CLI Week 4

Question 1

Lobar Pneumonia: Community Acquired Acute

Answer 1

• Organisms: Streptococcus pneumoniae (95% - hence pneumococcal vaccine), Haemophilus influenza (gram negative bacteria, less common in general, more common in COPD).
  
  • Klebsiella can be suspected in aged, diabetics, alcoholics
• Typical History: normal adult (20-50)
  
  • 1-3 days
  • High fever
  • Pleuritic chest pain
  • Rusty sputum
• Normally unilateral – can be whole lobe or just a segment – diffuse consolidation
• Complications uncommon
• More common in males

Question 2

Broncho Pneumonia: Nosocomial/Hospital Acquired

Answer 2

• Organisms: H. influenza (more common in nosocomial than lobar), Klebsiella, Pseudomonas, E. coli, Staph aureus, Strep pneumoniae (less common than in lobar)
• Occurs in a diseased lung or person – sick adult, old or very young
  
  • High fever, rusty sputum, pleuritic chest pain
• Look For: Patchy. Bilateral, lower lobes more common
  
  • Crosses anatomical borders! Due to damage to alveolar walls and spreading
• NOTE: Pathogenetic phases are unclear – can have different phases throughout lung
• Complications are common
• Both genders

Question 3

Phases of Pneumonia: Pathogenesis – Lobar Pneumonia

Answer 3

1. Congestion – Day 1
   
   1. Blood vessels enlarge – more blood – congestion – fluid leakage starts and accumulates in alveoli
   2. SOB because alveoli walls become thick with blood plus plasma accumulates in alveolar lumen
   3. Inflammatory mediators cause fever, chest pain, SOB = signs of Pneumonia
   4. Microscopy: thickened wall of alveoli, plasma in lumen
2. Red hepatisation – Day 2
   
   1. Lung appears red and solid like a liver
   2. Because RBCs start leaking in to the lumen by diapedesis
   3. Red lung = Pneumonitis
   4. Microscopy: Alveolar lumen filled with RBCs and some WBCs
3. Grey hepatisation – Day 4
   
   1. Neutrophils and WBCs start eating away bacteria and remove dead tissue
   2. Microscopy: lumen filled with all WBCs
4. Resolution – Day 8
   
   1. Lung mostly back to normal, some macrophages and lymphocytes remaining
   2. Clear lumen except for some remaining macrophages

Question 4

Lab diagnosis

Answer 4

Strep pneumoniae:

• Gram positive
• Circular colonies
• Alpha/partial haemolysis – dark green
• NOTE: clearing around central disc of optochin

Strep pyogenes:

• Gram positive
• Circular pinpoint colonies
• Beta/complete haemolysis
• Bright clear area around colony

Tuberculosis:

• Primary TB:
  
  • Initial infection
  • 90% asymptomatic
  • Infection walled off in Ghon Focus
• Secondary TB:
  
  • Reactivation of bacteria in the Ghon Focus when host is immunocompromised eg HIV, old age
  • Much more widespread inflammation – particularly upper lobes of lungs, often cavitation
• Miliary TB:
• Anergic TB:
  
  • When a patient has TB but a negative skin test
• Scrofuloderma: - see right
  
  • Cutaneous TB from underlying infection eg LN, bones or joints
  • Causes a Cold Abscess- so a big lump of pus but without the usual redness, heat or pain
• Atypical Mycobacteria:
  
  • Any of the 30 different acid-fast mycobacteria that do not cause TB or leprosy
  • Most Common:
    
    • Mycobacterium marinum – ‘fish tank granuloma’ from water
    • Mycobacterium avium-intracellulare – from birds or pigs

Question 5

COPD: Obstructive

Answer 5

• Emphysema + Chronic Bronchitis
• Most commonly caused by smoking
• Steps:
  
  • 1. Smoke irritants
  • 2. Epithelial irritation/damage
  • 3. Excess mucus production
  • 4. Inflammation
       * Emphysema: alveolar damage is by neutrophils and macrophages – Proteases – loss of elastic recoil – less pressure – equal pressure point moves lower – collapse in non-cartilaginous airway – obstruction. Acinus – alveoli/resp bronchioles.
       * Bronchitis: mucosal inflammation – mucus gland hyperplasia – inflammation – ciliary loss from damage to epithelium – retention of mucus – more inflammation – also smooth muscle spasm. Large airways.

Question 6

Restrictive Lung Disorders:

Answer 6

Restrictive Lung Disorders:

• Both FEV1 and FVC low so ratio is normal, but decreased TLC
• Pathology:
  
  • Damage by particles between 1-5 microns – lung injury to Type 1 pneumocytes – in response Type 2 Pneumocytes secrete fibroblast GF – inflammation and fibrosis of interstitium = stiff lung, restricts air entry and exit
• Idiopathic Pulmonary Fibrosis – unknown cause
• Pneumoconioses – dusts –
  
  • Silicosis – sand
  • Asbestosis – type of silicosis
  • Sarcoidosis – reaction to unknown antigen – from immune dysregulation

Question 7

• Other types of pneumonia‐ Interstitial, Atypical, chemical, lipoid pneumonia etc.

Answer 7

• Interstitial pneumonia ®
  
  • Pathophysiology ® idiopathic lung disease characterised by sudden onset fo dyspnoea and rapid development of respiratory failure. It involves the alveolated lung parenchyma in a bilateral, generally symmetric and fissue fashioin.
  • Microscopy ® diffuse alveolar damage with subsequent honeycomb fibrosis.
  • Gross ® cobblestoning of the pleural surface, associated with progressive fibrosis.
• Atypical
  
  • Caused by ® Legionella pneumophilia, Mycoplasma pneumoniae, Chlamydophila pneumonia
  • Affects people udner 40
  • Risk factors ® smoking, old age, weak immune system, chornic illness
  • Symptoms ® chills, cough, headache, fever, muscle stiffness, loss of appetitie, shortness of breath, rapid breathing
• Chemical ® Aspiration pneumonia
  
  • Inflammation of the lung caused by aspirating or inhaling irritants (usually gastric contents into the lungs).
  • Not infectious. Two types ® acute or chronic.
  • Symptoms ® cough and dyspnoea
  • Lung inflammation and infection (bacterial pneumonia or abscess), or airway obstruction.
  • Risk factors ® impaired cognition or level of consciousness, impaired swallowing, vomiting, GI devices and procedures, dental procedures, respiratory devices and procedures, GORD.
• Lipoid pneumonia
  
  • A type of pneumonia that develops when lipids enter the bronchial tree.
  • The disorder is sometimes called cholesterol pneumonia
  • It is either from exogenous or endogenous causes ®
    
    • Exogenous ® inhaled nose drops with an oil base for example
    • Endogenous ® from the body itself ® when the airway is obstructed, it is often the case that distal to the obstruction, lipid-laden macrophages (foamy macrophages) and giant cells fill the lumen of the disconnected airspace.

Question 8

• Acute Lung injury (ARDS, HMD).
• Atelectasis
• Bronchiectasis

Answer 8

• Acute Lung injury (ARDS, HMD).
  
  • Acute respiratory distress syndrome
    
    • Life threatening disease in critically ill patients. Manifestations of an inflammatory response of the lung to both direct and indirect insults and are characterised by severe hypoxemia, hypercapnia, diffuse infiltration in the chest x-ray and reduction in pulmonary compliance.
    • Triggered by various pathologies ® trauma, pneumonia and sepsis for example.
• Atelectasis
  
  • The collapse or closure of a lung resulting in reduced or absent gas exchange. It may effect part or all of the lung. Usually not bilateral.
  • Blockage of the air passages or by pressure on the outside of the lung, causing diminished volume. For example a tumour can be externally pushing the lung causing blockage.
• Bronchiectasis
  
  • Chronic infection in the airways causing them to widen and become flabby, thickened and scarred. This results in the affected person becoming more prone to recurrent respiratory tract infections. Characterised by a chronic cough.

Question 9

exchange in lungs and tissues

Answer 9

1. exchange in lungs and tissues

• External respiration (pulmonary gas exchange):
  
  • Partial pressure gradients of O₂ and CO₂ drive the diffusion of these gases across the respiratory membrane
  • A steep oxygen partial pressure gradient exists across the respiratory membrane because the P_O2 of deoxygenated blood in the pulmonary arteries is only 40 mmHg, as opposed to a P_O2 of approximately 104 mmHg in the alveoli à oxygen diffuses rapidly from the alveoli into the pulmonary capillary blood
  • Equilibrium – that is, a P_O2 of 104 mmHg on both sides of the respiratory membrane – usually occurs in 0.25 second (one-third of the time a RBC spends in a pulmonary capillary à blood can flow through the pulmonary capillaries three times as quickly and still be adequately oxygenated
  • Carbon dioxide diffuses in the opposite direction along a much gentler partial pressure gradient of about 5 mmHg (45 mmHg to 40 mmHg) until equilibrium occurs at 40 mmHg; expiration then gradually expels carbon dioxide from the alveoli
  • Although O₂ pressure gradient for oxygen diffusion is much steeper than the CO₂ gradient, equal amounts of these gases are exchanged as CO₂ is 20 times more soluble in plasma and alveolar fluid than O₂
• Internal respiration (capillary gas exchange in tissues):
  
  • Partial pressure and diffusion gradients are reversed from external respiration
  • Tissue cells continuously use O₂ for their metabolic activities and produce CO₂; as P_O2 is always lower in tissues than it is in systemic arterial blood (40 mmHg versus 100 mmHg), O₂ moves rapidly from blood into tissues until equilibrium is reached
  • Simultaneously, CO₂ moves quickly along its pressure gradient into blood à venous blood leaving the tissue capillary beds and returning to the heart has a P_O2 of 40 mmHg and a P_CO2 of 45 mmHg

Question 10

Blood gas and electrolytes in health and disease

Answer 10

• Normal values for arterial blood gas (ABG):
  
  • pH – 7.35-7.45
  • paO₂ – 75-100 mmHg
  • pCO₂ – 35-45 mmHg
  • HCO3^- - 22-26 mmol/L
• Changes in blood gases:
  
  • Metabolic acidosis – can be caused by either an increase in circulating acids and/or a loss of base (HCO3^-). These include:
    
    • Renal failure (unable to excrete acids or hydrogen)
    • Lactic acidosis (increase in circulating acids)
    • Keto-acidosis (increase in circulating acids)
    • Diarrhoea (HCO3^- loss)
  • Metabolic alkalosis – can be caused by an increase in HCO3^- or loss of metabolic acids. These include:
    
    • Prolonged vomiting (acid loss)
    • GI suctioning (acid loss)
    • Hypokalaemia (hydrogen excreted to maintain electrolyte balance)
  • Respiratory acidosis – caused by increased CO₂ levels which is then converted to an acid (hydrogen) as the body tries to compensate by excreting acids via the kidneys. These include:
    
    • Hypoventilation (sedatives/sedation/opiates)
    • Depression of respiratory centre in brain stem via trauma
    • Pneumonia
    • Pulmonary oedema
    • Asthma
  • Respiratory alkalosis – caused by a hyperventilation, the body getting rid of too much CO₂, for example:
    
    • Anxiety
    • Hypoxaemia (caused by heart failure)
• Normal ranges for electrolytes:
  
  • Sodium – 137-147 mmol/L
  • Potassium – 3.5-5.0 mmol/L
  • Chloride – 96-109 mmol/L
  • Calcium – 2.25-2.65 mmol/L
  • Glucose:
    
    • Random – 3.0-7.7 mmol/L
    • Fasting – 3.0-6.0 mmol/L

Question 11

Pulmonary function testing (PFT)

Answer 11

1. Pulmonary function testing (PFT)

• PFT measures:
  
  • Tidal volume (VT) – this is the amount of air inhaled or exhaled during normal breathing
  • Minute volume (MV) – this is the total amount of air exhaled per minute
  • Vital capacity (VC) – this is the total volume of air that can be exhaled after inhaling as much as you can
  • Functional residual capacity (FRC) – this is the amount of air left in lungs after exhaling normally
  • Residual volume – this is the amount of air left in the lungs after exhaling as much as you can
  • Total lung capacity – this is the total volume of the lungs when filled with as much air as possible
  • Forced vital capacity (FVC) – this is the amount of air exhaled forcefully and quickly after inhaling as much as you can
  • Forced expiratory volume (FEV) – this is the amount of air expired during the first, second, and third seconds of the FVC test
  • Forced expiratory flow (FEF) – this is the average rate of flow during the middle half of the FVC test
  • Peak expiratory flow rate (PEFR) – this is the fastest rate that you can force air out of your lungs

• Flow volume loops provide a graphical illustration of a patient’s spirometric efforts. Flow is plotted against volume to display a continuous loop from inspiration to expiration. The overall shape of the flow volume loop is important in interpreting spirometric results.
  
  • In normal patients, after a small amount of gas has been exhaled, the flow is limited by airway compression and determined by the elastic recoil of the lung and resistance upstream, of that point
  • In restrictive disease (interstitial lung disease, kyphoscoliosis), the maximum flow rate is reduced, as is the total volume expired. The flow is abnormally high in the latter part of expiration because of increased recoil
  • In obstructive diseases (COPD/asthma), the flow rate is very low in relation to lung volume, and a scooped-out appearance is often seen following the point of maximal flow

Question 12

Anatomy of the lobes of the lung. Why does aspiration occur on right side?

Answer 12

• Each lung is surrounded by pleurae and connected to the mediastinum by vascular and bronchial attachments (lung root)
• The two lungs differ in shape and size because the apex of the heart is slightly to the left of the median plane. The left lung is smaller than the right, and the cardiac notch is moulded to and accommodates the heart
• The left lung is subdivided into superior and inferior lobes by the oblique fissure, whereas the right lung is partitioned into superior, middle and inferior lobes by the oblique and horizontal fissures
• the trachea divides to form the right and left main (primary) bronchi; the right main bronchus is wider, shorter and more vertical than the left. Consequently, it is more common for an inhaled foreign object to get stuck there

Question 13

Spread of infectious disease – Mechanisms of spread.

Answer 13

Ways infectious diseases can spread:

1. Droplet
   
   • Talking, coughing, sneezing and releasing droplets into the air which can only travel a short distance (approx. 1 metre)
   • Touching nose or mouth with droplet-contaminated hands
   • Examples:
     
     • Cold, flu, meningococcal disease
2. Aerosol (airborne)
   
   • When infected person talks, breathes, coughs or sneezes with tiny particles containing infectious agents in the air
   • Aerosols can travel long distances on air currents – remain suspended in air for minutes to hours
   • Examples:
     
     • Varicella, measles, TB
3. Faecal-oral
   
   • Microscopic faecal particles taken in by mouth of another person
     
     • From soiled hands to mouth
     • Indirectly by objects, surfaces, food or water soiled with faeces
   • Examples:
     
     • Giardia, hep A, rotavirus, salmonella
4. Skin or mucous membranes
   
   • Directly when skin or mucous membranes comes into contact w/ skin of mucous membrane of another person
   • Indirectly when skin or mucous membrane comes in contact w/ contaminated surfaces
   • Examples:
     
     • Scabies, head lice, conjunctivitis, cold sores, warts
5. Blood or other body fluids e.g. urine, saliva, breast milk
   
   • When blood/body fluids from infected person comes into contact with:
     
     • Mucous membrane (kissing, breast feeding, sexually)
     • Bloodstream (needle stick, break in skin)
   • Examples:
     
     • Hep B, hep C, HIV, CMV, infectious mononucleosis
6. Sexually
   
   • Genital to genital; oral to genital; genital to anal
   • Chlamydia, genital herpes, genital warts, gonorrhoea, syphilis etc.
7. Vertical transmission
   
   • Mother to child
   • Examples:
     
     • Varicella, hep B, rubella
8. Insects (vector)
   
   • RRV, BFV, dengue, malaria

Question 14

Revision of physiology of Respiration, Blood gases and Pulse Oximetry.

Answer 14

Revision of physiology of Respiration, Blood gases and Pulse Oximetry.

Respiration and ventilation

• Inspiration and expiration
• Lungs kept inflated by natural elasticity of chest wall – and strong force between parietal and visceral pleura, as well as negative intrapleural pressure keeping lungs patent
• Dalton’s Law of Partial Pressures
  
  • Total pressure exerted by mixture of gas is sum of pressures exerted independently of each gas in mixture
  • Partial pressure of each gas is directly proportional to percentage of gas in the mixture
    
    • E.g. 20-21 of air is oxygen, 79% is nitrogen, the rest is mixture of others
• Henry’s Law
  
  • When gas is in contact with liquid, gas will dissolve in liquid in proportion to its partial pressure
    
    • Therefore the greater concentration of gas, the faster it will go into solution in liquid (i.e. nitrogen more likely to dissolve into liquid)
    • E.g. if P_CO2 in pulmonary capillaries is higher than in lungs, CO₂ diffuses out of blood and enters air in alveoli
  • Oxygen is only 1/20^th as soluble as carbon dioxide
• From Henry’s Law, partial pressure gradients of oxygen and carbon dioxide drive the diffusion of these gases across the respiratory membrane
  
  • Essentially, there is more carbon dioxide in the blood and less in the alveolar space, and vice versa for oxygen
• Molecular oxygen carried bound to Hb in RBCs – amount of oxygen bound to Hb depends on PO₂ and PCO₂ of blood, blood pH and other factors.
  
  • Some oxygen dissolved in plasma
• Carbon dioxide can be transported three ways in the blood:
  
  • Dissolved in plasma
  • Chemically bound to Hb
  • Primarily: bicarbonate ions in plasma

• Pulse oximetry = test used to measure oxygen saturation of blood
  
  • Non-invasive and cheap
  • Uses light to measure – Hb absorbs light therefore the more light is absorbed, the higher the concentration of Hb

Question 15

Metabolic and respiratory acidosis.

Answer 15

Metabolic acidosis:

• Low blood pH and not enough HCO₃^- levels to take on H⁺ ions
• Common causes include:
  
  • Accumulated lactic acid during exercise or shock (lactic acidosis)
  • DKA
  • Too much alcohol (acetic acid)
  • Kidney failure

Respiratory acidosis:

• Common cause of acid-base imbalance and most often occurs when someone breathes shallowly or when gas exchange is affected by diseases such as pneumonia or CF
  
  • CO₂ accumulates in the blood resulting in more conversion bicarb and H⁺ ions, reducing pH

Question 16

Clinical assessment of lung function

Answer 16

1. Spirometry: Measures flow in and out of lungs (ventilation) but cannot assess residual volume (volume in lungs that remains following maximal expiration)

Forced Expiration

FEV1 (forced expiratory volume in 1sec )

• Take maximal inspiration and forcefully expire
• Result likely to be less than slower expiration since forceful expiration causes small airway collapse (gas trapping) thus less volume of air exhaled

Functional vital capacity

FVC/ VC

• Total amount of air that can be exhaled after maximal inspiration

Flow volume curve

Measures inspiratory and expiratory flow as function of exhaled volume rather than against time

• Simple, reproducible
• Can calculate FEV1, FVC, PEF

1. Forced expiratory time (FET): measure the time taken for the patient to exhale forcefully and completely through open mouth after maximal inspiration.
   
   • Normal time <3sec
   • Increased FET- airway obstruction
   • If >9sec and significant smoking Hx à more predictive of COPD
   • Less accurate than spirometry or peak flow meter
2. Peak flow meter: simple gauge measuring maximum flow rate of expired air. Take full breath in but focus on rapid forced expiratory puff through mouth (rather than prolonged expiration). Value recorded is peak expiratory flow (PEF)

• Normal- 600L/min young men ; Normal- 400L/min young women
• Value depends on age, sex, height
• Airway obstruction (COPD, asthma) à reduced and variable PEF
• Most useful for serial estimates of lung function

Question 17

Clinical diagnosis of COPD

Answer 17

Clinical diagnosis of COPD

• Spirometry- FEV1/FVC <70% = obstructive indicative of conditions like:
  
  • Loss of elastic recoil (alveolar wall destruction and loss of elastic fibres) à asthma, COPD
  • Narrowed airways

COPD = Scooped out appearance

• Difficult to expire air from collapsed airways – prolonged expiration
• Increased RV from hyperinflation and gas trapping in collapsed airways

NOTE expiratory time is important for lung emptying, thus during exercise

• RR increases, reducing expiratory time à progressive increases in FRC à ‘dynamic hyperinflation’ à causes COPD exercise limitations

Pulmonary oedema

< >Spirometry- flow volume curve

Question 18

Clinical diagnosis of acute pneumonia

Answer 18

Clinical diagnosis of acute pneumonia

Symptoms:

• fever, rigors, anorexia, dyspnoea, cough, purulent sputum, haemoptysis, pleuritic chest pain

Signs:

• fever, cyanosis, confusion, tachypnoea/cardia, diminished lung expansion (consolidation), increased vocal fremitis, bronchial breathing, pleural rub

Investigations:

• CXR- consolidation (localised to lobes or sporadic)
• O₂ sats
• CBC, U&E, LFT, CRP
• Blood cultures if temp >38 degrees celcius

Question 19

Clinical assessment and definition/diagnosis of acute and chronic bronchitis

Answer 19

Clinical assessment and definition/diagnosis of acute and chronic bronchitis

Acute bronchitis

Chronic bronchitis

Clinical assessment

• Dry hacking cough
• Increased mucous production
• Sore chest
• Absence of fever or low grade fever

Blue bloater

• Hx recurrent respiratory tract infections (prone)
• Increasing SOB
• Loose cough worse in morning after waking
• Mucoid/mucopurulent sputum
• Resonance on percussion
• Hyper-inflated chest and reduced expansion
• Reduced breath sounds. Wheezes and crackles

Definition

Common, symptoms present 3-4days after URTI and resolve 2-3wks later.

• Usually viral aetiology
• Excessive sputum production – at least 3 months in a year for past 2 or more yrs.
• Airway irritation (smoking) inducing Irreversible hyperplasia of airway smooth muscle and hypertrophy of goblet cells. Reduced lumen size
• Inflammation induced destruction of airway epithelia- loss of cilia – no muscociliary escalator- mucous stasis

Diagnosis

• Clinical history
• ‘Rattling sound’ when listening to lungs
• Biopsy- look for hypertrophic changes in glands, hyperplasia of smooth muscle and loss of cilia
• CXR- may not always be useful unless significant fluid accumulation
• Lung function tests

Question 20

Clinical assessment and definition/diagnosis of COPD/emphysema

Answer 20

COPD/emphysema- pink puffer

Clinical assessment

• Increased AP diameter (barrel chest from gas trapping)
• May have tracheal tug if severe
• Pursed lip breathing
• Use of accessory muscles
• May be ‘drowsy’ from CO2 retention
• Hyper resonant on percussion
• Early inspiratory crackles

Definition

COPD/emphysema are obstructive conditions. Breakdown of alveolar walls and associated capillaries. Smoking- increases elastases and proteases (tissue destruction). May have genetic defect with alpha-1 antitrypsin deficiency (less inhibition of elastase activity)

• Pink puffer- can get air in so well oxygenated, but cannot exhale
• Alveolar disease- loss of radial traction – airway collapse on expiration- gas trapping

Diagnosis

• Obstructive condition: increased airway resistance
• Decreased VC, FEV1 (gas trapping less exhaled)
• Increased TLC, RV, FRC (gas trapping)
• FEV1/FVC <80%

• CXR- see more than 6 anterior ribs (more than 9 posterior ribs)
• Darker lung fields from more gas inside lung (trapped)
• Low flat diaphragm

Question 21

First line treatment of a patient with exacerbation of COPD

Answer 21

Normal COPD treatment

1. Smoking cessation, healthy lifestyle, immunisation
2. Bronchodilators to target obstruction (increases FEV1)
3. Long term O₂ therapy to counteract hypoxia
4. Pulmonary rehabilitation program

COPD exacerbation

• Usually due to infection – bacterial (50%), viral or both
  
  • Commonly Haemophilis influenza, Streptococcus pneumoniae, Moraxella catarrhalis
  • Antibiotics: recommended only if Hx of more purulent sputum, or if consolidation confirmed by CXR, or clinical signs of pneumonia

Question 22

Bronchiectasis- major problem in indigenous communities and recognition and misdiagnosis

Answer 22

• Pathological dilation of bronchi à impaired mucous clearance, prone to chronic infection (mucous stasis provides perfect conditions to harbor infection)
• Bronchiectasis commonly occurs if a patient has a Hx of chronic cough and purulent sputum since childhood. Caused by recurrent childhood infections such as:
  
  • Pertussis
  • Pneumonia
  • measles
• Major problem in indigenous communities- less likely to seek medical advice for URTI, common to acquire GAS infections – repeated pharyngitis. Overcrowding and reduced hygiene increases risk of repeated bouts of communicable disease
• Recognition:
  
  • Confirmed existing condition that predisposes risk of bronchiectasis development
    
    • CF, immune deficiency, primary ciliary dyskinesia
  • Purulent foul smelling sputum, sometimes bloodstained
  • Chronic respiratory symptoms can be non specific- no accurate way to distinguish between COPD, asthma and bronchiectasis (MISDIAGNOSED)
  • Spirometry findings can appear normal despite bronchiectasis (MISDIAGNOSED)
  • Confirmed by CT scan: indigenous communities have less access

Question 23

Clinical assessment of acute respiratory distress, how bad is it?

Answer 23

Clinical assessment of acute respiratory distress, how bad is it?

Severity of acute respiratory distress

• Unable to talk in full sentences
• Drowsiness from hypercapnia
• Stridor from upper airway obstruction
• Prominent use of accessory muscles – scalenes, sternocleidomastoid, intercostal recession, abdominal breathing
• SpO₂ <95%

Side note: Acute respiratory distress syndrome

Overview: ARDS can lead to respiratory failure and multiple organ failure. Pneumonia (viral or bacterial is most common cause), sepsis, gastric content aspiration and major trauma can precipitate ARDS. Clinically characterised by:

• Increased permeability pulmonary oedema
• Severe arterial hypoxemia
• Impaired CO₂ excretion

Survival improved by using lung protective ventilation

Question 24

• Interpretation of ABGs

Answer 24

NORMAL VALUES

pH

7.35-7.45

CO2

35-45 mmHg

O2

70/80-100mmHg

O2 sats

96-100%

HCO3

22-28mEq/L

Base excess

-3 à + 3

pH low = acidotic

pH high = alkalotic

CO2 = respiratory component, bicarbonate = metabolic component

Bicarbonate buffer system

note: increase CO2 and get compensatory rise in bicarb (kidneys reabsorb bicarb – takes a few days)

CO2 is not acidic but carbonic acid is (volatile acids – can be excreted by lungs)

Metabolic acids = fixed acids (not volatile – cant excrete via the lungs) e.g. lactate

Types of abnormalities:

• Acute resp acidosis (no renal compensation)
• Chronic resp acidosis (with renal compensation) e.g. COPD
• Respiratory alkalosis e.g. hyperventilation
• Metabolic acidosis
  
  • 2 TYPES: high anion gap and normal anion gap
  • pretty much compensate straight away (resp compensation is quick) patient will hyperventilate to get rid of CO2
• Metabolic alkalosis e.g vomiting, diuretics (low potassium means kidneys preserve potassium at expense of HCl)
  
  • Can be saline responsive or saline non-responsive
  • Saline responsive: diuretics, persistent vomiting, persistent NGT loss (low volume à increased aldosterone à Na reabsorption with loss of potassium and hydrogen, high chloride in urine ** if you give fluid – this stops happening **)
  • Saline unresponsive: due to excess mineralocorticoid activity from steroids/tumor à patients wont be hypovolaemic but will have high aldosterone, low urine chloride **need to give these patients lots of potassium so that kidneys retain hydrogen in exchange for excretion of potassium** if give fluid it wont help because aldosterone remains high causing Na reabsorption with loss of potassium and hydrogen.
• Mixed

METABOLIC ACIDOSIS:

Anion gap = (Na+K) – (HCO3 + Cl) positives – negatives, positives must equal negatives so the anion gap is the unmeasured anions present in the serum (lactate, ketones, toxins, drugs, renal acids)

• Raised anion gap (>11mEq/L) = high anion gap metabolic acidosis
  
  • Causes: GOLDMARK acronym
    
    • G – glycols (ethylene glycol, propylene glycol)
    • O – oxoproline (paracetamol metabolite)
    • L – L-lactate (responsible for lactic acidosis)
    • D – D-lactate
    • M – methanol
    • A- aspirin
    • R –renal failure
    • K – ketoacidosis (starvation, alcohol, diabetes)
• can have a metabolic acidosis without anion gap = NORMAL ANION GAP metabolic acidosis
• Normal anion gap metabolic acidosis à HCO3 loss (e.g. diarrhea) with Cl replacement
  
  • Causes = USEDCRAP acronym
    
    • U – uretoenterostomies
    • S – small bowel fistula
    • E – excess chloride (HCl infusion)
    • D – diarrhea
    • C – carbonic anhydrase inhibitors
    • R – renal tubular acidosis
    • A – addison’s disease
    • P – pancreatoenterostomies

Question 25

* **Clinical assessment of acute resp failure and sepsis**

Answer 25

Acute respiratory failure: * Type 1: hypoxaemia but no hypercapnia e.g. diffusion problem * Type 2: hypoxaenia and hypercapnia e.g. neuromuscular issue, reduced breathing effort from a drug or brain stem lesion * Look at ABGs, is it type I or 2? * Gold standard for diagnosis of acute respiratory failure (excluding those patients who have chronic respiratory failure) = pO2 less than 60mmHg on ABGs * SpO2 of 91% or below = respiratory failure (don’t apply to chronic resp failure patients) * Clues on examination: cant speak in full sentences, ALOC (GCS score), cyanotic (central and/or peripheral), plethora (vasodilation due to hypercapnia – in type II), tripoding, may have increased or decreased RR, pulsus paradoxus Sepsis ![]()

Question 26

* **Infective causes of pneumonia:**

Answer 26

* Common bacterial 1. Streptococcus.pneumoniae * Causes 90% of CAP * Encapsulated (increased risk if asplenic) * Gram pos diplococcus * Alpha haemolytic * Usually Optochin sensitive; (\>14mm) if not test if bile soluble (they will be) * Vaccine available * Serotype 3 pneumococci can cause complications 1. H.influenzae * Encapsulated and unencapsulated forms * Encapsulated form: can be life threatening in children (esp post-viral infection) * Increased risk if have COPD (most common cause of COPD exacerbation), cystic fibrosis, bronchiectasis * Gram negative coccobacillus 1. Pseudomonas aeruginosa * Gram negative rod * Usually nosocomial but can be CAP in cystic fibrosis patients * Immunocompromised * Necrotizing infection of lung parenchyma and pulmonary capillaries * Propensity to invade blood vessels and become extrapulmonary 1. Klebsiella pneumoniae * Gram negative rod * Most common cause of gram neg bacterial pneumonia * Especially affects chronic alcoholics * Thick gelatinous à Red currant jelly sputum * Tropical 1. Melioidosis * Burkholderia pseudomallei = gram negative soil dwelling bacteria * Indigenous, immunocompromised (diabetics/alcholics) most at risk * Vietnam and north Australia * Can be acute or chronic * Most common presentation is pneumonia (others include: skin lesions, lung nodules) * Note: can cause acute septicaemia (need to consider it as a cause to be able to treat) * Need to culture on Ashdown agar 1. Leptospirosis * Spirochaete bacteria * Spread by direct or indirect contact with animal urine (water/soil) – esp rats * Mostly in farmers, vets, abattoir workers * systems involved: symptoms can be mild like headaches, muscle aches and fevers à or severe like meningitis, bleeding from lungs (severe pulmonary haemmorhage syndrome) , kidney failure + bleeding (weil’s disease) * Aspiration pneumonia * Alcoholic/ debilitated with poor gag/cough reflex/comatose (GORD does not cause it) * Chemical (gastric contents) + infective (anaerobic bacteria e.g. bacteroides/fusobacterium from oral cavity) * Cause of lung abscess * Necrotizing and fulminant pneumonia – high mortality * Viral: atypical pneumonia 1. Influenza * Influenza A/B * Influenza pneumonia can cultivate a secondary staph aureus pneumonia in adults and children à very nasty with high incidence of complications * Epidemics (antigenic drift), pandemics (antigenic shift) 1. Human Metapneumovirus * Important in kids, elderly ad immunocompromised * 2^nd most common cause of pneumonia in children under 5 * Atypical: symptoms outweigh findings (no alveolar exudate but wall thickening due to inflammatory infiltrates leads to lack of O2 diffusion across to pulmonary capillaries) 1. Mycoplasma pneumoniae * Young adults/children * Positive cold agglutin test * Symptoms outweigh radiological findings (no consolidation – no alveolar exudate) = MAX symptoms MIN signs * Erythema multiforme may develop * Mild rise in WCC, dry cough, less sputum * Slow gradual onset of malaise, fever, headaches (days à weeks) * Use macrolide antibiotics (roxithromycin, erythromycin) 1. Legionella pneumophila (legionnaires disease) * Pipes/watercooling systems * Nosocomial/hospital acquired * Increased risk if immunocompromised e.g chronic illness, organ transplant recipient * Can be severe with high fatality rate * Rapid diagnosis: urine antigens * Tuberculosis * Mycobacterium tuberculosis – intracellular in macrophages * Granulomas with T cells, giant cells, macrophages containing TB bacilli, B cells (walls off the bacteria – but.. inflammatory response of host to bacteria is what causes symptoms) (note: HIV – lose T cells which means easier for TB to disseminate – not walled off) * Primary TB: form of disease in a previously unexposed and unsensitized patient * Lower/middle lobes * More LN involvement * Cavitation is rare * Most people with TB infection wont get symptoms – latent TB * Secondary TB: pattern of disease arising in a previously sensitized host (esp with HIV). Reactivation usually due to immunocompromised state. * Upper lobes * Less LN involvement (bacilli more walled off) * Sensitized T cells cause more tissue damage à cavitation * Military TB: can be pulmonary or systemic military TB * Pulmonary military TB: organisms drain through lymphatics into the lymphatic ducts which empty into venous circulation à enter RA and RV and pumped to lungs à widely disseminated through lung parenchyma * Systemic military TB: organisms disseminate into systemic arterial system to almost all body organs (esp liver, bone marrow, spleen, adrenals, meninges, kidneys, fallopian tubes and epididymis) à potts disease (spine), tuberculous meningitis, scrofuloderma (skin TB due to tuberculous lymphadenitis). Lupus vulgaris (skin), osteomyelitis * Important symptoms: chronic cough, night sweats, weight loss, haemoptysis * History: Travel hx – esp PNG, occupation (silicosis increases risk) * Ziehl neelsen stain for acid fast bacilli * RIPE treatment method – rifampicin, isoniazid, pyrazinamide, ethambutol (for 2 months) then only isoniazid and rifampicin for following 6 months * MDR/XDR forms – changes treatment course

Question 27

* **First line treatment of patient with an exacerbation of COPD. What prescriptions would the patient need?**

Answer 27

* Standard: ABCs (fix as you go) * Controlled oxygen therapy – be careful not to give too much (lose hypoxic drive to breath which they rely on due to lack of sensitivity to hypercapnia) * Inhaled beta2 agonists + anti-cholinergic drugs (bronchodilators) * Steroids (note: research shows that it helps COPD exacerbated by pneumonia – don’t worry about immunosuppressing them, antibiotics for the organism, steroid for the inflammation) * Antibiotics – broad spectrum e.g. doxycycline, trimethroprin-sulfamexazole and amoxicillin clavulanate potassium (others if more severe e.g. penicillins, fluroquinolones, third generation cephalosporins or aminoglycosides) * +/- ventilator assistance

Question 28

* **Interpreting chest xrays**

Answer 28

![]() D = document * Name, date, gender, hospital number * Type of film: AP/PA, erect/supine, inspiratory/expiratory * Look at quality of _exposure/penetration_ (thoracic discs through heart) and any _rotation_ (clavicles equal distance from spinous process), _inspiration (_5-6 anterior ribs/ 8-10 posterior ribs) C = chest 1. **L**ungs: all lobes esp apices 1. Infiltrates? Masses? Air bronchograms (air filled bronchi made visible by opacification of surrounding alveoli)? Increased interstitial markings? Absence of normal markings? Increased vascularity ? 2. **A**irways 1. Trachea: central or deviated? 2. Angle of carina 3. **M**ediastinum 1. Heart: cardiothoracic ratio, heart position (normal = 2/3 L, 1/3 to R), heart borders (silhouette margins) \*\*if AP cant comment on heart size – magnified) 1. Great vessels: aorta, pulmonary arteries, SVC/IVC (size, shape) 2. Lymph nodes 1. **D**iaphragm 1. Shape/contour 2. Hemidiaphragm levels 3. Costophrenic and cardiophrenic angles (any blunting?) 4. Any air under the diaphragm ? pneumoperitoneum 2. **A**nd pleura 1. Any thickening or pleural reflections? B = bones and soft tissues * # * subcutaneous emphysema? A = abdomen and review * stomach bubble? * Gas under diaphragm e.g. pneumoperitoneum ? (bowel perf) Extras = PICC line, ETT, catheters, chest drain, NG tube, ECG electrodes, oxygen device

Question 29

* Red flags in pneumonia

Answer 29

* Red flags in patient: * Fever and constant sweats * Brown, rusty colour of sputum * Tachycardia, hypotensive, tachypnoea, low O₂ sat 90%, cant speak in full sentences * Asthma and COPD history * Multiple risk factors: smoker, diabetic * From tropical region * Evidence of sepsis à progression to septic shock with low BP for this patient

Question 30

**How would a severely ill patient in respiratory distress be treated in a remote area:**

Answer 30