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MD3001 > Week 9 > Flashcards

Week 9 Flashcards

1
Q

Causes for abnormalities:

  • Increased translucency (too black)
  • Opacification (too white)
  • Solid white
A

Increase translucency: Air, loss of tissue density

Opacification: Fluid, increased tissue e.g. lymphadenopathy

Solid white: Hardware e.g. Pacemaker, Endotracheal tube (ETT), NG tube, chest drain

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2
Q

What is consolidation?

A

Replacement of normal air space gas with fluid or solid material

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3
Q

Causes of consolidation?

A 
Pus due to infection
Blood due to pulmonary haemorrhage
Fluid due to pulmonary oedema
Cells due to lung cancer
Protein due to alveolar proteinosis
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4
Q

What is atelectasis?

A

Aka: Collapse, pneumothorax
Definition: Reduction in inflation of all or part of the lung

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5
Q

Suspect atelectasis if on x-ray you see… (6)

A
  1. Volume loss
  2. Displacement of trachea
  3. Displacement of diaphragm
  4. Displacement of lung fissures
  5. Compensatory over inflation of non-collapsed lung
  6. Crowding of vessels and bronvhi
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6
Q

Causes of deviated trachea?

A
  1. Pneumonectomy/ lobectomy
  2. Lobar collapse
  3. Tension pneumothorax
  4. Pleural effusion
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7
Q

Pulmonary oedema signs found on XCR

A 
A: Alveolar oedema (Bat's wing)
B: Kerley B lines
C: Cardiomegaly
D: Upper lobe diversion
E: Pleural effusions
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8
Q

For a pleural effusion:

  • Describe the abnormality shown in the chest xray?
  • What clinical signs might you find on examination?
  • How would you manage the acute problem?
  • Suggest 2 further investigations you might request?
A

CXR abnormality: Area of whiteness expanding over mid and lower zones
Clinical signs: Increased RR, low sats, dull to percussion, decreased vocal resonance
Acute management: O2 delivery, drain fluid
Further 2 investigations: CT scan send fluid to lab for investigation to identify fluid

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9
Q

What lobes and fissures are present in the right lung?

A

Fissures: Horizontal and oblique
Lobes: Superior, middle and inferior

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10
Q

What lobes and fissures are present in the left lung?

A

Fissures: Oblique
Lobes: Upper and lower

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11
Q

Stucture in left lung that is the equivalent to the right middle lobe?

A

The lingula

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12
Q

Course of the:

  • Oblique fissure?
  • Horizontal fissure?
A

Oblique: From 3rd thoracic vertebrae to 6th costochondral junction
Horizontal: From 4th right CC to meet the oblique fissure as it follows course of 6th rib

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13
Q

Structures and arrangement of the right and left lung hilum?

A

o Bronchus (most posterior, identified by the small plates of hyaline cartilage)
o Pulmonary artery (Anterosuperior to bronchus)
o Pulmonary veins (superior vein is most anterior structure in hilum, inferior vein is most inferior structure)
o Lymph nodes
o Branches of bronchial arteries and pulmonary nerve plexus

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14
Q

What is pKa?

A

Defined as the pH at which 50% is ionised and 50% is unionised in the reaction

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15
Q

What direction of reaction is favoured if the normal pH is higher than the pKa?

A

Favoured to the high so there would be more products vs reactants

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16
Q

The _____ levels of bicarbonate can be changed by breathing

A

Absolute

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17
Q

What components of the following respiratory equation contribute to respiratory and metabolic acid-base disturbances?

A

Respiratory: CO2, H20
Metabolic: HCO3-, H+

i.e.
Rise in PCO2 -> Respiratory acidosis
Rise in HCO3- -> Metabolic alkalosis

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18
Q

What are the 4 causes for acid-base disturbances?

A
  1. Increase CO2
  2. Decrease CO2
  3. Increase non-volatile acid / decrease base
  4. Increased base / decreased non-volatile acid
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19
Q

What 2 organs offer compensation for acid-base disturbances?

A

Lungs via alters ventilation (quick)

Kidneys via altered excretion of bicarbonate (2-3 days)

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20
Q 
Respiratory acidosis:
How does it arise?
Acid-base disturbance?
Compensation?
Cause?
A

How does it arise:
-Results from an increase in PCO2 in hypoventilation (so less CO2 being blown away)

Acid-base disturbance:

  1. Increase in PCO2
  2. Increase in H+, lowering of pH
  3. plasma HCO3- levels increase to compensate for H+ concentration

Compensation: Renal. Increase HCO3- reabsorption and production to raise pH

Causes:

  • COPD
  • Blocked airway
  • Lung collapse
  • Injury to chest wall
  • Drugs reducing respiratory drive e.g. morphine
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21
Q 
Respiratory alkalosis:
How does it arise?
Acid-base disturbance?
Compensation?
Cause?
A

How does it arise:
Results from a decrease in PCO2 generally caused by alveolar hyperventilation (more CO2 being blown away).

Acid-base disturbance:
Causes a decrease in H+ thus a rise in pH

Compensation: Renal. Reduced reabsorption and production of HCO3-. Lowers pH back to normal as H+ increases

Causes:

  • Increase ventilation from hypoxic drive in pneumonia, diffuse interstitial lung diseases, high altitude, mechanical ventilation
  • Hyperventilation in brainstem damage, infection driving fever
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22
Q

Metabolic acidosis:
Acid-base disturbance?
Compensation?
Cause?

A

Acid-base disturbance:

  • Result of excess of H+ in the body, reducing equation to left so reduces HCO3 levels
  • PCO2 normal as respiration normal

Compensation: Respiratory

  • Low pH detected by peripheral chemoreceptors
  • Increases ventilation which lowers PCO2
  • Shifts bicarbonate equation further to left, lowering H+ further
  • pH increases to normal
  • Cannot fully correct the pH so excess H+ needs to be removed or HCO3- restored

Causes:

  • Loss of HCO3
  • Exogenous acid overloading, endogenous acid production
  • Failure to secrete H+ e.g. renal failure
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23
Q

Effect of high ventilation on PCO2

A

Increased ventilation –> lowers PCO2 as CO2 is being blown off

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24
Q

Metabolic alkalosis:
Acid-base disturbance?
Compensation?
Cause?

A

Acid-base disturbance:

  • Increase in HCO3- concentration or fall in H+
  • Removing H+ increased HCO3- levels are equation driven to the right
  • Raises pH

Compensation: Respiratory

  • Increase in pH detected by peripheral chemoreceptors
  • Decreases ventilation which raises PCO2
  • Equation driven further to right
  • pH lowers to normal
  • Ventilation cannot reduce enough to correct imbalance. Hence renal response is to secrete less H+

Causes:

  • Vomiting (loss of HCl from stomach)
  • Ingestion of alkali substances
  • Potassium depletion (e.g. diuretics)
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25
Q

What are the 3 central principles of antibiotic use?

A
  1. Anti-bacterials target processes that humans do not possess (e.g. bacterial cell well)
  2. Anti-bacterials target processes that humans possess by the bacterial versions are sufficiently different
  3. The toxicity of anti-bacterials is greater to bacteria than it is to humans (selective toxicity)
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26
Q

What are the 5 main classes of antimicrobial drugs?

A
  1. Beta-lactam and cephalosporin
  2. Glycopeptide
  3. Cyclic peptide
  4. Phosphonic acid
  5. Lipopeptides
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27
Q

Beta-lactam and cephalosporin:
Target?
Mechanism?
Example?

A

Target: Penicillin binding proteins
Mechanism: Preventing peptidoglycan cross-linking
Example: Penicillin G, flucloxacillin

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28
Q

Glycopeptide:
Target?
Mechanism?
Example?

A

Target: C-terminal D-Ala-D-Ala
Mechanism: Prevents transglycolation and transpeptidation
Example: Vancomycin, Teicoplanin

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29
Q

Glycopeptide:
Target?
Mechanism?
Example?

A

Target: C-terminal D-Ala-D-Ala
Mechanism: Prevents transglycolation and transpeptidation. Inhibits synthesis of peptidoglycan
Example: Vancomycin, Teicoplanin

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30
Q

What 3 drugs act as bacterial cell wall inhibitors? What does this cause?

A

Drugs:

  1. B-lactams
  2. Vancomycin
  3. Bacitracin

Inhibiting bacterial cell wall synthesis normally leads to the death of the bacteria.
The osmotic pressure in the cytoplasm of bacteria is high and the cytoplasmic membrane does not remain intact when the other rigid cell wall is damaged

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31
Q

What 3 drugs act as bacterial cell wall inhibitors? What does this cause?

A

Drugs:

  1. B-lactams
  2. Vancomycin
  3. Bacitracin

Inhibiting bacterial cell wall synthesis normally leads to the death of the bacteria.
The osmotic pressure in the cytoplasm of bacteria is high and the cytoplasmic membrane does not remain intact when the other rigid cell wall is damaged

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32
Q

Health hazards associated with being in hospital

A

HIA infections: Can be reduced by the implementation of hospital infection control guidelines
Bed rest: Highly unphysiologic, PE, bed sores, muscle loss (particular issue in elderly)

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33
Q

Effect of hospitalisation on adults

A
  1. Unfamilar environment: Limited privacy, stressful, staff wear uniforms
  2. Entering into the “role of a patient”
  3. Loss of control: Reactance (anger) due to restrictions placed upon inpatients. RLOC
  4. Depersonalisation
  5. Institutionalisation occurs in patients with long hospital stay
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34
Q

Issues related to hospitalisation of children

A
  1. Separation anxiety or distress:
    - Stages of separation: Protest -> despair -> Detachment
    - Height of distress seen at 15 months
  2. Illness misconception: Illness as punishment for being “bad”
  3. Faulty illness representation e.g. a haemophilia bug
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35
Q

What is the RLOC?

A

Recovery Locus Of Control scale.

Higher score boosts recovery

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36
Q

What is depersonalisation?

Why does depersonalisation happen?

A

Depersonalisation is when your patient is treated as though he or she were either not present or not a person
Why?
-Distancing mechanism of doctor
-Due to burnt out doctors

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37
Q

What is institutionalisation

A

Institutionalisation: Number of roles of person can adopt is reduced when in hospital

When leaving hospital there is a fear of not being able to adapt to different roles

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38
Q

Strategies to improve hospital experience for children?

A
  1. Outpatient treatment when feasible
  2. Preparation for hospitalisation
  3. Unrestricted parental visits
  4. Nursing staff provide support and education to parents about care
  5. Reduce number of staff dealing with one child
  6. Communicate with the child as well as the parents
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39
Q

Impacts on behaviour of hospitalisation of children? (3)

A
  • May regress sharply
  • Nightmares
  • Irritable
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40
Q

Explain some of the reasons why the NHS has become overstretched, year on year

A
  1. Increase in life expectancy
  2. Increasing costs of treatments
  3. Patient’s expectations increase
  4. Increase cost of admin and salaries
  5. Free means less constraints on demand
  6. Increase in negligence cases
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41
Q

Explain different strategies that could be used in NHS resource allocation

A

Rationing: The discretionary allocation of scare resources

  1. Equal access to treatment
  2. Rationing according to clinical need
  3. Maximising health gains (QALY)
  4. Discriminating according to age
  5. Taking individual responsibility for ill health into account
  6. Rationing according to ability to pay
  7. Singling out certain types of excluding treatment
  8. Dilution of care
  9. Random allocation
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42
Q

Outline the role of NICE

A

National Institute for Health and Clinical Excellence

Produce evidence-based guidance and advice for health, public heath and social care practitioners

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43
Q

Outline the role of SMC and describe its involvement in NHS rationing

A

SMC= Scottish Medicines Consortium

Ensures all new drugs are god value for money

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44
Q

Describe what a ‘QALY’ is?

What is its use in the decision-making process to purchase health care resources?

Strengths and weaknesses?

A

QALY= Quality of adjusted life year
Theory = consequentialism (utilitarianism)
Quality of life x life expectancy (before + after) then cost it

Use:

  • Beneficial healthcare activity = positive No. of QUALs
  • Efficient healthcare activity = cost per QALY is low
  • Quantity + quality = Overall welfare of patient

Weaknesses:

  • How do you define QOL
  • Only welfare?
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45
Q

Describe the work of NICE in their technology appraisals and their role in NHS rationing

A

4 technology appraisal recommendations possible:

  1. Recommended for use in NHS
  2. Restricted use to certain categories of patients
  3. Use confined to clinical trials
  4. Should not be used in NHS
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46
Q

What are the different branches of penicillins?

A
  1. Penicillins G&V
    - Gram positive and gram negative Cocci
    - Gram positive rods
    - Spirochaetes
  2. B-lactams-resistant penicillins
  3. Broad-spectrum penicillins
  4. Extended-spectrum penicillins
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47
Q

Structure and function of carbapenems?

A

Structure:

  • Broad antibacterial spectrum (broader than other penicillins and cephalosporins)
  • Resistant to the typical B-lactamases

Function:

  • Active against both gram positive and gram negative bacteria and anaerobes
  • Poorly active against MRSA
  • Targets bacteria cell wall
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48
Q

Mechanisms of bacterial resistance to the b-lactam antibiotics

A
  1. Destruction by B-lactamase e.g. S. aureus
  2. Failure to reach target enzyme e.g. Pseudomonas
  3. Failure to bind to the transpeptidase e.g. S. pneumoniae
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49
Q

B-lactamase inhibitors
Classes?
Inhibitors?
Use?

A

3 classes of B-lactamases (A.B and C)

B-lactam compounds, Clavulanic acid and sulbactam, are strong inhibitors of Class A

Use: Co-administration of B-lactamase inhibitors with B-lactam antibiotic is an alternative to B-lactam-resistant antibiotics

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50
Q

Cepholasporins:
Uses?
Examples?

A

Uses: Similar to penicillin and are often alternatives.

Used to treat: Septicaemia, pneumonia, meningitis, biliary tract infections, urinary tract infections, sinusitis

Examples: Cefalexin, cefuroxime, cefotaxime, cefadroxil

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51
Q 
Vancomycin:
Drug class?
Mechanism?
Development of resistance?
Uses?
A

Drug class: Glycopeptide antibiotic

Mechanism: Binds to the peptide chain of peptidoglycan (in bacterial cell wall). Interferes with the elongation of the peptidoglycan backbone.

Resistance development: Very specific interaction with D-Ala-D-Ala which leads to minimal resistance development

Uses: MRSA, resistant streptococci and enterococci

52
Q

Bacitracin:
Drug class?
Mechanism?
Clinical uses?

A

Drug class: Cyclic peptide

Mechanism: Interferes with the dephosphorylation of the lipid carrier which moves the early cell wall components through the membrane

Clinical uses: In an ointment to treat infections of the skin and eye by streptococci and staphylococci

53
Q

Bacterial folate antagonists:

  • Name 2 examples
  • Mechanism?
  • Therapeutic uses?
A

Sulphonamides and trimethoprim

Mechanism:

  • Inhibition of the folate pathway in bacteria which is key in cell metabolism
  • Bacteria make it, we receive in our diet
  • Bacteria are susceptible targets … “selective toxicity”

Therapeutic uses:

  • Urinary tract infections
  • Co-trimoxazole (combination of sulphamethoxazole and trimethoprim)
  • In combination with other drugs to treat opportunistic infections in AIDS
54
Q

Macrolides e.g. Erythromycin and clarithromycin:

  • Inhibitors of…
  • Uses as an alternative to…
  • Clinical uses
  • Side effects
A
  • Inhibitors of bacterial ribosomal actions
  • As an alternative to penicillin where patients are penicillin sensitive

Clinical uses:

  • Chlamydia Legionella
  • Lower respiratory tract infections
  • Diphtheria
  • Diarrhoea
  • Limited gram-neg spectrum
  • H. influenza
  • Helicobacter pylori (in combo)

Side effects:
Erythromycin- Gut disturbances, hypersensitivity reactions, hearing disturbances, GT prolongation

55
Q

Clindamycin:
-Drug class?
-Uses?
Side effects?

A

Lincosamide class

Uses:

  • Gram-pos Cocci inc staphylococci
  • In combo against anaerobic sepsis and necrotising fasciitis
  • Staphylococcal infections of joints and bones
  • In eye drop to treat staphylococcal conjunctivitis

Side effects:
-GI disturbances
-Psuedomembraneous colitis
(due to clindamycin-resistant C. diff)

56
Q

Aminoglycoside:

  • Inhibitors of…
  • Uses?
  • Side effects?
  • Pharmacokinetics?
  • Caution in use?
A

Inhibitors of bacterial ribosomal actions

Uses:
-UTIs
-Septicaemia
-Pneumonia
-Respiratory and intra-abdominal infections
(Due to pseudomonas)

Side effects:

  • Renal toxicity
  • Ototoxicity (damage and destruction of the sensory cells of the cochlea and vestibular organ of the ear)
  • Neuromuscular block

Pharmacokinetics:

  • Polar agent confined to extracellular fluid
  • Doesn’t cross BBB
  • Excreted by kidney
  • Administered intravenously

Cautions:

  • Elderly
  • With renal failure or other renal toxic drugs
  • In severe sepsis (that is causing acute renal failure)
57
Q

Tetracyclines:
Inhibitors of …..
Uses?
Side effects?

A

Inhibitors of bacterial ribosomal actions

Uses:

  • COPD
  • Chronic acne
  • Rickets
  • Mycoplasma and chlamydial infections
  • Brucellosis
  • Cholera
  • Resistant gram neg infection

Side effects:

  • Gut upsets
  • Hepatic and renal dysfunction
  • Photosensitivity
  • Binding to bone and teeth causing staining; dental hypoplasia and bone deformities
  • Vestibular toxicity (dizziness and nausea)
58
Q

Chloramphenicol:
Inhibitors of…
Risk?
Only used in?

A

Inhibitors of bacterial ribosomal actions
Risk: Aplastic anaemia
Only used in serious infection e.g. meningitis and brain abscess

59
Q

What is topoisomerase IV?

A

Tetrameric enzyme involved in chromosomal partitioning.

Catalyses relaxant of supercoiled DNA and unknotting of duplux

60
Q

What is DNA gyrase?

A

A tetrametic enzyme which forms a transient covalent bond with DNA.

  1. Breaks the DNA
  2. Passes the DNA through break
  3. Repairs break

DNA gyrase = type II topoisomerase

Target for quinolone antibacterial which make lethal DNA breaks

61
Q

Fluroquinolones:
Main action?
Most common?
Uses?

A

Antibiotics which affect Topoisomerase II.

Ciprofloxacin is most commonly used

  • Gram neg bacteria
  • H. influenza
  • N. gonorrhoea
  • Diarrhoea
  • Salmonella
62
Q

Metronidazole
Main function?
Action?
Uses:

A

Antibiotics which affect Topoisomerase II.

Under anaerobic conditions it generates toxic radicals that damage bacterial DNA

Uses:

  • Sepsis secondary to bowel disease
  • Pseudomembraneous colitis
  • In combo to Helicobacter pylori which gives rise to peptic ulceration
63
Q

Nitrofurans

  • Useful feature
  • Clinical use?
A

Broad spectrum so resistance is rare

Treats UTIs

64
Q

Polymixins:
Mechanisms?
Clinical use?

A

Mechanism: Interacts with phospholipids of cell membrane and disrupts its structure. Eventually cell membrane is breached and there is loss of its intracellular constituents

Use: Topical use for cutaneous Pseudomonas infections

65
Q

Describe the main types of vaccine preparations in use

LAKERD

A

Live: Organisms capable of normal infection and replication. Not used against pathogens that can cause severe disease.

Attenuated: Organisms is live, but ability to replicate and cause disease reduced by chemical treatment or growth-adaptation in non-human cell lines (MMR)

Killed: Organism killed by physical or chemical treatment. Incapable of infection or replication, but still able to provoke strong immune response (B.pertussis, typhoid)

Extract: Materials derived from disrupted or lysed organism. Used when risk of organism surviving inactivation steps (Flu, pneumococcal, diptheria, tetanus)

Recombinant: Genetically engineering to alter critical genes. Often can infect and replicate but does not induce associated disease

DNA: Naked DNA injected. Host cells pick up DNA and express pathogen proteins that stimulate immune response

66
Q

Essential characteristics of vaccines

A

Stimulate neutralised antibodies to prevent re-infection

67
Q

Essential characteristics of vaccines

A

Stimulate correct arm of immune response i.e. antibodies or effector T cells
Stimulate neutralised antibodies to prevent re-infection

68
Q

In general which vaccines are the most effective?

A

Live or attenuated
Why? These organisms express proteins and stimulate the immune response in a manner which most closely resembles normal infection

69
Q

What is herd immunity?
Reason for occurance?
Example

A

When a pool of unimmunised individuals is created that cab become victim to disease.

Why? Vaccinations create unawareness of risks of disease. Leads to vaccination rates fallen. Plus public debate on side effects

E.g. Measles

70
Q

Why is ‘reverse vaccinology” offered?

A

For MenB vaccine
The capsular polysaccharide antigen (that is normally a good target) is similar is structure to a sugar found on NCAM (an important neuronal membrane protein)
Hence antibodies could cause autoimmunity

71
Q

Role of dendritic cells in vaccination?

A
  1. On activation, they migrate to lymph nodes and activate T cells
  2. Express Pattern Recognition Receptors (PRR) , members of the Toll-Like Receptor family (TLR)
  3. Activation increases their ability to capture and process antigen and immunogens

[Activate when DC encounters antigens in periphery]

72
Q

Describe the normal host defence mechanisms of the respiratory tract and how these influence infection

A 
Saliva
Mucus
Cilia
Nasal secretions
Antimicrobial peptides
73
Q 
Common cold:
Transmission?
Causative agents?
Clinical features?
Treatment?
A

Transmission: Aerosol, virus-contaminated hands

Causative agents: Rhinoviruses, Coronaviruses

Clinical features:

  • Tiredness
  • Pyrexia
  • Malaise
  • Sore nose and pharynx
  • Nasal discharge
  • Secondary bacterial infection

Treatment: No vaccine

74
Q

Acute pharyngitis and tonsillitis:

Causative agents

A

Causative agents:
Viruses: Epstein-Barr virus (EBV) and cytomegalovirus (CMV)
Bacteria: Streptococcus pyogenes

75
Q 
Cytomegalovirus:
Transmission?
Causative agents?
Clinical features?
Diagnosis?
Treatment?
A

Transmission: Body secretions and organ transplants

Causative agents: Virus can reactivate and cause disease when cell-mediated immunity is compromised

Clinical features: Asymptomatic

Diagnosis:

  • 2’ infection= IgM in blood
  • CMV pneumonitis =CMV antigen in BAL (Broncho-Alveolar Lavage)

Treatment: Ganciclovir, foscarnet, cidofovir

76
Q 
Epstein-Barr Virus (EBV) (Glandular fever):
Transmission?
Pathophysiology?
Incidence?
Causative agents?
Clinical features?
Diagnosis?
Treatment?
Complications?
A

Transmission: Saliva and aerosol

Pathophysiology: Replicates specifically in B lymphocytes

Incidence: Occurs in 2 peaks, illness lasts 4-14 days

Clinical features

  • Occurs in 2 peaks, illness lasts 4-14 days
  • Causes glandular fever (Fever, headache, malaise, sore throat, anorexia, swollen tonsils, red dots on soft palate, pus)
  • Splenomegaly

Diagnosis:
-Detection of heterophile antibodies (IgM) specific for RBV in monospot test

Treatment?

  • No antibiotics
  • No contact sports or heavy lifting

Complications:

  • Burkitt’s lymphoma
  • Nasopharngeal carcinoma
  • Guillain- Barre syndrome
77
Q 
Tonsillitis:
Transmission?
Incidence?
Causative agents?
Clinical features?
Diagnosis?
Treatment?
A

Transmission: Aerosol

Causative agents: Streptococcus pyogenes (gram pos)

Incidence: Mainly in children

Clinical features:

  • Susceptible to treatment with penicillin
  • Fever, pain in throat, enlargement of tonsilts, tonsillar lymphadenopathy

Diagnosis?

Treatment?

78
Q

What are the 6 complications than can occur with Streptococcus pyogenes?

A
  1. Scarlet fever
  2. Peritonsillar abscess
  3. Otitis media/ sinusitis
  4. Rheumatic heart disease
  5. Glomerulonephritis
  6. Tonsillitis
79
Q 
Parotitis:
Transmission?
Incidence?
Causative agents?
Clinical features?
Diagnosis?
Treatment?
Prevention?
Complications?
A

Transmission: Droplet spread and fomites

Incidence: School-aged children and young adults

Causative agents: Mumps virus

Clinical features:

  • Fever
  • Malaise
  • Headache
  • Malaise
  • Anorexia
  • Trismus
  • Pain and swelling of parotid gland

Diagnosis:

  • Based on clinical features
  • IgM serology can be performed from saliva, CSF or urine

Treatment:

  • Mouth care
  • Nutritional
  • Analgesia

Prevent: MMR vaccine

Complications: CNS involvement

80
Q

What is trismus?

A

The reduced opening of the jaws caused by spasm of the muscles of mastication

81
Q 
Acute epiglottitis:
Transmission?
Incidence?
Causative agents?
Clinical features?
Diagnosis?
Treatment?
A

Transmission?
Incidence: Young children

Causative agents: Haemophilus influenza (gram neg)

Clinical features:

  • High fever
  • Oedema of epiglottis
  • Airflow obstruction = breathing difficulties
  • Bacteraemia

Diagnosis:

  • DO NOT examine throat or take throat swabs (precitates complete airway obstruction)
  • Blood cultures to isolate H. influenza

Treatment:

  • Life threatening emergency
  • Requires urgent endotracheal intubations
  • IV antibiotics
82
Q 
Diphtheria:
Transmission?
Incidence?
Causative agents?
Clinical features?
Diagnosis?
Treatment?
Prevention?
A

Transmission: Aerosol

Incidence: Rarely in developed countries. Childhood

Causative agents: Corynebacterium diphtheria 
(Only toxin producing strains cause disease)
Clinical features:
-Sore throat
-Fever
-Formation of pseudomembrane 
-Lymphadenopathy
-Oedema of anterior cervical tissue

Diagnosis:
-Clinical features

Treatment:

  • Prompt anti-toxin therapy administered intramuscularly
  • Concurrent antibiotics (penicillin or erythromycin)
  • Strict isolation

Prevention:

  • Childhood immunisation with toxoid vaccine
  • Booster when traveling to endemic areas
83
Q

Laryngitis and tracheitis:

  • Viral origin
  • Symptoms in adults and chidlren
A

Viral origin:

  • Parainfluenza virus
  • Respiratory syncytial virus
  • Influenza virus
  • Adenovirus

Symptoms in adults: Hoarseness, retrosternal pain
Symptoms in children: Dry cough, inspiratory stridor

84
Q 
Whooping cough:
Transmission?
Incidence?
Causative agents?
Clinical features?
Diagnosis?
Treatment?
Prevention?
Complications?
A

Transmission: Aerosol

Incidence: In children <5 yrs. In developed countries.

Causative agents: Bordetlla pertussis (Gram neg) in cilia

Clinical features:

  • Catarrhal stage (1 week): Highly contagious, malaise, mucoid rhinorrhoea, conjunctivitis
  • Paraoxysmal stage (1-4 weeks): Inspiratory whoop, Mucus secretion and oedema compromises RT

Diagnosis:

  • “Whoop”
  • Bacterial isolation
  • NAAT

Treatment:

  • In catarrhal stage = Erythromycin
  • In paroxysmal stage: Not antibiotics. Isolation and supportive care

Prevention:
-Vaccine
Complications?

85
Q

What is rhinorrhea?

A

Rhinorrhea or rhinorrhoea is a condition where the nasal cavity is filled with a significant amount of mucus fluid

86
Q

Difference between centrilobular and panacinar emphysema?

A

Centrilobular emphysema: Begins in the respiratory bronchioles and spreads peripherally.

Panacinar: Destroys the entire alveolus uniformly and is predominant in the lower half of the lungs.

87
Q

Name 3 interstitial lung diseases?

A
  1. Hypersensitivity pneumonitis: Type III and IV, Bird fancier, Farmer’s lung
  2. Sarcoidosis: Type IV (cell mediated)
    Clinical features include Granulomas; Hilar lymphadenopathy, raised ACE
  3. Idiopathic pulmonary fibrosis (UIP- Usual Interstitial Pneumonia): Presents as honeycomb lung
88
Q

Main type of benign lung cancer?

A

Mesenchymoma

  • Arising from mesenchyme
  • Non-invasive
89
Q

Where does primary malignant lung cancers develop?

A

Epithelium* and pleura

*[Importance of metaplasia and dysplasia]

90
Q

Difference between metaplasia and dysplasia?

A

Metaplasia: The conversion of one cell type into another; e.g., squamous metaplasia, in which non-keratinised squamous epithelium replaces ciliated columnar cells in the bronchi of smokers.

Dysplasia: An abnormality of development; in pathology, alteration in size, shape, and organization of adult cells.

91
Q

Where are the main locations of secondary cancers from lung cancer?

A
  1. Sarcoma
  2. Renal carcinoma
  3. Lymphoma
92
Q

What are the different forms of primary epithelial cancer in the lung?
How are they diagnosis?
How are they classified?

A
  1. Squamous (NSCLC)
  2. Adenocarcinoma (NSCLC)- Affects glandular structure in epithelia
  3. Small cell undifferentiated (SCLC)
  4. Carcinoid; In neuroendocrine system. “Atypical” is smoking related and tends to be malignant
  5. Large cell undifferentiated

Diagnosis:

  • Radiology (determines size change)
  • Cytology
  • EBUS (EndoBronchial UltraSound)
  • Biopsy

Classification:

  • Grade
  • Stage TNM
93
Q

What is the molecular pathology and treatment for epithelial cancers?

A

Molecular pathology:
Chromosomal rearrangements leading to oncogenic tyrosine kinase activation.
Cancers that harbour tyrosine kinase gene rearrangements express activated fusion kinases that drive the initiation and progression of malignancy
These cancers become dependent on continued signalling from the oncogenic fusion kinase

Mutations of:
-EGFR (epidermal growth factor receptor)
-B-RAF
-RAS
\+ ALK rearrangements

Treatment:
-Tyrosine-kinase inhibitors e.g. ALK (Anaplastic lymphoma kinase) inhibitors
-

94
Q

How are antibodies involved in cancer immunotherapy?

A

They inhibit the suppressing effects of PDL (programmes death ligation). Allowing cancer cells to be killed by immune system

95
Q

What is mesothelioma?

A

Mesothelioma is a rare cancer caused by asbestos that forms in the internal lining (pleura) of the lungs, abdomen, or heart

96
Q

1kPa =

A

7.5mmHg

97
Q

Acid-base disturbances occur when… (3)

A
  1. Ventilation problem
  2. Renal function problem
  3. Overwhelming acid or base load that they body cannot handle
98
Q

What are the normal values for the following:

  • pH
  • pO2
  • pCO2
  • Bicarbonate (standard)
A

pH = 7.35 - 7.45
pO2 = 12 - 13kPa
pCO2 = 4.5 - 5.6 kPa
Bicarbonate (standard) = 22 - 26 mmol/l

99
Q

How is standard bicarbonate calculated?

A

Form the actual bicarbonate but assuming 37C and pCO2 of 5.3kPa

100
Q

Adverse effects of high oxygen levels

A
  1. Increases risk of hypercapnic respiratory failure in acute exacerbations of COPD
  2. Increased mortality in cardiac arrest survivors
  3. Increased mortality in intensive care patients
  4. Increased mortality in acute severe asthma
  5. Generates free radicals
    - -> Lung toxicity (resulting in atelectasis and irritation of mucous membranes)
101
Q

What are the British Thoracic Society guidelines for oxygen administration?

A

Oxygen is a treatment for hypoxia not dyspnoea alone

In an unstable medical emergency give high O2 conc then titrate to target once stable.
Targets:
-94-98% (normally)
-88-92% (in type 2 respiratory failure)

102
Q

What are the therapeutic uses for high inspired conc of O2?

A

Pneumothorax

CO poisoning

103
Q

Normal alveolar -arterial gradient is less than ____

A

3kPa

104
Q

What is the P/F ratio?

A

PaO2 / FiO2

FiO2= Fraction of Inspired Oxygen

P/F ratio > 50 = healthy
P/F ratio < 40 = acute lung injury
P/F ratio <26.7 = ARDS

105
Q

If the pH and pCO2 are changing in opposite
directions this suggests a __________
If the pCO2 and pH are changing in the same
direction, the primary problem is probably
________

A

Opposite direction of pH and pCO2 = RESPIRATORY PROBLEM

Same direction of pH and pCO2 = METABOLIC PROBLEM

106
Q

What is compensation?

A

Altering of function of the respiratory or renal system in an attempt to correct an acid-base imbalance
The body will never overcompensate

107
Q 
If pCO2 and HCO3
- move in the \_\_\_\_ direction
compensation is possibly occurring 
• If both values move in opposite directions
more than 1 \_\_\_\_\_\_ must be present
A 
If pCO2 and HCO3
- move in the SAME direction
compensation is possibly occurring
(remember pH ∞ bicarbonate/pCO2)
• If both values move in opposite directions
more than 1 PATHOLOGY must be present
108
Q

Causes of hyperventilation

A

Acute severe asthma
Pulmonary embolism
Pulmonary oedema

109
Q

Explain how the different forms of tuberculosis occur

A

[]

110
Q

Acute bronchitis:
What is it?
Due to?
Secondary infections?

A

What is it? Inflammation of the tracheobronchial tree

Usually due to infection:

  • Rhinovirus
  • Coronovirus
  • Adenovirus
  • Mycoplasma pneumonia

Secondary infections:

  • Streptococcus pneumonia
  • Haemophilus influenzae
111
Q

Chronic bronchitis:

-Characteristics?

A

Characterised by cough and excessive mucus secretion in tracheobronchial tree

112
Q

Pneumonia:

  • Definition?
  • Diagnosis?
  • Assess to LRT
  • Difference between children and adult
  • 4 different anatomical classes?
  • Clinical features?
A

Defined as inflammation of the substance of the lungs

Confirmed on chest radiograph

Access to LRT by inhalation of microbes or by aspiration of normal flora of the URT

Age is important:

  • Children is mainly viral. Neonatal pneumonia caused by Chlamydia trachmatis from moth during birth
  • Adults is mainly bacterial. Aetiology varies with age, underlying disease, occupational and geographic risk factors

Classes: Lobar, broncho-, interstitial, necrotising

Clinical features: Dry cough, malaise, fever, productive sputum

113
Q

What makes “atypical pneumonia” different?

A 
Failure of patient to respond to treatment with penicillin
Causes:
-Mycoplasma pneumonia
-Legionella pneumophilia
-Chlamydia pneumoniae
114
Q
  • Common causes of viral pneumonia?

- Common causes of bacterial pneumonia?

A

Viral pneumonia causes:

  • Influenza virus
  • Measles
  • Coronavirus
  • CMV

Bacterial pneumonia causes:

  • Streptococcus pneumonia
  • Mycobacterium tuberculosis
  • Staph. aureus
115
Q

Legionnaire’s disease

  • Cause
  • Clinical features
  • Pathophysiology?
  • Transmission
  • Occurrence?
  • Diagnosis
A

Cause: Legionella pneuomophila (gram neg)

Clinical features:

  • Tachypnoea
  • Purulent sputum
  • CXR shows consolidation

Pathophysiology:

  • Secretes protease causing lung damage
  • Severe systemic infection with pneumonia

Transmission: Aerosol

Occurence: In outbreaks

Diagnosis

  • Gram staining of sputum
  • Recognition of serotype-specific fluorescent antibody
  • Culture of legionella on cysteine extract agar
  • Detection of antigen in urine
  • 4-fold rise in antibody
116
Q

Measles:

  • Clinical features
  • 2’ complications?
  • Cause?
  • Transmission?
  • Location of replication?
  • Diagnosis?
  • Treatment?
  • Prevention?
A

Clinical features:

  • Fever
  • Runny nose
  • Koplik’s spots
  • Characteristic rash

Complications:

  • Neurological
  • Giant cell (Hecht’s) pneumonia in the immunocompromised

Cause: Paramyxovirus

Transmission: Aerosol

Replicates in LRT

Diagnosis:

  • Serology for measules-specific IgM
  • Virus isolation
  • Viral RNA detection

Treatment:

  • Ribavirin for severe cases
  • Antibiotics for 2’ infection

Prevention: Immunisation with live/attenuated MMR

117
Q

Define endemic?

A

Present in a community at all times, at a relatively low to medium frequency but at a steady state

118
Q

Define epidemic?

A

Sudden severe outbreak within a region or a group

119
Q

Define pandemic?

A

Occurs when a epidemic become widespread and affects a whole region, a continent or the entre world

120
Q

Influenza virus:

  • Cause
  • 3 types?
  • What contributes to the variety of types?
  • Nucleic acid structure?
  • What are the genetic changes during spread?
  • Diagnosis?
  • Treatment?
A

Cause: Orthomyxovirus

3 types:
A- Epidemics and pandemics, anima reservioir
B- Epidemics, no animal hosts
C- Minor respiratory illness

Type-specific antigens on cell surface, Haemagglutinin (H) and Neuraminidase (N)

Single stranded RNA. Reassortment gives rise to novel combinations of H and N antigens

Genetic changes:

  1. Antigenic drift. Small point mutations in the H and N antigens occurs constantly. Allows replication despite immunity to preceding strains.
  2. Antigenic shift. Sudden major change based on recombination between two different virus strains when they infect the same cell. Produces virus with novel surface glycoproteins. Can cause new pandemic.

Diagnosis:
-Nasopharyngeal aspirate (Direct immunofluorescence, culture, NAAT detection)

Treatment:

  • Amantadine
  • Zanamavir
  • Oseltamvir
121
Q

4 features that make a pandemic

A
  1. Antigenic shift
  2. Lack of immunity
  3. Attack rate is high - it spreads rapidly
  4. Mortality can be high
122
Q

What s the difference in the antigens of season swine flu and pandemic swine flu?

A

Seasonal flu- Different serotypes (e.g. H3, B, H1)

Pandemic flu- Almost exclusively pandemic H1N1

123
Q

Influenza vaccination:

  • Name
  • Difference between yearly vaccine?
  • Give to who?
A

Name: “Tamiflu”

Antigenic variation mens a new vaccine is required each year.
New vaccine is based on the predicted strains
Recombination methods speed up the process of developing a new vaccine

Given to: Elderly, immunosuppressed and those with respiratory risk

124
Q

What does SARS stand for?

A

Severe Acute Respiratory Syndrome (SARS)

125
Q

SARS:
Symptoms?
Transmission?

A

Symptoms:

  • Sudden onset of high fever
  • Dry cough
  • Chills and shivering
  • Muscle aches
  • Breathing difficulties

Transmisson:

  • Droplets
  • Faeces
  • Infected animals
126
Q 
What is SARS Co-V?
How is it identified?
Nucleic acid structure?
Treatment
Vaccine available?
A

SARS Co-V= SARS Coronavirus

Identified by:

  • Virus isolation in cell culture
  • Electron microscopy
  • Molecular techniques

Nucleic acid:

  • Enveloped
  • RNA virus

Characteristic “halo”

Treatment:

  • No specific anti-viral treatment available
  • Ribavirin, corticosteroids, interferons

Whole inactivated virus vaccine and recombinant vaccine now been developed

127
Q 
TB
Associated with?
Clinical features of primary, military and post-primary TB?
Causative agent?
Transmission?
Diagnosis?
Treatment 
Prevention?
A

Associated with:

  • AIDS
  • Increased use of immunosuppressives
  • Decreased socio-economic conditions
  • Multiple drug resistance (MDR)
  • Overcrowding and poor nutrition

Clinical features:
Primary- Symptomless, cough, wheeze, small transient pleural effusion may occur
Miliary- Results from acute diffuse dissemination of bacillus. Fatal without treatment
Post-primary- Malaise, fever, weight loss, sputum abnormal, pleural effusion

Causative agent: Mycobacterium tuberculosis. Neither gram neg or pos. Obliqate aerobe (found in well-aerated upper lobes of lungs)

Transmission: Spread by inhalation of organisms from dust/aerosols

Diagnosis: Mantoux test
-Detects latent TB infection
-Tuberculin injected intradermally. Immune response if individual previously exposed to bacterium
Or
-Identifying ACID-FAST BACILLI in sputum smears

Treatment:

  • Combination therapy- Isoniazid, rifampicin, ethambutol, pyrazinamide. Prevents emergence of resistance
  • Prolonged therapy- To eradicate slow-growing organisms

Prevention:

  • Childhood immunisation
  • Live attenuated BCG vaccine
  • Prophylaxis with isoniazid for 1 year

MD3001 (12 decks)

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