A previously exposed individual to the antigen is said to be “sensitized”

65
Q

What is the effector phase?

A

Pathologic reaction upon re-exposure to the same
antigen and activation of the memory cells of the
adaptive immunity

66
Q

Describe the time of onset of type 2 hypersensitivity reaction

A

Usually develops 5 to 12 hours following exposure to the antigen

67
Q

What is the mechanism of hypersensitivity type 2 reactions?

A

IgM or IgG antibody binds to cell bound antigen
Cause complement activation, causing cascade of complement proteins resulting in:
Cell lysis (MAC)
Neutrophil recruitment (C3a/C5a)
Opsonisation ( C3b)
Also get tissue damage via antibody dependent cell cytotoxicity (NK cells)

68
Q

What is plasmapheresis? When is it used?

A

Used to treat conditions driven by type 2 hypersensitivity such as myasthenia gravis, goodpastures syndrome and Graves’ disease.

Take blood and remove the cellular component from the plasma. Discard the plasma and replace the plasma with a substitution fluid. Removes the cytokines and autoantibodies.

69
Q

What is the time of onset of type 3 hypersensitivity?

A

Usually develops within 3-8 hours after exposure to antigen

70
Q

What are the key factors that determine the pathogens is of immune complexes formed in type 3 hypersensitivity reactions

A
  1. Size = Intermediate size immunocomplexes are hardest to clear
  2. Host response = complement deficiency and low affinity antibody
  3. Local tissue factors.
71
Q

What are the signs and symptoms of SLE?

A

Systemic = low-grade fever and photosensitivity
Psychological = fatigue and loss of appetite
Ulcers
Butterfly rash
Pericardial rub
Pleuritic rub
Poor circulation to extremities - slow capillary refill time
Arthritis
Muscle aches

72
Q

What is the time of onset of type 4 hypersensitivity reactions?

A

Usually develops 24 to 72 hours after exposure to allergen

Immune System (4 decks)

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