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Respiratory system > Non- infectious respiratory diseases > Flashcards

Non- infectious respiratory diseases Flashcards

1
Q

What substances can embolise? State when each is most likely to occur

A
  • Thrombus (esp DVT)
  • Tumours (renal cell carcinoma)
  • Air (after IV injection)
  • fat (after bone breaks)
  • amniotic fluid (after childbirth)
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2
Q

Why may someone with a PE not have signs of a DVT?

A
  • many DVT are symptomatic
  • may not have come from a thrombus
  • the thrombus may not have come from a leg vein
  • the whole thrombus may have moved so they had a DVT which caused their PE but its in the lungs now
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3
Q

What are the risk factors for DVT?

A

Sedentary lifestyle/ immobilisation, age, surgery, cancer, obesity, smoking, heart failure, COCP, pregnancy, long haul travel

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4
Q

What are the most common signs and symptoms for a PE?

A
  • SOB
  • pleuritic chest pain
  • cough
    less likely: fever, haemoptysis, syncope, unilateral leg pain
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5
Q

How may PE cause death? (3)

A
  • right ventricular overload and failure
  • respiratory failure
  • pulmonary infarction
    Will likely get 2 or all off these processes happening.
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6
Q

How can a PE lead to RV failure and death?

A
  • if more then 30% of capillary bed occluded, the pulmonary pressure increases
  • this increases afterload on RV
  • also get pulmonary odema due to pulmonary hypertension
  • acute heart failure as RV starts to fail to pump/ may get ischaemic and arrhythmias, leads to shock and so sudden death
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7
Q

How can PE lead to respiratory failure?

A

You get a V/Q mismatch, so blood is diverted, hyperventilation ensures CO2 is blown off enough in good alveoli, but O2 cannot be compensated for so they get hypoxic (T1 resp failure).
This excasterbates the shock youve already got due to RV failure.

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8
Q

Why is infarction due to PE quite rare?

A

Generally you’ve got good collateral blood flow from bronchial arteries supplying the tissues.

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9
Q

What are the differentials for a PE?

A

MI, Pneumothorax, pneumonia, pleurisy

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10
Q

What physical signs may be present that indicate a PE?

A

Pleural rub (also in pneumonia and pleurisy). Raised JVP (also in other causes of right sided heart failure)

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11
Q

How should a PE be investigated? (5)

A
  • CXR (should be normal if PE but excluded pneumonia)
  • ECG (T wave inversion in V1-4,2,4 and aVF, also excludes MI)
  • ABG
  • D- dimer (if no risk factors and normal D Dimer its probably not a PE)
  • CT pulmonary angiography (CTPA)
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12
Q

How should PE be treated?

A
  • Oxygen
  • heparin
  • haemodynamic support (may not wanna give blood/ fluids as overloads RV)
  • Resp support (may need to ventilate)
  • Exogenous fibrionolytics (streptokinase, tPA)
  • Percutaneous catheter directed thrombectomy
  • Surgical pulmonary embolectomy
  • Long term warfarin for at least 3 months until risk factors can be removed
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13
Q

Define asthma?

A

a chronic inflammatory disorder of the airways involving inflammatory symptoms with widespread but variable airway obstruction and an increase in airway responsiveness to a variety of stimuli. The obstruction may be reversible spontaneously or with treatment

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14
Q

what are the 5 defining features of asthma?

A
  • chronic inflammation
  • susceptibility
  • variable airflow obstruction
  • hyperresponsiveness
  • reversibility
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15
Q

Briefly describe the pathophysiology of an asthma attack?

A

Antigen is inhaled, macrophages present it to TH2, TH2 release cytokines, this attracts mast cells and oesinophils and active B cells to secrete IgE, this reacts with antigens to cause mast cell degranulation which causes bronchioconstriction, vasodilation (which causes odema and increased mucous production)

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16
Q

Why do asthmatics react to non allergic stimulates/ irritants like cold air, fumes, deoderants ect?

A

Because the inflammation persists and means that you become hyperresponsive to these stimulants, meaning you get an exaggerated response

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17
Q

Some believe there is a late phase response to asthma attacks/ exasterbations, what is this?

A

This is a second attack 3-12 hrs later which occurs due to other cells reaching the tissue and starting to release cytokines again.

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18
Q

How does inflammation in asthma cause airway obstruction? (5)

A
  • mucosal swelling (odema)= narrower lumen
  • thickening of bronchial walls due to inflammatory cells infiltration
  • mucous overproduction
  • bronchioconstriction
  • epithelium is shed due to some of the cytokines, making the mucous thicker
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19
Q

Poorly controlled asthma leads to (often unreversible) airway remodelling, describe the changes which occur:

A
  • hypertophy and hyperplasia of smooth muscle
  • hypertrophy of mucous glands
  • thickening of basement membrane
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20
Q

How is asthma diagnosed?

A
  • Wheeze present

- FEV1/ FVC ratio < 70 which is improved when given bronchiodilators

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21
Q

How does asthma most commonly present?

A
  • classicaly in young pts but can be any age
  • wheeze
  • short of breath
  • non productive cough
  • chest tightness
  • atopic history
  • worse at night
  • symptoms vary over time and intensity
  • may be triggered by excersize, smoke, infections, perfumes ect
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22
Q

Why so asthma symptoms tend to be worse at night?

A

Cortisol and adrenaline drop so less immune surpression and natural bronchiodilation respectively

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23
Q

What else may asthma that presents acutely be?

A
  • pneumonia
  • infections
  • anamiea
  • shock
  • PE
  • pneumothoax
  • COPD exasterbation
24
Q

What else might a chronic presentation of asthma be?

A
  • bronchiectasis
  • deconditioning
  • obesity
  • heart failure
  • sleep apnoea
  • anxiety
  • carcinoma
  • TB
  • COPD
25
Q

What are the red flag symptoms for chronic respiratory diseases?

A
  • sputum changes in colour, consistancy or volume
  • haemoptysis
  • weight loss
  • ankle swelling
  • severe fatigue
  • inability to speak or swallow properly
  • night sweats
  • finger clubbing
26
Q

How is chronic asthma treated (generally) ?

A

SIMPLE

  • stop smoking
  • inhaler technique
  • pharmacotherapy
  • lifestyle management
  • education
27
Q

How do the brown and the blue inhalers work and what’s in them?

A

brown- budesonide, which is a corticosteroid and will reduce inflammation and prevent symptoms arising
Blue- salbutamol which is a B2 agonist so causes vasodilation and will relieve attacks

28
Q

How is acute severe/ acute life threatening asthma treated?

A

O SHIT ME
- Oxygen

  • Salbutamol (nebulised)
  • Hydrocortiosone
  • Ipratropium (antimuscarinic)
  • Theophylline (phosphodiesterase inhibitors- less breakdown of cAMP= more cAMP= more relaxation)
  • Magnesium
  • Escalate (probably need ICU for ventilation if descends to T2 resp failure)
29
Q

What does a silent chest suggest in someone whos having an asthma attack?

A

theyre very unwell and need immediate treatment because part of their lung has completely been blocked and will soon collapse/ is already collapsed

30
Q

What two diseases make up COPD?

A

Emphysema and chronic bronchitis

31
Q

What two things can cause COPD?

A
  • Smoking- 90% of time
  • a1 anti trypsin deficiency- trypsin more active, breakdown of elastin in alveoli–> empysema
  • sometimes pollution but very rare
32
Q

How does cigarette smoking lead to COPD?

A

It causes:

  • enlargement of mucous glands
  • increased number of goblet cells
  • cilary dysfunction -> this + increased mucus is why you get chronic infections, cough and obstruction
  • breakdown of elastin
  • destruction of alveolar walls-> large airspaces (bullae)
  • vascular bed changes leading to pulmonary hypertension
33
Q

Why do you get airway obstruction and wheeze in COPD?

A
  • increased mucous

- loss of elastin and lung parenchyma which normally hold airways open on expiration

34
Q

Why do you get a barrel chest with COPD?

A
  • less elastin to less inward pull opposing outward force from ribs
  • also means less recoil, leading to air trapping in lungs and hyperinflation
35
Q

How does COPD normally present?

A
  • smoking history
  • gradual onset of persistant, productive cough which is worse in the morning and progressive shortness of breath
  • barrel chest
  • tachypnoea
  • use of accessory muscles
  • hyperresonant to precuss
  • wheeze
36
Q

What investigations should be done for COPD?

A
  • spirometery to show irreversibily reduced FEV1/FVC ratio
  • CXR: flattened diaphragm, hyperlucent lungs, increased chest wall thickness, also rules out cancer, pneumonia, pneumothorax
  • ABG if needed to asses need for O2
  • a1 antitrypsin level
37
Q

How is COPD managed? (7 interventions)

A
  • stop smoking
  • pulmonary rehab (exercise)
  • vaccines
  • good nutrition and keep weight normal
  • inhaled bronchodilators and corticosteroids may help to extent
  • long term oxygen treatment- continuous o2 for 16hrs increases survival rate
  • if COPD limited to certain areas you can remove large bullae surgically
38
Q

How may an acute exacerbation of COPD be managed?

A
  • ABG and pulse oxymetry to monitor resp failure
  • low flow oxygen (incase theyre in o2 drive)
  • nebulized brochodilators
  • oral steroids
  • antibiotics if infection caused exacerbation
  • invasive/ non invasive ventilation
39
Q

What is bronchiectasis?

A

Chronic dilation of one or more bronchi, these bronchi exhibit poor mucus clearance so there is a predisposition to infection.

40
Q

What are the 3 main causes of bronchiectasis?

A
  • post infections (TB, whooping cough and H. influenza are main ones)
  • immune deficiency
  • genetic/ mucocillary clearance defects (cystic fibrosis, primary cilary dyskenisa)
  • obstruction due to foreign body, tumours ect
  • toxic insult
  • rheumatoid arthritis
41
Q

How is bronchiectasis diagnosed?

A

Signet ring sign on chest CT

42
Q

What are signs and symptoms of bronchiectasis?

A
  • chronic cough
  • high sputum production
  • breathlessness on exertion
  • nasal symptoms
  • chest pain
  • fatigue
  • frequent chest infections
  • sometimes haemoptysis and wheese
43
Q

How is bronchiectasis managed?

A
  • Treat underlying cause
  • physiotherapy to clear mucus
  • antibiotics
  • flu vaccines, bronchodilators may help
  • pulmonary rehab if dyspnea
44
Q

Describe the genetic basis of cystic fibrosis?

A

Autosomal ressesive defect in CFTR gene meaning less extrusion of Cl- at mucous membranes and so less water in mucus, making mucous secretions thicker

45
Q

How is cystic fibrosis diagnosed?

A
  • History
  • Screening test
  • saltier sweat
46
Q

How may cystic fibrosis present?

A
  • +ve heel prick test
  • muconium ileum (delay in passing mecuonium, vomiting after birth)
  • interstitial malabsorbtion (failure to thrive)
  • recurrent chest infections
47
Q

What systems are affected by cystic fibrosis?

A
  • resp (bronchiectasis, infections, cough, SOB)
  • Pancreas (insufficeincy diabetes, less secretion)
  • intestine (less pancreatic secretion= malabsorbtion, distal obstructions)
  • liver disease
  • heart failure
  • repro (no vas deferense)
  • osteoporosis
  • high salt sweat
48
Q

How is cystic fibrosis managed?

A
  • no smoking
  • avoid other CF pts due to infection risk
  • avoid friends w/ infections
  • avoid jacuzzis due to pseudomonas risk
  • clean and dry nebulisers properly
  • flu vaccines
  • NaCl tablets in hot water/ vigerous exercise
  • Physio to maintain lung health and move mucus
  • some targeted gene therapies are emerging
  • mental health management
49
Q

What could cause a pleural effusion (6)

A
  • less absorbtion of pleural fluid (more protein- nephrotic syndrome, liver failure// lymphatic obstruction// increased venous pressure (heart failure))
  • more production (Inflammation- PE, infection, cancer)
50
Q

What can be inferred about a bilateral pleural effusion?

A

probably due to pressure changes- venous pressures, oncotic pressures ect

51
Q

What is the difference between a transudate and an exudate and the causes of each?

A

Exudate is cloudy and contains protein- therefor due to inflammation or lymphatic obstruction

52
Q

How is pleural effusion treated?

A

Aspirate fluid w/ needle 5th ICS axiallary line, upper boarder of rib

53
Q

What could cause a pneumothorax?

A
  • opening in chest wall- trauma, inserting central line, breast aspiration
  • opening in lung- trauma (rib fracture), high pressure ventilation, lung cancer, COPD, bronchiectasis, asthma, ruptured blebs and bullae
  • opening in both- stab wound
54
Q

What are the risk factors for blebs?

A

young, tall, thin, smoking

55
Q

How are pneumothorax treated?

A

chest drain in 5th ICS mid axillary line- under water straw- air is pushed out on expiration but cant be sucked in on inspiration due to water seal

56
Q

How can a pneumothorax develop into a tension pneumothorax?

A

When the hole creates a flap which allows air in on inspiration and out on expiration so gas cant escape- the volume of air within the pleural space will build up.

57
Q

How is tension pneumothorax treated?

A

canula in 2nd ICS at mid clavicular line

Respiratory system (9 decks)

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