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Respiratory Flashcards

Asthma Lung cancer Acute Bronchitis & Pneumonia (Chest infections) Sarcoidosis & TB COPD ILD (Pulmonary fibrosis) Asbestos-related lung diseases Obstructive Sleep Apnoea (OSA) Infectious mononucleosis

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USMLE® Step 1 flashcards
1
Q

QoL complications - Asthma (Childhood vs adulthood development)

A

Childhood - growth stunt, higher risk of learning disability
Adulthood - higher risk of depression, increased sick days
Both - obesity, medication side effects, lingering cough spells

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2
Q

What is the definition of asthma?

A

chronic respiratory condition associated with airway inflammation and reversible airway obstruction

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3
Q

characteristic symptoms of asthma?

A

Wheeze, cough, chest tightness, worsening cough at night (Diurnal pattern), SOB & variable expiratory airflow limitation.

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4
Q

Common triggers for exacerbation of asthma?

A

changes in weather, drugs (NSAIDs & beta-blockers), exercise, allergens and viral respiratory infections

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5
Q

What is the term used for “onset of severe asthma symptoms, which can be life-threatening”

A

Asthma exacebation

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6
Q

Prevalence of asthma?

A

Affects 12% of UK population.
Incidence - children > adults. In childhood, boy > girls but by adulthood, girls > boys.
Occupational asthma account for 9-15% of adult-onset asthma - most common industrial lung disease in developed world

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7
Q

Risk factors of asthma - development or persistence?

A

Non-modifiable factors
- Age – childhood > adults
- Sex – development boys > girls, persistence into adulthood women > men
- Ethnicity
- Family/ Medical history – atopic diseases (incl. asthma), Respiratory disease in childhood, premature birth associated low birth weight
Modifiable risk factors
- Social conditions – poverty stricken, environment with high pollutant/ allergens/ dampness, exposure to inhaled particulates, workplace exposure – floor dust & isocyanates
- Diet – childhood obesity
- Smoking/alcohol - smoking
- Physical activity
- Medication – NSAIDs & beta-blockers

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8
Q

Prognosis - asthma?

A

Growing out - male children, early onset (< 2 yr old) without other atopic diseases (likely to be asymptomatic by 6-11)

Worse prognosis - early onset asthma in atopic children. Severe/ frequent symptoms -> more likely to persist (eg. wheeze)

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9
Q

Examples of atopic diseases?

A

Asthma, eczema, allergic rhinitis or allergic conjunctivitis

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10
Q

Complications - asthma?

A

Death, respiratory complications and impaired QoL (from suboptimal control - fatigue & underperformance)

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11
Q

Eg. of respiratory complications of asthma?

A

Irreversible airway changes, pneumonia, pulmonary collapse (atelectasis), respiratory failure, pneumothorax& status asthmaticus (repeated attacks with non-response to treatment)

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12
Q

Diagnosis - Asthma

A

Clinical judgement from…

  1. History - presence of hallmark symptoms
  2. Personal/ FHx of atopic conditions - use previous results (skin-prick, >4% blood eosinophilia, raised allergen specific igE)
  3. FeNO test results - confirm eosinophilic inflammation
  4. Spirometry, BDR, PEF readings
  5. Direct bronchial challenge test with histamine or methacholine (special referral)
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13
Q

Positive Values for FeNO test - Asthma

A

Steroid-naive adults >= 40 ppb
5-16 yrs >= 35 ppb

May be affected by empirical treatment with ICS

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14
Q

3 objective tests for airway obstruction - Asthma

A 
Spirometry (FEV1/FVC) - all symptomatic age > 5.
Bronchodilator reversibility (BDR) - Age > 5 with obstructive spirometry.
Variable Peak Expiratory Flow (PEF) readings - support diagnosis of diagnostic uncertainty.
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15
Q

Spirometry Results Criteria - Asthma

A

Normal FEV1/FVC > 70%

Airflow limitation: FEV1/FVC < 70% or lower limit of normal

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16
Q

BDR results criteria - asthma

A

Adults: Improvement in FEV1 of 12% or more with increased volume of > 200ml in response to beta-2-agonist/ corticosteroids. Strong indication - improvement of 400 mL in FEV1

Children: FEV1 improvement of 12% or more

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17
Q

Auscultation finding - Asthma

A

Expiratory polyphonic wheeze

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18
Q

High risk occupations - Asthma?

A

Laboratory work, baking, animal handling, wedding and paint spraying

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19
Q

Prevalence - Lung cancer & mesotheliomas

A

Lung cancer: 3rd most common cancer in UK (behind breast & prostate)
Seen in both sex ~1:1

Mesothelioma: new diagnosis - men: female 5:1

Cigarette smoking = biggest cause. 80% of lung cancer is preventable

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20
Q

Histology - lung cancer

A

Non-small cell lung cancer (80%): adenocarcinoma (40%), squamous cell carcinoma (20%), large cell carcinoma (10%) & others

Small cell lung cancer (SCLC - 20%) - cells contain neurosecretory granules -> release neuroendocrine hormones responsible for paraneoplastic syndromes

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21
Q

Which lung cancer is highly associated with paraneoplastic syndromes & why?

A

Small cell lung cancer (SCLC - 20%) - cells contain neurosecretory granules -> release neuroendocrine hormones responsible for paraneoplastic syndromes

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22
Q

Presentation - Lung cancer

A

Systemic signs: fatigue, weight loss, appetite loss

Respiratory: SOB, haematemesis, chest pain, cough, recurrent pneumonia

Peripheral: finger clubbing, lymphadenopathy (often supraclavicular nodes)

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23
Q

Causes of finger clubbing

A 
Cyanotic heart disease, Cystic fibrosis
Lung cancer, lung abscess
Ulcerative colitis
Bronchiectasis
Benign mesothelioma
Infective endocarditis, idiopathic pulmonary fibrosis
Neurogenic tumours
GI disease - biliary cirrhosis, IBD - UC, liver cirrhosis, coeliac
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24
Q

Investigations - Lung cancer

A

First line: CXR (2ww)
Imaging: Contrast staging CAP CT (metastasis), PET-CT
Bronchoscopy with EBUS - endoscopy allowing detailed assessment of tumour in bronchi and Us-guided biopsy
EGFR-TK mutation testing

Histological diagnosis - bronchoscopy/ percutaneous biopsy

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25
Q

CXR findings - Lung cancer

A

Airway: hilar enlargement
Breathing: peripheral opacity - visible lesion in lung field, pleural effusion, collapse

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26
Q

CXR - ABCD approach

A

Airway: trachea, carina, bronchi and hilar structures
Breathing: lung and pleura
Cardiac: heart size and borders
Diaphragm: including assessment of costophrenic angles
Everything else: mediastinal contours, bones, soft tissues, bones, valves, pacemakers and review areas

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27
Q

Prognosis - lung cancer and mesothelioma

A

5 year survival

Non-small cell lung cancer has better prognosis than small cell lung cancer

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28
Q

Treatment options - Non-small cell lung cancer

A

First line: Surgery - lobectomy (first line), segmentectomy or wedge resection
Radiotherapy (Stereotactic ablative body radiotherapy (SABR): curative if early enough
Chemotherapy: adjuvant chemo or as palliative treatment to improve survival and quality of life in later stages
Systemic treatments: Oncogene directed (metastatic NSCLC with mutation), immunotherapy (metastatic NSCLC with no mutation ad PDL1 > 50%), cytotoxic chemotherapy (Metastatic, nil mutation, PDL1 <50%)

Endobronchial treatment with stents and debulking - palliative treatment to relieve bronchial obstruction caused by lung cancer

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29
Q

Treatment - Small cell lung cancer (SCLC)

A

Chemotherapy and radiotherapy

Endobronchial treatment with stents and debulking - palliative treatment to relieve bronchial obstruction caused by lung cancer

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30
Q

Extrapulmonary manifestations - non-small cell lung cancer

A

Recurrent laryngeal nerve palsy: present with hoarse voice. Cause - cancer pressing on/ affecting recurrent laryngeal nerve as it passes though mediastinum

Phrenic nerve palsy due to nerve compression causes diaphragm weakness and presents as shortness of breath.

Superior vena cava obstruction is a complication of lung cancer. It is caused by direct compression of the tumour on the superior vena cava. It presents with facial swelling, difficulty breathing and distended veins in the neck and upper chest. “Pemberton’s sign” is where raising the hands over the head causes facial congestion and cyanosis. This is a medical emergency.

Horner’s syndrome is a triad of partial ptosis, anhidrosis and miosis. It is caused by a Pancoast’s tumour (tumour in the pulmonary apex) pressing on the sympathetic ganglion

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31
Q

What is the sign associated with superior vena cava obstruction which is a medical emergency

A

Pemberton’s sign - raising hands over head leads to cyanosis and facial congestion

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32
Q

Paraneoplastic syndromes assoc. with small cell lung cancer

A

SIADH: caused by ectopic ADH secretion by a small cell lung cancer and presents with hyponatraemia.

Cushing’s syndrome can be caused by ectopic ACTH secretion by a small cell lung cancer.

Hypercalcaemia caused by ectopic parathyroid hormone from a squamous cell carcinoma.

Limbic encephalitis. This is a paraneoplastic syndrome where the small cell lung cancer causes the immune system to make antibodies to tissues in the brain, specifically the limbic system, causing inflammation in these areas. This causes symptoms such as short term memory impairment, hallucinations, confusion and seizures. It is associated with anti-Hu antibodies.

Lambert-Eaton myasthenic syndrome. Immune system attacks neuromuscular junctions (voltage-gated calcium channels sited on the presynaptic terminals in motor neurones.)

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33
Q

What are the main neuroendocrine secretions of small-cell lung cancer

A

Hormones: ADH, ACTH, PTH
Antibodies: Anti-Hu (limbic encephalitis)

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34
Q

Lambert-Eaton Myasthenic Syndrome - Cause and Presentation

A

Antibodies secreted against SCLC also targets and affect voltage-gated calcium channels on presynaptic terminals in motor neurones in neuromuscular junction.

Presentation: weakness (esp. proximal muscles), intraocular muscles -> diplopia, levator muscles -> ptosis and pharyngeal muscles -> slurred speech and dysphagia.
Other symptoms: dry mouth, blurred vision, impotence and dizziness from automatic dysfunction.

Reduced tendon reflexes. A notable finding - reflex become temporarily normal for a short period following a period of strong muscle contraction. For example, the patient can maximally contract the quadriceps muscle for a period, then have their reflexes tested immediately afterwards, and display an improvement in the response. This is called post-tetanic potentiation.

In older smokers with symptoms of Lambert-Eaton syndrome consider small cell lung cancer.

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35
Q

What is mesothelioma?

A

Lung malignancy affecting the mesothelial cells/ mesothelium (of the pleura)

It is strongly linked to asbestos inhalation. There is a huge latent period between exposure to asbestos and the development of mesothelioma of up to 45 years. The prognosis is very poor. Chemotherapy can improve survival but it is essentially palliative.

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36
Q

Mesothelioma: Possible sites

A

Lung pleura (pleural), pericardium (pericardial), lining of the abdomen (peritoneal) & sac surrounding testes (testicular)

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37
Q

Mesothelioma: Presentation

Think about possible sites affected

A

Cancer red flags - fatigue, weight loss, anorexia, fever (large portion of energy depleted), night sweats

Respiratory: Chest pain (pleural effusion), Cough, dyspnoea, hemoptysis

Abdominal: abdominal mass, jaundice, ascites, vomiting and constipation (umbilical hernia)

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38
Q

Mesothelioma: Diagnosis & Histology (3 main malignant types)

A

CXR with biopsy confirmation

Epitheliod mesothelioma - uniform, sharply defined and square to tubular in configuration. They feature prominent nuclei and divide quickly but tend to stick together. This means it takes longer for them to spread throughout the body. The epithelial cell type accounts for more than 50% of all mesothelioma cases and up to 70% of cases.

Sarcomatous - Spindle-shaped sarcomatoid cells typically lack defining structure and have an irregular configuration. They spread more quickly than epithelial cells because they don’t tend to stick together as they grow. This rare cell type characterizes 10% to 20% of cases.

Biphasic - Malignant mesothelioma is considered biphasic when it contains epithelial and sarcomatoid cells. Each cell type must account for at least 10% of the tumor mass to receive a biphasic diagnosis. The biphasic (mixed) cell type accounts for 20% to 30% of mesothelioma cases.

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39
Q

Mesothelioma: Prognosis of 3 main malignant subtypes

A

Epitheliod mesothelioma: Slower rate of metastasis. Most responsive to treatment -> better prognosis

Sarcomatous mesothelioma: poor respose to treatment. Most negative prognosis

Biphasic: prognosis dependant on epithelial cells: sarcomatoid cells

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40
Q

Mesothelioma: Treatment

A

CHEMOTHERAPY (pemetrexed, cisplatin, carboplatin)
SURGERY (pleurectomy/ decortication, extrapleural pneumonectomy or pericardectomy) with RADIATION and/or CHEMO

Advances diffused mesothelioma: Chemotherapy + radiotherapy

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41
Q

Risk factors - Lung cancer

A

Non-modifiable risk factors

  • Age: peak 75-90
  • Sex: male>female
  • Personal/ FHx: chronic lung conditions (COPD), immunodeficiency & genetic loci

Modifiable risk factors

  • Social: low socioeconomic status, passive smoking
  • Smoking/ alcohol - duration, intensity and cessation onset
  • Exposures: occupational - asbestos & radon, indoor cooking fumes
  • Occupation: plumbers, ship-builders, carriage workers, carpenters
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42
Q

Common tumour sites for different NSCLC pathophysiology

A

Adenocarcinoma: originated from mucus-producing glandular tissue, more peripherally located (deep inhalation of particulates)

Squamous cell carcinoma: originated form bronchial epithelium; centrally located

Large cell cancer: heterogenous group, undifferentiated

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43
Q

Lung cancer - oncogenes mutation important for directed treatments

A

EGFR: 15-30% of adenocarcinoma, female, Asian ethnicity, non-smokers
ALK: 2-7% of NSCLC, younger patients, non-smokers
ROS1: 1-2% of NSCLC, younger patients, non-smokers
BRAF: 1-3% of NSCLC, smokers

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44
Q

Presentations of asso. paraneoplastic syndrome (+ condition name) for SCLC

A

Hyponatremia (SIADH), Cushing’s, hypercalcaemia (PTH)
Limbic encephalitis: ST memory impairment, hallucinations, confusion and seizures
Focal weakness (Lambert-Eaton myasthenic syndrome)

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45
Q

Asthma: Management goal & how achieve Asthma

A
  1. Reduce airway eosinophilic inflammation: ICS & Leukotriene receptor antagonist (reduce T2 inflammation)
  2. Acute symptomatic relief (smooth muscle relaxation): Beta-2-agonist (SABA) & Anticholinergic therapies
  3. Severe asthma: steroid sparring therapies - Biologic targeted to IgE (Anti-IgE antibody) or biologics targeted to airway eosinophils (Anti-IL-5 antibodies or Anti-IL5 receptor antibody) In5
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46
Q

Treatment: Asthma step-up plan

A
  1. PRN reliever (SABA)
  2. Add regular preventer (low dose ICS)
  3. Initial add-on therapy: add inhaled LABA or LTRA
  4. Additional controller therapies: ?increasing ICS to medium dose OR ?Adding LTRA. If no LABA response, consider stopping LABA
  5. Specialist therapies: refer
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47
Q

Why is respiratory viral infections a risk factor to asthma exacebations and not bacteria?

A

Prolonged infection leads to decreased IFN-a,b,d

Decreased IFN -> decreased viral replication inhibition -> increased viral replication -> prolonged illness and asthma severity

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48
Q

Asthma treatment - Anti-IgE antibody example

A

Omalizumab - for severe eosinophilic asthma (blood Eos =>300 cells/mcl in last 12 months)

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49
Q

Role of skin prick aeroallergen test for asthma diagnosis

A

Not diagnostic test for asthma.

Done after official diagnosis to identify triggers

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50
Q

Possible reasons for uncontrolled asthma that should be considered before stepping up treatment

A

Patient factors: lack of adherence, suboptimal inhaler technique, smoking (passive / active), psychological factors

Doctor factors: alternative diagnosis

Environmental or seasonal factors

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51
Q

Definition - Pneumonia

A

Infection of the lung tissue. It causes inflammation of the lung tissue and sputum filling the airways and alveoli

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52
Q

X-ray finding - Pneumonia

A

Lung consolidation

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53
Q

Pneumonia - 3 main classifications

A

Community Acquired Pneumonia - developed outside hospital

Hospital Acquired Pneumonia - developed > 48hr after admission

Aspiration Pneumonia

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54
Q

Presentation - Pneumonia

A

Systemic - fatigue, febrile, delirium, SEPSIS

Respiratory: SOB, productive cough w/ sputum, Haemoptysis, pleuritic chest pain

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55
Q

Clinical signs (+ chest examination) - Pneumonia

A

Sepsis: tachypnoea, tachycardia, hypotension, hypoxia

Fever, Confusion

Sounds: Bronchial breath sounds, Focal coarse crackles, Dullness to percussion

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56
Q

Explain characteristics of 3 main chest exam. results for Pneumonia

A

Bronchial Breath sounds: harsh breath sounds equally loud on inspiration and expiration. Caused by consolidation of lung tissue in airway

Focal coarse crackles: air passing through sputum

Dullness to percussion: lung tissue collapse and/or consolidation

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57
Q

Pneumonia - Severity Scoring system. What is the difference between CAP and HAP

A

CAP: CRB-65 and HAP: CURB-65

CURB-65 does not count urea

The CURB 65 score predicts mortality (score 1 = under 5%, score 3 = 15%, score 4/5 = over 25%). The scoring system is there to help guide whether to admit the patient to hospita

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58
Q

What is CURB-65 criteria consist of?

A

Confusion (new disorientation in person, place or time),
Urea > 7
Respiratory rate >= 30
Blood pressure <90 systolic or <=60 diastolic
65 - age >=65

The CURB 65 score predicts mortality (score 1 = under 5%, score 3 = 15%, score 4/5 = over 25%). The scoring system is there to help guide whether to admit the patient to hospital:

Score 0/1: Consider treatment at home
Score ≥ 2: Consider hospital admission
Score ≥ 3: Consider intensive care assessment

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59
Q

Pneumonia - Common causes and other causes/ associations

A

Common: Streptococcus pneumonia (50%) & haemophilias influenzae (20%)

Other causes: Moraxella catarrhalis - in immunocompromised patients/ with chronic pulmonary disease, Pseudomonas aeruginosa - CF/ bronchiectasis patients, Staphylococcus aureus - CF patient’s

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60
Q

Common diseases (via direct tissue invasion) caused by Staphylococcus aureus

A

Skin infections, Pneumonia, Endocarditis, Osteomyelitis, Infectious (septic) arthritis

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61
Q

Definition - Atypical Pneumonia

A

The definition of atypical pneumonia is pneumonia caused by an organism that cannot be cultured in the normal way or detected using a gram stain.

They don’t respond to penicillins and can be treated with macrolides (e.g. clarithomycin), fluoroquinolones (e.g. levofloxacin) or tetracyclines (e.g. doxycycline)

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62
Q

Treatment for atypical pneumonia

A

They don’t respond to penicillins.

Can be treated with macrolides (e.g. clarithomycin, erythromycin), fluoroquinolones (e.g. levofloxacin) or tetracyclines (e.g. doxycycline)

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63
Q

Causes of atypical pneumonia

Legions of psitacci MCQs

A

Legionella pneumophilia (Legionnaires’ disease): typically by infected water supplies or air conditioning units. Can cause SIADH -> hyponatraemia (low. The typical exam patient has recently had a cheap hotel holiday and presents with hyponatraemia.

Mycoplasma pneumoniae.: This causes a milder pneumonia and can cause a rash called erythema multiforme characterised by varying sized “target lesions” formed by pink rings with pale centres. It can also cause neurological symptoms in young patient in the exams.

Chlamydia psittaci: This is typically contracted from contact with infected birds. The MCQ patient is a from parrot owner.

Chlamydophilia pneumoniae: The presentation might be a school aged child with a mild to moderate chronic pneumonia and wheeze. Be cautious though as this presentation is very common without chlamydophilia pneumoniae infection.

Coxiella burnetii AKA “Q fever”. This is linked to exposure to animals and their bodily fluids. The MCQ patient is a farmer with a flu like illness.

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64
Q

What is the rash associated with atypical pneumonia? What is the bacteria?

A

Erythema Multiforme - target lesions

Mycoplasma pneumoniae

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65
Q

What are the 2 most common conditions associated with erythema multiforme?

A

Herpes Simplex Virus (HSV) & Mycoplasma pneumoniae (Atypical pneumonia)

66
Q

Who does Pneumocystis jiroveci (PCP) pneumonia mainly affect?

A

Immunocompromised patients.

Particularly important in patients with poorly controlled or new HIV with a low CD4 count.

67
Q

What is PCP pneumonia?

A

Fungal Pneumonia - Pneumocystis jiroveci.

Treatment is with co-trimoxazole (trimethoprim/sulfamethoxazole) known by the brand name “Septrin”. Patients with low CD4 counts are prescribed prophylactic oral co-trimoxazole to protect against PCP.

68
Q

Presentation - Pneumocystis Jiroveci

A

It usually presents subtly with a dry cough without sputum, SOB on exertion and night sweats.

69
Q

When is MRI necessary for Lung cancer Inx

A

Pancoast tumours (superior sulcus tumours) - Inx extent of disease

70
Q

Definition - Acute bronchitis

A

Lower respiratory tract infection causing inflammation in bronchial airways.
No evidence of pneumonia

71
Q

Pneumonia vs acute bronchitis

A

Pneumonia: inflammation of lung tissue. Air sacs become filled with microorganisms, fluid and inflammatory cells

Bronchitis inflammation of bronchial airways

72
Q

CRB-65 score - Interpretation

A

Score 0: community treatment should be considered

Score 1-2: hospital assessment should be considered

Score 3: Urgent admission to hospital required

73
Q

Acute Bronchitis - Causes

A

Most commonly Viral infection - rhinovirus, enterovirus, coronavirus, influenza A & B, parainfluenza, human metapneumovirus, RSV and adenovirus

Bacterial (1 in 100 cases) - streptococcus pneumoniae, haemophillus influenza, mortadella catarrhalis and atypical bacteria

74
Q

Which viral pathogens can cause pneumonia

A

Influenza A & B

adenovirus , coronavirus, RSV

75
Q

Prevalence - Chest infections

A

Acute Bronchitis: 44 per 100 in adult population. Most occur in autumn or winter

CAP: 220,000 adults diagnosed annually. 5-10 per 1000 adult population

76
Q

Prognosis & Complication: Acute Bronchitis

A

Mainly self-limiting illness
Cough usually lasts about 2-3 weeks and most people recovery fully with no residual symptoms.

Around 1/4 - cough >4 week and some persist (<6 months) = post-bronchitis syndrome

Complication: pneumonia

77
Q

Chest infection - asso. Symptoms

A

Wheeze, SOB, pleuritic pain, fever

78
Q

Acute bronchitis - when is immediate Abx indicated

Which Abx (adults)

A

Patient is systemically very unwell

People at higher risk of complications: pre-existing comorbidities (heart, lung, kidney, liver or neuromuscular disease, immunosuppression)

First line: doxycycline 200mg first day and 100mg once for 4 days (5 day course)

Alternative (if pregnant): amoxicillin, clarithromycin or erythromycin

79
Q

Defintion - Sarcoidosis

A

Multisystem inflammatory disease of unknown origin characterised by presence of non-caseating granuloma in affected organs.

Granculomas = nodules of inflammation full of macrophages and T lymphocytes. Cause is unknown

80
Q

Acute Sarcoidosis - Extra-pulmonary manifestations

A

erythema nodosum (eg. nodules on shin)

81
Q

Prevalence - Sarcoidosis

A

UK incdence: 5/100 000
Sex: females > males
Age: young adulthood and around 60
Ethnicity: more common in afro-carribean

Common MCQ: patient is a 20-40 year old black woman presenting with a dry cough and shortness of breath. They may have nodules on their shins suggesting erythema nodosum.

82
Q

Why is Sarcoidosis more common in afro-carribean population?

A

Due to ethic variation in HLA-B28 gene. Making sarcoidosis racially determined.

83
Q

Sarcoidosis: organs most commonly involved

A

Skin, eyes (esp. iritis) & respiratory tract

84
Q

Sarcoidosis - Cause

A

Unknown aetiology

May relate to dist inhalation and significant genetic contribution (suggested by increased incidence in monozygotic twins)

Associated with leukocyte antigen HLA-B8 (particularly complications with erythema nodosum and arthritis)

85
Q

Sarcoidosis - pathophysiology

A

Non-caseating granulomas = pathogenic lesion

Lymphocytic alveolitis occurs in lung -> lymphocyte-stimulated recruitment of macrophages -> organised into granulomas -> inflammation and long-term damage of lung

86
Q

Presentation: Acute vs Chronic sarcoidosis

A

Acute sarcoidosis: erythema nodosum, arthralgia (joint stiffness), bilateral Hilar lymphanopathy, no lung fibrosis

Chronic sarcoidosis: slowly progressive breathlessness. Associated with progressive pulmonary fibrosis. nil EN. nil BHL

87
Q

Sarcoidosis: prognosis (+ acute vs chronic)

A

Acute has better prognosis than chronic: better prognosis 80% resolution in 1 year.

2/3 of white and 1/3 of black patients recover with no treatment.

Worse prognosis in… older age of onset, more widespread disease & in Afro-carribean.

Fewer than 3% mortality (arrhythmias or CNS involvement)

Complicaitons: pulmonary fibrosis and pulmonary hypertension

88
Q

Sarcoidosis: Investigations

A

Lab tests: FBC - lymphopaenia in active disease & thrombopenia. Raised ESR, calcium. raised ACE (product of macrophages), immunologlobins and serum soluble IL-2 receptor.

Imaging: CxR, HRCT, MRI - CNS involvement

Pulmonary function tests

Histology (gold standard) - Bronchoscopy + EBUS

89
Q

Sarcoidosis: Affected organs

A

Intrathoracic (90%) : bilateral Hilar lymphanopathy, pulmonary fibrosis/ infiltrates & pulmonary nodules

Liver: liver nodules, cirrhosis & cholestasis (granulomas common but clinical symptoms rare)

Hepetosplenomegaly

Eyes (20%): uveitis, conjunctivitis & optic neuritis

Skin (15%): erythema nodosum, lupus pernio, granulomas develop in scar tissue

Heart (5%): BBB, Heart block, VT, HF. 10-20% abnormal ECG

Kidneys (5%): Kidney stones (hypercalcaemia), nephrocalcinosis & interstitial and glomerulonephritis

CNS (5%): nodules, pituitary involvement (Diabetes insipidus), Encephalopathy

PNS (5%): facial nerve palsy, mononeuritis multiplex

Bones (2%): Arthralgia (joint stiffness), arthritis, myopathy

Hypercalcaemia - 1,25-dihydroxyvitamin D release by macrophages

90
Q

Sarcoidosis: Complications

A

Pulmonary hypertension,
Pulmonary fibrosis

Can develop in a few patients

91
Q

Sarcoidosis: Presentation syndromes

A

Lofgren’s syndrome: BHL + arthritis/arthralgia + EN + fever

Uveo-parotid fever = Heerfordt’s syndrome: Uveitis + parotid enlargement + CN palsies + subacute meningitis + systemic symptoms

92
Q

Sarcoidosis: CXR classification

A

Grade 0: normal
Grade 1: BHL (65%)
Grade 2: BHL & pulmonary infiltration
Grade 3: nil BHL, pulmonary infiltration

Grade 0: extra-thoracic symptoms
Grade 3: intra-thracic symptoms

93
Q

Sarcidosis: Differential diagnosis

A

TB, Lymphoma, hypersensitivity pneumonitis, HIV, toxoplasmosis, Histoplasmosis

94
Q

Sarcoidosis: Management

A

No treatment: first line in patients with no/ mild symptoms (resolve spontaneously)

Oral steroids (prednisolone): first one where treatment is required. Given between 6-24 months. patients should be given bisphosphonates to protect against osteoporosis on LT steroids

Immunosuppressants: methotrexate and azathioprine (2nd line)

Lung transplant: required in severe pulmonary disease

95
Q

Sarcoidosis: Indication for Prednisolone. Dosage?

Long term treatment

A
  1. Progression of pulmonary fibrosis
  2. Hypercalcaemia
  3. Threatening vital organs eg. cardiac, renal, liver
96
Q

Erythema nodosum (EN): disease association

A

EN can be associated with streptococcal infection, TB, sarcoidosis, drugs, IBD and histoplasmosis.

97
Q

COPD: Definiton

A

non0reversible, long term deterioration of airflow in lung caused by lung tissue damage.

Characterised by the fixed for partially reversible airway obstruction

98
Q

COPD: Main cause of exacerbations

A

Often triggered by infection -> infective exacerbations

Low ventilation of lungs -> more prone to infections

99
Q

COPD: Prevalence

A

COPD: 4th leading cause of mortality worldwide
M=F (historically M > F)

Occupational exposure - 15% of cases

100
Q

COPD: Risk factors

A

Non-modifiable

  • Age
  • Sex: females more susceptible to harmful effects of tobacco smoke
  • Genetics: alpha-1-antitypsin deficiency (less common cause) -> early onset of COPD
  • PMH: asthma

Modifiable

  • Environment: inner city pollutants, indoor air pollutants (burning wood and other biomass materials)
  • Smoking = major cause
  • Occupational exposure: dusts, certain fumes and chemicals
101
Q

COPD: prognostic factors

A

Severity of COPD on spirometry (FEV1),

Lifestyle: smoking, low BMI (muscle wasting and cachexia),

Multi-morbidity and frailty

Severity and burden of symptoms eg breathlessness, CAT score & exercise capacity

102
Q

COPD: Complications

A

Low QoL, Depression & anxiety (loneliness)

Cardiovascular: Cor pulmonale (RHF 2dary to lung disease causes by pulmonary hypertension as consequence of chronic hypoxia), 2dary polycythemia (chronic hypoxia)

Respiriatory: frequenct chest infections (esp. pneumonia), respiratory failure, pneumothorax, lung cancer

Systemic: muscle wasting ans cachexia

103
Q

COPD: Presentation in history

A

Suspect COPD in age > 35 with risk factor with (>) one symptoms:
SOB(persistent, progressive over time and worse on exertion), chronic cough, regular sum production, frequent LRTI & wheeze

General signs: weight loss, anorexia & fatigue, waking up at night with breathlessness, ankle swelling,

104
Q

COPD: Clinical assessment

A

RF Type I “pink puffer”: cachexic, anxious

RF Type II “blue bloater”: large, quiet

Plethoric (high Hb), lip pursing, cyanosis, bouding pulse (CO2 retention), cor pulmonale (raised JVP), hyperinflated chest, warm hands and metabolic flap, wheeze and crackles during auscultation

105
Q

COPD: Diagnosis

A

History and presentation

Confirmation of diagnosis: Spirometry

  • Confirmation of persistent airflow obstruction: post bronchodilators FEV1/FVC <0.7
  • Consider other causes in older people without typical COPD symptoms with FEV1/FVC < 0.7
  • Consider COPD in younger people who have symptoms of COPD, even if FEV1/FVC > 0.7
106
Q

COPD: MRC Dyspnoea Scale

A

Assess impact of breathlessness

Grade 1: breathless on strenuous exercise
Grade 2: breathless on walking up hill
Grade 3: breathless that slows on the flat
Grade 4: stop to catch their breath after walking 100m on flat
Grade 5: unable to leave house due to breathlessness

107
Q

COPD: Severity grading for airflow obstruction

A

Grading using FEV1

Stage 1: FEV1 >80% of predicted
Stage 2: 50-79% of predicted
Stage 3: 30-49% of predicted
Stage 4 (very severe): <30% of predicted

108
Q

ILD: definition

A

Interstitial lung disease is an umbrella term to describe conditions that affect the lung parenchyma (the lung tissue) causing inflammation and fibrosis.

109
Q

Fibrosis: definiton

A

Fibrosis involves the replacement of the normal elastic and functional lung tissue with scar tissue that is stiff and does not function effectively.

110
Q

Diagnosis: ILD

A

Combination of clinical features & HRCT of thorax

HRCT report: “ground glass” appearance with ILD

Lung biopsy if diagnosis unclear

111
Q

ILD: HRCT diagnosis

A

“Ground glass” appearance

112
Q

ILD: Management

A

Non-curative (irreversible damage).. supportive & aim to prevent progression

Remove/ treat underlying cause

  • Lung transplant… consider risk
  • Smoking cessation

Supportive

  • Advanced care planning and palliative care where appropraite
  • Home O2 where hypoxic at rest
  • Physiotherapy and pulmonary rehabilitation
  • Pneumococcal and flu vaccine
113
Q

ILD: Difference types

A

Pulmonary fibrosis: idiopathic, drug induced, secondary
Asbestosis
Hypersensitivity Pneumonitis (EAA)
Cryptogenic Organising Pneumonia

114
Q

Idiopathic pulmonary fibrosis: diagnosis & management

A

Idiopathic: no clear cause. insidious SOB onset & dry cough over 3 months.

Progressive fibrosis

Presentation: insidious onset of SOB and dry cough over more than 3 months. It usually affects adults over 50 years old.

Examination: bibasal fine inspiratory crackles and finger clubbing.

Prognosis: poor with a life expectancy of 2-5 years from diagnosis.

Management: Pirfnidone (antifibrotic and antiinflammatory) and Nintedanib (monoclonal Ig targeting tyrosine kinase)

115
Q

Drug induced fibrosis: Key drug causes

A

Amiodarone,
Cyclophosphamide,
Methotrexate,
Nitrofuratonin

116
Q

Secondary PF: Condition Causes

A

Alpha-1 antitrypsin deficiency
Rheumatoid Arthritis
SLE
Systemic sclerosis

117
Q

EAA: Defintion

A

Hypersensitivity pneumonitis is a type III hypersensitivity reaction to an environmental allergen that causes parenchymal inflammation and destruction in people that are sensitive to that allergen.

118
Q

EAA: Diagnosis

A

Bronchoalveolar lavage involves collecting cells from the airways during bronchoscopy by washing the airways with fluid then collecting that fluid for testing.

Histology: raised lymphocytes and mast cells in hypersensitivity pneumonitis.

119
Q

EAA: specific causes

A

Bird-fanciers lung: a reaction to bird droppings

Farmers lung: a reaction to mouldy spores in hay

Mushroom workers’ lung: a reaction to specific mushroom antigens

Malt workers lung: a reaction to mould on barley

120
Q

Cryptogenic Organising Pneumonia: information

A

Previously known as bronchiolitis obliterans organising pneumonia. It involves a focal area of inflammation of the lung tissue.

Cause: idiopathic or triggered by infection, inflammatory disorders, medications, radiation or environmental toxins or allergens.

Presentation: Very similar to infectious pneumonia with shortness of breath, cough, fever and lethargy. It also presents on similarly to pneumonia on a chest xray with a focal consolidation.

Diagnosis: often delayed due to the similarities to infective pneumonia. Lung biopsy is the definitive investigation. Treatment is with systemic corticosteroids.

121
Q

Asbestosis: Definition

A

Asbestosis is lung fibrosis related to the inhalation of asbestos. Asbestos is fibrogenic, meaning it causes lung fibrosis. It is also oncogenic, meaning it causes cancer. The effects of asbestos usually take several decades to develop.

122
Q

Asbestos inhalation: Complications

A

Benign: Pleural plaques, pleural thickening, benign pleural effusions

ILD: asbestosis

Malignant disease: mesothelioma and adenocarcinoma

Suffers are eligible for compensation if they develop asbestos related health conditions (except isolated pleural plaques). All patients that die with known exposure to asbestos need to be referred to the coroners.

123
Q

Asbestosis: Diagnosis

A

Presentation: insidious onset of SOB & reduced exercise tolerance, cough +/- sputum and wheeze. fine bilateral inspiratory crackles, flinger clubbing & cor pulmonate

Inx: Pulmonary function tests - reduced gas transfer, reduced lung volumes, restrictive ventilatory defect & exercise-related hyperaemia.
CXR - maybe normal, usually bilateral lower zone, interstitial changes often with pleural plaques and thickening. HRCT more sensitive
Histology: not required

124
Q

Asbestosis: managemnet

A

No specific treatment available.

Management therefore includes treatment for COPD and cor pulmonale

Lifestyle: smoking cessation, influenza and pneumococcal immunisation and prevention of further exposure to asbestos.

125
Q

Diffuse pleural thickening: causes

A

Asbestos exposure

Lung: previous haemothorax, TB

Intervention: chest surgery, radiation

Infection and exposure to drugs eg. methysergide

126
Q

Bronchiestasis: Definition

A

Permanent dilation and thickening of airways. Often associated with superadded respiratory infection.

Characterised by chronic cough, excessive sputum production, bacterial colonisation and recurrent acute infections.

127
Q

Bronchiectasis: 3 main morphological classifications

A

Cylindrical bronchiectasis: enlarged and cylindrical

Varicose bronc: irregular bronchi with areas of dilation and constriction

Saccular/ cystic: dilated bronchi form clusters of cysts. Most severe form and often found in CP patients.

128
Q

Bronchiectasis: method of severity classification Historically vs now)

A

Historically: volume of sputum produced

Now: radiological appearance on CT scan

129
Q

Bronchiectasis: Characteristics

A

It may be widespread throughout the lungs (diffuse) or more localised (focal).

The affected airways are inflamed and easily collapse. There is an impairment of airflow and drainage of secretions, leading to the accumulation of a large amount of mucus in the lungs.
The mucus collects bacteria, predisposing to frequent and often severe LRTIs.

130
Q

Bronchiectasis: prevalence

A

Women > men (70% women)

Higher in older age groups (>60 yrs)

131
Q

Bronchiectasis: Causes

A

Chronic inflammation of airways.

Post-infection (most common cause): Measles; pertussis; bronchiolitis; pneumonia; TB; HIV.
Immunodeficiency: e.g. HIV infection, hypogammaglobulinaemia
Connective tissue disease: RA, Sjogren’s syndrome, systemic sclerosis, SLE, EDS, Marfan’s syndrome,
Asthma,
ABPA,
Gastric aspiration,
Congenital defects: CF (upper lobe dominant), primary ciliary dyskinesia, a1- antitrypsin deficiency, yellow nail syndrome,
Bronchial obstruction by lymphadenopathy, tumour or inhaled foreign bodies,
IBD

132
Q

Bronchiectasis: pathophysiology

A

Continued inflammation destroying their elastic and muscular structure. followed by poor mucus clearance, and bacterial colonisation of collected mucus. This then can progress, as chronic infection causes further inflammation in a cyclical fashion. Ending in tissue damage with further progressive lung damage.

133
Q

Bronchiectasis: which structures are destroyed leading to dilation

A

Elastic and muscular

134
Q

Bronchiectasis: 2 main diseases more likely to lead to localised.

A

Bronchial obstruction & bronchopneumonia

135
Q

Bronchiectasis: presentation

A

Classic: chronic cough with large volume of mucopurulent sputu. ‘Unpleasant breath’

Non-specific: dyspnea, chest pain, haemoptysis. can progress to RF & cor pulmonlae

Signs: coarse crackles (70%) - early inspiration and often in lower zones, large airway rhonchi (44%), wheeze (34%), clubbing (infrequent)

History: chronic condition, daily expectoration of large volumes of v. purulent sputum, haemoptysis (unexplained)

136
Q

Bronchiectasis: Inx

A

Gold standard: HRCT - bronchial wall dilation (‘signet ring’ sign), bronchial wall thickening

Radiological: CXR - normal/ ring/ tubular opacities, tramlines and fluid levels.

Sputum microbiology

Bloods: confirm infection/ presence of co-morbidity

Immune function test

Lung function tests: Spirometry, BDR, PEF

137
Q

Bronchiectasis: Management

A

Airway clearance techniques and mucolytics.
Chest physiotherapy and devices such as a flutter valve may aid sputum expectoration and mucus drainage.

Antibiotics should be prescribed according to bacterial sensitivities. Patients known to culture Pseudomonas will require either oral ciprofloxacin or suitable IV antibiotics.
If ≥3 exacerbations a year consider long-term antibiotics (may be nebulized).

Bronchodilators (eg nebulized salbutamol) may be useful in patients with asthma, COPD, CF, ABPA (p177).

Corticosteroids (eg prednisolone) and itraconazole for ABPA.

Surgery may be indicated in localized disease or to control severe haemoptysis.

138
Q

OSA: Prevalence

A

1/30 rising to 1/4 in BMI >30

Risk Factors: age, male, obesity, hypothyroidism, alcohol and smoking

139
Q

OSA: Common Causes

A

Mainly by pharyngeal obstruction (neck circumference >= 40 cm), enlarged tonsils or retrognathia (set back mandibular)

140
Q

OSA: pathophysiology

A

Obstruction of the airway (mainly pharynx) leads to episode of apnea (>10s of non-breathing) at night (as many as 100).
Causes frequent waking, often forgotten by patient, giving saw-tooth pattern of sleep.

141
Q

OSA: Presentation

A

Snoring, gasping, and choking during sleep. Often noticed by partner.
Morning headache.
Daytime sleepiness.
Cognitive or personality changes may also be seen.
Apnoeic episodes lead to sympathetic nervous system spikes, causing ↑BP.
Kids with OSA due to large tonsils are often hyperactive not sleepy.

142
Q

OSA: Inx

A

Initial examination:
Epworth Sleepiness Scale (ESS): initial screen, with a score >10 grounds for referral to a sleep service.
Neck circumference and BMI. Also check nasal patency, tongue size, and oropharynx for large tonsils or other obstructions.
Metabolic: BP, glucose.

Polysomnography (PSG = standard diagnostic test: Various physiological measures are taken during sleep. Can include EEG, electro-oculogram (EOG), air flow sensors, chest and abdominal movement sensors, pulse oximetry, EMG, and ECG. Can be in hospital (‘attended’) or at home (‘unattended’).

Respiratory PSG – leaves out the neurophysiology (EEG, EOG, EMG) – is usually sufficient and can be done at home.
Calculates the Apnoea-Hypopnea Index (AHI), the number of apnoeas or hypopneas per hour. Alternative is the Respiratory Distress Index (RDI), which also includes respiratory-effort related arousals.
Diagnosis of OHA by AHI score: mild ≥5, moderate ≥15, severe >30.

Other options, if indicated: TFT, ABG and lung function tests as there may be co-morbid respiratory disease & Nasolaryngoscopy

143
Q

OSA: Management

A

Lifestyle: lose weight below trigger (below BMI 30), exercise, stop smoking and alcohol

CPAP:

144
Q

TB: Causative agent

A

Mycobacterium tuberculosis

Alcohol, acid fast bacterium (AAFB)

145
Q

TB: Histology

A

Caseating granulomatous.

Ghon’s complex: Ghon’s focus (site of localised inflammation) + regional lymphadenopathy
Ranke’s complex: Ghon’s focus fibrosis, calcification

146
Q

TB: Primary vs Post-primary infection

A

Primary TB: non-sensitive patients.

  • Sites of Ghon’s focus: sub-pleural in mid lung zone, pharynx & terminal ilium
  • Lymph involvements: hilar, cervical & mesenteric
  • Fibrose & calcifies

Most patients asymptomatic, rarely cause pleural effusion or bronchial obstruction

Post-primary TB: Tuberculin sensitive patients.
Lesions may: be fibrotic & calcifies, cause bronchial obstruction -> collapse, blood dissemination

147
Q

TB: Primary vs Post-primary infection

A

Primary TB: non-sensitive patients.

  • Sites of Ghon’s focus: sub-pleural in mid lung zone, pharynx & terminal ilium
  • Lymph involvements: hilar, cervical & mesenteric
  • Fibrose & calcifies

Most patients asymp

Post-primary TB: Tuberculin sensitive patients.
Lesions may: be fibrotic & calcifies, cause bronchial obstruction -> collapse, blood dissemination

148
Q

TB: Presentation (Common)

A

Symptoms present only in established disease

Non-specific: malaise, slight fever, anorexia & weight loss

Specific: haemoptysis, dry cough (+ mucoid in later), SOB on exertion, pleuritic pain
Lung auscultation: crepitation (esp. apical), consolidation, pleural effusion/ cavitation

149
Q

TB: Complications (pulmonary & extra-pulmonary)

A

Lung: pulmonary fibrosis & calcification, colaspe, pneumothorax, pleural effusion
CNS: meningitis, cerebral abscess
Skin: lupus vulgaris, erythema nodosum
Cardiac: pericarditis
GI: terminal ileitis, peritonitis, hepatitis, obstructive jaundice
Renal: haematuria, pyuria, pyelonephritis
Bone & Joints: spinal TB, Pott’s disease

Miliary TB: blood dissemination -> involving lung, adrenals and spleen

150
Q

TB: Risk factors

A

Immunosuppressed patients: HIV, DM, malnutrition, aging, Immunosuppressant (RA, steroid)
Substance abuse: ETOH, IV drug use
Low income countries: Pakistan, India, hostel dwelling (in & out)

151
Q

TB: Radiological finding

A

Reactive TB: apical consolidation (High O2 tension - M. TB aerobe)
. changing ‘soft’ shadows
. cavitation

152
Q

TB: Management

A

Prophylaxis: BCG vaccination
Latent TB: Isoniazid 6-8 mth
Active TB: 1st line anti-TB - isoniazid, rifampin, pyraziamide, ethambutol
Multi-drug resistant TB: 2nd line: amikacin, kanamycin & capreomycin

153
Q

TB: Diagnosis

A

Screening test: Mantoux test (PPD intradermal injection) - 48-72 hr post-injection measurement
Imaging: CXR - Ranke’s complex or cavities

Diagnostic: sputum or bronchial wash culture (AAFB) - at least 3 tests and 1 early morning test.

154
Q

Miliary TB: Definition

A

Miliary tuberculosis refers to clinical disease resulting from bacteraemia (blood dissemination) of Mycobacterium tuberculosis and is characterized by the presence of small, firm white nodules resembling millet seeds

155
Q

Infectious mononucleosis: Causative pathogen

A

EBV (Epstein-Barre virus)

Main target: B lymphocytes and epithelial cells in larynx

156
Q

Infectious mononucleosis: Presentation

A

Classic triad: fever & malaise (prominent), cervical lymphadenopathy (esp. posterior neck triangle), tonsillar exudate

Other: Macular-papule rash, hepatosplenomegaly, sore throat, muscle and joint pain.

157
Q

Why should Abx (esp. which) be avoided in young patients with sore throat?

A

Most URTI are caused by virus.

Ampicillin & Amoxicillin - causes macular papule rash in infectious mononucleosis (glandular fever)

158
Q

DD for macular-papule rash

A

Infectious mononucleosis

Mumps & rubella

159
Q

Infectious mononucleosis: Diagnosis

A

Blood film: lymphocytosis with absolute/ relative (>50%) mononuclear cells (atypical: large an irregular nuclei)
Positive Paul Bunnel/ monospot test
Acute infection: high IgM, Post infection: IgG

Thrombocytopenia & abnormal LFTs common (rarely severe)

160
Q

Infectious mononucleosis: Complications

A

Splenic rupture
EBV associated with Hodgkin’s Burkitt’ s lymphoma
Neurological syndromes: GBS, cranial nerve palsy, peripheral/optic neuropathy
EBV manifestations: Lung (pneumonia), Heart (myocarditis), Stomach (gastric pseudo lymphoma), GI (hepatitis & pancreatitis)

161
Q

Infectious mononucleosis: Management

A

Mainly supportive: antipyretics and analgesics.. .avoid aspirin -> can cause reye’s disease

Where tonsils obstruct airway -> prednisolone 40mg/day for 5-10 days

Thrombocytopenia: IV Ig (IV immunoglobulins)

Medical Conditions (8 decks)

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