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Phase 2a > Respiratory > Flashcards

Respiratory Flashcards

1
Q

What is FEV1?

A

The volume of air that can be forcibly expired in 1 sec

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2
Q

What is FVC?

A

The total volume of air that can be forcibly exhaled after maximum inhalation

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3
Q

If FEV1 is reduced so the FEV1/FVC is <0.7, what does this suggest?

A

Patient can’t expire air quickly enough, obstructive - asthma, COPD

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4
Q

What would it suggest if FVC was reduced so FEV1/FVC is >0.8?

A

Restriction - pulmonary fibrosis

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5
Q

What is type 1 respiratory failure?

A

low pO2 and low normal pCO2 -PE

fibrosis causes, lung fails to fill properly

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6
Q

What is type 2 respiratory failure?

A

Low pO2 and high pCO2 - hypoventilation
Obstruction causes can’t remove CO2 properly - codp , asthma

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7
Q

What is Chronic Obstructive Pulmonary Disease, COPD?

A

COPD is a disease state that is characterised by airflow obstruction, usually is progressive and isn’t fully reversible

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8
Q

What are the risk factors of COPD?

A
  • smoking
    -air pollutants
    -Alpha 1 Antitrypsin deficiency
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9
Q

What is alpha 1 anti trypsin?

A

A protein produced in your liver that helps protect your lungs - inhibits neutrophil elastase which degrades elastin

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10
Q

What are the 3 associations of the pathology of COPD?

A
  1. Chronic bronchitis
  2. Emphysema
  3. A1AT deficiency
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11
Q

What is Chronic bronchitis?

A

Hypertrophy and hyperplasia of mucous secreting glands. Chronic inflammation cells infiltrate bronchi and bronchioles causing luminal narrowing. Restricts airflow

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12
Q

What are the 3 pathophysiology changes in chronic bronchitis?

A

1.Mucus hypersecretion
2. cilliary dsyfunction
3.narrowed lumen
All increases the chance of infection and traps air inside

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13
Q

What would chronic bronchitis present with?

A

cough for 3+ months , over 2+ years with sputum

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14
Q

What is blue bloater associated with?

A

Chronic bronchitis - it is the typical presentation

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15
Q

What is Emphysema?

A

Destruction of elastin layer in alveoli ducts/ sacs and respiratory bronchioles. Elastin usually keeps walls open during expiration. Without elastic this causes air trapping and expiratory airflow limitation. Also large air sacs are called Bullae

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16
Q

What is pink puffer associated with?

A

The typical presentation of a patient with Emphysema

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17
Q

What is A1AT deficiency?

A

Autosomal codominnat inheritance. A1AT degrades neutrophil elastae to protect excess damage to elastin layer especially in the lungs. If this is deficient then NE levels are high causing panacinar Emphysema.

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18
Q

What is the typical presentation of someone with COPD?

A

Typically older patient with a chronic cough, with purulent sputum and extensive smoking history and Contant dyspnoea.
Blue boater or pink puffer presentation or usually both.

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19
Q

What is the presentation of a blu bloater?

A
  • Chronic purulent cough
    -dyspnoea
    -cyanosis
    -obesity
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20
Q

What is the presentation of a pink puffer?

A

pursed lip breathing
Barrel shaped chest
Hyperesonance

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21
Q

What is the dyspnoea grading scale MRC?

A

used to assess the baseline disability due to dyspnoea
1 - difficulty breathing during strenuous exercise
2/3
4 - difficulty when just doing minor tasks

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22
Q

What are the investigations for COPD?

A

Pulmonary function tests - spirometry = If FEV1/FVC <0.7 suggests COPD
-Irreversible on bronchodilators-
(<12% improved FEV1)
DlCO( diffusing capacity of CO across lung) = low in COPD
CXR- May show flattened diaphragm from hyperventilation and bullae formation

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23
Q

What are the treatments for COPD?

A
  1. Smoking cessation
  2. Vaccines - influenza/pneumoccal
  3. Short acting beta 2 agonists - Salbutamol
    4.Short acting beta 2 agonist and long acting beta 2 agonist - salmeratol and long acting anticholinergic agonist -tiotropium bromide
  4. SAB2A +LAB2A + LAM3A + ICS - inhaled corticosteroids
  5. Oxygen therapy - 15hr a day for 3 weeks if severe - <88%/90%
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24
Q

What are beta agonists?

A

Bronchodilators - increased cAMP = smooth muscle relaxation

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25
Q

What are anticholinergics?

A

Bronchodilators - promotes cGMP degradation = smooth muscle relaxation

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26
Q

What causes a COPD exacerbations?

A

Respiratory tract infections

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27
Q

How would you treat a COPD exacerbation?

A

Oxygen - titrate to improve hypoxaemia ( target saturation = 88-92% for COPD patient and 94-98% for normal)
- nebuliser salbutamol and ipatropium bromide
-ICS and Abx

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28
Q

What is Asthma?

A

Chronic reversible airway disease characterised by reversible airway obstruction, airway hyper responsiveness, inflamed bronchioles and mucus hyper secretion.

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29
Q

What is the epidemiology of Asthma?

A

-Commonly starts in childhood (3-5)
-More common in developed countries

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30
Q

What are the types of asthma?

A

Allergic - 70%
and non-allergic - 30%

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31
Q

What is allergic asthma?

A

IgE mediated; extrinsic Type 1 Hypersensitivity
- due to environmental trigger(Pollen, smoke, mould, antigens)
-consider genetics and hygiene hypothesis
- often early presentation

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32
Q

What is non-allergic asthma?

A

Non IgE mediated; intrinsic
- may present later in life, harder to treat
-associated with smoking

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33
Q

What are the triggers for asthma?

A

infection
allergens
cold weather
exercise
drugs - BB, aspirin

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34
Q

What is atopic triad?

A

atopic rhinitis
Asthma
Eczma
These 3 conditions together is known as atopy

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35
Q

What is samter’s triad?

A

A disease characterised by the triad:
- nasal polyps
-asthma
-aspirin sensitivity

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36
Q

What is the pathology of asthma?

A

Overexpressed TH2 cells in airways exposed to trigger –> TH2 cytokine release IL3,4,5,13, IgE production and eosinophils recruitment –> IgE mast cell degradation:
-histamines
-Leukotriene
-Tryptase
Esonphilia release of toxic proteins e.g MBP —>

This causes bronchial constriction and mucus hyper secretion and over time = chronic remodelling

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37
Q

What is chronic remodelling?

A

bronchial scarring decreases lumen size and increases mucus secretion

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38
Q

What is the presentation of someone with asthma?

A

Wheeze, cough, chest tightness, SOB
- typically episodic with triggers and diurnal variation
- often younger patient

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39
Q

What would show if you do a microscopy of mucus that had been coughed up? ASTHMA

A

curschmanns spirals
Charcot leyden crystals

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40
Q

What are the episodes classed as?

A

Moderate - PEF = 50-75%
Severe - PEF= 33-50% / can’t finish sentences
Life threatening - PEF -<33%, low consciousness
Fatal - hypercapnic

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41
Q

What are the investigations for asthma?

A

FeNO is high
and spirometry shows obstruction = FEV1/FVC<0.7
- but bronchodilator reversible = >12% FEV1 increase = asthma

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42
Q

What is FeNO test?

A

FeNO devices are used to diagnose asthma. FeNO devices measure fractional exhaled nitric oxide in the breath of patients. Nitric oxide is a biomarker for asthma which provides an indication of the level of inflammation in the lungs.

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43
Q

What is the treatment for Asthma?

A
  1. SAB2A
  2. SAB2A + ICS
    BEFORE DRUG ADDITION ASSESS TECHNIQUE AND COMPLIANCE
  3. SAB2A +ICS + LTRA
    4.SAB2A + ICS +LAB2A -/+ LTRA
  4. Increase ICS dose
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44
Q

What is LTRA?

A

Leukotriene receptor antagonist - Montelukast

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45
Q

What is the treatment for asthma exacerbations?

A

OSHITME :

  • O2
    -Nebulised SAB2A
    -ICS Hydrocortisone
    -IV MgSO4 - bronchodilation
    -IV theophylline
    -MgSO4 IV
    -escalate

BIPAP - bilevel positive airway pressure
+/- Abx - if infection present

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46
Q

What is the epidemiology of lung tumours?

A
  • Bronchial carcinoma most common
    -M>F
    -1/3 of all cancer deaths
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47
Q

What are common metastases sites?

A
  • bone
  • liver
    -adrenals
    -brain
    -lymph nodes
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48
Q

What are the types of Lung cancers?

A

Pleura = mesothelioma
Lung parenchyma= bronchial - Small cells or non small cells (squamous, adenocarcinoma, carcinoid, large cell)

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49
Q

What is Mesothelioma?

A

Malignancy of the pleura

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50
Q

What is the cause of mesothelioma?

A

Asbestos - typically doesn’t present until decades after exposure - latent period

Typically males, 40-70

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51
Q

What is the presentation of mesothelioma?

A

Cancer Sx - Weight loss, night pain
Lung Sx - shortness of breath, persisted cough, pleuritic chest pain
- tumour may press on nearby structures - recurrent laryngeal (hoarse voice)
- also signs of metastases-bone pain

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52
Q

What is the diagnosis for mesothelioma?

A

-CXR + CT - imaging first line - pleural thickening (+/- effusion)
-CA - 125 (Cancer antigen 125) high level - non specifically raised in many tumours; sensitive but not specific
-Lung Biopsy = diagnostic

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53
Q

What is the treatment for mesothelioma?

A

-Aggressive tumour BUT isn’t like to metastasise as affects pleura; pleura isn’t found everywhere in the body
- usually palliative
-If found early can try surgery, chemo/ radio ( generally resistant)

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54
Q

What is Bronchial carcinoma?

A

Malignancy of lung parenchyma - can be either small cell (15%) or non small cell(85%)

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55
Q

What are the risk factors of bronchial carcinoma?

A
  • smoking
    -asbestos
    -coal
    -ionising radiation
    -lung disease already present
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56
Q

Who is affected by small cell bronchial carcinoma?

A

Exclusively smokers

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57
Q

What is associated by SCLC?

A

Paraneoplastic syndromes:
-ectopic ACTH –> cushings
-Ectopic ADH –> SIADH
-Lambert Eaton syndrome (autoimmune disorder of nmj)

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58
Q

What is SCLC?

A
  • fast growing- early mets
    -central lung lesions
  • most agressive
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59
Q

What are the types of non small cell bronchial carcinoma?

A
  • squamous
    -Adenocarcinoma
    -Carcinoid tumours
    -Large cell
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60
Q

What is Squamous cell carcinoma?

A
  • 25%
    -mostly smokers
    -affects central lung, lesions with central necrosis
    May secrete PTH -> hypercalcemia
    -arise from lung epithelium
    -locally spread mostly
    -late mets
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61
Q

What can cause hypertrophic pulmonary osteoarthropathy?

A

Squamous cell carcinoma as secretes PTH so hypercalcemia.
- clubbing
-arthritis
-periostitis
Biggest cause of secondary HPO = adenocarcinoma

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62
Q

What is adenocarcinoma?

A

-40%
-commonly asbestos
-affect peripheral lung
-arise from mucus secreting glandular epithelium
-Mets common -> bone, brain, adrenals, lymph nodes,liver

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63
Q

What causes carcinoid tumour?

A

Associated with genetics; MEN1 mutation and neurofibromatosis 1.

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64
Q

What is carcinoid tumour?

A

Neuroendocrine tumour secretes serotonin, arise in GIT and sometimes lung.
Symptoms only appear when Liver mets present

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65
Q

What are the general symptoms of Bronchial carcinomas?

A

chest pain, cough, haemoptysis, cancer Sx, signs of mets (hoarse voice,horners syndrome, Pemberton sign)

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66
Q

what is the diagnosis of bronchial carcinoma?

A

-Imaging first line - CT,CXR
-Diagnostic -bronchoscopy/ lung biopsy
-MRI - staging TNM

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67
Q

What are the treatments for small cell carcinoma?

A

More aggressive so if early consider chemo/radio
Metastasised = palliative

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68
Q

What is the treatment for non small cell carcinoma?

A

Less aggressive - early surgical excision
Metastasised = chemo/radio
Mab therapy cetuximab

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69
Q

Why are secondary lung tumours more common/likely than primary lung tumours?

A

Lungs oxygenate 100% blood therefore all blood comes to the lungs therefore higher mets risk. ESP: breast, kidney, bowel and bladder cancers

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70
Q

What is a Pancoast tumour?

A

Tumour in lung apex metastasises to necks sympathetic plexus - causing horners syndrome ; ptosis, myosis, andhidrosis

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71
Q

What is a BALT lymphoma?

A

A non hodgkin lymphoma originate in bronchi (bronchial associated tissue lymphoma)

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72
Q

What is a pulmonary embolism?

A

where the pulmonary artery circulation is blocked by a blood clot, typically a DVT

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73
Q

What are the risk factors of a PE?

A

anything affecting the virchows triad + FHx

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74
Q

What is the virchows triad?

A

3 components of thrombus formation
- endothelial injury
-venous statsis
-hypercoaguability

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75
Q

What causes endothelial injury?

A
  • smoking
    -HTN
    -trauma
    -vascular catheters
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76
Q

What causes venous stasis?

A
  • immobility (long flight)
    -post surgery
    -varicose veins
    -AF
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77
Q

what causes hypercoaguability?

A
  • acquired: pregnancy, obesity, malignancy
    -inherited: factor v leiden, antiphospholipid syndrome, Protein c+s deficiency
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78
Q

What is the pathology of a pulmonary embolism?

A

DVT embolisms and enters right side of heart via IVC -> occluding pulmonary artery small vessels causing A-a gradient to increase and a V/Q mismatch (ventilation with no perfusion) - this causes reactive bronchoconstriction therefore dyspnoea and smaller airways ->embolus incraeses pulmonary blood pressure -> pul HTN -> RV strain/ RH

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79
Q

What is A-a gradient?

A

The Alveolar–arterial gradient, is a measure of the difference between the alveolar concentration of oxygen and the arterial concentration of oxygen

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80
Q

What is a V/Q mismatch?

A

happens when part of your lung receives oxygen without blood flow or blood flow without oxygen

LOW- no ventilation with perfusion

High - ventilation, no perfusion

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81
Q

What is the presentation of a pulmonary embolism?

A

-Classically sudden onset SOB + pleuritic chest pain with swollen painful calf (DVT) and Hx of immobility
-Haemoptysis
-increased JVP
-tachycardia and dyspnoea
-signs of RHF= hypotensive, tachycardia, peripheral oedema

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82
Q

What are the investigations for PE?

A

Wells score = <4 - unlikely so do D-dimer = <500ng/ml PE unlikely

> 4 PE likely - Gold standard -CTPA - clot = PE and no clot exclude PE

-ECG
-CXR - usually normal (Ddx pleural effusion = visible on CXR)

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83
Q

What is D-dimer?

A

measures plasmin therefore measures clot burden - sensitive but not specific

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84
Q

What is the wells score?

A

the most widely used clinical decision tool for the diagnosis of deep vein thrombosis (DVT) - 8point maximum

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85
Q

What are the ECG characteristics?

A

S1Q3T3 =
- S waves deep in lead 1
-Q waves deep in lead 3
-T waves inverted in lead 3
RBBB V1-3 -> RSR pattern due to right axis deviation
-sinus tachycardia

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86
Q

What is the treatment for PE?

A

Haemodynamically stable = 1st line - DOAC - apixaban (LMWH if DOAC CI)
2nd Line - warfarin

Haemodynamically unstable = Thrombolysis (clot busting)
- alteplase If fails - catheter embolectomy

87
Q

What is the prophylaxis for PE?

A
  • compression stockings
    -regular walking
88
Q

What is pneumonia?

A

Fluid exudation into alveoli due to inflammation from an infection - typically bacterial but can be viral.

89
Q

What are the two forms of pneumonia?

A

Community acquired pneumonia -CAP

Hospital acquired pneumonia -HAP

90
Q

What is community acquired pneumonia?

A

In the community or <48hr in a hospital

91
Q

What bacteria causes CAP?

A

-S.pneumonia - mc
-H.influenza
-mycoplasma pneumonia - causes atypical pneumonia
-others:
-S.aures
-Legionella
-chlamydia pneumonia

92
Q

What is strep pneumonia?

A
  • gram postive cocci
    -alpha haemolytic
    -optochin sensitive
93
Q

What fungi can cause pneumonia?

A

Pneumocystis jiroveci - in immunocompromised patients - AIDS defining illness

94
Q

What is HAP?

A

Hospital acquired pneumonia, >48hr of hospital admission

95
Q

What bacteria causes HAP?

A

P. auerginosa
E.coli.
Klebsiella
ALL of the above gram negative aerobic bacilli
(MRSA)

96
Q

How can you get pneumonia?

A

Typically from inhaled pathogens, can also be from aspiration.

97
Q

What are the risk factors of pneumonia?

A
  • immunocompromised (HIV, long term steroids)
    -IVDU(s.aures)
    respiratory pre existing disease
    -v.young/ old
98
Q

What is typical pneumonia?

A

Bacteria invades + exudate forms inside alveoli lumen + sputum

99
Q

What is atypical pneumonia?

A

Bacteria invades + exudate forms in interstitial of alveoli + dry cough

100
Q

What is the presentation of pneumonia?

A
  • productive cough with rusty coloured sputum (purilent)
    -pyrexic due to infection
    -pleuritic chest pain - worse with breathing and cough
    -tachypnoea, dyspnoea( tachycardia and hypotension)
  • confusion in elderly

ATYPICAL - dry cough, low grade fever

101
Q

What is the diagnosis of pneumonia?

A

-1st line diagnostic: CXR shows consolidation - airbronchogram -air fused bronchi made visible by specified fluid filled surrounding alveoli
-Sputum sample + culture
-CAP assess severity

102
Q

How do you assess the severity of CAP?

A

CURB65:

Confusion - abbreviated mental test
Urea nitrogen >7mmol/L
Respiration Rate>30/min
BP - low systolic <90mmHg or diastolic <60
Age >65

103
Q

What would happen if the score was 1?

A

3% mortality - Outpatient, oral Abx and discharge

104
Q

What would happen if the patient scored 2?

A

Consider short hosp stay + Abx

105
Q

What would happen if the patient scored 3 and above?

A

15% mortality, Hospital. –> ICU +IV abx

106
Q

What is the treatment for pneumonia?

A

02 (stats 94-98%, broad spec Abx, Analgesia (NSAIDS) for pleuritic chest pain

107
Q

What antibiotics would be used for CAP - CURB 0-2?

A

Amoxicillin

108
Q

What antibiotics would be prescribed for CAP - CURB 3 to 5?

A

CoAmoxiclav + Clarithromycin

109
Q

What would be needed to treat legonella?

A

Clarithromycin - notifiable disease

110
Q

What is aspiration pneumonia?

A
  • seen in presentation with stroke, bulbar palsy and myasthenia gravis
    -Aspiration of gastric contents into lungs can be fatal due to destructiveness of gastric acid
111
Q

What is the epidemiology of tuberculosis?

A
  • top infectious killer in the world
  • global incidence on the decline
    -Most commonly seen in Africa and Asia
112
Q

What is tuberculosis?

A

Granulomatous caseating disease, caused by mycobacteria

113
Q

What are the 4 species that make up mycobacterium complex?

A
  • M. tuberculosis
    -M. africanum
    -M. microtis
    -M.bovis

These cause TB

114
Q

Where is tuberculosis most common?

A
  • South Asia (India ,China, Pakistan) and Africa

-1.7billion worldwide have TB (mostly latent)

115
Q

How is TB spread?

A

Airborne

116
Q

What are the risk factors of TB?

A
  • country + travel associated
  • immunocompromised (HIV)
  • IDVDU
    -smoking + alcohol
    -Ascending age
117
Q

What are MTC features?

A
  • non motive and non spore forming
    -mycocilic acid capsule
  • stain acid fast bacilli with ziehl Nielsen - go red
    -resistant to phagocyte killing
  • slow growing 15-20hr
118
Q

What is the pathology of tuberculosis?

A

TB phagocytosed but resist killing therefore form granuloma –> T cells recruited and central region of granuloma undergoes caseating necrosis –> forms primary Ghon focus in upper parts of the lung(increased ventilation)–> Ghon focus spreads to nearby lymph nodes - Ghon complex (in most infection contained within granulomas, but TB doesn’t die - known as latent TB) –> if TB spreads systemically = Miliary TB

119
Q

What is the presentation of tuberculosis?

A

If symptomatic (not latent as latent =Asx)

-Characteristic night sweats and weight loss
-Pyrexia, chest pain and patient looks very unwell
-extrapulmonary - meningitis, skin change, TB pericarditis Sx, joint pain

120
Q

What is the diagnosis for tuberculosis?

A

-Mantoux skin test - (red lump if TB) (latent or active)
-Sputum culture 3x - the acid fast bacilli = bright red with ziehl Neelson stain
-CXR biopsy

121
Q

What is the treatment for TB?

A

RI2PE6:

Rifampicin - 2months - SE: haematuria
Isoniazid - 2months -SE: peripheral neuropathy
Pyramidine - 6months - SE: hepatitis
Ethambutol - 6months-SE: eye problems - optic neuritis
Refer to public health England

122
Q

What is an interstitial lung disease ?

A

interstitial lung disease (ILD) is an umbrella term used for a large group of diseases that cause scarring (fibrosis) of the lungs. The scarring causes stiffness in the lungs which makes it difficult to breathe and get oxygen to the bloodstream.

123
Q

What is a granulomatous ILD?

A

Sarcoidosis

124
Q

What is an inhalational ILD?

A

Hypersensitivity pneumonitis
Pneumoconiosis (Asbestos/silicosis)

125
Q

What are idiopathic pneumonias ILD?

A

Pulmonary fibrosis -most common ILD
Non pulmonary fibrosis

126
Q

What are conn tissue ILD?

A

Scleroderma, R.A

127
Q

What are drug induced ILD?

A

Amiodarone, biemycin

128
Q

What are other ILD?

A

Good pastures, vasculitis

129
Q

What is pulmonary fibrosis?

A

-Commonest ILD, seen in older men who smoke, idiopathic - unknown cause

130
Q

what are the risk factors of pulmonary fibrosis?

A

smoking, occupational (e.g dust), drugs(methotrexate), Viruses (EBV,CMV)

131
Q

What is the pathology of pulmonary fibrosis?

A

pulmonary fibrosis is progressive scarring –> type 1 respiratory failure

132
Q

What is the presentation of pulmonary fibrosis?

A

exertion dyspnoea, dry unproductive cough

133
Q

What is the diagnosis for pulmonary fibrosis?

A

Spirometry = restriction; FEV1/FVC >0.7 BUT FVC lower than normal <0.8
Gold standard imaging = CT chest= ground glass lungs - traction bronchiolectasis

134
Q

What is traction bronciolectasis?

A

dilation of bronchioles due to airway damage

135
Q

What is the treatment for pulmonary fibrosis?

A

smoking cessation + vaccines
Pirfenidone , nintendinib - help slow down the process of scarring
Surgery- lung transplant

136
Q

What is pneumoconiosis?

A

Occupationally acquired interstitial lung disease caused by inhalation of mineral dust.

137
Q

What is silicosis?

A

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

138
Q

What is asbestosis?

A

Inhalation of asbestos; affects pleura ; mesothelioma

139
Q

What is sarcoidosis?

A

Multi system granulomatous disease with lung involvement. Characterised by non caseating granulomas throughout the body.

140
Q

What is the epidemiology of sarcoidosis?

A

Common in women 20-40y.o African Caribbean

141
Q

What is the presentation of sarcoidosis ?

A
  • fever, fatigue
    -dry cough, dyspnoea
    -eye lesions (anterior uveitis), lupus permio- blue-red nodules on nose and cheeks
    -erythema nodosum
    -bilateral hilar lympadenopathy
142
Q

What is the diagnosis for sarcoidosis?

A

-CXR (staging 1-4) - shows bilateral hilar adenopathy + pulmonary infiltrates
- Diagnostic : biopsy shows non caseating granuloma
-Serum Ca high
-Serume ACE high

143
Q

What is the treatment for sarcoidosis?

A

Early stages - self resolving
Later stages, 2-4 (symptomatic) = corticosteroids

144
Q

What is lofgren syndrome?

A

A subset of sarcoidosis
Triad of :
-erythema nodosum
-bilateral hilar adenopathy
-fever

145
Q

What is hypersensitivity pneumonitis?

A

T3 hypersensitivity; immune antibody- antigen complex deposition in lung tissues causing immune hyper response.

146
Q

What are the risk factors of hypersensitivity pneumonitis?

A

occupation (e.g farmer_, bird keeping

147
Q

What are the types of of hypersensitivity pneumonitis ?

A

Farmers lung - (mc) - mouldy hay
Pigeon fancier’s lung - bird droppings
Malt worker’s lung
Cheeseworker’s lung
Humidifier fever

148
Q

What is the treatment for hypersensitivity pneumonitis?

A

remove allergen

149
Q

What is good pastures syndrome?

A

T2 autoimmune hypersensitivity response

150
Q

What is the pathology of goodpasture’s syndrome?

A

Autoantibodies ANTIGBM attack lungs and kidneys - lung fibrosis, glomerulonephritis

151
Q

What is the diagnosis of good pasture’s syndrome?

A

lung and kidney biopsy = damage + Ig deposition
Serum Anti - GBM positive

152
Q

What is the treatment of goodpasture’s syndrome?

A

supportive
corticosteroids
plasma exchange - rid of anti - GBM

153
Q

What is Wegener’s granulomatosis (Granulomatosis with polyangitis)

A

Granulomatosis vasculitis where small and medium blood vessels become inflamed typically affecting the ENT< lungs and kidneys.
c-ANCA associated vasculitis

154
Q

What is the presentation of GPA?

A

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

155
Q

What is the diagnosis of GPA?

A

cANCA positive

156
Q

What is the treatment for GPA?

A

Corticosteroids
Immunosuppression - rituximab

157
Q

What is Bronchiectasis?

A

permanent dilation of bronchioles and excessive mucus in them - usually affects lower lobes

158
Q

What is the pathology of bronchiectasis?

A

irreversible dilation, loss of cilia and mucus hyper secretion, increased risk of infection as low muco-ciliary clearance

159
Q

What are the risk factors of bronchiectasis?

A

-most common after an infection (TB,pneumonia)
-CF,HIV

160
Q

What is the presentation of bronchiectasis?

A

productive cough with lots of sputum, dyspnoea

161
Q

What is the diagnosis of bronchiectasis?

A

Imaging - CXR -
-High Resolution CT gold standard = dilated thickened bronchi (signet ring sign) + cysts at end of bronchioles
-Spirometry = obstructive FEV1/FVC <0.7
-sputum culture. - (check infection) - H.influenza , pseudomonas aeruginosa, s.aures, s.pneumonia

162
Q

What is the treatment for bronchiectasis?

A

non curative
conservative - chest physio and stop smoking
bronchodilators
Abx for infections
H.influenza and s.pneumonia = Amoxocillin
Pseudomonas aeruginosa = ciprofloxacin
S.aures= flucloxacillin

163
Q

What is cystic fibrosis?

A

Autosomal recessive condition, a mutation in the CFTR gene on chromosome 7 which causes a defective CFTR production. Most commonly the F508 mutation.

164
Q

What does CFTR stand for?

A

Cystic fibrosis transmembrane conductance regulator

165
Q

What are the risk factors of cystic fibrosis?

A

FHx, caucasians - mostly diagnosed in childhood - 90% before 8 years old

166
Q

What is the pathology of CF?

A

Defective CFTR gene - normally secretes CL- (actively)and Na+(+H2O) (passively) into ductal secretions therefore making them thin and watery. Now they are thicker with high retention of Na+ and Cl-.
Lung - impaired mucociliary clearance as mucus is extra thick therefore stagnation causing an increase in infection risk and difficulty breathing and increased risk of bronchiectasis .

167
Q

What is the presentation of cystic fibrosis?

A

Resp - thick sticky sputum cough, recurrent upper respiratory infection, bronchiectasis
Neonates - Meconium ileus (earliest stool too thick to pass through bowel –> bowel obstruction) + failure to thrive
GIT- thick secretions, pancreatic insufficiency, bowel obstruction
Other - salty sweat, atrophy of vas deferens + epididymis (infertility)

168
Q

What is the diagnosis for cystic fibrosis?

A

-Sweat test - Na+ and Cl- >60mmol/L in children
-Fecal elastase negative/ low = normally elastase produced by pancreas + found in faeces; obstruction in CF may mean negative
-FHx, genetic testing - F508 mutation

169
Q

What is the treatment for CF?

A

Non curative :
Conservative - chest phscion, no smoking
Drugs - mucolytics, bronchodilators, pancreatic enzyme replacements

170
Q

What is the treatment for CF?

A

Non curative :
Conservative - chest phscion, no smoking
Drugs - bronchodilators, pancreatic enzyme replacements, prophylactic antibiotics

171
Q

What antibiotic is used for Staphylococcus aureus?

A

Flucloxacillin

172
Q

what antibiotic is used to treat Haemophilus influenza?

A

Amoxicillin

173
Q

What antibiotic is used to treat pseudomonas aeruginosa?

A

Ciprofloxacin

174
Q

What is pharyngitis?

A

Inflammation of pharynx +/- exudate

175
Q

What are the causes of pharyngitis?

A

Viral - EBV, adenoviruses
Bacterial - group A haemolytic strep; streptococcus pyogenes

176
Q

What is the presentation of pharyngitis?

A

sore throat + fever
Viral = +cough + nasal congestion
Bacterial = +exudate

177
Q

What is sinusitis?

A

inflamed mucosa of nasal cavity and nasal sinuses

178
Q

What are the causes of sinusitis?

A

mostly viral (10 days, non purulent discharge )

Sometimes bacterial >10 days, purulent -S.pneumonia (40%), H.influenza(30%)

179
Q

What is Otitis media?

A

-inflamed middle ear, typically children
-bacterial or viral

180
Q

what is the diagnosis of otitis media?

A

otoscope shows inflamed erythematous tympanic membrane

181
Q

What can be linked to Meningitis contagious spread?

A

Sinusitis and otitis media

182
Q

What is epiglottitis?

A

Inflammation of epiglottis; obstructs airway. Mostly children <5

183
Q

What is the most common cause of epiglottitis?

A

H. influenza

184
Q

What is the presentation of epiglottitis?

A

Tripoding (leant forward, mouth open and tongue out=max air in), sore throat, SOB

185
Q

What is whooping cough?

A

chronic cough caused by bordetella pertussis (gram neg bacillus) - mainly children 90% - <5 years old

186
Q

What is the pathology of whooping cough?

A

Bordetella has a high virulence
-Hemaggultuinin and fimbree adhere to urt
-adenylate cyclase toxin inhibits phagocyte chemotaxis
-pertussis toxin inhibits alveolar macrophages

187
Q

What is the presentation of a whooping cough?

A

classic inspiratory whoop

188
Q

What is croup/laryngobronchitis?

A

An occasional complication of URT infections, particularly those caused by parainfluenza and measles - most severe in children under 3

189
Q

What is the presentation of croup/laryngobronchitis?

A

hoarse voice, barking cough, inspiratory stridor - high pitched wheeze when inhaling

190
Q

What is the treatment for coup?

A

single dose dexamethasone

191
Q

What is pleural effusion?

A

excess fluid accumulated between visceral and parietal pleural layers

192
Q

What is transudative fluid?

A

Low protein - <25g/L
Due to high hydrostatic pressure or low oncotic pressure - usually from liver cirrhosis, nephrotic syndrome
- transparent fluid

193
Q

What is exudative fluid?

A

High protein >35g/L
Due to inflammation causing high vascular permeability e.g cancer, TB, pneumonia
-cludy fluid

194
Q

What is light criteria?

A

used to determine whether a pleural effusion is exudative or transudative -when protein level between 25-35

195
Q

What is the presentation of pleural effusion?

A

Generic dyspnoea, pleuritic chest pain, cough, low breathing sounds
- dull percussion(high fluid) on ipsilateral side

196
Q

What is the diagnosis of pleural effusion?

A

-Gold standard - CXR - low costophrenic angles (blunting), excess fluid appears white +/- tracheal dilation
-Thoracentesis (aspiration of pleural fluid) = sample pleural fluid - pH,Lactase,WCC,Microscopy, transudate or exudate

197
Q

What is the treatment for pleural effusion?

A

Chest drain
- if recurrent - pleurodesis Surgical fusing of pleural layers to prevent fluid building )

198
Q

What is pneumothorax?

A

Excess air accumulation in pleural space, causing ipsilateral collapse

199
Q

What is the pathology of pneumothorax?

A

-Can be primary - spontaneous or secondary to trauma
pleural space normally a vacuum (and air)
- breach in pleura (trauma)e.g subpleural bullae burst, abnormal connection (fistula) between pleural space and airways

200
Q

What is the presentation of pneumothorax?

A

Typical presentation= tall thin males with connective tissue disorders (Marfans,50) +/- smokers, some kind of trauma

201
Q

What are the symptoms of pneumothorax?

A

SOB, one sided sharp pleuritic chest pain, low breathing sounds
- hyper resonant percussion ipsilaterally as air increase

202
Q

What is the diagnosis of pneumothorax?

A

GS, 1st line - CXR - excess fluid appears black, tracheal deviation to other side

203
Q

What is the treatment for pneumothorax?

A

-small self healing
-Larger - needle decompression(suck out with syringe)
- chest drain(more longer term treatment, one way air removal)
-surgical - pleurodosis if recurrent

204
Q

What is simple pneumothorax?

A
  • Non medical emergency, little tracheal deviation
    -air can flow in and out of valve between alveoli and Plura therefore doesn’t or is unlikely to worsen with every breath
205
Q

What is tension pneumothorax?

A

-Medical emergency
-air can flow into pleural space but can’t leave therefore increase in intra pleural pressure with every breath( can even press on heart and cause cardiac Sx)

206
Q

What is the treatment for tension pneumothorax?

A

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

207
Q

What is pulmonary hypertension?

A

resting mean pulmonary arterial pressure >25mmHg measured with right heart catheterisation. Often results RHF; cor pulmonale

208
Q

What is the pre capillary cause of pulmonary hypertension?

A

Pulmonary emboli, primary pulmonary HTN

209
Q

What is the the post capillary cause of pulmonary hypertension?

A

LV failure

210
Q

How does chronic hypoxia cause pulmonary hypertension?

A

COPD, altitude

211
Q

What is the pathology of pulmonary hypertension?

A

Reactive pulmonary vasoconstriction when hypoxia ( all causes cause hypoxia due to low perfusion to tissues) –> increased pulmonary vascular resistance and pressure therefore endothelial damage –> RVH and failure

212
Q

What is the presentation of pulmonary hypertension?

A

Initially - exertion dyspnoea and fatigue
Then RHF signs :
-increased JVP
-peripheral oedema
-Louder S2 than normal

213
Q

What is the diagnosis of pulmonary hypertension?

A

CXR - RVH - enlarged proximal pulmonary artery
ECG- RA dilation, peaked p waves
Echo - RVH
Diagnostic (GS) - right heart catheter (>25mmHg)

214
Q

What is the treatment for pulmonary hypertension?

A
  • phosphodiesterase 5 inhibitor (sildenafil)
    -CCB - amlodipine
    -Endothelin-1 antagonists
    =Diuretic for oedema

Phase 2a (9 decks)

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