Module A Flashcards
A 84 year old women presents with a respiratory rate of 20 breaths per minute, blood pressure 84/56, urea plasma content is 12mmol/L. An abbreviated mental state test gives a score of 5. What is the patients CURB-65 score. How would you commence treatment. No known penicillin allergies.
Confusion score < 8 = 1 point Urea plasma > 7mmol/L = 1 point Respiratory rate > 30breaths/min = 0 Blood pressure systolic < 90 diastolic < 60 = 1 Age > 65 = 1
Total = 4, hence severe pneumonia
Treat with benzylpenicillin and clarithromycin (500mg/12h IV). Consider admitting to ITU.
What are the typical causes of HAP?
1) Staphylococcus aureus (60% of cases)
2) Escherichia coli
3) Pseudomonas aeruginosa and other gram negative bacteria.
4) Acinetobacter spp
What are the atypical organisms that can cause CAP?
1) Legionella pneumophilia 1 and 6
2) Mycoplasma pneumoniae
3) Chlamydia trachomatis
4) Chlamydia psittaci
5) Pneumocystis jiroveci
6) Respiratory viruses: RSV, influenza, parainfluenza.
How would you treat CAP caused by Legionella pneumophilia?
Fluroquinolone, combine with clarithromycin or rifampicin if severe.
How would you treat CAP caused by pneumocystis jiroveci?
High dose of co-trimoxazole (sulphamethoxazole and trimethoprim)
Where are pseudomonas aeruginosa and Escherichia coli normally found?
In the GI tract.
What is the aetiology of bronchiectasis?
Genetic: CF
Post infective: TB, Whooping cough, severe pneumonia
Immunosupressive: hypogammagloblinaemia, HIV
Mucociliary clearance abnormalities: Primary ciliary dyskinesia.
Toxic assault: aspiration
What are the typical organisms that cause CAP?
1) Streptococcus pneumoniae
2) Haemophilus influenzae
3) Moraxella catarrhalis
4) Staphylococcus aureus
What mycobacteria contribute to the mycobacteria tuberculosis complex?
1) Mycobacterium tuberculosis
2) Mycobacterium bovis
3) Mycobacterium africana
4) Mycobacterium microli
Describe the lung sounds you would hear in bronchiectasis
Coarse crackles during inspiration and expiration
Describe briefly the pathogenesis of bronchiectasis
- An initial assault is needed to damage the airways (usually infectious), this causes changes to the lung anatomy which following a secondary infection allows colonisation that perpetuates inflammatory changes. Importantly this damages the mucociliary escalator preventing airway clearance and causing further damage.
- Major airways and bronchioles are involved in mucosal oedema, inflammation and ulceration.
- Mucus accumulation causes blockage of the bronchioles resulting in reduced lung volume.
- Chronic host inflammatory response causes release of ROS and neutrophil elastin. This encourages neo-vasularisation that are perfused at systemic pressures.
- These vessels are torturous and easily bleed resulting in intermittent haemoptysis.
What symptoms (6) are associated with COPD?
1) Productive cough with white / clear sputum
2) Wheeze
3) Breathlessness
4) Frequent chest infections
5) Nocturnal hypoxia, occurs most commonly during the REM stage of sleep.
6) Symptoms are exacerbated in cold weather or following exposure to environmental pollutants.
What is bronchiectasis?
Permanent dilatation of the airways due to destruction of the muscle and elastic tissue.
How may lung function tests change in COPD
1) FEV1 will be decreased resulting in a FEV/FVC less than 70% of the predicted value.
2) PEFR may be reduced.
What are the signs and symptoms of bronchiectasis?
- Cough
- purulent, tenacious and daily sputum
- Pleuritic pain during infectious episodes
- Intermittent haemoptysis.
- Course inspiratory and expiratory sounds
- Airflow obstruction wheeze.
What is the definition of HAP?
A lung parenchyma infection that develops >48h after hospital admission.
What are the symptoms and signs of pneumonia (8)?
1) pleuritic chest pain 2) purulent sputum 3) productive cough 4) haemoptysis 5) bronchial breathing 6) coarse crackles 7) Loss of chest resonance 8) Tachypnoea
What signs are associated with COPD?
1) In mild cases there may be no symptoms just quite wheezing noises.
2) In severe cases patient is tachypnoeic with prolonged expiratory phase. Lips may be pursed during expiration.
3) Recruitment of accessory muscles.
4) Reduced chest expansion.
5) Hyper inflation of the lungs (resulting in reduced chest expansion as the lungs are already inflated)
6) Loss of dullness when percussing over the liver and stomach (due to hyperinflation)
7) In some patients, signs of hypercapnia: asterixis, bounding pulse, peripheral dilation.
What is the treatment and side effects of treatment for tuberculosis?
Induction phase, 2 months:
- Rifampicin, turns secretions orange, induces Cy450 enzymes, hepatoxicity.
- Isoniazid: peripheral nerve damage if patient deficient in pyridoxine (B6) can also cause drug induced lupus.
- Ethambutol, causes optic neuritis affecting red-green colour first,
- Pyrizinamide: gout, rash and hepatoxicity.
What is bronchiolitis? What is the major causative agent?
Inflammation of the bronchioles typically affecting young children < 6months of age. Most commonly caused by RSV.
How would you treat bronchiolitis in a premature child with chronic lung disease?
Palivizumab
What are the investigations (6) you would order for bronchiectasis, what are the features you would look for and their sensitivities?
1) Chest x-ray, 50% sensitivity. Look for tram-lines and ring shadows indicating thickened airways. Gloved-finger bronchioles indicates consolidation around thickened airways.
2) HRCT, 97% sensitivity. Look for bronchioles that are larger than their accompanying arteries, bronchial wall thickening and dilation in the peripheries.
3) Sputum cultures.
4) Ig M, E, G, and A
5) Aspergillus précipitants
6) Pulmonary function tests with reversibility.
What are the symptoms of bronchiolitis (6)?
1)Tachypnoea 2)tachycardia 3)costal recession 4)temperature 5)expiratory wheeze 6)cyanosis
What drugs would you use to treat heart failure?
1) Diuretics: loop diuretics (furosemide 40mg/24h PO, bumetanide 1-2mg/24h PO) SE: K decrease renal impairment.
2) ACE-I, consider in all those with left ventricular systole dysfunction. If cough use angiotensin receptor antagonists
3) beta blockers
4) mineralocorticoid receptor antagonists, spironolactone (25mg/24h PO)
Why is LDL a strong independent CV risk factor?
It is pro-inflammatory, stimulates macrophages to become foam cells causing atherosclerosis.
What measurement or ratio is the best predictor of vascular event risk?
Non HDL cholesterol (TC-HDL).
What is the Friedewald equation?
LDL = TC - HDL - (TG/2.2)
all concentrations are given as mmol/L
Non HDL cholesterol is a better predictor of vascular event risk.
What concentration of HDL is protective against CVD, what concentration results in increased risk?
> 2mmol/L protective
<1mmol/L increased CVD risk
What are the secondary causes of hypercholesterolaemia? What drugs can also cause it?
Hypothyroidism Nephrotic Syndrome Cholestasis Paraproteinaemias Anorexia and bulimia Ciclosporin, sirolimus and some antiepileptics
What are the signs and symptoms of hypercholesterolaemia?
Xanthalasma
Tendon xanthromas
Corneal arcus <45yo
Abdominal obesity
What polymorphisms contribute most the the genetic risk of developing T1DM?
HLA-DQ8 14x increase
HLA-DQA301 and HLA-DRB401
CTLA-4
PTPN22
What auto antigens are primarily targeted in T1DM (4)?
1) Insulin
2) IA-2 protein tyrosine phosphatase
3) Glutamic acid decarboxylase
4) Zinc transporter 8
What are the signs and symptoms of T1DM?
1) Polyurea
2) Polydisia
3) Weightloss
4) Blurred vision related to fluctuations in blood sugars
5) Symptoms of DKA
6) Family history of autoimmune diseases.
What investigations are used to diagnose T1DM?
Random glucose test >11mol/L Fasting glucose test (no calorie intake for 8h) >6.8mmol/L 2h plasma glucose test >11mmol/L Urine ketones HBA1c ≥48mmol/L
What is the treatment for T1DM?
1) Basal-bolus insulin
2) + mealtime correction doses
3) Pramlintide
What does pramlintide do?
A synthetic form of the hormone amylin that is secreted from the pancreatic beta cells alongside insulin. Increases gastric emptying time, reduces glycogen release, and reduced food intake by suppressing apatite.
What are the signs and symptoms of T2DM?
1) Frequent candidate infections
2) UTIs
3) skin infections (abscesses / cellulitis)
What are the diagnostic investigations for T2DM?
1) HbA1c ≥48mmol/L
2) Fasting plasma glucose >11.1mmol/L
3) 2h post load glucose after 75g oral glucose dose >11.1mmol/L.
What is the treatment for T2DM?
1) Metformin monotherapy
2) Metformin + DPP4 inhibitor (sitagliptin) / sulphonylurea (glimepiride) / thiazolidendione (pioglitazone) / SGLT-2i (gliflozin)
3) If HbA1c ≥58mmol/L with double therapy add a third drug or insulin therapy
4) If triple therapy is not tolerated and insulin contraindicated use: metformin + sulphonylurea + GLP1 mimetic.
How would you diagnose DKA (4 + viii)?
1) VGB pH <7.35
2) Hyperglycaemia > 11.1mmol/L
3) Ketoaemia > 3mmol/L OR ketourea >2+ on dipstick.
4) Severe DKA if:
i) ketones >6mmol/L
ii) venous HCO3- <5mmol/L
iii) pH <7
iv) GSC <12
v) O2 <92% ORA
vi) SBP <90mmHg
vii) pulse >100 / <60
viii) Anion gap >16
How would you manage DKA?
1) 2 large bore cannulate, 1L 0.9% saline over 1h.
2) Conduct relevant investigations
3) Insulin, 50 unit to 50ml 0.9% saline, infuse continually at 0.1unit/kg/h. Continue patients regular long acting insulin. Aim for a fall in blood ketones of 0.5mmol/L/h or a rise in venous bicarbonate of 3mmol/L/h. If not achieved increase insulin infusion by 1unit/h until target achieved.
4) Check CBG and ketones hourly, check VBG at 2h, 4h, 8h, 12h and 24h at least.
5) Continue fluids, assess need for K (3.5-5.5 give 40mmol with each litre of fluid)
6) Consider catheter if not passed urine, aim for 0.5ml/kg/h. Start LMWH.
7) to avoid hypoglycaemia give 125ml 10% glucose alongside saline when CBG reaches <14mmol/L
8) Continue fixed rate insulin until ketones <0.6mmol/L, venous pH <7.3 and venous bicarbonate >15mmol/L. Urine ketones may remain elevated after DKA resolved always check blood ketones.
What are the key symptoms of DKA (5)?
1) Gradual drowsiness
2) Vomiting
3) Anorexia
4) ketotic breath
5) Kussmaul hyperventilation
What is Hyperosmotic Hyperglycaemic State (HHS)
A hyper osmotic state with hyperglycaemia and volume depletion in the absence of ketoacidosis.
What are the symptoms of HHS?
1) Altered mental state
2) Dry mucus membranes
3) Tachycardia
4) Hypotension
What investigations can be used to diagnose HHS?
1) CBG >33mol/L
2) Serum ketones normal or low
3) Serum urea raised due to volume depletion
4) Serum osmolality >320mmol/kg
5) ABG pH >7.3
How would you manage HHS?
Rehydrate slowly using 0.9% saline over 48h. When urine starts to flow add K.
Only use insulin if glucose does not fall by 5mmol/L/h during rehydration. Start slow 0.05u/kg/h using fixed rate intravenous insulin infusion.
Keep blood glucose between 10-15mmol/L in the first 24h to reduce the risk of cerebral oedema.
What are the possible complications of DKA
1) cerebral oedema
2) Aspiration pneumona
3) hypokalaemia
4) Hypomagnesaemia
5) hypophosphateaemia
6) Thromboembolism
What is the treatment of acute suspected HF?
1) Sit patient up
2) Provide appropriate oxygen
3) Provide IV furosemide 40-80mg bolus
4) Give IV GTN 0-10mg/h
5) Diamorphine bolus (2.5-5mg) + antiemetic (metoclopramide 10mg bolus)
6) Monitor urinary output
7) CPAP if T1RF
8) Ionotrope if patient is in cardiac shock
9) Use echo to confirm heart failure diagnosis and start prognostic treatment.
A patient presents with structural signs of heart failure but no symptoms what is the appropriate AHA category and treatment? What are the major side effects of these drugs?
Category B, start the patient on ACEI (ramipril, captopril, enalopril, or lisinopril) or if appropriate use a beta blocker (carvedilol, bisoprolol). If intolerant to ACEI use ARB (candesartin, losartin)
SE:
- ACEI: hypotension, hyperkalaemia, renal failure (constricts the efferent renal arteriole), angio-oedema, bronchospasm (cough)
- Beta blockers: bradycardia, hypotension, heart block, cold extremities, impotence, and fluid retention.
A patient presents with symptoms of heart failure and structural heart abnormalities. Describe the possible symptoms, the AHA classification, the initial treatment and how this treatment can be escalated. Describe the drug side effects.
Symptoms LHF: Pulmonary congestion - cough - SOB - Orthopnoea - Paroxysmal nocturnal dyspnoea - Reduced exercise tolerance - Haemoptysis Systemic hypoperfusion - Low blood pressure / postural hypotension - Fatigue
Symptoms of RHF Systemic congestion - Ankle swelling - Weight gain - Abdominal distension - Cardiac cachexia
AHA C, start on both ACEI (ramipril, captopril, enalopril, lisinopril) and Beta blockers (carvedilol, bisoprolol), in severe heart failure LVEF < 35% use a mineralocorticoid antagonist (spironolactone, eplerenone) eplerenone is indicated if MI HF.
SE
- ACEI: renal failure (efferent constriction), hypotension, hyperkalaemia, angio-oedema, bronchospasm.
- Beta blocker: bradycardia, heart block, hypotension, cold extremities, impotence, fluid retention.
- Mineralocorticoid antagonist: hyperkalaemia, hyponatraemia, renal failure, gynaecomastoid, (spironolactone, impotence).
What would prescribe to a patient with AHA C heart failure who is intolerant to ACEI and ARB or a patient of african-carribean decent on ACEI or ARB?
Hydralazine or isosorbide dinitrate (vasodilators)
What are the possible aetiologies of heart failure?
- Vasculature: hypertension, CHD, Stunning
- Infective / inflammatory: myocarditis (viral: coxsackie and adenovirus), Chagas, Lymes disease, and infective endocarditis. Sarcoid, amyloidosis,
- Trauma
- Autoimmune: rheumatic heart disease.
- Metabolic: Selenium deficiency, iron overload (haemachromatosis), Beri-beri (thiamine deficiency).
- Iatrogenic: anthracyclines, abstruzimab.
- Neoplasm
- Congenital heart disease
- Degenerative: cardiac myopathy (most commonly dilated), valvular disease.
What are the signs of left and right sided heart failure?
Left:
- Cold extremities
- Hypotension
- Weak peripheral pulses, pulses alternans
- Tachycardia
- Tachypnoea
- Fine basal crackles
- Wheeze
- Weak first heart sound
- Sounds 3 ± 4
Right:
- Ascites
- Peripheral oedema
- JVP
- Liver congestion.
What cell types make up the respiratory epithelium (4)?
Pseudostratified ciliated columnar cells, goblet cells, kulchitsky cells, reserve cells.
What is bronchogenic carcinoma?
Lung cancer
What type of cancer has the highest mortality?
Bronchogenic carcinoma. Accounts for 27% of cancer deaths.
What are the risk factors associated with bronchogenic carcinoma (6)
1) Tabacco smoking
2) Industrial exposure, asbestos.
3) Radiation exposure.
4) Air pollution, radon gas and car exhaust fumes.
5) Genetics
6) Rarely may occur due to residual scarring following respiratory disease.
What are the symptoms of bronchogenic carcinoma, what causes these symptoms?
1) Cough due to mucosal irritation.
2) Dyspnoea due to obstruction of the airway and atelectasis.
3)
In which individuals can 1st degree heart block or kibitz type two be a normal finding in?
Young people with a high vagal tone.
Obstruction of which artery would most likely produce ischaemia resulting in heart block?
Right coronary artery, typically produces the branches that supply the AVN and SAN.
How can disease occur as a result of complicated atheromatous plaques (3)?
1) If the plaque ruptures or erodes the prothrombotic plaque contents is exposed to the circulation, this causes thrombosis, micro emboli and possible vessel occlusion.
2) Blood can haemorrhage into the plaque causing expansion of the obstruction.
3) Plaques weaken the underlying media this leads to aneurysmal dilation and possible rupture of the artery.
What are the major modifiable risk factors for the development of atheromatous disease?
1) Smoking
2) Diabetes
3) Hypertension
4) Dyslipidaemia
What are the complications of atherosclerosis?
CVS: Ischaemia (MI), AAA.
Brain: TIA, stoke, cerebrovascular dementia
Renal: renal artery stenosis
Gastro: abdominal claudication, ischaemic colitis, small bowel infarction.
Lower Limb: claudication, infarction and ischaemia.
When can angina pectoralis lead to dyspnoea?
In diabetics where neuropathy has altered the innervation of the heart, makes angina diagnosis difficult and requires exclusion of differentials.
What are the possible causes of stable angina?
1) CAD
2) Hypertrophic cardiomyopathy
3) Severe AS
A patient presents with central chest pain radiating to the left jaw that occurs repeatedly during exertion, following the cessation of activity the pain usually fades after 1-2 minutes. The patient has never experienced pain whilst at rest. She describes that she often experiences pain when climbing several flights of stairs at work. What is the most likely diagnosis and stage of disease?
Stable angina stage 3 (Canadian CV society)
A 65 year old women with atypical angina symptoms presents in A&E, she is currently a smoker and has a history of diabetes and hypertension. What is their risk of CAD and what would be the appropriate next investigation? Given a positive result what would be the possible next investigation?
Intermediate risk, recommend non invasive investigations such as stress echocardiography, myocardial perfusion scintigraphy, stress MRI, CT coronary calcium score. If one of these investigation yields a positive result then consider a coronary angiography.
What is the first line treatment for stable angina?
- Beta blocker or dihydropryidine calcium channel blocker such as nifedipine, amlodipine or felodipine.
- If a patient cannot tolerate a beta blocker of CCB, use a long acting nitrate such as ivabradine, nicorandil, or ranolazine.
What is the secondary prevention applied in stable angina patients?
1) aspirin
2) ACEI in diabetics.
What is the second line treatment for stable angina?
1) Beta blocker / CCB (first line treatment)
2) Add ivabradine (funny channel blocker), nicorandil (nitrate + ca channel blocker) or ranolazine (blocks the late Na onward current reducing Ca overload and therefore decreasing diastolic wall stress).
When would a patient with stable angina be referred for revascularisation therapy?
1) Do not respond to pharmacological treatment.
2) Stenosis is in a prognostically significant area such as the left main stem or affecting all three vessels.
What is the immediate management for ACS?
1) Attach ECG
2) Offer GTN
3) Give oxygen if required.
4) Establish IV access
5) Morphine 2.5-5mg and anti-emetic
5) Give aspirin 300mg and clopidogrel 300mg (tricagrelor)
6) Determine STEMI or NSTEMI
What is the immediate treatment for STEMI?
1) PCI, if 12h since onset of symtpoms. If PCI can not be delivered within 120mins proceed immediately to fibrinolysis. PCI should still be considered >12h if there is evidence of ongoing ischaemia (e.g. the patient still has symptoms).
- Fibrinolysis should be given with thrombolysis.
2) If reprofusion therapy can not be applied give LMWH (fondaparinux) / unfractionated heparin if angiography planned in the next 24h.
What is the immediate treatment for NSTEMI?
1) complete risk assessment (GRACE score)
2) Give LMWH (fondaparinux) / unfractionated heparin if planned angiography in next 24h.
3) If still in pain give IV nitrates.
4) If patient is going to receive angiography based on intermediate or high CVD risk score but has already received LMWH also give heparin. Also give glycoprotein IIb/IIIa inhibitor.
5) Give an oral beta blocker, bisoprolol (2.5mg), unless patient is already on verapamil.
What is the secondary prevention for patients following ACS?
- Beta blocker offer for 12 months.
- ACEI continue indefinitely, check U&Es
- statin
- Aspirin for life
- Clopidogrel / ticagrelor may be continued for 1 year unless on DOAC.
- Angiography / PCI to NSTEMI with high GRACE score.
- If heart failure mineralocorticoid antagonist eplerenone improves outcomes after an MI.
- Continue LMWH until discharge
How many major and minor scores are present in the following history? What is the probable diagnosis?
Patient presents with a fever of 38.1˚C, sweating, and chest pain. On examination there are no peripheral stigmata but auscultation indicates a new late diastolic murmur. Dip stick of the urine shows raised protein and glomerulonephritis. CRP is raised. The patient appears ill at rest.
The patient has one major factor (new murmur), and two minor factors (glomerulonephritis and pyrexia).
This indicates a possible IE (1 major and 1 minor)
Not enough evidence for a definite diagnosis (2 major / 1 major and 3 minor)
Modified Duke’s Criteria
A patient is diagnosed with IE, they have a prosthetic valve, what is the initial antibiotic treatment?
Vancomycin and gentamicin
In order of incidence what are the causes of IE?
1) Vivians Streptococci: S.mutans, S.sanguis, and S.mitis. S.bovis, and S.milleri. All cause alpha haemolysis
2) Staphylcoccus aureus and staphylococcus epidermis, coagulase negative.
3) Enterococci.
4) HACEK bacteria: Haemophillus spp, Actinobacillus, actinomyetemcomitans, Cardiobacterium hominis, Eikenella spp, and Kingella
5) Culture negative
A patient develops IE 5 months after a valve replacement, which to organisms are the most likely causative agents and what is the best antibiotic therapy assuming they are the infectious agent.
Coagulase negative bacteria such as staphylococcus aureus or staphylococcus epidermis. Treat with flucloxacillin 12mg daily + gentamicin for 4-6 weeks.
If MRSA or MRSE us vancomycin 1g bd + gentamicin / rifampicin.
What ECG changes may be present following a PE?
1) New RAD
2) New RBBB
3) S wave in lead 1
4) Q wave with T wave inversion in lead 3.
