Brainscape's Knowledge GenomeTM

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


See full index

Medicine Year 3 > Respiratory Medicine > Flashcards

Respiratory Medicine Flashcards

1
Q

What is Anaphylaxis?

A

SERIOUS allergic reaction
• Sensitised individual exposed to specific antigen

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

Causes of anaphylaxis and angio-oedema

A

insects bites/ stings, food, medications

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

Immunology of anaphylaxis

A

IgE → antigen → mast cell & basophils ‡ → histamine ↑ → body response

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

Anaphylaxis symptoms?

A

Pruritus, urticaria & angioedema

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

Anaphylaxis treatment

A

• Remove trigger, maintain airway, 100% O2
• Intramuscular adrenaline 0.5 mg
(Repeat every 5 mins as needed to support CVS)
• IV hydrocortisone 200mg
• IV chlorpheniramine 10 mg
• If hypotensive: lie flat and fluid resuscitate
• Treat bronchospasm: NEB salbutamol
• Laryngeal oedema: NEB adrenaline

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Asthma Severity?

A

Mild:
• No features of severe asthma
• PEFR >75%
Moderate:
• No features of severe asthma
• PEFR 50-75%
Severe (if any one of the following):
• PEFR 33 – 50% of best or predicted
• Cannot complete sentences in 1 breath
• Respiratory Rate > 25/min
• Heart Rate >110/min
Life threatening (if any one of the following):
• PEFR < 33% of best or predicted
• Sats <92% or ABG pO2 < 8kPa
• Cyanosis, poor respiratory effort, near or fully silent
chest
• Exhaustion, confusion, hypotension or arrhythmias
• Normal pCO2
Near Fatal:
• Raised pCO2

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Acute Asthma management

A

ABCDE

Aim for SpO2 94-98% with oxygen as needed, ABG if
sats <92%

5mg nebulised Salbutamol (can repeat after 15 mins)

40mg oral Prednisolone STAT (IV Hydrocortisone if
PO not possible)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Severe asthma treatment

A

Nebulised Ipratropium Bromide 500 micrograms
 Consider back to back Salbutamol

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Life threatening or near fatal asthma

A

 Urgent ITU or anaesthetist assessment
 Urgent portable CXR
 IV Aminophylline
 Consider IV Salbutamol if nebulised route ineffective

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

What is Asthma?

A

Asthma is a chronic inflammatory disease of the airways
• Airway obstruction that is reversible (but not completely so in some subjects), either spontaneously or with treatment
• Increased airway responsiveness (airway narrowing) to a variety of stimuli

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Asthma pathophysiology

A

Airway epithelial damage – shedding and subepithelial fibrosis, basement membrane thickening
• An inflammatory reaction characterised by eosinophils, T-lymphocytes (Th2) and mast cells. Inflammatory mediators released include histamine, leukotrienes, and prostaglandins
• Cytokines amplify inflammatory response
• Increased numbers of mucus secreting goblet cells
and smooth muscle hyperplasia and hypertrophy
• Mucus plugging in fatal and severe asthma

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Asthma safe discharge criteria

A

PEFR >75%
• Stop regular nebulisers for 24 hours prior to
discharge
• Inpatient asthma nurse review to reassess inhaler
technique and adherence
• Provide PEFR meter and written asthma action plan
• At least 5 days oral prednisolone
• GP follow up within 2 working days
• Respiratory Clinic follow up within 4 weeks
• For severe or worse, consider psychosocial factors

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Asthma Triggers

A

• Smoking
• Upper respiratory tract infections – mainly viral
• Allergens – pollen, house dust mite, pets
• Exercise – also cold air
• Occupational irritants
• Pollution
• Drugs – aspirin, beta blockers (including eye drops)
• Food and drink – dairy produce, alcohol, orange
juice
• Stress
• Severe asthma – consider inhaled heroin, pre-menstrual, psychosocial aspects

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Eosinophilia causes

A

Some patients with asthma have eosinophilic inflammation which typically responds to steroids. However, there are several differentials of eosinophilia:
• Airways inflammation (asthma or COPD)
• Hayfever / allergies
• Allergic Bronchopulmonary Aspergillosis
• Multiple courses of antibiotics for chronic infections
• Eosinophilic Granulomatosis with Polyangiiitis
• Eosinophilic Pneumonia
• Parasites e.g. Hookworm
• Lymphoma
• SLE
• Hypereosinophilic syndrome

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

What is COPD

A

COPD is characterised by airflow obstruction. The airflow obstruction is usually progressive, not fully reversible and does not change markedly over several months. The disease is predominantly caused by smoking.

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

COPD Pathophysiology

A

COPD is an umbrella term which encompasses emphysema and chronic bronchitis.

Mucous gland hyperplasia
Loss of cilia function
Emphysema - alveolar wall destruction causing irreversible enlargement of air spaces distal to the terminal bronchiole.
Chronic inflammation and fibrosis of small airways.

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

COPD causes

A

Smoking
• Inherited α-1-antitrypsin deficiency
• Industrial exposure, e.g. soot

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

Outpatient COPD management

A

COPD Care Bundle’
• SMOKING CESSATION
• Pulmonary Rehabilitation
• Bronchodilators
• Antimuscarinics
• Steroids
• Mucolytics
• Diet
• LTOT if appropriate
• LUNG VOLUME REDUCTION if appropriate

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

COPD Long term oxygen therapy

A

Extended periods of hypoxia cause renal and cardiac damage – can be prevented by LTOT
• LTOT to be used at least 16 hours/day for a survival benefit
• LTOT offered if pO2 consistently below 7.3 kPa, or below 8 kPa with cor pulmonale
• Patients must be non-smokers and not retain high levels of CO2
• O2 needs should be balanced with loss of independence and reduced activity which may occur • Note: oxygen is not a treatment for breathlessness; it is a treatment to help prevent organ hypoxia.

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

Pulmonary rehabilitation

A

MDT 6-12 week programme of supervised exercise, unsupervised home exercise, nutritional advice, and disease education

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

COPD exacerbation treatment

A

ABCDE approach

Oxygen:
- aim for target SaO2 94-98% but if any evidence of acute (raised pCO2 on ABG) or previous Type 2 Respiratory Failure, then target SaO2 88-92%
• NEBs – Salbutamol and Ipratropium
• Steroids – Prednisolone 30mg STAT and OD for 7
days
• Antibiotics if raised CRP / WCC or purulent sputum
• CXR
• Consider IV aminophylline
• Consider NIV if Type 2 respiratory failure and pH
7.25-7.35
• If pH <7.25 consider ITU referral

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

Community acquired pneumonia - typical causative organisms

A

streptococcus pneumonia; haemophilus influenza, moraxella catarrhalis

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

Community acquired pneumonia atypical organisms

A

legionella pneumphila, chlamydia pneumoniae, mycoplasma pneumoniae

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

Hospital acquired pneumonia causative organisms

A

organisms include e. coli, MRSA, pseudomonas

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

Pneumonia management

A

Use CURB-65 score to direct antibiotic treatment in accordance with local trust guidance.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

Pneumonia investigations

A

CXR
FBC, U&E, CRP,
Sputum
Blood cultures if febrile

High CURB-65 score; initiate atypical pneumonia screen,

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

Legionnaire’s disease

A

form of pneumonia, usually caused by Legionella pneumophila. Association with infected water in showers or hot tubs – ask your patient if there is a history of recent travel or stay in a hotel? Associated with higher CURB-65 scores.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

Pneumonia follow up

A

• HIV test
• Immunoglobulins
• Pneumococcal IgG serotypes
• Haemophilus influenzae b IgG
• Follow up in clinic in 6 weeks with a repeat CXR to ensure resolution

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

Non-resolving pneumonia causes

A

CHAOS
• Complication – empyema, lung abscess
• Host – immunocompromised
• Antibiotic – inadequate dose, poor oral absorption • Organism – resistant or unexpected organism not
covered by empirical antibiotics
• Second diagnosis – PE, cancer, organising
pneumonia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

Haemoptysis differentials

A

Infection:
• Pneumonia
• Tuberculosis
• Bronchiectasis / CF
• Cavitating lung lesion (often fungal) Malignancy:
• Lung cancer
• Metastases Haemorrhage:
• Bronchial artery erosion
• Vasculitis
• Coagulopathy Others:
• PE

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

TB clinical features

A

Often fever and nocturnal sweats (typically drenching)
Weight loss (weeks – months)
Malaise
Respiratory TB: cough ± purulent sputum/ haemoptysis, may also present with pleural effusion Non-Respiratory TB: Skin (erythema nodosum); Lymphadenopathy; Bone/joint; Abdominal; CNS (meningitis); Genitourinary; Miliary (disseminated); Cardiac (pericardial effusion)

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

TB risk factors

A

Past history of TB
Known history of TB contact
Born in a country with high TB incidence
Foreign travel to country with high incidence of TB Evidence of immunosuppression–e.g. IVDU, HIV, solid organ transplant recipients, renal failure/ dialysis, malnutrition/ low BMI, DM, alcoholism

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

Management of TB part 1

A

ABCDE approach & aim to culture whenever possible
• Admit to a side room& start infection control measures (e.g. masks & negative pressure room)
• If productive cough: x3 sputum samples for AAFB
(acid-alcohol fast bacilli – acid-fast stain also called
Ziehl-Neelsen stain) &TB culture
• (If no productive cough & pulmonary TB suspected
consider bronchoscopy)
• Routine bloods (especially LFTs) & include HIV test
and vitamin D level

34
Q

Management of TB part 2

A

Consider CT chest if pulmonary TB suspected but clinical features/ CXR not typical
• If diagnosis between pneumonia and TB not clear: start antibiotics for pneumonia (as per CURB-65) whilst investigating possibility of TB.
• If patient critically unwell and high likelihood of TB (no time to wait for sputum results) then start anti-TB therapy AFTER sputum samples sent.
• Notify case to TB nurse specialists (support patient in investigation, during treatment, public health issues and initiate contact tracing)
• TB culture can take 6-8 weeks. So, treatment is often started before a culture confirmed diagnosis can be made. A novel PCR test (Gene Xpert) is available in some centres which can give immediate information regarding drug sensitivities or resistance.

35
Q

Anti TB therapy

A

Standard regimen is with 4 antibiotics for the first two months (Rifampicin, Isoniazid, Pyrazinamide, Ethambutol) followed by 4 months on two antibiotics (Rifampicin, Isoniazid)
Treatment for a minimum of 6 months in total (can vary – see NICE/ BTS guidelines)
Patient’s weight is important: dose of anti-TB antibiotics is weight dependent
Check baseline LFT’s and monitor closely Check visual acuity before giving Ethambutol Compliance is crucial and Directly Observed Therapy (DOT) sometimes used for patients Provide leaflets on treatment & ensure patient is aware of common and serious side effects (see below)
Pyridoxine also given (while on Isoniazid) as prophylaxis against peripheral neuropathy
If CNS TB suspected MRI Brain is the test of choice, (more likely to identify tubercles than CT)

36
Q

TB treatment side effects

A

Rifampicin – Hepatitis, rashes, febrile reaction,
orange/red secretions (N.B. contact lenses), many drug interactions including warfarin and OCP
Isoniazid – Hepatitis, rashes, peripheral neuropathy, psychosis
Pyrazinamide – Hepatitis, rashes, vomiting, arthralgia
Ethambutol – Retrobulbar neuritis
Management Principles for Respiratory TB
• ABCDE approach & aim to culture whenever possible
• Admit to a side room& start infection control measures (e.g. masks & negative pressure room)
• If productive cough: x3 sputum samples for AAFB
(acid-alcohol fast bacilli – acid-fast stain also called
Ziehl-Neelsen stain) &TB culture
• (If no productive cough & pulmonary TB suspected
consider bronchoscopy)
• Routine bloods (especially LFTs) & include HIV test
and vitamin D levels
Leicester Medical School Phase II Respiratory Medicine Booklet
14
Therefore, MUST do a baseline visual acuity test and LFT’s which must be monitored closely

37
Q

What is Bronchiectasis?

A

Chronic dilatation of one or more bronchi. The bronchi exhibit poor mucus clearance and there is predisposition to recurrent or chronic bacterial infection

38
Q

Bronchiectasis gold standard investigation?

A

Gold standard diagnostic test = High Resolution CT

39
Q

Bronchiectasis causes?

A

Post infective – whooping cough, TB
 Immune deficiency – Hypogammaglobulinaemia
 Genetic / Mucociliary clearance defects – Cystic
fibrosis, primary ciliary dyskinesia, Young’s syndrome (triad of bronchiectasis, sinusitis, and reduced fertility), Kartagener syndrome (triad of bronchiectasis, sinusitits, and situs inversus)
 Obstruction – foreign body, tumour, extrinsic lymph node
 Toxic insult – gastric aspiration (particularly post lung transplant), inhalation of toxic chemicals/gases
 Allergic bronchopulmonary aspergillosis
 Secondary immune deficiency – HIV, malignancy
 Rheumatoid arthritis
 Associations – inflammatory bowel disease; yellow
nail syndrome

40
Q

Blood tests identify Bronchiectasis in newly diagnosed?

A

Immunoglobulin levels
 Cystic Fibrosis Genotype
 Aspergillus IgE / IgG and Total IgE
 HIV test
 Rheumatoid Factor
 Auto Antibodies
 Alpha-1-antitrypsin level

41
Q

Bronchiectasis Common Organisms

A

Haemophilus influenzae
• Pseudomonas aeruginosa
• Moraxella catarrhalis
• Stenotrophomonas maltophilia
• Fungi – aspergillus, candida
• Non-tuberculous mycobacteria
• Less common - Staphylococcus aureus (think about
CF)

42
Q

Bronchiectasis Management

A

Treat underlying cause
• Physiotherapy – mucus / airways clearance
• Sputum for routine culture as well as nontuberculous
mycobacteria
• 10-14 days antibiotics according to sputum cultures / sensitivities for acute exacerbations (infections)

Amoxicillin - Haemophilus Influenzae
Ciprofloxacin - Pseudomonas aeruginosa

Long-term (prophylactic) antibiotics for patients with recurrent infective exacerbations
Supportive – flu / covid vaccines, bronchodilators if required
Pulmonary Rehab – MRC Dyspnoea Score >3

43
Q

Allergic Bronchopulmonary Aspergillosis

A

Caused by aspergillus fumigatus exposure
• Aspergillus is a common fungus found indoors and
outdoors
• ABPA is a combination of types 1 and 3 hypersensitivity reactions following inhalation of fungal spores i.e. it is not a fungal infection
• Repeated damage from these immunological reactions leads to bronchiectasis (often upper lobe)
• ABPA is seen more in patients with Asthma, Bronchiectasis and Cystic Fibrosis
• Diagnosis is made by a combination of symptoms (often dry cough and wheeze) along with positive blood tests (raised Aspergillus IgE level as well as a high Total IgE – these are often accompanied by a high eosinophil level too)
• Treatment (steroids) may be required if ongoing symptoms and high total IgE level

44
Q

What is Cystic Fibrosis

A

CF Definition
CF is an autosomal recessive disease leading to mutations in theCysticFibrosisTransmembraneConductanceRegulator (CFTR). This can lead to a multisystem disease (most commonly affecting the respiratory and gastrointestinal systems but can affect any part of the body with CFTR) characterised by thickened secretions.

45
Q

Diagnosing CF

A

One or more of the characteristic phenotypic features -
• Or a history of CF in a sibling
• Or a positive newborn screening test result
And
• An increased sweat chloride concentration
(> 60 mmol/l) – SWEAT TEST
• Or identification of two CF mutations – genotyping
• Or demonstration of abnormal nasal epithelial ion
transport (nasal potential difference)

46
Q

Presentation of Cystic Fibrosis

A
  1. Meconium ileus
    • In 15-20% of newborn CF infants the bowel is
    blocked by the sticky secretions. There are signs of intestinal obstruction soon after birth with bilious vomiting, abdominal distension and delay in passing meconium.
  2. Intestinal malabsorption
    • Over 90% of CF individuals have intestinal
    malabsorption. In most this is evident in infancy. The main cause is a severe deficiency of pancreatic enzymes.
  3. Recurrent Chest infections
  4. Newborn screening
47
Q

Cystic Fibrosis complications

A

1.Respiratory Infections
- Needs aggressive therapy with physio and antibiotics
- Patientsoftenreceiveprophylacticantibioticstomaintain
health
2.Low Body Weight
- needs careful monitoring
- may be consequence of pancreatic insufficiency (lack of
pancreatic enzymes), therefore in those patients give
pancreatic enzyme replacement therapy
- highcalorieintakeandoftenextrasupplements - may need NG or PEG feeding
3.Distal Intestinal Obstruction Syndrome (DIOS)
- DIOS vs. constipation – faecal obstruction in ileocaecum
versus whole bowel
- Duetointestinalcontentsinthedistalileumandproximal
colon (thick, dehydrated faeces)
- Mostoftenduetoinsufficientprescriptionofpancreatic
enzymes or non-compliance, also salt deficiency / hot
weather
- Oftenpresentswithpalpablerightiliacfossamass
(faecal)
- Diagnosis:Symptoms,palpableRightIliacFossaMass,
AXR demonstrating faecal loading at junction of small
and large bowel
- Treatment:POGastrografin–thisworksbydrawing
water across the bowel wall by osmosis into the bowel lumen, aiming to rehydrate the dehydrated faecal mass and allow it to pass
4. CF Related Diabetes

48
Q

Cystic Fibrosis lifestyle advice

A

No smoking
• Avoid other CF patients
• Avoid friends / relatives with colds / infections
• Avoid jacuzzis (pseudomonas)
• Clean and dry nebulisers thoroughly
• Avoid stables, compost or rotting vegetation – risk of
aspergillus fumigatus inhalation
• Annual influenza immunisation
• Sodium chloride tablets in hot weather / vigorous
exercise

49
Q

Cystic Fibrosis management

A

No smoking
• Avoid other CF patients
• Avoid friends / relatives with colds / infections
• Avoid jacuzzis (pseudomonas)
• Clean and dry nebulisers thoroughly
• Avoid stables, compost or rotting vegetation – risk of
aspergillus fumigatus inhalation
• Annual influenza immunisation
• Sodium chloride tablets in hot weather / vigorous
exercise

50
Q

Pneumothorax types

A

Air in pleural cavity

1.Spontaneous
i.Primary (no lung disease) ii.Secondary (lung disease) 2.Traumatic
3.TENSION: emergency
4.Iatrogenic (e.g. post central line or pacemaker insertion)

51
Q

Pneumothorax risk factors

A
  • Pre-existing lung disease
  • Height
  • Smoking/ Cannabis
  • Diving
  • Trauma/ Chest procedure
  • Association with other conditions e.g. Marfan’s
    syndrome
52
Q

Pneumothorax management

A

 Primary – If symptomatic and rim of air >2cm on
CXR give O2 and aspirate. If unsuccessful consider re-aspiration or intercostal drain. Remove drain after full re-expansion / cessation of air leak.
 Secondary – as above but lower threshold for ICD  If persistent air leak >5 days (bronchopleural
fistula) refer to thoracic surgeons
 Discharge advice – No flying or diving until
resolved

53
Q

Pleural effusion approach

A

•CXR
•ECG
•Bloods: FBC, U&E’s, LFT’s, CRP, Bone profile, LDH, clotting
•ECHO (if suspect heart failure) •StagingCT(withcontrast)ifsuspectexudativecause

54
Q

Pleural Effusin Diagnosis

A

Ultrasound guided pleural aspiration
- Biochemistry (protein, pH, LDH) - Cytology
- Microbiology (including AAFB)
N.B. Never insert a chest drain unless the diagnosis is well established (e.g. known metastatic lung cancer) otherwise draining all fluid off may hinder the opportunity to obtain pleural biopsies. Only indication for urgent chest drain insertion for a new effusion would be an underlying empyema (pH of pleural fluid <7.2 or visible pus on aspirate).
Consider Thoracoscopy or CT Pleural Biopsy

55
Q

Causes of Transudate effusions (pleural protein <30 g/L)

A

Common:
 Heart failure
 Cirrhosis
 Hypoalbuminaemia (nephrotic syndrome or
peritoneal dialysis) Less common:
 Hypothyroidism, mitral stenosis, pulmonary embolism
Rare:
 Constrictive pericarditis, superior vena cava
obstruction, Meig’s syndrome

56
Q

Causes of Exudate effusions >30 g/L

A

Malignancy
 Infections – parapneumonic, TB, HIV (kaposi’s) Less common:
 Inflammatory (rheumatoid arthritis, pancreatitis, benign asbestos effusion, Dressler’s, pulmonary infarction/pulmonary embolus), Lymphatic disorders, Connective tissue disease
Rare:
 Yellow nail syndrome, fungal infections, drugs

57
Q

Interstitial lung disease

A

Umbrella term describing a number of conditions that affect the lung parenchyma in a diffuse manner including:
 Usual Interstitial Pneumonia (UIP)
 Non-specific Interstitial Pneumonia (NSIP)
 Extrinsic Allergic Alveolitis
 Sarcoidosis
 Several other conditions

58
Q

On PFT for ILD?

A

Usually a restrictive pattern

59
Q

Investigations for interstitial lung disease?

A

ANA – connective tissue disease OR SLE
ENA – connective tissue disease
Rh F – Rheumatoid Arthritis
ANCA – Vasculitis
Anti-GBM – Pulmonary Renal disease ACE – Sarcoidosis
Ig G to serum precipitins e.g. pigeon, budgie – Extrinsic Allergic Alveolitis
HIV

60
Q

UIP?

A

Commonest type of Pulmonary Fibrosis Usually Idiopathic
Classical Findings:
 clubbing, reduced chest expansion
 Auscultation – fine inspiratory crepitations (like pulling Velcro slowly) – usually best heard basal / axillary areas
 Cardiovascular – may be features of pulmonary hypertension

61
Q

Extrinsic Allergic Alveolitis?

A

Also known as Hypersensitivity Pneumonitis
• Inhalation of organic antigen to which the individual has been sensitised
Clinical Presentation:
–ACUTE – short period from exposure, 4-8 hrs. Usually reversible: spontaneously settle 1-3 days. Can recur. –CHRONIC – chronic exposure (months – years). Less reversible.
Common Drug causes:
 Amiodarone
 Bleomycin
 Methotrexate
 Nitrofurantoin
 Penicillamine

62
Q

Sarcoidosis?

A

• Multisystem inflammatory condition of unknown cause
• Non-caseating granulomas (Histology important)
• Immunological response
• Commonly involves Resp system BUT can affect nearly all organs
• 50% get spontaneous remission, others get progressive disease
Investigations:
• PFTs: (obstructive until) fibrosis
• CXR: 4 stages
• Bloods: renal function, ACE, Calcium
• Urinary Calcium
• Cardiac involvement: ECG, 24 tape, ECHO, cardiac MRI • CT/MRI head: headaches – Neuro sarcoid

63
Q

Treatment for interstitial lung disease?

A

• Multisystem inflammatory condition of unknown cause
• Non-caseating granulomas (Histology important)
• Immunological response
• Commonly involves Resp system BUT can affect nearly all organs
• 50% get spontaneous remission, others get progressive disease
Investigations:
• PFTs: (obstructive until) fibrosis
• CXR: 4 stages
• Bloods: renal function, ACE, Calcium
• Urinary Calcium
• Cardiac involvement: ECG, 24 tape, ECHO, cardiac MRI • CT/MRI head: headaches – Neuro sarcoid

64
Q

Lung cancer clinical features

A

Asymptomatic, incidental finding
• Any respiratory symptom/systemic deterioration
• Superior Vena Caval Obstruction
• Horner’s syndrome
• Metastatic disease – liver, adrenals (Addison’s),
bone, pleural, CNS
• Paraneoplastic – clubbing, hypercalcaemia,
anaemia, SIADH, Cushing’s syndrome, Lambert-
Eaton myasthenic syndrome
• Increased risk of thrombo-embolic disease

65
Q

Risk factors for lung cancer

A

Large number of smoking pack years
• Airflow obstruction
• Increasing age
• Family history of lung cancer
• Exposure to other carcinogens, e.g. asbestos

66
Q

Performance status lung cancer

A

WHO scale
Gives an indication of patient’s level of fitness
• 0 Normal - Fully active without restriction
• 1 Restricted in physically strenuous activity but
ambulatory and able to carry out light work e.g.,
light house work, office work
• 2 Ambulatory and capable of all self-care but
unable to carry out any work activities. Up and
about more than 50% of waking hours
• 3 Capable of only limited self-care, confined to
bed or chair more than 50% of waking hours
• 4 Completely disabled. Cannot self-care. Totally
confined to bed or chair
• 5 Dead

67
Q

Lung cancer investigations

A

Bloods – FBC, U&E, Calcium, LFT’s, INR
• CXR
• Staging CT – Spiral CT Thorax and Upper Abdo helps to stratify TNM stage

Histology options
• US guided neck node FNA for cytology if
lymphadenopathy
• Bronchoscopy – endobronchial, transbronchial,
endobronchial ultrasound (if mediastinal
lymphadenopathy) • CT Biopsy
• Thoracoscopy if pleural effusion present
PET Scan
• MDT Decision if patient is a surgical candidate
and initial CT suggestive of low stage
• Helps to detect small metastases not seen on
staging CT

68
Q

Lung cancer Histology

A

Classified primarily into two groups which account for about 95% of cases
1. Small cell (oat cell) lung cancer (SCLC)
2. Non-small cell lung cancer (NSCLC)
- includes squamous cell, adenocarcinoma, and large cell carcinoma, bronchoalveolar cancer
Others -, bronchial gland ca, carcinoid tumour

69
Q

Lung cancer treatment

A

Curative surgery for stages I & II – assuming fit for surgery
• Surgery & adjuvant chemotherapy clinical trial for stage IIIa – assuming fit for surgery & chemo
• Chemotherapy – consider in patients with stage III/IV disease and PS 0-2
• Radiotherapy – curative (CHART = continuous hyperfractionated accelerated radiotherapy) for people not fit for surgery OR palliative
• Palliative Care
• Do nothing / watch & wait

70
Q

Non-small cell lung cancer survival

A

All NSCLC – 15-23%
• Stage 1 following surgical resection – 65-80% • Stage II following surgical resection – 50-60% • Stage III – 20%
• Stage IV – 1-5%

71
Q

Small cell lung cancer treatment and prognosis

A

Rapid growth rate and almost always too extensive for surgery at time of diagnosis
• Mainstay of treatment is chemotherapy
• Also palliative radiotherapy
• Untreated – median survival is 8-16 weeks
• Combination chemotherapy – median survival 7-
15 months

72
Q

What is obstructive sleep apnoea?

A

Upper airway obstruction during sleep
 Clinical definition = upper airway narrowing,
provoked by sleep, causing sufficient sleep fragmentation to result in significant daytime symptoms, usually excessive sleepiness
 Most patients with significant OSA are male, and tend to have a combination of upper body obesity (collar size >17 in), and a relatively undersized or set back mandible

73
Q

Sleep Apnoea pathophysiology

A

Upper airway patency depends on dilator muscle activity. All muscles relax during sleep (including pharyngeal dilators).
 Some narrowing of the upper airway is normal
 Excessive narrowing can be due to either an
already small pharyngeal size during awake state which undergoes a normal degree of muscle relaxation during sleep causing critical narrowing OR excessive narrowing occurring with relaxation during sleep

74
Q

Causes of small pharyngeal size in sleep apnoea?

A

Fatty infiltration of pharyngeal tissues and external pressure from increased neck fat and/or muscle bulk
 Large tonsils
 Craniofacial abnormalities
 Extra submucosal tissue, e.g. myxoedema

75
Q

Causes of excessive narrowing of the airway during sleep?

A

Obesity may enhance residual muscle dilator action
 Neuromuscular disease with pharyngeal involvement may lead to greater loss of dilator muscle tone, e.g. stroke, MND, myotonic dystrophy
 Muscle relaxants – sedatives, alcohol
 Increasing age

76
Q

Clinical effects of sleep apnoea

A

Severe OSA leads to repetitive upper airway collapse, with arousal required to re-activate the pharyngeal dilators. There may be associated hypoxia and hypercapnia which are corrected during the inter-apnoeic hyperventilatory period.
 Recurrent arousals lead to highly fragmented and unrefreshing sleep – snoring and apnoea attacks often witnessed by partner
 Excessive daytime sleepiness results (Epworth Sleepiness Scale score >9)
 With every arousal there is a rise in BP, often over 50 mmHg. It is not clear if this damages the CVS. There is also a rise in daytime BP.
 Nocturia
 Less common - Nocturnal sweating, reduced
libido, oesophageal reflux

77
Q

Epworth sleepiness scale?

A

Points for following:0=would never doze, 1=slight chance, 2=moderate chance, 3=high chance
-Sitting & reading
-Watching TV
-Sitting in a public place, e.g. theatre
-Passenger in a car for an hour
-Lying down to rest in the afternoon
-Sitting & talking
-Sitting quietly after lunch without alcohol
-In a car, while stopped in traffic

78
Q

Diagnosis of sleep apnoea?

A

Overnight oximetry alone
 Limited sleep study – oximetry, snoring, body
movement, heart rate, oronasal flow, chest/abdominal movements, leg movements – usual study of choice
 Full polysomnography – limited study plus EEG, EMG

79
Q

Management of sleep apnoea?

A

Treatment is given based on symptoms/quality of life – NOT on severity seen on sleep study
-Also consider livelihood, e.g. driving as occupation SIMPLE APPROACHES:
-Weight loss, sleep decubitus rather than supine, avoid/reduce evening alcohol intake
FOR SNORERS & MILD OSA:
-Mandibular advancement devices, consider
pharyngeal surgery as last resort FOR SIGNIFICANT OSA:
-Nasal CPAP, consider gastroplasty/bypass, and rarely tracheostomy
FOR SEVERE OSA & CO2 RETENTION:
-May require a period of NIV prior to CPAP if
acidotic, but compensated CO2 may reverse with CPAP alone

80
Q

Driving with sleep apnoea?

A

Tell all patients with OSA to NOT drive while sleepy; stop and have a nap. On diagnosis the patient should notify the DVLA
 The doctor can advise drivers to stop altogether (e.g. HGV drivers)

81
Q

CPAP?

A

Usually given via nasal mask, but can use mouth/nose masks
 Upper airways splinted open with approximately 10cm H2O pressure – this prevents airways collapse, sleep fragmentation, and ultimately daytime somnelence
 Also opens collapsed alveoli and improves V/Q matching

82
Q

CPAP vs BIPAP (NIV)

A

CPAP supplies constant positive pressure during inspiration and expiration and is therefore not a form of ventilatory support. It can be used to treat OSA and helps oxygenation in some patients with acute respiratory failure, e.g. pulmonary oedema
 Non-invasive ventilation (NIV) does provide ventilatory support with two levels of positive pressure (bilevel) – pressure support provided between selected inspiratory and expiratory positive pressures (IPAP & EPAP). They can also be set up with back up rates so the machine operates when the respiratory rate drops below a fixed level.

Medicine Year 3 (3 decks)

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