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MD3001 > Week 9 > Flashcards

Week 9 Flashcards

1
Q

What can be the cause of a CXR being too black or black in the wrong place?

A

Increased Translucency:

  • Air (gas)
  • Loss of tissue density
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2
Q

What can be the cause of a CXR being too white or white in the wrong place?

A

Opacification:

  • Fluid
  • Increased tissue ie. lymphadenopathy
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3
Q

What can be the cause of a CXR being really really white or very radio opaque?

A

Patient may have a pacemaker, Endotrachial tube, Nasogastric tube, Sternal wiring, CVP line, chest drain, prosthetic heart valves

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4
Q

What is the definition of Consolidation?

A

Replacement of normal air space gas with fluid or solid material

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5
Q

What are the 5 causes of consolidation and what can they be due to?

A
  1. Pus- infection (pneumonia)
  2. Blood- pulmonary haemorrhage
  3. Fluid- pulmonary oedema
  4. Cells- lung cancer
  5. Protein- alveolar proteinosis
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6
Q

What is the definition of a collapsed lung or atelectasis?

A

Reduction in inflation of all or part of the lung

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7
Q

What are the signs to look for on X-ray for a collapsed lung/atelectasis?

A
  • Volume loss
  • Displacement of trachea
  • Displacement of diaphragm
  • Displacement of lung fissures
  • Compensatory over inflation of non collapsed lung
  • Crowding of vessels & Bronchi
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8
Q

What are the causes of a deviated trachea? (towards & away from pathology)

A
  • Towards pathology: pneumonectomy/Lobectomy, lobar collapse
  • Away from pathology: tension pneumothorax, massive pleural effusion
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9
Q

In ABCDEFGH of examining a CXR what does A stand for?

A

AIRWAY:

  • Trachea position and length
  • Bifurcation of bronchi and main bronchi at T4
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10
Q

In ABCDEFGH of examining a CXR what does B stand for?

A

BREATHING:

  • Good inspiration the dome of right diaphragm should be between 5th-6th ribs
  • Lung fields
  • Opacities
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11
Q

In ABCDEFGH of examining a CXR what does C stand for?

A

CARDIAC:

  • Heart should be no more than 1/2 diameter of chest, 1/3 right of sternum, 2/3 to left
  • Check what makes up the right and left borders
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12
Q

In ABCDEFGH of examining a CXR what does D stand for?

A

DIAPHRAGM:

  • Stomach bubble
  • Below right diaphragm for free air
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13
Q

In ABCDEFGH of examining a CXR what does E stand for?

A

EXTERNAL STRUCTURES:

  • Ribs
  • Thoracic spine
  • Clavicles
  • Scapulae
  • Heads of both humeri
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14
Q

In ABCDEFGH of examining a CXR what does F stand for?

A

FAT & SOFT TISSUE:

  • Breast shadows
  • Subcutaneous fat for signs of surgical emphysema
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15
Q

In ABCDEFGH of examining a CXR what does G stand for?

A

GREAT VESSELS:

  • Aortic arch, pulmonary arteries & veins
  • Calcium deposits in elderly
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16
Q

In ABCDEFGH of examining a CXR what does H stand for?

A

HIDDEN AREAS:

  • Apices
  • Mediastinum for widening ie. adenopathy, aortic dissection, mediastinal emphysema
  • Behind heart for lingular pneumonia
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17
Q

How do you calculate plasma pH?

A

pH = pKa + log[HCO3-] / [CO2]

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18
Q

What is the definition of pKa?

A

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

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19
Q

H2CO3 ↔ HCO3- + H+

What happens to this equation if H+ rises?

A

Equation is driven to the left

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20
Q

H2CO3 ↔ HCO3- + H+

What happens to this equation if H+ falls?

A

Equation is driven to the right

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21
Q

What is the pKa for carbonic acid/bicarbonate?

A

6.1

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22
Q

What is the normal pH for the body?

A

7.4

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23
Q

If you increase CO2 what happens to H2CO3?

A

H2CO3 increases

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24
Q

Where in the equation is Respiratory Acid-base disturbances/disorders?

A

CO2 + H2O

- Primary change is to CO2 levels

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25
Q

Where in the equation is Metabolic Acid-base disturbances/disorders?

A

H2 + HCO3

- Primary change is to bicarbonate

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26
Q

What pH is defined as acidosis?

A

< 7.35

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27
Q

What pH is defined as alkalosis?

A

> 7.45

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28
Q

What are the 2 causes for acidosis?

A
  1. Rise in PCO2

2. Fall in HCO3-

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29
Q

What are the 2 causes for alkalosis?

A
  1. Fall in PCO2

2. Rise in HCO3

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30
Q

How is compensation achieved?

A

Lungs and kidneys may try return any acid-base disturbance towards normal

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31
Q

What are the ways that the lungs and kidneys can compensate?

A
  1. Respiratory system alters ventilation, this happens quickly
  2. Kidneys alter excretion of bicarbonate, this takes 2-3 days
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32
Q

What does Renal Compensation do during respiratory acidosis?

A

Increased HCO3 reabsorption and increased HCO3 production which raises pH towards normal

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33
Q

What are clinical causes of respiratory acidosis?

A
  • COPD
  • Blocked airway (foreign body/tumour)
  • Lung collapse
  • Injury to chest wall
  • Drugs reducing respiratory drive ie. morphine, anaesthetics
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34
Q

What does Renal Compensation do during respiratory alkalosis?

A

Reduced HCO3 reabsorption & reduced HCO3 production, thus plasma HCO3 levels fall, compensating for lower H+, moving pH back towards normal

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35
Q

What are the clinical causes of respiratory alkalosis?

A
  • Increased ventilation, from hypoxic drive in pneumonia, diffuse interstitial lung diseases, high altitude, mechanical ventilation
  • Hyperventilation from brainstem damage, infection driving fever
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36
Q

What does metabolic acidosis result from?

A

Excess H+ in the body, which reduces HCO3- levels

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37
Q

What does Respiratory Compensation do during metabolic acidosis?

A
  • Lower pH is detected by peripheral chemoreceptors, causes increase in ventilation which lowers PCO2.
  • Bicarbonate equation driven to left, reducing HCO3- and H+ further.
  • Decrease H+ drives pH up.
  • Respiratory cannot fully compensate, H+ needs to be removed or HCO3- needs to be restored by kidneys (2-3days)
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38
Q

What are the clinical causes of metabolic acidosis?

A
  • Loss of HCO3 from gut e.g. diarrhea
  • Exogenous acid overload e.g. aspirin
  • Endogenous acid overload e.g. ketogenesis
  • Failure to secrete H+ e.g. renal failure
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39
Q

What does respiratory acidosis result from?

A

Increase in PCO2 caused by hypoventilation or ventilation/perfusion mismatch

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40
Q

What does respiratory alkalosis result from?

A

Decrease in PCO2 due to alveolar hyperventilation, decreasing H+, raising pH

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41
Q

What does metabolic alkalosis result from?

A

Increase HCO3 concentration or fall in H+

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42
Q

What does Respiratory Compensation do during metabolic alkalosis?

A
  • Increase pH detected by peripheral chemoreceptors
  • Decreases ventilation and raises PCO2
  • Increase H+ & HCO3
  • Renal response is to secrete less H+
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43
Q

What are the clinical causes of metabolic alkalosis?

A
  • Vomiting, loss of HCl from stomach
  • Ingestion of alkali substances
  • Potassium depletion (diuretics)
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44
Q

What is Selective toxicity?

A

Toxicity of antibacterial is greater than it is to human

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45
Q

What are the bacterial cell wall inhibitor subclasses?

A
  • Beta-Lactam
  • Cephalosporin
  • Glycopeptides
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46
Q

What group of cell wall inhibitors work by inhibiting synthesis of peptidoglycan?

A

Glycopeptides (e.g. vancomycin, teicoplanin)

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47
Q

What groups of bacterial cell wall inhibitors work by inhibiting cross linkage of peptidoglycan?

A
  • Penicillins,
  • Cephlosporins
  • Carbapenems
  • Monobactams
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48
Q

What 3 groups of pathogens can be treated by penicillins G & V?

A
  1. Gram positive and Gram negative cocci
  2. Gram positive rods
  3. Spirochaetes
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49
Q

Give examples of beta lactamase resistant penicillins?

A
  • Methicillin
  • Oxacillin
  • Nafcillin
  • Dicloxacillin
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50
Q

Give examples of broad spectrum penicillins?

A
  • Ampicillin

- Amoxicillin

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51
Q

Give examples of extended spectrum antibiotics?

A
  • Carbenicillin
  • Ticaracillin
  • Azlocillin
  • Piperacillin
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52
Q

What bacteria do extended spectrum penicillins cover?

A

All of broad spectrum and Pseudomonas Aeruginosa

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53
Q

Describe Carbapenems?

A
  • Broad spectrum
  • Resistant to typical beta-lactamases
  • Bind Beta-lactamases and acylate the enzyme inactivating it
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54
Q

What are Carbapenems poorly active against?

A
  • MRSA

- Bacteria lacking cell wall

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55
Q

What are the 3 main mechanisms of resistance in beta lactam antibiotics?

A
  • Destruction by Beta-lactamase ie. s. aureus
  • Failure to reach target enzyme due to changes in bacterial outer membrane porins and polysaccharide components of gram negative bacteria ie. pseudomonas Spp
  • Failure to bind to transpeptidases ie. S. pneumoniae
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56
Q

What is an alternative approach to the use of Beta-lactamase-resistant antibiotics?

A

Co-administration of Beta-lactamase inhibitors & Beta-Lactam antibiotic

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57
Q

Describe Cephalosporins?

A
  • Same as penicillins
  • Classified by generation
  • Cell wall inhibitor
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58
Q

What do Cephalosporins treat?

A
  • Septicaemia
  • Pneumonia
  • Meiningitis
  • Biliary tract infections
  • UTIs
  • Sinusitis
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59
Q

Give examples of cephalosporins?

A
  • Cephalexin
  • Cefuroxime
  • Cefotaxime
  • Cefadroxil
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60
Q

Describe Vancomycin?

A
  • Glycopeptide antibiotic
  • Binds to peptide chains of peptidoglycan & interferes with elongation of peptidoglycan backbone (D-ala-D-ala interaction is specific so little resistance)
  • Cell wall inhibitor
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61
Q

What is Vancomycin usually used to treat?

A
  • MRSA

- Resistant Streptococci & Enterococci

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62
Q

Describe Bacitracin?

A
  • Polypeptide
  • Bactericidal (kills bacteria)
  • Interferes with dephosphorylation of lipid carrier which moves the early cell wall components through the membrane
  • Cell wall inhibitor
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63
Q

What can Bacitracin be used in?

A

Ointment to treat infections of skin & eye by Streptococci & Staphylococci

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64
Q

What are the main Bacterial Folate Antagonists?

A
  • Sulphonamides

- Trimethoprim

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65
Q

How do Bacterial Folate Antagonists work?

A
  • Inhibit folate pathway in bacteria important in cell metabolism as bacteria can’t ingest folate (selective toxicity as we take in through diet)
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66
Q

What is Trimethoprim commonly used for?

A

Community UTI’s

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67
Q

What 2 antibiotics are combined to make Co-trimoxazole?

A

Sulphamethoxazole & Trimethoprim

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68
Q

What is Co-trimethoprim used to treat?

A
  • Toxoplasmosis
  • Opportunistic infections in AIDs
  • Resistant salmonella & thyphoid
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69
Q

What 2 drugs are used in combination to treat drug resistant Malaria and Toxoplasmosis?

A

Sulphamethoxazole & Pyrimethamine

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70
Q

What are the main Macrolides?

A

Erythromycin & Clarithromycin

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71
Q

When are Macrolides used?

A
  • Alternative to penicillin in sensitive patients
  • Management of community acquired lower RTI
  • Corynebacterium (diphtheria)
  • Camphylobacter (diarrhea)
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72
Q

What are side effects of Erythromycin?

A
  • Gut disturbances
  • Hypersensitivity
  • Transient hearing disturbances
  • Rarely cholestatic jaundice
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73
Q

What are side effects of Clarithromycin?

A
  • Gut disturbances
  • Hypersensitivity
  • Transient hearing disturbances
  • QT PROLONGATION
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74
Q

What are side effects of Clindamycin?

A
  • GI disturbances

- Pseudomembraneous colitis

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75
Q

What are the uses of clindamycin (lincosamide class)?

A
  • Against gram-positive cocci ie. staphylococci
  • Wide range of anaerobic species ie. Bacteriosides sp.
  • Combination against anaerobic sepsis, necrotizing fasciitis, staphylococcal infections of joints and bones
  • Eye drop for staphylococcal conjunctivitis
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76
Q

Give examples of Aminoglycoside antibiotics?

A
  • Streptomycin
  • Gentomycin
  • Kanamycin
  • Neomycin
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77
Q

What conditions may Aminoglycosides be used to treat?

A
  • Enterobacteriaceae and Pseudomonas (septicaemia and serious UTI)
  • Hosptial aquired pneumonia, respiratory and intraabdominal infections due to Pseudomonas
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78
Q

What are common side effects of aminoglycosides?

A
  • Renal toxicity due to damage of kidney tubules
  • Ototoxicity with progressive destruction of sensory cells in cochlea and vestibular organ of the ear (vertigo, ataxia, loss of balance & auditory disturbances)
  • Neuromuscular block
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79
Q

Describe the pharmacokinetics of Aminoglycosides?

A
  • Polar agent confined to extracellular fluid
  • Doesn’t cross BBB
  • Excreted by kidney
  • IV administration
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80
Q

Describe the uses of Tetracylines?

A
  • 1st choice in Mycoplasma & chlamydial infections, Lyme disease
  • COPD
  • Management of resistant gram-negative infection
  • Chronic acne
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81
Q

What are side effects of Tetracyclines?

A
  • Gut upsets
  • Hepatic & renal dysfunction
  • Photosensitivity
  • Binding to bone & teeth causing staining
  • Vestibular toxicity=dizziness
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82
Q

Describe Chloramphenicol?

A
  • Broad spectrum
  • Inhibits protein synthesis
  • Only used in serious infections
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83
Q

What are the side effects of Chloramphenicol?

A

Rarely causes aplastic anaemia

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84
Q

What is Chloramphenicol used to treat?

A

Meningitis and brain abscesses when other agents cannot be used

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85
Q

What does Topioisomerease IV do?

A
  • Involved in chromosomal partitioning
  • Catalyses ATP dependent relaxation of negatively & positively supercoiled DNA and untknotting of unknicked suplex DNA
  • No action against super-coiling
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86
Q

What does DNA gyrase do?

A
  • Tetrameric enzyme consisting of 2 GryA and 2 GyrB subunits
  • Transient covalent bond with DNA
  • Breaking DNA & passing DNA through break
  • Repairing the break
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87
Q

What is the spectrum of activities of Fluoroquinolone?

A

Ciprofloxacin most commonly used against Enetrobacteriaceae (gram -ve), H influenzae, N gonorrhoea, camphylobacter (diarrhoea), pseudomonas aeruginosa & salmonella

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88
Q

Name some Quinolone antibiotics?

A
  • Naladixic acid
  • Norfloxacin
  • Ciprofloxaxin
  • Moxifloxacin
  • Gatifloxacin
  • Gemifloxacin
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89
Q

Describe Metronidazole?

A
  • Anaerobic conditions generates toxic radicals that damage bacterial DNA
  • Active against anaerobic bacteria ie. Bactericides, Clostridia
  • Treat anaerobic infections ie. sepsis secondary to bowel disease
  • Treat pseudomembraneous colitis
  • Used with other drugs (omeprazole, amoxicillin) to treat Helicobacter pylori infections which give rise to peptic ulceration
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90
Q

What spectrum of bacteria is Nitrofurans active against?

A

Broad Spectrum

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91
Q

How do Polymixins work?

A

Cationic detergent properties, interact with phospholipids of cell membranes, causing breach and loss of intracellular contents

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92
Q

What is the use of Nitrofurantoin?

A

UTI due to Enterobacteriaceae

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93
Q

What is the use of Polymixins?

A

Topical use for cutaneous Pseudomonas infections

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94
Q

What are the 2 main health hazards of hospitalisation?

A
  1. HAI Infections (nosocomial) i.e MRSA, MSSA, E coli, C difficile - Can be reduced by implementation of hospital infection control guidelines
  2. Bed Rest - deterioration in CV fitness, loss of muscle, problem in elderly
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95
Q

What can healthcare staff try and improve on for patients feeling a loss of control whilst in hospital?

A
  • Behavioural control
  • Cognitive control
  • Decision control
  • Informational control
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96
Q

What is the definition of “Depersonalisation”?

A

When your patient is treated as though he or she were either not present or not a person

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97
Q

What is the definition of “Institutionalisation”?

A

In normal life people adopt a variety of roles each day, in hospital the variety of roles decreases

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98
Q

Give a summary on the experience of being a patient?

A
  • Unfamiliar environment
  • Role of being a patient
  • Complain about losing control
  • Staff often depersonalise patients
  • Institutionalisation if patient is in hospital for long period
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99
Q

What are the stages of separation anxiety in a hospitalised child?

A
  1. Protest (upset, distressed)
  2. Despair (withdrawn, hopelessness)
  3. Detachment (behaviour returned to normal, child will reject primary care giver)
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100
Q

What are the impacts of hospitalisation on a childs behaviour?

A
  • May regresses sharply
  • Nightmares
  • Irritable
  • May not occur until returned home
  • Misconceive illness
  • Faulty illness representation
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101
Q

How can be improve experience of hospital for children?

A
  • Day surgery/outpatient treatment
  • Preparation for hospital
  • Unrestricted parental visits
  • Nursing staff supporting and educating parents to care for their child in hospital
  • Reduce nursing staff dealing with particular child
  • Communicate with child & Parent
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102
Q

What are the 3 Steps in Pasteur’s Principle for vaccines?

A
  1. Isolate
  2. Inactivate
  3. Inject
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103
Q

What are the essential characteristics of vaccines?

A
  • Effective protection without risk of disease/severe side effects
  • Long-lived protection
  • Stimulate correct arm of immune response ie. antibodies, effector T cells
  • Stimulate neutralising antibodies to prevent reinfection
  • Stable for long-term storage and transport
  • Affordable
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104
Q

What is a Live Vaccine?

A

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

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105
Q

What is a Attenuated Vaccine?

A

Organism is live, but ability to replicate and cause disease reduced by chemical treatment or growth-adaption in non-human cell lines (measles, mumps, rubella)

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106
Q

What is a Killed Vaccine?

A

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

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107
Q

What is an Extract Vaccine?

A

Materials derived from disrupted or lysed organism ie. capsular polysaccharides. Used when risk of organism surviving inactivation steps (flu, pneumococcal, diptheria, tetanus)

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108
Q

What is a Recombinant Vaccine?

A

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

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109
Q

What is a DNA Vaccine?

A

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

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110
Q

What is the most effective vaccines?

A
  • Live / Attenuated

- They express proteins and stimulate immune response closely resembling normal infection

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111
Q

What is Herd Immunity?

What are the potential problems with it?

A
  • You don’t need to vaccinate all of the population (90-95%) because the unvaccinated people have a very slim chance of actually catching the disease
  • Population remains essentially resistant
  • Problems are that vaccination rates fall below 90-95% and disease rates can increase
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112
Q

What is the definition of DTaP/IPV/Hib Vaccinations?

A

Diptheria, tetanus, pertussis, inactivated Polio vaccine, haemophilus influenzae type B

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113
Q

What is the DTaP/IPV Vaccination?

A

Booster vaccine for diptheria, tetanus, pertussis, Polio

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114
Q

What is the Td/IPV Vaccination?

A

Booster vaccine for tetanus, diptheria, polio

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115
Q

When is the Pneumococcal Vaccination offered?

A

> 65yr

116
Q

When is the Flu Vaccination offered?

A

Elderly & at risk patients

117
Q

When is the DTaP/IPV/Hib and MenC Vaccinations offered?

A

2,3,4 month olds (2 injections in total)

118
Q

When is the MMR Vaccination offered?

A

~13months (1 injection)

119
Q

When is the DTaP/IPV and MMR Vaccinations offered?

A

3yr 4month –> 5yr olds

2 injections in total

120
Q

When is the Td/IPV Vaccination offered?

A

13yr –> 18yr old

1 injection

121
Q

What is the problem with creating a vaccine for Meningococcus B?

A
  • Capsular polysaccharide which would be target antigen of vaccine is very similar to sugar of NCAM- important neural membrane protein
  • Antibodies could cause autoimmunity
122
Q

What are Dendritic cells (DCs) ?

A
  • Antigen presenting cells - Process antigen material & present it on the cell surface to T cells
  • Act as messengers between the innate & adaptive immune systems
  • Express Pattern Recognition Receptors (PRR) which are from Toll-like receptor family (TLR)
123
Q

What is TLR4?

A

Lipopolysaccharide, heat shock proteins

124
Q

Describe the 3 step process of dendritic cell function?

A
  1. Encounters antigen in periphery, becomes activated
  2. Migrates to lymph node
  3. Activates T cells to become effector cells
125
Q

What/ When is an Adjuvent used?

A

Added to vaccines to increase immune response to vaccine

126
Q

What are the common (>50%) normal microbiota or the respiratory tract?

A
  • Bacteroides spp.
  • Candida albicans
  • Oral Streptococci
  • Haemophilus influenzae
127
Q

What are the occasional (<10%) normal microbiota of the respiratory tract?

A
  • Streptococcus pyogenes
  • Streptococcus pneumoniae
  • Neisseria meningitidis
128
Q

What are the normal microbiota of latent state in tissues of respiratory tract?

A
  • Herpes Simplex Virus type 1 (HSV)
  • Epstein-Barr virus (EBV)
  • Cytomegalovirus (CMV)
  • Mycobacterium tuberculosis
129
Q

What are the respiratory tract host defences?

A
  • Saliva
  • Mucus
  • Cilia
  • Nasal secretions
  • Antimicrobial peptides
130
Q

What is Acute Coryza/ Rhinitis/Common cold?

A
  • Irritation & inflammation of the mucous membrane inside the nose
  • Seasonal in early autumn & mid/late spring
    (40% rhinovirus, 30% coronavirus)
131
Q

How is the common cold transmitted?

A
  • Aerosol

- Virus-contaminated hands

132
Q

What are the clinical features of the common cold?

A
  • Tiredness
  • Pyrexia
  • Malaise
  • Sore nose & pharynx
  • Profuse, watery nasal discharge becoming mucopurulent (pus)
  • Sneezing in early stages
  • Secondary bacterial infection occurs in minority
  • MILD, NO VACCINE!
133
Q

What are the viral causative agents for Acute Pharyngitis & Tonsillitis?

A
  • Epstein-Barr virus (EBV)
  • Cytomegalovirus (CMV)
  • Herpes Simplex virus type I (HSV-1)
  • Rhinovirus
  • Coronavirus
  • Adenovirus
134
Q

What are the bacterial causative agents for Acute Pharyngitis & Tonsillitis?

A
  • Streptococcus pyogenes
  • Haemophilus influenzae
  • Corynebacterium dephtheriae
135
Q

Describe Cytomegalovirus (CMV)?

A
  • Transmission in body secretions & organ transplants
  • Asymptomatic/mild
  • Can be reactivated
  • Diagnose IgM in blood
  • Diagnose CMV pneumonitis CMV Ag in BAL
  • Treatment with ganciclovir, foscarnet, cidofovir
136
Q

Describe Epstein-Barr Virus (EBV)?

A
  • Replicates in B lymphocytes (CD21 receptor)
  • Causes glandular fever
  • Transmitted in saliva & aerosol
137
Q

What are the clinical features of Glandular Fever?

A
  • Fever
  • Headache
  • Malaise
  • Sore throat
  • Anorexia
  • Palatal petechiae
  • Cervical lymphadenopathy
  • Splenomegaly
  • Mild hepatitis
138
Q

How do you detect IgM antibodies for Glandular Fever (EBV)?

A
  • Monospot test

- If negative consider HIV conversion

139
Q

How do you treat Glandular Fever?

A
  • Not with antibiotics!

- Contact sports/heavy lifting avoided during 1st month of illness until any splenomegaly has resolved

140
Q

What can be the complications of Glandular Fever?

A
  • Burkitt’s Lymphoma
  • Nasopharyngeal carcinoma
  • Guillain-Barre Syndrome
141
Q

Describe Tonsillitis?

A
  • Streptococcus pyogenes
  • Transmission aerosol
  • Children mainly
  • Can become asymptomatic carrier
  • Treat with Penicillin
142
Q

What are the clinical features of Tonsillitis?

A
  • Fever
  • Pain
  • Enlargement of tonsils
  • Tonsillar lymphadenopathy
143
Q

What can be the complications of Streptococcus pyogenes?

A
  • Scarlet fever
  • Peritonsillar abscess
  • Otitis media/sinusitis
  • Rheumatic heart disease
  • Glomerulonephritis
144
Q

What are the clinical features of Parotitis?

A

SCHOOL-AGE & YOUNG ADULTS

  • Fever
  • Malaise
  • Headache
  • Anorexia
  • Trismus (spasm of jaw)
  • Pain & swelling
145
Q

Describe Parotitis?

A
  • Mumps virus
  • Paramyxovirus family
  • Transmission by droplet spread & fomites
  • Diagnosed by IgM serology performed from saliva, CSF/Urine
146
Q

What are the Treatments for Parotitis?

A
  • Mouth care
  • Nutritional
  • Analgesia
147
Q

What can be done to prevent Parotitis?

A

MMR vaccine

148
Q

What can be the complications of Parotitis?

A
  • CNS involvement

- Epididymo-orchitis (~30% infected after puberty)

149
Q

Describe Acute Epiglottitis?

A
  • Haemophilus influenza
  • Young children
  • Hib vaccine prevents it
150
Q

What are the clinical features of Acute Epiglottitis?

A
  • High fever
  • Massive oedema of epiglottis
  • Severe airflow obstruction
  • Bacteraemia
151
Q

How do you diagnose Acute Epiglottitis?

A

DONT examine throat/take swabs as this will precipitate complete obstruction of airway

152
Q

What is the treatment for Acute Epiglottitis?

A
  • EMERGENCY
  • Urgent endotracheal intubation
  • Intravenous antibiotics (ceftriaxone/chloramphenicol)
153
Q

Describe Diphtheria?

A
  • Rare
  • Children
  • May affect adults in countries where childhood vaccination is poor
  • 3-5% of healthy throats
  • Incubation period 2-7days
154
Q

What are the clinical features of Diphtheria?

A
  • Sore throat
  • Fever
  • Formation of pseudomembrane
  • Lymphadenopathy
  • Oedema of anterior cervical tissue (bull-neck)
155
Q

How do you diagnose Diphtheria?

A

Made on clinical grounds as therapy is usually urgently required

156
Q

What is the treatment for Diphtheria?

A
  • Anti-toxin therapy intramuscularly
  • Concurrent antibiotics (penicillin/erythromycin)
  • Strict isolation
157
Q

How do you prevent Diphtheria?

A
  • Immunisation with toxoid vaccine

- Booster doses given if travelling

158
Q

Describe Laryngitis & Tracheitis?

A
  • May spread down from URT

- Viral origin (parainfluenza, respiratory syncytial, influenza virus & adenovirus)

159
Q

What are the clinical features of Laryngitis & Tracheitis in adults?

A
  • Hoarseness

- Retrosternal pain

160
Q

What are the clinical features of Laryngitis & Tracheitis in children?

A
  • Dry cough

- Inspiratory stridor (croup)

161
Q

Describe Whooping Cough?

A
  • 90% children <5
  • Uncommon in developed countries
  • Transmission aerosol
  • Incubation period 1-3 weeks
162
Q

What are the clinical features of Whooping Cough at catarrhal stage (1 week)?

A
  • Highly contagious
  • Malaise
  • Mucoid rhinorrhoea
  • Conjunctivitis
163
Q

What are the clinical features of Whooping Cough at Paroxysmal stage (1-4 weeks)?

A
  • Sudden attack of coughing with inspiratory “whoop”

- Lumen of respiratory tract compromised by mucus secretion & mucosal oedema

164
Q

How do you diagnose Whooping Cough?

A
  • Characteristic “whoop”
  • Bacterial isolation from nasopharyngeal swabs
  • NAAT
165
Q

How do you treat Whooping Cough?

A
  • Catarrhal stage: erythromycin
  • Paroxysmal stage: antibiotics have NO effect
  • Isolation
  • Supportive care
166
Q

How do you prevent Whooping Cough?

A

Whole cell vaccination

167
Q

What is Bordetella pertussis?

A
  • Gram negative aerobic coccobacillus
  • Attaches & replicated in ciliated respiratory epithelium
  • NO invasion of deeper structures
  • Specific attachment due to surface components i.e. filamentous haemagglutinin (FHA)
168
Q

What are the toxic factors of Bordetella pertussis?

A
  • Pertussis toxin (Ptx)
  • Adenylate cyclase toxin
  • Tracheal cytotoxin
  • Endotoxin
169
Q

Describe Acute Bronchitis?

A
  • Inflammation of tracheobronchial tree
  • Rhinovirus, Coronovirus, Adenovirus, Mycoplasma pneumoniae
  • Secondary infections: Streptococcus pneumoniae, Haemophilus influenzae
170
Q

Describe Chronic Bronchitis?

A
  • Cough & excessive mucus secretion in tracheobronchial tree
  • Anatomical disturbance of respiratory system
  • Immune deficit: SCID
  • Ciliary deficit: Kartegener syndrome, smoking
  • Excessively thick mucus: CF
171
Q

Describe Pneumonia?

A
  • Inflammation of the substance of the lungs
  • Lower respiratory tract by inhalation of aerosolised microbes / aspiration of normal flora of the upper respiratory tract
172
Q

What is the cause of Pneumonia in children?

A
  • Mainly viral

- Neonates may develop pneumonia caused by Chlamydia trachoma’s acquired from mother during birth

173
Q

What is the cause of Pneumonia in adults?

A

Mainly bacterial

174
Q

List the common causes of Viral Pneumonia

A
  • Influenza virus
  • Measles
  • Coronavirus
  • Parainfluenza virus
  • Respiratory syncytial virus (RSV)
  • Cytomegalovirus (CMV)
  • Adenovirus
175
Q

List the common causes of Bacterial Pneumonia?

A
  • Streptococcus pneumoniae
  • Mycobacterium tuberculosis
  • Haemophilus influenza
  • Pseudomonas aeruginosa
  • Staphylococcus aureus
176
Q

What is Atypical Pneumonia?

Give examples?

A

FAILURE TO RESPOND TO PENICILLIN

  • Mycoplasma pneumonia
  • Legionella pneumophilia
  • Chlamydia psittaci
  • Chlamydia pneumoniae
  • Coxiella burnetii
177
Q

What is Lobar Pneumonia?

A

Involvement of distinct region of the lung ie. lobe

178
Q

What is Bronchopneumonia?

A
  • Diffuse, patchy consolidation

- Associated with bronchi & bronchioles

179
Q

What is Interstitial Pneumonia?

A
  • Invasion of lung interstitium

- Usually characteristic of viral infection

180
Q

What is Necrotising Pneumonia?

A

Lung abscesses & destruction of parenchyma

181
Q

What are the clinical features of Streptococcus Pneumoniae?

A 
INITIALLY:
- Abrupt onset
- Rigors
- Fever
- Malaise
- Tachycardia
- Dry cough
FOLLOWED BY:
- Productive cough and rusty sputum
- Spiky temp
- Lobular consolidation
182
Q

What are the clinical features of Mycoplasma Pneumoniae?

A
  • Fever
  • Dry cough
  • Dyspnoea
  • Lymphadenopathy
183
Q

What are the clinical features of Haemophilus Influenzae?

A
  • Mainly children
  • Consolidation/patchy bronchopneumonia
  • Persistent purulent sputum & malaise
184
Q

How is Pneumonia diagnosed?

A

Chest X-ray

185
Q

Describe Legionnaires disease?

A
  • Legionella pneumophila
  • Secretes protease causing lung damage
  • Transmitted by aerosol, not person-person
  • Outbreaks
186
Q

What are the clinical features of Legionnaires disease?

A
  • Tachypnoea
  • Purulent sputum
  • Chest X-ray consolidation
187
Q

How is Legionnaires Disease diagnosed?

A
  • Gram staining of sputum
  • Recognition with serotype-specific fluorescent antibody
  • Culture of Legionella on cystine yeast extract agar
  • Detection of antigen in urine
  • 4-fold rise in antibody
188
Q

Describe Measles?

A
  • Paramyxovirus
  • Spread via aerosol
  • Multisystem infection
  • Replicates in Lower respiratory tract
  • Incubation 10-14days
  • May result in neurological complications
  • Can cause “giant cell” pneumonia in immunocompromised
189
Q

What are the clinical features of Measles?

A
  • Fever
  • Runny nose
  • Koplik’s spots
  • Characteristic rash
190
Q

How do we diagnose Measles?

A
  • Serology for measles-specific IgM
  • Virus isolation
  • Viral RNA detection
191
Q

How do you treat Measles?

A
  • Severe: ribavirin treatment

- Antibiotics for secondary bacterial infections

192
Q

How do you prevent Measles?

A

Live, attenuated MMR vaccine

193
Q

Describe Influenza Virus?

A
  • Orthomyxovirus
  • There are 3 types
  • Type-specific antigen on cell surface (spikes)
  • Single-stranded RNA
194
Q

What are the 3 types of Influenza Virus?

A
  • Type A: epidemics & pandemics, animal reservoir
  • Type B: epidemics, no animal hosts
  • Type C: minor respiratory illness
195
Q

What are the 2 type-specific antigens on cell surface of an Influenza Virus?

A
  • Heamagglutinin (H)

- Neuraminidase (N)

196
Q

What happens to Influenza Virus during Antigenic Drift ?

A
  • Small point mutations in H & N antigens occurs constantly
  • Allows virus to multiple in individuals with immunity to preceding strains
  • New subtype can re-infect community
  • Occurs with all influenza types
197
Q

What happens to Influenza Virus during Antigenic shift?

A
  • Sudden major change based on recombination between 2 different virus strains when they infect the same cell
  • Produces virus with novel surface glycoproteins
  • New strain can spread through previously immune populations= new pandemic
198
Q

What makes a pandemic?

A
  • Antigenic shift
  • Most people have no immunity
  • Attack rate is high
  • Mortality can be high
  • Spreads rapidly
199
Q

How do you diagnose Influenza?

A 
Nasopharyngeal aspirate:
- Direct immunofluorescence
- Culture
- NAAT detection
Serum:
- Serology
200
Q

How do you treat Influenza?

A
  • Amantadine
  • Zanamavir
  • Oseltamivir (“Tamiflu”)
201
Q

How do you manage Influenza?

A
  • Rest, warmth, hydration, analgesia
  • Anti-viral treatment within 48hrs
  • Antibiotics for secondary bacterial infection
202
Q

How do you prevent Influenza?

A
  • Killed vaccine ~70% efficacy

- Different strains of antigen each year in anticipation of latest strain to emerge so need different vaccine each year

203
Q

Describe Swine Flu?

A
  • H1N1 virus
  • Older people infected
  • Vaccine had contained H1N1 components
  • Infection largely limited to <40years
  • Attack rate high but mortality low because of immunity
204
Q

What does “SARS” stand for?

A

Severe Acute Respiratory Syndrome

205
Q

What are the clinical features of SARS?

A
  • High fever
  • Cough
  • Shortness of breath
  • CXRs consistent with pneumonia
206
Q

How is SARS transmitted?

What is SARS incubation period?

A
  • Droplets, faeces, infected animals

- 2-7days

207
Q

What is SARS-associated Coronavirus (SARS CoV)?

A
  • Enveloped
  • RNA virus
  • Characteristic “halo”
  • Receptor for spike protein is ACE2
208
Q

What is SARS-associated Coronavirus (SARS CoV) identified by?

A
  • Virus isolation in cell culture
  • Electron microscopy
  • Molecular techniques
209
Q

How do you treat SARS?

A
  • Ribavirin
  • Corticosteroids
  • Interferons
  • Anti-retroviral therapies ie. protease inhibitors
  • Whole inactivated virus vaccine & recombinant vaccine now developed
210
Q

What is Tuberculosis (TB) associated with?

A
  • AIDS
  • Increased use of immunosuppressive drugs
  • Decreased socio-economic conditions
  • Increased immigration from areas of high endemicity
  • Multiple drug resistance (MDR)
  • Overcrowding & poor nutrition
211
Q

What bacteria causes Tuberculosis?

A

Myobacterium tuberculosis

212
Q

What are the clinical features of Primary Tuberculosis?

A
  • Usually symptomless
  • Cough & Wheeze
  • Small transient pleural effusion
213
Q

What are the clinical features of Miliary Tuberculosis?

A
  • Acute diffuse dissemination of bacillus

- Fatal without treatment

214
Q

What are the clinical features of Post-Primary Tuberculosis?

A
  • Onset of symptoms over weeks/months
  • Malaise
  • Fever
  • Weight loss
  • Mucoid, purulent or blood-stained sputum
  • Pleural effusion
215
Q

How do we diagnose Tuberculosis?

A

MANTOUX TEST:

  • Latent TB infection
  • Tuberculin injected intradermally
  • Immune response if previously exposed to bacterium
  • Induration (palpable hardened area) measured after 48-72hrs
216
Q

How is bacterial growth measured on cultures?

A

Actively respiring bacteria consume O2 from media allowing fluorescence to be detected

217
Q

How do you treat Tuberculosis?

A 
Combination therapy:
- Isoniazid, ridampicin, ethambutol, pyrazinamide
Prolonged therapy:
- Min 6months
- Eradicate slow-growing organisms
218
Q

How do you prevent Tuberculosis?

A
  • Childhood immunisation
  • Live, attenuated BCG vaccine (Bacille Calmette-Guerin)
  • Prophylaxis with isoniazid for 1yr
219
Q

What bacteria cause Fungal infections?

A
  • Aspergillus fumigatus

- Pneumocystis jiroveci

220
Q

List 4 Parasitic infections?

A
  • Ascaris
  • Strongyloides
  • Schistosoma
  • Echinococcus granulosus
221
Q

List some smoking related lung diseases?

A
  • COPD
  • Emphysema
  • Chronic Bronchitis
222
Q

What are the 2 types of emphysema and describe them?

A
  1. Centrilobular (localised)- primarily the upper lobes. Loss of respiratory bronchioles in proximal portion of acinus. Typical for smokers.
  2. Panacinar (unlocalised)- all lung fields, particularly bases. Loss of all portions of acinus (respiratory bronchiole –> alveoli)
223
Q

List 3 Interstitial lung diseases?

A
  1. Hypersensitivity pneumonitis
  2. Sarcoidosis
  3. Idiopathic pulmonary fibrosis (UIP)
224
Q

Describe Hypersensitive pneumonitis?

extrinsic allergic alveolitis

A
  • Inflammation of alveoli within lung caused by hypersensitivity to inhaled organic dusts
  • Type III and IV
  • Bird fancier
  • Farmers lung
225
Q

Describe Sarcoidosis?

A
  • Small patches of red and swollen tissue, called granulomas
  • Cell mediated
  • US black>white
  • Granulomas
  • Hilar lymphadenopathy
  • Raised angiotensin converting enzyme
226
Q

Describe Idiopathic pulmonary fibrosis (UIP)?

A
  • Lungs become scarred and breathing increasingly difficult
  • Post Viral?
  • Other systemic disease
  • Part of a spectrum?
  • Honeycomb lung
227
Q

Give examples of Benign Lung Tumours?

A
  • MESENCHYMOMA
  • Papilloma
  • Inflammatory myoblastic tumour
228
Q

Give examples of Primary Malignant Lung Tumours?

A
  • EPITHELIUM (metaplasia/dysplasia)
  • Vessels
  • Muscles
  • Cartilage
  • Lymphoid
  • Pleura
229
Q

What is metaplasia & Dysplasia?

A
  • Metaplasia: change of 1 mature cell type to another mature cell type
  • Dysplasia: enlargement of organ/tissue by proliferation of cells of an abnormal type
230
Q

Give examples of Secondary Malignant Lung Tumours?

A
  • Sarcoma
  • Renal Carcinoma
  • Lymphoma
231
Q

Give examples of Primary Epithelial malignant lung tumours?

A
  • Squamous
  • Adeno (glands)
  • Small cell undifferentiated
  • Carcinoid
  • Large cell undifferentiatied
232
Q

List how you can diagnose Primary Epithelial lung tumours?

A
  • Radiology
  • Cytology
  • EBUS (Endobronchial ultrasound)
  • Biopsy
  • Grade
  • Stage TNM
233
Q

Describe Squamous Epithelial Malignant Lung Tumours? (NSCLC)

A
  • Non-small cell lung cancer is a disease in which malignant cells form in tissues of lung
  • ~40%
  • Risk in Smoking, Air pollution, Asbestos
  • Fibrosing lung disease
  • TNM
234
Q

Describe Adenocarcinoma Lung Tumour? (NSCLC)

A
  • ~40%

- Risk in Smoking, Lung scar, Air pollution, Asbestos

235
Q

Describe Adenocarcinoma-bronchoalveolar Lung Tumour? (NSCLC)

A
  • Variant of adenocarcinoma
  • Pattern of spread
  • Intrapulmonary dissemination
236
Q

Describe Small Cell Undifferentiated Lung Tumours (SCLC)?

A
  • Neuroendocrine
  • Paraneoplastic effects: may produce bioactive amines or peptides i.e. ADH, PTN-like peptides, ACTH
  • Neurological ie. demyelination
237
Q

What is NSCLC?

A
  • Non-small cell lung cancer - A disease in which malignant cells form in tissues of lung
238
Q

Describe Carcinoid Lung tumours?

A
  • Malignant spectrum
  • “Typical” towards less aggressive end of spectrum
  • “Atypical” smoking related, tends towards malignant end of spectrum
239
Q

Describe Mesothelioma Lung Tumours?

A
  • Asbestos: crocidolite
  • Incidence rising
  • Long lag period 20-40yrs
  • Male:Female 5:1
  • Significance of fibrous pleural plaques
240
Q

What is the main form of primary malignant lung tumours?

A

Epithelium

241
Q

What does staging refer to in terms of tumour?

A

TNM staging

Tissue, lymph Nodes and Metastasis

242
Q

What does grade refer to in quantifying tumours?

A

Amount of differentiation (undifferentiated being abnormal, primitive and aggressive)

243
Q

What may Carcinoid tumours produce?

A

Amines such as noradrenaline resulting in panic attack

244
Q

How many mmHg does 1kPa equal?

A

7.5mmHg

245
Q

What buffers the pH in the body?

A
  • Proteins
  • Haemoglobin
  • Carbonic acid and Bicarbonate
246
Q

Where is acid/base excreted?

A
  • Lungs

- Kidneys

247
Q

Which 3 scenarios result in disturbances in acid base balance?

A
  • Problems with ventilation
  • Problems with renal function
  • Overwhelming acid/base load that body can’t handle
248
Q

What is the body’s normal pH value?

A

7.35-7.45

249
Q

What is the body’s normal pO2 value?

A

12-13kPa

250
Q

What is the body’s normal pCO2 value?

A

4.5-5.6kPa

251
Q

What is the body’s normal bicarbonate value?

A

22-26mmol/l

252
Q

Give 2 examples of endogenous acids?

A
  • Ketoacidosis

- Lactic acidosis

253
Q

Give 2 examples of exogenous acids?

A
  • Methanol

- Aspirin

254
Q

Which test is used to check arterial sufficiency to the hand?

A

Allan’s test

(hand elevated & patient clench their fist ~30secs. Pressure applied over ulnar & radial arteries. Still elevated, the hand is then opened)

255
Q

What is the difference between Actual v Standard Bicarbonate?

A

Standard bicarbonate is calculated from the actual bicarbonate but assuming 37oC and a pCO2 of 5.3kPa

256
Q

If CO2 is high, how will bicarbonate be affected?

A

Increased

257
Q

What is Step 1 in assessing acid/base balance?

A

Assess the oxygenation & look at pO2

258
Q

What are the different adverse effects of high O2 levels?

A
  • Increases risk of hypercapnic (abnormally elevated CO2) respiratory failure in acute exacerbations of COPD
  • Increased mortality in survivors of cardiac arrest, intestine care patients, acute severe asthma
  • Generates free radicals causing lung problems
  • Ocular toxicity
  • Myocardial damage
  • Neuro damage
259
Q

What can a high pO2 do to the lungs?

A
  • Lung toxicity
  • Collapse of alveoli due to atelectasis
  • Irritating to mucous membranes
260
Q

What is the normal target range of O2 saturation?

A

94-98%

261
Q

What is the target range for O2 saturation in patients with type 2 respiratory failure?

A

88-92%

262
Q

What are the 2 therapeutic uses of high inspired concentration of O2?

A
  • Pneumothorax

- Carbon monoxide poisoning

263
Q

What may result in low O2 saturation but high O2 intake?

A

Problem with oxygenation (alveolar arterial gradient)

264
Q

What is the normal Alveolar-arterial (A-a) gradient in kPa?

A

<3kPa

265
Q

What fraction should the arterial pO2 be of the inspired pO2 in a fit healthy adult?
(PaO2/FiO2)

A

2/3

266
Q

What else is the PaO2/FiO2 ratio known as?

A

P/F ratio

kpa divided by inspired fraction of O2

267
Q

What is the P/F ratio of a healthy person?

A

> 50

268
Q

What is the P/F ratio of a person with acute leg injury?

A

<40

269
Q

What is the P/F ratio of a person with acute respiratory distress (ARDS)?

A

<26.7

270
Q

What is Step 2 in assessing acid/base balance?

A

Assess pH

271
Q

What is the pH of acidaemia?

A

<7.35

272
Q

What is the pH of alkalaemia?

A

> 7.45

273
Q

What is Step 3 in assessing acid/base balance?

A

Determine the primary problem

274
Q

If pH and pCO2 are changing in the opposite direction what does this suggest?

A

Respiratory problem

275
Q

If pH and pCO2 are changing in the same direction what does this suggest?

A

Metabolic problem

276
Q

What is Step 4 in assessing acid/base balance?

A

Is compensation occuring?

277
Q

What is Compensation?

A

Altering of function of the respiratory or renal system in an attempt to correct an acid-base imbalance

278
Q

Can the body ever overcompensate?

A

NO

279
Q

If CO2 and bicarbonate move in the same direction what does this usually indicate?

A

Compensation is possibly occuring

280
Q

If pCO2 and bicarbonate move in opposite directions what does this indicate?

A

More than 1 pathology is present

281
Q

In chronic respiratory acidosis what is the compensation?

A

Kidneys retain bicarbonate (takes a few days to reach maximal value)

282
Q

What are 4 possible causes of hyperventilation?

A
  1. Acute severe asthma
  2. Pulmonary embolism
  3. Pulmonary oedema
  4. Anxiety attack
283
Q

What can cause an abnormal level of central respiratory drive?

A
  • Hypoxia
  • Stimulation lung mechanoreceptors/chemoreceptors
  • Direct stimulation of respiratory centre
  • Psychogenic
284
Q

In what 2 situation may chronic respiratory alkalosis occur?

A
  1. High altitude- hypoxaemia induced

2. Hyperventilation- compensation occurs by renal excretion of bicarbonate

285
Q

Why do you look at the pO2 first?

A

Because hypoxia kills a patient the fastest

286
Q

Can O2 be used as a treatment for hypoxia and dyspnoea?

A

Hypoxia- YES

Dyspnoea- NO

MD3001 (15 decks)

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