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CP3 > resp > Flashcards

resp Flashcards

1
Q

Signs of CO2 retention

A

dizzieness, flap, headache, tired, confused,

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2
Q

describe a blue boater

A

not breathless and cyanosed.
Rely on oxygen to stimulate respiratory effort as insensitive to CO2
Usually have cor pulmonale
Blood gas will show type 2 resp failure (CAREFUL with oxygen therapy)
Chronic bronchitis

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3
Q

describe a pink puffer

A 
sensitive to CO2 - low CO2
increased resp rate and heart rate, using resp muscles
usually not cyanosed
thin
type 1 resp failure 
Emphysema
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4
Q

What are the stages of COPD

A
  1. 80% FEV
  2. 50-80% FEV
  3. 30-40% FEV
  4. <30% very serious
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5
Q

WHat is the treatment for COPD >50%

A
  1. SABA or SAMA
  2. SABA/ SAMA + LABA/LAMA (cant have LAMA + SAMA)
  3. SABA/ SAMA + LABA/LAMA + ICS
  4. SABA + LABA + ICS + LAMA
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6
Q

What is the treatment for COPD <50%

A
  1. SABA or LAMA
  2. SABA/LAMA + LABA + ICS
    or SABA + LAMA + ICS
  3. SABA + LABA + LAMA + ICS
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7
Q

other treatments for COPD

A 
oral theophyline
pulmonary rehabilitation
mucolytics
nutritional supplements
long term home oxygen therapy
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8
Q

criteria for home oxygenation

A

<92 dats on air, FEEV <30, cor pulmonale, polychthaemia

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9
Q

Management of acute COPD in hospital and community

A

Community: 30mg pred 7-14 days. oral Abx if ? pneumo, safety net 6 weeks and optimise treatment once stable

Hospital: oxygen titrated , can have IV Abx, salbutamol nebs, ipatropium nebs, PO pred, sputum culture and CXR, theophyline, bloods ECG,
- Theophylline level at admission (if the person is on theophylline)
last line bipap

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10
Q

Causes of bronchiectasis

A 
- TB pneumonia flu
 SLE, RA, Marfans (connective tissue disorders)
- A1at, CF
- tumour
- immune deficiencies e/g
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11
Q

Management of bronchiectasis

A
  • Stop smoking
  • Physiotherapy
  • Postural drainage
  • Antibiotics for exacerbations
  • Immunisations
  • Bronchodilators
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12
Q

Management of CF

A
  • Physiotherapy, bronchodilators and antibiotics, antibiotics (same as bronchiectasis)
  • Mucolytics
  • airway clearence devices
  • lung transplant if resp failure
  • creon, ADEK vits
  • liver transplant if cirrhosis
  • fertility counselling and genetic counselling
  • treatment of DM
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13
Q

Criteria for HAP

A

develops >48h after admission

OR thats gone home but been hospitalised >10 days previously

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14
Q

WHich organisms predispose to CAP

A
  • s pneumo, Hib
  • Mycoplasma, chlymidia, legionella
  • influenza and parainfluenza
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15
Q

Which organisms predispose to HAP

A
  • Klebsienna, S. aureus, Pseudomonas, enterobacteria
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16
Q

How do you investigate suspected pneumonia

A
  • FBC, CRP, U+E, LFT
  • CXR
  • Sputum sample
  • Urine (legoinella)
  • PCR (mycoplasma and chlymidia)
  • Serum IgM (mycoplasma)
  • Blood cultures
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17
Q

How do you treat CURB 1-3

How does the treatment change if aspiration is considered

A 
0/1 = oral amoxicillin OP
2 = oral amoxicillin + clarithromycin Inpatient 
3 = IV clarithromycin and IV co-amoxiclav inpatient 10 days

Follow up Xray 6 weeks!!

Aspiration? metronidazole

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18
Q

How do you manage HAP

A 
mild = oral doxycycline
severe = oral co-trimoxazole

Follow up X ray 6 weeks!!

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19
Q

Complications of pneumonia

A

abscess, effusion, empyema, bronciectasis, sepsis, collapse

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20
Q

Difference between lobar pneumonia and bronchopneumina

A

Lobar pneumonia - alveoli, CAP organisms

Bronchopneumonia - patchy, Old/ immunosuppressed/ ill, can cause BE/ fibrosis/ empyema

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21
Q

How would you investigate suspected active TB

A
  1. sputum samples: microscopy, PCR (cant diff between active and latent), culture (takes 6w)
    +/- bronchoscopy + biopsy
  2. CXR
22
Q

How would you investigate for latent TB

A

Mantoux test

Interferon-gamma release assay

23
Q

How is active TB managed

How is latent TB managed

A

Active: 6m isoniazid, rifampicin, 2m + pyrazinamide and ethambutol as well (RIPE)

  • CNS keep isonazid and rifampicin 12m
  • direct observation if poor adherence
  • Notifiable disease (household and close contacts traced and assessed)

LATENT: 3 months of rifampicin and isoniazid

24
Q

Where are the common sites of non pulmonary TB

A
  • lymphiatic (lymphadenopathy)
  • spine/ joints (arthritis)
  • renal tb (sterile pyuria)
  • meningitis
  • cutaneous (erythema nodosum)
  • pericarditis
25
Q

Cause of: (auscultation)

  1. reduced vocal resonance
  2. increased vocal resonance
  3. crackles
  4. bronchial breathing
  5. reduced breath sounds
  6. wheeze polyphonic
  7. wheeze monophonic
A
  1. pleural effusion, pneumothorax, collapse,
  2. pneumonia
  3. pulmonary oedema, pulmonary fibrosis, BE, pneumonia
  4. consolidation,
  5. acute life threatening asthma (hypoventilation), collapse, COPD (hyperinflation), pleural effusion, pneumothorax, obesity
  6. asthma, COPD, BE
  7. obstruction
26
Q

Cause of: (percussion)

  1. dullness to percussion
  2. hyperesonance
  3. unequal expansion
A
  1. pleural effusion, consolidation, collapse, tumour
  2. pneumothorax
  3. collapse, pneumonia, pneumothorax, effusion, fibrosis
27
Q

Name the types of pneumothorax

A

Spontaneous: 1y and 2y
Iatrogenic
Traumatic

28
Q

When would you treat a pneumothorax?

How do you treat

A

> 2cm of patient SOB
3 way tap aspiration 2nd ics. max 1500-2000ml

repeat CXR 24h and 7 days

29
Q

What are the last line treatments for pneumothorax that aren’t resolving with chest drains

A
  • apical pleurectomy + blebectomy

- talc pneurodesis if not fit for surgery

30
Q

What symptoms/ signs/ findings would suggest an empyema rather than pleural effusion

How are they treated

A
  • fever + pleural effusion signs
  • aspirated fluid is yellow and turbid, low glucose, high LDH, low pH <7.2

Abx and chest drain

31
Q

Which lung cancer is the most malignant. Which met early?

A

Small cell carcinoma are the most malignant.

SCC and large cell met early also

32
Q

Which lung cancers are paraneoplastic

A

small cell: ACTH, ADH

SCC: PTH

33
Q

WHat investigations would you do in someone with ? lung cancer

A

FBC (anaemia) LFT (mets) U+E (paraneoplastic), CXR, sputum/ pleural fluid cytology, staging CT, biopsy (CT guided if periperal via bronchoscopy if central)
PET scan if suspect mets

34
Q

what is hypertrophic pulmonary osteoarthrophy

A

clubbing and painful periosteitis of small joints in hands. 1y or 2y (cancer) usually non small cell + paraneoplastic lung cancer

35
Q

Name some local manifestations of lung cancer (invasion)

A
  • recurrent laryngeal nerve palsy
  • phrenic nn palsy
  • SVC obstruction
  • Pericarditis
  • Pancoast syndrome:
    horners
    shoulder pain or hand muscle atrophy
36
Q

WHat happens in SVC obstruction

A

JVP raised, raised arm BP, facial swelling

37
Q

Where do lung cancer metastasise to

A

Brain, bone, liver, adrenals BLAB

38
Q

Treatment of small cell and non small cell cancers

A

Non small cell: remove if >2cm from carina + adjuvent chemo. If more advanced can do chemo and radiotherapy

Small cell: chemo + radio but nearly always disseminated at presentation

39
Q

List the causes of interstitial lung disease

A

Exogenous:

  • asbestosis, silicosis, coal dust, nitrofurantoin, amiodarone, methotrexate, sulfasalazine,
  • pigeon, cheese factory (allergy), farmers
  • TB, fungal or viral infections

Endogenous:
- Sarcoidosis, rheumatoid arthritis, SLE, sjorgens, systemic sclerosis

Idiopathic (most common cause)

40
Q

Describe the clinical picture of interstitial lung disease

A
  • dry cough
  • SOB on exertion
  • reduced expansion
  • can have clubbing
  • fine end expiratory crackles and sometimes a wheeze

Decompensation = pulmonary hypertension and heart failure

41
Q

Investigations for interstitial lung disease?

A
  • FBC, ANA/ RF
  • CXR
  • High resolution CT
  • Spirometry (shows restrictive disease)
  • Bronchoalveolar lavage
  • Lung biopsy only if diagnosis uncertain
42
Q

Symptoms of extrinsic allergic alveolitis ?

Treatment?

How is diagnosis confirmed?

A

fever, rigors, myalgia
Dry cough, SOB, +/- wheeze

po Pred

CT/ CXR confirms interstitial disease, Bronchoalveolar lavage confirms diagnosis

43
Q

Describe pleural plaques

A

asbestosis

  • cause mild restrictive defecit
  • pleural thickening
  • non-progressive
  • can cause pleural effusions
44
Q

Describe pleural thickening

A

asbestosis, more severe than pleural plaques
affect >1/4 of pleural space
- Restrictive defecit with SOB
- can be progressive

45
Q

What is asbestosis

A

causes by heavy exposure

  • 5-10 years from exposure to disease
  • poor outcome
  • progressive
46
Q

Risks of OSA

A
  • hypertension
  • pulmonary hypertension and cor pulmonale
  • type 2 resp failure (can worsen existing disease)
47
Q

What are the complications of acidosis

A
  • negatively ionotropic on the heart
  • H+ into cells K+ out of cells > hyperkalaemia
  • confusion
48
Q

How would a patient with a lobectomy present

A

OVER LOBESTOMY SIDE

  • hyperresonant
  • reduced expansion
  • trachea towards
  • reduced air entry
49
Q

Causes of metabolic acidosis with a raised anion gap

A 
lactic aciosis
ketoacidosis
renal failure causing acidosis
alcohol
ingesting H+ e.g. antifreeze
50
Q

causes of metabolic acidosis with a normal anion gap

A

diarrhoea
renal tubular acidosis
ileostomy

51
Q

causes of metabolic alkalosis

A 
vomiting
conns
burns
diuretics
hypokalaemia

CP3 (6 decks)

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