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Haroon Phase 2A > Respiratory > Flashcards

Respiratory Flashcards

1
Q

What is COPD?

A

Progressively worsening, irreversible airflow obstruction

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2
Q

Types of respiratory failure and pathophysiology?

A

Type 1 = fibrosis related causes, lung fails to fill properly which results in ↓PaO2, ↓PaCO2 Type 2 = obstructive causes. Lung fails to remove CO2 properly which results in ↓PaO2 + ↑PaCO2.

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3
Q

Conditions that cause type 2 respiratory failure?

A

Asthma and COPD

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4
Q

Treatment for type one respiratory failure?

A

CPAP - continuous positive airway pressure

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5
Q

Treatment for type 2 respiratory failure?

A

BIPAP - bi positive airway pressure

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6
Q

Types of COPD?

A

Chronic Bronchitis Emphysema A1AT deficiency

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7
Q

Risk factors for COPD?

A

Cigarettes Air pollution Genetics (A1AT deficiency = auto recessive) Older males

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8
Q

Pathophysiology of chronic bronchitis?

A
  • Hypertrophy + hyperplasia of mucous glands (mucous is protective against damage) - Chronic inflammation cells infiltrate bronchi and bronchioles - This causes: - mucus hypersecretion - ciliary dysfunction - narrowed lumen (thus increased infection risk + airway trapping)
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9
Q

Typical presentation of chronic bronchitis?

A

Chronic purulent cough, dysponea for 3+months, over 2 years with sputum “blue bloater” (blue tint of skin and lips due to cyanosis and typically overweight- not a respectful term to use nowadays)

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10
Q

Pathophysiology of Emphysema?

A

Destruction of elastin layer in alveolar ducts/alveolar sacs/respiratory bronchioles - elastin keeps walls open during expiration (bernouli principle) - decreased elastin = air trapping distal to blockage

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11
Q

Types of Emphysema?

A

Centriacinar Emphysema Panacinar Emphysema Distal Acinar Irregular Emphysema

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12
Q

Most common type of Emphysema?

A

Centracinar emphysema very common in smokers

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13
Q

Most severe type of emphysema?

A

Panacinar emphysema caused by A1AT deficiency

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14
Q

What area of the lungs does centriacinar emphysema effect?

A

Respiratory bronchioles only

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15
Q

What area of the lungs does Panacinar emphysema effect?

A

respiratory bronchioles - alveolar ducts - alveolar sacs - alveoli

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16
Q

Pathophysiology of A1AT deficiency?

A

A1 antitrypsin degrades NE (neutrophil elastase) which protects excess damage to elastin layer especially in lungs - Deficiency (decreased liver production) = ↑NE = panacinar emphysema and liver issues

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17
Q

What is A1AT deficiency caused by?

A

Autosomal codominant inheritance

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18
Q

Typical patient presentation to suspect A1At deficiency in?

A

Younger/middle aged men with COPD symptoms but no smoking history

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19
Q

Symptoms of COPD?

A

Typically: - older patient - chronic cough - with (often) purulent (infectious) sputum - extensive smoking history (exception A1AT) - constant dyspnoea (not episodic)

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20
Q

Presentation of a pink puffer?

A

Minimal cough - Pursed lip breathing - Cachectic (muscle wastage) - Barrel Chest - Hyperesonant percussion

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21
Q

Complication of pink puffer patients?

A

Bullae rupture - if subpleural = pneumothorax

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22
Q

Do patients present with only blue bloater or pink puffer?

A

These aren’t separate conditions and most patients present with a mix of both

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23
Q

Dyspnoea grading scale MRC 1-5?

A

1- strenuous exercise 5- can’t do daily activities without SOB eg. change clothes

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24
Q

Main investigation to diagnose COPD?

A

Pulmonary function test: - Increasing fractional expired number indicates lung damage - FEV1:FVC <0.7 = obstruction on PFT spirometry

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25
Q

What are the 2 conclusions from the diagnostic test and the values associated with them?

A

Bronchodilator irreversible <12% ↑FEV1 = COPD Bronchodilator reversible >12% ↑FEV1 = Asthma

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26
Q

Other investigations to diagnose COPD?

A
  • DLCO (diffusing capacity of CO across lung) = low in COPD, normal in asthma - Genetic test for A1AT deficiency - ABG/ECF/CXR (may show flattened diaphragm + bullae formation)
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27
Q

Complications of COPD?

A

Cor pulmonale (RHS heart failure due to increased portal hypertension + infection risk)

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28
Q

Main pathogens in acute COPD exacerbations?

A

S.Pneumo - H.Influenzae(as these patients are increasingly susceptible to infection)

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29
Q

Treatment for COPD?

A
  • First smoking cessation + vaccines (influenza + pneumococcal) Long term management (more key): 1) SAB2A (salbuterol) 2) SAB2A + LAB2A (salmeterol) + LAM3A (tiotropium) 3) SAB2A + LAB2A + LAM3A + ICS *consider long term oxygen if v.severe - 15h+ for 3 weeks
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30
Q

When is oxygen given to severe COPD patients?

A

O2 <88% (55mmHg) or O2 <90% (60mmHg) with heart failure *for long term oxygen therapy must be non smoker and readings of <7.3KPa consistently

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31
Q

How to treat episodes of acute COPD exacerbation in hospital?

A
  • O2 target is 88-92% saturation - as these patients are chronic CO2 retainers, excess O2 = increased dead space= increased V/Q mismatch and CO2 retention => respiratory acidosis Treatment: - nebulised salbutamol + ipratropium bromide - ICS - Antibiotics
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32
Q

What is asthma?

A

Chronic reversible airway disease characterised by: - reversible airway obstruction - airway hyperresponsiveness - inflamed bronchioles - mucus hypersecretion

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33
Q

What increases the risk of susceptibility to asthma infection?

A

Hygiene Hypothesis = Growing up in a very hygienic environment

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34
Q

What are the types of asthma and prevalence?

A

1) Allergic (70%) 2) Non allergic (30%)

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35
Q

What does allergic asthma entail?

A
  • IgE mediated - Extrinsic - T1 hypersensitivity - Due to environmental trigger (pollen, smoke etc.) - Often early presentation –> childhood diagnosis - Consider genetics + hygiene hypothesis
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36
Q

What does non-allergic asthma entail?

A

Non IgE mediated - Intrinsic - may present later - Harder to treat - Associated with smoking (like COPD)

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37
Q

What are the triggers for asthma?

A

infection - Allergen - Cold weather - Exercise - Drugs (Beta blockers, aspirin)

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38
Q

What is the atopic triad?

A

1) Atopic rhinitis 2) Asthma 3) Eczema (some people have 3 conditions synonymously - known as ATOPY)

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39
Q

What is Somter’s triad?

A

1) nasal polyps 2) asthma 3) aspirin sensitivity

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40
Q

What is the pathophisiology of Asthma?

A
  • overtime = chronic remodelling (bronchial scarring —> decreased lumen size —> increased mucus)
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41
Q

What happens with asthma overtime?

A

=> chronic remodelling bronchial scarring —> decreased lumen size —> increased mucus

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42
Q

Symptoms of asthma?

A

Wheeze - Cough (typically dry) - Chest tightness - SOB (shortness of breath) - typically episodic w/triggers and diurnal variation - Often younger patient

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43
Q

What may be found in microscopy of mucus in asthma?

A

May show Curschmann’s spirals + Lexton Charcot crystals

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44
Q

How can asthma episodes be classified?

A
  • Moderate (PEF 50-75%) - Severe (PEF 33-50%) - can’t finish sentences - Life Threatening (PEF <33%) - decreased consciousness - Fatal (hypercapnic pKa 6+)
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45
Q

Investigations to diagnose asthma?

A

Spirometry: FeNO ↑ and spirometry shows obstruction (FEV1:FVC <0.7) => Ratio will determine if its bronchodilator reversible/irreversible

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46
Q

What does bronchodilator reversible indicate, give relevant values

A

Diagnosis = asthma >12% FEV1↑

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47
Q

What does bronchodilator irreversible indicate, give relevant values

A

Diagnosis = COPD <12% improved FEV1

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48
Q

Give examples for SABA, LABA, SAMA, LAMA?

A

SABA = salbutamol LABA = salmeterol SAMA = ipratropium bromide LAMA = tiotropium bromide

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49
Q

Define SABA, LABA, SAMA, LAMA?

A

SABA = short acting beta agonist LABA = long acting beta agonist SAMA = short acting muscarinic antagonist LAMA = long acting muscarinic antagonist

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50
Q

Treatment guidelines for asthma?

A

1) SAB2A (PRN) 2) SAB2A + ICS (hydrocortisone) (before adding more meds, review inhaler technique + compliance) 3) SAB2A + ICS + LTRA (leukotriene receptor antagonist eg. Montelukast) 4) SAB2A + ICS + LAB2A +/- LTRA 5) increase ICS dose =very very important!!

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51
Q

Treatment for exacerbations in asthma?

A

OHSHITME - O2 - SABA (nebuslised) - Hydrocortisone (ICS) - IV MgSO4 (bronchodilation) - Theophylline IV - MgSO4 IV - Escalate (also BIPAP as asthma patients and +/- antibiotics if infection present)

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52
Q

The locations of primary lung cancer?

A

img

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53
Q

Location of primary metastasis sites?

A

Bone - liver - Adrenals (usually asymptomatic) - Brain - Lymph nodes

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54
Q

What is mesothelioma?

A

Malignancy of pleura

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55
Q

Cause of mesothelioma?

A

Asbestos! - doesn’t present till decades after exposure (latent period)

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56
Q

Who does mesothelioma tend to affect?

A

Males, 40-70yrs old

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57
Q

Symptoms of Mesothelioma?

A

Cancer symptoms: 1) weight loss 2) tired all the time 3) night pain Lung symptoms: - shortness of breath - persistent cough - pleuritic chest pain - tumour may press on nearby structures - recurrrent laryngeal (hoarse voice) - signs of metastasis e.g bone pain

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58
Q

Investigations to diagnose mesothelioma?

A

CXR + CT: 1st line - pleural thickening +/- effusion CA-125 (cancer antigen 125) increased - sensitive not specific - (non specifically raised in many tumours) Biopsy = diagnostic

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59
Q

Treatment for mesothelioma?

A

Very aggressive tumour => usually palliative BUT doesn’t distantly metastasise as pleura isn’t everywhere - If found early can try surgery + chemo/radiotherapy ( but generally resistant)

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60
Q

What is bronchial carcinoma?

A

Primary malignancy of lung parenchyma

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61
Q

Types of bronchial carcinoma and prevalence of each?

A

Small cell (15%) Non small cell (85%)

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62
Q

What is BALT lymphoma?

A

A non Hodgkin lymphoma originating in bronchi (Bronchial Associated Tissue Lymphoma)

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63
Q

Who does small cell bronchial carcinoma affect?

A

Exclusively smokers

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64
Q

Causes of small cell bronchial carcinoma?

A

Paraneoplastic syndromes: - Ectopic ACTH -> cushings - Ecoptic ADH -> SIADH - Lambert Eaton syndrome (autoimmune disorder of NMJ)

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65
Q

Features of small cell bronchial carcinoma?

A

Fast growing - early metastases - Central lung lesions

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66
Q

Types of non small bronchial cancers and prevalence?

A
  • Squamous (25%) - Adenocarcinoma (40%) - Carcinoid tumour - Large cell
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67
Q

Features of squamous cell bronchial carcinoma?

A
  • Mostly affects smokers - Affects central lung, lesions with central necrosis - May secrete PTHrP -> hypercalcemia - Arise from lung epithelium - Late metastases, locally spread mostly
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68
Q

What condition is heavily associated with non small cell lung carcinoma?

A

Hypertrophic Pulmonary Osteoarthropathy - a paraneoplastic syndrome - usually squamous cell carcinoma

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69
Q

Key features of Hypertrophic Pulmonary Osteoarthropathy?

A

Clubbing - Arthritis - Periostitis

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70
Q

What does adenocarcinoma in situ mean?

A

Stage 0 => not yet spread

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71
Q

What are the features of adenocarcinoma?

A

Commonly asbestos caused (also in smokers but less so than Squamous) - affects peripheral lung - Arises from mucous secreting glandular epithelium - metastases common in: Bone, Brain, Adrenals, Lymph nodes, liver

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72
Q

What is carcinoid tumour associated with?

A

Genetics: - MEN1 mutation - Neurofibromatosis 1

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73
Q

What is a carcinoid tumour?

A

Neuroendocrine tumour (secretes serotonin) - Arises in GIT and sometimes lung - Symptoms only appear when liver metastases are present

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74
Q

What is the biggest cause of secondary hypertrophic osteoarthritis?

A

Adenocarcinoma Triad: - Clubbing - Arthritis - Long bone swelling

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75
Q

General symptoms of bronchial carcinoma?

A
  • Chest pain - Cough - Haemoptysis (cough up blood from lungs/bronchial tubes) - cancer symptoms - Signs of metastases: - hoarse voice - recurrent laryngeal nerve - Pemberton sign - mediastinal mass - Homer’s syndrome - Pancoast tumour
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76
Q

What is a Pancoast tumour?

A

Tumour in lung apex metastasises to neck’s sympathetic plexus => causing horner’s syndrome: - ptosis - myosis (XS pupil constriction) - anhidrosis (lack of sweat) *typically on half the face

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77
Q

Investigations to diagnose bronchial carcinoma?

A

Imaging is 1st line - CXR, CT Diagnostic - bronchoscopy + biopsy Staging is done by MRI (TNM)

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78
Q

Treatment of small cell bronchial carcinoma?

A

More aggressive; - If early = consider chemo/radio (often unsuccessful) - If metastasised = palliative

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79
Q

Treatment of non small cell carcinoma?

A

Less aggressive - If early = surgical excision - If metastasised = chemo +/- radio Eg. MAb therapy- Cetuximab vs epidermal growth factor

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80
Q

Are secondary or primary lung tumours more common?

A

Secondary are much more common

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81
Q

Why are secondary lung tumours more common?

A

Lungs oxygenate 100% blood => all blood comes to lungs so higher metastasis risk - Especially in the breast, kidney, bowel, bladder

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82
Q

What is a pulmonary embolism?

A

Pulmonary artery circulation blocked by blood clot - typically embolising from a DVT

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83
Q

Risk factors for PE?

A
  • Anything affecting Virchow’s triad - Fmily history
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84
Q

Pathophysiology of PE?

A

1) DVT embolises + enters right heart via IVC 2) Occluding pulmonary artery small vessels - decreased V/Q= vent with no perfusion => reactive bronchoconstriction causing increased dyspnoea and smaller airways) 3) Embolus = increased pulmonary BP Pulmonary htn –> RV strain = cor pulmonale + right heart failure

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85
Q

Symptoms of PE?

A
  • Sudden onset SOB - Chest pain (pleuritic) w/swollen painful calf (from DVT) - History of immobility (after surgery/flight) - ↑JVP - Tachypnoea
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86
Q

Signs of RH failure?

A

1) Hypotensive 2) Tachycardic 3) Peripheral oedema

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87
Q

Investigations to diagnose PE

A
  • ECG - DUSS shows DVT (vein doesn’t compress when squeezed) - CXR is usually normal
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88
Q

ECG characteristics of PE?

A

S1Q3T3: - S waves deep in lead I - Q waves very deep in lead III - T waves inverted in lead III - RBBB V1-3 = RSR pattern due to right axis deviation - Sinus Tachycardia

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89
Q

Treatment of PE if patient is haemodynamically stable?

A

Anticoagulants: 1st line = DOAC (apixaban) or LMWH (if DOAC CI) 2nd line = Warfarin

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90
Q

Treatment of PE if patient is haemodynamically unstable?

A

Thrombolysis (clot busting) i.e alteplase - If that fails catheter embolectomy

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91
Q

Differential diagnosis for PE?

A

Pleural effusion + pneumothorax which are visible on CXR

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92
Q

Prophylactic treatment for PE?

A
  • Compression stockings - Regular walking, - SC LMWH
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93
Q

Name two types of lower respiratory infections?

A

Pneumonia - TB

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94
Q

What is Pneumonia?

A

Fluid exudation into alveoli Due to inflammation from infection - typically bacterial but can be viral

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95
Q

Two types of Pneumonia?

A

1) CAP - community acquired pneumonia 2) HAP - hospital acquired pneumonia (>48h of hospital admission)

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96
Q

The common bacterial causes of CAP?

A

S.pneumoniae (most common) - H.Influenzae - Mycoplasma pneumoniae (causes atypical Pneumonia)

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97
Q

The rarer bacterial causes of CAP and treatment?

A
  • S.Aureus - Legionalla (comes from spain) - Chlamydia pneumoniae (atypical pneumonia) => not b lactam susceptible so use macrolide to treat (clarithromycin)
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98
Q

Viral causes of pneumonia?

A

H. flu - CMV

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99
Q

Fungal causes of Pneumonia?

A

P.jirovecci -> only in immune compromised patients eg. HIV

100
Q

Bacterial causes of HAP?

A

P.puruginosa - E.coli - Klebsiella All gram -ve aerobic bacilli also MRSA

101
Q

Why is HAP normally more severe than CAP?

A

Increased severity as many of the causes are multi drug resistant (MDR)

102
Q

How do people typically get infected with pneumonia?

A

Typically from inhaled pathogens, can also be from aspiration

103
Q

Risk factors of pneumonia?

A
  • Immunocompromised (HIV/long term steroids) - IVDU (S.aureus) - Pre existing respiratory disease - Very young/old
104
Q

Pathophysiology of typical pneumonia?

A

Bacteria invades and exudate forms inside alveoli lumen - SPUTUM

105
Q

Pathophysiology of atypical pneumonia?

A

Bacteria invades and exudate forms inside interstitium of alveoli - dry Cough (eg M.pneumoniae)

106
Q

Symptoms of typical pneumonia?

A

Productive Cough with nasty coloured SPUTUM (purulent) - Pyrexia- Due to infection - pleuritic Chest pain, worse w/breathing + Cough - Tachypnoea - Dyspnoea - Tachycardia - Hypotension - Confusion in elderly

107
Q

Symptoms of atypical pneumonia?

A

dry Cough - low grade fever

108
Q

Investigations to diagnose Pneumonia?

A

1st line diagnostic = CXR shows consolidation - Can show “Air bronchogram” = air-filled bronchi (dark) being made visible by the opacification of surrounding alveoli (grey/white) = diagnostic sign - Sputum sample + culture to ID organism (gram stain, Ziehl Nielsen stain)

109
Q

Which causes of pneumonia show multilober lesions on CXR?

A

S.pneumoniae - S.Aureus - Legionella

110
Q

What are the types of pneumonic lesions on CXR?

A

Multilobar - Multiple abscesses - Upper lobe

111
Q

Which cause of pneumonia can cause multiple abscesses on CXR?

A

S.aureus

112
Q

Which cause of pneumonia can cause upper lobe pneumonic lesions on CXR?

A

Klebisella but exclude TB first

113
Q

Scores for assessing severity of CAP?

A

CURB 65 - scored out of 5 - 1 = 3% mortality, outpatients - 2 = consider short hospital stay and antibiotics - ≥3 = 15% mortality, hospital ICU stay

114
Q

How to assess severity of CAP?

A

CURB 65 - Confusion - Abbreviated Mental Test Score (AMTS) ≤8/10 - Urea nitrogen >7mmol/L - Respiratory rate >30 - BP <90/60mmHg (either <90 sys or <60 dys) - 65+ y/o

115
Q

Treatment for Pneumonia?

A
  • O2 (stats 94-98%) - Broad spectrum antibiotics - Analgesia (NSAIDS) for pleuritic chest pain unless COPD
116
Q

Antibiotic guidelines for CURB 0 to 2?

A

Amoxicillin

117
Q

Antibiotic guidelines for CURB 3 to 5?

A

Co-amoxiclav +Clarithromycin

118
Q

Exceptions with antibiotic treatment for pneumonia?

A

Legionella needs clarithromycin 1st line and its a notifiable disease (PHE)

119
Q

What is aspiration pneumonia and which patients is it seen in?

A

aspiration of gastric contents into lungs => can be fatal due to destructiveness of gastric acid - seen in patients with stroke, Bulbar palsy and Myasthenia gravis

120
Q

What is TB?

A

Granulomatous caseating disease, caused by mycobacteria

121
Q

Causes of TB?

A

Many mycobacteria species (eg M.Leprae- Leprosy) but 4 species are known as mycobacterium tuberculosis complex (MTC) which cause TB

122
Q

Mycobacterium Tuberculosis Complex?

A

1) M.tuberculosis 2) M.africanum 3) M.microtis 4) M.bovis (from unpasteurised milk) =most common causes of TB

123
Q

Where is TB most common in world?

A

South Asia (India, China, Pakistan) - Sub-Saharan Africa

124
Q

Epidemiology of TB?

A

1.7bn people worldwide (mostly latent)

125
Q

How is TB spread?

A

Airborne

126
Q

Risk factors for TB?

A

Country + travel association (eg.India) - Immunocompromised - Homeless/crowded housing - IVDU - smoking + alcohol - Increased age

127
Q

Features of MTC (mycobacterium tuberculosis complex)?

A
  • Non motile + non spore forming - Mycolic acid capsule - Resistant to phagosome killing - Slow growing (15-20 hrs)
128
Q

Pathophysiology of TB?

A

1) TB phagocytosed but resist killing, thus forming caseous granulomatous 2) T cells recruited + central region of granuloma undergoes caseating necrosis (primary Ghon focus in upper parts of lung) 3) Ghon focus (lesion) spreads to nearby lymph nodes - ghon complex 4) 2 possibilities: if TB spreads systemically = Miliary TB OR in most infection is contained within granulomas but not dead = latent TB

129
Q

Can latent TB be symptomatic?

A

No can only be asymptomatic

130
Q

Symptoms of non-latent TB?

A
  • Characteristic night sweats + weight loss - Pyrexia, chest pain and patient will look unwell - Extrapulmonary: - Meningitis (meningism + fever) - Skin changes - TB pericarditis symptoms - Joint pain
131
Q

Investigations to diagnose TB?

A
  • Mantoux skin (tuberculin) test - to ID latent or active TB - Sputum culture 3x +ve = acid fast bacilli, bright red w/ Ziehl Nielsen - CXR - Biopsy
132
Q

Treatment of TB?

A

RIPE: 2266 Rifampicin - 2 months, SE: haematuria Isoniazid - 2 months, SE: peripheral neuropathy (tingly hands/feet) Pyrimidine - 6 months, SE: hepatitis Ethambutol - 6 months, SE: eye problems (optic neuritis)

133
Q

What are Interstitial lung diseases?

A

Group of chronic lung disorders characterised by inflammation and scarring that make it hard for lungs to get enough oxygen

134
Q

Give the 6 types of chronic ILDs and examples

A

1) granulomatous = sarcoidosis 2) Inhalational = hypersensitivity pneumonitis, pneumoconiosis 3) Idiopathic pneumonias = pulmonary fibrosis + Non-pulmonary fibrosis 4) connective tissue = scleroderma, RA 5) Drug induced = amiodarone, bleomycin 6) Other = Goodpasture’s, vasculitis

135
Q

Most common interstitial lung disease?

A

Pulmonary Fibrosis

136
Q

Who is pulmonary fibrosis most commonly seen in?

A
  • Older men 60+ - Smoke
137
Q

Cause for pulmonary fibrosis?

A

Often Idiopathic

138
Q

Risk factors for pulmonary fibrosis?

A

smoking - occupational (eg. Dust) - Drugs (methotrexate) - Viruses (EBV, CMV)

139
Q

Pathophysiology for pulmonary fibrosis?

A

Pulmonary fibrosis (progressive scarring) —> T1 respiratory failure

140
Q

Symptoms of pulmonary fibrosis?

A

Exertional dysponea - dry unproductive Cough

141
Q

Investigations to diagnose pulmonary fibrosis?

A
  • Spirometry = restriction - FEV: FVC >0.7 BUT FVC decreased (<0.8 normal) - Gold standard = High res CT (chest) = GROUND GLASS lungs + traction bronchiectasis
142
Q

Treatment for pulmonary fibrosis?

A

smoking cessation + vaccines - Pirfenidone, Nintendinib - surgery (lung transplant)

143
Q

How is pmeumoconiosis acquired?

A

Occupationally acquired

144
Q

Two causes of pneumoconiosis?

A

Silicosis - Asbestosis

145
Q

What is silicosis?

A

Inhalation of silicon dioxide, egg shell calcification at hilar lymph nodes

146
Q

What is asbestosis?

A

Inhalation of asbestos which affects pleura - causes mesothelioma and T1 respiratory failure

147
Q

What is Sarcoidosis?

A

Idiopathic granulomatous disease

148
Q

Risk factors for sarcoidosis?

A
  • Women - 20-40yrs old - Afro Caribbean
149
Q

Symptoms of sarcoidosis?

A
  • Fever - Fatigue - Respiratory: dry cough, dysponoea - Other: eye lesions (uveitis), lupus pernio (blue- red nodules in nose + cheeks)
150
Q

Investigations to diagnose sarcoidosis?

A
  • CXR (staging 1-4) shows bilateral hilar adenoathy + pulmonary infiltrates - Diagnostic = biopsy shows non caseating granuloma Also increase in serum calcium and serum ACE (granulomas)
151
Q

Name a subset of sarcoidosis?

A

lofgrens syndrome (systemic acute sarcoidsis)

152
Q

Symptoms of Iofgren’s syndrome?

A

Triad of: 1) acute polyarthiritis 2) erythema nodosum 3) bilateral hilar adenopathy

153
Q

Treatment for Sarcoidosis?

A

Early stages = self resolving Symptomatic patients = corticosteroids

154
Q

What is hypersensitivity pneumonitis?

A

T3 hypersensitivity: - immune (Ab-Ag) complex deposition at lung tissues - causes immune hyperresponse

155
Q

Risk factors for hypersensitivity pneumonitis?

A

Occupation (e.g farming) - Bird keeping

156
Q

Most common type of hypersensitivity pneumonitis?

A

Farmer’s Lung - due to mouldy hay

157
Q

5 types of hypersensitivity pneumonitis?

A
  • Farmer’s lung - mouldy hay - Pigeon fancier’s lung - avian protein, bird droppings - Malt workers lung - Cheese workers lung - Humidifier fever
158
Q

Treatment for hypersensitivity pneumonitis?

A

Remove allergen

159
Q

What is Goodpasture’s syndrome?

A

T2 autoimmune hypersensitivity response

160
Q

Pathophysiology of Goodpasture’s?

A
  • presence of autoantibodies to the alpha-3 chain of type IV collagen - anti Glomerular basement membrane disease (anti-GBM) - attack lungs + kidneys = lung fibrosis + glomerulonephritis
161
Q

Investigations to diagnose Goodpasture’s?

A

1) Lung + kidney biopsy = damage + Ig deposition 2) Serology = anti-GBM +ve (anti glomerular basement membrane)

162
Q

Treatment for Goodpasture’s?

A

1) Supportive, 2) Corticosteroids 3) Plasma exchange (get rid of anti GBMs antibodies)

163
Q

Another name for Wegener’s granulomatosis?

A

Granulomatosis with polyangiitis

164
Q

What is Wegener’s granulomatosis?

A

Granulomatosis vasculitis affecting small and medium vessels - typically causes ENT, lung and kidney symptoms

165
Q

What is associated with Wegener’s granulomatosis?

A

C-ANCA vasculitis

166
Q

Symptoms of Wegener’s granulomatosis?

A

ENT = saddle shaped nose, ear infection Lungs = diffuse alveolar haemorrhage => haemoptysis Kidney = glomerulonephritis => haematuria

167
Q

Investigations to diagnose Wegener’s granulomatosis?

A

c-ANCA +ve

168
Q

Differential diagnosis for Wegener’s granulomatosis?

A

1) Microscopic polyangiitis (MPA) 2) Eosinophilic granulomatosis with polyangiitis (EGPA) but these are both mostly p ANCA positive

169
Q

Treatment for Wegener’s granulomatosis?

A

Corticosteroids - Immunosuppression e,g Rituximab

170
Q

What is bronchiectasis?

A

Permanent dilation of bronchioles - Excessive mucus in them

171
Q

Which lobes does bronchiectasis usually effect?

A

Usually effects lower lobes

172
Q

Symptoms of bronchiectasis?

A

Productive cough with lots of sputum and dyspnoea

173
Q

Risk factors for bronchiectasis?

A

most Commonly occurs post infection e.g TB, Pneumonia - CF - HIV - ABPA (Allergic bronchopulmonary aspergillosis)

174
Q

Pathophysiology of bronchiectasis?

A
  • Irreversible dilation - Loss of cilia - Mucus hypersecretion - ↑increased risk of infection (as decreased muco-cilliary clearance)
175
Q

Investigations to diagnose bronchiectasis?

A

Imaging: - CXR - HRCT (Gold standard) - dilated thickened bronchi (signet ring sign) - cysts at the end of bronchioles Spirometry = obstructive - FEV1:FVC <0.7 - Sputum culture (check infection)

176
Q

Infective organisms that can cause bronchiectasis and treatment?

A

H.Influenzae - S.pneumoniae - P.aeruginosa Use antibiotics eg. amoxicillin

177
Q

Treatment of bronchiectasis?

A

Non curative *conservative - Chest physio + smoking cessation *drug - bronchodilators to manage symptoms consider antibiotics If infection

178
Q

What is Cystic Fibrosis?

A
  • Auto recessive mutation on chromosome 7 - Changes f508 gene which codes for CFTR Protein
179
Q

Risk factors for cystic fibrosis?

A

Family History - Caucasians

180
Q

Pathophysiology of Cystic fibrosis?

A

Defective CFTR gene - Normally secretes CL- actively & Na+ passively (+H20) into ductal secretions making them thin + watery => With defective gene, ductal secretions are thicker with increased Na+ and Cl- retention

181
Q

What happens to the lungs in CF?

A

Impaired mucocilliary clearance as mucus extra thick ↑stagnation = ↑infection risk and difficulty breathing and ↑risk of bronchiectasis

182
Q

When is CF mostly diagnosed?

A

In childhood (90% before 8 y/o)

183
Q

Symptoms of CF?

A
  • Resp: thick + sticky sputum cough, recurrent upper respiratory tract infection, bronchiectasis GIT: thick secretions, pancreatic insufficiency, bowel obstruction Other : - males = atrophy of vas deferens + epididymis - very salty sweat
184
Q

Symptoms of CF in neonates?

A

Meconium ileus (bowel obstruction Due to earliest stool being too thick to pass through) - failure to thrive

185
Q

Investigations to diagnose CF?

A
  • Sweat test (Na+ and Cl- >60mmol/L in children) - Faecal elastase -ve/↓ (= obstruction as normally elastase produced by pancreas + found in faeces) - fHx, genetic testing (mutation in f508)
186
Q

Common infections in CF patients?

A

S.Aureus - H.Influenzae - P.aeroginosa (same as bronchiectasis)

187
Q

Treatment for CF?

A

Non curative - Conservative -> chest physio, no smoking - Drugs -> anti mucolytic, bronchodilator, pancreatic enzyme replacements + fat soluble vitamin supplements

188
Q

What is pleural effusion?

A

Excess fluid accumulation between visceral + parietal pleura layers

189
Q

How is fluid in pleural effusion categorised?

A

Fluid is either: 1) Transudative 2) Exudative

190
Q

What is transudative fluid?

A

↓Protein; <25 g/L - Due to ↑increased hydrostatic pressure or ↓oncotic pressure - TRANSparent fluid E.g congestive heart failure, liver cirrhosis, nephrotic syndrome

191
Q

What is exudative fluid?

A

↑Protein; >35g/L - Due to inflammation causing ↑vascular permeability - Cloudy e.g cancer, TB, pneumonia

192
Q

What is the Light’s criteria?

A

Used to determine if fluid is exudative when protein is 25-35g/L and therefore in the grey area

193
Q

Symptoms of Pleural effusion?

A

Generic: dyspnoea, pleuritic chest pain, cough, ↓breathing sounds - Dull percussion (↑increased fluid) on ipsilateral side

194
Q

Differential diagnosis for pleural effusion?

A

Pneumothorax however this has a hyper resonant sound when listened to, not dull percussion on ipsilateral side

195
Q

Investigations to diagnose Pleural effusion?

A

GS + 1st line: CXR = ↓costophrenic angles (‘blunting’) - excess fluid appears white +/- tracheal deviation Thoracentesis = aspiration of pleural fluid - tells us pH, lactate, WCC, trans or exudate

196
Q

Treatment of Pleural effusion?

A

Chest drain - If recurrent = pleurodesis - surgical fusing of pleural layers to prevent Fluid build up

197
Q

What is Pneumothorax?

A

Excess air accumulation in pleural space => causing ipsilateral collapse of lung

198
Q

Typical pneumothorax patient?

A

Tall thin males with connective tissue disorders (marfan’s, ED) +/- smokers, with some kind of trauma

199
Q

Types of pneumothorax?

A

Primary (spontaneously with no underlying cause) - Secondary (to a trauma or pathology)

200
Q

Pathophysiology of Pneumothorax?

A

pleural space Normally a vacuum - Breach in pleura ( Due to trauma or conn. tissue disorder) e.g subpleural bullae burst = abnormal connection between pleural space + airways (fistula)

201
Q

Symptoms of pneumothorax?

A

SOB - One sided sharp pleuritic Chest pain - decreased breathing sounds - Hyper resonant percussion ipsilaterally (Due to Increased air)

202
Q

Two types of pneumothorax?

A

1) Simple pneumothorax 2) Tension pneumothorax

203
Q

Differences between simple and tension pneumothorax?

A

Simple: - Non medical emergency, little tracheal deviation - Air can flow in/out of valve between alveoli + pleura => Unlikely to worsen with every breath Tension: - Medical emergency with contralateral tracheal deviation - One way valve (air into pleural space, not out) => worsens with each breath

204
Q

Investigations to diagnose pneumothorax?

A

Gold standard + 1st line:CXR = Excess fluid appears black + Tracheal deviation to other side * CT is more sensitive so useful in detecting smaller pneumothoraxes

205
Q

Treatment for smaller pneumothoraxes?

A

Self healing

206
Q

Treatment for larger pneumothorax?

A

Needle Compression (suck air out with a syringe) + Chest drain (One way air removal, air can only leave so longer term treatment) surgical treatment If its recurrent = pleurodesis

207
Q

What to do if tension pneumothorax is obvious?

A

Avoid chest xray and go straight to treatment

208
Q

Treatment for tension pneumothorax?

A

Insert large bore cannula into 2nd intercostal space at midclavicular line - needle decompression first and then chest drain

209
Q

What is Cor Pulomonale?

A

Right ventricle enlargement due to long term pulmonary (artery) hypertension => Leads to right heart failure

210
Q

What is pulmonary hypertension?

A

resting mPAP >25mmHg measured with heart catheterisation

211
Q

What does pulmonary hypertension often result in?

A

RHS heart failure (cor pulomonale)

212
Q

Causes of pulmonary hypertension categorised?

A

Pre capillary = pulmonary emboli, Primary pulmonary hypertension - capillary + lung = COPD, asthma - post capillary = LV failure - Chronic hypoxemia = COPD, altitude

213
Q

Pathophysiology of pulmonary hypertension?

A
  • Reactive pulmonary vasocontriction when hypoxic -> ↑increased vascular resistance and pressure => thus endothelial damage -> RVH + (right heart) failure
214
Q

How does a patient present with pulmonary hypertension?

A

Initially = exertional dyspnoea and fatigue Then right heart failure signs

215
Q

Signs of right heart failure?

A

Increased JVP - peripheral oedema - v waves prominent on JVP - louder S2 than normal

216
Q

Investigations to diagnose pulmonary hypertension?

A

CXR = RVH, enlarged proximal pulmonary artery ECG = RA dilation (p.pulmonary, peaked P waves > 2.5mm) ECHO = RVH Diagnostic (GS) = right heart catheter (>25mmHg)

217
Q

Treatment for pulmonary hypertension?

A
  • Phosphodiesterase-5 inhibitor (sildeiaful = viagra). - CCB (amlodipine) - Endothelin-1-antagonists/prostagladin analogues - Diuretics for oedema
218
Q

What is pharyngitis?

A

Inflammtion of pharynx +/- exudate

219
Q

Causes of pharyngitis?

A

Viral - EBV, adenoviruses Bacterial - group A beta haemolytic strep = s.pyogenes

220
Q

Bacteria that often causes otitis media and pharyngitis?

A

Streptococci => treatment is amoxicillin - aka flucloxacillin

221
Q

Symptoms of pharyngitis?

A

Sore throat + fever If viral = + cough + nasal congestion If bacterial = + exudate

222
Q

What disease should be ruled out when considering pharyngitis?

A

Rheumatic Fever - especially in children if bacterial

223
Q

What is rheumatic fever?

A

Systemic inflammatory disease - typically 2-4 weeks post group A strep infection

224
Q

What is sinusitis?

A

Inflamed mucosa of nasal cavity + nasal sinuses

225
Q

Cause of sinusitis?

A
  • Mostly viral causes (<10 days non purulent discharge) - Sometimes bacterial (>10 days, purulent)
226
Q

Bacterial causes of sinusitis and prevalence?

A

S.Pneumo (40%) H.Influenzae (30%) (self limiting)

227
Q

Treatment for bacterial causes of sinusitis?

A

Amoxicillin

228
Q

What is Otitis media?

A

Inflamed middle ear - typically in children

229
Q

Cause if otitis media?

A

Bacterial or viral

230
Q

Investigations to diagnose otitis media?

A

Otoscopy shows inflamed erythrmatous tympanic membrane

231
Q

What can sinusitis and Otitis media be linked too?

A

Meningitis contagious spread (direct to meninges, not through blood)

232
Q

What is epiglottitis?

A

Inflammation of epiglottis = obstructs airways = Mostly occurs in kids under 5

233
Q

Most common cause of epiglottitis?

A

H.influenzae

234
Q

Symptoms of epiglottitis?

A
  • TRIPODING (leant forward, mouth open, tongue out = max air in) - Sore throat - SOB
235
Q

Investigations to diagnose epiglottitis?

A

Gold standard= laryngoscopy XR = lateral radiograph => thumb print sign

236
Q

What is whooping cough?

A

Chronic cough caused by bordella pertussis (gram -ve bacilli) - Mainly in children

237
Q

Prevalence of whooping cough

A

90% of case under 5 years old

238
Q

Pathophysiology of whooping cough?

A

↑bordella virulence - Haemagglutinin + fimbrae adhere to URT - Adenylate cyclase toxin inhibits phagocyte chemotaxis - Perctussis toxin inhibits alveolar macrophages

239
Q

Symptoms of whooping cough?

A

Characteristic violent cough

240
Q

What is croup/laryngobronchitis?

A

Occasional complication of URTI particularly from parainfluenza + measles infection (children <3y/o)

241
Q

Symptoms of Croup/laryngobronchitis?

A

Hoarse voice + barking Cough (Croup) - Stridor (high pitched Wheeze when inhaling)

242
Q

Treatment for croup/laryngobronchitis?

A

Single dose dexamethasone

243
Q

What does type 1 respiratory failure entail?

A

Normal pCO2 with low pO2 indicates type 1 respiratory failure (only one is affected) (low PO2 indicates hypoxia and respiratory failure)

244
Q

What does type 2 respiratory failure entail?

A

Raised pCO2 with low pO2 indicates type 2 respiratory failure (two are affected)

245
Q

if there has been compensation in acidosis/alkalosis, is it acute or non acute?

A

Non acute -acute doesn’t occur with compensatory mechanisms

246
Q

What does an ABG tell us in terms of resp system?

A

Resp failure = acute or chronic

Haroon Phase 2A (14 decks)

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