Respiratory system

Question 1

Describe the action of salbutamol, including indications, dosage and side effects:

Answer 1

Selective beta 2 adrenergic receptor agonist, works as a stimulant and bronchodilator which relaxes the smooth muscle of the small/medium airways.
Indications: acute asthma, anaphylaxis, B-blocker OD, smoke inhalation, eCOPD. No contra’s.
Dosage: 5mg for an adult, 2.5mg in paeds.
Side effects: tremors, tachy, palpitations, headaches, muscle cramps, peripheral vasodilation.

Question 2

Describe the action of ipratropium bromide (atrovent), including indications, dosage and side effects:

Answer 2

Bronchodilating, anti-muscarinic. Acetylcholine antagonist which blocks muscarinic cholinergic receptors decreasing cyclic guanosine monophosphate (cGMP) production - decreasing smooth muscle contraction of the airways.
Indications: acute severe/life threatening asthma unresponsive to salbutamol, eCOPD.
Contraindications: nil in emergency, cautions glaucoma, preg. prostatic hyperplasia.
Dosage: 500mcg in 2ml, single dose.
Side effects: nausea, dry mouth, arrhythmias, tachy, dizzy.

Question 3

List the time critical features of an exaccerbation of COPD that would require an ASHICE

Answer 3

Extreme dyspnea - cyanosis, unable to talk in full sentences, tripoding
Extreme tachypneoa 
Sats <88% consistently despite treatment
Major ABCDE problems 
Agitation 
Symptoms persisting despite treatment

Question 4

List the features of acute severe asthma

Answer 4

PEF 33-50% below expected

Unable to talk in full sentences

Tachycardia 110+ adults, 125+ in 5 y/o+, 140+ in 2-5y/o

Resp rate 25+, 30+, 40+ (as above)

Question 5

List the features of life threatening asthma

Answer 5

Altered GCS 
Arrhythmia 
Exhaustion 
Low BP
Cyanosis 
Silent chest 
Reduced resp effort
Sats <92%

Question 6

What is the treatment for asthma?

Answer 6

High flow O2
Salbutamol nebulisers 
Ipratropoum nebuliser
HYC
ADX
ASHICE required?

Question 7

What are the main causes of respiratory pathophysiology?

Answer 7

> Genetic: asthma and CF

> Environmental: smoking -> lung Ca, COPD, emphysema, air pollution -> chronic bronchitis

> Occupation: mesothelioma, lung Ca, pmeumoconiosis, asbestosis

> Infection: influenza, TB, pneumonia

Question 8

Describe the pathophysiology of cystic fibrosis:

Answer 8

Autosomal recessive, 1:2500.

Mutation of cystic fibrosis transmembrane conductance regulation gene (CFTR) on chromosome 7
-> abrmomal water/electrolyte transmembrane movement.

Links with chronic pancreatitis, bronchiecstasis, DM, M inferility.

Question 9

List how CF may affect different body systems:

Answer 9

Resp: bronchiecstasis, bronchitis, haemoptysis, reactive airway disease, increased resp secretions.

Cardiac: RVH, pulm A dilation.

Pancreas: pancreatitis, DM, insulin deficiency.

Reproductive: inferility, delayed puberty.

Bone: arthritis, osteoporosis, growth failure.

Intestinal; intusussception, rectal prolapse, appendicitis.

Question 10

List the predisposing factors for a respiratory infection:

Answer 10

Cough reflex: those w/ conditions that affect the cough reflex, strokes, surgery, NM disorders.

Cilia defects: smoking

Mucosal disorders: CF, bronchitis.

Immunosuppression: loss of lymphocytes.

Macrophage function damage: smoking, occupational exposure, hypoxia.

Pulmonary oedema: -> alveolar flooding.

Question 11

What is the difference between a primary and secondary respiratory infection.

Answer 11

Primary: no predisposing conditions, usually healthy individuals.

Secondary: local or systemic body defences are weakened -> HIV/AIDS.

Question 12

Describe the pathophysiology of asthma

Answer 12

Inflammatory airway disease associated w/ reversible episodes of smooth muscle over-reactivity.
Bronchial tree has increased irritability - paroxysmal narrowing of the airway -> spontaneous or treatment reversal.
Mucus membrane/muscle of bronchi become thickened -> mucus glands enlarge reducing air flow to lower tract, walls swell causing inflammatory exudate influx.
During attacks bronchospasm and secretion of thick sticky mucus causes narrowing -> partial expiration -> hyperinflation and wheezing.
Mucus plugs can completely obstruct - hypoxia, resp failure, death.

Question 13

Outline the causes of asthma

Answer 13

Atopic, non-atopic, aspirin induced, occupational, allergic bronchopulmonary aspergillosis.

Atopic (extrinsic): atopic (type 1) hypersensitivity to foreign proteins, absorption by bronchial mucosa stimulates antibody binding to mast cell surface, second exposure releases histamine -> bronchospasm and mucus secretion. Attacks less severe w/ age.

Non-atopic (intrinsic): later adulthood, chronic upper airway inflammation, bronchitis, occupation, aspirin may induce, attacks more severe w/ age, irreversible lung damage, impaired vent, pulm HTN, R HF.

Question 14

Outline what bronchitis is

Answer 14

Infections which affect the trachea, larynx and lungs

Usually viral

Characterised by cough, dyspnoea, tachypnoea, xs sputum prod.

Laryngotracheobronchitis - croup -> severe: cough, dyspnoea, tachypnoea, seal bark cough.

Question 15

Describe the pathophysiology of acute bronchitis

Answer 15

Viral infection weakens defences allowing bacteria already in the tract to colonise -> infect bronchi

Extremes of age - downward spread -> bronchiolitis, bronchopneumonia

Common cause of IECOPD -> deterioration of pulm function -> cough, purulent sputum

Air pollutants can cause chemical injury -> smoke, Cl

Question 16

Describe the pathophysiology of chronic bronchitis

Answer 16

Progressive condition, commonly starts in middle age, cough for 3/12 for 2 successive years.
Prolonged irritation of the bronchial epithelium, worsened by cold/damp.
Causes - smoking and recurrent acute bronchitis.
Hyperventilate w/ accessory muscle use to achieve ‘normal’ blood gases.
Common bacteria include Haemophilus influenzae, Streptococcus pneumoniae.
Exaccerbation changes -> increase vol of mucus glands blocking the small airways impairing mucociliary escalator, oedema due to swelling of airway wall, reduced cilia function as cilia are damaged and non-ciliated endothelial cells replace leading to mucus accumulation, fibrosis of airway leading to reduced airflow -> all lead to dyspnoea, SOBOE, inc WOB.
Condition worsens impairing ventilation, leading to hypoxia, pulm HTN, R HF.
Later stages inflammation affects the alveoli and bronchioles -> emphysema -> COPD.

Question 17

Outline the pathophysiology of emphysema

Answer 17

Long term inflammation (chronic bronchitis) -> destruction of elastic tissue -> progressive lung expansion as recoil ability is lost -> barrel chest
Irreversible distention of the bronchioles, alveolar ducts and alveoli -> red. SA for GE.
Microscopically - lungs become full of large irregular cavities from damage.
2 types - Panacinar and centrilobar.
1/3 lung capacity lost before sympto.
S/S: weight loss, dyspnoea, R HF, prod cough, recurrent infections.

Question 18

Describe the term chronic obstructive pulmonary disorder (COPD)

Answer 18

Umbrella term - chronic progressive resp conditions inc asthma, chronic bronchitis, emphysema.

CB/emphysema normally co-exist to a degree.

Irreversible & persistent damage to small airways.

Significant resp impairment -> red. lung function -> red. vital capacity.

Causes -> GASES
Genetics: alpha -1 antitrypsin deficiency -> loss of protease protection
Air pollution.
Smoking.
Exposure: occupation.
Second-hand smoking.

Question 19

Outline the pathophysiology of pneumonia, inc common signs and symptoms:

Answer 19

> Infection/inflammation of the distal airways leading to formation of inflammatory exudate as pulmonary defence mechanisms fail to protect the lungs.
Polymorphs, lymphocytes and macrophages appear in greater no. in the blood.
Bacteria causing: Streptococcus pneumoniae, Staphylococcus aureus, Mycobacterium tuberculosis.

Signs and symptoms:
Body wide - fever, chills.
Resp - prod cough, haemoptysis, dyspnoea, pleuritic CP.
CNS - headaches, loss of appetite.
CVS - low BP, tachy.
Gastric - N&V.
MSK - joint pain, muscular aches and fatigue.

Question 20

List the risk factors for pneumonia:

Answer 20

> Impaired cough reflex -> secretions.
Damaged epithelial lining -> cilia function.
Impaired alveolar phagocytosis -> red. macrophage activity.
Hospitalisation -> antibiotic resistance exposure.
Extremes of age
Immobility -> unable to expel mucus.

Question 21

Describe bronchopneumonia

Answer 21

Patchy presentation -> inflamed bronchioles spreading to alveoli.
Fibrous exudate accumulates.
Leukocyte influx.
Common in elderly, infants, Ca, HF, CVA pts.
Often become septic with fever and red LOC.
Audible crackles.

Question 22

Describe lobar pneumonia

Answer 22

Infection in the lobules, 1/+.
Streptococcus pneumoniae -> watery exudate.
Fills lobule, overflows and fills adjacent lobules.
Inflamed visceral pleura -> pleuritic pain (sudden onset).
Abx treatment, or self-resolves in 2-3/52.

Question 23

What is the treatment for pneumonia?

Answer 23

BAPP:
Breathing -> maintain sats.
Antibiotics.
Pain relief -> pleuritic CP.
Pneumococcal vaccines.

Question 24

What is Legionnaires disease?

Answer 24

Respiratory infection caused by Legionella pneumophila, transmitted in water droplets in humidifiers and cisterns.
USA 1976.
S/S -> cough, dyspnoea, CP, myalgia, headache, C, nausea, D&V.
5-20% fatality.
Erythromycin.

Question 25

Describe what pulmonary tuberculosis is:

Answer 25

Caused by Mycobacterium tuberculosis.
Predisposing conditions - chronic alcoholism, DM, HIV/AIDS.
Humans host -> spread inhalation.
Can lay dormant.
Clinical features vary on stage, extent and disease activity - night sweats, weight loss, chronic cough, fever, bronchopneumonia, resp distress.
Lesions 10mm in D will destroy lung tissue leaving calcified nodule.
Can be no clinical consequences, organism may be host for years.

Question 26

Outline the pathophysiology of pulmonary embolism (PE):

Answer 26

Occlusion of pulmonary vasculature, commonly arterial -> S/M, multiple or massive.
Caused by DVT, thrombus, air, fat, Ca cells, bone fragments following trauma.
-> pulmonary infarct.
Pathophys pathways:
- Platelet factor release - serotonin/thromboxane A2 -> vasoconstriction.
- Decreased alveolar perfusion - hypoperfusion -> red. GE.
- Decreased surfactant - vent/perfusion mismatch -> hypoxia/dyspnoea.
Risk factors - immobilisation, preg, post-op, travel, HF, malignancies, contraceptives.
Prevention key - ambulation post-op, thrombo-embolic deterrent stockings, leg exercises.
Ax - Wells, sinus tachy, S1Q3T3, D-dimer, CTPA.
Treatment - O2, fluids, heparin, fibrinolytic agents, surgical thrombectomy.

Question 27

Describe carcinoma of the lung, inc common symptoms and treatment options:

Answer 27

Most common Ca, worst survival -> 4-7% rate in 5yrs.
<90% lung tumours are carcinomas, 10% operable.
Mets -> lymph nodes, bone, brain, liver, adrenal glands.

Symptoms:
Severe weight, pleuritic CP, dyspnoea, cough, haemoptysis.

Treatment: stage dependent
Surgical removal best chance, only option if small tumour and no mets.
Combined w/ chemo can lead to remission.

Question 28

What is mesothelioma?

Answer 28

Lung Ca associated w/ asbestosis -> v’ poor prognosis.

Involves both pleural layers.

Obliterates pleural cavity, compresses the lung as it grows.

Mets in hilar and mesenteric lymph nodes, other lung, liver, thyroid, bone, skeletal muscle, adrenal glands and brain.

Question 29

Outline what pneumoconiosis is:

Answer 29

Prolonged exposure to inhaled organic dusts -> inflammation and fibrosis of lung tissue.
Particles in bronchioles -> macrophage response -> fibrosis.
^ risk if smoker.

Types:
Coal workers - coal dust, common in miners, potentially fatal resp impairment.
Silicosis - silicon particles.

Question 30

What are the four causes of lung collapse:

Answer 30

> Obstruction of an airway (absorption collapse):
vol of collapse depends on size of obstruction, distally to obstruction air is trapped & absorbed -> lung collapse -> secretions -> infection -> abscess. Short-term collapse -> few affects. Long-term - fibrosis, permanent collapse. Sudden collapse - foreign body. Gradual - tumour.

> Impaired surfactant function: prem babies unable to produce surfactant -> unable to expand lungs. Vent until able to produce -> neonatal RDS. ARDS -pulm oedema dilutes surfactant in alveoli -> atelectasis -> gravely ill.

> Pressure collapse: pneumothorax, tension pneumothorax, haemothorax, pleural effusion.

> Alveolar hypoventilation: normal rest breathing some lobules collapsed as low tidal vol, re-expand on deep inspiration. Non-physiological causes post-op collapse after chest/abdo surgery, pain restricts expansion - secretions collect, chest infection risk.

Question 31

Explain what the four types of lung pressure collapse are:

Answer 31

> Pneumothorax: air in pleural cavity, spontaneous -> primary (unknown cause/recurrent in young/healthy) secondary (visceral pleura ruptures due to lung disease. Traumatic -> penetrating trauma to pleura.

> Tension pneumothorax: complication as flap/1-way valve between lung and pleura develops, air taken into cavity in inspiration, not escape in expiration, air accumulates and forces mediastinum and organs to other side -> cardiac arrest.

> Haemothorax: blood in pleural cavity, trauma, AAA.

> Pleural effusion: xs fluid in pleural cavity due to ^ hydrostatic P - (HF, ^ blood vol), ^ capillary permeability due to inflammation, decreased plasma osmotic P (nephrotic syndrome, cirrhosis), impaired lymph drainage.