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Respiratory Conditions Flashcards

1
Q

How would you describe pleuritic pain and how is this pain localised?

A

Pain is localised because the parietal pleura is irritated and is innervated by the intercostal nerve and phrenic nerve.

Feel:

  • sharp pain
  • worse on inspiration and coughing
  • shoulder tip pain (phrenic nerve) and/or thoracic wall pain (intercostal nerve)
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2
Q

Do you hear a wheeze greater on inspiration or expiration?

Explain

A

Expiration because the intrathoracic airways become narrow on expiration, in conjunction with the obstruction in the intrathoracic airway, the wheeze is heard.

Obstruction can be due to foreign body, mucous, oedema, bronchial SM contraction

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3
Q

What is stridor and when is it heard greater (inspiration or expiration)?

A

Stridor is a high pitched continuous harsh sound heard predominantly on inspiration as there is an obstruction in the extrathoracic airway

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4
Q

What are the common clinical presentations of a COPD patient and why?

A 
Breathing with pursed lips (to prolong gas exchange so more air can be expelled from small airways than be trapped)
Use of accessory muscles (forced inspiration and expiration to get more air into lungs)
CLEAR sputum (also get this in CHRONIC BRONCHITIS)
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5
Q

In emphysema, why are the lungs hyperinflated and why is the chest wall hyperextended (AP diameter>Lat. diameter - barrel chest)?

A

Due to the trapping of air in the small airways (this air is not expelled)

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6
Q

Describe how air would sound in the chest on percussion and describe possible conditions that could correspond with that air sound

A

Resonant: normal
Hyper-resonant: pneumothorax (air in pleural space)
Dull: pneumonia (consolidation - exudate in airways)
Stony dull: pleural effusion

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7
Q

If this breath sound is heard in the lower respiratory tract what condition may the patient have and what would the air sound like in the chest?

A

Bronchial breath sounds
Pneumonia
Dull

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8
Q

What does a pleural rub sound like and what condition does the patient have?

A

Rub hands against ear (coarse, scratching)

Pleurisy/pleuritis (inflammation of the pleura)

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9
Q

Describe the different crackle sounds and what condition the patient could have?

A

Fine: pneumonia
Mid coarse: pulmonary fibrosis
Coarse: COPD, bronchiectasis

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10
Q

In pneumonia how would the:

A) air sound
B) breath sound
C) crackles sound

On the chest?

A

A) dull
B) bronchial
C) fine

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11
Q

Pulmonary embolism definition

A

When a substance (typically a thrombus) has entered the right side of the heart and lodged in the pulmonary artery

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12
Q

What causes fat embolism syndrome and what is its triad?

A

LT long bone fracture

Brain: neurological abnormalities (confusion)
Lung: hypoxaemia (fat emboli)
Skin: petechial rash

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13
Q

What is the main cause of a pulmonary emboli?

A

DVT from popliteal or pelvic vein

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14
Q

Name 4 risk factors for a thrombo-embolism and why?

relate to Virchow’s triad

A
  • pregnancy (stasis)
  • long haul flight (stasis)
  • COCP (oestrogen increases livers synthesis of clotting factors)
  • obesity (fat so have more oestrogen so same as above, also increased stasis and impaired circulation due to fat on vessel wall)
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15
Q

List symptoms of a pulmonary embolus

A 
Dyspnoea
Cough
Pleuritic chest pain
Haemoptysis
Syncope
Unilateral leg pain
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16
Q

List signs of a pulmonary embolus

A 
Tachycardia
Tachypnoea
Cyanosis
Decreased breath sounds
Fever
Loud P2 (result of kpa r. side>l. side)
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17
Q

Name 4 conditions where breath sounds will be reduced or absent

A

pppa

Pulmonary embolism
Asthma
Pleural effusion
Pneumothorax

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18
Q

A) Acute right ventricular overload
B) Respiratory failure
C) Pulmonary infarction
are all clinical outcomes of a pulmonary emboli, how do they come about?

A

A) + inotropes (to ↑BP)-> RV overload + PA vasoconstriction -> PA ↑kpa-> RV dilation

B)RV output ↓ so get V/Q mismatch

C) emboli lead to alveolar haemorrhage, get triad + wedge on CXR.

1) haemoptysis
2) pleural effusion
3) pleuritis

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19
Q

What is the treatment for a pulmonary embolism?

A

Immediate Heparin or LMWH

Oxygen

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20
Q

Describe the pathology of a pneumothorax and why the lung collapses?

A

Breach in chest wall or lung leads to air from the atmosphere (higher kpa) now entering the pleural cavity (lower kpa). Air keeps flowing down the [gradient] until the pressures are =. Lung then collapses due to unopposed elastic recoil of the chest wall.

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21
Q

How do you treat a large spontaneous pneumothorax that is symptomatic?

A

Place CHEST DRAIN in safe triangle found in the 5th ICS at the MAL. Chest drain is connected to an underwater seal that is open to the air/suction to prevent inspiration of air when patient is inspiring.

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22
Q

Name the borders of the safe triangle of the chest

A

Lateral border of pectoralis major
Anterior border of latissimus dorsi
Nipple line

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23
Q

Why do patients with a tension pneumothorax have a raised Jugular Venous Pressure?

A

Due to intra-pleural pressure being higher than atmospheric pressure (as a result of the flap on the chest wall, preventing air from escaping the intra-pleural space) so venous return is impaired so RA is increasing its force of contraction to try and increase the CO and this causes JVP to rise

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24
Q

What is the treatment for a tension pneumothorax?

A

Insert a cannula in the 2nd ICS MCL, remove this once a chest drain with underwear seal has been placed into the 4th ICS MAL

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25
Q

What is empyema?

A

Pus in pleural cavity

Can be a result of pneumonia. Bacteria enters the pleural space

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26
Q

What is chylothorax?

A

Lymphatic fluid in pleural cavity from lymphatic duct - a result of trauma

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27
Q

Name 3 causes of an exudate pleural effusion

A

Infection (TB, Pneumonia)
Cancer
Pulmonary infarction (due to pulmonary embolism)

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28
Q

Describe the pathogenesis of PRIMARY TB and POST PRIMARY TB

A

inhale aerosol containing Mycobacterium tuberculosis -> engulfed by alveolar macrophages (Ghon’s focus) -> MT enters local/MS lymph nodes -> Primary complex (Ghon’s focus + LN infection) (-> PRIMARY TB, active 5%) -> containment of infection -> latent infection -> 95% cure or reactivation and get POST PRIMARY TB

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29
Q

How does extrapulmonary tuberculosis occur?

A

TB bacilli enters lymph drainage to venous system thus enabling its haematogenous spread

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30
Q

What is the difference between latent and active TB?

What is the similarity between latent TB and active TB?

A

Latent TB, you are not infectious and you are asymptomatic, sputum smear and culture is -, normal CXR

You have the MTB infection in both, tuberculin skin test + and interferon gamma test +

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31
Q

Name 6 symptoms of tuberculosis

A 
Cough
Malaise
Fever
NIGHT SWEATS
Weight loss
Lethargy
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32
Q

What is tuberculin?

A

A protein released by Mycobacterium Tuberculosis

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33
Q

3 side effects of Rifampicin

A

Orange urine
Paraesthesia
Myalgia

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34
Q

Side effects of Isoniazid

How do you prevent this side effect?

A

Peripheral neuropathy

Take vitamin B6

35
Q

Side effect for Pyrazinamide

A

Hepatitis

36
Q

What drug gives you the side effect of optic neuritis?

A

Ethambutol

37
Q

What is alpha 1 anti-trypsin deficiency?

A

An autosomal recessive disease, where the liver is unable to synthesis a1 anti-trypsin so elastase in the lungs remain active and continuously breakdown elastin in the alveolar so the air space remains dilated as there is no elastic recoil (Emphysema)

38
Q

What are the causes of COPD?

A

Noxious particles or gases:

1) cigarette
2) air pollution
3) alpha 1 anti-trypsin deficiency

39
Q

What are the late signs of Chronic Obstructive Pulmonary Disease and what are their causes?

A

Flapping tremor as a result of hypercapnia due to hypoventilation

Cor pulmonale as a result of pulmonary hypertension due to pulmonary artery vasoconstriction and vascular SM hypertrophy

Central cyanosis as a result of hypoxia due to hypoventilation

40
Q

How do you treat an acute exacerbation of COPD?

A

Nebulised bronchodilator
24-28% O2 with ABG (don’t want to become too hypercapnic)
Oral high dose prednisolone
AMOXICILLIN (H. influenzae and S. pneumoniae)

41
Q

Name 3 less common MO’s that cause community acquired pneumonia

A

Staphylococcus aureus
Haemophilius influenzae
Mycoplasma pneumoniae

42
Q

Name 3 bacteria that can cause nosocomial pneumonia

A
  1. Gram - bacteria
  2. Staphylococcus aureus
  3. Methicillin resistant staphylococcus aureus
43
Q

Name the 3 opportunistic MO’s that cause pneumonia in an immunocompromised person

A

Pneumocystis jiroveci
Cytomegalovirus
Aspergillus spp.

44
Q

Name 3 drugs that could be given to treat CAP.

How long should the treatment be for a mild case and a severe case?

A

Mild: 3-7 days
Severe: 7-10 days
Amoxicillin or Doxycycline or Erythromycin/Clarithromycin

45
Q

What is the treatment for Aspiration pneumonia?

A

Mild - severe: IV Co-Amoxiclav

46
Q

What is the treatment for Nosocomial pneumonia?

A

IV Co-Amoxiclav then Piperacillin/Tazobactam

47
Q

Why is the FVC reduced in a restrictive respiratory condition (lung fibrosis)

A

The lung is stiff so can’t expand properly and force air out

48
Q

What is Young’s syndrome?

You Be So Rong

A

A triad that encompasses bronchiectasis, sinusitis and reduced fertility

49
Q

What is Kartagener’s syndrome?

Kome Be Sweet Sweety

A

A triad that encompasses bronchiectasis, sinusitis and situs inversus

50
Q

Name 2 gram negative bacteria that are commonly responsible for infections in the bronchiectasis?

A

Haemophilus influenzae and Psuedomonas aeruginosa

51
Q

What 2 conditions, that do not primarily effect the respiratory system is associated with bronchiectasis?

A

Inflammatory bowel disease and Rheumatoid arthritis

52
Q

A part from the lungs, name 4 other sites that the lack of the cystic fibrosis transmembrane conductance regulator can cause issue and what does it cause?

A 
Vas deferens (infertility)
Pancreatic duct (acute pancreatitis)
Common bile duct (biliary cirrhosis)
Sweat glands (heat shock)
53
Q

Name 4 common clinical presentations of cystic fibrosis

A
  1. Meconium ileus (bilious vomitus, abdominal distention, delayed meconium passing)
  2. Intestinal malabsorption (pancreatic enzymes blocked by mucus plug in pancreatic duct)
  3. Recurrent chest infections
  4. Phenotype screening of newborns
54
Q

What drugs makeup Orkambi and what gene mutation of Cystic fibrosis does it help the most?

What are the mechanisms of each drug?

A

Lumacaftor (transports CFTR protein to apical surface of epithelial cell) + Ivacaftor (binds to CFTR protein, keeping it open so increases Cl- entering ion channel)

Help people with Phe508del mutation

55
Q

Name 5 conditions that can lead to a V/Q <1 (hypoventilation) and briefly discuss their reasons

  • ↓PaO2 ↑PaCO2 in alveoli*
A 
Obstructive (asthma *bronchus isn’t wide* + COPD)
Pulmonary oedema (fluid in alveoli)
RDS (low surfactant so alveoli don’t expand)
Pneumonia (exudate in alveoli)
56
Q

Why is PCO2 in plasma directly proportional to PaCO2 in the alveoli?

5.3 kPa

A

Because CO2 is very soluble in plasma and it has no carrier molecule

57
Q

Why do conditions with a V/Q mismatch (<1) have ↓PaO2 but normal/low PaCO2?

Why do they hyperventilate?

A

↓PaO2: due to O2 not being very soluble in plasma, it is taken up by its carrier molecule Hb so the [O2] in the plasma will be low post hyperventilation

Normal/low PaCO2: CO2 has no carrier molecule and it is 20x more dissolvable in plasma than O2 so [CO2] in plasma can be returned back to normal post hyperventilation

You hyperventilate in order to increase the ventilation to the alveoli as the perfusion>ventilation

58
Q

Hypoxia definition

A

Low oxygen levels in the tissues

59
Q

What is central cyanosis?

A

Blueish discolouration of oral mucosa, lips and tongue as a person is hypoxaemic so there is a high concentration of deoxyhaemoglobin present in arteries (O2 sat: <85% and PaO2: <5kPa)

60
Q

What is peripheral cyanosis?

A

Blueish discolouration of fingers and toes because there is poor local circulation

61
Q

What is Type 1 Respiratory failure?

A

Hypoxaemia (<8 kPa) caused by gas exchange impairment at the alveolar-capillary membrane with a low O2 sat of <90%

PaCO2 is normal or low

62
Q

What is Type 2 Respiratory failure?

A

Hypoxaemia caused by respiratory pump failure (hypoventilation) with hypercapnia present (PaCO2 >6.5kPa)

63
Q

In a V/Q mismatch of <1, the alveoli PaO2 is low and PaCO2 is high, does this leads to vasodilation or vasoconstriction of the pulmonary capillary?

And why?

A

Vasoconstriction so alveoli that are better ventilated get better perfusion

64
Q

What is the treatment ladder for an adult with chronic asthma?

A
  1. Preventer inhaler: Low dose inhaled corticosteroid
  2. MART: (1 + LABA (Salmeterol)
  3. Controller inhaler: (medium dose ICS + LTRA)
65
Q

Discuss the vicious cycle of bronchiectasis

A

Bronchodilation leads to mucus accumulation, impaired ciliary function and increased risk of infection. Infection leads to inflammation and destruction of elastin and smooth muscle cells of the bronchial wall which leads to more dilation

66
Q

With metabolic alkalosis, are you hyperkalaemic or hypokalaemic?

And why?

Would you get increased or decreased K+ excretion at DCT?

A

Hypokalaemic

As ↑H+ leaving cell so ↑K+ entering cell so get ↑K+ excretion at DCT

67
Q

You have metabolic acidosis and a normal anion gap.

Why is the anion gap normal?

A

HCO3- is replaced by Cl-

68
Q

What change will lead to the anion gap increasing?

Being closer to 18mmol.-1

A

HCO3- levels decreasing and being replaced by another anion from a metabolic acidosis cause e.g. lactic acid

69
Q

What are the pCO2 and pO2 levels in a person with diffuse lung fibrosis?

Why does pCO2 have this level?

What cells thicken the interstitium?

A

pCO2: normal (20x more soluble than O2 so can get get through thickened interstitium (thickened by collagen, elastin and fibrinogen) to pulmonary capillary easily
pO2: low

70
Q

How does congestive cardiac failure cause a transudate pleural effusion?

A

Increases HP at venous end of parietal capillary leads to more fluid being forced out of the capillary into the pleural cavity

71
Q

How does a lung cancer cause a exudate pleural effusion?

A

Inflammation of the pleural capillary leads to increased permeability of pleural capillary wall so more protein leave capillary and enter pleural cavity

72
Q

A part from a B-2 agonist, what other drug can you give to combat muscle spasms in asthma?

What class of drug is it and what receptor does it inhibit?

A

Ipratropium - an antimuscarinic (inhibits mACHR)

73
Q

Name 5 Paraneoplastic syndromes that can occur in lung cancer

F CASH

A

Anaemia

Hypercalcaemia

Cushing’s syndrome

SIADH

Finger clubbing

74
Q

Describe what a subcutaneous emphysema or a crepitus is and when it is typically felt.

A

SE/C is felt on the chest wall and it feels like rice kripsies, it has a crackling sensation when you touch it.

(This is the sensation of air under the skin)

Felt in PNEUMOTHORAX (until proven otherwise)

75
Q

What is the definition of Costochondritis?

Is it typically unilateral or can it affect more than one rib?

A

Inflammation of the costochondral junction OR costosternal joints of the anterior chest wall. Typically affects more than one rib.

76
Q

What is the definition of Tietze’s syndrome?

Is it typically unilateral or can it affect more than one rib?

A

Swelling of the costochondral junction OR costosternal joints of the anterior chest wall. Typically unilateral.

77
Q

How do you differentiate between Costochondritis and Tietze’s syndrome (2)?

Both are musculoskeletal causes of chest pain

A

Pain in Tietze’s syndrome is more localised, whereas the pain in Costochondritis is more diffuse.

Tietze’s syndrome is more common in people under 40, whereas Costochondritis is more common in people over 40 (but Costochondritis is more common than Tietze’s syndrome overall).

78
Q

What are 4 symptoms of pneumonia?

A
  1. Cough with sputum production
  2. Pleuritic chest pain
  3. Wheeze
  4. Dyspnoea
79
Q

Discuss 2 causes of lung/lobar collapse.

A
  1. Obstruction- e.g. secondary to pneumonia or foreign body present
  2. Airway obstruction- e.g. enlarged lymph nodes (due to cancer or TB)
80
Q

What can be the long term effect of steroids on the bone?

A

Weakens the bone, leading to osteoarthritis

81
Q

How are aortic dissections described?

A

Central crushing chest pain that radiates to their back. Pain often described to have a tearing sensation

82
Q

What is Samter Syndrome and what is the typical clinical triad?

A

Samter syndrome is Aspirin-induced asthma

Triad:

  1. Nasal polyps
  2. Aspirin intolerance
  3. Asthma
83
Q

What is Pott’s disease?

MRI is the gold standard investigatory tool

A

Infection of the vertebral body and intervertebral disc by Mycobacterium Tuberculosis

Respiratory (5 decks)

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