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Life Protection > Week 19 - TB > Flashcards

Week 19 - TB Flashcards

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
Q

What is a Ghon complex?

A 
Ghon focus (lesion) + lymph node
Sign of primary tuberculosis
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26
Q

What is miliary TB?

A

TB in another part of the body

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27
Q

Describe intestinal TB - causes

A

Can be secondary to pulmonary TB, swallowed from infected sputum

Primary cause is milk infected with M. bovis (now rare)

28
Q

How does milliary TB cause damage around the body?

A

Chronic granulomatous tissue damage

29
Q

Describe the immune response to TB - the good and the bad

A

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
Q

Overview of general pathogenesis of TB (active) - simple steps

A

PICTURE IN FOLDER

31
Q

Outline Koch’s postulates

A

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
Q

How do you diagnose TB?

A 
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
Q

Management of TB

A

Rifampicin, Isoniazid, Pyrazinamide, Ethambutol (initial 2 months)

Further 4 months with Rifampicin, Isoniazid

34
Q

Treatment side effects - rifampicin

A 
hepatitis
rash
GI upset
intermittent Rx can give rise to flu like symptoms
drug interactions - OCP/prednisolone
35
Q

Treatment side effects - isoniazid

A

rash
peripheral neuropathy
hepatitis

36
Q

Treatment side effects - Ethambutol

A

dose related optic neuropathy

37
Q

Treatment side effects - Pyrazinamide

A 
hepatitis
facial flushing
rash
nausea & anorexia
arthralgia
high uric acid
38
Q

Expectations with treatment

A

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
Q

Considerations if patients are not improving

A

Compliance, AMR

40
Q

Does TB have caesating or non-caesating granulomas?

A

Either, but more things cause non- so more tests / clarity needed

41
Q

What are the roles of complement? (8)

A 
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
Q

Complement system overview

A

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
Q

Which complement factor is involved in opsinisation?

A

C3b opsonises bacteria, which tags it for killing

44
Q

Roles of C3b (3)

A

Opsonises bacteria
Vasodilator
Activates phagocytes

45
Q

How can bacteria stop the complement process?

A

Bacteria binds Factor H (regulator molecule) so that the complement system can’t act on the surface

46
Q

What does protein A do?

A

Binds antibody wrong way round which makes it useless

defense mechanism of bacteria

47
Q

Summary of antibacterial roles of antibodies

A

PICTURE IN FOLDER

48
Q

Summary of types of immune response to bacteria (based on location)

A

PICTURE IN FOLDER

49
Q

Pathogenesis and defence response of neisseria meningitidis

A

PICTURE IN FOLDER

50
Q

Pathogenesis and defence response of mycobacterium tuberculosis

A

PICTURE IN FOLDER

51
Q

Pathogenesis and defence response of staph aureus

A

PICTURE IN FOLDER

52
Q

Overview of types of cells - macrophages, PMN, NK cells, dendritic cells, CD8, CD4, B cells

A

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
Q

What is hypersensitivity?

A

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
Q

Outline the types of hypersensitivity reactions

A

Type 1: Immediate (IgE) / allergic
Type 2: Antibody mediated (IgM, IgG)
Type 3: Immune complex mediated
Type 4: T cell mediated

55
Q

Describe type 1 hypersensitivity reaction

A

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
Q

Examples of type 1 hypersensitivity reaction (what can cause)

A

Hay fever, atopic dermatitis, allergic asthma, pollen, dust mites, animal dander, food (peanuts, eggs), chemicals (penicillin), insect venom
Asthma (kind of, also chronic)

57
Q

What is the series of events in SENSITISATION in type 1 hypersensitivity reaction

A 
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
Q

What is the series of events in SUBSEQUENT EXPOSURE TO ALLERGEN in type 1 hypersensitivity reaction

A

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
Q

What happens during the activation of mast cells

A

Release of preformed mediators - histamine and enzymes
Production and secretion of lipid mediators
Production and release of cytokines

60
Q

What happens with the late reaction of type 1 hypersensitivity reaction?

A

SLIDE IN FOLDER

61
Q

What is anaphylaxis?

A

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
Q

What is a type 2 hypersensitivity reaction?

A

Antibodies to cell-bound antigens (self-antigen)

MECHANISMS
Opsonisation and phagocytosis
Complement and Fc receptor mediated inflammation
Antibody-mediated cellular dysfunction

63
Q

Types of type 2 hypersensitivity reactions (conditions)

A 
Autoimmune haemolytic anaemia
Agranulocytosis
Autoimmune thrombocytopenic purpura
transfusion reactions
haemolytic disease of newborn
Organ transplant rejection
64
Q

What occurs in antibody-mediated cellular dystunction in type 2 hypersensitivity reactions? (2 condition examples)

A

There is no inflammation, they just make particular antibodies more or less effective
EXAMPLES
Blocking antibodies - Myasthenia gravis
Stimulating antibodies - Graves disease

65
Q

What is a type 3 hypersensitivity reaction?

A

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
Q

What is type 4 hypersensitivity reaction?

A

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
Q

System for assessing a chest x-ray

A

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

Life Protection (5 decks)

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