Week 1 - I'm Not Having A Doctor in My House

Adam
Trytell
Week 1: I don’t want a doctor in my house

MICROBIOLOGY OF PNEUMONIA 3
UNDERSTAND THE UNDERLYING MICROBIOLOGY OF PNEUMONIA AND RECOGNISE MAJOR
PATHOGENIC MICROORGANISMS IN SPUTUM GRAM STAINS AND APPROPRIATE STAINED TISSUES 3
APPRECIATE THE DIFFERENT SPECTRUM OF CAUSATIVE ORGANISMS BETWEEN (A) COMMUNITY
ACQUIRED AND HOSPITAL ACQUIRED PNEUMONIA AND (B) PNEUMONIA IS IMMUNE-‐COMPETENT
VS IMMUNE-‐COMPROMISED HOST 4
UNDERSTAND MECHANISMS OF ACTION OF MAJOR ANTIBIOTICS 5
BE AWARE OF THE MICROBIOLOGICAL SPECTRUM OF MAJOR ANTIBIOTICS 7
BE AWARE OF VIRULENCE FACTORS AND RESISTANCE MECHANISMS FOR RESPIRATORY TRACT
PATHOGENS 9
DEFENCE OF LOWER RESPIRATORY TRACT AGAINST INFECTION 11

BE AWARE OF MAJOR MUCOSAL AND SYSTEMIC DEFENCE MECHANISMS 11
APPRECIATE HOW PARTICULAR IMMUNE DEFECTS PREDISPOSE TO INFECTION WITH CERTAIN
TYPES OF PATHOGENS USING GLUCOCORTICOID TREATMENT AS AN EXAMPLE 13
APPRECIATE THE EFFECT OF IMMUNE DEFECTS ON RESPONSE TO TREATMENT 13
PATHOLOGY OF PNEUMONIA 14

UNDERSTAND THE PATHOLOGY (MACROSCOPIC, MICROSCOPIC, PATHOPHYSIOLOGY) OF THE
DIFFERENT TYPES OF PNEUMONIA AND RELATE THESE TO CLINICAL AND RADIOLOGICAL SIGNS 14
DIAGNOSIS OF PNEUMONIA 17

PREDICT THE MOST LIKELY RANGE OF PATHOGENS FROM THE CLINICAL HISTORY 17
UNDERSTAND THE PRINCIPLES OF CHOOSING EMPIRIC ANTIBIOTIC THERAPY 17
RECOGNISE THE IMPORTANCE OF MICROBIOLOGICAL DIAGNOSIS IN MANAGEMENT 17
RESPIRATORY FAILURE 18
UNDERSTAND THE PATHOPHYSIOLOGY OF ACUTE RESPIRATORY FAILURE IN SEVERE PNEUMONIA
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DIAGNOSIS AND MANAGEMENT OF PNEUMONIA 20

RECOGNISE CLINICAL SIGNS OF PNEUMONIA 20
RECOGNISE RADIOLOGICAL SIGNS OF PNEUMONIA 20
BE ABLE TO ASSESS THE CLINICAL SEVERITY OF ACUTE PNEUMONIA 22
BE ABLE TO PRIORITISE HISTORY, CLINICAL EXAMINATION, INVESTIGATIONS, AND TREATMENTS
APPROPRIATELY IN THE ACUTE MANAGEMENT OF VERY SICK PATIENTS 23
BE FAMILIAR WITH CLINICAL METHODS OF OBTAINING SAMPLES FOR MICROBIOLOGICAL
INVESTIGATION 23
UNDERSTAND PRINCIPLES OF SUPPORTIVE MANAGEMENT AND CLINICAL MONITORING 23

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Adam Trytell
EPIDEMIOLOGY OF COMMUNITY ACQUIRED PNEUMONIA 24

BE ABLE TO CONTRAST THE RISK FACTORS, PREVALENCE AND OUTCOMES OF COMMUNITY
ACQUIRED PNEUMONIA IN THE PRE-‐ANTIBIOTIC AND ANTIBIOTIC ERAS 24
BE AWARE OF THE EXTENT TO WHICH PNEUMONIA AND OTHER RESPIRATORY INFECTIONS AND
DISEASES ACCOUNT FOR MORBIDITY AND MORTALITY IN THE AUSTRALIA POPULATION AS A
WHOLE, AND IN THE INDIGENOUS POPULATION. SUGGEST REASONS FOR OBSERVED DIFFERENCES
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PREVENTION; IMMUNISATION 25
OUTLINE THE RATIONALE FOR POPULATION-‐BASED PREVENTION 25
DISCUSS THE EPIDEMIOLOGICAL AND SCIENTIFIC BASIS OF INFLUENZA AND PNEUMOCOCCAL
VACCINATION 25
PATIENT’S EXPERIENCE OF ILLNESS (MEDICAL SOCIOLOGY) 26

OUTLINE FACTORS (EG. PSYCHOSOCIAL, CULTURAL, ENVIRONMENTAL, ECONOMIC, GENDER, AGE)
THAT MAY INFLUENCE AN INDIVIDUAL’S ADAPTATION TO AND EXPERIENCE OF ILLNESS 26
REFUSAL OF TREATMENT 27

ANALYSE THE NEED FOR THE DOCTOR TO INTERPRET PATIENT TREATMENT REFUSALS 27
EXPLAIN THE DIFFERENCE BETWEEN OVER-‐RIDING A PATIENT’S REFUSAL OF TREATMENT AND
TREATING A PATIENT WITHOUT CONSENT 27
EXTRA LEARNING OBJECTIVE: RESPIRATORY CONTROL 28
EXTRA LEARNING OBJECTIVE: CLINICAL REASONING AND THE MURTAGH

METHOD 31
EXTRA LEARNING OBJECTIVE: PRESCRIBING DRUGS 33
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Adam Trytell

Microbiology of pneumonia

Understand the underlying microbiology of pneumonia and recognise major pathogenic
microorganisms in sputum Gram stains and appropriate stained tissues

Community Acquired Pneumonias
− Often a bacterial infection follows an upper respiratory tract viral infection
− Pathophysiology;
o Bacterial invasion of the lung parenchyma causes the alveoli to fill with
inflammatory exudate causing consolidation of the pulmonary tissue
− Predisposing factors;
o Age: <16 or >65 years
o Co-‐morbidities: HIV infection, diabetes mellitus, chronic kidney disease,
malnutrition, recent viral respiratory infection
o Other respiratory conditions: CF, bronchiectasis, COPD, obstructing lesion
o Lifestyle: cigarette smoking, excess alcohol, IV drug use
o Iatrogenic: immunosuppressant therapy (including prolonged corticosteroids)

Streptococcus Pneumonia
− Most common cause of CAP
− Virulence factors
o Contain polysaccharide capsule
o Lacks catalase (increased peroxide and inhibits normal flora)
o IgA protease
o Autolysis
o Pili that mediates adherence to epithelium
− Gram-‐stained sputum
o Numerous neutrophils containing Gram-‐positive, lancet-‐shaped diplococci
− Treatment
o Respond rapidly to penicillin (be wary for resistance)

Haemophilus Influenzae
− Exists in two forms; encapsulated (5%) and unencapsulated (95%)
− Virulence factors
o Pili mediate adherence to respiratory epithelium
o Secretion of a factor disorganizes ciliary beating
o Protease released degrades IgA
o Capsule protects H. Influenzae from complement if in the blood
stream
− Gram-‐stained sputum
o Gram-‐negative
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Moraxella Catarrhalis
− Increasingly recognizes as a cause of bacterial pneumonia, especially in the elderly

Staphylococcus Aureus
− An important cause of secondary bacterial pneumonia is children and adults following viral
respiratory illness (eg: measles in children and influenza in children and adults)
− S. Aureus is associated with high incidence of complications (eg: lung abscess and empyema)

Klebsiella Pneumoniae
− Most frequent cause of Gram-‐negative bacterial pneumonia
− Commonly affects debilitated and malnourished people, particularly alcoholics
− Thick, gelatinous sputum due to the abundant viscid capsular polysaccharide it produces

Pseudomonas Aeruginosa
− Most commonly causes nosocomial infections, commonly occurs in CF and patients who are
neutropenic and has the ability to invade blood vessels

Legionella Pneumophila
− Common in individuals with predisposing conditions and can be quite severe
− Rapid diagnosis via antigens in the urine or a positive fluorescent antibody test on sputum
samples

Appreciate the different spectrum of causative organisms between (a) community acquired and
hospital acquired pneumonia and (b) pneumonia is immune-‐competent vs immune-‐
compromised host

Community-‐Acquired Acute Pneumonia Atypical Community-‐Acquired Pneumonia
− Streptococcus pneumonia − Mycoplasma pneumonia
− Haemophilus influenza − Chlamydia spp
− Moraxella catarrhalis − Coxiella burnetti
− Staphylococcus aureus − Viruses
− Legionella pneumophila o RSV, parainfluenza virus
− Enterobacteriaceae (Klebsiella pneumonia) (children), influenza A and B
− Pseudomonas spp (adults), adenovirus (military
recruits), SARS virus

Nosocomial Pneumonia Aspiration Pneumonia
− Gram-‐negative rods belonging to − Anaerobic oral flora (Bacteroides,
Enterobacteriaceae (Klebsiella spp., Prevotella, Fusobacterium,
Serratia marcescens, Escherichia coli) Peptostreptococcus), admixed with aerobic
and Pseudomonas spp., Staphylococcus bacteria (Streptococcus pneumonia,
aureus (usually penicillin resistant) Staphylococcus aureus, Haemophilas
influenza and Pseudamonas aeruginosa)

Pneumonia in an Immunocompromised Host

− Cytomegalovirus

− Pneumocystic carinii

− Mycobacterium avium-‐intracellulare

− Invasive aspergillosis

− Invasive candidiasis
− Usual bacterial, viral and fungal organisms listed above
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Understand mechanisms of action of major antibiotics

Targets for antibacterial drugs
− Cell wall synthesis
o Penicillins, cephalosporins, glycopeptides, carbapenems, monobactams, isoniazid,
and bacitracin
− DNA integrity
o Metronidazole, quinolones (DNA gyrase inhibitors)
− DNA dependent RNA polymerase
o Rifampicin
− Protein synthesis (50S)
o Macrolides, lincosamides, lincomycin, chloramphenicol
− Protein synthesis (30S)
o Aminoglycosides, tetracyclines
− Folic acid metabolism
o Trimethoprim, sulphonamides

Antibacterial drugs that inhibit cell wall synthesis

Penicillins (benzylpenicillin, amoxicillin, phenoxymethylpenicillin and flucloxacillin)
− Mechanism of Action
o Target the ‘Penicillin Binding Proteins (PBP)’ in bacterial wall, including
transpeptidases. This results in irreversible inactivation of transpeptidase via
blocking cross-‐linking of peptide chains attached to peptidoglycan backbone
− Bacteriocidal to growing cells (autolysis), bacteriostatic for entire populations

Cephalosporins (cefadroxil, cefuroxime and ceftriaxone)
o Bacteriocidal drugs containing a β-‐lactam that inhibit bacterial wall synthesis
similar to penicillins
− Generations (I-‐V) are defined on spectrum of activity, with later generations having
expanded activity against gram negative bacteria (but decreased against gram positive)

Carbapenems (ertapenem, Imipenem)
o Binds to penicillin-‐binding proteins, preventing bacterial wall synthesis.
Carbapenems are able to circumvent β-‐lactamase by binding it with high affinity and
acylating the enzyme, rendering it inactive
− Carbapenems have the broadest antibacterial spectrum compared with other β-‐lactam drugs

Monobactams (aztreonam)
o Binds to penicillin-‐binding proteins, inhibiting synthesis of bacterial cell wall,
thereby blocking peptidoglycan crosslinking

Glycopeptide (vancomycin)
o Bacteriocidal drugs that inhibit peptidoglycan synthesis, with possible effects on
RNA synthesis

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Antibacterial drugs that inhibit bacterial nucleic acids

− Antifolates; affect DNA metabolism
− Quinolones; affect DNA replications and packaging
− Rimfampicin; affects transcription

Quinolones (ciprofloxacin, nalidixic acid)
o Bactericidal drugs that inhibit prokaryotic DNA gyrase, preventing packaging DNA
into supercoils that is essential for DNA replication and repair
− Cannot give quinolones with theophylline, this will prevent toxicity

Metronidazole (tinidazole)
− Mechanism of action
o Bactericidal drug that is metabolized to an intermediate that inhibits bacterial DNA
synthesis and degrades existing DNA. It is selective as it’s intermediate is not
produced in mammalian cells
− Should not be given to pregnant women

Rifampicin
o Bactericidal drug that inhibits DNA-‐dependent RNA polymerase

Antibacterial drugs that inhibit protein synthesis

Aminoglycosides (gentamicin, streptomycin, netilmicin, amikacin)
o Bacteriocidal drugs the bind irreversibly to the 30S portion of the bacterial
ribosome. This inhibits the translation of mRNA to protein and causes more frequent
misreading of the prokaryotic genetic code

Tetracyclines (tetracycline, minocycline, doxycycline)
o Bacteriostatic drugs that work by selective uptake into bacterial cells due to active
bacterial transport systems not possessed by mammalian cells. The tetracycline then
binds reversibly to the 30S subunit of the bacterial ribosome, interfering with the
attachment of tRNA to the mRNA ribosome complex

Macrolides (erythromycin, clarithromycin, azithromycin)
o Bacteriostatic/bacteriocidal drugs that reversibly bind to the 50S subunit of the
bacterial ribosome, preventing translocation movement of ribosome along mRNA

Chloramphenicol
o Bacteriocidal/bacteriostatic drug depending on the bacterial species. It reversibly
binds to the 50S subunit of the bacterial ribosome, inhibiting the formation of
peptide bones

Lincosamine (clindamycin)
o Similar to macrolides
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Adam Trytell
Folate synthesis inhibitors

o Folate is an essential co-‐factor in the synthesis of purines
and DNA. Bacteria, unlike mammels, but synthesize their
own folate from para-‐aminobenzoic acid. This pathway
can be inhibited at two points;
§ Sulfonamides: inhibits dihydrofolate synthetase
§ Trimethoprim; inhibits dihydrofolate reductase
o Both drugs are bacteriostatic. Sulfonamides are used for
simple urinary tract infections (UTIs), where as
trimethoprim and co-‐trimoxizole (trimethoprim and
sulfamethoxazole) are used for UTIs and respiratory tract infections

Be aware of the microbiological spectrum of major antibiotics

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Be aware of virulence factors and resistance mechanisms for respiratory tract pathogens

Virulence factors for Respiratory Pathogens
− Establishment (staying in)
o Polysaccharide capsule: inhibits phagocytosis and adhere to surfaces
o Fimbrae: found on some Gram-‐negative organisms, allows attachment
o Adhesins: glycolipids/lipoproteins allows adherence to tissue
o Virions: lytic virus fills a host cell with virions until it bursts open and pours
the virions into the intercellular fluid. This process repeats until not host
cells remain
− Defeating the host defences
o Passive defences
§ Capsule: protects against phagocytosis
§ Cell walls: defends against host defences (ie: increasing adherence
to host target cells and resisting against hostile environment))
o Active defences
§ Enzymes;
• Leukocidins: destroy white blood cells (ie: neutrophils and
macrophages)
• Hemolysins; membrane-‐damaging toxins that disrupt the
plasma membrane of host cells and cause the cells to lyse
• Coagulase; causes fibrin clots to form in the blood of the host
• Kinsase; break down fibrin and dissolve clots
• Hyaluronidase/collagenase; break down connective tissue and
collagen in host, allowing the infection to spread
§ Penetrating inside host cells (hiding from the immune response)
• Invasin; alters configuration of host cells cytoskeleton, allowing
pathogen to invade the host cell and use the cells cytoskeleton
• Cadherin; pathogen is able to use host cell cadherin to move from
cell to cell without exposing itself to the host’s immune defences

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− Damaging the host

o Damage due to presence of bacteria
§ Direct damage; destruction is localized to the site of infection and host
defences respond in a timely and potent manner, limiting damage
§ Indirect damage; seen in serious infections and involves systemic disease.
Toxins are soluble in aqueous solutions and move through blood/lymph
• Exotoxins; produced by Gram-‐positive organisms and leave the
pathogen cells and enter host cells
o Cytotoxins; kill cells that they come in contact with
o Neurotoxins; interfere with neurological transmission
o Enterotoxins; affect the lining of the digestive system
• Endotoxins; part of the cell wall of Gram-‐negative bacteria and are
active only after the bacteria containing them have been killed; as
they are released into the bloodstream of the host. All endotoxins
cause the same symptoms, chills, fever, muscle weakness and
aches, however large amounts can cause disseminated
intravascular clotting (IDC), using up clotting elements which may
predispose the host to bleeding
o Damage as a by-‐product of host response

Mechanisms of Antibiotic Resistance

Intrinsic Resistance
− Species or genus specific

Acquired Resistance
− Present in only certain strains or species of a genus
o Gene mutation
o Plasma transfer
o Transposons: DNA incorporated into chromosome (more secure) or plasmids
(resistance transferred quicker)
o DNA acquisition
§ Conjugation: cell-‐to-‐cell contact via ‘sex pili’
§ Transformation: Take up naked DNA from environment and incorporate
into genome
§ Transduction: Plasmid DNA enclosed by bacteriorphage (bacterial virus),
transferred to another bacterium of the same species
− Decrease uptake
o Outer membrane protein block
o Alternation of binding proteins (ie: PBP for β-‐lactams)
o Alterations in porin molecules, decreasing entry into gram negative bacilli
− Increased antibiotic extrusion/efflux
o Active export from cell
− Enzymatic modification/inactivation
o β-‐lactamases of gram positive and negative bacteria
o Aminoglycoside modifying enzymes
− Alteration of antimicrobial target site
− Overproduction of target
− Bypass pathways
o Development of pathways to bypass reaction
inhibited by antibiotics
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Defence of lower respiratory tract against infection

Be aware of major mucosal and systemic defence mechanisms

Mucosal Immunity
− Major compartments of the immune system;
o Systemic; lymph nodes and spleen, lymphatic vessels
o Skin associated lymporeticular tissue (SALT)
o Mucosa associated lymphoreticular tissue (MALT)
− Mucosal tissues are characterised by permeability or by fine structures associated with the
higher sensory powers, especially sight and smell and with production
− Key features of the mucosal defence
o Mucus; must be of a particular consistently, selectively allowing particles to pass
o Specialised immune response; part of this is due to IgA
o IgA
o MALT – GALT, NALT, BALT
o Intraepithelial lymphocytes
o Cryptogenic lymphocytes; behave like cells that can determine tolerance
o Tolerance
− Major features of failure in mucosal immunity
o Serious and/or recurrent infection
o Chronic inflammation
o Malignancy
o Allergy
− Major challenge
o Immunisation

Barrier function
− The overall structure of mucosa closely
approximates the skin. Although an epithelial
tissue, mucosa differs from skin in the
permeability of the structure and it’s massive
surface area

Non-‐immune exclusion
− Mucus, enzymes (secreted by Paneth cells and
PMN)
− Natural antimicrobials (ie: defensins)
− Motility
− Cilia
− Commensals

Immunoglobulin A
− A ‘benign’ immunoglobulin that binds to
mucus and optimises viscosity, neutralises
foreign antigens, does not active the
complement cascade, may also block IgG
induced complement activation (hence anti-‐
inflammatory) and can induce pathogen
killing when required

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Mucosal epithelium
− Mucosal epithelium is composed of several cell
types including;
o Mucus producing goblet cells
o Antigen sampling M cells; interspaced
between enterocytes and in close
contact with sub-‐epithelial lymphocytes
and dendritic cells
o Intraepithelial lymphocytes
o Intraepithelial dendritic cells
o Intraluminal macrophages

Mucosal T cells
− Lymphocytes of mucosal tissue are predominantly T cells and are phenotypically unusual
with high proportion of γδ T cells compared with other lymphoid tissues. The cells are of
several distinct phenotypes and produce characteristic cytokines that are responsible for the
class switch to IgA
− Some of the T cells develop in the cryptopatches of gut epithelium rather than the thymus,
however most muscosal T cells migrate to the mucosa from peripheral blood as naïve T cells

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Appreciate how particular immune defects predispose to infection with certain types of
pathogens using glucocorticoid treatment as an example

Impairment of Host Defence Mechanisms;
− Loss/suppression of cough reflex
o Coma, general anaesthetic, pain, neuromuscular disease, kyphoscoliosis,
endotracheal tube and drugs
− Injury to mucociliary blanket/escalator
o Smoke, viral, alcohol, hot corrosive gases, obstruction and cystic fibrosis
− Decrease in macrophage function
o Alcohol, smoking, anoxia, oxygen toxicity and phagocyte killing defects
− Impairment of immune system
o Chronic debilitating disease, immune deficiency, immune suppression; drugs/AIDS,
leukopaenia, aging
− Unusual virulent microbes

Action of glucocorticoids:
− Metabolic actions;
o Carbohydrates -‐ decreased uptake and utilisation of glucose (hyperglycaemia)
o Proteins -‐ increased catabolism, reduced anabolism
o Lipids -‐ permissive effect on lipolytic hormones and redistribution of fat as per
Cushing’s syndrome!
− Regulatory actions;
o Hypothalamus and anterior pituitary -‐ negative feedback action resulting in reduced
release of endogenous glucocorticoids
o Cardiovascular -‐ reduced vasodilation, decreased fluid exudation
o Musculoskeletal -‐ decreasing osteoblast and increasing osteoclast activity
− Inflammation and immunity;
o Acute inflammation -‐ decreased influx and activity of leukocytes
o Chronic inflammation -‐ decreased activity of mononuclear cells, decreased
angiogenesis, less fibrosis
o Lymphoid tissues -‐ decreased clonal expansion of T and B cells, decreased action of
cytokine-‐secreting T cells, switch from TH1 to T H2 response!
− Mediators;
o Decreased production and action of cytokines
o Reduced generation of eicosanoids (messengers to CNS for inflammation)
o Decreased generation of IgG
o Decrease in complement components in the blood
o Increased release of anti-‐inflammatory factors such as interleukin-‐10 and annexin 1
− Overall effects;
o Reduction in the activity of the innate and acquired immune systems
o Decrease healing and diminution in the protective aspects of the inflammatory
response

Appreciate the effect of immune defects on response to treatment

− The course of treatment may need to me more aggressive to account for the patients immune
defects, such that the immune response has less of a role in the destruction of the pathogen
− The course of treatment may need to be less aggressive as the patient may not be able to
handle the treatment given and their ability to start a healing process may be severely limit
the positive outcomes of the treatment
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Pathology of pneumonia

Understand the pathology (macroscopic, microscopic, pathophysiology) of the different types of
pneumonia and relate these to clinical and radiological signs

Community Acquires Acute Pneumonia

Lobar Pneumonia
− Acute bacterial infection resulting in fbrinosuppurative consolidation of a large portion of a
lobe or an entire lobe. May spread through pores of Kohn (alveolar connections)
− Common in healthy young adults and has an acute onset
− Pathogens involved:
o Pneumococci (90%), Klebsiella, Staph, Strep, Haemophilus influenza, Proteus and
Pseudomonas
− Pathology: Stages of the inflammatory response
o Congestion (1-‐2 days)
§ Lung is heavy, boggy and red
§ Characterised by vascular engorgement, intra-‐alveolar fluid with few
neutrophils, numerous bacteria and vascular congestion
§ Clinically; fine crackles and watery sputum
o Red hepatisation (2-‐4 days)
§ Characterized by massive confluent
exudation with red cells
(congestion), neutrophils and fibrin
filling the alveolar spaces
§ On examination, appears distinctly
red, firm and airless with a liver-‐like
consistency (hence the term
hepatisation)
§ Clinically; bronchial breathing and
rusty sputum
o Gray hepatisation (4-‐8 days)
§ Disintegration of red cells and the
persistence of a fibrinosuppurative
exudate gives the gross appearance of
a grayish brown, dry surface
§ Clinically; moist rhonchi
o Resolution (8 days)
§ Consolidated exudate within the
alveolar spaces undergoes progressive
enzymatic digestion to produce a
granular, semifluid debris that is
resorbed, ingested by macrophages,
coughed up or organised by fibroblasts
growing into it
− Complications
o Pleural effusion
o Empyema
o Organisation of exudate (carnification)
o Abscess formation
o Bacteraemia; endocarditis, meningitis, arthritis
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Bronchopneumonia
− Inflammation of conducting airways (terminal bronchioles)
− Often the cause of death of the elderly in conjunction with a
debilitating illness
− Pathogens involved;
o Staph, Strep, Pneumococci, Haemophilus, Pseudomonas,
Coliforms, Candida, Mucor and Aspergiullus
− Pathology;
o Patchy consolidation of acute suppurative inflammation.
May occur in one lobe but is more often multilobar and
frequently bilateral and basal because of the tendency of
secretions to gravitate into the lower lobes
o Well-‐developed lesions are usually 3-‐4cm in diameter,
slightly elevated, dry, granular, gray-‐red to yellow and
poorly delineated at their margins
o Necrosis centrally; tends to be more destructive than
lobar pneumonia
o Histologically; reaction usually elicits a suppuratives,
neutrophil-‐rich exudate that fills the bronchi, bronchioles
and adjacent alveolar spaces
− Complications;
o Abscess formation
o Empyema
o Suppurative pericarditis
o Metastatic abscesses

Clinical course
− Major symptoms of CAP; abrupt onset of high fever, shaking
chills, productive cough of mucopurulent sputum, haemoptysis,
pleuritic pain and pleural friction rub
− Clinical picture is dramatically modified by the administration of
antibiotics. Treated patients may be relatively afebrile with few
clinical signs 48-‐72 hours after the initiation of antibiotics

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Atypical (Interstitial) Pneumonia

− A combination of atypical presentation and atypical organisms, usually CAP
− Clinically defined based on the presence of extra-‐pulmonary manifestations
− Transmitted via droplet spread (inhalation) in children and young adults and generally is of
insidious onset following at URTI
− Clinical presentation
o Moderate sputum production
o No evidence of consolidation
o Moderate elevation of WCC
o Lack of alveolar exudate
o CXR: more impressive than expected with lower lung fields, bilateral and perihilar
− Pathology;
o Predominant in the interstitial nature of the inflammatory reaction, virtually
localized within the walls of the alveoli. Alveolar septa are widened and edematous
and usually have a mononuclear inflammatory infiltrate of lymphocytes, histiocytes
and occasionally plasma cells (neutrophils may be present acutely)
o Alveoli may be free from exudate, but many patients may have intra-‐alveolar
proteinaceous material (cellular exudate) and a characteristically pink hyaline
membrane lining the alveolar walls. These changes reflect alveolar similar (similar
to ARDS). Eradication of infection is followed by reconstitution of normal lung
architecture

Clinical course
− Clinical course extremely varies and even patients with well established pneumonias may
have few localization symptoms
− Cough may be absent and the major manifestations may consist only of fever, headache,
muscle aches and pains in legs
− Oedema and exudation are both strategically located to cause mismatching of ventilation and
blood flow and thus evoke symptoms out of proportion to the scanty physical findings

Viral Pneumonia
− Uncommon in healthy adults
− Pathogens;
o Influenza A, B
o RSV
o Rhinovirus
− Predisposing factors;
o Alcohol
o Malnutrition
o Immunodeficiency/immunosuppression
− Pathology;
o Interstitial inflammation
o Viral inclusions

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Diagnosis of pneumonia

Predict the most likely range of pathogens from the clinical history

− Patients with CAP due to typical bacteria CAP pathogens present with pulmonary symptoms,
while patients with CAP due to atypical CAP pathogens present with a variety of pulmonary
and extrapulmonary findings (eg: CAP plus diarrhoea)
− Patients with bacterial CAP typically present with fever, usually with a productive cough and
pleuritic chest pain
− Patients with atypical CAP present acutely and have 1 or more extrapulmonary features,
which is due to it’s aetiology
− Patients with legionella pneumonia may have a productive or non-‐productive cough. In
contrast, patients with pneumonia due to M pneumonia or Chlamydophila pneumonia usually
present with a non-‐productive cough
− During a clinical history, it is important to elicit;
o Clinical signs/symptoms
o Location of contraction of infection
o Exposure to soils
o Risk factors:
§ Diabetes
§ Immuno-‐compromised
§ Cystic fibrosis
§ Alcohol abuse
§ IVDU
§ Hospitalization
§ Chronic renal failure
§ Chronic lung disease

Understand the principles of choosing empiric antibiotic therapy

− Empirical antibiotic therapy is employed one the basis of choosing an antibiotic that will
treat the most probable organism based on the patients clinical signs, history and
radiological investigations
− It is employed as it is important to begin therapy early to avoid the patient deteriorating

Recognise the importance of microbiological diagnosis in management

− Microbiological diagnosis is important to narrow the antibiotic treatment
− Based on the MINDME principle of ABS treatment
o Microbiology
o Indication
o Narrowest spectrum possible
o Dosage needs to be adequate to achieve MIC
o Minimize duration of treatment
o Ensure monotherapy where possible

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Respiratory Failure

Understand the pathophysiology of acute respiratory failure in severe pneumonia

Respiratory failure is inadequate gas exchange by the respiratory system, with the result that
levels of arterial oxygen, carbon dioxide or both cannot be maintained within their normal ranges

Type 1 Respiratory Failure (failure of the lung parenchyma)
− Hypoxia without hypercapnia (CO2 may be normal or low) that is caused by V/Q mismatch
− Classification;
o PaO2: low (> 55-‐60 mmHg)
o PaCO2: normal or low (<50 mmHg)
− Caused by conditions that affect oxygenation;
o Low ambient oxygen (ie: high altitude)
o V/Q mismatch
o Alveolar hypoventilation (ie: neuromuscular disease)
o Diffusion problem
o Shunt

Type 2 Respiratory Failure (failure of the pump)
− Hypoxia with hypercapnea and is caused by inadequate alveolar ventilation
− Classification
o PaO2: decreased (55-‐60 mmHg)
o PaCO2: increased (>50 mmHg)
− Caused by conditions that build up CO2 but cannot get rid of it. These include;
o Increased airway resistance (ie: COPD, pulmonary disease and asthma)
o Reduced breathing effort (ie: drug effects, obesity, brainstem lesion)
o Decreased area of lung available for gas exchange (ie: chronic bronchitis)
o Neuromuscular conditions (ie: GBS, myasthenia gravis, motor neuron disease)
o Deformed (ie: kyphoscoliosis), rigid (ie: ankylosing spondylitis) or flail chest

Respiratory Failure in Severe Pneumonia
− During an infection such as pneumonia, the acute inflammatory response will result in an
increase in cytokine production à vasodilation of pulmonary arterioles à increased blood
flow to fight infection à poorly ventilated areas receive a large blood flow à V/Q mismatch
à blood in corresponding pulmonary venules low in oxygen
− In healthy lung, vasodilation of arterioles in well-‐ventilated areas increases gas transport.
Poorly ventilated lung areas result in vasoconstriction, decreasing blood flow to the areas

Monitoring of respiratory failure
− Use of accessory muscles
− Intercostal recession
− Tachypnoea and tachycardia
− Sweating
− Pulsus paradoxus -‐ decrease in systolic BP during inspiration
− Inability to speak, unwillingness to lie flat
− Agitation, restlessness, diminished conscious level
− Asynchronous respiration
− Paradoxical respiration
− Respiratory alternans (change in muscle usage breath-‐to-‐breath)

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Adam Trytell
Types of Respiratory Failure

Hypoxaemia
− Mechanisms
o Impaired diffusion
o Ventilation-‐perfusion mismatch
o Hypoventilation
o Shunt
o Reduced inspiratory oxygen
concentration
− Effects
o Symptoms of hypoxaemia result from
cerebral dysregulation (non specific)

Hypercapnoea
− Mechanisms
o Hypoventilation
o Ventilation-‐perfusion mismatch
− Effects
o Increased cerebral blood flow (leading to headache, raised ICP and papilloedema)
o Restlessness, tremor, slurred speech, asterixix and bounding pulse
o High levels à respiratory depression and unconsciousness

Treatment of respiratory failure
− Specific; treat the underlying cause/disease process
− General supportive management
o Correct hypoxaemia: oxygen therapy
o Deal with hypercapnoea: NIV and mechanical ventilation
o Nutrition
o Prevent DVT
o Monitor patient

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Adam Trytell
Diagnosis and management of pneumonia

Recognise clinical signs of pneumonia

Clinical features of CAP
− Cough: may be dry or productive and haemoptysis can occur (in pneumococcal pneumonia,
sputum is characteristically rust-‐coloured)
− Breathlessness: alveoli fill with pus and debris, impairing gas exchange. Coarse crackles are
often heart on auscultation as well as bronchial breath sounds over consolidated lung
− Fever: if fever is swinging, this suggests empyema
− Chest pain: commonly pleuritic in nature due to plural inflammation
− Extrapulmonary features:
o Haemolysis (mycoplasma pneumonia)
o Thrombocytopenia
o Myalgia, arthralgia and malaise (legionella and mycoplasma)
o Myocarditis and pericarditis (mycoplasma pneumonia)
o Headache (legionella pneumonia)
o Abdominal pain, diarrhoea and vomiting
o Labial herpes simplex reactivation (pneumococcal pneumonia)
o Skin rashes (mycoplasma pneumonia)
− Other:
o Confusion
o Recurrent falls

Recognise radiological signs of pneumonia

Description of plain radiograph films
− Airway
o Is the trachea midline and are there any para-‐tracheal masses or tracheal deformity?
o Can you identify the carina and the right/left bronchi?
− Bones/soft tissues
o Clavicles, scapulae, ribs, humeri
o Fractures, deformities, soft tissue masses, subcutaneous emphasema?
− Cardiac
o Size; should be <50% of thoracic diameter on PA film
o Shape; elongated or otherwise?
o Silhouette – any loss of heart border?
− Diaphragm
o Right higher than left by 1-‐3cm?
o Preservation of costo-‐phrenic angles and hemi-‐diaphragm borders?
− Equal volume
o Both lungs should be roughly equal volume, count the ribs!
− Fine detail
o Check the apices, lung markings, masses, consolidation, effusion, pneumothorax and
mediastinal shift?
− Gastric bubble
o Present or absent? Size <0.5cm air
− Hilum/hardware
o Widened?
o Hilar masses
o Any tubes, catheters, pacemakers, wires and monitor stickers
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Adam Trytell
Normal Chest Xray

Pneumonia
Lobar pneumonia Bronchopneumonia

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Adam Trytell

Be able to assess the clinical severity of acute pneumonia

Pneumonia Severity Index

CURB-‐65

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Adam Trytell
Be able to prioritise history, clinical examination, investigations, and treatments appropriately in
the acute management of very sick patients

1. Oxygen therapy
2. Dehydration management (establish IV)
3. Antibiotics treatment
4. Analgesia
5. Co-‐morbidity treatment (e.g. Diabetes)

Be familiar with clinical methods of obtaining samples for microbiological investigation

− Throat swab
o Used to diagnose whether or not pharyngitis is bacterial (it’s mostly viral)
− Nasopharyngeal swab
o Useful for isolation of Bordetella pertussis in whopping cough
− Sputum
o Sample is difficult to obtain as it is commonly contaminated by saliva, mouth and
URT (abundance of squamous epithelium cells = contaminated by saliva)
− Blood
o Used in cases of acute pneumonia, cultures should be taken to maximize changes of
isolation of causative organisms
− Nasal swab
o Used to determine carrier status for S. aureus
− Pleural fluid aspirate (pneumonia with pleural effusion)
− Percutaneous trans-‐trancheal aspiration (under local)
o For patients with pneumonia who can’t expectorate sputum

Understand principles of supportive management and clinical monitoring

− Supportive management:
o Nurse patient while seated
o Encourage coughing to eject sputum
o Give analgesia if required
o Provide physiotherapy to help with sputum ejection
− Clinical monitoring:
o ABG -‐ to assess & monitor degree of respiratory failure
o Blood biochemistry -‐ to assess electrolyte imbalance & correct if necessary

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Adam Trytell
Epidemiology of community acquired pneumonia

Be able to contrast the risk factors, prevalence and outcomes of community acquired pneumonia
in the pre-‐antibiotic and antibiotic eras

− Sharp drop in the incidence of pneumonia after the introduction of antibiotics
− Increase in 2000 since the introduction of automated coding to assign pneumonia as the
cause of death rather than a contributing cause of death

Be aware of the extent to which pneumonia and other respiratory infections and diseases
account for morbidity and mortality in the Australia population as a whole, and in the Indigenous
population. Suggest reasons for observed differences

− Currently accounts for 10-‐20 per 100,000 deaths for males and females in Australia
− Risk factors for pneumonia:
o Age over 50 years
o Alcoholism
o Asthma
o COPD
o Dementia
o Heart failure
o Immunosupression
o Indigenous background
o Location is also a key factor -‐ tropical settings
o Institutionalisation
o Seizure disorders
o Smoking
o Stroke

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Adam Trytell
Prevention; Immunisation

Outline the rationale for population-‐based prevention

− The cost of treating a condition is outweighed by the cost of prevention of that condition
o E.g. The cost of treating elderly with influenza is $10,000 per person and 100 people
are affected by it each year (total cost = $1,000,000)
− The Influenza vaccine costs $20 per person and will decrease the incidence of influenza in
the elderly by 50%
− To vaccine 100 people will cost $2000 but in doing so you will save $500,000 in treating
people who end up getting influenza

Discuss the epidemiological and scientific basis of influenza and pneumococcal vaccination

− Minimize the incidence of pneumonia
− Decrease the severity of pneumonia once a patient has contracted the disease

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Adam Trytell
Patient’s experience of illness (Medical sociology)

Outline factors (eg. Psychosocial, cultural, environmental, economic, gender, age) that may
influence an individual’s adaptation to and experience of illness

Explanatory model of illness
− What do you think has caused your illness (ideas)
− Why did it start when it did (ideas)
− What do you think your sickness does to you (concerns)
− How severe is your sickness (concerns)
− What kind of treatment should you receive (ideas)
− What are the most important results you expect from treatment (expectations)
− What are the chief problems your sickness has caused for you (ideas)
− What do you fear the most about the sickness (concerns)

Social determinants of health
− Personal
o Income
o Employment
o Culture
o Social cohesion
− Community
o Transport
o Education
o Housing
− Government
o Political stability
o Access to services

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Adam Trytell
Refusal of treatment

Analyse the need for the doctor to interpret patient treatment refusals

Criteria for refusal of treatment
− Valid refusal of treatment requires the satisfaction of the same conditions as consent to
treatment. Decisions must be;
o Voluntary; patient must not be acting under duress
o Informed; patient has received sufficient information to make the decision
o Made by a competent person; who is someone that can;
§ Comprehend and retain relevant information
§ Understand nature and effects of decisions
§ Evaluate information and predicted consequences in relation to one’s
situation, goals and values
§ Offer reasons for one’s decisions (justification)
§ Communicate one’s decision to others
§ Ability to follow through with decision
o For a specific procedure

Values in medical ethics
− Autonomy; the patient has the right to refuse or choose their treatment
− Beneficence; a practitioner should act in the best interest of the patient
− Non-‐maleficence; first, do no harm
− Justice; concerns the distribution of scare health resources, and the decision of who gets
what treatment (fairness and equality)

Explain the difference between over-‐riding a patient’s refusal of treatment and treating a patient
without consent

− Overriding a patient’s refusal of treatment:
o Deeming the patient competent and performing refused treatment. Not only over-‐
riding the patients’ autonomy (strong paternalism), it is also illegal and may result in
a charge of battery (assault)
− Treating a patient without consent:
o Most often occurs in the context of emergency treatment. In this case treatment is
legal under the doctrine of necessity (and proportion) and complies with the ethic
principles of beneficence and non-‐maleficence

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Adam Trytell
Extra Learning Objective: Respiratory Control

Mechanisms of Respiratory Control
− Automatic control
o Pacemaker cells in the medulla send off regular impulses via the cervical and
thoracic spinal cord to the diaphragm and external intercostals respectively
− Voluntary control
o Located in the cerebral cortex and sends messages via cortico-‐spinal tracts to the
respiratory motor neurons
o Cortex is influence by; speech, gases, water and
emotion

Respiratory Centre
− Main area is the medullary rhythmicity center
o Inspiratory area fires for two seconds every five
seconds
o Expiration occurs when the inspiratory area stops
fire and is inactive during quiet breathing
− Signals are sent from/to the;
o Pneumotaxic area, which will increase length of
inspiration if damaged
o Apneustic area

Medullary Systems
− Pattern generation
o Small groups of synaptically linked cells located in
the pre-‐Bötzinger complex responsible. If these cells
become hypoxic you begin to gasp for air, if you are
subject to opioids they slow down
− Impulses are modified by neurons in the pons and afferents
in vagal fibres coming from the lungs. The whole synthesis
area is known as the Pneumotaxic centre

Apneustic centre
− Located in the in the lower pons, the apneustic centre promotes inspiration by stimulation of
the neurons in the medulla, providing a constant stimulus
− Apneustic centre sends signals to the dorsal respiratory centre in the medulla to delay the
‘switch off’ signal of the inspiratory ramp provided by the penumotaxic centre of the pons
− Apneustic centre controls the intensity of breathing by sending positive impulses to
inspiratory neurons and is inhibited by pulmonary stretch receptors

Pneumotaxic Centre (Pontine Respiratory Group)
− The PRG antagonises the apneustic entre, cyclically inhibiting inspiration, via limiting the
burst of action potentials in the phrenic nerve. Thus effectively decreasing the tidal volume
and regulating respiratory rate (this also stops lungs overinflating)
− Absence of the PRG results in increased depth of respiration and decreased respiratory rate

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Adam Trytell
Chemical Regulations

Central
− In or near the medulla oblongata; monitor changes in CSF
− Chemoreceptors are located on the ventral medullary surface against spinal fluid and
monitor H+ levels including the brain CSF. Small changes of H+ are not seen in the CSF due to
a lack of buffering systems. Any increase in PCO2 stimulates these chemoreceptors to cause
the inspiratory area to become highly active and increase respiratory rate
− As the brain gets signals from both the blood and CSF, it is able to compare the two
− The ventilator response to CO2 has an upper limit of 7%, any higher than this will result in
CNS depression, leading to decreased respiratory rate, headache, confusion and coma

Peripheral
− Aortic and carotid bodies
o Aortic; via vagus (CN X) nerve
o Carotid bodies; via right and left glossopharyngeal (CN IX) nerves
− When in hypoxic conditions, Type 1 cells are excited and release dopamine to nerve. It is
thought that Type 2 cells may act like glial cells

Sensory Feedback
− Reflexes from the periphery provide feedback for fine-‐tuning of breathing, which adjusts
frequency and tidal volume to minimise the work of breathing
− Pulmonary sensory receptors can be divided into 3 groups;
o Slowly adapting
o Rapidly adapting
o C fibre endings (more protective in function)
− All three types of afferent fibres lie predominantly in the vagus nerve, although some pass in
the sympathetic nerves to the spinal cord

Slowly adapting receptors
− Sensory terminals lie within the smooth muscle layer of conducting airways and respond to
airway stretch (aka: pulmonary stretch receptors)
− Their role is to sense lung volumes and when stimulated increase their firing rate as long as
the stretch is imposed (they adapt slowly)
− Stimulation of these receptors causes an excitation of the inspiratory off-‐switch neurons and
a prolongation of expiration

Rapidly adapting receptors
− Sensory terminals are found in the larger conducting airways and are stimulated by lung
inflation and deflation, their firing rate rapidly declines when a volume change is sustained
− Due to their rapid adaptation, bursts of activity occur in proportion to the change of volume
and the rate at which that change occurs
− The nerve endings also respond to irritation of the airways, by touch or noxious substances
− Receptors are also stimulated by histamine, serotonin and prostaglandins released locally in
response to allergy and inflammation

Hering:Breuer reflex
− Located in the walls of bronchi and
bronchioles are stretch receptors that send
inhibitory impulses via vagus nerve to the
inspiratory centre and apneustic area when
overstretched
− These reflexes are usually involved in
breathing at rest or when tidal volumes are
<1000mL
− This is a protective mechanism for the over-‐
inflation of the lungs

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Adam Trytell
Involuntary Control
− Several additional sensory stimuli can affect the activities of the respiratory centres;
o Sudden pain or immersion in cold water can produce a temporary apnoea
o Chronic pain can lead to an increase in the respiratory rate
o Vomiting and swallowing involve autonomic adjustments in respiratory activity to
prevent entrance of foreign objects into the trachea
o Increased body temperature due to fever/exertion will increase respiratory rate
o Reduction in body temperature has the opposite effect and reduces respiratory rate

Breath Holding
− Voluntary inhibition of respiration does not last as the rise is arterial PCO2 and fall in PO2 will
result in a ‘Breaking Point’ in which respiratory will recommence. If you remove the carotids
you could hold your breath for longer. Blowing off CO2 will also delay the breaking point
− Psychological factors play a role; if you’re told you’re good at holding you breath, you will be!

Periodic breathing
− If you hyperventilation and ‘wash out’ CO2 and then perform a few shallow breaths,
breathing cycles will last a while before normal breathing is resumed
− If you swim under water for a long period of time, death occurs much faster due to low O2
levels and low CO2 levels, thus no respiratory drive; this is know as “Shallow Water Blackout”

Coughing and Sneezing
− Coughing and sneezing involves a period of apnoea followed by a forceful expulsion of air.
Cough is instigated by irritation of the wall of the nasal cavity, larynx, trachea or bronchi
− Coughing
o Lungs still full of air and the glottis is closed à expiratory muscles forcibly contract,
creating sufficient pressure to blast air out of the respiratory passageways when the
glottis is reopened (velocities up to 965km/h)
− Sneezing
o Similar to coughing but with the glottis open

Asphyxia
− Acute hypercapnia and hypoxia develop together, resulting in stimulation of respiration, a
sharp rise in blood pressure and heart rate, as well as rise in catecholamine levels and pH fall
− If prolonged, respiratory effort ceases, blood pressure falls and heart slows which may result
in organ damage and ventricular fibrillation. Cardiac arrest follows in 4-‐5 minutes

Drowning (asphyxia caused by immersion, usually in water)
− In approximately 10% of cases, the first gasp of water triggers laryngospasm, preventing
water entering lungs. Otherwise the glottis is relaxes and water enters the lungs à asphyxia
o Ocean water is hypertonic; removes water from lungs/body increasing the chance of
resuscitation as there is less cell damage
o Fresh water is hypotonic; enters the body and ruptures red cells etc.
− Diving reflex;
o When cold water hits the face; heart rate drops by 25%, peripheral vasoconstriction
and blood shift allows survival for extended periods in cold (<21°C) for extended
periods (occurs in mammals but is poor)

Exercise
− Increased CO2 plays a large role. As blood lactate accumulates it is buffered in the blood and
CO2 is liberate. As O2 debt builds up respiration will suffer until the debt is paid off!
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Adam Trytell
Extra Learning Objective: Clinical Reasoning and the Murtagh method

Clinical Reasoning; Refers to a process in which the therapist, interacting with the patient,
structures meaning, goals and health management strategies based on clinical data, client choices
and professional judgement and knowledge

Clinical reasoning involves;
− The doctor acquiring clinical data from the patient
− The doctor applying knowledge and professional judgement to structure meaning (and make
a diagnosis)
− The doctor interacting with the patient to establish goals
− The doctor interacting with the patient to institute a management plan

Murtagh method
1. What is the probable diagnosis?
2. What serious disorders must not be missed? RED FLAGS
3. What conditions are often missed (pitfalls)?
4. Could this patient be one of the ‘masquerades’ in general practise?
5. Is the patient trying to tell me something else?

The probably diagnosis
− Common things are common and the GP has an awareness of the epidemiology of the
patterns of disease in his geographical area of practise. The GP will compare the pattern of
symptoms with the patterns of diseases prevalent in the area

What seriously disorders must not be missed?
− These disorders may not be common in the GPs area, but can be lethal and therefore must be
excluded!!
o Vascular
§ Arterial
• Cardiac; acute coronary syndromes
• Cerebral; CVA, TIA, SAH
• Aneurysms; abdominal, cerebral
§ Venous
• DVT, PE, Axillary vein thrombosis
§ Arteritis
• Giant Cell arteritis/temporal arteritis
• Vasculitis
§ Bleeding
• Ectopic
• Anticoagulants
o Infective
§ Meningo-‐encephalitis
§ Septicaemia
§ Meningococcus
§ HIV infection
§ Infective endocarditis
§ Avian flu/SARS/prion
§ Clostridia infections
§ Pneumonia

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Adam Trytell
o Malignant neoplasms
§ Major primaries (colon, lung, breast, melanoma, kidney and prostate)
§ Occult (ovary, pancreas, caecum, lung, kidney, lymphoma, leukaemia,
cervix)
§ Metastatic (colon, lung, breast, melanoma)
§ Para-‐neoplastic effects (lung, kidney, pancreas, hepatoma)
o Psychiatric
§ Imminent or probable suicide
− RED FLAGS
o History
o Signs
§ Age > 50 years
§ Pallor
§ Sudden onset
§ Cyanosis
§ Past history of cancer
§ Altered conscious state
§ Fever > 37.8°C
§ Cold extremities
§ Weight loss
§ Tachypnoea
§ Drug and alcohol abuse
§ Tachycardia
§ Travel, especially overseas
§ Fever > 38°C
§ Neurological deficit
§ Poor capillary refill > 2 secs
§ Vomiting
§ Altered conscious state/cognition
§ Failure to improve
§ Use of anticoagulants, biologicals or steroids

What conditions are often missed? – The pitfalls!
− Abscess − Herpes zoster − Migrane
− Allergies − Faecal impaction − Paget’s disease
− Chronic fatigue syndrome − Foreign bodies − Pregnancy
− Coeliac disease − Giardiasis − Sarcoidosis
− Domestic abuse − Haemochromatosis − Seizure disorders
− Drugs − Malnutrition − Tourette’s syndrome
− Menopause syndrome

The seven primary masquerades Another seven masquerades
− Depression − Chronic renal failure
− Diabetes mellitus − Malignancy
− Drugs (Iatrogenic, Substance abuse, OTC) − HIV/AIDS
− Anaemia − Baffling bacterial infection
− Thyroid and other endocrine diseases o Syphilis, TB
o Hypo-‐/hyper-‐thyroid − Baffling viral/protozoan infection
o Sex hormone deficiency o EB, Malaria
− Spinal dysfunction (Spondylotic pain) − Neurological problems (parkinson’s, GBS, MS)
− UTI − Connective tissue disorders and vasculitis (SLE)

Is the Patient trying to tell me something?
− Hidden agenda − Conflict at home/work
− Ticket of entry − Bullying
− Masked depression − Sexual issues (inc. STIs)
− Underlying anxiety/fears − Munchausen’s

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Adam Trytell
Extra Learning Objective: Prescribing drugs

The process of rational treatment
− Define the problem
− Specify the treatment objectives (once determined the root cause of the problem)
− Choose the treatment; choice of drug is based on a number of factors
o Efficacy: will the drug be effective in treating the problem?
o Safety: is the drug safe to use in this instance? Considering comorbidities and other
drugs that the patient is currently taking
o Suitability: might there be a compliance issue with this patient?
o Cost: is the drug too expensive? Are there cheaper alternatives?
− Start the treatment
o Write an accurate and legible prescription and give the patient clear instructions
− Monitor progress
o Review the patient regularly and decide whether to stop, continue or change
treatment

Therapeutic Goods Administration
− Regulatory body for therapeutic goods available in Australia and is responsible for
conducting assessment and monitoring activities to ensure that therapeutic goods available
in Australia are of an acceptable standard and that access to therapeutic advances in a timely
manner

Pharmaceutical Benefits Scheme
− The PBS is a programme of the Australian Government that provides subsidised prescription
drugs to residents of Australia. It ensures that Australian residents have affordable and
reliable access to a wide range of necessary medicines

Standard for the Uniform Scheduling of Medicines and Poisons
− A document used in the regulation of drugs and poisons in Australia

Scheduling
− Schedule 1: Intentionally left blank
o Schedule level is now defunct and has been set aside for possible future use
− Schedule 2, 3, 4 and 8: Therapeutics Human and Veterinary
o Schedule 2: Substantially safe in used but where advice or counselling is available if
necessary. Are for minor ailments that can be easily recognised by the consumer and
do not require medial diagnosis or management (ie: paracetamol and Claritin)
o Schedule 3: Pharmacist only medications that are safe in used but require
professional advice or counselling by a pharmacist. Are for ailments that can be
identified by the consumer and verified by a pharmacist, they do not require medical
diagnosis and do not require medical management (ie: cold and flu, ventolin)
o Schedule 4: Prescription only medication that must be used/supplies by or on the
order of persons permitted to prescribe and should be available from pharmacists
on prescription. Requires professional medical, dental or veterinary management
and monitoring and is for ailments that require professional management.
Prescriptions are only available for 12 months and accessible by pharmacy staff
o Schedule 8: Controlled drugs that are for therapeutic use and have high potential
for abuse and addiction. All S8 drugs require a doctor to have a S8 permit before
prescribing treatment. Furthermore, they have to be securely locked in a safe and a
register has to be kept (ie: morphine and cocaine)
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Adam Trytell
− Schedule 5, 6 and 7: Pesticides, Domestic, Industrial, Veterinary chemicals

o Schedule 5: Drugs and poisons that have low toxicity/concentration, low-‐to-‐
moderate hazard, can cause only minor adverse effects and require caution with
handling, storage or use (ie: lomotil and promethazine)
o Schedule 6: Drugs and poisons with moderate-‐to-‐high toxicity, which may cause
death or severe injury if ingested, inhaled or inhaled with skin or eyes (ie: arsenic)
o Schedule 7: Drugs and poisons that and high-‐to-‐extremely high toxicity and can
cause death or severe injury at low exposures. They require special precautions in
their manufacture, handling or use and may require special regulations restricting
their availability, possession or use. They are too hazardous for domestic use or by
untrained persons (ie: cyanide, paraquot and yellow phosphorus)
− Schedule 9: Only for medical or scientific research
o Drugs and poisons that, by law, may only be used for research purposes. The sale,
distribution, use and manufacture of such substances without a permit is strictly
prohibited by law. Permits for research uses on humans must be approved by a
recognised ethics committee on human research (ie: heroin and cannabis)

Special cases in prescribing
− Prescribing for children
o Age impacts pharmacokinetics and pharmacodynamics, rate of gastric emptying and
absorption and clearance from the body
− Prescribing for the elderly
o It is common that the elderly have impaired renal function, changes in drug
receptors and target organs, higher prevalence of disease (leading to polypharmacy)
and a higher incidence of non-‐compliance due to confusion or forgetfulness
− Prescribing for palliative care
o Control of pain and other symptoms is paramount. Accurate diagnosis is imperative
and you must be aware of opioid side effects such as diarrhoea, nausea and vomiting
− Prescribing for pregnant women
o Drugs can be damaging to the foetus at certain stages of pregnancy, as well as having
adverse effects at labour or on the neonate
− Prescribing for breastfeeding women
o Be aware that if a drug enters breast milk in pharmacologically significant doses in
the mother that is could be toxic to the baby, it may also suppress lactation or
suppress the infants sucking reflex
− Prescribing for renal impairment
o Renal impairment renders some drugs ineffective (ie: frusemide) or toxic (ie:
methotrexate) unless a dose adjustment is made. An active/toxic metabolite may
form and clearance must be considered

Medical errors
− Wrong drug error
− Extra dose error
− Omission error
− Wrong dose/strength error
− Wrong route error
− Wrong time error
− Wrong dosage error

34

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Week 1: I don’t want a doctor in my house

DEFENCE OF LOWER RESPIRATORY TRACT AGAINST INFECTION 11

PATHOLOGY OF PNEUMONIA 14

DIAGNOSIS OF PNEUMONIA 17

DIAGNOSIS AND MANAGEMENT OF PNEUMONIA 20

EPIDEMIOLOGY OF COMMUNITY ACQUIRED PNEUMONIA 24

PATIENT’S EXPERIENCE OF ILLNESS (MEDICAL SOCIOLOGY) 26

REFUSAL OF TREATMENT 27

EXTRA LEARNING OBJECTIVE: RESPIRATORY CONTROL 28

EXTRA LEARNING OBJECTIVE: CLINICAL REASONING AND THE MURTAGH

EXTRA LEARNING OBJECTIVE: PRESCRIBING DRUGS 33

Understand mechanisms of action of major antibiotics

Antibacterial drugs that inhibit bacterial nucleic acids

Folate synthesis inhibitors

− Damaging the host

Defence of lower respiratory tract against infection

Pathology of pneumonia

Atypical (Interstitial) Pneumonia

Types of Respiratory Failure

Diagnosis and management of pneumonia

Normal Chest Xray

Lobar pneumonia Bronchopneumonia

Epidemiology of community acquired pneumonia

Patient’s experience of illness (Medical sociology)

Refusal of treatment

Extra Learning Objective: Respiratory Control

Extra Learning Objective: Clinical Reasoning and the Murtagh method

Extra Learning Objective: Prescribing drugs

− Schedule 5, 6 and 7: Pesticides, Domestic, Industrial, Veterinary chemicals

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