Brainscape's Knowledge GenomeTM

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


See full index

RESPIRATORY > CORE CONDITIONS > Flashcards

CORE CONDITIONS Flashcards

1
Q

Asthma: Description

A

Inflammation of the bronchioles. Obstructive respiratory disease because inflamed bronchioles obstruct air flow.
Bronchial wall contracts, mucosal surfaces become inflamed and mucus production increases

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

Asthma: Epidemiology

A

5-8% prevalence. More common in children. Can, grow out of it, be lifelong or be adult-onset

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

Asthma: Aetiology and RFx

A
  • Allergic asthma (ATOPIC) associated with eczema and hayfever
  • Exercise induced
  • Cold weather induced
  • Drug induced (NSAIDs)
  • Stress/emotion reduced
  • RF: smoking, infection, Beta-blockers

Mast cells degranulate and release histamine and IgE. Basophils may also degranulate and levels rise.

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

Asthma: Presentations (signs and symptoms)

A
  • Intermittent dyspnoea
  • Wheeze on expiration
  • Cough (often worse at night and evening)
  • Sputum
  • Tachypnoea
  • Hyperinflated chest
  • Hyper-resonant percussion
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Asthma: Differentials

A 
Pulmonary Oedema 
COPD
Large airway obstruction
SVC obstruction
Pneumothorax 
PE 
Bronchiectasis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Asthma: Ix and Dx

A
  • PEF, Sputum Culture,
  • BLOODS: FBC, U&E and CRP, cultures for infection
  • ABG (might show decreased PaCO2 and PaO2 - due to hyperventilation)
  • Decreased FEV1 and FVC, Increased RV.
  • *There should be a >15% improvement in PEF after B2 agonists. ASTHMA IS REVERSIBLE
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Asthma: Treatments

A
  • Short-acting beta2 agonist (salbutamol)
  • Steroid Inhalers (beclamethasone)
  • Long-acting beta2 agonists (salmeterol)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

COPD: Description

A

Progressive, obstructive disorder. Combination of chronic bronchitis and emphysematous change.

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

COPD: Types

A

Two types of presentation depending on whether bronchitis or emphysema is main problem:

  • PINK-PUFFER: usually younger, less advanced. Bronchitis main problem
  • BLUE-BLOATER: have much less alveolar ventilation, very lowPaO2 and PaCO2. Cyanosed. At risk of cor pulmonale
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

COPD: Epidemiology

A

10-20% of over 40%

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

COPD: Aetiology/Risk Factors

A

Almost always caused by smoking

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

COPD: Presentation (signs and symptoms)

A
  • Persistent SOB worse on exertion
  • Cough with sputum
  • Wheeze
  • Tachypnoea
  • Accessory muscle use
  • Hyperinflation
  • Cyanosis
  • Cor Pulmonale
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

COPD: Ix and Dx

A 
FBC
CXR (hyperinflation, decreased vascular markings)
ECG: RVH (cor pulmonale)
ABG (reduced PaO2)
FEV1 <80% expected, increased TLC and RV
Spirometry with trial steroids
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

COPD: Treatments

A 
Stop smoking, treat sx.
IRREVERSIBLE
Weight loss
Mucolytics 
Inhalers (Beta2Ags and steroids)
Long term steroids: prednisolone PO or beclametasone Inhaled
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Bronchial Carcinoma: Description

A

Mostly squamous cell tumours, some are adenocarcinomas.

SMALL CELL or LARGE CELL. Small cell more common

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

Bronchial Carcinoma: Epidemiology

A

19% of all cancers

27% of all deaths

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

Bronchial Carcinoma: Aetiology/Risk factors

A

Most often smoking

Asbestos, Chromium, arsenic, iron oxides and radiation also RFs

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

Bronchial Carcinoma: Presentation (Signs and Symptoms)

A
  • Cough + Haemoptysis
  • Weight loss
  • Dyspnoea
  • Chest Pain
  • Recurrent or slowly resolving pneumonias
  • Clubbing
  • Anaemia
  • Lymphadenopathy (supra-clavicular and axillary)
  • Pleural effusions on CXR
  • METS
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

Bronchial Carcinoma: Complications

A

Can be P/C

  • Horner’s Syndrome (apical tumours/Pancoast tumours compress sympathetic chain: ptosis, miosis, anhidrosis)
  • Brain sx (mets)
  • Bone pain (mets)
  • Lambert-Eaton (AI attacking neuromuscular junction, proximal limb muscle weakness)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

Bronchial Carcinoma: Differentials

A
  • COPD +/- acute exacerbation
  • Pneumonia
  • TB
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

Bronchial Carcinoma: Ix and Dx

A
  • CXR (consolidation and effusions and poss. visible tumour)
  • Sputum sample
  • CT to stage the tumour
  • Aspiration for cytology
  • Bronchoscopy
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

Bronchial Carcinoma: Treatment

A

Different depending on whether it is small cell or non-small cell. NSCLC less likely to be disseminated (spread throughout lungs) hence better for excision and chemo/radio

SCLC can be treated with chemo/radio but invariably relapse
- CYCLOPHOSPHAMIDE, VINCRISTINE

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

Bronchial Carcinoma: Prognosis

A

NSCLC: 505 2 year survival (without spread.
SCLC: median survival is 3 months to 1.5 years if treated

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

Pneumothorax: Description

A

Air in pleural space - one lung might collapse.
Tension pneumothorax is when puncture trauma creates a one-way valve through which air can enter pleural space but not leave

25
Q

Pneumothorax: Aetiology and Risk Factors

A

Can be spontaneous (more common in thing young men)
Secondary to pathology:
- Asthma, COPD, TB, Pneumonia, Lung abscesses
- Connective Tissue disorders
- Recent Surgeries

26
Q

Pneumothorax: Presentation (signs and symptoms)

A
  • Sudden onset dyspnoea
  • Pleuritic pain
  • Hyper-resonant to percussion
  • Lack of tactile or audible vocal fremitus
  • Absent breath sounds
  • Reduced expansion
  • Sudden deterioration of COPD patients
27
Q

Pneumothorax: IX and Dx

A
  • CXR will show it (actual pneumothorax, deviated trachea ONLY IN TENSION)
28
Q

Pneumothorax: Treatment

A

Don’t wait for CXR to commence treatment. Chest drain (4-6th IC space mid-axillary line). Risk of damaging lymph and long thoracic nerve - winged scapula)

29
Q

Pleural Effusion: Description

A

Collection of fluid in pleural cavity. Can impact expansion of lung and hence ventilation. Can be in isolation or as part of other conditions (trauma, heart failure, thoracic cancers)

30
Q

Pleural Effusion: Types

A

TRANSUDATES: watery, <25g/dL protein)
EXUDATES: >35g/dL protein

31
Q

Pleural Effusion: Aetiology/ RFs

A

Can be a sign of other pathology:

  • Congestive heart failure
  • Bronchial Carcinomas or other cancers
  • Chest trauma

TRANSUDATE more likely when there is high pressure in pulmonary venous system (congestive HF, constrictive pericarditis and fluid overload, hypoproteinaemia and hypothyroidism)

EXUDATE more likely secondary to infection, inflammation or mass (Pneumonia, TB, RA, SLE, Lymphoma, mesothelioma, carcinoma)

32
Q

Pleural Effusion: Presentation (signs and symptoms)

A

Small ones are usually found incidentally. But sx are…

  • Dyspnoea
  • Pleuritic chest pain
  • Absent breath sounds
  • STONY Dull percussion
  • Decreases expansion
  • Decreased tactile vocal fremitus and resonance
  • May show tracheal dev. AWAY and bronchial breathing above effusion
33
Q

Pleural Effusion: IX and Dx

A

Clinical diagnosis: Stony dullness and absent breath sounds

  • CXR shows opacity at lung bases (loss of costs-phrenic angle)
  • Can aspirate effusion (identify exudate or transudate)
34
Q

Pleural Effusion: Treatment

A

usually resolve self, can consider chest drain if very large
- Pleurodesis in recurrence with tetracycline, bleomycin or talc

35
Q

Lobar Pneumonia: Description

A

Infection in lung usually confined to one lobe.

36
Q

Lobar Pneumonia: Aetiology and Risk Factors

A

MOST COMMON CAUSATIVE ORGANISM: Streptococcus pneumoniae followed by haemophilus influenzae
ATYPICALS: legionella, chalmydia, mycoplasma

Spread via aerosolised mucus droplets, particularly at risk if you have another lung pathology (esp COPD and ASTHMA)

37
Q

Lobar Pneumonia: Presentations (symptoms)

A

Fever, Rigors, Sweats, Malaise, Productive cough, Dyspnoea, Green sticky sputum, haemoptysis, Pleuritic chest pain

38
Q

Lobar Pneumonia: Signs

A
  • Cyanosis, bronchial breathing, tachypnoea, dull percussion, increased vocal fremitus/resonance, pleural rub
39
Q

Lobar Pneumonia: Ix and Dx

A

CXR shows consolidation
O2 Sats <92 suggest severe
BLOODS: FBC, U&E, LFT, CRP, Cultures, ABG

40
Q

Lobar Pneumonia (CAP): CURB65

A
  • Confusion: AMTS <8 then 1 point
  • Urea >7mmol/L 1 point
  • Resp rate >30 1 point
  • Blood Pressure <90/60mmHg 1 point
  • > 65yo 1 point
41
Q

Lobar Pneumonia: Treatment and Management

A

CAP: Empirical Amoxicillin for 7-10 days
- Clarithromycin for atypical cover and penicillin allergy

Oxygen therapy

42
Q

Pulmonary Embolus: Description

A

Clot or other mass lodges in pulmonary arteriole, partially or fully occluding it and restricting lung perfusion. There is then a V/Q mismatch and a decrease in gas exchange. usually acute or sub-acute

43
Q

Pulmonary Embolus: Aetiology and RF

A

Most commonly comes from DVT. Clot forms due to haemostats (incompetent valves) travels up IVC into R side of heart and then into lungs.
Can also be caused by RA or RV thrombus due to AF or MI

RF: immobility, OCP, Long haul flight, obesity, diabetes, smoking, pregnancy, previous PE, malignancy

44
Q

Pulmonary Embolus: Presentation (signs and symptoms)

A 
Sudden onset SOB, syncope, pleuritic chest pain, haemoptysis.
Tachypnoea 
Tachycardia 
Hypotension
Raised JVP
Pleural rub
Pleural effusion
45
Q

Pulmonary Embolus: Ix and Dx

A

CXR (usually normal might show small effusion or wedge shaped opacity)
CT Chest with contrast might be able to track pulmonary arteries
BLOODS: FBC, U&E, baseline clotting. D-DIMERS(negative D-Dimer excludes PE). ABG might show decr. PaO2 and PaCO2

46
Q

Pulmonary Embolus: Differentials

A

Pneumonia
Pneumothorax
TB

47
Q

Pulmonary Embolus: Treatment and Management

A

LMWH for anti-coag then start warfarin. Stop heparin when INR >2. Continue warfarin for minimum of three months and aim for INR of between 2-3.

  • Thrombolyse massive PEs (alteplase)
  • LMWH (tinza or dalteparin) goes to ALL immobile patients prophylactically
48
Q

Interstitial Lung Disease: Description

A

Lung parenchyma becomes stiff and less elastic due to chronic inflammation and/or pulmonary fibrosis. Build up of scar tissue

49
Q

Interstitial Lung Disease: Aetiology and RFs

A

THREE MAIN CATEGORIES:
Those of known cause:
- Occupational (cola workers, pigeon-fanciers, asbestosis)
- Drugs: nitrofurantoin, bleomycin, amiodarone
- Hypersensitivity: Extrinsic allergic alveoli’s
- Infections: TB and recurrent pneumonia scarring
- GORD
Those of associated systemic disorder:
- Sarcoidosis
- SLE or RA
- UC, renal tubular acidosis, AI thyroid disease
Idiopathic

50
Q

Interstitial Lung Disease: Presentation (signs and symptoms)

A
  • Dyspnoea on exertion
  • Non productive cough
  • Tachypnoea
  • Tachycardia
  • Fine crackles
  • Reduced expansion
  • Restrictive spirometry
51
Q

Interstitial Lung Disease: Ix and Dx

A

CXR

52
Q

Interstitial Lung Disease: Treatment and management

A

Treat cause

53
Q

Extrinsic Allergic Alveolitis: Description

A

Inhalation of allergens leading to hypersensitivity. If this is chronic then granuloma can form and there will be damage to the parenchyma

  • Pigeon-fanciers lung is a type of EAA
  • Farmers are also prone (due to hay)
54
Q

Industrial Dust Diseases: Descriptions

A

Coal Workers’ Pneumoconiosis (CWP): very common can cause chronic bronchitis and multiple round opacities
Progressive massive Fibrosis: progression of CWP causing progressive dyspnoea, fibrosis and cor pulmonate
Caplan’s syndrome: pneumoconiosis-like nodules from RA
Silicosis: Caused by inhalation of silicone particles (metal miners or pottery). Increased risk of TB
Asbestosis: white asbestos is least fibrogenic and blue the mosts. Progressive dyspnoea, clubbing, fine-end resp crackles and pleural plaques
Malignant Mesothelioma: tumour of pleura caused by asbestos. treat with PEMETREXED

55
Q

Type 1 Respiratory Failure

A 
Resp Failure is when gaseous exchange is inadequate 
Type 1 is Hypoxia (PaO2 <8kPa) with a NORMAL OR LOW PaCO2. Causes include:
- Pneumonia 
- Pulmonary oedema 
- PE 
- Asthma 
- Emphysema 
- Pulmonary fibrosis 
- ARDS
56
Q

Type 2 Respiratory Failure

A

Hypoxia PaO2 <8kPa WITH HYPERCAPNIA
Usually caused when there is alveolar hypoventilation
- COPD and asthma (sometimes severe pneumonia)
- Reduced respiratory drive (sedative drugs or CNS tumour)
- Neuromuscular disease (cervical cord lesion, Guillain-Barré)

57
Q

Respiratory failure symptoms

A

HYPOXIA: dyspnoea, restlessness, agitation, reduced consciousness, cyanosis
HYPERCAPNIA: headache, peripheral vasodilation, tachycardia, bounding pulse

58
Q

Respiratory Failure: Treatment

A

ALWAYS GIVE O2 to type 1 and treat cause.
For those with type 2 respiration could be driven by hypoxia and so do NOT give O2 because it will depress breathing rate and worsen resp failure.

RESPIRATORY (2 decks)

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