Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Phase 2A revision > RESPIRATORY > Flashcards

RESPIRATORY Flashcards

1
Q

Define pneumonia

A

Inflammation of the substance of the lungs .

It is an acute lower respiratory tract infection

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

How can pneumonia be anatomically classified?

A
  1. Bronchopneumonia = diffuse, patchy infection of different lobes
  2. Lobar pneumonia = localised consolidation of a single lobe
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

How can pneumonia be aetiologically classified?

A
  1. Community acquired pneumonia = person with no underlying immunosuppression or malignancy
  2. Hospital acquired pneumonia = >48 hours after hospital admission
  3. Aspiration pneumonia = acute aspiration of gastric contents into lungs
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Briefly describe the pathophysiology of pneumonia

A
  • invasion and overgrowth of a pathogen in lung parenchyma
  • overwhelming of host immune defences
  • production of intra-alveolar exudates
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

What can cause pneumonia to be severe?

A
  1. Excessive inflammation
  2. Lung injury
  3. Resolution failure
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Name 3 groups of people who might be at risk of pneumonia

A
  1. Elderly
  2. Children
  3. COPD patients
  4. Immunocompromised people
  5. Nursing home residents
  6. alcoholics
  7. IV drug users
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Name 3 pathogens that can cause community acquired pneumonia (CAP)

A
  1. Streptococcus pneumoniae (most common)
  2. Haemophilus influenzae
  3. Mycoplasma pneumoniae
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Name 3 pathogens that can cause hospital acquired pneumonia (HAP)

A

mainly gram negative

  1. Pseudomonas aeruginosa
  2. E.coli
  3. Klebsiella penumoniae
  4. Staphylococcus aureus
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

which pathogen can cause pneumonia in immunocompromised patients

A

pneumocystis jiroveci

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

What symptoms might you see in someone with pneumonia?

A 
SOB
cough
sputum
fever
pleuritic chest pain
delirium
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

What signs might you see in someone with pneumonia?

A
  • increased resp rate and HR
  • hypotension
  • decreased O2 saturation
  • dull to percuss
  • increased tactile fremitus
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

What investigations might you do on someone you suspect has pneumonia?

A
  • FBC, U&E, CRP– increased WCC, urea and CRP
  • Sputum culture - MC+S
    Chest X ray: localised/widespread consolidation, effusion, abscesses, empyema
    Multi-lobar – strep pneumoniae, s. aureus
    Multiple abscesses – s. aureus
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

How can you assess the severity of community acquired pneumonia?

A

CURB65 score (1 point for each)

  • Confusion
  • Urea (>7 mmol/L)
  • Respiratory rate (> 30/min)
  • BP (<90/60 mmHg)
  • Age >65
Scores
0-1 = mild (outpatient treatment) 
2 = admit to hospital 
3-4 = severe, admit and monitor closely 
5 = ITU transfer
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

How can pneumonia be prevented?

A

polysaccharide pneumococcal vaccine - protests against 23 serotypes
Smoking cessation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

What is the treatment for someone with mild CAP (CRUB65 score 0-1)?

A

oral amoxicillin at home

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

What is the treatment for someone with moderate CAP (CRUB65 score 2)?

A

consider hospitalising, amoxicillin (IV or oral) + macrolide (clarithromycin)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

What is the treatment for someone with severe CAP (CRUB65 score 3-5)?

A

consider ITU,

IV Co-Amoxiclav + macrolide (clarithromycin)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

What is the treatment for someone with Legionella pneumoniae?

A

Fluoroquinolone + clarithromycin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

What is the treatment for someone with Pseudomonas aeruginosa pneumonia?

A

IV ceftazidime + gentamicin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

A 66 y/o patient presents to you with fever and a productive cough. On examination you notice they are their confused. Their vital signs are: RR - 35; BP - 80/55 and HR: 130. You measure their urea and it comes back at 8mmol/L

a) What is this patients CURB65 score?
b) Where should they be treated?
c) Describe the treatment for this patient

A

a) Their CURB65 score is 5
b) This patient should be treated in hospital and admitted to critical care
c) The patient should be given IV co-amoxiclav and clarithromyocin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

Give 3 potential complications of pneumonia

A
  1. Respiratory failure
  2. Hypotension
  3. Empyema
  4. Lung abscess
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

Define bronchiectasis

A

Chronic infection of the bronchi/bronchioles leading to permanent dilation and thinning of the airways

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

Describe the pathophysiology of bronchiectasis

A

Failed mucociliary clearance and impaired immune function means microbes easily invade and cause infection

This causes inflammation and progressive lung damage

Bronchitis –> bronchiectasis –> fibrosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

What can cause bronchiectasis?

A
  1. Congenital = Cystic fibrosis
  2. Idiopathic (50%)
  3. Post infection - (most common)
    • pneumonia,
    • TB,
    • whopping cough
  4. Bronchial obstruction
  5. RA
  6. Hypogammaglobulinaemia
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

Which bacteria might cause bronchiectasis?

A
  1. Haemophilus influenza (children)
  2. Pseudomonas aeruginosa (adults)
  3. Staphylococcus aureus (neonates often)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

Give 3 symptoms of bronchiectasis

A
  1. Chronic productive cough
  2. Purulent sputum
  3. Intermittent haemoptysis
  4. Dyspnoea
  5. Fever, weight loss
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

Give 3 signs of bronchiectasis

A
  1. Finger clubbing
  2. Coarse inspiratory crepitate (crackles)
  3. Wheeze
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

What investigations might you do on someone to determine whether they have bronchiectasis?

A

CXR = kerley B lines, dilated bronchi with thickened walls, multiple cysts containing fluid

High resolution CT = bronchial wall dilation

Spirometry = obstructive lung disease

Sputum culture - h.influenzae is most common

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

Describe the treatment for bronchiectasis

A
  1. Antibiotics
  2. Anti-inflammatories (azithromycin)
  3. Bronchodilators (nebulised salbutamol)
  4. Chest physio - physical training
  5. Surgery = lung resection or transplant
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

Give 3 possible complications of Bronchiectasis

A
  1. Pneumonia
  2. Pleural effusion
  3. Pneumothorax
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

A lady who has recently had pneumonia presents to you with SOB and chronic cough. She is producing copious amounts of purulent sputum. What is the likely diagnosis?

A

Bronchiectasis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

Describe the pathogenesis of Cystic fibrosis

A

Autosomal recessive defect in chromosome 7 coding CFTR protein (F508 deletion = most common mutation)

  • Cl- transport affected
  • Decreased Cl secretion and increase Na reabsorption this causes an increase H2O reabsorption –> thickened mucus secretion
  • in the lungs, this leads to dehydrated airway surface liquid, mucus stasis, airway inflammation and recurrent infection
  • this leads to progressive airway obstruction and bronchiectasis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

What are the main systemic consequences of CF?

A

Pancreatic insufficiency = dehydrated secretion –> enzymes stagnation
GI = intraluminal water deficiency –> concentrated bile
Resp = thick mucus can’t be cleared –> infection risk and inflammatory damage

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

How is CF passed on?

A

Autosomal recessive condition

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

How does neonate present with CF?

A
  • Failure to thrive
  • Meconium ileus - bowel obstruction due to thick meconium
  • Rectal prolapse
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

How do children/young adults present with CF?

A
  • Cough and wheeze
  • Recurrent infections
  • Haemoptysis
  • Pancreatic insufficiency
  • Malabsorption
  • Male infertility
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

What are 3 possible respiratory complications of CF?

A
  1. Pneumothorax
  2. Respiratory failure
  3. Cor pulmonale
  4. Bronchiectasis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

Give 3 signs of CF

A
  1. Clubbing
  2. Cyanosis
  3. Bilateral coarse crepitations
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
39
Q

Name 3 associated conditions with CF

A
  1. Osteoporosis
  2. Arthritis
  3. Vasculitis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
40
Q

What investigations might you do to diagnose cystic fibrosis?

A

heel prick test - newborns

Sweat test = Na and Cl < 60 mmol/L

Genetic screening for common mutations

Faecal elastase - tests pancreatic enzyme function

Absent vas deferent and epididymis (males)

Microbiology - for infections

Spirometry

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
41
Q

What is the management of CF?

A
  1. Physical therapies (airway clearance) and surveillance
  2. Antibiotics for infections and prophylaxis
  3. Bronchodilators
    - B2 agonist (SALBUTAMOL) and inhaled corticosteroids (BECLOMETASONE)
  4. Pancreatic enzymes replacement (creon)
  5. ADEK vitamin supplements
  6. Screening for consequent conditions - osteoporosis
  7. Bilateral lung transplant
    • must not have m. abscessus
  8. Vaccinations - flu and pneumococcal
  9. high calorie, high fat diet
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
42
Q

Infection with a gram negative bacteria is a particular concern in patients with CF. What is this organism and how can infection be prevented?

A
  • Pseudomonas Aeruginosa

- Nebulised anti-pseudomonal antibiotic therapy and regular sputum cultures

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
43
Q

Malignant bronchial tumour can be divided into 2 groups, what are they?

A
  1. Non small cell lung carcinoma (80%)

2. Small cell lung carcinoma (20%)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
44
Q

What type of malignant bronchial tumour tends to have a worse prognosis?

A

Small cell lung carcinomas - often metastasise

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
45
Q

From what cells are small cell carcinomas derived from and what is the significance of this?

A

Neuroendocrine cells

Can secrete peptide hormones - ACTH, PTHrP, ADH, HCG

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
46
Q

Give the cell types the make up non-small cell lung cancers

A
  1. Squamous cell (20%) - arise from epithelial cells + associated with keratin production
  2. Adenocarcinoma (40%) - originate from mucus-secreting glandular cells
  3. Large cell
  4. carcinoid tumours
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
47
Q

what are the risk factors of lung cancer

A
  1. Smoking = main cause
  2. Asbestos
  3. Radon exposure
  4. Coal products
  5. pulmonary fibrosis
  6. HIV
  7. genetic factors
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
48
Q

Which type of NSCC is most common in smokers?

A

Squamous cell carcinoma - it is most stronlgy associated with cigarette smoking

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
49
Q

Which type of malignant bronchial tumour fits into TNM staging?

A

Non small cell carcinoma

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
50
Q

What does TNM stand for in lung cancer?

A 
T = size/invasion = T1 (<3cm) --> T2 (>3cm) --> T3 (chest wall/diaphragm) --> T4 (heart + vessels)
N = nodal involvement = N1 (hilar) --> N2 (ipsilateral mediastinal) --> N3 (contralateral mediastinal)
M = metastases = M0 (no metastases) --> M1 (metastases)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
51
Q

where does lung cancer commonly metastasise to?

A
  1. Bone
  2. Brain
  3. Lymph nodes
  4. Liver
  5. Adrenal
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
52
Q

which cancers most commonly metastasise to the lungs?

A

breast
bowel
kidney
bladder

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
53
Q

Give 4 symptoms of local disease lung cancer

A 
Persistent cough 
Shortness of breath
Haemoptysis
Weight loss
Chest pain, wheeze, recurrent infections
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
54
Q

Give 4 symptoms of lung cancer that has metastasised

A
  1. Bone pain
  2. Headaches
  3. Abdominal pain
  4. Seizures
  5. Neuro deficit - Confusion
  6. Weight loss
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
55
Q

What are paraneoplastic syndromes?

A

they are conditions which occur as a side effect of the tumour and occur in 10% of patients

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
56
Q

Give 3 examples of paraneoplastic syndromes due to lung cancer

A
  • ↑PTH -> Hyperparathyroidism
  • ↑ADH -> SIADH
  • ↑ACTH -> Cushing’s disease
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
57
Q

Name 3 differential diagnosis’s of lung cancer

A
  1. Oesophageal varices
  2. COPD
  3. Asthma
  4. Pneumonia
  5. Bronchiectasis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
58
Q

What investigations might you done on someone to determine whether they have lung cancer?

A

First line:
- CXR - central mass, hilar lymphadenopathy, pleural effusion
(a negative CXR does not rule out cancer)

  • CT chest, liver & adrenal glands – for staging
  • Sputum cytology - malignant cells in sputum
    (high specificity but mixed sensitivity)

diagnostic = biopsy + histology

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
59
Q

What is the treatment for NSCLC?

A
  • Surgical excision for peripheral tumours with no metastatic spread
  • Curative radiotherapy is an alternative if respiratory reserve is poor - complications include radiation pneumonitis + fibrosis
  • Chemotherapy +/- radiotherapy for more advanced disease e.g. with monoclonal antibodies e.g. CETUXIMAB
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
60
Q

What is the treatment for SCLC?

A

Limited disease = chemo + radio
Extensive = palliative chemo + care

• Superior vena cava stent + radiotherapy + dexamethasone for superior
vena cava obstruction

• Endobronchial therapy - used to treat symptoms of airway narrowing:

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
61
Q

Give 4 possible complications of lung cancer

A
  1. SVC obstruction
  2. ADH secretion –> SIADH
  3. ACTH secretion –> Cushing’s
  4. Serotonin secretion –> carcinoid
  5. Peripheral neuropathy
  6. Pathological fractures
  7. Hepatic failure
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
62
Q

Describe asthma

A

Chronic, inflammatory condition, causing episodes of reversible airway obstruction, due to:
Bronchoconstriction
Excessive secretion production

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
63
Q

What are the 3 characteristic features of asthma?

A
  • Airflow limitation - usually reversible spontaneously or with treatment
  • Airway hyper-responsiveness
  • Bronchial inflammation with T lymphocytes, mast cells, eosinophils with associated plasma exudation
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
64
Q

what are the causes of asthma?

A

Hypersensitivity of the airways, triggered by various factors:
Cold air,
exercise
Cigarette smoke
Air pollution
Allergens: pollen, cats, dogs, horses, mould
Time of day: early morning, night

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
65
Q

What is the mechanism behind hyper-reactivity?

A

Neurogenic inflammation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
66
Q

Describe neurogenic infalmmation

A

Sensory nerve activation initiates impulses which stimulates CGRP (pro-inflammatory)
this activates mast cells and innervates goblet cells

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
67
Q

Describe the process of airway remodelling in asthma

A
  1. Hypertrophy and hyperplasia of smooth muscle cells narrow the airway lumen
  2. Deposition of collagen below the BM thickens the airway wall
  3. metaplasia occurs with an increase in number of mucus-secreting goblet cells
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
68
Q

What type of T cell is involved in asthma?

A

CD4+

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
69
Q

What 2 categories can asthma be divided into?

A
  1. Allergic asthma (extrinsic), atopic, IgE and mast cell involvement
  2. Non allergic asthma (intrinsic)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
70
Q

Define atopy

A

The tendency to develop IgE mediated response to common aeroallergens

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
71
Q

What is allergic asthma?

A

When an innocuous allergen triggers an IgE mediated response
Immune recognition processes are faulty –> increase IgE, IL3,4,5, production

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
72
Q

What is non-allergic asthma?

A

Airway obstruction induced by exercise, cold air and stress
it is associated with both smoking/non-smoking
it is also associated with obesity

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
73
Q

Extrinsic asthma: what happens when IgE binds to mast cells?

A

Vasodilative substances are released causing bronchoconstriction, oedema, bronchial inflammation and mucus hyper-secretion

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
74
Q

Name 4 factors that can exacerbate asthma

A
  1. Allergens
  2. Viral infection
  3. Cold air
  4. Exercise
  5. Stress
  6. Cigarette smoke
  7. Drugs - NSAIDs/BB
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
75
Q

What occupations can be associated with an increase risk of developing asthma?

A
  1. Paint sprayers
  2. Animal breeders
  3. Bakers
  4. Launder workers
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
76
Q

What other atopic conditions are associated with asthma?

A

Eczema

Hayfever

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
77
Q

What are the symptoms of asthma?

A
  1. Episodic cough
  2. Expiratory wheeze
  3. SOB
  4. often worse at night (and in the morning)
  5. Chest tightness
  6. dyspnoea
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
78
Q

What are the signs of asthma?

A
  1. Tachypnoea - rapid breathing
  2. Audible wheeze
  3. Widespread polyphonic wheeze
  4. Cough
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
79
Q

What are the signs of an acute asthma attack?

A
  1. Can’t complete sentences
  2. HR > 110 bpm
  3. RR > 35/min
  4. PEF < 50% predicted
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
80
Q

What are the signs of a life threatening asthma attack?

A
  1. Hypoxia = PaO2 <8 kPa, SaO2 <92%
  2. Silent chest
  3. Bradycardia
  4. Confusion
  5. PEFR < 33% predicted
  6. Cyanosis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
81
Q

Give 3 differential diagnosis’s of asthma

A
  1. COPD
  2. Bronchial obstruction
  3. Pulmonary oedema
  4. Pulmonary embolism
  5. Bronchiectasis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
82
Q

What investigations might you do someone to determine whether they have asthma?

A
  1. PEFR
  2. Spirometry with reversibility testing (>5 years)
    - Obstructive pattern:
    • FEV1 <80% of predicted normal (reduced)
    • FVC = normal
    • FEV1/FVC ratio <0.7
      Peak flow measurement (reduced)
  3. CXR
  4. Atopy = skin prick, RAST
  5. Bloods = high IgE, Eosinophils
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
83
Q

What is the long-term guideline mediation regime for asthma?

A
  1. SABA
  2. SABA + ICS
  3. SABA + ICS + LTRA
  4. SABA + ICS + LABA continue LTRA if needed (stop LTRA in children)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
84
Q

Give 3 possible complications of asthma

A
  1. Exacerbation
  2. Pneumothorax
  3. Pneumonia
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
85
Q

Define COPD

A

Progressive obstructive disorder (FEV1/FC < 70%) that is irreversible
long-term deterioration in air flow through the lungs, caused by damage to lung tissue (almost always due to smoking)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
86
Q

What can COPD be sub-divided into?

A
  1. Chronic bronchitis

2. Emphysema

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
87
Q

What is the clinical diagnosis of chronic bronchitis?

A

Cough/sputum for >3 months in 2 consecutive years

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
88
Q

Describe the pathophysiology of chronic bronchitis

A

Airway inflammation –> fibrosis and luminal plugs –> decreased alveolar ventilation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
89
Q

Would a patient with chronic bronchitis be a ‘pink puffer’ or a ‘blue bloater’?

A

Blue bloater
Patient have low PaO2 and high PaCo2 –> cyanosis –> cor pulmonale
Cyanosis = blue

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
90
Q

Describe the pathophysiology of emphysema

A

Dilation and destruction of the lung tissue distal to the terminal bronchioles
Enlarged alveoli + loss of elastic recoil = increased alveolar ventilation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
91
Q

Would a patient with emphysema be a ‘pink puffer’ or a ‘blue bloater’?

A

Pink puffer
Breathless but not cyanosed
Type 1 respiratory failure
Normal or near normal PaO2 and normal or low PaCO2

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
92
Q

What are the main cells responsible for inflammation in COPD?

A

Neutrophils and macrophages

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
93
Q

What type of T cell is involved in COPD?

A

CD8+

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
94
Q

What can cause COPD?

A
  1. Genetic = alpha 1 antitrypsin deficiency
  2. Smoking = major cause
  3. Air pollution
  4. Occupational factors = dust, chemicals
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
95
Q

Name 4 symptoms of COPD

A
  1. Dyspnoea
  2. Cough +/- sputum
  3. Expiratory wheeze
  4. Weight loss
  5. SOB
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
96
Q

Give 4 signs of COPD

A
  1. Tachypnoea
  2. Barrel shaped chest
  3. Hyperinflantion
  4. Cyanosis
  5. Pulmonary hypertension
  6. Cor pulmonale
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
97
Q

Give 3 differential diagnosis’s for COPD

A
  1. Asthma
  2. HF
  3. Pulmonary embolism
  4. Bronchiectasis
  5. Lung cancer
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
98
Q

What investigations might you do to diagnose someone with COPD?

A 
Spirometry = FEV1:FVC < 0.7
CXR = hyperinflation, bullae, flat hemi-diaphragms, large pulmonary arteries 
CT = Bronchial wall thickening, enlarged air spaces 
ECG = RA and RV hypertrophy 
ABG = decreased PaO2 +/- hypercapnia
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
99
Q

Give 3 factors that can be used to establish a diagnosis of COPD

A
  1. Progressive airflow obstruction
  2. FEV1/FVC ratio < 0.7
  3. Lack of reversibility
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
100
Q

What are the treatments for COPD?

A

general:

  • stop smoking (refer to cessation services)
  • pneumococcal vaccine
  • annual flu vaccine

step 1:
- SABA (salbutamol or terbutaline) or SAMA (ipratropium bromide)

step 2:

  • If no asthmatic / steroid response:
    • LABA (salmeterol)
    • LAMA (tiotropium)
  • If asthmatic / steroid response:
    • LABA (i.e. salmeterol)
    • ICS (i.e. budesonide)

step 3:
- long term oxygen therapy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
101
Q

Give 3 advantages and 1 disadvantage of using ICS in the treatment of COPD?

A

Advantages

  1. Improve QOL
  2. Improve lung function
  3. Reduce the likelihood of exacerbations

Disadvantages:
1. There is an increased risk of pneumonia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
102
Q

Give 3 possible complications of COPD

A
  1. Exacerbations
  2. Infection
  3. Respiratory failure
  4. Cor pulmonale
  5. Pneumothorax
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
103
Q

Define exacerbation of COPD

A

An acute event characterised by worsening symptoms beyond normal day to day variation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
104
Q

Give 2 potential consequences of exacerbations of COPD/asthma

A
  1. Worsened symptoms
  2. Decreased lung function
  3. Negative impact of QOL
  4. Increased mortality
  5. Huge economic cost
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
105
Q

What is the likely cause for an exacerbation of COPD?

A

Viral URTI

Bacterial infections

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
106
Q

What are the aims of treatment for exacerbations of COPD?

A
  1. Minimise the impact of the current exacerbation

2. Prevent subsequent exacerbations

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
107
Q

What is the treatment for an exacerbation of COPD?

A

Steroids (hydrocortisone / prednisolone)
+
nebulised bronchodilators (salbutamol / ipratropium bromide)
+
antibiotics

Physiotherapy → sputum clearance

If severe:
IV aminophylline (bronchodilator),
NIV (CPAP / BIPAP)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
108
Q

Give 3 ways in which subsequent exacerbations of COPD can be prevented

A
  1. Smoking cessation
  2. Vaccination
  3. LABA/LAMA/ICS
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
109
Q

A young person presents to you with breathlessness, wheeze and cough. There appears to be inflammation of the airways. When you do a spirometry test the results are variable. You ask the patient to do a peak flow diary and the results of this show diurnal variation. Is the patient likely to have asthma or COPD?

A

Asthma
Although breathlessness, wheeze and cough are symptoms of both asthma and COPD the fact that the spirometry results are variable is a large indication that this person has asthma!
The patient is also young and COPD tends to be more common in older people

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
110
Q

An older person presents to you with breathlessness, wheeze and cough. There appears to be inflammation and fibrosis of the airways and also alveolar disruption. You ask the patient to do a peak flow diary and the results of this are all abnormal. Is the patient likely to have asthma or COPD?

A

COPD
Although breathlessness, wheeze and cough are symptoms of both asthma and COPD the fact that the spirometry results are consistently abnormal is a large indication that this person has COPD; in asthma there would be diurnal variation. Fibrosis and alveolar disruption are also signs of COPD and the fact that the patient is an older patient also makes COPD the more likely diagnosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
111
Q

Give 3 functions of pleura

A
  1. Allows movement of the lung against the chest wall
  2. Coupling system between the lungs and chest wall
  3. Clearing fluid from the pulmonary interstitium
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
112
Q

What does the pleural fluid contain?

A

Protein - albumin, globulin, fibrinogen

Mesothelial cells, monocytes and lymphocytes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
113
Q

How much fluid is contained within the healthy pleural space?

A

15ml

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
114
Q

What produces and reabsorbs pleural fluid?

A

Parietal pleura

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
115
Q

Name 3 diseases associated with the pleura

A
  1. Pleural effusion
  2. Pneumothorax
  3. Pleural plaques
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
116
Q

Define pleural effusion

A

Excess accumulation of fluid in the pleural space

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
117
Q

Name the types of pleural effusion

A
  1. Transudate = extravascular fluid with low protein content (<25 g/L)
  2. Exudate = protein rich fluid (>35 g/L)
  3. Chylothorax = lymph in pleural cavity
118
Q

what are the causes of a transudate pleural effusion?

A

fluid movement (systemic causes)

  1. Heart failure
  2. fluid overload
  3. Peritoneal dialysis
  4. Constrictive pericarditis
  5. hypoproteinaemia
    • cirrhosis
    • hypoaluminaemia
    • nephrotic syndrome
119
Q

Name 3 causes of a exudate pleural effusion

A

inflammatory (local causes)

  1. Pneumonia
  2. Malignancy
  3. TB
  4. pulmonary infarction
  5. lymphoma
  6. mesothelioma
  7. asbestos exposure
  8. MI
120
Q

How does a pleural effusion present?

A
  • SOB especially on exertion
  • Dyspnoea
  • Pleuritic chest pain
  • cough
  • Loss of weight (malignancy)
  • Chest expansion reduced on side of effusion
  • In large effusion the trachea may be deviated away from effusion
  • Stony dull percussion note on affected side
  • Diminished breath sounds on affected side
  • Decreased tactile vocal fremitus (vibration of chest wall when speaking)
  • Loss of vocal resonance
121
Q

How might you diagnose a pleural effusion?

A

1st line: CXR =
blunt costophrenic angles, fluid in lung fissures, meniscus, tracheal and mediastinal deviation

USS - identify pleural fluid

aspiration (thoracentesis/pleural tap)

  • purulent = empyema (pus)
  • turbid (cloudy) = infected
  • milky = chylothorax
122
Q

How would you treat a pleural effusion?

A

Dependent on cause
Fluid overload or congestive HF - diuretic
Infective - antibiotics
Large effusions often need aspiration or drainage

123
Q

What can you do if recurrent pleural effusions occur?

A

Pleurodesis (stick pleura together)

124
Q

What is a pneumothorax?

A

Accumulation of air in the pleural space which can lead to partial or complete lung collapse

125
Q

How can pneumothorax be classified?

A 
Spontaneous pneumothorax
Traumatic pneumothorax
Iatrogenic pneumothorax
Lung Pathology
Tension pneumothorax
126
Q

How does a pneumothorax present?

A
  • Sudden onset dyspnoea and pleuritic chest pain
  • as the pneumothorax enlarges the patient becomes more breathless and may develop pallor and tachycardia
  • Reduced expansion
  • Hyper-resonant percussion
  • Diminished breath sounds
127
Q

What investigation might you do in someone you suspect to have a pneumothorax?

A

CXR = translucency and collapse

ABG = in dyspnoeic patients check for hypoxia

128
Q

What is the treatment for a pneumothorax?

A
  • Small primary spontaneous PTX (visible rim ≤ 2cm) and not SOB
  • Consider discharge and follow up CXR in review
    Large primary spontaneous PTX (visible rim >2cm) and/or SOB
  • Needle aspiration
    If not <2cm on repeat CXR insert chest drain and supplemental O2 if needed, admit.
  • Secondary Pneumothorax – requires chest drain if large/ needle aspiration if small, admission and high flow O2
129
Q

Name a possible complication of a pneumothorax

A

Tension pneumothorax

130
Q

Describe the pathophysiology of a tension penumothorax

A

Pleural tear creates 1 way valve - air only goes into cavity –> increased unilateral pressure –> respiratory distress, shock and cardiac arrest

131
Q

What is the treatment for a tension pneumothorax?

A 
Put out cardiac arrest call
Start high flow O2
Immediate decompression
Unless tension PTX due to trauma:
“Insert a large bore cannula into the pleural space through the second intercostal space in the mid-clavicular line”

Hiss sound confirms diagnosis

132
Q

Define interstitial lung diseases

A

Distant cellular infiltrate and extracellular matrix deposition in lung distal to the terminal bronchioles - disease of the alveolar/capillary interface

133
Q

What are 5 major categories of interstitial lung disease

A
  1. Associated with systemic disease - rheumatological
  2. Environmental aetiology - fungal, dusts
  3. Granulomatous disease - sarcoidosis
  4. Idiopathic - idiopathic pulmonary fibrosis
  5. Other
134
Q

What are the 4 major features of interstitial lung disease?

A
  1. Cough
  2. Dyspnoea
  3. Restirictve spirometry
  4. Abnormal CXR/CT
135
Q

Would pulmonary function tests taken from someone with interstitial lung disease show a restrictive or obstructive pattern?

A

Restrictive

Decreased gas transfer and a reduction in PaO2

136
Q

What is the pathology of interstitial lung disease?

A

Increased fibrous tissue within the lung parenchyma resulting in increased stiffness and decreased expansion

137
Q

What kind of disease is sarcoidosis?

A

Granulomatous disease - type of interstitial lung disease

138
Q

Describe the pathophysiology of sarcoidosis

A

Chronic inflammation –> non-caseating granuloma in various body sites

Typical sarcoid granulomas consist of focal accumulations of epithelioid cells, macrophages and lymphocytes - mainly T cells

139
Q

Describe the epidemiology of sarcoidosis

A

Women > men
Aged 20-40 years old
African-Caribbean’s are affected more frequently and more severely than Caucasians

140
Q

Give 3 pulmonary symptoms of sarcoidosis

A
  1. Dry cough
  2. Progressive SOB
  3. Wheeze
  4. Chest pain
141
Q

What is the effect of sarcoidosis on the skin?

A

Erythema nodosum

142
Q

What is the effect of sarcoidosis on the eyes?

A

Uveitis

143
Q

What is the effect of sarcoidosis on the bone?

A

Arthralgia

144
Q

What is the effect of sarcoidosis on the liver?

A

Hepatosplenmeagly

145
Q

What investigations might you do in someone who you suspect to have sarcoidosis?

A

Bloods = increase ESR, lymphopenia, increase CAE, raised LFTs

Bronchoalveolar lavage = increased lymphocytes

Lung tissue biopsy = diagnostic = non-caseating granulomata (increased lymphocytes in active disease and increased neutrophils in pulmonary fibrosis)

CXR = staging

146
Q

How can you stage sarcoidosis?

A

Using CXR
Stage 1 = bilateral hilar lymphadenopathy (BHL)
Stage 2 = pulmonary infiltrates with BHL
Stage 3 = pulmonary infiltrates without BHL
Stage 4 = progressive pulmonary fibrosis, bulla formation and bronchiectasis

147
Q

How do you treat acute sarcoidosis?

A

NSAIDs and bed rest

148
Q

How do you treat sarcoidosis?

A

do not treat symptomatic stage 1, and asymptomatic stage 2 or 3
patients with BHL do not need treatment - most recover spontaneously

acute = bed rest and NSAIDs

prednisolone orally
if severe = IV methylprednisolone
if steroid resistant = methotrexate (requires close monitoring)

lung transplant in severe cases

149
Q

Give 2 possible differential diagnosis’s for sarcoidosis

A
  1. Lymphoma

2. Pulmonary TB

150
Q

What is idiopathic pulmonary fibrosis?

A

Progressive fibrosis in the alveoli that limits the patients ability to respire

Formation of scar tissue in lungs with no known cause.

151
Q

Describe the pathophysiology of idiopathic pulmonary fibrosis

A

repetitive injury to the alveoli epithelium causes wound healing mechanisms to become uncontrolled

this leads to fibroblast over-production and increased fibrosis

this leads to a loss of elasticity and ability to perform gas exchange is impaired -> restrictive lung disease and progressive respiratory failure

152
Q

what are the risk factors of idiopathic pulmonary fibrosis?

A
  • cigarette smoking
  • infectious agents - CMV, Hep C, EBV
  • occupational dust exposure
  • drugs - methotrexate, imipramine
  • GORD
  • genetic predisposition
153
Q

what are the clinical features of idiopathic pulmonary fibrosis

A
  1. Dry cough
  2. SOB on exertion
  3. Systemic = malaise, weight loss, arthralgia
  4. Cyanosis
  5. Finger clubbing
  6. bibasal crackles (Inspiratory crackles/crepitus)
  7. dyspnoea
154
Q

What investigations might you do in someone you suspect to have idiopathic pulmonary fibrosis?

A

ABG = type 1 respiratory failure

Bloods = raised CRP, immunoglobulins and check autoantibodies

CXR/CT = degreased lung volume + honeycomb lung

High resolution CT = ground glass appearance

Spirometry = restrictive

Lung biopsy = confirmation

155
Q

What is the treatment for idiopathic pulmonary fibrosis?

A

Pharmacological: Pirfenidone, nintedanib - antifibrotic

Non pharmacological: Smoking cessation, physiotherapy, vaccines up to date

Lung transplantation last resort

156
Q

what are the possible complications of idiopathic pulmonary fibrosis

A
  1. Respiratory failure

2. Cor pulmonale

157
Q

Define pulmonary hypertension

A

A disease of the small pulmonary arteries characterised by vascular proliferation and remodelling. It results in a progressive increase in pulmonary vascular resistance (PVR)

Increase in mean pulmonary arterial pressure >25 mmHg and secondary right ventricular failure

158
Q

What can cause an increase in mPAP?

A

Increase resistance to flow

Increased flow rate

159
Q

what are the causes of pulmonary hypertension

A
  • pre-capillary
    • multiple small PE’s
    • left-to-right shunts
    • primary
  • capillary
    • emphysema
    • COPD
  • Post-capillary
    • backlog of blood causes secondary hypertension
    • LV failure
  • chronic hypoxaemia
    • living at high altitude
    • COPD
160
Q

what is the clinical presenation of pulmonary hypertension

A

initial features - due to an inability to increase cardiac output

  • exertional dyspnoea
  • lethargy and fatigue
  • ankle swelling
  • Accentuated pulmonic component to the 2nd heart sound
  • Tricuspid regurgitation murmur
  • peripheral oedema, cyanosis
  • cor pulmonale
161
Q

What investigations might you do in someone to determine whether they have pulmonary hypertension?

A

Initial tests:
- CXR - Enlarged main pulmonary artery, enlarged hilar vessels and pruning.

  • ECG - right ventricular hypertrophy,right axis deviation, right atrial enlargement. (A normal ECG does not rule out the presence of significant pulmonary hypertension)
  • TTE - (trans-thoracic echocardiogram)

Diagnostic test: Right heart catheterisation

162
Q

Describe the treatment of pulmonary hypertension

A 
General supportive therapy:
       Treat underlying cause
       - Oral anticoagulants - WARFARIN
       - diuretics for oedema
       - oxygen 
       - oral CCBs
       - Supervised exercise training
       Avoiding pregnancy

In treatment-resistant patients:
Balloon atrial septostomy - produces right-to-left shunting that decompresses the right atrium and right ventricle, increases systemic cardiac output, and decreases systemic arterial oxygen saturation
Lung transplantation

163
Q

Give a possible complication of pulmonary hypertension

A

Cor pulmonale (RS HF) –> pleural effusion + death

164
Q

what are the features of mycobacterium tuberculosis bacteria?

A
  • Aerobic, non-motile, non-sporing, slightly curved bacilli with a thick waxy capsule
  • Acid-fast bacilli – turns red/pink with Ziehl-neelsen stain
  • Slow growing
  • Resistant to phagolysosomal killing and able to remain dormant
165
Q

What mycobacterium can cause abdominal tuberculosis?

A

Mycobacterium bovis

- found in unpasteurised milk

166
Q

How is TB transmitted?

A

Aerosol transmission

167
Q

Describe pulmonary infection of TB

A

Bacilli settle in lung apex

Macrophages and lymphocytes mount an effective immune response that encapsulate and contains the organism forever

168
Q

Describe the pathogenesis of pulmonary TB disease

A

TB spread via respiratory droplets as it is an airborne infection
1. Alveolar macrophages ingest bacteria and the rods proliferate inside.

  1. Drain into hilar lymph nodes 🡪 present antigen to T lymphocytes 🡪 cellular immune response.
  2. Delayed hypersensitivity reaction 🡪 tissue necrosis and granuloma formation: caseating.
    • Primary Ghon Focus
    • Ghon Complex – Ghon focus + lymph nodes
169
Q

Describe the disease course of TB

A

Primary infection –> latent TB –> reactivation/immunocompromised

170
Q

Where in the lung is granuloma cavity most likely to develop in TB?

A

Apex of the lung = more air and less blood supply and less immune cells

171
Q

Give 3 risk factors for TB

A
  1. Living in a high prevalence area
  2. IVDU
  3. Homeless
  4. Alcohol
  5. HIV +ve
172
Q

What systemic symptoms might you see as a result of TB?

A
  1. Weight loss
  2. Night sweats
  3. Anorexia
  4. Malaise
  5. low grade fever
173
Q

What pulmonary symptoms might you see as a result of TB?

A 
Productive cough
Haemoptysis
Cough >3 weeks (dry or productive)
Breathlessness
Sometimes chest pain
174
Q

Name 3 places where TB might spread to?

A
  1. Bone and joint = pain and swelling
  2. Lymph nodes = pain and discharge
  3. CNS = TB meningitis
  4. Biliary TB = disseminated
  5. Abdominal TB = ascites, malabsorption
  6. GU TB = sterile pyuria, WBC in GU tract
175
Q

What investigations might you do to determine whether someone has TB?

A

Inflammatory markers = raised CRP, hyperalbuminaemia, thromobocytosis, high B cell count
CXR = consolidation, collapse, pleural effusion
Microbiology - sputum/biopsy = Ziehl-Neelson stain and culture

176
Q

A special culture medium is needed to grow TB, what is it called?

A

Lowenstein Jenson Slope

177
Q

What test might you do to diagnose latent TB?

A

Tuberculin skin test (Mantoux)
Intradermal injection –> stimulates type 4 hypersensitivity reaction

interferon gamma release assay -> detect response of WBC to TB antigens
(rapid results and less likely to give false positives)

178
Q

What might a lymph node biopsy from someone with TB show?

A

Caseating granuloma

179
Q

What is the drug treatment commonly used for TB?

A

RIPE
RI = 6 months
PE = for first 2 months

R = rifampicin
I = isoniazid 
P = pyrazinamide
E = ethambutol
180
Q

Give 2 potential side effects of Rifampicin

A
  1. Red urine
  2. Hepatitis
  3. Drug interaction - it’s an enzyme inducer
181
Q

Give 2 potential side effects of Isoniazid

A
  1. Hepatitis

2. Neuropathy

182
Q

Give 2 potential side effects of Pyrazinamide

A
  1. Hepatitis
  2. Gout
  3. Neuropathy
183
Q

Give a potential side effect of Ethambutol

A

Optic neuritis

184
Q

Why is compliance so important when taking TB medication?

A

Resistance and relapse likely if non-compliant

185
Q

Why does TB treatment need to last 6 months?

A

Ensure all dormant bacteria have ‘woken up’ and been killed

186
Q

Give 2 factors that can increase the risk of drug resistance in TB

A
  1. If the patient has had previous treatment
  2. If they live in a high risk area
  3. If they have contact with resistant TB
  4. If they have a poor response to therapy
187
Q

How can TB be prevented?

A
  1. Active case finding
  2. Detect and treat latent TB
  3. Vaccination = BCG
188
Q

What is Whooping cough caused by?

A

Bordatella pertussis (gram -ve coccobacilli) - rod

189
Q

Describe the disease course of whooping cough

A

7-10 day incubation –> 1-2 week catarrhal stage –> 1-6 week paroxysmal stage

190
Q

What are the symptoms of whooping cough?

A

Paroxysmal cough - sudden and severe

Vomiting after cough

191
Q

What is the treatment of whooping cough?

A

Clarithromycin - in catarrhal or early paroxysmal stages

  • have little effect on disease course in paroxysmal stage
192
Q

How can you prevent whooping cough?

A

Pertussis vaccination

8, 12 and 16 weeks and a pre school booster

193
Q

Give 2 possible complications of whooping cough

A
  1. Pneumonia
  2. Encephalopathy
  3. Sub-conjunctival haemorrhage
194
Q

What is the difference between bronchitis and bronchiolitis?

A 
Bronchitis = inflammation of bronchi epithelium due to irritant and chemical 
Bronchiolitis = Inflammation of bronchioles and increased mucus secretion due to RSV infection
195
Q

A patient presents with breathlessness. On examination they have absent breath sounds and their chest produces a stony dull sound on percussion. They have a PMH of heart failure. What is the likely cause of their symptoms?

A

Pleural effusion

196
Q

what is the epidemiology of cystic fibrosis?

A

• One of the most commonest lethal autosome RECESSIVE conditions in
CAUCASIANS, 25% condition and 50% carrier risk
- Much less common in Afro-Caribbean and Asian people
- Multi-system disease although respiratory problems are usually the most prominent
- Most people with CF also have pancreatic insufficiency

197
Q

what are the risk factors for cystic fibrosis?

A
  • Family history

- Caucasian

198
Q

what is CFTR and what is it’s function?

A

• Transport protein on membrane of epithelial cells that acts as a chloride
channel
• Transports chloride ions
• Normally; it actively exports NEGATIVE IONS especially Cl- and Na+ passively follows causing an osmotic gradient and movement of water out of the cell and into the mucus

199
Q

what is the clinical presentation of the alimentary effects of cystic fibrosis?

A

• Thick secretions
• Reduced pancreatic enzymes (due to mucus blocking pancreatic duct)
• Pancreatic insufficiency (diabetes mellitus & steatorrhoea (fatty stools
since enzymes not released to digest fat)
• Distal intestinal obstruction syndrome - bowel obstruction (equivalent of
meconium ileus) resulting in reduced GI motility
• Reduced bicarbonate (HCO3-)
• Maldigestion & malabsorption thus poor nutrition (associated with
pulmonary sepsis)
• Cholesterol Gallstones (in increased frequency) & cirrhosis
• Increased incidence of peptic ulcers & malignancy

200
Q

what is transudate pleural effusion?

A
  • transparent (less protein)
    • Pleural fluid protein is less than 30g/L since vessels are normal so only
    fluid is able to leak out and not protein
    • Occurs when the balance of hydrostatic forces in the chest favour the accumulation of pleural fluid i.e. increased pressure due to the backing up of blood in left sided congestive heart failure
201
Q

what is exudate pleural effusion?

A
  • exudes proteins
  • Pleural fluid protein is more than 30g/L since endothelial cells of vessels are more apart meaning fluid and protein is able to leak out
  • Occurs due to the increased permeability and thus leakiness of pleural
    space and or capillaries usually as a result of inflammation, infection or
    malignancy
202
Q

what is the epidemiology of pleural effusion?

A
  • Seen in adults and less commonly in children
  • Recurrent pleural effusions are seen malignant mesothelioma
  • Pleural effusions are transudates or exudates
203
Q

what are the risk factors for pleural effusion?

A
  • Previous lung damage

- Asbestos exposure

204
Q

what are the risk factors for pneumothorax?

A 
Smoking
Family history
Male
Tall and slender build
Young age 
Presence of underlying lung disease
205
Q

what is the pathophysiology of pneumothorax?

A

Normally intrapleural pressure is negative

When there is a bridge between alveoli and pleural space or atmosphere and pleural space

Flow of air in until communication closed or gradient closed.

206
Q

what is the clinical presentation of a tension pneumothorax?

A 
Cardiopulmonary deterioration:
Hypotension – imminent cardiac arrest
Respiratory distress
Low sats
Tachycardia
Shock
Severe chest Pain
207
Q

what are the clinical features of a tension pneumothorax?

A

Tracheal deviation to contralateral side

Ipsilateral reduced breath sounds
Hyperresonance on percussion

Hypoxia

208
Q

what is the epidemiology of pneumothorax?

A
  • Occurs spontaneously or secondary to chest trauma
  • Spontaneous pneumothorax is most common in young males
  • Generally a pneumothorax is MUCH MORE COMMON in MALES
  • Often patients are tall and thin
  • Caused by the rupture of a pleural bleb/sub-pleural bulla(serous filled blister),
    usually apical (top) thought to be due to congenital defects in the connective
    tissue of the alveolar walls
209
Q

what are the causes of pneumothorax?

A
  • In patients over 40 years of age the usual cause is underlying COPD
  • Other/rarer causes include:
    • Bronchial asthma
    • Carcinoma
    • Breakdown of a lung abscess leading to bronchopleural fistula
    • Severe pulmonary fibrosis with cyst formation
    • TB
    • Pneumonia
    • Cystic fibrosis
    • Trauma (penetrating or rib fracture)
    • Iatrogenic e.g. pacemakers or central lines
210
Q

what is the catarrhal phase of whooping cough?

A
  • Patient highly infectious
  • Cultures from respiratory cultures are positive in 90% of cases
  • Malaise
  • Anorexia
  • Rhinorhoea (nasal cavity congested with significant amount of mucus)
  • Conjunctivitis
211
Q

what is the paroxysmal phase of whooping cough?

A

• Begins 1 week later from catarrhal phase
• Coughing spasms
• Classic inspiratory whoop is only seen in younger individuals in whom
the lumen of the respiratory tract is compromised by mucus secretion
and mucosal oedema
• These coughing spasms usually terminate in vomiting
• Cough for more than 14 days

212
Q

what are the investigations for whooping cough?

A
  • Chronic cough and one clinical feature indicated pertussis
  • Chronic cough and history of contact or microbiological diagnosis is used
    to confirm pertussis
  • Suggested clinically by the characteristic whoop and history of contact with
    an infected individual
  • PCR test
  • But culture of a nasopharyngeal swab = definitive diagnosis
213
Q

what is the epidemiology of whooping cough?

A

Mainly a disease of childhood with 90% of cases occurring below 5 years of age

214
Q

what is the pathophysiology of whooping cough?

A
  • Highly contagious and spread by droplet infection

- In early stages it is indistinguishable from other upper respiratory tract infections

215
Q

what are the signs of TB?

A 
Signs of bronchial breathing
Dullness to percuss
Decreased breathing
fever
crackles
216
Q

what is the treatment for pneumonia?

A

Maintaining O2 Sats between 94-98%
In COPD patients: maintain O2 sats between 88-92%
Analgesia: paracetamol or NSAIDs
IV fluids

217
Q

which bacteria causes rusty sputum in pneumonia?

A

strep pneumoniae

218
Q

what is atypical pneumonia?

A

Bacterial pneumonia caused by atypical organisms that are not detectable on Gram stain and cannot be cultured using standard methods.

219
Q

what are the common organisms that cause atypical pneumonia?

A

Mycoplasma pneumoniae,
Chlamydophila pneumoniae,
Legionella pneumophila
coxiella burnetii

220
Q

what are the characteristic symptoms of atypical pneumonia?

A

headache
low-grade fever
cough
malaise

221
Q

what is the mechanism of action for rifampicin for TB?

A

bactericidal - blocks protein synthesis

222
Q

what is the mechanism of action of isoniazid for TB?

A

bactericidal - blocks cell wall synthesis

223
Q

what is the mechanism of action for pyrazinamide for TB?

A

bactericidal initially, less effective later

224
Q

what is the mechanism of action for ethambutol

A

bacteriostatic - blocks cell wall synthesis

225
Q

what antibiotics are used for bronchiectasis?

A
  • pseudomonas aeruginosa = oral ciprofloxacin
  • h.influenzae = oral amoxycillin, co-amoxyclav or doxycycline
  • staph aureus = flucloxacillin
226
Q

what is the pathophysiology of goodpasture’s syndrome?

A

Specific autoimmune disease caused by a type II antigen-antibody reaction leading to diffuse pulmonary haemorrhage, glomerulonephritis (and often acute kidney injury and chronic kidney disease)

  • There are circulating anti-glomerular basement membrane (anti-GBM) antibodies
227
Q

what is the characteristic presentation of COPD?

A 
productive cough
white or clear sputum
wheeze
SOB
following many years of smoking
228
Q

what are the systemic effects of COPD?

A 
hypertension
osteoporosis
depression
weight loss
reduced muscle mass with general weakness
229
Q

where does squamous cell carcinoma of the lung arise from?

A
  • epithelial cells typically in the central bronchus
230
Q

what is squamous cell carcinoma associated with the production of?

A

associated with the production of keratin

231
Q

where does small cell lung cancer arise from?

A

Arises from endocrine cells typically in the central bronchus

232
Q

what is small cell lung cancer associated with the production of?

A

Secretes polypeptide hormones

233
Q

which is the most common lung cancer in non-smokers?

A

adenocarcinoma

234
Q

where does adenocarcinoma arise from?

A

mucus-secreting glandular cells

235
Q

which is more common, primary lung cancer or metastatic lung cancer from elsewhere?

A

Cancer metastasising from elsewhere is more common than a primary lung tumour

236
Q

what is the pathophysiology of pulmonary hypertension?

A

The main vascular changes are:
Vasoconstriction
Smooth-muscle cell and endothelial cell proliferation
Thrombosis

237
Q

what are the different types of emphysema?

A

centri-acinar emphysema
pan-acinar emphysema
irregular emphysema

238
Q

what is centri-acinar emphysema?

A
  • Distension and damage of lung tissue is concentrated around the respiratory bronchioles, whilst the more distal alveolar ducts and alveoli tend to be well preserved
  • Extremely common
239
Q

what is pan-acinar emphysema?

A
  • Less common
  • Distension and destruction affect the whole acinus and in severe cases the lung is just a collection of bullae
  • Associated with alpha-1 antitrypsin deficiency
240
Q

what is irregular emphysema?

A

• Scarring and damage that affects the lung parenchyma

patchily, independent of acinar structure

241
Q

what are the signs of emphysema?

A 
Dyspnoea / Tachypnoea
Minimal cough
Pink skin, pursed-lip breathing
Accessory muscle use
Cachexia
Hyperinflation (barrel chest)
Weight loss (due to increased work of breathing and cachexia)
242
Q

what are the complications of emphysema?

A

Pneumothorax due to bullae

243
Q

what are the symptoms of emphysema?

A
  • Chronic productive cough
    - Purulent sputum
  • Dyspnoea
  • Cyanosis (hypoxaemia)
    - Can cause secondary polycythemia
    - May develop pulmonary hypertension (reactive pulmonary vasoconstriction)
  • Peripheral oedema
  • Obesity
  • Haemoptysis
244
Q

what are the investigations for IE COPD?

A

ABG

  • CO2 retention → acidosis
  • Raised pCO2 + low pO2 = T2RF

Chest X-Ray, sputum culture + sensitivities for antibiotic therapy, FBC + U&E

245
Q

what is the epidemiology of asthma?

A
  • Commonly starts in childhood between the ages 3-5 years and may either worsen or improve during adolescence
  • Peak prevalence between 5-15 years
  • more common in developed countries
246
Q

what is extrinsic (atopic) allergic asthma?

A
  • Occurs most frequently in atopic individuals

- Childhood asthma often accompanied by eczema

247
Q

what is intrinsic allergic asthma?

A
  • Often starts in middle-aged and attacks are usually triggered by respiratory infections
248
Q

what are the genetic factors for asthma?

A
  • Genes controlling the production of cytokines IL-3,-4,-5,-9 & -13
  • ADAM33 is associated with airway hyper-responsiveness and tissue remodelling
249
Q

what are the environmental factors for asthma?

A

• Early childhood exposure to allergens and maternal smoking has a
major influence on IgE production
• Growing up in a ‘clean’ environment may predispose towards an IgE
response to allergens whereas growing up in a ‘dirtier’ environment may
allow the immune system to avoid developing allergic responses

250
Q

what are the risk factors for developing asthma

A
  • Personal history of atopy
  • Family history of asthma or atopy
  • Obesity
  • Inner-city environment
  • Premature birth (low birth weight, not breast-fed)
  • Socio-economic deprivation
  • exposure to allergens
251
Q

which drugs can trigger asthma attacks?

A

NSAIDs and aspirin

beta blockers - results in bronchoconstriction which results in airflow limitation and potential attack

252
Q

what is the acute management of asthma?

A
  1. oxygen
  2. salbutamol nebuliser
  3. ipratropium bromide nebuliser
  4. hydrocortisone IV or oral prednisolone
  5. IV magnesium sulfate
  6. aminophylline / IV salbutamol
253
Q

give 2 examples of SABAs

A
  • salbutamol (partial agonist)

- terbutaline

254
Q

what is the mechanism of action for SABAs?

A
  • are beta-2 selective

- bind to B2 receptor causing more cAMP which leads to more bronchodilation

255
Q

how long do SABAs last for?

A

4 hours

256
Q

give 2 examples of LABAs

A
  • salmeterol

- formoterol (full agonist)

257
Q

what is the mechanism of action for LABAs?

A
  • are beta-2 selective
  • bind to B2 receptor causing more cAMP which leads to more bronchodilation
  • are longer acting since more lipophilic so remain in the body for longer
258
Q

give an example of a SAMA

A

ipratropium

259
Q

what is the mechanism of action for SAMA?

A
  • Act on airway M3 receptors

- prevent ACh from binding since they bind to the M3 receptor thereby blocking ACh action

260
Q

give an example of a LAMA

A

tiotropium

261
Q

what is the mechanism of action for LAMA?

A
  • Act on airway M3 receptors
  • prevent ACh from binding since they bind to the M3 receptor thereby blocking ACh action
  • has high affinity and disassociates slowly from muscarinic receptors
262
Q

what is the mechanism of action for ICS?

A
  • They reduce the number of inflammatory cells in the airways
  • Suppress production of chemotactic mediators
  • Reduce adhesion molecular expression
  • Inhibit inflammatory cell survival in the airway
  • Suppress inflammatory gene expression in airway epithelial cells
263
Q

what are the side effects of ICS?

A

Loss of bone density
Adrenal suppression
Cataracts
Glaucoma

264
Q

what is the effect of interaction between beta-2 agonists and glucocorticoids in the treatment of asthma?

A
  • glucocorticoids increase the transcription of B2-receptor gene, resulting in increased expression of cell surface receptors
  • Long acting B2 agonists increase the translocation of GR from cytoplasm to the nucleus after activation by glucocorticoids
  • Leads to greater overall efficacy and need for lower doses
265
Q

what are the advantages of inhaled drugs?

A
  • lungs are robust -> can handle repeated exposure
  • very rapid absorption
  • large SA
  • fewer drug metabolising enzymes
  • non-invasive port of entry
  • fewer systemic side effects
266
Q

what are the risk factors for developing pneumonia?

A
  • under 16 or over 65
  • HIV infection
  • DM
  • CF
  • COPD
  • smoking
  • excess alcohol
  • IVDU
  • immunosuppressant therapy
267
Q

what is a Ghon complex?

A

Ghon focus + lymph nodes

268
Q

what are the extra-pulmonary manifestations of lung cancer?

A

Recurrent laryngeal nerve palsy - hoarse voice

Superior vena cava obstruction - facial swelling, distended veins in neck and upper chest, Pemberton’s sign

Horner’s syndrome - ptosis, miosis, anhidrosis

269
Q

what is a PE?

A

occlusion of a pulmonary artery by an embolic thrombus.

270
Q

what is the pathophysiology of a PE?

A

clot breaks off from venous thrombus → IVC → RA → RV → pulmonary arteries

271
Q

what are the causes/risk factors of PE?

A

Increased age
Immobility e.g. post-surgery, long haul flights
Pregnancy
Active malignancy
DVT
Family history of VTE
Congenital and acquired thrombotic disorders

272
Q

what is the clinical presentation of PE?

A

SYMPTOMS
Acute onset SOB
Cough +/- haemoptysis
Pleuritic chest pain

SIGNS
DVT
hypoxia
tachycardia
increased resp rate
low grade fever
haemodynamic instability -> hypotension
273
Q

what scoring system is used to measure the risk of PE?

A

Wells score

274
Q

what are the investigations for PE?

A

D-dimer
CTPA spiral with contrast
ABG

275
Q

what is the management for PE?

A
  • if investigations are delayed start anticoagulation

1st line = apixaban/rivaroxaban

LMWH for 5 days followed by dabigatran
3 months for provoked
>3 months for unprovoked

IVC filter

276
Q

what is the management for haemodynamic instability caused by a PE?

A
  • IV thrombolysis - alteplase
  • catheter directed thrombolysis
  • embolectomy
277
Q

what is pharyngitis?

A

rapid onset of sore throat and inflammation of the pharynx (with or without exudate)

278
Q

what are the most common causes of pharyngitis?

A

group A strep = most common

EBV

279
Q

what are the clinical features of pharyngitis?

A 
Sore throat → difficulty swallowing
Fever 
Headache
Joint pain/ muscle ache
Skin rashes
Swollen lymph nodes in neck
280
Q

what are the clincial features of pharyngitis that suggest a viral cause?

A

runny nose, blocked nose, sneezing, cough

281
Q

what are the clinical features of pharyngitis that suggest a bacterial cause?

A

fever, pharyngeal exudate, cervical lymphadenopathy, absence of cough + runny nose

282
Q

what are the investigations for pharyngitis?

A

rapid antigen detection test (RADT)

throat culture

283
Q

what is the management for pharnygitis?

A

group A strep = phenoxymethylpenicillin (clarithromycin if allergic to penicillin)

viral = self resolving, supportive care

284
Q

what is sinusitis?

A

inflammation of the mucous membrane of the nasal cavity and paranasal sinuses - also known as acute rhinosinusitis.

285
Q

what are the most common causes of sinusitis?

A

Common infectious agents:
Streptococcus pneumoniae
Haemophilus influenzae
Rhinoviruses

286
Q

what are the risk factors for sinusitis?

A

nasal pathology e.g. septal deviation or nasal polyps
recent local infection e.g. rhinitis or dental extraction
swimming/diving
smoking

287
Q

what is the clinical presentation of sinusitis caused by bacteria?

A 
symptoms > 10 days
purulent nasal discharge
nasal obstruction
dental/facial pain
headache
288
Q

what is the clincial presentation of sinusitis caused by virus?

A

symptoms < 10 days
clear nasal discharge
fever
sore throat

289
Q

what are the investigations for sinusitis?

A

clincial diagnosis

290
Q

what is the management for sinusitis?

A

Symptom management with analgesia and intranasal decongestants

intranasal corticosteroids considered if symptoms have been present for >10 days

Antibiotic therapy not normally required but may be given for severe presentations (phenoxymethylpenicillin first-line)

Phase 2A revision (38 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions