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Medicine Year 2 2 > Respiratory > Flashcards

Respiratory Flashcards

1
Q

CHRONIC OBSTRUCTIVE PULMONARY DISEASE

What features show it is more likely a patient has COPD than Asthma?

A

1) Onset >35
2) Smoking/pollution related
3) Chronic Dyspnoea
4) Sputum production

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2
Q

What is Chronic Bronchitis?

A
  • Cough and sputum production for 3+ months in 2 consecutive years
  • Permanent narrowing of the airways
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3
Q

What are the causes of Chronic bronchitis?

A
  • mucous gland hypertrophy and hyperplasia

- bronchial wall inflammation and mucosal oedema

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4
Q

How would a patient appear if they had Chronic Bronchitis?

A

’ Blue Bloaters’

  • Overnight
  • Peripheral Oedema
  • Cyanosed
  • Low PaO2 and high PaCO2
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5
Q

why should we be careful when giving O2 therapy to someone with Chronic bronchitis?

A

They rely on their hypoxic drive to breath as their respiratory centres are insensitive to CO2. If we take their hypoxic drive away by giving O2 this could be fatal to the patient

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6
Q

What is Emphysema?

A

Dilation and destruction of alveolar walls distal to terminal bronchioles

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7
Q

What does dilation and destruction of alveolar walls lead to?

A

1) Decreased elastic recoil (keeps airways open during expiration)
2) Increased air trapping = increased dead space

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8
Q

How does a patient with Emphysema appear?

A

‘Pink Puffer’

  • thin
  • hyperinflated chest
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9
Q

How is Respiration driven?

A

an increase in PaCO2

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10
Q

Pathology of Cigarette smoke and what it causes

A

1) - Mucous gland hypertrophy
- increase in immune cells (neutrophils, macrophages, lymphocytes)
- release of inflammatory mediators (elastases, proteases, IL-1, TNF-8)

2) This increase in inflammation breaks down the lung parenchyma

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11
Q

CHRONIC OBSTRUCTIVE PULMONARY DISEASE

Signs and Symptoms?

A

symptoms

1) Chronic productive cough
2) Wheeze
3) Dyspnoea

signs

1) Breathless
2) Tachypnoea
3) Prolonged expiration
4) hyperinflated chest
5) Decreased lung expansion
6) Use of accessory muscles
7) wheeze

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12
Q

CHRONIC OBSTRUCTIVE PULMONARY DISEASE

Diagnosis?

A

1) FEV1/FVC= <0.7

2) INCREASED TLC and RV

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13
Q

CHRONIC OBSTRUCTIVE PULMONARY DISEASE

What can be seen on bloods, CXR and ABG

A

bloods= increased packed cell volume

CXR= hyperinflated lungs and flat diaphragm

ABG= decreased PaO2

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14
Q

CHRONIC OBSTRUCTIVE PULMONARY DISEASE

Stages of COPD?

A

stage 1= <80% FEV1 - predicted
stage 2= 50-79% FEV1
stage 3= 30-49% FEV1
stage 4= <30% or <50% FEV1 if respiratory failure

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15
Q

CHRONIC OBSTRUCTIVE PULMONARY DISEASE

What must all diagnosed patients receive

A

Steroid Trial:

Oral prednisolone for 2 weeks and if FEV1 rises by >15% COPD is steroid responsive

therefore they may benefit from long term inhaled corticosteroids

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16
Q

CHRONIC OBSTRUCTIVE PULMONARY DISEASE

Treatment?

A
  • cessation of smoking and BMI control
  • SAB2A and LAB2A if persists
  • short acting antimuscarinic (ipratropium) may be enough for mild
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17
Q

CHRONIC OBSTRUCTIVE PULMONARY DISEASE

treatment of severe?

A

1) LAB2A
2) Corticosteroids
3) Long term oxygen therapy

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18
Q

CHRONIC OBSTRUCTIVE PULMONARY DISEASE

What is an acute exacerbation?

A 
respiratory failure/ 
2/3 of:
1) Worsening dyspnoea
2) Worsening wheeze
3) Increased coughing
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19
Q

CHRONIC OBSTRUCTIVE PULMONARY DISEASE

treatment of an acute exacerbation?

A

Low conc 02 through venturi mask (SaO2 88-92%)

Abx if infective

  • salbutamol
  • prednisolone
  • ipratropium
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20
Q

ASTHMA

Characteristics?

A

1) bronchial muscle contraction - triggered by stimuli
2) Mucosal swelling and inflammation - mast degranulation = mediator and histamine release
3) Increased mucous production

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21
Q

ASTHMA

Classifications?

A

Eosinophilic- Extrinsic (atopic) - allergens proven by +ve skin prick reactions

& Intrinsic

Non- eosinophilic

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22
Q

ASTHMA

Aetiology?

A
  • Individuals who readily develop IgE against common allergens
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23
Q

ASTHMA

Genetic Cause?

A

IL-4 clusters on chromosome 5. this produces IL-3,4,5 &13

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24
Q

ASTHMA

Environmental cause?

A

childhood exposure to allergens (hygiene hypothesis)

if you grow up in a clean area your risk is increased

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25
Q

ASTHMA

Pathology of the inflammation?

A
  • Mast cells, eosinophils, T-lymphocytes and dendritic cells increased in bronchial wall

1) T- cells release IL-3,4,5 &13
2) IL-4 &13 produce IgE instead of B-cells/ antibodies
3) IgE attaches to mast cell= degranulation when inhaled allergens are encountered
4) Inflammatory mediator and histamine released

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26
Q

ASTHMA

Pathological changes to the airway

A
  • Bronchial Smooth muscle undergoes hypertrophy and hyperplasia
  • airway wall thickened by deposition of collagen below the basement membrane
  • metaplasia of respiratory epithelium
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27
Q

ASTHMA

How many people suffer in the U.K?

A

5-8%(more in developed countries (hygiene hypothesis)

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28
Q

ASTHMA

Precipitants?

A
  • fumes
  • exercise
  • viral infections
  • cold air
  • Beta blockers
  • NSAIDS
  • smoking
  • stress
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29
Q

ASTHMA

Clinical features?

A

1) Wheeze
2) Dyspnoea
3) Tight chest
4) tachypnoea

these all vary diurnally (daily)

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30
Q

ASTHMA

what jobs may increase your chance of developing or worsening asthma?

A
  • animal handlers
  • food processors
  • paint sprayers
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31
Q

ASTHMA

Diagnosis?

A

2 week peak flow diary - 3 each morning and 3 each night- best score

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32
Q

ASTHMA

Non medical treatment?

A
  • stop smoking
  • avoid allergens
  • avoid beta blockers/ NSAIDs
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33
Q

ASTHMA

Step by step treatment?
can move up and down the steps accordingly

A

1) Short acting beta 2 agonist (salbutamol- BASELINE)
2) Inhaled corticosteroids (ICS)
3) Add LTRA
4) Add long acting beta2 agonist + - LTRA
5) Increased dose of ICS, SAB2A, LAB2A +- LTRA
6) Trial addition of theophylline / muscarinic receptor antagonist
- Refer to asthma clinic and specialist may recommend PO prednisolone

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34
Q

ASTHMA

What is an LTRA?

A

leukotriene receptor agonist

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35
Q

ASTHMA

Features of an acute attack?

A

1) Pulse <110bpm
2) Respiratory rate >25
3) Cant complete sentences

4) PEF 35-50% predicted

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36
Q

ASTHMA

When may an attack be life threatening / fatal?

A
  • cyanosis
  • silent chest
  • bradycardic
  • PEF <33% predicted
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37
Q

ASTHMA

Treatment of an acute attack?

A
  • nebulised salbutamol and ipratropium
  • prednisolone
  • O2 through venturi (24%)
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38
Q

ASTHMA

When can someone be discharged after a severe attack?

A
  • PEF >75%
  • Diurnal variation <25%
  • Stable for 24 hrs +
  • once discharged give PO prednisolone to be taken OD
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39
Q

LUNG CANCER

What are 95% of all lung tumours?

A

Bronchial Carcinoma’s

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40
Q

LUNG CANCER

Risk Factors?

A
  • smoking
  • asbestos
  • radiation (radon)
  • arsenic
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41
Q

LUNG CANCER

Types?

A

Small cell and non-small cell

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42
Q

LUNG CANCER

Subtypes of Non-small cell?

A

Squamous
Adenocarcinoma
Large Cell
Small Cell

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43
Q

LUNG CANCER

What does Squamous Lung Cancer present as?

A

It presents AS an obstructive lesion leading to infection

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44
Q

LUNG CANCER

What is Adenocarcinoma associated with?

A

asbestos and non smokers. occurs peripherally

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45
Q

LUNG CANCER

WHat is LArge Cell?

A

poorly differentiated tumour that metastasizes early

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46
Q

LUNG CANCER

What is small cell?

A

it arises from endocrine cells and secretes polypeptide hormones

also metastases early so a poor prognosis

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47
Q

LUNG CANCER

Epidemiology?

A

`19% of all cancers. 27% of all cancer deaths. poor prognosis

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48
Q

LUNG CANCER

Local Effects?

A
  • cough
  • dyspnoea
  • haemoptysis
  • chest pain
  • slowly resolving/ recurrent pneumonia
  • weight loss/ anorexia
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49
Q

LUNG CANCER

Invasive Effects?

A

1) Arm pain (brachial plexus)
2) Facial plethora
3) Horner’s Syndrome (stellate ganglion)
4) Hoarseness (Left recurrent laryngeal)
5) Pleural effusion (pleura)

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50
Q

LUNG CANCER

Common sites for Mets?

A
  • bone
  • brain
  • liver
  • pleura
  • lymph nodes
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51
Q

LUNG CANCER

Commonly secreted hormones from the tumour and their effects?

A 
ACTH = Cushing's
PTH = Hypercalcaemia
ADH = SIADH
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52
Q

LUNG CANCER

3 steps to an Investigation?

A

1) Confirm diagnosis
2) Assess spread
3) Stage the tumour

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53
Q

LUNG CANCER

Investigations?

A

1st = CXR then CT of chest to stage it, then PET scan to check for Mets

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54
Q

LUNG CANCER

Staging?

A 
primary tumour (T0-T4)
regional nodes (N0-N3)
distant mets (M0-M1)
T0
T1
T2
T3
T4
N0
N1
N2
N3
M0
M1
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55
Q

LUNG CANCER

Describe the 4 numbered stages

A

Stage 1= T1/T2, N0, MO

Stage 2= T1, T2, N1 OR T3

Stage 3= T3, N1, M0 OR T1-T3, N2

Stage 4= T1-T4, N0-N3, M1 (instant stage 4 if distant metastases)

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56
Q

LUNG CANCER

Treatment of non-small T1/T2

A

Curative surgery or curative radiotherapy

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57
Q

LUNG CANCER

What occurs before any surgery occurs?

A

WHO Performance status: ECG&PFTs to assess if they are fit enough to actually have the surgery and recover

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58
Q

LUNG CANCER

What happens post op?

A

radio/chemo therapy

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59
Q

LUNG CANCER

How is radiotherapy given?

A

3x every day for 12 days.

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60
Q

LUNG CANCER

Treatment of Stage 3/4?

A

palliative radio/chemo

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61
Q

LUNG CANCER

WHat is palliative radiotherapy good for?

A

local symptoms such as bone pain and haemoptysis

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62
Q

LUNG CANCER

What is palliative chemo good for

A

Systemic symptoms and maintaining quality of life right up until death

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63
Q

LUNG CANCER

Side effects of Chemo?

A
  • alopecia
  • nausea + vomiting
  • Peripheral neuropathies
  • Bone marrow suppression
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64
Q

LUNG CANCER

Side effects of Radiotherapy?

A
  • Fatigue
  • Anorexia
  • cough
  • oesophagitis
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65
Q

treatment for small cell LUNG CANCER?

A

palliative chemo/ radio

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66
Q

PNEUMONIA

Which groups are at risk?

A
  • old people
  • IVDU
  • alcoholics
  • diabetics
  • immunocompromised (AIDs)
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67
Q

PNEUMONIA

Aetiology? (typical and hospital acquired)

A

TYPICAL:

  • S.aureus
  • H.influenzae
  • S.pneumoniae
  • Klebsiella pneumoniae

HOSPITAL:
S.aureus
-ve enterobacteria

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68
Q

PNEUMONIA

Epidemiology and what is the mortality rate in hospital?

A

5-11 per 1000 people

21% mortality

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69
Q

PNEUMONIA

Symptoms?

A

1) fever
2) Sweats
3) pleuritic pain
4) Purulent cough
5) weakness
6) Dyspnoea

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70
Q

PNEUMONIA

Signs?

A

1) Confusion
2) Tachycardia
3) Tachypnoea
4) Lung consolidation features e.g. ( crackles, dull percussion and bronchial breathing)

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71
Q

PNEUMONIA

Tests?

A

CXR- to see for consolidation (follow up to check for cancer/complications)
Bloods ( increased WCC and CRP)
Sputum test for MC&S
Green swab for flu

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72
Q

PNEUMONIA

How is the severity determined?

A

CURB-65 1 point each for:

  • confusion
  • urea >7mmol/L
  • resp rate >30
  • Age >65
  • BP <90 systolic/ <60 diastolic
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73
Q

PNEUMONIA

For the CURB-65 what do the different scores represent?

A 
0-1=  home treatment
2= hospital treatment
3-5= severe/ ITU/ Mortality is 15-40%
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74
Q

PNEUMONIA

Type 1 respiratory failure is common after pneumonia. what is the cycle of draining an infected pleural effusion

A

pneumonia causes a pleural effusion, exudate produced and this needs to be drained

signs of infection =
if exudate is yellow, smelly, acidic

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75
Q

PNEUMONIA

Treatment of Mild, moderate and severe?

A

mild= PO amoxicillin

moderate= PO amoxicillin + PO clarithromycin

severe= IV cefuroxime and IV clarithromycin

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76
Q

PNEUMONIA

Who is eligible for Vaccine?

A
  • age over 65
  • people with chronic conditions (heart and lung e.g.)
  • Diabetes Mellitus
  • Immunosuppressed (AIDS)
  • People on Chemo
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77
Q

TUBERCULOSIS

Epidemiology?

A
  • in UK African and indian immigrants are common
  • Biggest killer of a single infectious disease in the world. 2 million deaths a year
  • biggest cause of death for people with HIV
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78
Q

TUBERCULOSIS

Cause?

A

mycobacterium tuberculosis =primary tuberculosis that is spread by aerosols

79
Q

TUBERCULOSIS

Pathophysiology?

A

1) Bacteria ingested by macrophages become granulomas which are the primary focus (these are recognised by exudation and neutrophil infiltration)
2) Also occurs in mediastinal lymph node (primary complex)
3) Typical Granulomatous LEsions form
4) They are calcified/ walled off = bacteria remains latent?

80
Q

TUBERCULOSIS

What is Dissemination and where is it likely to spread after dissemination?

A

When the bacteria fails to stay contained

Spreads into lungs, CNS, Bone, abdomen , Commonly= lymphadenopathy

81
Q

TUBERCULOSIS

What is Dissemination to the lungs and CNS called?

A

lung: Miliary TB

CNS= TB meningitis

82
Q

TUBERCULOSIS

Most people present with post-primary TB, what symptoms may they have?

A
  • weight loss
  • night sweats

Pulmonary:

  • Over 3 week cough
  • Haemoptysis
  • Dyspnoea
  • chest pain

Takes 4-8 weeks to develop

83
Q

TUBERCULOSIS

Complications?

A

1) Pleural effusion
2) Pericardial effusion
3) Lung collapse
4) Lung consolidation (becomes solid)

84
Q

TUBERCULOSIS

Investigations?

A

1st CXR = see cavitating lesion in upper lobes + loss of volume

Sputum test by coughing or broncho-alveolar lavage

85
Q

TUBERCULOSIS

What is the name of the sputum test and what culture medium is used?

A

Zeihl-Neeson Test with a Lowenstein Jenson culture medium

86
Q

TUBERCULOSIS

Latent TB tests?

A

1) Mantoux test

2) Interferon- Gamma testing

87
Q

TUBERCULOSIS

Treatment of latent TB?

A

Isoniazid for 6 months

88
Q

TUBERCULOSIS

Treatment of Non Drug resistant TB?

A

First 2 months:

1) Rifampicin
2) Isoniazid
3) Pyrazinamide
4) Ethambutol

then another 4 months with:

1) Rifampicin
2) Isoniazid

89
Q

TUBERCULOSIS

Side effects of Rifampicin?

A

pink urine, low platelets, induces CYP450, Flu symptoms

90
Q

TUBERCULOSIS

Side effects of Isoniazid?

A

neuropathy, low WCC, inhibits CYP450

91
Q

TUBERCULOSIS

Side effects of Pyrazinamide?

A

rash and arthralgia

92
Q

TUBERCULOSIS

Side effects of Ethambutol

A

Optic Neuritis

93
Q

PULMONARY EMBOLISM

Pathophysiology?

A

1) Embolism obstructs ventricular outflow tract
2) Increased in pulmonary vascular resistance
3) Right heart failure
4) Lung tissue is ventilated but not perfused - impaired gas exchange

94
Q

PULMONARY EMBOLISM

Risk factors?

A

1) Recent flight
2) Recent surgery / immobilization
3) Recent fracture
4) Pregnant or the pill
5) Cancer
6) Heart failure

95
Q

PULMONARY EMBOLISM

Features?

A

Small-medium: Tachycardia, tachypnoea, pleuritic chest pain, breathlessness, syncope

Large: SAME but also cyanosis, pale and sweaty and distended/ increased JVP

96
Q

PULMONARY EMBOLISM

What is the Name of the pre test probability test?

A

wells score

97
Q

PULMONARY EMBOLISM

Diagnostic tests?

A

cxr- normal or decreased vascular markings

ECG- inverted T IN v1-v4, tachycardia, RBBB

ABG- type 1 respiratory failure

98
Q

PULMONARY EMBOLISM

Gold standard imaging?

A

CTPA= CT pulmonary angiography

99
Q

PULMONARY EMBOLISM

what is given to people of low risk and high risk of PE?

A

low risk = d-dimer

high risk = LMWH (low molecular weight heparin)

100
Q

PULMONARY EMBOLISM

Treatment of small?

A

1st - D-dimer test
if that is positive do a CTPA
if that is positive give warfarin/ NOAC

101
Q

PULMONARY EMBOLISM

Treatment of medium?

and what should be given if they’re compromised?

A

LMWH

+ O2, morphine and fluids if they’re compromised

102
Q

PULMONARY EMBOLISM

Treatment of large?

A

Thrombolysis (alteplase)

103
Q

PULMONARY EMBOLISM

How long is treatment?

A

Normally 3 months, 6 months if idiopathic

maybe lifelong if they’re recurrent

104
Q

RESPIRATORY FAILURE

How is type 1 defined?

A

PaO2<8kPa

105
Q

RESPIRATORY FAILURE

How is type 2 defined?

A

PaO2<8kPa

PaCO2>6kPa

106
Q

RESPIRATORY FAILURE

Cause of Type 1?

A

Ventilation- perfusion mismatch

may be due to Asthma, COPD, Pulmonary oedema, Pneumonia, Pulmonary Fibrosis

107
Q

RESPIRATORY FAILURE

Cause of Type 2?

A

Alveolar Hypoventilation

1) Pulmonary (Fibrosis, COPD, Asthma)
2) Reduced respiratory flow (trauma, opiates)
3) Neuromuscular (Myasthenia Gravis, Guillan Barre)
4) Thoracic wall disease (kyphoscoliosis)

108
Q

RESPIRATORY FAILURE

Investigations? (ABG already done)

A

CXR, FBC, U+E, Spirometry, CRP

109
Q

RESPIRATORY FAILURE

Treatment of type 1?

A

treat underlying cause + high saturated O2 through venturi 35-60%

110
Q

RESPIRATORY FAILURE

Treatment of type 2?

A

treat hypoxia first as patient can rely on the respiratory drive to breathe if they have hypoxia

24% O2 through venture then ABG every 20 mins to check if its working, Titrate O2 up slowly

111
Q

RESPIRATORY FAILURE

There are two types of severe treatment. Name them

A

Type 1: Continuous Positive Airways Pressure (CPAP)

Type 2: Bilevel Positive Airways Pressure (BiPAP)

112
Q

URT INFECTIONS

Causes of Sinusitis?

A

Bacteria: H influenzae, S pneumoniae

Virus: Rhinovirus, Coronavirus

113
Q

URT INFECTIONS

Symptoms of Sinusitis?

A

Headache, frontal pain, Nasal discharge

114
Q

URT INFECTIONS

Pharyngitis causes?

A

S.aureus, H.influenzae, S,pyogenes, S.pneumoniae

virus: EBV and Adenoviruses

115
Q

What is EBV?

A

Epstein-Barr Virus

116
Q

URT INFECTIONS

Criteria for Pharyngitis?

A

1) Tonsillar exudate
2) No cough
3) Fever

117
Q

URT INFECTIONS

What is Croup?

A

Laryngo tracheobronchitis

118
Q

URT INFECTIONS

What is Laryngo Tracheobronchitis caused by and how is it treated?

A

Parainfluenza viruses and steroids with O2 therapy

119
Q

INFLUENZA

WHat are the two proteins found on the influenza virus?

A

Haemagglutinin (H)

Neuraminidase (N)

120
Q

What is the function of Haemagglutinin?

A

Sticking onto the host respiratory cell/ epithelium

121
Q

what is the function of Neuraminidase?

A

Lysis of host cell so the virus can be released

122
Q

Why is Influenza A worse than B?

A

it has less robust genetics so mutates much more frequently

123
Q

What is Antigenic Drift?

A

Small mutations so only small changes made to the virus so small infection

124
Q

What is Antigenic Shift?

A

Complete change in the proteins H&N so it is unrecognisable to the immune system = infection

125
Q

INFLUENZA

How is it transmitted?

A

Aerosols and droplets

126
Q

INFLUENZA

Symptoms?

A

1) Myalgia
2) Fever
3) Tired
4) Headache
5) Sore throat
6) Dry cough

127
Q

INFLUENZA

Diagnosed?

A

by green swab

128
Q

INFLUENZA

Treatment?

A

Paracetamol, bed rest and fluids

129
Q

INFLUENZA

When does Antigenic Drift happen a lot?

A

Seasonally e.g. every year new vaccine needs to be made

130
Q

INFLUENZA

What would cause an influenza pandemic?

A

when Antigenic Shift occurs

131
Q

What is Alpha- 1 antitrypsin?

A

Alpha1 - antitrypsin is a protease inhibitor inactivated by cigarette smoke.

132
Q

BRONCHIECTASIS

What is it?

A

• Chronic infection of the bronchi and bronchioles

133
Q

BRONCHIECTASIS

What is bronchiectasis a result of, and give 5 causes for this.

A

A result of chronic inflammation

CAUSES
genetic conditions (CF, immotile cilia), 
childhood infections (Pertussis), 
chronic lung infections (TB), 
idiopathic
immunodeficiency.
134
Q

BRONCHIECTASIS

Give 4 symptoms and 2 signs a person with bronchiectasis may have.

A 
Chronic purulent cough, 
dyspnoea, 
wheeze, 
recurrent chest infections, 
haemoptysis.

Signs are clubbing and crackles.

135
Q

BRONCHIECTASIS

What is gold standard investigation and what would spirometry likely show?

A

CT chest is gold standard (CXR can be used too). obstructive

136
Q

BRONCHIECTASIS

Give 3 organisms commonly causing acute exacerbations

A

S aureus, H influenzae, P aeruginosa

137
Q

BRONCHIECTASIS

Give 3 non-pharmacological and 3 pharmacological rx.

A

Non-drug:
flu + pneumococcal vaccines
physiotherapy
stop smoking.

Drugs:
mucolytics,
Abx,
SABAs.

138
Q

HYPERSENSITIVITY PNEUMONITIS

What is it?

A

Inhalation of allergens (fungal spores or avian proteins) provokes a hypersensitivity reaction

139
Q

HYPERSENSITIVITY PNEUMONITIS

Causes?

A
  • Farmers lung
  • malt workers lung
  • mushroom workers lung
  • cheese washers lung
  • wine makers lung
140
Q

HYPERSENSITIVITY PNEUMONITIS

Acute phase?

A

alveoli are infiltrated with acute inflammatory cells

141
Q

HYPERSENSITIVITY PNEUMONITIS

Chronic exposure?

A
  • granuloma formation

- obliterative bronchiolitis

142
Q

HYPERSENSITIVITY PNEUMONITIS

treatment of acute and chronic?

A

Acute
• Remove allergen and give O2
• Oral prednisolone

Chronic
• Avoid exposure – facemask
• Long-term steroids often achieve CXR and physiological improvement
• Compensation may be payable

143
Q

HYPERSENSITIVITY PNEUMONITIS

Investigations? Acute and chronic

A

Acute
• Bloods – FBC , raised ESR, ABGs
• CXR – upper-zone consolidation
• Lung function tests

Chronic
• Blood tests
• CXR – upper zone fibrosis; honeycomb lung

144
Q

HYPERSENSITIVITY PNEUMONITIS

Acute clinical presentation?

A 
•	4-6h post exposure
o	Fevers
o	Rigors
o	Myalgia
o	Dry cough 
o	Dyspnoea
o	Crackles (no wheeze)
145
Q

HYPERSENSITIVITY PNEUMONITIS

Chronic clinical presentation?

A 
•	Chronic
o	Increasing dyspnoea
o	Weight loss
o	Exertional dyspnoea
o	Type I respiratory failure
o	Cor pulmonale
146
Q

CYSTIC FIBROSIS

Epidemiology?

A

1/20 caucasians carry, 1/2000 affected.

147
Q

CYSTIC FIBROSIS

Where is the genetic problem?

A

Deletion mutation in a gene on chromosome 7 that encodes the CF transmembrane conductance regulator (CFTR) protein

148
Q

CYSTIC FIBROSIS

Pathophysiology of the gene defect?

A

Mutations affect the cystic fibrosis transmembrane conductance regulator (CFTR).

Lead to impaired Cl- and H2O transport across cell membranes

leading to viscosity of secretions.

149
Q

CYSTIC FIBROSIS

Give 4 places CFTR is found

A

Lungs, pancreas, GIT, reproductive tract.

150
Q

CYSTIC FIBROSIS

Common presenting features?

A

Recurrent respiratory infections

small intestine obstruction in the young

failure to thrive

cough

haemoptysis

wheeze

Bilateral coarse crackles

151
Q

CYSTIC FIBROSIS

Give 2 pancreatic symptoms and one reproductive.

A

Pancreatic: DM and steatorrhoea.

Reproductive: infertility

152
Q

CYSTIC FIBROSIS

Investigations?

A

Sweat test – sweat sodium and chloride >60mmol/L; chloride > sodium

Genetics – screen for known common CF mutations – family screening + counselling

Faecal elastase – screens for pancreatic dysfunction

153
Q

CYSTIC FIBROSIS

Treatment?

A 
Chest
•	Regular physiotherapy
o	Postural drainage
o	Active cycle breathing techniques
o	Forced expiratory techniques
•	Abx for acute infective exacerbations
•	Bronchodilators
GI
•	Pancreatic enzyme replacement
•	Fat soluble vitamin supplements
•	Ursodeoxycholic acid – for impaired liver function
•	Cirrhosis = liver transplant
Other
•	Treat CF-related diabetes
•	Screen for/treat osteoporosis
•	Treat arthritis, sinusitis, vasculitis
•	Fertility and genetic counselling
154
Q

SARCIODOSIS

What is it?

A

A multisystem granulomatous disorder of unknown cause.

155
Q

SARCIODOSIS

What group are affected more frequently and more severely?

A

afro-caribbeans

156
Q

SARCIODOSIS

What is the most common way it presents?

A

Symptomless found incidentally on a CXR with bilateral hilar

lymphadenopathy, ± fibrosis and pulmonary infiltrates (latter 2 less common early on).

157
Q

SARCIODOSIS

Give 2 lung symptoms, 1 skin, 2 eye, 1 bone, 1 cardiac.

A

Lung: Dyspnoea, dry cough. Skin: Erythema nodosum. Eye: Uveitis, conjunctivitis. Bone: Polyarthralgia.
Heart: Bundle branch block.

158
Q

SARCIODOSIS

What is the diagnostic test and what is found? What are 2 other blood tests you would look for? What will lung function tests show?

A

Biopsy is diagnostic: non-caseating granuloma. Look for increased ACE and hypercalcaemia (due to granulomas). Lung function tests can show a restrictive defect.

159
Q

SARCIODOSIS

When is treatment indicated and what is given?

A

Parenchymal lung disease on CXR, ocular, cardiac or neurologcal involvement, or hypercalcaemia. Treated with prednisolone.

160
Q

SARCIODOSIS

Prognosis?

A

60% resolve in 2 years

161
Q

3 holistic lung tests?

A

6 minute walking test. Incremental shuttle walking test. Cardio-respiratory exercise testing.

162
Q

What is Mesothelioma?

A

Tumour of mesothelial cells that usually occur in the pleura, caused by asbestos exposure

163
Q

Mesothelioma clinical presentation, investigation and treatment?

A
  • chest pain
  • dyspnoea
  • weight loss

CXR/CT

Chemo

164
Q

PLEURAL EFFUSIONS

What is it?

A

excessive fluid in pleural space

165
Q

PLEURAL EFFUSIONS

How is Transudates and exudates defined?

A

Transudates : <25g/L protein

Exudates : >35g/L

166
Q

PLEURAL EFFUSIONS

what do you call blood in the pleura?
what do you call pus in the pleura?

A

Haemothorax

Empyema

167
Q

PLEURAL EFFUSIONS

Cause of Transudates?

A

1) Increase venous pressure e.g.g HF
2) Hypalbuminaemia
3) Hypothyroidism

168
Q

PLEURAL EFFUSIONS

Cause of exudates?

A

1) TRauma
2) Cancer
3) Infection (TB, Pneumonia, SLE)

169
Q

PLEURAL EFFUSIONS

Signs and symptoms?

A 
Breathless
Reduced breath sounds
Dull percussion
Reduced chest wall movement
Tracheal deviation
170
Q

PLEURAL EFFUSIONS

Diagnostic tests?

A

1st CXR- dense shadows with blunt angles

2nd- aspiration of fluid, send for cytology, bacteriology, protein, glucose, pH

171
Q

PLEURAL EFFUSIONS

treatment?

A

Transudates- treat cause

Exudates = Drain

Drain if symptomatic and surgery if persistent

172
Q

PNEUMOTHORAX

What is it?

A

Air in pleural space = collapsed lung

173
Q

What is a Tension Pneumothorax?

A

pleural tear acts as a one way valve so air can go in but not out

174
Q

How does a tension pneumothorax cause a cardiac arrest?

A

Unilateral increase in pleural pressure = increased respiratory distress = shock and cardiac arrest

175
Q

Treatment of tension pneumothorax?

A

1st - needle decompression at 2nd intercostal space at midclavicular line

176
Q

PNEUMOTHORAX

Difference between tension and normal?

A

Tracheal deviation away from side of pneumothorax in tension

177
Q

PNEUMOTHORAX

Aetiology?

A
  • COPD
  • asthma
  • Pneumonia
  • TB
178
Q

PNEUMOTHORAX

How may a spontaneous one occur?

A

thin young man - rupture of sub-pleural bulla

179
Q

PNEUMOTHORAX

Clinical features?

A

1) Pleuritic chest pai
2) dyspnoea
3) Decreased breath sounds
4) Hyper- resonant percussion
5) Reduced expansion

180
Q

PNEUMOTHORAX

Diagnostics?

A

CXR - pleural linings, no lung markings, shifted mediastinum

181
Q

PNEUMOTHORAX

Treatment?

A

1st - Aspirate
2nd - chest drain

primary = >2cm + breathless = Aspirate

secondary = >2cm + breathless + over 50 = intercostal drain

182
Q

PULMONARY HYPERTENSION

What is it?

A
  • Pulmonary arterial pressure of over 25mmHg at rest and secondary RV failure
183
Q

PULMONARY HYPERTENSION

What is the normal mean pulmonary arterial pressure and mean arterial pressure? (MPAP and MAP)

A

MPAP = 10-14mmHg

MAP= 90mmHg

184
Q

PULMONARY HYPERTENSION

Aetiology?

A

Occurs due to increase in pulmonary vascular resistance or increase in pulmonary blood flow

185
Q

PULMONARY HYPERTENSION

causes?

A

Drugs = methotrexate, amiodarone

HIV, portal HTN, autoimmune rheumatic e.g. RA

Heart - valvular heart disease, systolic/diastolic failure

Lung- COPD, fibrosis

186
Q

PULMONARY HYPERTENSION

Symptoms?

A

initial - Exertional dyspnoea and fatigue

Proegresses to : RV failure, cor pulmonale = increased JVP, Hepatomegaly, peripheral oedema

187
Q

PULMONARY HYPERTENSION

Signs?

A

Loud pulmonary 2nd sound, RV heave

188
Q

PULMONARY HYPERTENSION

Diagnostic tests?

A

CXR- enlarged proximal pulmonary arteries

ECG- RVH, P pulmonale - peaked p waves

189
Q

PULMONARY HYPERTENSION

Treatment?

A

1st

oxygen
warfarin
diuretics = oedema
oral CCBs = pulmonary vasodilators

190
Q

What drugs will reduce pulmonary resistance?

A

Sildenafil

191
Q

PULMONARY HYPERTENSION

Worst case scenario treatment?

A

Lung and heart transplant - unlikely

192
Q

Name some lung consolidation features

A

Bronchial breathing, dull percussions, crackles

193
Q

BRONCHIECTASIS

What does the inflammation lead to?

A
  • Abnormal and permanent dilation of these airways
  • Leads to impaired clearance of bronchial secretions
  • Secondary bacterial infection
  • May be localised to a lobe or generalized
194
Q

Complications of TB (other organs)

A

Meningitis
Addison’s
Hepatitis

Medicine Year 2 2 (15 decks)

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