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Week 4 Flashcards

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1
Q

What are the 4 functions of the complement system?

A
  • Pathogen killing (mediated by MAC)
  • Pathogen opsonisation and phagocytosis (mediated by C3b)
  • Mast cell degranulation (mediated by C3a and C5a)
  • Immune complex solubilisation
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2
Q

What is the difference between immunisation and vaccination?

A

Immunisation - process by which an individual develops memory/immunity to a disease

Vaccination - deliberate administration of antigenic material to induce immunity

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3
Q

How does empyema develop? What is the mortality rate?

A

57% of all patients with pneumonia will develop some pleural fluid.

Starts as a simple parapneumonic effusion

  • clear fluid
  • pH > 7.2
  • LDL < 1000
  • glucose >2.2

Becomes a complicated parapneumonic effusion

  • pH < 7.2
  • LDL > 1000
  • glucose <2.2
  • Requires chest drain

Progresses to empyema

  • Frank pus present
  • Mortality rate is 20%
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4
Q

What type of Hypersensitivity is associated with TB? What is classically seen?

A

Type IV (delayed hypersensitivity)

Granuloma formation with necrosis (caseating)

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5
Q

Opportunistic pathogen associated with patients with AIDS/immunosuppression?

Treatment?

A

Pneumocystis jirovecii pneumonia (PCP)

Treatment - Co-trimoxazole (+/- prophylaxis)

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6
Q

Describe the immunoglobulin profiles in primary vs secondary infection

A

Primary - IgM initially, followed by a slower rise in IgG

Secondary - Same IgM response, but much larger IgG response at the same time

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7
Q

Bronchiectasis - clinical signs and symptoms

A

Productive cough with green/yellow sputum

Occasionally may present with haemoptysis

Frequent bronchial infections, breathlessness

Bad breath (possibly indicating infection)

Crepitations may be heard on auscultation

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8
Q

What bacteria commonly colonise the upper respiratory tract? Gram +ve and Gram -ve examples

A

Gram +ve

  • Strep pneumoniae (alpha haemolytic)
  • Strep pyogenes (beta haemolytic)
  • Staph aureus

Gram -ve

  • Haemophilus influenzae
  • Moraxella catharalis
  • many more
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9
Q

What is the causative organism of Whooping cough?

What is the treatment? What if the patient is pregnant?

A

Bordetella pertussis, gram negative coccobacillus

If the cough has been present for more than 3 weeks, Clarithromycin (Erythromycin if pregnant)

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10
Q

What are some conditions that could result in Bronchiectasis?

A

CF

Bronchial obstruction

Young’s syndrome, Kartagener’s syndrome

Immunodeficiency

Rheumatoid arthritis

Idiopathic in >50% of cases

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11
Q

What are the most common causative organisms of TB?

A

Mycobacterium tuberculosis and Mycobacterium bovis

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12
Q

What are some important points to bear in mind when using Rifampicin?

A

It colours all bodily fluids orange

Prompts rapid breakdown of all steroid molecules, including hormonal contraception

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13
Q

Scenario - middle-aged woman has had a persistent cough, has had frequent chest infections throughout our life and is on numerous antibiotics.

Diagnosis?

A

CF or Bronchiectasis.

Oh, and she mentions her sister has CF… follow with genetic testing looking for common CF gene mutations (F508del, G551D)

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14
Q

Secondary TB is reinfection/reactivation of latent disease. When this occurs, how does the infection typically present (location)?

A

Typically remains localised, often in the apices of the lungs. Can spread however via the airways or blood stream.

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15
Q

Chronic Bronchial Sepsis - clinical presentation

A

All the hallmarks of bronchiectasis but no appearance on CT

Often younger patients, mainly women, often involved in childcare

Others are older, with COPD/airway disease

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16
Q

Primary immunodeficines are more common than secondary, true or false?

A

False

Primary are rare, affectin 1:10,000 live births

Secondary are often subtle and involve more than one component of the immune system

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17
Q

Empyema - diagonsis

A

CXR - don’t forget lateral!

Ultrasound sonography - preferred investigation, simple bedside testing

CT - differentiate between empyema and abscess

(note D sign on CXR)

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18
Q

What are the potential negative effects of tuberculosis treatment?

A

Both Rifampicin and Isoniazid are associated with liver dysfunction (more frequently in women)

Steroid use can also lead to the reactivation of latent TB

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19
Q

Phagocytic cells (e.g. neutrophils and macrophages) are particularly important in defence against…

A

Bacteria and fungi

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20
Q

How do vaccines work?

A

Generate a memory B and T cell response in 14-21 days.

Most of these cells will die off via apoptosis in the absence of pathogen, but a small number will become memory cells

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21
Q

What is Leukocyte Adhesion Deficiency (LAD)?

A

Rare primary immunodeficiency, defect in leucocyte integrins (CD18)

Failure in neutrophil adhesion and migration

Characterised by leukocytosis (raised WBCs) and localised bacterial infections

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22
Q

Intra-pulmonary abscess - clinical signs

A

Lethargy, tiredness, weakness

Weight loss is common

Cough +/- sputum

High mortality if left untreated

Usually there is a preceding illness i.e. pneumonia, aspiration/foreign body, post-virus

(note fluid level in picture)

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23
Q

How does Kostmann syndrome present?

A

Infections - usually within 2 weeks of birth

Fever, irritability, oral ulceration, failure to thrive

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24
Q

Briefly outline the idea behind memory B and T cell reactivation

A

Resting cells become activated

Clonal expansion occurs

Cells differentiate into Effector or Memory cells

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25
What pathogen causes epiglottitis in children? What's the treatment? How do you test for this organism?
*Haemophilus influenzae* Type B (HiB) Treatment - Ceftriaxone (cephalosporin, inhibits bacterial cell wall synthesis) Testing: * gram staining shows gram -ve coccobacillus * grows on blood agar (haemophilus = blood loving)
26
What's the difference between an abscess and empyema?
Abcess - collection of pus in a **newly formed cavity** e.g. intra-pulmonary Empyema - collection of pus in a **pre-existing anatomical cavity** e.g. the pleural space
27
What is affected in Cystic Fibrosis? How does this result in pathology?
Cystic Fibrosis Transmembrane Receptor (CFTR) doesn't function correctly, meaning Chloride ions remain on the outside of cells. This results in mucous becoming much thicker due to H2O flowing into the cell
28
What is Young's Syndrome?
Encompasses a combination of conditions, such as bronchiectasis, reduced fertility and rhinosinusitis. Functioning of the lungs is usually normal but the mucous lining the resp tract is abnormally viscous.
29
Bronchiectasis - treatment
Initially * Flu vaccine? Pneumococcal vaccine? * Reactive antibiotics Colonised with persistent bacteria * Prophylactic antibiotics * Neb gentamicin, colomycin * Alternate between oral and IV antibiotics
30
What is the difference between pulmonary and miliary TB?
Miliary tuberculosis (TB) is the widespread dissemination of Mycobacterium tuberculosis via hematogenous spread.
31
What immunoglobulins are involved in complement fixing?
IgG and IgM
32
What is Chronic Granulomatous Disease (CGD)? How is it tested for?
Failure of oxidative killing mechanisms by phagocytes Characterised by persistent accumulation of neutrophils, activated macrophages and lymphocytes, but inability to clear organisms - **granuloma formation** Recurrent deep bacterial infections, especially Staph, aspergillus, pseudomonas Test - nitroblue tetrazolium (NBT), can neutrophils kill via oxidative free radicals?
33
What is an adujvant ?
Mixture of inflammatory substances used to prompt an immune response for inactivated vaccines Consist of aluminium hydroxide/toxins/other pathogens etc.
34
Empyema - Treatment
Antibiotics * Broad spectrum - IV amoxicillin and metronidazole initially * Follow with oral antibiotics for specific bacteria
35
*Moraxella catarrhalis* is a gram positive/negative bacilli/coccus/coccobacilli
Gram negative, coccus
36
What are the tissue changes seen in 1) Primary TB and 2) Secondary TB?
1. Primary TB 1. **Ghon focus** in the peripheray of the mid zone of the lung (see image) 2. Large hilar lymph nodes (granulomatous) 2. Secondary TB 1. Fibrosing and **cavitating apical lesion** (cancer is differnetial)
37
What are the some of the forms of Chronic Pulmonary Infection?
Intrapulmonary abscess Empyema Chronic bronchial sepsis Bronchiectasis CF
38
Desribe Bronchopneumonia. Think causative organisms, clinical setting and complicatons.
* Infection staring in the airways and spreading to adjacent alveolar lung * Most often seen in patients with **pre-existing disease** * Causative pathogens are more varied than lobar - *Strep. pneumoniae, Haemophilus influenzae, Staph.,* anaerobes, coliforms * Classically seen in * COPD * Cardiac failure * Complication of viral infection (e.g. influenza) * Aspiration of gastric contents * Complications are the same as lobar, but **abscess formation** is the main complication
39
What are the two common gene deletions in CF patients?
F508del G551D
40
What is Bronchiectasis? What commonly causes it and why is it a problem?
* Abnormally fixed dilatation of the bronchi * Ususally due to fibrous scarring following infection (pneumonia, TB, CF etc.), but can also be due to a tumour causing chronic obstruction * CF is thought to be the cause in up to 50% of cases * Purulent (pus) secretions accumulate in the dilated airways
41
Two tests for TB?
Tuberculin Skin Test - false +vs and -vs Interferon Gamma Release Assay - highly sensitive
42
What bacteria are typically found in an empyema?
Mostly aerobes (anaerobes in 13% of cases) Gram +ve * *Strep milleri* * *Staph aureus* Gram -ve * *E. coli* * *Pseudomonas* * *Haemophilus influenzae* * *Klebsiella*
43
What disease was variolation vaccination used in? Did it work? What was developed as an alternative
Small pox - small amount of a dried pustule administerd to healthy individuals Yes it worked, but 1/100 died Jenner's vaccinia vaccine - contained cowpox
44
What is Kostmann syndrome? What is Reticular Dysgenesis?
Both cause a failure to produce neutrophils Kostmann - Severe congential neutropaenia, neutrophils fail to mature. Autosomal recessive. RG - Failure of stem cells to differentiate along the myeloid lineage
45
What are the three complement activating pathways? Briefly, how does each one work?
All revolve around C3 ⇒ C3b + C3a * Classical Pathway * Activation via antigen-antibody complexes * C1, C2, C3 and C4 involved: C1 + C4 - C2 = C3 * Alternative Pathway * Spontaneous hydrolysis of C3 to C3b * Mannose-Binding Lectin Pathway * MBL is produced in the liver as part of the acute phase response, binds mannose (e.g. on bacterial cells) and converts C3 ⇒ C3b + C3a Mnemonic - CMA Classical - Complex (immune) activated MBL - Microbe Manose Alternative - Alien particles
46
Desribe Lobar pneumonia. Think causative organisms, clinical setting and complicatons.
* Confluent consolidation involving a **complete lung lobe** * Usually due to ***Strep pneumoniae*** but can also be due to others * Usually community acquired and classically in **otherwise healthy young adults** * Classical acute inflammatory response * exudation of fibrin-rich fluid ⇒ neutrophil infiltration, followed by macrophage infiltration ⇒ resolution * Complications - organisation (fibrous scarring), abscess, brochiectasis, empyema
47
Why might a latent TB infection reactivate?
* Reduced T cell function * increasing age * immunosuppressive therapy (steroids, chemo) * immunocompromisation (HIV) * Reinfection at a high dose, or with a more virulent organism
48
How many people are carriers of the CF mutation? If both parents are carriers, what are the chances their child will have CF?
1/25 (autosomal recessive) If both parents are carriers, 25% of child having CF
49
What is an Inactivated vaccine? What are the drawbacks?
Exposure to an inactivated form of the pathogen, cannot replicate Generally not as effective as live vaccines Immune response is primarily antibody based (no T cells) and may diminish over time Requires multiple doses to stimulate response
50
What is the treatment of TB?
2 RIPE 4 RI 2 months * Rifampicin * Isoniazid * Pyrazinamid * Ethambutol 4 months * Rifampicin * Isoniazid
51
What are the Sepsis 6?
**BUFALO** B - take blood cultures U - measure urine output F - provide fluids A - give IV antibiotics L - measure lactate O - give oxygen to keep SaO2 over 94%
52
Complications of CF
Bronchiectasis Biliary obstruction and obstructive hepatitis Pancreatic dysfunction Infertility in males
53
What is Kartagener Syndrome?
Rare, ciliopathic, autosomal recessive disorder. Affects the cilia in the resp tract, leading to abnormal function/immotility
54
Of all the people that are exposed to TB, what % will develop any kind of disease?
10% will develop disease, 5% being primary TB infection and 5% being reactivation of latent disease
55
What have been shown to reduce exacerbation rates in bronchiectasis?
Low dose macrolides - clarithromycin, azithromycin 3 times a week
56
Tuberculosis - associations and diagnostic tests
Associations * Immunocompromised/immunosuppressed individuals * **Recent travel** from high risk areas Diagnostic tests * Microscopy - acid fast, Ziehl-Neelsen stain, Mycobacteria appear red * PCR * Culture * Immune reaction
57
Tuberculosis - clinical features
* Long term cough * Chest pain * Sputum +/- haemoptysis * Weakness/fatigue * Weight loss * Fever and chills * Night sweats
58
How does Bronchiectasis present in spirometry?
As an obstructive condition - impaired clearance of secretions
59
What are the classical radiological signs of pulmonary tuberculosis?
Upper lobe predominance Cavity formation Tissue destruction Scarring and shrinkage Calcified lymph nodes
60
What is the classical histological appearance of tuberculosis?
Multinucleate giant cell granulomas Caseating (cheesy) necrosis
61
What drug can be used in the G551D mutation variant of CF? How does it work?
Ivacaftor In the G551D mutation, the CFTR works normally, however the channel is non-functioning. Ivacaftor is a CFTR potentiator, and improves chloride delivery. Expensive!!!
62
CF - clinical presentation
Salty skin Intestinal blockages and filled sinuses Fibrotic pancreas Failure to thrive Recurrent bacterial lung infections Gallbladder/liver disease Congenital bilateral **absence** of vas deferens.
63
What is a Live Attenuated vaccine?
"Weakened" form of a wild type pathogen Organism must replicate to be effective Examples - BCG, MMR, chicken pox, smallpox, polio Very similar to natural infection, but potentially not as safe as inactive vaccines and harder to store

Respiratory (11 decks)

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