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Immunity Flashcards

1
Q

List stimulants of an acute inflammatory reaction

A 
Micro organisms
Trauma (surgical incision)
Ischaemic necrosis
Radiation damage - sunburn
Chemical damage- acid/alkali
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2
Q

3 purposes of an acute inflammatory reaction

A

Destroy/neutralise damaging agent
Liquefy/remove dead tissue
Prepare damaged area for healing

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3
Q

How does an acute inflammatory reaction occur?

A

Production of inflam exudate from blood from capillaries near damaged area
Consists of:
FLUID- dilute toxins, carry nutrients, mediators, antibodies
FIBRIN- speculative role
NEUTROPHILS- phagocytose living tissue/necrotic tissue
few macrophages, lymphocytes

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4
Q

Stages in exudate formation

A
  1. BV near damaged tissue become dilated
    Blood flow increases then slows down

Axial flow pattern of blood lost
Why?
Substances released from dead tissue into bv–> VESSELS DILATE

  1. Endo cells swell and retract, vessels leak, perm inc
  2. Water, salt, proteins leak into damaged area
    Fibrinogen important protein
  3. Neutrophils marginate and emigrate
  4. Neuts stick to endo cells, neuts migrate through caps to damaged area
  5. Fibrin polymerises in tissue, from fibrinogen released from vessel in exudate.
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5
Q

Describe 4 types of clinical exudate

A
  1. Serous- excess fluid accum eg pericardial sac. Forms a blister
  2. Purulent- in meninges- live and dead neutrophils
  3. Fibrinous- shaggy exudate on pericardium- adhesions following surgery
    Pink staining fibrin- abcesses, boils, cellulitis
  4. Fibrinopurulent
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6
Q

List the mediators of inflammation

A

Vascular changes- prostaglandins, NO, histamine, 5HT, bradykinin, leukotriene
Cellular changes- leukotriene, PG, bradykinin

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7
Q

List the consequences of an acute inflam reaction

A 
A boil shows
Rubor
Dolor 
Tumor
functio laesa
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8
Q

How does acute inflammation manifest in a clinical setting?

A

Malaise, fever, pain, rapid pulse
Raised ESR
Neutrophil leukocytes
Increased acute phase proteins eg IL1, CRP

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9
Q

Define chronic inflammation and list 3 circumstances it arises

A

Occurs if damaging stumilus persists, complete healing can’t occur
Organisation repair still happens- inflam and prolif- still damage as stimuli not removed
Tissue infiltrated by immune effector cells eg MP- always heals by scarring
eg PEPTIC ULCERS
protective stomach mucosa damaged, tissue exposed to gastric acid
Tissue necrosis–> acute inflam, exudate formation and granulation. More damage
If continues- bleed/perforation
Stops- scar

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10
Q

List pathological features of chronic inflammation

A

Resolution
Abcess formation
Fibrous repair

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11
Q

Describe resolution and its outcome

A

Exudate eliminates agent, both removed by macrophages
Local cells grow so tissue function goes back to normal eg tubular necrosis of kidney, sunburn and LOBAR PNEUMONIA
No damage to alveolar architecture, exudate forms in alveolar air sacs
Liquefied exudate is resorbed
Alveolar lining cells regrow

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12
Q

Describe an abcess

A

Large accum of liquid purulent exudate (pus) where tissue damage causes necrosis
Usually due to bacteria - staphylococcus

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13
Q

Describe fibrous repair

A

Same inflam and MP phase as resolution
Prolif- new cap vessels form by budding from nearby vessels and support new cells
New caps redundant–> regress
Normal structure/function not restored

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14
Q

Describe organisation and repair

A 
Caps grow into damaged area
Fibroblasts migrate into area and multiple
Fibroblasts synthesis collagen
New capillaries regress
Fibroblasts regress

Macrophages phag solid debris, enzymes liquefy resr
Caps grow into damaged area by budding, fibroblasts move in
New caps dominate histology, residual inflam cells remain
Fibroblasts prolif and excrete collagen
Most new caps regress
Fibs align and secrete lots of collagen

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15
Q

Describe granulomatous inflammation

A

Special form of chron inflam where neutrophils are ineffective

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16
Q

Describe TB as an example of granulomatous inflammation

A

MP involved in early response
Aggregate around agent
Assoc with surrounding lymphocytes and fibroblasts, form a granuloma

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17
Q

How does TB get better?

A

Fibroblasts around tubercle prolif, make a collagenous shell, prevent spread of organism

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18
Q

How does TB get worse?

A

Necrosis expands and can’t be contained by granuloma

May be spread by lymphatics, veins, bronchi

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19
Q

How are macrophages activated?

A

By gamma interferon

  • leak from caps near damage, phag solid debris
  • secrete inflam mediators eg protease hydrolyses
  • Cytokines IL1 and TNFa move up conc gradient–>infection
  • Secrete growth factors
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20
Q

Outline how acute inflam, inflam exudate, gran tissue and fibrous scar are interlinked as the most common outcome of tissue damage

A 
Tissue damage-->
acute inflam
Exudate formation
Granulation
Fibrous repair
Debris removed, new vessels and support cell grown
Collagen layed down. matures
Gran tissue--> scar
Vascular, fibrovascular, collagenous
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21
Q

List examples of how system repair can fail

A 
Exudate causes symptoms- meningitis, pericarditis
Continuing infection- wound infection
Foreign or uncleared necrotic material
Diabetes- tissue necrosis and ischaemia
Denervation
Steroid therapy
Previous irradiation
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22
Q

Describe how brain necrosis differs from basic repair processes

A 
No fibroblasts in brain parenchyma
Can't make collagen
Necrosis undergoes liquefaction. MP turn it into liquid
and phag debris 
Dead area- liquid. 
Astrocytes form a wall
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23
Q

Describe how bone fractures heal

A

Defect fills with blood- HAEMATOMA
Debris phagocytosed, haematoma organised like exudate
Defect filled with vascular then fibrovascular tissue
Osteoprogenitor cells develop, converted into osteoblasts and synth osteoid collagen
Calcified to woven bone
Woven and healthy old bone form continuity
Active remodelling–> strong lamellar bone–> max strength

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24
Q

Distinguish the sources of the antigens recognised, and the materials damaged by, the adaptive response in antimicrobial immunity, allergy and autoimmunity.

A

Recognised as foreign, damages foreign marerial, immunity
Recognised as foreign, damages self cell- allergy/hypersensitivity
Recognised as self, damages self- autoimmunity, hypersensitivity

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25
Describe the role of IgE and mast cells in type 1 hypersensitivity
- TH2 makes IL4, causes Ig class switching to IgE - Complement activates mast cells, IgE crosslink - Mast cell FceR has high affinity for IgE- bind, crosslink, histamine granules released - Preformed granule mediators released eg histamine, heparin, tryptase within 5 mins or - New formed eg arachidonic acid, leukotrienes, PGI2 in 5-30 minutes Smooth muscle contraction and inflammation
26
List examples of type 1 hypersensitivity
``` Atopic allergy eg Asthma Allergic rhinitis Eczema Food allergies Bee stings ```
27
Explain the role of Th2 cells in promoting IgE production and eosinophil development
APCs take up antigens, process and present via HLA Class II which interacts w CD4 t cells Th2 cells promote type 1 via IL4 Genetic assoc- atopy sufferers have higher levels of IgE Th2 makes IL5- activates eosinophils
28
Describe systemic anaphylaxis - ALLERGENS - ENTRY ROUTE - RESPONSE
Allergens: Drugs, venom, peanuts, serum Route of entry: IV- directly or through oral Response: edema, vascular perm increases, tracheal occlusion, circulatory collapse, death
29
Describe acute urticaria | wheal-and-flare
Allergens: Insect bites, allergy testing Route: Subcutaneous Response: Local increase in blood flow and vascular perm
30
Describe allergic rhinitis - hayfever
Allergens: Pollen, dust mite faeces Entry: inhalation Response: Edema of nasal mucosa and irritation
31
Describe asthma
Allergens: pollen, danders(cat), dust mite faeces- D pteronyssinus Route: inhalation Response: bronchial constriction, increased mucous prod, airway inflam
32
Describe food allergies
Allergens: Nuts, milk, eggs, peanuts, shellfish, peanuts Route: oral Response: vom, diarrhoea, pruritis, urticaria, anaphylaxis
33
Outline the skin prick test
``` How to tell what allergens and immune cells are involved in a reaction Immediate reaction- IgE Immediate and late- IgE and T cells Delayed- Th1 eczematous- IgE and Th2 ```
34
Outline type 2 hypersensitivity
Driven due to entry of foreign tissue/recognition of self So ALLERGY or AUTOIMMUNITY IgA, IgM and IgG bind to cell surface membranes and connective tissue components Activate complement Trigger neutrophils to release digestive products and reactive O2 species Cell lysis and membrane leakage Allergic- haemolytic disease of newborn- enlargement of foetus liver, spleen, blood transfusion reactions GIVE ANTI D Autoimmune- MG, graves, thrombocytopoenia
35
Outline the mechanism of type III hypersensitivity
Immune complex mediated Antibody mediated, ineffective removal of immune complexes. IgM, IgA or IgG-->tissue inflam or necrosis Soluble Ig cross link, form lattice structure (immune complex) Activate complement and neutrophils--> tissue damage Allergy- dermatitis, herpetiformis, allergic alveolitis or autoimmunity- SLE, RA
36
Describe Extrinsic allergic alveolitis
Production of antibodies to counteract inhaled fungal spores Farmers lung Immune complexes form, deposited in lungs, activation of neutrophils and tissue damage Mediated by IgG- shortness of breath due to fibrosis of tissue Asthma mediated by IgE- wheezing
37
Describe type IV hypersensitivity
``` eg contact dermatitis, tuberculosis, leprosy Cell mediated- Th1, MP, Tc, CD8+, MHC class 1 ``` APCs activate Th cells Th1 secrete IL2- activate Tc cells and IFN-gamma to activate macrophages-- granuloma formation Macrophages become epitheloid cells then multinucleated giant cell Tc causes cell lysis
38
List types of allergic and autoimmunity type IV hypersensitivity
Allergic- contact derm, acute graft rejection, tuberculosis, leprosy Autoimmune- thyroiditis, Addison's disease, Gastritis- pernicious anaemia, T1DM
39
Describe contact dermatitis
``` Response to nickel or chromate Plant products- poison ivy Small allergens- haptens Bind to body proteins Skin patch test- 2-4 days ```
40
Explain the immunological basis of tissue transplant rejection
Individuals are different Transplanted tissue destroyed by immune system- foreign material TYPE 4 hypersensitivity reaction Triggered by HLA proteins on graft tissue cells HLA class1 and 2
41
Distinguish primary and secondary immunodeficiencies
Primary- due to inherited mutations in genes with immunological functions. Autosomal recessive Secondary- due to environmental insults/disease process
42
Features of characteristic infections due to immunodeficiency
Serious Persistent Unusual-opportunistic Recurrent
43
Causes of bacterial infections
Deficiencies in antibodies, complement, phagocytes-- abcess formation
44
Causes of viral/fungal infections
T cell defects, | graft vs host disease
45
Outline features of primary immunodeficiency
``` Tretable Several types Affect more adults than children Generally underdiagnosed- diagnosis late or delayed Chronic infections eg bronchiecstasis ```
46
Outline features of secondary immunodeficiency
Lymphoproliferative disease Loss of IgG (renal/gut) Malnutrition Immunosuppressive drugs
47
Explain nature and consequences of DiGeorge syndrome as an example of a primary T cell defect
Defective thymus development due to developmental defect in 3rd and 4th pharyngeal arches - fungal/viral infections, graft vs host disease - 22q11 defect CATCH 22 Cleft palate, abnormal face- dysmorphic features, thymichypoplasia heart abnormalities- CHD hypocalcaemia due to defective parathyroids
48
Describe Myasthenia Gravis And symptoms
Autoantibodies specific to Ach receptors of neuromuscular junction block Ach binding Induce internalisation of receptor Extreme weakness, fatigue, lack of nerve stim or muscle contraction
49
Outline features of AIDS
AIDS- Secondary T cell deficiency, caused by HIV Asymptomatic for years then early symptoms Persistent generalised lymphadenopathy
50
Outline features of HIV
HIV1 and 2 are opportunistic retroviruses Transmitted by blood/sex Infect Th cells, bind to CD4 molecules Progressive CD4 T cell decline, worsening immune function and susceptibility
51
Outline nature of SCID
Treat: bone marrow transplant/gene therapy Inherited stem cell defect- lack of function of B and T cells Primary immunodeficiency
52
What are the main causes of neutrophil defects?
Lack of production due to 1: Kostmanns, cyclic neutropenia 2: leukemia, cancer, chemo, infections
53
How can neutrophils be defected?
Destroyed peripherally Abnormal function eg leucocyte adhesion deficiency Chronic granulamtous disease/hyper IgE syndrome
54
Describe the consequences of complement deficiency
Immune complex disease- bac infection | Recurrect Neisserial infection
55
List 4 main categories of secondary immunodeficiencies
Iatrogenic- immunosuppressants, removal of lymphoid tissue by surgery/radiation Malignancies- leukemia, lymphoma, myeloma Infections- HIV, chronic malaria, measles Malnutrition- Protein loss disease, chronic disease (renal failure), burns
56
Describe how Grave's disease induces hyperthyroidism
Usually TSH from pit--acts on thyroid gland to make T3/4 Grave's antibodies bind to TSH receptor on thyroid follicular cells, stim thyroid production Excessive TH prod--hyperthyroidism If TSH is inhibited- no effect
57
Describe how Grave's opthalmology develops
Inflammatory disease of extra ocular tissue Mucopolysaccharides produced Associated oedema behind eyes, eyes bulge out Cross reaction between thyroid and ocular autoantigen
58
Describe how pretibial myxoedema develops | Which condition is it due to
Deposition of mucopolysaccharides in subcutaneous connective tissue Swelling in front of skin
59
Describe the immunological basis of Hashimoto's thyroiditis
Autoimmune destruction of thyroid gland- hypo | Lymphocytic infiltration of thyroid- goitre
60
Describe the immunological basis of Atrophic thyroiditis
Antibodies block TSH receptors Destruction and fibrosis of thyroid tissue Causes hypothyroidism
61
With which other diseases does autoimmunity to thyroid overlap?
Endocrine/organ specific diseases eg pancreatic islets gastric tissues
62
Explain the basis of pernicious anaemia (cockblock)
Type 4 hypersensitivity Autoimmune destruction of parietal cells and antibodies destroy INTRINSIC FACTOR Antibodies bind to IF, block B12 interactions Inhibit binding of IF to ileal receptors Parietal cell destruction decreases IF prod and decreases B12 absorption form gut B12 needed tor RBC production-- megaloblastic anaemia
63
Explain the basic of T1DM
Autoreactive Tc cells target and destroy B cells in pancreatic islets React against autoantigens eg insulin, glutamic decarboxylase, glucagon, somatostatin
64
Describe autoimmune haemolytic anaemia
Autoantibodies specific to erythrocytes | Surface antigens oposonise erythrocytes- induce complement activation and destruction by phagocytes
65
Describe Pemphigus
Antibodies bind to intercellular substance (cadherin)of skin epidermis Blistering inflam reaction
66
Describe the nature of systemic lupus erythrematous (SLE)
Autoantibodies to range of ubiquitis cellular components Anti nuclear antibodies One AMA is DNA specific-autoantigen/antibody complex forms- DNA/antiDNA deposit in tissues causing damage eg skin, kidney glomeruli, joints, CNS
67
Describe the nature of rheumatoid arthritis
Immune complexes formed by rheumatoid factors- IgG and IgM Autoantibodies which are IgG specific-damage joints RF agglutinate IgG coated beads and can be detected in pt blood samples

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