Brainscape's Knowledge GenomeTM


Top Flashcards (Certified)
All Flashcards

Year 3 Medicine > Respiratory > Flashcards

Respiratory Flashcards

(100 cards)

Start Studying
1
Q

What are the causes of Respiratory acidosis?

A
  • Hypoventilation e.g. neuromuscular diseases
  • “Alveolar hypoventilation” e.g. COPD
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

What should the A-a values be ?

A
  • Young healthy people: <2 kPa
  • Older people: <4 kPa
  • >4 kPa- lung pathology
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

What happens in anaphylaxis?

A

Immunological response: – 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

Symptoms of Anaphylaxis and Angioedema?

A
  • Pruritus, urticaria & angioedema
  • Hoarseness, progressing to stridor & bronchial obstruction
  • Wheeze & chest tightness from bronchospasm
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

How is Anaphylaxis treated?

A
  • Remove trigger, maintain airway, 100% O2
  • Intramuscular adrenaline 0.5 mg (Repeat every 5 mins as needed to support CVS)

Management following stabilisation:

  • non-sedating oral antihistamines, in preference to chlorphenamine
  • Serum tryptase levels are sometimes taken in such patients (remain elevated for up to 12 hours)
  • Referral to a specialist allergy clinic
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

How is mild to moderate asthma defined?

A
  • Mild: No features of severe asthma; PEFR >75% Moderate:
  • No features of severe asthma; PEFR 50-75%
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

How is severe asthma defined?

A
  • PEFR 33-50%
  • Cannot complete sentences in 1 breath
  • RR > 25/min
  • HR >110 BPM
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

How is life threatening asthma defined?

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

How is acute asthma managed?

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)

If severe:

  • Nebulised Ipratropium Bromide 500ug
  • Consider back to back Salbutamol If life threatening or near fatal:
  • Urgent ITU or anaesthetist assessment
  • Urgent portable CXR
  • IV Aminophylline
  • Consider IV Salbutamol if nebulised route ineffective
  • Magnesium sulphate
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

What are some of the signs and sx of COPD?

A

Symptoms

  • Cough + sputum
  • Dyspnoea
  • Wheeze
  • Wt. loss

Signs

  • Tachypnoea
  • Prolonged expiratory phase
  • Hyperinflation
    • ↓Cricosternal distance (normal = 3 fingers)
    • Loss of cardiac dullness
    • Displaced liver edge
    • Wheeze
  • May have early-inspiratory crackles
  • Cyanosis
  • Cor pulmonale: ↑JVP, oedema, loud P2
  • Signs of steroid use
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

How are COPD Exacerbations treated?

A
  • ABCDE
  • Oxygen: - via a fixed performance face mask due to risk of CO2 retention - aim for SaO2 88-92% (use ABGs)
  • NEBs – Salbutamol and Ipratropium
  • Steroids – Prednisolone 30mg STAT and OD for 7 days
  • Abx 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
12
Q

How is pneumonia investigated?

A
  • Bedside: urine CAP (pneumococcal and legionella ), ECG?, sputum sample MC+S
  • Bloods: FBC, UE, CRP, LFT
  • Imaging: CXR
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

What are the signs + sx of pneumonia?

A
  • Sx: Fever, rigors, Malaise, anorexia, Dyspnoea, Cough, purulent sputum, haemoptysis, Pleuritic pain
  • Signs: ↑RR, ↑ HR, Cyanosis, Confusion,
    • Consolidation: ↓ expansion, Dull percussion, Bronchial breathing, ↓ air entry, Crackles, Pleural rub , ↑VR
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

What aids in the diagnosis of pneumonia?

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

What antibiotics are used for the treatment of pneumonia?

A
  • ABCDE - appropriate management
  • Antibiotics
    • CURB65 score 0 or 1 (low severity): amoxicillin 500mg TD 5 days
      • Atypical: Doxycycline (e.g. legionella)
    • CURB65 score 2: Amoxicillin 500mg TD 5 days + Clarithromycin 500 mg BD 5 days
      • Atypical: Doxycycline
    • CURB65 score 3 to 5: Co-amoxiclav (500/125 mg 3 times a day orally or 1.2 g 3 times a day IV) and Clarithromycin (500 mg twice a day orally or IV for 5 days)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

What is considered a massive haemoptysis?

A
  • >240mls in 24 hours OR
  • >100mls / day over consecutive days
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Define the Management of Massive Haemoptysis?

A
  • ABCDE
  • Lie patient on side of suspected lesion (if known)
  • Oral Tranexamic Acid for 5 days or IV
  • Stop NSAID’s / aspirin / anticoagulants •
  • Antibiotics if any evidence of respiratory tract infection
  • Consider Vitamin K
  • CT aortogram – interventional radiologist may be able to undertake bronchial artery embolisation
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

How is a tension pneumothorax detected?

A
  • Hypotension
  • Tachycardia
  • Deviation of the trachea away from the side of the pneumothorax
  • Mediastinal shift away from pneumothorax
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

How is a tension pneumothorax managed?

A
  • Large bore intravenous cannula into 2nd ICS MCL
  • Chest drain into the affected side: 4th ICS MAL
  • Give high flow 02 and admit
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

What are some of the sx of a PE?

A
  • Chest pain (pleuritic)
  • SOB
  • Haemoptysis
  • Low cardiac output followed by collapse (if Massive PE)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

What are some of the Major Risk Factors of a PE?

A
  • Surgery – Abdominal/pelvic; Knee/ hip replacement; Post-op spell on ITU
  • Obstetric – Late pregnancy; C- section
  • Lower Limb – Fracture; Varicose veins
  • Malignancy – Abdominal/ Pelvic/ Advanced/ Metastatic
  • Reduced Mobility
  • Previous proven VTE
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

How is a PE managed?

A
  • ABCDE
  • Oxygen if hypoxic
  • Fluid resuscitation (if hypotensive)
  • Thrombolysis: if haemodynamically unstable (large PE) - 100mg alteplase IV; (2nd: streptokinase)
  • Anticoagulation
    • LMWH - Dalteparin on admission
    • After admission:
      • 1st line: DOAC - provoked 3 months, unprovoked life long
      • 2nd: LMWH (bridging) + warfarin (check INR 2-3 - warfarin needs 5 days to be effective and is prothombotic)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

How do sx and management change for a massive PE?

A
  • Hypotension/ imminent cardiac arrest
  • Signs of right heart strain on CT / Echo
  • Consider thrombolysis with IV alteplase
  • Consider Thrombolysis Contraindications
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

What are some of the absolute contraindications of thrombolysis?

A
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
What are some of the relative contraindications of thrombolysis?
26
What are the characteristics of asthma?
* Asthma is a **chronic inflammatory disease** of the airways * Airway obstruction that is **reversible**, either spontaneously or with treatment * Increased **airway responsiveness** (airway narrowing) to a variety of stimuli
27
Asthma Pathophysiology
* **Airway epithelial damage** – shedding and subepithelial fibrosis, basement membrane thickening * An inflammatory reaction characterised by eosinophils, **T-lymphocytes (Th2)** + 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
28
How is Acute Asthma Managed?
* ABCDE * Aim for SpO2 94-98% with 02 as needed, ABG if sats \<92% * **5mg nebulised Salbutamol** (can repeat after 15 mins) * **40mg oral Prednisolone STAT** (IV Hydrocortisone if PO not possible) * *Severe: ipratroprium bromide 500mg + back to back salbutamol* * *Life threatening fatal: IV aminophylline. IV salbutamol*
29
What are the histological features of asthma?
* Thickening of basement membrane * Mucosal thickening * Mucus plugging * Bronchial wall smooth muscle hypertrophy
30
How do you treat severe or life threatening asthma?
* If severe: Nebulised **Ipratropium Bromide 500 micrograms** * Consider back to back **Salbutamol** If life threatening or near fatal * Urgent ITU or anaesthetist assessment * Urgent portable **CXR** * **IV Aminophylline** * Consider **IV Salbutamol** if nebulised route ineffective * **Magnesium sulphate**
31
Criteria for safe asthma discharge after exacerbation
* 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
32
What are the NICE guidelines for chronic asthma management?
1. SABA 2. +ICS 3. +LTRA 4. +LABA 5. +SABA=/- LTRA
33
What is Eosinophilia
* 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 * Drugs * Churg-Strauss / vasculitis * Eosinophilic Pneumonia * Parasites * Lymphoma * SLE * Hypereosinophilic syndrome
34
What is the COPD definition?
* 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
35
What is the pathophysiology of COPD?
* **COPD** is an umbrella term which encompasses **emphysema** and **chronic bronchitis** * **Mucous** gland hyperplasia * Loss of **cilial** function * **Emphysema** – alveolar wall destruction causing irreversible enlargement of air spaces distal to the terminal bronchiole * **Chronic inflammation** (macrophages and neutrophils) and fibrosis of small airways
36
What are the common causes of COPD?
* Smoking * Inherited α-1-antitrypsin deficiency * Industrial exposure, e.g. soot
37
What outpatient COPD management?
* COPD care bundle * Smoking cessation * Pulmonary Rehabilitation * Bronchodilators * Antimuscarinics * Steroids * Mucolytics * Diet * LTOT if appropriate * Lung volume reduction if appropriate General Measures * Stop smoking * Specialist nurse * Nicotine replacement therapy * Bupropion, varenicline (partial nicotinic agonist) * Support programme * Pulmonary rehabilitation / exercise * Influenza and pneumococcal vaccine Medications: * Mucolytics -Consider if chronic productive cough * E.g. Carbocisteine (CI in PUD) * Breathlessness and/or exercise limitation * SABA and/or SAMA (ipratropium) PRN * SABA PRN may continue at all stages Exacerbations or persistent breathlessness * FEV1 ≥50%: LABA or LAMA (tiotropium) (stop SAMA) * FEV1 \<50%: LABA+ICS combo or LAMA * Persistent exacerbations or breathlessness: LABA+LAMA+ICS * Roflumilast / theophylline (PDIs) may be considered * Consider home nebs LTOT: Aim: PaO2 ≥8 for ≥15h / day (↑ survival by 50%) Surgery * Recurrent pneumothoraces * Isolated bullous disease * Lung volume reduction
38
What are the three types of pneumonia?
* Community Acquired * Hospital Acquired * Others, e.g. aspiration
39
How is CAP diagnosed?
* **CURB-65 score** * **ABX** according to CURB-65 score and patient allergies * **ABCDE** approach - Even if CURB-65 score is low do not ignore signs of sepsis * NO DELAY in initiating Abx (or IV fluids if indicated) + / - **Paracetamol** * **ITU referral** if high CURB-65 score
40
What other tests are used for CAP diagnosis?
* **CXR** * Bloods: **FBC, U&E, CRP** and **sputum** cultures * **Blood cultures** if febrile * If **high CURB-65 score -** * **Urinary CAP screen -** Atypical pneumonia screen – **legionella** * **ABG** if low sats
41
What tests are used in a Pneumonia Follow Up?
* HIV test * Immunoglobulins * Pneumococcal **IgG** serotypes * Haemophilus **influenzae** **b IgG** * Follow up in clinic in **6 weeks** with a **repeat CXR** to ensure resolution
42
Causes of a non-resolving pneumonia
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
43
What are some of the clinical features of Tuberculosis?
* 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)
44
What are the risk factors of TB?
* 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 * Immunosuppression–e.g. IVDU, HIV, solid organ transplant recipients, renal failure/ dialysis, malnutrition/ low BMI, DM, alcoholism
45
What are the differential diagnosis of Haemoptysis?
* **Infection**: Pneumonia, Tuberculosis, Bronchiectasis / CF, Cavitating lung lesion (often fungal) * **Malignancy**: Lung cancer, Metastases Haemorrhage, Bronchial artery erosion, Vasculitis, Coagulopathy * **Others**: PE
46
What investigations are performed for TB?
* CXR * Sputum acid-fast bacilli (AFB) smear * sputum culture * Bloods: FBC * Gastric aspirate * Bronchoscopy and bronchoalveolar lavage (BAL) * Tuberculin skin testing (TST) * Interferon-gamma release assays (IGRAs)
47
How is respiratory TB managed?
* ABCDE * Side room & start infection control measures * Productive cough: x3 sputum samples for AAFB&TB culture (early morning samples) * No productive cough & pulmonary TB suspected consider **bronchoscopy** * Bloods: **LFTs, HIV test + Vit D levels** * Pulmonary TB: **CT chest** * Military TB: **MRI brain/spine** followed by **LP** * If diagnosis between pneumonia and TB not clear: start Abx for pneumonia (CURB-65) whilst investigatingTB. * Pt critically unwell and high likelihood of TB (no time to wait for sputum results): **start anti-TB therapy** AFTER sputum samples sent. * Notify case to TB nurse specialists TB culture can take 6-8 weeks
48
How is Latent TB diagnosed?
* Mantoux test (tuberculin skin test (TST)) * Interferon Gamma Test
49
How is Pulmonary TB treated (ATT - AntiTB therapy)?
* **4 antibiotics for the 1st 2 months: (RIPE)** Rifampicin, Isoniazid, Pyrazinamide, Ethambutol * **Followed by 4 months on 2 ABx:** Rifampicin, Isoniazid * Dose of anti-TB antibiotics is weight dependent * Check baseline **LFT’s** and monitor closely * Check visual acuity before giving Ethambutol * **Pyridoxine:** 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
50
What are some of the major side effects of TB drugs?
* **Rifampicin** – Hepatitis, rashes, febrile reaction, orange/red secretions (N.B. contact lenses), drug interactions w/ warfarin and OCP * **Isoniazid** – Hepatitis, rashes, peripheral neuropathy, psychosis * **Pyrazinamide** – Hepatitis, rashes, vomiting, arthralgia * **Ethambutol** – Retrobulbar neuritis Do baseline visual acuity and LFTs
51
What is CF?
* **Autosomal recessive** disease leading to mutations in the **Cystic Fibrosis Transmembrane Conductance Regulator (CFTR)**. * This leads to a multisystem disease affecting the **respiratory** and **GI** systems * Characterised by **thickened secretions**
52
How if CF diagnosed?
* History of CF in a sibling OR * Positive newborn screening test result * And * Increased sweat chloride concentration - SWEAT TEST * Identification of 2 CF mutations – genotyping * Abnormal nasal epithelial ion transport Other Ix: * Bloods: FBC, LFTs, clotting, ADEK levels, glucose TT * Sputum MCS * CXR: bronchiectasis * Abdo US: fatty liver, cirrhosis, pancreatitis * Spirometry: obstructive defect * Aspergillus serology / skin test (20% develop ABPA)
53
How does CF present itself?
1. **Meconium ileus:** * **I**nfant bowel blocked by sticky secretions. * **Intestinal obstruction** after birth with bilious vomiting, abdominal distension and delay in passing meconium 2. **Intestinal malabsorption** * Evident in infancy. * Main cause is a **severe deficiency of pancreatic enzymes** 3. **Recurrent Chest infections** 4. **Newborn screening**
54
What are some of the common CF complications?
1. **Respiratory Infections:** physio, Abx and sometimes prophylactic ABx 2. **Low Body Weight:** bc of pancreatic insufficiency 3. **Distal Intestinal Obstruction Syndrome (DIOS):** faecal obstruction in ileocaecum versus whole bowel. RIF mass. 4. **CF Related Diabetes**
55
What are the signs and sx of CF?
* Nose: nasal polyps, sinusitis * Resp: cough, wheeze, infections, bronchiectasis, haemoptysis, pneumothorax, cor pulmonale * GI: * Pancreatic insufficiency: DM, steatorrhoea * Distal Intestinal Obstruction Syndrome * Gallstones * Cirrhosis (2O biliary) * Other: male infertility, osteoporosis, vasculitis Signs * Clubbing ± HPOA * Cyanosis * Bilateral coarse creps
56
What life style advice should be given to those with CF?
* 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
57
How is CF managed?
* **Conservative**: physiotherapy * **Pharmacological**: abx, mucolytics, bronchodilators * **GI**: pancreatic enzyme replacement (CREON), give fat soluble vitamins (DEAK) * **Other**: treatment of CF related diabetes * **Advanced lung disease**: oxygen, diuretics * Dornase Alfa
58
What is the pleural cavity?
* Potential space created by pleural surfaces * Serous membrane that folds back on itself to give: –Outer pleura = PARIETAL (attached to chest wall) –Inner pleura = VISCERAL (covers lungs)
59
What can end up in the pleural cavity?
* **Pneumothorax** = air in pleural cavity * **Pleural effusion** = fluid in pleural cavity * **Empyema** = infected fluid in pleural cavity * **Pleural tumours** = benign vs malignant * **Pleural plaques** = discrete fibrous areas * **Pleural thickening** = scarring/ calcification causing thickening (benign vs malignant)
60
What are the different types of pneumothorax?
1. Spontaneous 2. Primary (no lung disease) 3. Secondary (lung disease) 4. Traumatic 5. TENSION: emergency 6. Iatrogenic (e.g. post central line or pacemaker insertion)
61
What are risk factors for pneumothorax?
* Pre-existing lung disease * Height - Smoking/ Cannabis * Diving * Trauma/ Chest procedure * Connective tissue disorders: Ehlers danlos, Marfan’s syndrome
62
How are pneumothorax managed?
* **Primary** * \<2cm rim of air: discharge and review in 2-4 weeks * \>2cm rim of air: 1. **Aspirate** (2ICSMCL) + oxygen 2. (If aspirate unsuccessful) - **Chest** **drain** (4ICSMAL) * **Secondary** * \<1cm air: admit for 24 hr * 1-2cm air: aspiration -\> chest drain * \>2cm: chest drain
63
How do you deal with Pleural Effusions?
* ***Ultrasound guided pleural aspiration*** * CXR * ECG * Bloods: FBC, U&E’s, LFT’s, CRP, Bone profile, LDH, clotting * ECHO (if suspect heart failure) * Staging CT (with contrast)
64
What are the causes of transudate effusions?
* Heart failure * Cirrhosis * Hypoalbuminaemia (nephrotic syndrome or peritoneal dialysis) * less common: Hypothyroidism, mitral stenosis, pulmonary embolism
65
What is Interstitial Lung Disease?
* 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 - Important to take a comprehensive occupational / environmental history - Typically restrictive lung diseases on PFT’s
66
What investigations for interstitial lung disease?
* **Bloods**: FBC (neutrophilia); ↑EST; ABGs; serum antibodies * ANA ENA Rh F ANCA Anti-GBM ACE Ig G to serum precipitins (HIV) * **CXR:** upper-zone mottling/consolidation; hilar lymphadenopathy (rare) * **Lung function tests:** Reversible restrictive defect; reduced gas transfer during acute attacks.
67
What are the classification presentation findings of interstitial lung disease?
* 3Cs: Clubbing, coughing, course crackles * Reduced **chest expansion** * **Auscultation** – fine inspiratory crepitations - basal / axillary areas * **Cardiovascular** – may be features of pulmonary hypertension
68
What are the types of interstitial lung disease?
* Sarcoidosis * Usual Interstitial Pneumonia (UIP) * Non-specific Interstitial Pneumonia (NSIP) * Extrinsic Allergic Alveolitis * Sarcoidosis
69
What is Extrinsic Allergic Alveolitis?
* Hypersensitivity Pneumonitis * Inhalation of organic antigen to which the individual has been sensitised * Presentation: * **ACUTE** – *Alveoli are infiltrated with acute inflammatory cells* * Short period from exposure, 4-8 hrs. reversible: spontaneously settle 1-3 days. Can recur. * **CHRONIC** – *granuloma formation and obliterative bronchiolitis* * *​C*hronic exposure (months – years). Less reversible
70
What are the causes of Exudate effusions?
* **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
71
What is Light's criteria?
* The **Light's Criteria** for **Exudative** Effusions determines if pleural fluid is exudative * Use if pleural fluid protein level is between **25-35 g/L** * Exudate if: * Pleural fluid/ serum **protein** \> 0.5 * Pleural Fluid/ Serum **LDH** \> 0.6 * Pleural fluid LDH \> 2/3 of the upper limit of normal
72
How would you investigate extrinsic allergic alveolitis? What would you see ?
Acute * **Bloods**: FBC, raised ESR, ABG * **CXR**: * Upper zone mottling/ consolidation * Hilar lymphadenopathy * Patchy, nodular infiltrates * Fine reticulation may also occur * **LFTs**: reversible and restrictive Chronic * **CXR:** upper zone fibrosis, honeycomb lung, * LFT: persistent changes * BAL: increased **lymphocytes** and **mast cells**
73
How would you treat Extrinsic allergic alveolitis?
* Remove allergen * Oxygen * Steroids: prednisalone Po
74
What are the causes of extrinsic allergic alveolitis?
* **Bird-fancier’s** and **pigeon-fancier’s lung** (proteins in bird droppings). * **Farmer’s** and mushroom worker’s lung (Micropolyspora faeni, Thermoactinomyces vulgaris). * **Malt worker’s lung** (Aspergillus clavatus). * **Bagassosis** or **sugar worker’s lung** (Thermoactinomyces sacchari)
75
What are some of the symptoms of extrinsic allergic alveolitis?
Fever Chills Malaise Weight loss Anorexia Bibasalar rales/ diffuse rales Clubbing
76
What is Sarcoidosis?
* **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
77
What are the clinical features of sarcoidosis?
* Acute: Erythema nodosum, Polyarthralgia * Sx: * Dry cough * Dyspnoea * Reduced exercise tolerance * Chest pain * Fatigue and arthralgia
78
How is sarcoidosis investigated?
* Pulmonary Function Tests: (obstructive until) fibrosis * **CXR**: 4 stages * Bloods: renal function, ↑ESR, lymphopenia, ↑LFTs, ↑serum ACE in ~60% (non-specific), ↑Ca2+, ↑immunoglobulins. * 24h urine: Urinary Calcium * **Cardiac involvement:** ECG, 24 tape, ECHO, cardiac MRI * **CT/MRI head: headaches** – Neuro sarcoid * **Other tests:** Bronchoalveolar lavage (bal), USS, Bone X Ray
79
What are the four CXR stages of sarcoidosis?
1. Normal 2. BHL 3. BHL + pulmonary infiltrates 4. BHL - pulmonary infiltrates 5. Fibrosis + distortion
80
How do you treat sarcoidosis?
* Most recover spontaneously * Acute: bed rest, NSAIDs * Corticosteroid: **prednisalone** (if calcium elevated, uveitis, neurological, or parenchymal involvement)
81
What are the ILD Treatment Principles?
* Depends on underlying pathology * Occupational exposure – remove * Drug associated – avoid * Stop smoking * ? N-Acetylcysteine ? Immunosuppressant ? Pirfenidone * Transplantation * Treatment of infections (atypical) * Oxygen * MDT * Palliative care
82
What investigations would you perform for CF?
* CXR * High-resolution chest CT * Bloods: FBC * Sputum culture and sensitivity *Others* * Bronchial biopsy and electron microscopy of cilia * Cystic fibrosis transmembrane regulator (CFTR) protein gene mutation testing * Swallow study * pH monitoring of oesophagus
83
What is bronchiecstasis?
* Bronchiectasis is the **permanent dilation of bronchi** due to the destruction of the elastic and muscular components of the bronchial wall * It is often caused as a consequence of **recurrent and/or severe infections** secondary to an underlying disorder. * Pt present with a **chronic cough** and **sputum** production
84
How does bronchiestasis present?
* Productive cough more than 8 weeks: sputum production * Crackles, high-pitched inspiratory squeaks and bronchi * Other: fatigue, haemoptysis, rhinosinusitis, weight loss * Clubbing
85
How is bronchiecstasis investigated?
* **CXR** * **High-resolution chest CT** * Bloods: FBC, UE, CRP, Se Ig, Aspergillus precipitins, RF, α1-AT level * Spirometry * **Sputum** culture and sensitivity * Others (for cause): serum a1-antitrypsin deficiency, sweat chloride test (CF), RF (RA), HIV Ab * **Bronchoscopy + mucosal biopsy**
86
What are the signs of bronchiestasis?
* Clubbing * Coarse inspiratory creps * Wheeze * Purulent sputum * Cause * Situs inversus (+ PCD = Kartagener’s syn.) * Splenomegaly: immune deficiency
87
What signs would indicate bronchiecstasis on a HRCT scan?
* **Tram-track** sign * **Signet** ring sign * String of **pearls** sign * Cluster of **grapes** sign
88
What are some of the common organisms causing bronchiectasis?
* H Influenzae * Pseudomonas Aeruginosa * Moraxella catarrhalis * Fungi * Non tuberculous myobacterial * Less common - staph
89
How would you manage bronchiecstasis?
* Acute: * **1st line:** exercise and nutrition, * **Airway clearance therapy** (maintenance of oral hydration, postural drainage, percussion, vibration, and the use of oscillatory devices), * **Bronchodilator** (salbutamol) * **Mucoactive agent e.g.** Nebulised hypertonic saline * **Acute** exacerbation (mild to moderate): + short term oral abx (**amoxicillin**) - Treatment course: **14 days.** * **Pulmonary rehab** * **Physiotherapy** * **Treat underlying cause** * CF: DNAase * ABPA: Steroids * Immune deficiency: IVIg
90
What are some of the symptoms + signs of lung cancer?
* Cough * Chest pain * Haemoptysis * Dyspnoea * Weight loss * Hoarseness of voice
91
What are some of the clinical complications of lung cancer?
* Recurrent laryngeal nerve palsy; phrenic nerve palsy * SVC obstruction * Horner’s syndrome (Pancoast’s tumour) * Rib erosion * Heart: Pericarditis; AF. * Metastatic: brain; bone (bone pain, anaemia, ↑Ca2+); liver; adrenals (Addison’s). * Paraneoplastic syndrome: clubbing, hypercalcaemia, anaemia, SIADH, Cushing's, Lambert Eaton myasthenic syndrome
92
What are some of the RFs for lung cancer?
* Smoking * Airflow obstruction * Age * FMH of lung cancer * Carcinogens/ occupationl exposure
93
What are some of the investigations you would do for lung cancer?
* **Bloods**: FBC, UE, CRP, LFT, Ca2+, INR * **Cytology:** sputum, pleural fluid * Imaging * **CXR**: peripheral nodule; hilar enlargement; consolidation; lung collapse; pleural effusion; bony secondaries * * **Staging CT** (chest abdo pelvis) * **PET scan** (if MDT confirms needed) - for small mets Histology / biopsy * US guided neck FNA for cytology * Bronchoscopy - endobronchial, transbronchial, (EBUS) endobronchial US * CT biopsy * Thoracoscopy * Bronchoscopic alveolar lavage (BAL)
94
What is used for the treatment of Pneumocystic Jiroveci pneumonia?
Co-trimoxazole
95
How are primary and secondary pneumothoraxes managed? Not tension
96
What are some common causes of BHL?
* **Infection**: TB, mycoplasma * **Malignancy**: lymphoma, carcinoma, mediastinal tumours * **ILD**: extrinsic allergic alveolitis, sarcoidosis
97
When is LTOT offered to COPD patients?
* p02 consistently \<7.3 / 8 with cor pulmonale * Pt must be non smokers and not retain high levels of C02
98
What are the signs of lung cancer?
Chest * Consolidation * Collapse * Pleural effusion General * Cachexia * Anaemia * Clubbing and HPOA (painful wrist swelling) * Supraclavicular and/or axillary LNs Metastasis * Bone tenderness * Hepatomegaly * Confusion, fits, focal neuro * Addison’s Complications * Local * Recurrent laryngeal N. palsy * Phrenic N. palsy * SVC obstruction * Horner’s (Pancoast’s tumour) * AF Paraneoplastic * Endo * ADH → SIADH ( euvolaemic ↓Na+) * ACTH → Cushing’s syndrome * Serotonin → carcinoid (flushing, diarrhoea) * § PTHrP → 1O HPT (↑Ca2+, bone pain) – SCC Rheum - Dermatomyositis / polymyositis Neuro * Purkinje Cells (CDR2) → cerebellar degeneration * Peripheral neuropathy Derm * Acanthosis nigricans (hyperpigmented body folds) * Trousseau syndrome: thrombophlebitis migrans
99
How is lung cancer managed?
NSCLC * Surgical Resection * Rx of choice for peripheral lesions c¯ no metastatic spread = stage I/II (~25%) * Need good cardiorespiratory function * Wedge resection, lobectomy or pneumonectomy * ± adjuvant chemo * Curative radiotherapy * If cardiorespiratory reserve is poor * Chemo ± radio for more advanced disease * Platinum-based regimens: MAbs targeting EGFR (e.g. cetuximab) or TKI (e.g. erlotinib) SCLC * Typically disseminated @ presentation * May respond to chemo but invariably relapse Palliation * Radio: bronchial obstruction, haemoptysis, bone or CNS mets * SVCO: stenting + radio + dexamethasone * Endobronchial therapy: stenting, brachytherapy * Pleural drainage / pleurodesis * Analgesia
100
What Ix are used for COPD?
* BMI * Bloods: FBC (polycythaemia), α1-AT level, ABG * CXR * Hyperinflation (\> 6 ribs anteriorly) * Prominent pulmonary arteries * Peripheral oligaemia * Bullae * ECG: * R atrial hypertrophy: P pulmonale * RVH, RAD * Spirometry: FEV1 \<80%, FEV1:FVC \<0.70, ↑TLC, ↑RV * Echo: PHT

Year 3 Medicine (11 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2025 Bold Learning Solutions. Terms and Conditions