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Flashcards in WEEK 9 Deck (156):

What is the terminology used to describe a part of a CXR that is too black/black in the wrong place? What pathology does this suggest?

Increased translucency
- air (gas)
- loss of tissue density


What is the terminology used to describe a part of a CXR that is too white/white in the wrong place? What pathology does this suggest?

- fluid
- increased tissue e.g. lymphadenopathy (at hilum)


If part of a CXR is really, really white or very radio opaque, what could this suggest?

- pacemaker
- endotracheal tube
- nasogastric tube
- sternal wiring
- prosthetic heart valves
- CVP line
- chest drain


When describing any abnormality, how do you explain WHERE said abnormality is?

Using ZONES (upper, middle and lower)
Also specify if left or right sided abnormality


What is consolidation?

Replacement of normal air space gas with fluid/solid material


If a normal airspace is filled with (i) pus (ii) blood (iii) fluid (iv) cells (v) protein, what disease(s) could this suggest?

(i) infection (pneumonia)
(ii) pulmonary haemorrhage
(iii) pulmonary oedema, drowned lung
(iv) lung cancer
(v) alveolar proteinosis


What is atelectasis? (also can be referred to as collapse but the former is preferred)

Reduction in inflation of all or part of the lung


What on a CXR would make you suspect atelectasis? (HINT: there's 6 things)

Volume loss
Displacement of trachea
Displacement of diaphragm
Displacement of lung fissures
Compensatory over inflation of non collapsed lung
Crowding of vessels and bronchi


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

(i) pneumonectomy/lobectomy, lobar collapse
(ii) tension pneumothorax, (massive) pleural effusion, or any mass effect.


What does the ABCDE mneumonic stand for with regards to abnormalities seen on a CXR of a pt with pulmonary oedema?

A - alveolar oedema (bat wings)
B - kerley B lines
C - cardiomegaly
D - upper lobe diversion
E - pleural effusions


What is pneumoperitoneum?

When there is significant air underneath the peritoneum of the diaphragm


What does air in the soft tissues suggest?

Subcutaneous emphysema


What are the hidden areas when examining a CXR?

Behind the heart
Mediastinum: widening, adenopathy, mediastinal emphysema

But remember the hilum too!


What condition pushes the trachea away, has increased opacity, is dull to percuss on examination and decreases vocal resonance?

Pleural effusion


What is the pKa for carbonic acid/bicarbonate?



Describe a Davenport Diagram

pH<7.35 = acidosis
pH>7.45 = alkalosis
AB shows plasma pH changes as CO2 changes
CD shows plasma pH change when non-volatile acid (lactic acid, those derived from phosphate etc) is added/removed (static PCO2)
NOTE: volatile acid = CO2 based


What are the causes fo acid base disturbances?

increased CO2
Decreased CO2
Increased non-volatile acid/decreased base
Decreased non-volatile acid/increased base


What type of disorder is it if the primary change is to (i) CO2 levels (ii) bicarbonate?

(i) respiratory disorders
(ii) metabolic disorders


What is (i) acidosis (ii) alkalosis caused by?

(i) rise in PCO2, fall in HCO3-
(ii) fall in PCO2, rise in HCO3-


What are the 2 ways the lungs and kidneys try to return any disturbances to normal (i.e. compensation)?

1. Respiratory system alters ventilation - immediate response
2. Kidneys alter excretion of bicarbonate - takes 2-3 days


What are the various causes of respiratory acidosis?

Blocked airway - foreign body/tumour
Lung collapse
Injury to chest wall
Drugs reducing respirator y drive e.g. morphine, general anaesthetics, barbituates


What is the 2 compensations done for respiratory acidosis?

An increase in PCO2 causes increase in H+ so plasma HCO3- levels increase to compensate for increased H+
Renal - increased HCO3- reabsorption and increased HCO3- production, raising pH to normal


Respiratory acidosis results form an increase in PCO2 which is caused by what 2 things?

1. Hypoventilation (less CO2 being blown away)
2. V/Q mismatch


Respiratory alkalosis results from a decrease in PCO2 generally caused by what?

Alveolar hyperventilation
- more CO2 being blown away
Decrease in H+ and therefore rise in pH


What renal compensation is done for respiratory alkalosis?

reduced HCO3- reabsorption and reduced HCO3- production
- thus plasma HCO3- levels falls fall, compensating for lower H+, moving pH back towards normal


What are the causes of respiratory alkalosis?

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


What does metabolic acidosis result from?

Excess of H+ in the body, which reduces HCO3 levels.
Respiration is unaffected, therefore PCO2 is initially normal.


How is metabolic acidosis compensated for?

Lower pH detected by PCRs,
=> increase in ventilation which lowers PCO2.
Bicarbonate equation is driven further to the left, lowering H+ and HCO3-
concentration further
Decrease in H+ conc moves pH towards normal
Resp compensation can't fully correct pH, HCO3 and H+, so excess H+ needs to be removed or HCO3- restored (by slow renal compensation)


What are the causes of metabolic acidosis?

loss of HCO3- e.g. form gut in diarrhoea
Exogenous acid overloading (aspirin overdose), endogenous acid production (ketogenesis)
Failure to secrete H+ e.g. in renal failure


What does metabolic alkalosis result from?

Increase in HCO3- conc or fall in H+
- raising pH


How is metabolic alkalosis compensated for?

increase in pH detected by PCR - decreases ventilation which raises PCO2
Eqn is driven further to the right, increasing H+ and HCO3-
Increase in H+ moves pH towards normal
Resp. compensation is often small - ventilation cannot reduce enough to correct imbalance
Renal response to secrete less H+


What are the causes of metabolic acidosis?

Vomiting - loss of HCl from stomach
Ingestion of alkali substance
Potassium depletion


What are the 3 bacterial cell wall inhibitors?

- the osmotic pressure in cytoplasm of bacteria is high and membrane doesn't remain intact when cell wall is damaged


What are the classes of antibiotics active against the cell membrane? Give names examples.

1. Beta-lactam and cephalosporin
- pen. G, Fluclox, Tazobactam
2. Glycopeptide
- vancomycin, teicoplanin
3. Cyclic peptide
- bacitracin, polymyxin
4. Phosphonic acids
- fosphomycin
5. Lipopepides
- daptomycin


What is the (i) target and (ii) mechanism for Beta-lactams and cephalosporins?

(i) penicillin binding proteins
(ii) preventing peptidoglycan crosslinking


What is the (i) target and (ii) mechanism for glycopeptides?

(i) C-terminal D-Ala-D-Ala
(ii) prevents transglycolation and transpeptidation


What is the (i) target and (ii) mechanism for cyclic peptides?

(i) C55 - isoprenyl pyrophosphate
(ii) prevents carriage of building-blocks of peptidoglycan cell wall outside fo the inner cel membrane


What is the (i) target and (ii) mechanism for phosphonic acids?

(i) murA protein
9ii) inhibits first stage of peptidoglycan synthesis


What is the (i) target and (ii) mechanism for lipopepides?

(i) cell wall stress stimulation
(ii) calcium-dependent membrane depolarisation


What is the difference between penicillin G and V?

G is only administered parentally but V can be given orally


Give examples of B lactamase resistant penicillins, what spectrum do they target?

Methicillin, oxacillin, cloxacillin, dicloxacillin, naficillin
- same spectrum as ordinary penicillins


Give examples of B lactamase resistant penicillins, what spectrum do they target?

Methicillin, oxacillin, cloxacillin, dicloxacillin, naficillin
- same spectrum as ordinary penicillins


Give examples of broad spectrum penicillins.

Ampicillin and amoxicillin
- same as G and V but also beta lactamase free strains of H.influenzae, N.gonorrhoeae, E.coli, salmonella, sinusitis


Give examples of extended spectrum penicillins

Carbenicillin, ticaracillin, azlocillin, piperacillin
- covers borad spectrum bacteria plus pseudomonas aeruginosa


What is the structure and function of carbapenems?

Broad spectrum (more so than penicillins and cephalosporins)
Resistant to typical beta-lactamases as they bind to them, which acetylates it => inactive
Active against both Gram +ve and -ve bacteria and anaerobes but poorly active against MRSA
- it is NOT active against bacterial without a cell wall


What are the different beta-lactamase inhibitors?

There's 3 classes of beta-lactamases (A, B and C)
Clavulanic acid and salbactam = strong class A inhibitors NOT B and C


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

the co-administration of beta-lactamase inhibitors with a beta-lactam antibiotic


What are cephalosporins? What conditions are they used to treat? Give examples.

Cefalexin, cefurtaxime, cefotaxime, cefadroxil
Basically same as penicillins hence why they are often used as alternatives.
There are fewer of them and they are classed by generation
used against septicaemia, pneumonia, meningitis, biliary tract infections, UTIs, sinusitis


What is vancomycin? What is its MoA? What is it used to treat?

It binds to the peptide chain of the peptidoglycan. It interferes with the elongation of the peptidoglycan backbone
It's a very specific interaction with D-Ala-D-Ala which explains the minimal development of resistance
MRSA and resistant streptococci and enterococci


What is bacitracin? What is its MoA? What is it used to treat?

Polypeptide that is bactericidal
It interferes with the dephosphorylation of the lipid carrier which moves the early cell wall components through the membrane
Ointment to treat skin and eye infections by streptococci and staphylococci


What are the 2 types of bacterial folate antagonists? What is their MoA?

Sulphonamides and Trimethoprim
- inhibit folate pathway in bacteria = selective toxicity target
Sulphonamides act on PABA
Trimethoprim acts on dihydrofolic acid


What are the therapeutic uses of sulphonamides and trimethoprim?

T - community UTIs
Can be combined to treat toxoplasmosis - Co-trimoxazole
Used in combo with other drugs for opportunistic infections in AIDS pts e.g. pneumonia


Name 2 examples of macrolides. What are they used for? What is their MoA?

Used as penicillin alternative. Active against mycoplasma Chlamydia Legionella, used in management of community acquired lower resp tract infection
Active against:
- H.influenzae, corynebacterium (diptheria), camphylobacter (diarrhoea), chlamydia trachomatis, toxoplasma gondii (in pregnancy)
Also against helicobacter pylorii in combo with other agents


What are the adverse events/ side effects of (i) erythromycin (ii) clindamycin?

(i) Mild gut disturbances, hypersensitivity reactions, transient hearing disturbances and rarely cholestatic jaundice
(ii) Mild GI disturbances but pseudomembranous colitis can occur and can be fatal


What is the lincosamide class of clindamycin active against? What is it used to target/treat?

Active against gram +ve cocci including staphylococci, and a wide range of anaerobic species including bacteroides species
Used in eye drops for staphylococcal conjuctivitis
In combo against anaerobic sepsis and necrotising fasciitis, for staph infection of joints and bones


What are aminoglycosides used to treat? What side effects can occur?

They are reserved for treatment of serious infections
- enterobacteriaceae and pseudomonas (septicaemia and serious UTIs)
- hospital acquired pneumonia, resp and intra-abdominal infections due to pseudomonas
- brucellosis, yersinia pestis (plague)
Side Effects: renal toxicity due to damage of kidney tubules. Ototoxicity which can result in vertigo, ataxia and loss of balance as well as auditory disturbances (deafness). Neuromuscular block if drug is given with a neuromuscular blocker


What are the pharmacokinetics of aminoglycosides? (HINT: there's 4 points)

1. Polar agent confined to ECF
2. Doesn't cross BBB
3. Excreted by kidney
4. Must be administered IV


When should you be cautious about the use of aminoglycosides?

elderly, renal failure, severe sepsis which is causing acute renal failure


What are the uses of tetracyclines?

Rickettsial, mycoplasma and chlamydial infections, brucellosis, cholera, plague and Lyme disease
Tigecycline used in resistant gram -ve infection
Used in COPD and chronic acne


What are the side effects of tetracyclines?

Gut upsets
Hepatic and renal dysfunction
Binding to bone and teeth causing staining, dental hypoplasia and bone deformities
Vestibular toxicity (dizzy and nausea)


When is chloramphenicol used?

Limited to indications for serious infections when no other drug is suitable (because of its low risk of aplastic anaemia)
indications = meningitis and brain abscess


What is topoisomerase IV?

Tetrameric enzyme of 2 ParC and 2 ParE sub-units
Involved in chromosomal partitioning as it catalyses ATP dependent relaxation of negatively and positively supercoiled DNA and unknotting of un-nicked duplex DNA


What is DNA gyrase?

Tetrameric enzyme consisting of two GryA and two GyrB subunits
Forms a transient covalent bond with DNA, breaking the DNA and then passing the DNA through the break, repairing the break


The most commonly clinically used quinolones are fluoroquinolones, what is the most commonly used fluoroquinolones.

Ciprofloxacain = most commonly used atm
Good against enterobacteriaceae and H. influenzae.
A single dose can cure gonorrhoea (beta lactamase producing N. gonorrhoea)
Camphylobacter (diarrhoea)
Pseudomonas aeruginosa


What is the uses of (i) Naladixic acid (ii) Norfloxacin and ciprofloxacin (iii) moxifloxacin, gatifloxacin and gemifloxacin?

(i) UTI
(ii) Systemic infection
(iii) Acute lower respiratory tract infection


What is metronidazole? What is its MoA? What is it used to treat?

An antiprotozoal agent
Under anaerobic conditions it generates toxic radicals such as bacteriodes, clostridia and some streptococci
Treats anaerobic conditions (e.g. sepsis secondary to bowel disease)
Treats pseudomembranousu colitis
Used with other drugs (omeprazole, amoxicillin) to treat H. pylori - gives rise to peptic ulceration


What is nitrofurans (nitrofuratoin)? What is it used to treat?

MoA unkown but has broad spec of activity against bacteria and resistance is rare
Treats UTIs due to enterobacteriaceae


What is polymixins? What is their MoA? What are they used to treat?

Branched chain decapeptides with cationic detergent properties
MoA involves interaction with phospholipids of the cell membrane and disruptioni of its structure, membrane eventually breached and loss of intracellular material
Topical use for cutaneous pseudomonas infections


What are some of the health hazards associated with being in hospital? (HINT: there's 2)

1. Nosocomial infections (MRSA, E coli, C difficile)
2. Bed rest
- deterioration in CV fitness, loss of muscle strength
- particular problem in elderly


What are the 5 effects of hospitalisation on adults?

1. Unfamiliar environment
2. Entering the role of the patient
- wearing night-clothes all day, no control over lights, meals etc, allowing body to be examined
3. Loss of control
- restrictions placed upon inpatients
- behavioural, cognitive, decision, informational control
- "the stomach ulcer in bed 9"
5. Institutionalisation
- people normally adopt a variety of roles each day but in hospital this variety is reduced


What are some of the specific issues related to the hospitalisation of children? (HINT: there's 3 issues)

1. Separation distress
- protest, despair, detachment
2. Illness misconceptions
- illness is a punishment for being "bad"
3. Faulty representation


What are the main types of vaccine preparations currently in use? Describe them. (HINT: there's 6 types)

1. LIVE - organisms capable of normal infection and replication. Not used against pathogens that can cause severe disease
2. ACCENTUATED - organism is live, but ability to replicate and cause disease reduced by chemical treatment or growth-adaptation in non-human cell lines (MMR)
3. KILLED - killed by physical/chemical treatment. Can't infect or replicate, but can still provoke immune response (B.pertussis, typhoid)
4. EXTRACT - derived from disrupted/lysed organism. Used when risk of organism surviving inactivation steps (flu, pneumococcal, diptheria, tetanus)
5. RECOMBINANT - genetically engineered to alter critical genes. Can infect and replicate but not induce disease
6. DNA - naked DNA injected, host cells pick up and express pathogen proteins which stimulate immune response


What type of vaccine(s) is best? Why is this the case?

- they express proteins and stimulate the immune response in a manner which most closely resembles normal infection


What does activation of DC's do?

Increases their ability to capture and process antigen and immunogens, and also attract and activate T cells


What is TLR9? When it is included with HepB or flu vaccines what is the result?

CpG (cytosine-phosphate-guanosine)
- increased antibody or IFN gamma secretion


What are the different strategies that could be used in NHS resource allocation? Describe their strengths & weaknesses.

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 excluded treatment
8. Dilution of care
9. Random allocation


What is the role of NICE?

The national institute for health and care excellence
- provides evidence based guidance and advice for health, public health and social care practitioners
Examples of guidance given include clinical guidelines, technology appraisals, public health, interventional procedures


How is QALY measured?

QALY = quality adjusted life year
QoL x life expectancy (before + after), then cost it


What are the 4 technology appraisal recommendations possible from NICE?

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


What are the top 6 infections responsible for the greatest number of deaths in the world?

Acute respiratory infectiona
Diarrheal diseases


What are the normal respiratory tract host defences? (HINT: there's 5)

Cilia (muco-ciliary escalator/elevator)
Nasal secretions
Antimicrobial peptides


What is the common cold? How is it transmitted? What are its causative agents?

Acute coryza
Transmitted via aerosol or virus-contaminated hands
Agents = 40% rhinoviruses 30% coronaviruses


What are the clinical features of a common cold?

Slight pyrexia
Sore nose and pharynx
Profuse, watery nasal discharge becoming mucopurulent
Sneezing in early stages
Secondary bacterial infection occurs in minority


What are the causative agents of acute pharyngitis and tonsillitis?

VIRUSES: epstein-barr virus (EBV), Cytomegalovirus (CMV)
(HSV-1, rhinovirus, coronavirus, adenovirus)
BACTERIA: strep. pyogenes
(H. influenzae, corynebacterium diptheriae)


What is CMV? How is it transmitted? How is it treated?

Transmitted in body secretions and organ transplants
- asymptomatic or mild in healthy adults but can cause disease when cell-mediated immunity is compromised
Treatment with ganciclovir, foscarnet, cidofovir


Where does EBV replicate? What does it cause? How is it transmitted?

In B lymphocytes (CD21 receptor)
Causes glandular fever
Transmitted by saliva and aerosol


What are the 2 stages in life that EBV tends to arise? How long is incubation? How long does the illness last?

1-6 years old
14-20 years old
Incubation: 4-8 weeks
Illness: 4-14 days


What are the clinical features of glandular fever?

Fever, headache, malaise, sore throat, anorexia, palatal petechiae, cervical lymphadenopathy, splenomegaly, mild hepatitis


What treatment should be used for glandular fever?

NOT antibiotics
- avoid contact sports or heavy lifting should be avoided during the 1st month of illness and till any splenomegaly has resolved


What complications can arise from glandular fever? (HINT: there's 3)

Burkitt's Lymphoma
Nasopharyngeal carcinoma
Guillain-barre syndrome


What pathogen causes tonsillitis? How is it transmitted? How is it treated?

Streptococcus pyogenes
Transmission by aerosol
Treatment = penicillin
NOTE: there's becoming increasing resistance to erythromycin and tetracycline


What are the clinical features of tonsillitis?

Pain in throat
Tonsil enlargement
Tonsillar lymphadenopathy


What is streptococcus pyogenes? What complications can occur if carrying strep pyogenes?

Group A Strep
Gram +ve cocci in chains
- scarlet fever
- peritonsillar abscess
- otitis media/sinusitis
- rheumatic heart disease
- glomerulonephritis


Who does parotitis primarily affect? What are the clinical features associated?

School-aged children and young adults
Fever, malaise, headache, anorexia, trismus, severe pain and swelling of parotid gland(s)


What is parotitis caused by? How is it transmitted? What is diagnosis based on?

Mumps virus which is a part of the paramyxovirus family
Transmitted by droplet spread and fomites
Diagnosis based on clinical features - IgM serology performed in doubtful cases from saliva, CSF or urine


What is the (i) treatment (ii) prevention (iii) complications of parotitis?

(i) mouth care, nutritional, analgesia
(ii) active immunisation, MMR vaccine
(iii) CNS involvement, epididymo-orchitis


What is acute epiglottitis caused by? What are the clinical features?

Caused by Haemophilus influenzae and most often seen in young kids
CF: high fever, massive oedema of epiglottis, severe airflow obstruction resulting in breathing difficulties, bacteraemia


What is haemophilus influenzae?

Part of the pasteurellaceae family. Gram negative bacillus.
Present in nasopharynx of 75% healthy people


How is acute epiglottitis (i) diagnosed (ii) treated?

(i) Don't examine throat or take throat swabs - this will cause complete obstruction of airway. Instead take blood cultures to isolate H. influenzae
(ii) LIFE THREATENING EMERGENCY, need ET intubation and IV antibiotics (ceftriaxone or chloramphenicol)


What pathogen causes diphtheria? What is the incubation period of diphtheria? What are the clinical features?

Corynebacterium diphtheriae
2-7 days
CF - sore throat, fever, formation of pseudomembrane, lymphadenopathy, oedema of anterior cervical neck tissue


How is diphtheria (i) diagnosed (ii) treated (iii) prevented?

(i) made on clinical grounds as therapy urgently needed
(ii) Prompt anti-toxin therapy IM. Antibiotics (penicillin or erythromycin) and strict isolation
(iii) Childhood immunisation with toxoid vaccine. Booster doses if travelling to endemic areas >10 years after primary vaccine


What are the 2 subunits of corynebacterium diphtheriae? How is it transmitted? What does it colonise?

Subunit A (Active) = clinical toxicity
Subunit B (Binding) = transports toxin to receptors on myocardial and peripheral nerve cells
Transmission - aerosol
Colonises pharynx, larynx and nose


What are the various viral origins of laryngitis and tracheitis? What does it present as in (i) adults (ii) children?

Parainfluenza virus
Respiratory syncytial virus
Influenza virus
(i) hoarseness and retrosternal pain
(ii) dry cough and inspiratory stridor (croup)


What pathogen causes whooping cough? How is it transmitted? How long is the incubation period?

Bordetella pertussis
Transmission = aerosol
Incubation = 1-3 weeks


What are the clinical features of whooping cough?

- highly contagious, malaise, mucoid rhinorrhoea, conjuctivitis
2. PAROXYSMAL STAGE (1-4 weeks)
- sudden outburst of coughing with an inspiratory "whoop". Lumen of resp tract compromised by mucus secretion and mucosal oedema


How is whooping cough (i) diagnosed (ii) treated (iii) prevented?

(i) clinically from "whoop". Bacterial isolation from nasopharyngeal swabs. NAAT
(ii) Catarrhal stage use erthromycin. But in paroxysmal stage antibiotics have no effect so simply isolation and supportive care
(iii) vaccine (whole cell)


What is Bordetella pertussis? What does it attach to and replicate in? What is this specific attachment due to?

Gram -ve aerobic coccobacillus.
Attaches to and replicates in respiratory epithelium but does not invade deeper structures
Specific attachment is due to surface components


What is acute bronchitis? What is it caused by?

Inflammation of tracheobronchial tree
Normally due to infection: rhinovirus, coronovirus, adenovirus, mycoplasma pneumoniae


What is chronic bronchitis characterised by? What effect does it have on the body?

Cough and excessive mucus secretion in tracheobronchial tree
Disturbs respiratory system
- immune deficit: SCID
- ciliary deficit: Kartegener syndrome; smoking
- excessively thick mucus: CF


What is bronchiolitis? What can it lead to? What is it caused by?

Children <2 years only
May lead to epithelial cell necrosis
Caused mainly by RSV (resp syncytial virus)


What pathogen causes pneumonia? What is it defined as? What is the difference of pneumonia in children and adults?

Strep. pneumoniae
Inflammation of the substance of the lungs
Mainly viral in children and neonates can acquire it from mother during birth (chlamydia trachomatis)
Mainly bacterial in adults and cause varies with age, occupation, underlying disease and geographical risk factors


What are the common causes of (i) viral (ii) bacterial pneumonia?

(i) influenza virus, measles, coronavirus, parainfluenza virus, RSV, CMV, adenovirus
(ii) strep. pneumoniae, myobacterium tuberculosis, H. influenzae, pseudomonas aeruginosa, staph. aureus


What is (i) interstitial (ii) necrotising pneumonia?

(i) invasion of lung interstitium, charactristic of viral infection
(ii) lung abscess and destruction of parenchyma


What is legionella pneumophila? What are the clinical features? How is it transmitted?

It causes legionnaire's . Is severe systemic infection with pneumonia
CF = tachypnoea, purulent sputum, CXR consolidation
Transmitted by aerosol but not person-person


What are the clinical features of measles? What pathogenic family is it a part of? How is it spread? How long is its incubation?

Fever, runny nose, koplik's spots and a characteristic rash
Part of paramyxovirus family
Spread via aerosol
Incubation = 10-14 days


How is measles (i) diagnosed (ii) treated (iii) prevented?

(i) serology for measles-specific IgM. Virus isolation and viral DNA detection
(ii) if severe, ribavirin
Antibiotics for secondary bacterial infections
(iii) highly effective, live, accentuated MMR vaccine


What are the 3 types of influenza virus? What are the 2 types of specific antigens on their cell surfaces?

TYPE A: epidemics and pandemics, animal reservoir
TYPE B: epidemics, no animal hosts
TYPE C: minor resp illness
Antigens = haemagglutinin (H) and neuraminidase (N)


What is (i) antigenic DRIFT (ii) antigenic SHIFT?

(i) small point mutations in the H and N antigens constantly occurs, allowing virus to multiply in individuals which had immunity to previous strains. This new sub-type can re-infect the community
(ii) major change based on recombination between 2 different strains when they infect the same cell, this produces a virus with novel surface glycoproteins. This new strain can spread through previously immune populations => new pandemic


How is influenza (i) diagnosed (ii) treated (iii) managed (iv) prevented?

(i) nasopharyngela aspirate - direct immunofluorescence, culture and NAAT detection
(ii) amantadine, zanamavir, oseltamivir
(ii) rest, warmth, hydration, analgesia. Anti-viral treatment w/in 48 hrs can decrease fever duration. Ab not given unless 2dary bacterial infection suspected


What is SARS? What are the symptoms? How is it transmitted?

Severe acute resp distress syndrome
High fever, cough, shortness of breath, CXRs consistent with pneumonia
Transmitted via droplets, faeces, infected animals


How is SARS treated?

No specific anti-viral treatment available: ribavirin, corticosteroids, interferons, antiretroviral therapies e.g. protease inhibs


What is TB associated with/ What are the clinical features of (i) primary TB (ii) miliary TB (iii) post-primary TB?

AIDS, increased use of immunosuppressants, decreased socio-economic conditions, increased immigration from areas of high endemicity, MDR, overcrowding and poor nutrition
(i) normally symptomless but can have cough and wheeze. Small pleural effusion may occur
(ii) fatal without treatment
(iii) symptoms onset over weeks/months: malaise, fever, weight loss, pleural effusion, mucoid, purulent or blood stained sputum


What is the mantoux test?

Used to detect latent TB infection.
Tuberculin is injected intradermally. Immune response occurs if individual has previously been exposed to myobacterium tuberculosis
An induration (palpable hard area) is measured after 48-72 hrs


How is the primary diagnosis made for M. tuberculosis?

From visualisisng acid-fast bacilli in sputum smears


What is the (i) treatment (ii) prevention for tuberculosis?

(i) Combination therapy (isoniazid, rifampicin, ethambutol, pyrazinamide)- prevents resistance BUT MDR-TB is a major global problem
Prolonged therapy- min 6 months to eradicate slow growing organisms
(ii) childhood immunisation with llve accentuated GCB vaccine


What are the types of (i) fungal infections (ii) parasitic infections?

(i) aspergillus fumigatus, pneumocystis jiroveci
(ii) ascaris, stronglyoides, schistosoma, echinococcus granulosus


What is COPD a combination of?

emphysema and chronic bronchitis


What part of the body does emphysema affect?What is the name of (i) localised (ii) systemic emphysema?

The acinus
(i) centrilobular emphysema
(ii) panacinar emphysema


What is hypersensitivity pneumonitis?

Caused by Type III and IV
- people who live around pigeons or farmers with grains tend to have the disease
Note: bronchodilators do not work


What is sarcoidosis?

cells in the body clump together to make small lumps called 'granulomas'
- most commonly in the lungs and lymph nodes


What are the types of benign lung cancer?

- benign tumour arising from mesenchyme


Where can primary malignant lung cancers arise?

- metaplasia and dysplasia


What are 3 types of secondary lung tumours?

Renal carcinoma


What are the types of primary epithelial lung tumours?
What are the tests done to diagnose?

Squamous, adeno, small cell undifferentiated, carcinoid, large cell undifferentiated
Diagnosis: radiology, cytology examination, EBUS (endobronchial ultrasound), biopsy


Describe primary epithelial (i) squamous (ii) adenocarcinoma (iii) adenocarcinoma-bronchoalveolar (iv) small cell undifferentiated (v) carcinoid tumours.

(i) associated with smoking, air pollution, asbestos
(ii) associated with smoking. Other influences are lung scars, air pollution and asbestos
(iii) cells drop off into mucus, it can present as what looks like pneumonia but its not
(iv) has origin from neuroendocrine cell and may have paraneoplastic effects (produce bioactive amines or peptides). Pt can have confusion and low sodium
(v) typical is less aggressive, atypical is smoking related and tends towards malignant end of spectrum


What do the checkpoint inhibitors PD1 and PDL1 do for lung cancer treatment?

PD1 = programme death1
PDL 1 = programme death ligase 1
These inhibitors interact and this interaction suppresses the immune response
- use antibodies to target PD1 and PDL1 to free immune system and allow to target the cancer
=> targeting the immune tolerance that allows the cancer cells to stay there


How is molecular pathology stratifying lung cancer for treatment?

Test the lung cancers for the following mutations:
- EGFR (epidermal growth factor receptor)
- ALK rearrangements


What is mesothelioma?

Asbestos generates oxygen free radicals which cause fibrosis (asbestosis)
Incidence is rising due to the long lag period of 20-40 years
Males:females 5:1 (due to men working in mining, ship building etc.)
Has fibrous pleural plaques


How many mmHg is 1kPa?

7.5 mmHg


What buffers maintain the bodies pH?

Carbonic acid/bicaronate


In what 3 situations do acid-base disturbances occur?

1. There's a problem with ventilation
2. There's a problem with renal function
3. Overwhelming acid or base load that the body cannot handle


What are the normal values for (i) pH (ii) pO2 (iii) pCO2 (iv) bicarb (standard)

(i) 7.35 - 7.45
(ii) 12 - 13 kPa
(iii) 4.5 - 5.6 kPa
(iv) 22 - 26 mmol/l


What does the standard bicarbonate reflect? What is the standard bicarbonate calculated from?

Reflects the metabolic component of the acid base balance
The actual bicarbonate but assuming 37 degrees and a pCO2 of 5.3 kPa


What is step 1 of the observation of the arterial blood gas results? Why is this step 1?

To look at the pO2
- hypoxia will kill you fastest
- if you find out the patient is hypoxic you stop analysis of blood gases immediately


What can occur in premature babies if the pO2 is too high?

immature retinopathy
- impaired vision as a result


What are the adverse effects of high oxygen levels?

- increases risk of hypercapnic respiratory failure in acute exacerbations of COPD
- generates free radicals which can result in lung toxicity (collapse of alveoli due to atelectasis, irritating to mucous membranes)


What are the oxygen targets (i) normally (ii) for type 2 resp failure?

(i) 94 - 98%
(ii) 88 - 92%


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

- high pO2 in aleoli forces nitrogen in pleural space to diffuse out pleural space and back into alveoli
- increase blood pO2 and forces CO2 to leave Hb


What is the relationship between age and pO2?

the older you are the lower your pO2 due to loss of elastic tissue


What is the P/F ratio? How is it calculated? What are the range of values and what do these values suggest?

PaO2/FiO2 (kpa divided by inspired fraction of oxygen)
P/F ratio >50 = healthy
P/F ratio <40 = acute lung injury
P/F ratio <26.7 = ARDS


What is step 2 of the observation of the arterial blood gas results?

Assess the pH
<7.35 = acidaemia
>7.45 = alkalaemia
pH between 7.35 and 7.45 can mean either normal or mixed acid base abnormality


What will the primary problem be if pH and CO2 are moving in the (i) opposite direction (ii) same direction?

(i) respiratory problem
(ii) metabolic problem


What is compensation?

Altering of function of the respiratory or renal system in an attempt to correct an acid base imbalance
pH is directly proportional to HCO3/pCO2
NOTE: the body will NEVER overcompensate


If pCO2 and HCO3- are moving in the same direction what may this suggest?

That (renal) compensation is occuring


What do the kidneys do in chronic respiratory acidosis?

They compensate by retaining bicarbonate
- this takes a few days to reach its max value


What are the 4 main causes of hyperventilation?

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