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CLS > Immunity > Flashcards

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
Q

Describe the role of IgE and mast cells in type 1 hypersensitivity

A
  • 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
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26
Q

List examples of type 1 hypersensitivity

A 
Atopic allergy eg
Asthma
Allergic rhinitis
Eczema
Food allergies
Bee stings
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27
Q

Explain the role of Th2 cells in promoting IgE production and eosinophil development

A

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
Q

Describe systemic anaphylaxis

  • ALLERGENS
  • ENTRY ROUTE
  • RESPONSE
A

Allergens: Drugs, venom, peanuts, serum
Route of entry: IV- directly or through oral
Response: edema, vascular perm increases, tracheal occlusion, circulatory collapse, death

29
Q

Describe acute urticaria

wheal-and-flare

A

Allergens: Insect bites, allergy testing
Route: Subcutaneous
Response: Local increase in blood flow and vascular perm

30
Q

Describe allergic rhinitis - hayfever

A

Allergens: Pollen, dust mite faeces
Entry: inhalation
Response: Edema of nasal mucosa and irritation

31
Q

Describe asthma

A

Allergens: pollen, danders(cat), dust mite faeces- D pteronyssinus
Route: inhalation
Response: bronchial constriction, increased mucous prod, airway inflam

32
Q

Describe food allergies

A

Allergens: Nuts, milk, eggs, peanuts, shellfish, peanuts
Route: oral
Response: vom, diarrhoea, pruritis, urticaria, anaphylaxis

33
Q

Outline the skin prick test

A 
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
Q

Outline type 2 hypersensitivity

A

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
Q

Outline the mechanism of type III hypersensitivity

A

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
Q

Describe Extrinsic allergic alveolitis

A

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
Q

Describe type IV hypersensitivity

A 
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
Q

List types of allergic and autoimmunity type IV hypersensitivity

A

Allergic- contact derm, acute graft rejection, tuberculosis, leprosy
Autoimmune- thyroiditis, Addison’s disease, Gastritis- pernicious anaemia, T1DM

39
Q

Describe contact dermatitis

A 
Response to nickel or chromate
Plant products- poison ivy
Small allergens- haptens
Bind to body proteins
Skin patch test- 2-4 days
40
Q

Explain the immunological basis of tissue transplant rejection

A

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
Q

Distinguish primary and secondary immunodeficiencies

A

Primary- due to inherited mutations in genes with immunological functions. Autosomal recessive
Secondary- due to environmental insults/disease process

42
Q

Features of characteristic infections due to immunodeficiency

A

Serious
Persistent
Unusual-opportunistic
Recurrent

43
Q

Causes of bacterial infections

A

Deficiencies in antibodies, complement, phagocytes– abcess formation

44
Q

Causes of viral/fungal infections

A

T cell defects,

graft vs host disease

45
Q

Outline features of primary immunodeficiency

A 
Tretable
Several types
Affect more adults than children
Generally underdiagnosed- diagnosis late or delayed
Chronic infections eg bronchiecstasis
46
Q

Outline features of secondary immunodeficiency

A

Lymphoproliferative disease
Loss of IgG (renal/gut)
Malnutrition
Immunosuppressive drugs

47
Q

Explain nature and consequences of DiGeorge syndrome as an example of a primary T cell defect

A

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
Q

Describe Myasthenia Gravis

And symptoms

A

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
Q

Outline features of AIDS

A

AIDS- Secondary T cell deficiency, caused by HIV
Asymptomatic for years then early symptoms
Persistent generalised lymphadenopathy

50
Q

Outline features of HIV

A

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
Q

Outline nature of SCID

A

Treat: bone marrow transplant/gene therapy
Inherited stem cell defect- lack of function of B and T cells
Primary immunodeficiency

52
Q

What are the main causes of neutrophil defects?

A

Lack of production due to

1: Kostmanns, cyclic neutropenia
2: leukemia, cancer, chemo, infections

53
Q

How can neutrophils be defected?

A

Destroyed peripherally
Abnormal function eg leucocyte adhesion deficiency
Chronic granulamtous disease/hyper IgE syndrome

54
Q

Describe the consequences of complement deficiency

A

Immune complex disease- bac infection

Recurrect Neisserial infection

55
Q

List 4 main categories of secondary immunodeficiencies

A

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
Q

Describe how Grave’s disease induces hyperthyroidism

A

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
Q

Describe how Grave’s opthalmology develops

A

Inflammatory disease of extra ocular tissue
Mucopolysaccharides produced
Associated oedema behind eyes, eyes bulge out
Cross reaction between thyroid and ocular autoantigen

58
Q

Describe how pretibial myxoedema develops

Which condition is it due to

A

Deposition of mucopolysaccharides in subcutaneous connective tissue
Swelling in front of skin

59
Q

Describe the immunological basis of Hashimoto’s thyroiditis

A

Autoimmune destruction of thyroid gland- hypo

Lymphocytic infiltration of thyroid- goitre

60
Q

Describe the immunological basis of Atrophic thyroiditis

A

Antibodies block TSH receptors
Destruction and fibrosis of thyroid tissue
Causes hypothyroidism

61
Q

With which other diseases does autoimmunity to thyroid overlap?

A

Endocrine/organ specific diseases eg
pancreatic islets
gastric tissues

62
Q

Explain the basis of pernicious anaemia (cockblock)

A

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
Q

Explain the basic of T1DM

A

Autoreactive Tc cells target and destroy B cells in pancreatic islets
React against autoantigens eg insulin, glutamic decarboxylase, glucagon, somatostatin

64
Q

Describe autoimmune haemolytic anaemia

A

Autoantibodies specific to erythrocytes

Surface antigens oposonise erythrocytes- induce complement activation and destruction by phagocytes

65
Q

Describe Pemphigus

A

Antibodies bind to intercellular substance (cadherin)of skin epidermis
Blistering inflam reaction

66
Q

Describe the nature of systemic lupus erythrematous (SLE)

A

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
Q

Describe the nature of rheumatoid arthritis

A

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

CLS (11 decks)

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