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Life Protection > Week 19 - TB > Flashcards

Week 19 - TB Flashcards

(67 cards)

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1
Q

What is chronic inflammation?

A

Long lasting inflammatory response (weeks, months)
May follow acute inflammation or not
Marked by significant tissue destruction

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2
Q

What are the potential causes of chronic inflammation?

A

Failure to close acute inflammatory reactions - Persistent infections

Misdirected inflammatory reaction - harmless environmental substances, autoimmune diseases

Underlies many disorders - cancer, atherosclerosis, alzheimer’s, etc

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3
Q

Acute vs chronic inflammation

A

Chronic involves adaptive more than acute
Chronic may include necrosis, fibrosis, scarring and angiogenesis
PICTURE FROM FOLDER

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4
Q

What sort of cells are most often involved in chronic inflammation?
What is their role?

A

Monocytes - which become macrophages in cell
Activate other cells, secrete inflammatory cytokines, produce growth factors (tissue repair)
Other cells can be there - depends on what the response is to

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5
Q

When are eosinophils involved in chronic inflammation?

A

infections with parasites, IgE-mediated allergic reactions

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6
Q

When are mast cells involved in chronic inflammation?

A

present in connective tissue, close to vessels

Involved in acute as well

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7
Q

When are neutrophils involved in chronic inflammation?

A

some types of chronic inflammation: suppurative inflammation (abscess, osteomyelitis); lung disease smoking/irritants

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8
Q

What is the cytokine that activates macrophages?

A

Interferon-gamma

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9
Q

Types of chronic inflammation (4)

A

Non-specific - H.Pylori associated gastritis
Autoimmune - Rheumatoid arthritis
Chronic suppurative - abscess, osteomyelitis
Chonic granulomatous - TB, sarcoidosis

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10
Q

Outline non-specific chronic inflammation

A

Acute inflammation fails to clear properly such as h.pylori which body tries to fight with neutrophils. They do not effectively fight it so start to attack epithelial cells, leading to ulceration

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11
Q

Outline inflammation in autoimmune disease

A

Immune response to self-antigens

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12
Q

Outline chronic suppurative inflammation

A

Persisting pus-forming inflammation

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13
Q

Outline chronic granulomatous inflammation

A

Usually develop when causing agent can’t be eradicated
Granuloma forms to isolate and prevent spread of agent (usually made up of macrophages, lymphocytes, fibroblasts, necrotic tissues)

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14
Q

Types of granulomas

A

Immune - Infection or autoimmune (usually T cell activation)
Foreign bodies - no T cells
Diseases of unknown aetiology - sarcoidosis

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15
Q

Potential outcomes of granulomatous inflammation

A

Causing agent eradicated - tissue healing with some scarring / fibrosis
Causing agent persists - ‘walled off’ by fibrous tissue, infection kept in check by T cells and macrophages

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16
Q

Stages of tissue repair (3)

A

Acute inflammation
Dead organisms / cells are phagocytosed and cleared
Organisation, formation of granulation tissue
Resolution, repair (scarring)

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17
Q

Outline healing of skin wounds - primary and secondary intention

A

Primary - small, limited to epithelial layer, regeneration

Secondary - more extensive, repair by regeneration and scarring

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18
Q

What are the functions of the lymphatic system?

A

Fluid balance (homeostasis)
Tissue immunosurveillance - immune response
Fat homeostasis

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19
Q

What are the mechanisms for chronic oedema?

A

Veins are dumping more fluid than lymphatics can drain

Lymphatic failure - lymph build up

Long standing increased venous filtration

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20
Q

What is tuberculosis?

A

Contagious, debilitating bacterial disease spread by airborne droplet nucleii for an infected person

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21
Q

What is the infectious dose of TB?

A

Only 1-3 organisms - very transmissible

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22
Q

What happens following initial infection with TB?

A

5% will progress to active infection
90% will have latent infection
About 10% of those with latent will have reactivated disease

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23
Q

Latent vs active TB infection - symptoms, spread, skin test, x-ray

A

PICTURE IN FOLDER

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24
Q

Risk factors for reactivation

A 
Malnutrition
Poverty
Immunosuppression
Diabetes
Old age
Poor health
HIV
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25
What is a Ghon complex?
``` Ghon focus (lesion) + lymph node Sign of primary tuberculosis ```
26
What is miliary TB?
TB in another part of the body
27
Describe intestinal TB - causes
Can be secondary to pulmonary TB, swallowed from infected sputum Primary cause is milk infected with M. bovis (now rare)
28
How does milliary TB cause damage around the body?
Chronic granulomatous tissue damage
29
Describe the immune response to TB - the good and the bad
Good - Innate immunity as macrophages try to kill ingested bacilli, adaptive response with CD8 and CD4 T cells, IFN-gamma Bad - Excessive response leads to overproduction of TNF-alpha leading to damage of healthy tissues by macrophages
30
Overview of general pathogenesis of TB (active) - simple steps
PICTURE IN FOLDER
31
Outline Koch's postulates
Working in anthrax, cattle Criteria designed to establish causative relationship between microbe and disease 1. Organism is in the lesions in ALL cases of disease 2. Isolate organism and cultivate it outside host 3. Produce the same disease if pure culture is injected into healthy subject 4. Recover microbe from experimentally infected host Does NOT work for many organisms - M.leprae, treponema pallidum (syphillus)
32
How do you diagnose TB?
``` Blood - Interferon-gamma blood test Chest x-ray PCR - GeneXpert looks at TB DNA and looks for Rifampcin resistance Sputum smear, culture Bronchoscopy Biopsy ```
33
Management of TB
Rifampicin, Isoniazid, Pyrazinamide, Ethambutol (initial 2 months) Further 4 months with Rifampicin, Isoniazid
34
Treatment side effects - rifampicin
``` hepatitis rash GI upset intermittent Rx can give rise to flu like symptoms drug interactions - OCP/prednisolone ```
35
Treatment side effects - isoniazid
rash peripheral neuropathy hepatitis
36
Treatment side effects - Ethambutol
dose related optic neuropathy
37
Treatment side effects - Pyrazinamide
``` hepatitis facial flushing rash nausea & anorexia arthralgia high uric acid ```
38
Expectations with treatment
Non-infectious within 2 weeks (90% fall in number of viable organisms) Temperature settled and feeling better Gaining weight at 1mth with sputum smear negative Sputum culture negative by 2mths
39
Considerations if patients are not improving
Compliance, AMR
40
Does TB have caesating or non-caesating granulomas?
Either, but more things cause non- so more tests / clarity needed
41
What are the roles of complement? (8)
``` induces inflammatory response promotes chemotaxis increases phagocytosis by opsonisation increases vascular permeability mast cell degranulation lysis of cell membranes activates macrophages (C3a) Removal of immune complexes ```
42
Complement system overview
IgM or IgG bind, complement unit bind, complement pathway activated which leads to MAC tunnel in microbe surface, creates hole/pore that causes lysis
43
Which complement factor is involved in opsinisation?
C3b opsonises bacteria, which tags it for killing
44
Roles of C3b (3)
Opsonises bacteria Vasodilator Activates phagocytes
45
How can bacteria stop the complement process?
Bacteria binds Factor H (regulator molecule) so that the complement system can't act on the surface
46
What does protein A do?
Binds antibody wrong way round which makes it useless | defense mechanism of bacteria
47
Summary of antibacterial roles of antibodies
PICTURE IN FOLDER
48
Summary of types of immune response to bacteria (based on location)
PICTURE IN FOLDER
49
Pathogenesis and defence response of neisseria meningitidis
PICTURE IN FOLDER
50
Pathogenesis and defence response of mycobacterium tuberculosis
PICTURE IN FOLDER
51
Pathogenesis and defence response of staph aureus
PICTURE IN FOLDER
52
Overview of types of cells - macrophages, PMN, NK cells, dendritic cells, CD8, CD4, B cells
Macrophages and neutrophils (PMNs) - phagocytose free bacteria & present antigen NK cells - kill infected cells showing antigen Dendritic cells - present antigen at lymph nodes Cytotoxic T cells CD8+ kill cells expressing antigen CD4 helper cells - activate macrophages & stimulate B cells B cells - antibodies
53
What is hypersensitivity?
Diseases caused by abnormal immune responses (excssive response to innocuous antigens) or response against self antigens (autoimmune) Misdirected, excessive, poorly controlled Leading to tissue damage
54
Outline the types of hypersensitivity reactions
Type 1: Immediate (IgE) / allergic Type 2: Antibody mediated (IgM, IgG) Type 3: Immune complex mediated Type 4: T cell mediated
55
Describe type 1 hypersensitivity reaction
Allergic response Fast immune reaction Triggered by exposure to allergen, which binds to IgE on surface of mast cell Most common Healthy subjects would respond to igM/igG, atopic subjects produce IgE
56
Examples of type 1 hypersensitivity reaction (what can cause)
Hay fever, atopic dermatitis, allergic asthma, pollen, dust mites, animal dander, food (peanuts, eggs), chemicals (penicillin), insect venom Asthma (kind of, also chronic)
57
What is the series of events in SENSITISATION in type 1 hypersensitivity reaction
``` SENSITISATION Antigen presenting cell brings antigen Th2 cell response Activation of B cells and IgE switch (from IgM) IgE production IgE binds to Fc receptors on mast cells ```
58
What is the series of events in SUBSEQUENT EXPOSURE TO ALLERGEN in type 1 hypersensitivity reaction
Allergen binds on IgE on mast cells Activation of mast cells, release of mediators Vascular and smooth muscle reactions within minutes Late phase reaction (inflammation) (2-24 hours)
59
What happens during the activation of mast cells
Release of preformed mediators - histamine and enzymes Production and secretion of lipid mediators Production and release of cytokines
60
What happens with the late reaction of type 1 hypersensitivity reaction?
SLIDE IN FOLDER
61
What is anaphylaxis?
Systemic response all over body Can happen with injection, insect bites, absorption through mucosa/skin Activation and degranulation of mast cells Clinical signs - Drop in blood pressure (shock), airway constriction, widespread oedema, vomiting, cramps, diarrhoea
62
What is a type 2 hypersensitivity reaction?
Antibodies to cell-bound antigens (self-antigen) MECHANISMS Opsonisation and phagocytosis Complement and Fc receptor mediated inflammation Antibody-mediated cellular dysfunction
63
Types of type 2 hypersensitivity reactions (conditions)
``` Autoimmune haemolytic anaemia Agranulocytosis Autoimmune thrombocytopenic purpura transfusion reactions haemolytic disease of newborn Organ transplant rejection ```
64
What occurs in antibody-mediated cellular dystunction in type 2 hypersensitivity reactions? (2 condition examples)
There is no inflammation, they just make particular antibodies more or less effective EXAMPLES Blocking antibodies - Myasthenia gravis Stimulating antibodies - Graves disease
65
What is a type 3 hypersensitivity reaction?
Immune complex-mediated hypersensitivity reaction Antibodies and antigens combine to form COMPLEX, get deposited in vessel wall which causes inflammation Arthritis, vasculitis, glomerulonephritis, SLE
66
What is type 4 hypersensitivity reaction?
Mediated by CD4 T cells, delayed type Th1, Th17 mediated autoimmune diseases - theumatoid arthritis, MS, IBD, psoriasis OR Mediated by CD8 T cells Type 1 diabetes, viral hepatitis, organ transplant rejection
67
System for assessing a chest x-ray
Adequacy - well centred, inspiration, exposure A- airway B - breathing, looking at zones not lobes C - cardiomediastinal contour (and hila) D - diaphragm E - everything else - bones, soft tissues, and upper abdomen

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