Immune System

Front 1

Skin immunity

Back 1

barrier, lysosyme (breaks down cell wall), pH (sweat), fatty acids (sebum - antifungal)

Front 2

Mucous membranes

Back 2

mucous (adhesion), ciliary action (clearing), saliva (hydrolases), stomach (pH, protease), small intestine (proteases, macrophages)

Front 3

First line innate response

Back 3

complement (alternative), macrophages, neutrophils

Front 4

Second line innate response

Back 4

inflammation (cytokines)

Front 5

List the 4 broad categories of the innate immune system

Back 5

phagocytes, cytokines (interleukins), interferon, complement

Front 6

Describe innate immunity

Back 6

Preexisting, not acquired, non-specific. Includes barriers, mucous membranes, phagocytes, cytokines, complement

Front 7

Describe the 2 main types of specific immunity (ie not innate)

Back 7

Passive: pre-formed antibodies or T-cells used to treat acute infection
Active: contact with infectious agent or antigen.

Front 8

How are pathogens remove from the respiratory tract via innate mechanisms

Back 8

Mucocilliary apparatus, macrophages, coughing,

Front 9

Which non-specific mechanism prevents adhesion of gonococci or E.coli to the urinary tract

Back 9

IgA antibodies

Front 10

What virulence factor does pneumococcus have to prevent phagocytosis

Back 10

Polysaccharide capsule

Front 11

List the hallmarks of chronic inflammation

Back 11

1) recurring injury & repair
2) fibrosis & angiogenesis
3) mononuclear cells: lymphocytes, monocytes, macrophages

Front 12

repeated cholelitiasis leading to repeated cholecystitis can lead to?

Back 12

chronic inflammation due to repeated acute inflammation

Front 13

List the 4 contributing factors to chronic inflammationa

Back 13

1) low antigenicity
2) prolonged exposute to antigen (eg autoimmune endogenous antigens)
3) antigen that cannot be broken down (endogenous - uric acid crystals, exogenoug - silica, asbestos)
4) virulance factors preventing complete phagocytosis

Front 14

What is the fate of monocytes in the absence of chemotactic factors (inflammation)

Back 14

1) adhesion -> extravasation
2) differentiation into Kupfer cells (liver), osteoclasts, tissue macrophages

Front 15

What is the fate of monocytes in the presence of chemotactic factors (inflammation)

Back 15

1) adhesion -> extravasation
2) activation -> growth, increased lysosymal & phagocytic activity
3) release of biologically active compounds -> NO2,

Front 16

What are biologically active compounds released by macrophages when activated

Back 16

1) tissue injury compounds: proteases, oxygen metabolites, NO
2) fibrosis: angiogenesis, fibrogenic, growth factors
3) remodelling collagenases

Front 17

List the ways mechanism by which macrophages contribute to chronic inflammation

Back 17

1) immobilisation at site by cytokines
2) proliferation
3) ongoing release of biologically active products causing tissue injury, fibrosis, angiogenesis, remodelling
4) phagocytosis and harbouring of antigenic agent it is unable to break down

Front 18

Describe the positive feedback cycle between macrophages and T-cells in chronic inflammation

Back 18

Activated macrophages release cytokines (TNF, IL1) recruiting T-cells releasing interferon-a recruiting more macrophages, cytotoxic T-cells & NK cells

Front 19

List 3 types of cells other than single macrophages that contribute to chronic inflammation

Back 19

1) eosinophils
2) mast cells -> fibrosis
3) giant cells

Front 20

Primary lymphoid organs

Back 20

1) thymus
2) bone marrow

Front 21

List the maturation steps of T-Cells

Back 21

1) migration of immature lymphocytes to cortex of thymus
2) maturation, migration to medulla and apoptosis of cells recognising self
3) return of mature T-cells back to secondary tissue (spleen, peyer's patches, lymph nodes)

Front 22

List the main regions within a lymph node and the major sites of lymphoid cells

Back 22

1) Cortex is fed by afferent lymphatics. Distal cortex contains follicles containing B cells and germinal centres. Cortex also has more proximal T-cell region
2) Medulla: B-cells, macrophages, medullary sinus & fed by artery & drained by vein

Front 23

How are MHC involved in recognition of self

Back 23

1) MHC1 on all nucleated cells
2) MHC2 on macrophages & T-cells)

Front 24

What is the MHC restriction of Th cells & the MHC co-receptor

Back 24

1) Th will only bind to MHC2 (no actual primary defence role - only binds to other lymphocytes and macrophages)<BR>2) Co-receptor expressed is CD4

Front 25

How do cytotoxic T-cells recognise antigenic cells

Back 25

cell exhibits:
1) MHC1
2) presented antigen

Front 26

How do cytotoxic T cells recognise & kill cells

Back 26

1) Recognise MHC1/antigen complex on cell surface
2) Inject perforin
3) inject proteases initiating apoptosis (granzymes)

Front 27

Describe the interactions between Th cells and cells expressing MHC2

Back 27

1) Interaction with macrophages -> interferon-Y secretion & activation of macrophage
2) interaction with B-cells -> IL4/IL5 secretion -> antibody production

Front 28

How are cells recruited in chronic inflammation

Back 28

macrophages IL1 TNF IF

Front 29

What are the 3 forms of giant cells

Back 29

1) Langhans (curved nucleus TB only)
2) touton
3) foreign body

Front 30

What cytotoxic agents are released in chronic inflammation

Back 30

free radicals, NO, prostaglandins

Front 31

Repair factors released in chronic inflammation

Back 31

TGF (transforming growth factor), PDGF (platelet derived growth factor)

Front 32

List the factors protecting the stomach mucosa

Back 32

alkkaline mucus(HCO3), prostaglandins, hormonal control (somatostatin)

Front 33

What are the hotile factors promoting peptic ulcer formation

Back 33

H.pylori, H+, pepsin, EtOH, NSAIDS, smoking

Front 34

which pair is most similar & why: exudate, transudate, ultrafiltrate, plasma

Back 34

Exudate & plasma are most similar because it is whole plasma leaked from capillaries during acute inflammation

Front 35

which mediators have the most effect on vascular permeability during 1) acute immediate inflammation (2) sustained inflammation

Back 35

1) reversible mediators: histamines, leukotrienes
2) irreversable: oxygen free radicals, proteases

Front 36

What is the difference between transudate and exudate

Back 36

1) transudate: normal passage of ultrafiltrate fluid through endothelium, minimal protein
2) exudate: (eg glue ear) abnormal passage of whole plasma containing immunoglobulins, fibrin, complement, proteins causing inflammation &amp; clotting

Front 37

What is the process of vascular margination of neutrophils

Back 37

1) Heavy neutrophils remail axial during high flow
2) Inflammation -> vasodilation & flow flow allowing margination of neutrophils

Front 38

What is the process of marginated neutrophils adhering to the endothelial surface

Back 38

Pavementing (adhesion) due to expression of CAMS (cell adhesion molecules)

Front 39

which cytokines upregulate cellular adhesion to the endothelium during acute inflammation

Back 39

1) endothelial ICAM 1 & 2 upregulated by IL1 & TNF-alpha
2) B cell integrins upregulated by complement

Front 40

What is erythrocyte sludging in acute inflammation

Back 40

Slow blood flow causes colums to form - rouleax

Front 41

What are the inflammatory amines

Back 41

Vasoactive amines of acute inflammation: histamine, seritonin (activatted by C3 & C5)

Front 42

What are arachidonic acid derivatives

Back 42

1) Leukotrienes
2) Prostaglandins

Front 43

Following acute inflammation, resolution occurs how?

Back 43

macrophages phagocytose & liquify debris, passed to lymphatics

Front 44

When is repaiir an outcome of acute inflammation

Back 44

when there has been tissue necrosis. Repair can be regenerative or fibrotic.

Front 45

What is supprative inflammation & what happens when it is walled off

Back 45

1) Exagerrated infiltration of neutrophils
2) Necrotic tissue & dead neutrophils = puss forms & exudates or
3) If walled off then an abcess forms

Front 46

Name the two leukocyte adhesion proteins expressed at sites of acute inflammation

Back 46

1) selectins (rolling adhesion)
2) adhesins (firming adhesion)

Front 47

Acute inflammation features several hallmarks. Name them and their cause

Back 47

mast cells (his, ser, PGs), endothelium (NO), tissue damage (kinins, vasoactive amines) ->
rubor (vasodilation
dolor (PGs, bradykinin)
calor (vasodilation)
loss of function (prolonged NO, neutrophils-> reactive oxides, lysosomes)
tumor (endothelial contraction -> venule leakage)

Front 48

What signs are expected when a fever "breaks"

Back 48

Raised hypothalamus set point returns to normal -> mechanisms to cool body down -> sweating, vasodilation.

Front 49

How does nornal flora become pathogenic

Back 49

Entry to abnormal places ie:
Skin commensals: broken skin -> enters vascularised layers and bloodstream
GI -> urinary tract
immunocompromised or broad spectrum antibiotics: candida -> Gi tract & respiratory system.

Front 50

What are the 4 virulencce factors by which bacteria can redistribute/recombine genetic material

Back 50

transduction: phage transfer
transformation: uptake of loose DNA
conjugation: transfer of plasmid via pillus
transposition: sequences of DNA moving within the bacterial genome

Front 51

Name 2 commensals of skin flora, one of which is an anaerobe

Back 51

1) Propionbacterium acnes (anaerobe)
2) Staphylococcus epidermidis

Front 52

What are some features lacking in normal commensal bacteria preventing them bocoming pathogenic

Back 52

virulence factors:
pilli, flagella, capsules, biofilms, exotoxins, invasins, genetic variability

Front 53

Describe the process of suppuration &amp; abcess formation

Back 53

1) Noxious agent -> necrosis
2) chemokines (IL-8, TNF-α and/or IL-1β) attract neutrophils, selectins (rolling adhesion), integrins (tight adhesion), transmigration into extracellular fluid -> chemotaxis
3) pyogenic membrane (fibrous exudate + necrotic tissue) forms abcess
4) migration; death of neutrophils + vasodilation (fluid seepage) -> puss -> tumor, rubor
5) resolution (bursting, granulation) or
6) chronic inflammation (granulating pyogenic membrane, infiltration of plasma cells &amp;amp; macrophages, inflammation &amp;amp; repair, fibrosis, calcification)

Front 54

What types or organisms are likely to infect with (1) B-cell deficiency and (2) t-cell deficiency

Back 54

1) Extracellular bacteria: eg Haemophilus & S.pneumoiae
2) Viruses, intracellular bacteria

Front 55

What factors lower host resistance to infection

Back 55

1) nutrition, ageing (lower concentrations of complement & lymphocytes
2) mechanical barriers: smoking (disruption, destruction of ciliated, columnar cells), burns, sutures, IDC, IV drug use
3) immunosuppression: HIV, steroids, cytotoxics
4) overwhelming: antibiotic over/misuse, large innoculum

Front 56

Give examples from 4 different classes of opportunistic pathogens

Back 56

Viral: CMV
Bacterial: Pseudomonas aureginosa
Fungal: Candida albicans
Protozoal: Cryptosporidium parvum

Front 57

How does P.aeruginosa become pathogenic in CF

Back 57

1) thick secretions form barrier to immune system
2) innate immune selective pressure -> biofilms
3) antibiotics -> resistance

Front 58

Describe Interferon-alpha

Back 58

Peptide released by cells infected with virus or lymphocytes responding to viral infection. Upregulate MHC 1 (NK cells) & 2 (CD4 Th -> Tc activation)

Front 59

Describe release and main effects (local and distal) of TNF1

Back 59

Released by macrophages in response to LPS, bacterial proteins, IL1
Responses
1) on other macrophages & self: IL1, PGE2 (inflammation, fever, increased phagocytosis)
2) local tissues: cardinal signs of acute inflammation
3) hypothalamus (fever, CTRF),

Front 60

Describe the immediate, early & late stages defense against a viral infection

Back 60

1) Immediate: lysing infected cells release interferon-a, macrophages activated and release TNF-a and IL1 -> inflammation, hypothalamus effects (fever, CTRF), MHC1&2 upregulated
2) Early: NK cells activated
3) Late: T-cells followed by plasma cells and increasing antibody titres.

Front 61

What type of virus is Hep A & what type of acquired immune response more effective

Back 61

1) picornavirus
2) humoral (IgM, IgG, IgA)

Front 62

With acute infection and prevention of reinfection by a virus, what is the order of humoral verses cell mediated immune response

Back 62

Acute infection: CM initially then humoral
Prevention of reinfection: humoral then CM

Front 63

How does influenza A & B evade humoral immunity provided by vaccination

Back 63

Antigenic drift: RNA virus more prone to mutations
Envelope epitope (HA) changes from season to season

Front 64

Describe antigenic shift

Back 64

1 Human and 1 animal (eg bird) virions infect a cell of an intermediate (eg pig) or human
Mixing of DNA or RNA (if influenza) causes new strain

Front 65

List 3 ways a virus can subvert the immune system

Back 65

1) cytokine mimicks (TNF-a, IL1)
2) Block interferon-a antiviral signalling
3) block movement of MHC1 to infected cell surface

Front 66

what th subclasses produce which acquired immune response

Back 66

Th1 -> CTL
th2 -> Bcells -> plasma cells -> antibodies

Front 67

What does presence of HBsAg indicate

Back 67

Active or persistent infection

Front 68

what does the presence of anti-HBsAg indicate

Back 68

Clearance of infection

Front 69

What does presence of anti-HBcAg indicate

Back 69

Previous infection

Front 70

What does presence of HBeAg indicate

Back 70

Envelope antigen present indicating whole virions present - carrier is highly infective

Front 71

Hep Delta antigen present

Back 71

If HepB carrier then superinfection with HepD -> fulminant (likely death) or severe acute -> chronic HepB with risk of cirrhosis and carcinoma

Front 72

What are 2 types of whole virus vaccines and give examples

Back 72

Attenuated: live virus (MMR, ADT)
Inactive (killed): (influenza, HepA)

Front 73

What are the requirements of an effective vaccine

Back 73

1) activates APCs
2) multiple epitopes covering most MHC polymorphism types

Front 74

What types of vaccines don't use whole viruses & comment on efficacy

Back 74

1) synthetic sub-unit (poor)
2) recombinant sub-unit (effective for Hep B & HPV)

Front 75

what are the problems associated with live vaccines

Back 75

1) immunocompromised & pregnant patients
2) genetic reversion within vaccinated host -> carrier of virulent organism eg polio

Front 76

What are the 3 causes of a chronic infection

Back 76

1) De novo (low antigenicity)
2) Following acute (unable to completely eradicate foreign matter)
3) Following recurrant acute

Front 77

What are the 3 causes of a chronic infection

Back 77

1) De novo (low antigenicity)
2) Following acute (unable to completely eradicate foreign matter)
3) Following recurrant acute

Front 78

List the immunological steps of chronic inflammation

Back 78

1) Adhesion & extravasation of monocytes at inflammation site in response to cytokines (TNFa, IL1)
2) Activation of macrophages by IFa
3) Harbour large matter by giant cells (Langhans horseshoe nuclei, foreign body, touton)
4) Recurring injury (proteases, oxygen metabolites, coagulation factors, NO)
4) Repair: angiogenesis factors-> angioblasts, growth factors (PSGF, FGF), granulation (fibroblasts)-> maturation & contraction -> fibrosis (dense collegen & elastin)

Front 79

Describe granulatomous inflammation

Back 79

Accumulations of macrophages with epithelioid appearance

Front 80

Describe a granuloma

Back 80

Aggregate of epithelioid macrophages, giant cells with necrotic tissue surrounded by T cells and plasma cells

Front 81

Describe the 2 types of mucosal repair processes

Back 81

Regeneration: intact matric framework allowing restoration

Front 82

List 2 types of acute inflammatory responses to pathogens that can cause harm to the host

Back 82

1) suppurative
2) necrotising

Front 83

What are the components of pus

Back 83

1) neutrophils
2) fibrin
3) plasma

Front 84

What are the stages of acute lobar pneumonia

Back 84

1) congestion
2) red hepatisation (fibrin stiffening with erythrocyte seepage)
3) grey hepatisation (erythrocytes die/reabsorbed, fibrin remains)
4) rsolution (breakdown of fibrin)

Front 85

List the loss of host defences that may allow lobar or bronchial pneumonia

Back 85

1) loss of cough reflex (cancer, stroke)
2) mucocilliary escalator impairment (smoking, CF, virus - RSV)
3) Accumulation of secretions (CF, asthma, CB)
4) Immunosuppresion (chemo, HIV)
5) Impairment of macrophages (smoke, alcohol)

Front 86

How is bronchopneumonia different from lobar pneumonia

Back 86

1) patchy
2) extension of bronchitis

Front 87

Explain pneumonia with extensive alveolar descruction

Back 87

necrotising pneumonia - typically staph in immunosuppressed. Often exotoxins produce necrosis

Front 88

Define an abcess

Back 88

1) prurulent matter
2) confined space

Front 89

Explain the process of otitis media with effusion

Back 89

1) viral infection of upper respiratory tract (pharynx, nasal cavity)
2) swelling of MALT tissues producing B-cells secreting IgA
3) blockage of entrance to pharyngoauditory tube by pharyngeal tonsil
4) trapped air reabsorbed by respiratory epithelium of auditory tube and middle ear
5) -ve pressure seeps clear serum into middle ear, causing "glue ear"

Front 90

Explain the process of bacterial infection of middle ear

Back 90

1) initial assault by virus: RSV or rhinovirus damages respiratory epithelium of auditory tube
2) Streptococcus pneumoniae has virulence factors evading phagocytosis (capsule) and migrates from nasopharynx
3) if not cleared by acute inflammatory response (neutrophils, influx of MALT tissue and IgA) then development into chronic supprative otitis media (macrophages, T-cells, basophils)

Front 91

Describe the 2 conductive hearing tests

Back 91

1) Weber: tuning fork centre forehead. Conductive if sounds better in affected ear. Sensoneural if sounds better in unaffected ear
2) Rinne: place on mastoid bone and 1cm away. If louder on contact then conductive hearing loss.

Front 92

What type of granuloma is formed in TB

Back 92

Caseating (ie necrotic tissue) granuloma

Front 93

List the sequence of apoptosis

Back 93

1) cell shrinkage
2) chromatin condensation (pyknosis)
3) nuclear fragmentation (karyorrhexis)
4) formation of blebs on cell membrane
5) breakdown of cell into vesicles

Front 94

List the 3 types of giant cells

Back 94

1) caseating (TB)
2) foreign body
3) touton (eg xanthelasma)

Front 95

When is perioperative antibiotic prophylaxis given and why

Back 95

Timing of 1hr pre is optimal and prophylactic use decreases infection rate of clean would 5x (0.8) and 10x for clean contaminated wound (1.3%). Less effective on contaminated wound 2x (10%)

Front 96

What are the non-surgical indications for AB prophylaxis

Back 96

1) immunocompromised (chemo, HIV - PCP, CMV)
2) Ascites (spontaneous bacterial peritonitis)
3) travellers to malaria endemic countries

Front 97

What type of antibiotic is given perioperatively and why

Back 97

1st gen cephalosporins because
1) less chance of allergic response
2) covers staph and strep

Front 98

Common scenarios of bacterial colonization

Back 98

Foley catheters
Wounds (take swabs)
High epithelial presence in urine
Tracheostomy (sputum culture)

Front 99

Where should swabs be taken to determine if resistant bacteria are present

Back 99

1) nasal (MRSA)
2) rectal (VRE)