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Medicine and Surgery Mushkies > Passmed General Medical Mushkies > Flashcards

Passmed General Medical Mushkies Flashcards

1
Q

How can you classify the causes of pleural effusion?

A

Transudate (<30g/L protein) and exudate (>30g/L protein)

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2
Q

What are the transudative causes of pleural effusion?

A
  1. Heart failure (most common transudate cause)
  2. Hypoalbuminaemia (liver disease, nephrotic syndrome, malabsorption)
  3. Hypothyroidism
  4. Meigs’ syndrome
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3
Q

What are the exudative causes of pleural effusion?

A
  1. Infection: pneumonia (most common exudate cause), TB, subphrenic abscess
  2. Connective tissue disease: RA, SLE
  3. Neoplasia: lung cancer, mesothelioma, metastases
  4. Pancreatitis
  5. Pulmonary embolism
  6. Dressler’s syndrome
  7. Yellow nail syndrome
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4
Q

What disease are bite and blister cells a feature of?

A

G6PDD

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5
Q

What drugs cause haemolysis in G6PDD?

A

Antimalarials e.g. primaquine
Ciprofloxacin
Sulph groups (sulphonamides, sulfonylureas, sulphasalazine)

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6
Q

What investigation do you do for phaeochromocytomas?

A

24hr urinary collection of catecholamines

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7
Q

What are 3 syndromes that phaeochromocytomas are associated with?

A
  1. MEN II
  2. NF
  3. vHL
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8
Q

What is the definitive management of phaeochromocytomas, and how does one prepare pts for it?

A
  1. Surgery is definitive treatment

2. Give alpha blocker (e.g. phenoxybenzamine) before giving a beta blocker (e.g. propranolol)

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9
Q

How do you treat ascites secondary to liver cirrhosis?

A

Spironolactone, with furosemide only being used as an adjuvant if needed

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10
Q

What is TIPS and what can it be used to treat?

A

Transjugular intrahepatic portosystemic shunt

Used to treat portal HTN, life threatening oesophageal varices, and ascites

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11
Q

What are some features of granulomatosis with polyangiitis (GPA, a.k.a Wegener’s Granulomatosis)

A
  1. Upper respiratory tract (epistaxis, sinusitis, nasal crusting)
  2. Lower respiratory tract (dyspnoea, haemoptysis)
  3. Glomerulonephritis = rapidly progressive, pauci-immune
  4. Saddle shaped nose deformity
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12
Q

What Ab is the marker for GPA?

A

cANCA

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13
Q

What is the management for GPA?

A

Steroids
Cyclophosphamide
Plasma exchange

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14
Q

What is achalasia?

A

Failure of oesophageal peristalsis and of relaxation of lower oesophageal sphincter (LOS) due to degenerative loss of ganglia from Auerbach’s plexus

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15
Q

What are the investigations for achalasia?

A
  1. Manometry
  2. Barium swallow = birds beak
  3. CXR = wide mediastinum, fluid level
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16
Q

What are the treatment options for achalasia?

A
  1. Intra-sphincteric injection of botulinum toxin
  2. Heller cardiomyotomy
  3. Balloon dilatation
  4. Drugs have limited effect
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17
Q

What is HBPM?

A

Home blood pressure monitoring

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18
Q

What is the PEP for Hep A?

A

HNIG (human normal immunoglobulin) or Hep A vaccine

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19
Q

What is the PEP for Hep B?

A
  1. HBsAg positive source: if the person exposed is a known responder to HBV vaccine then a booster dose should be given. If they are in the process of being vaccinated or are a non-responder they need to have hepatitis B immune globulin (HBIG) and the vaccine
  2. Unknown source: for known responders the green book advises considering a booster dose of HBV vaccine. For known non-responders HBIG + vaccine should be given whilst those in the process of being vaccinated should have an accelerated course of HBV vaccine
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20
Q

What is the PEP for Hep C?

A

Monthly PCR - if seroconversion then interferon +/- ribavirin

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21
Q

What is PEP for HIV?

A
  1. A combination of oral antiretrovirals (e.g. Tenofovir, emtricitabine, lopinavir and ritonavir) as soon as possible (i.e. Within 1-2 hours, but may be started up to 72 hours following exposure) for 4 weeks
  2. serological testing at 12 weeks following completion of post-exposure prophylaxis
  3. reduces risk of transmission by 80%
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22
Q

What is the transmission rate after a needlestick injury for HIV?

A

0.3%

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23
Q

What is the transmission rate after a needlestick injury for Hep B?

A

20-30%

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24
Q

What is the transmission rate after a needlestick injury for Hep C?

A

0.5-2%

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25
Q

What medication can worsen gout?

A

Thiazides

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26
Q

What is the STOPP-START Criteria (Gallagher et al., 2008)?

A

Outlines medications that we should consider withdrawing in the elderly

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27
Q

What is the BP target for pts <80y/o?

A

<140/90

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28
Q

What is the BP target for pts >80y/o?

A

<150/90

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29
Q

if a patient has progressive dysphagia what should you be thinking of?

A

Oesophageal carcinoma

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30
Q

What nerve can an oesophageal carcinoma damage?

A

Laryngeal nerve, leading to hoarsening of voice

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31
Q

How do pts with achalasia present?

A

Trouble with swallowing both solids and liquids equally

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32
Q

What do patients with oesophageal spasm typically present with?

A

Pain when swallowing

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33
Q

How does bulbar palsy present?

A

Symptoms of weakness, such as drooling, weak and wasted tongue, dysphonia and problems articulating.

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34
Q

Where are the majority of oesophageal carcinomas?

A

The middle third of the oesophagus

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35
Q

What is the most standard surgical procedure for management of oesophageal carcinoma?

A

Ivor- Lewis type oesophagectomy

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36
Q

What causes internuclear ophthalmoplegia?

A

A lesion of the medial longitudinal fasciculus (MLF), a tract that allows conjugate eye movement and connects the connects the IIIrd, IVth and VIth cranial nuclei

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37
Q

What are the signs of internuclear ophthalmoplegia?

A

Impairment of adduction of the ipsilateral eye. The contralateral eye abducts, however with nystagmus.

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38
Q

What are 2 causes of internuclear ophthalmoplegia?

A

MS and vascular disease

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39
Q

What would cause a metabolic ketoacidosis with a low or normal blood glucose?

A

Alcohol

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40
Q

What are the 3 stages of presentation of Churg-Strauss (eGPA)?

A
  1. Allergy with many patients having a history of asthma or allergic rhinitis. This inflammation of the nasal passages can lead to the development of nasal polyps.
  2. The second phase is eosinophilia
  3. Vasculitis itself which affects small and medium-sized blood vessels and therefore resulting in damage to many organs
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41
Q

What are the 4Hs of the reversible causes of cardiac arrest?

A
  1. Hypoxia
  2. Hypovolaemia
  3. Hyperkalaemia, hypokalaemia, hypoglycaemia, hypocalcaemia, acidaemia and other metabolic disorders
  4. Hypothermia
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42
Q

What are the 4Ts of the reversible causes of cardiac arrest?

A
  1. Thrombosis (coronary or pulmonary)
  2. Tension pneumothorax
  3. Tamponade – cardiac
  4. Toxins
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43
Q

What is the treatment for Bell’s palsy?

A
  1. Prednisolone 1mg/kg for 10 days w/in 72hrs

2. Lubricating eye drops

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44
Q

What is the definition for Bell’s palsy?

A

An acute, unilateral, idiopathic, facial nerve paralysis

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45
Q

Who is Bell’s palsy more common in?

A

Pregnant women

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46
Q

How can you classify the causes of SIADH?

A

MINDO
Malignancy = SCLC, pancreas, prostate
Infection = TB, pneumonia
Neurological = stroke, subarachnoid haemorrhage, subdural haemorrhage, meningitis/encephalitis/abscess
Drugs = sulfonylureas, SSRIs, TCAs, carbamazepine
Other = PEEP, porphyria

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47
Q

What type of tumour accounts for 5% of intracranial tumours and 90% of cerebellopontine angle tumours?

A

Vestibular schwannomas (acoustic neuromas)

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48
Q

In what condition do you see bilateral vestibular schwannomas?

A

NF2

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49
Q

What is the investigation of choice for acoustic neuromas?

A

MRI cerebellopontine angle

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50
Q

What is the anatomical basis for how vestibular schwannomas present?

A

CN 5, 7, 8

  1. cranial nerve VIII: vertigo, unilateral sensorineural hearing loss, unilateral tinnitus
  2. cranial nerve V: absent corneal reflex
  3. cranial nerve VII: facial palsy
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51
Q

What is the management for vestibular schwannomas?

A

Surgery
Radiotherapy
Observation

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52
Q

What could be the cause for unexplained petechiae and hepatosplenomegaly?

A

Leukaemia, and thus needs immediate assessment

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53
Q

What is a granuloma?

A

A collection of epithelialioid histiocytes

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54
Q

What is the 1st line test for pts with with suspected chronic HF?

A

NT-proBNP –>

  1. If levels are ‘high’ (>2000) arrange specialist assessment (including transthoracic echocardiography) within 2 weeks
  2. If levels are ‘raised’ (400-2000) arrange specialist assessment (including transthoracic echocardiography) echocardiogram within 6 weeks
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55
Q

What are some factors that can raise BNP levels?

A
  1. Cardiac = LVH, RVH, ischaemia, hypertrophy
  2. Resp = COPD
  3. Renal = CKD
  4. Hepatic = CLD
  5. DM, old age, sepsis
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56
Q

What are some factors that can lower BNP levels?

A
  1. Anti-hypertensives = ACEi, ARBs, BBs, Aldosterone antagonists, diuretics (i.e. all of them)
  2. Obesity
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57
Q

What are 3 adverse effects of statins?

A
  1. Myopathy (myalgia, myositis, rhabdomyolysis and asymptomatic raised creatine kinase)
  2. Liver impairment
  3. Intraceberal haemorrhage in pts who have previously had a stroke
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58
Q

How should pts be monitored whilst on statins?

A

Checking LFTs at baseline, 3 months and 12 months. Treatment should be discontinued if serum transaminase concentrations rise to and persist at 3 times the upper limit of the reference range

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59
Q

Which statins are more likely to cause myopathy?

A

Lipophilic statins such as simvastatin and atorvastatin

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60
Q

What are 2 contraindications to taking statins?

A
  1. Pregnancy

2. Macrolides (statins should be stopped until course is finished)

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61
Q

What are the indications for starting a statin?

A
  1. All people with established cardiovascular disease (stroke, TIA, ischaemic heart disease, peripheral arterial disease)
  2. Anyone with a 10-year cardiovascular risk >= 10%
  3. Patients with type 2 diabetes mellitus should now be assessed using QRISK2 like other patients are, to determine whether they should be started on statins
  4. Patients with type 1 diabetes mellitus who were diagnosed more than 10 years ago OR are aged over 40 OR have established nephropathy
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62
Q

When should statins be taken?

A

Statins should be taken at night as this is when the majority of cholesterol synthesis takes place. This is especially true for simvastatin which has a shorter half-life than other statins.

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63
Q

What are the statin doses for the prevention of cardiovascular disease?

A

Atorvastatin 20mg OD for primary prevention

Atorvastatin 80mg OD for secondary prevention

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64
Q

What are 5 sinister features of a headache which require further imaging (CT)?

A
  1. Vomiting more than once with no other cause.
  2. New neurological deficit (motor or sensory).
  3. Reduction in GCS
  4. Valsalva (associated with coughing or sneezing) or positional headaches.
  5. Progressive headache with a fever.
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65
Q

What can a pt with parkinsons who is NBM be given?

A

Dopamine agonist patch as rescue medication to prevent acute dystonia

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66
Q

What can be given to manage drooling in patients with parkinsons disease:

A

Glycopyrronium bromide

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67
Q

What are 6 parkinsons medications?

A
  1. L-DOPA
  2. Dopamine receptor agonists
  3. MAO-B inhibitors
  4. Amantadine
  5. COMT inhibitors
  6. Anti-muscarinics
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68
Q

What is L-DOPA usually combined with?

A

A decarboxylase inhibitor (e.g. carbidopa or benserazide) to prevent peripheral metabolism of levodopa to dopamine

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69
Q

What is an example of a MAO-B inhibitor and how does it work?

A
  1. Selegine

2. Inhibits the breakdown of dopamine secreted by the dopaminergic neurons

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70
Q

What is the MOA of amantadine?

A

Mechanism is not fully understood, probably increases dopamine release and inhibits its uptake at dopaminergic synapses

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71
Q

What is an example of a COMT inhibitor and how does it work?

A
  1. Entacapone, tolcapone

2. COMT is an enzyme involved in the breakdown of dopamine, and hence may be used as an adjunct to levodopa therapy

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72
Q

How can anti-muscarinics help in Parkinsons disease? What is an example?

A
  1. Help tremor and rigidity, and are used more to treat drug-induced parkinsonism
  2. E.g. procyclidine
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73
Q

What are some indications for haemodialysis?

A
  1. Pulmonary oedema
  2. Refractory hyperkalaemia
  3. Metabolic acidosis
  4. Uraemia
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74
Q

How does one officially diagnose AKI?

A
  1. A rise in serum creatinine of 26 micromol/litre or greater within 48 hours
  2. A 50% or greater rise in serum creatinine known or presumed to have occurred within the past 7 days
  3. A fall in urine output to less than 0.5 ml/kg/hour for more than 6 hours in adults and more than
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75
Q

What are 5 drugs that should be stopped during AKI as it may worsen renal function?

A
  1. ACEi
  2. ARBs
  3. Diuretics
  4. NSAIDs
  5. Aminoglycosides
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76
Q

What is the loss of the left heard border a classic sign of?

A

Left lingula consolidation

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77
Q

What are 6 causes of white shadowing on CXRs?

A
  1. Consolidation
  2. Pleural effusion
  3. Collapse
  4. Pneumonectomy
  5. Specific lesions e.g. tumours
  6. Fluid e.g. pulmonary oedema
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78
Q

Trachea pulled towards white-out?

A
  1. Pneumonectomy
  2. Complete lung collapse e.g. endobronchial intubation
  3. Pulmonary hypoplasia
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79
Q

Trachea central with white-out?

A
  1. Consolidation
  2. Pulmonary oedema (usually bilateral)
  3. Mesothelioma
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80
Q

Trachea pulled away from white-out?

A
  1. Pleural effusion
  2. Diaphragmatic hernia
  3. Large thoracic mass
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81
Q

4 features of acute moderate asthma?

A
  1. PEFR 50-75% best or predicted
  2. Speech normal
  3. RR < 25 / min
  4. Pulse < 110 bpm
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82
Q

4 features of acute severe asthma?

A
  1. PEFR 33 - 50% best or predicted
  2. Can’t complete sentences
  3. RR > 25/min
  4. Pulse > 110 bpm
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83
Q

5 features of acute life threatening asthma?

A
  1. PEFR < 33% best or predicted
  2. Oxygen sats < 92%
  3. Silent chest, cyanosis or feeble respiratory effort
  4. Bradycardia, dysrhythmia or hypotension
  5. Exhaustion, confusion or coma
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84
Q

Pt presents with acute asthma attack that is managed with salbutamol nebs, what should you discharge her on?

A
  1. Prednisolone 40mg OD 5d (w/ stat dose now)

2. Beclametasone inhaler 200mcg BD

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85
Q

What causes hypopigmentation and loss of sensation?

A

Leprosy

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86
Q

What is leprosy?

A

A granulomatous disease primarily affecting the peripheral nerves and skin, caused by Mycobacterium leprae

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87
Q

What determines the type of leprosy a patient will develop?

A

The degree of cell mediated immunity

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88
Q

If a patient has a low degree of cell mediated immunity, what kind of leprosy will they develop?

A

Lepromatous leprosy (‘multibacillary’), characterised by extensive skin involvement and symmetrical nerve involvement

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89
Q

If a patient has a high degree of cell mediated immunity, what kind of leprosy will they develop?

A

Tuberculoid leprosy (‘paucibacillary’), characterised by limited skin disease and asymmetric nerve involvement

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90
Q

What is the management for leprosy?

A

WHO-recommended triple therapy: rifampicin, dapsone and clofazimine

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91
Q

What is a CLO test?

A

Campylobacter-like organism test a.k.a. rapid urease test, is a rapid diagnostic test for Helicobacter pylori

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92
Q

What test is indicated for H.pylori detection post eradication therapy?

A

Urea breath test

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93
Q

What investigation still yields a positive result after H.pylori eradication therapy?

A

H. pylori serology

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94
Q

What 6 tests can be performed for H.pylori?

A
  1. Urea breath test
  2. Rapid urease test (CLO test)
  3. Serum antibody test
  4. Gastric biopsy
  5. Culture of gastric biopsy
  6. Stool antigen test
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95
Q

When can you not perform a urea breath test for H.pylori?

A

Within 4 wks of treatment with an antibiotic or within 2 weeks of an antisecretory drug (PPI)

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96
Q

What are 4 contraindications to lung cancer surgery?

A
  1. SVC obstruction
  2. FEV < 1.5
  3. Malignant pleural effusion
  4. Vocal cord paralysis
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97
Q

What is Wellen’s syndrome?

A

Deep arrowhead T wave inversion (biphasic T waves) in the anterior leads (esp V2 and V3) = precursor to a ruptured lesion in the LAD

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98
Q

What may cause shortening of the QTc interval?

A

Hypercalcaemia

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99
Q

What 3 presentations are included as part of ACS?

A

STEMI
NSTEMI
Unstable angina

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100
Q

What are 3 non-modifiable risk factors for MI?

A

Age
Male
FHx

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101
Q

What are 5 modifiable risk factors for MI?

A 
Smoking 
DM 
HTN
Hypercholesterolaemia 
Obesity
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102
Q

What artery supplies the anterior leads (V1-V4)?

A

LAD

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103
Q

What artery supplies the inferior leads (II, III, aVF)

A

RCA

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104
Q

What artery supplies the lateral leads (I, V5, V6)

A

LCX

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105
Q

What medications should you give a pt during a ACS?

A

Morphine
Metoclopramide
Aspirin
Clopidogrel

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106
Q

What are the 5 post-STEMI prescriptions? (secondary prevention)

A
  1. Atorvastatin 80mg
  2. Aspirin 75mg
  3. Clopidogrel 75mg
  4. ACEi (less risk of HF) e.g. ramipril
  5. BB (less risk of ventricular arrhythmia and HF) e.g. bisoprolol
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107
Q

What are the 2 main causes of ACS?

A
  1. Plaque rupture = 95%

2. Embolism = 5%

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108
Q

When should you give oxygen during an ACS?

A

If Sats <94%

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109
Q

What scoring system can be used to risk stratify pts during an NSTEMI?

A

GRACE score

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110
Q

What are 2 drugs than cause a nephrogenic diabetes insipidus?

A

Lithium and demeclocycline

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111
Q

What are the causes of cranial Diabetes Insipidus?

A
  1. Idiopathic
  2. Post head injury
  3. Pituitary surgery
  4. Craniopharyngioma
  5. Histiocytosis
  6. DIDMOAD
  7. Haemochromatosis
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112
Q

What is DIDMOAD?

A

The association of cranial DI, DM, Optic Atrophy and Deafness (a.k.a. Wolfram’s syndrome)

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113
Q

What are the causes of nephrogenic Diabetes Insipidus?

A
  1. Genetic = AQP2 mutation
  2. E- = hypercalcaemia, hypokalaemia
  3. Drugs = lithium, demeclocycline
  4. Tubulo-interstitial disease = obstruction, sickle cell, pyelonephritis
114
Q

How can you treat cranial DI?

A

Desmopressin

115
Q

How can you treat nephrogenic DI?

A

Thiazides, low salt/protein diet

116
Q

What is the U&E picture for a pt with rhabdomyolysis?

A
  1. AKI with disproportionately raised creatinine
  2. Raised CK
  3. Hypocalcaemia (myoglobin binds calcium)
  4. High phosphate (released from myocytes)
  5. Hyperkalaemia
  6. Metabolic acidosis
117
Q

What is the management for rhabdomyolysis?

A
  1. IV fluids to maintain good urine output

2. Urinary alkalinisation is sometime used

118
Q

What should pts with frequent exacerbations of COPD be given at home?

A

A home supply of prednisolone and an antibiotic (ask pt to contact you if they are required to use them)

119
Q

What are the general management strategies for COPD?

A
  1. Smoking cessation advice: including offering nicotine replacement therapy, varenicline or bupropion
  2. Annual influenza vaccination
  3. One-off pneumococcal vaccination
  4. Pulmonary rehabilitation to all people who view themselves as functionally disabled by COPD (MRC grade 3 and above)
120
Q

What is the first line treatment for COPD?

A
  1. SABA or SAMA
  2. for patients who remain breathless or have exacerbations despite using short-acting bronchodilators the next step is determined by whether the patient has ‘asthmatic features/features suggesting steroid responsiveness’
121
Q

What are the NICE criteria to determine whether a patient has asthmatic/steroid responsive features in COPD?

A
  1. Previous asthma/atopy
  2. High eosinophil count
  3. FEV1 variation over time
  4. Diurnal peak flow variation (at least 20%)
122
Q

If pt doesnt have asthmatic features/features suggesting steroid responsiveness, what is 2nd line treatment for COPD?

A

Add LABA + LAMA

123
Q

If pt has sthmatic features/features suggesting steroid responsiveness, what is the 2nd line treatment for COPD?

A
  1. LABA + inhaled corticosteroid (ICS)

2. if patients remain breathless or have exacerbations offer triple therapy i.e. LAMA + LABA + ICS

124
Q

What are 3 factors which may improve survival in pts with stable COPD?

A
  1. Smoking cessation
  2. LTOT if fit criteria
  3. Lung volume reduction surgery in selected patients
125
Q

What is required to diagnose tumour lysis syndrome?

A

A positive laboratory TLS and a positive clinical TLS (The Cairo-Bishop scoring system)

126
Q

What are the criteria for a positive laboratory TLS?

A

2 or more of the below within 7 days of chemotherapy or 3 days before:

  1. uric acid > 475umol/l or 25% increase
  2. potassium > 6 mmol/l or 25% increase
  3. phosphate > 1.125mmol/l or 25% increase
  4. calcium < 1.75mmol/l or 25% decrease
127
Q

What are the criteria for a positive clinical TLS?

A
  1. Increased creatinine (1.5x upper limit of normal)
  2. Cardiac arrhythmia/SCD
  3. Seizure
128
Q

What should pts at high risk of TLS be given?

A

IV allopurinol or IV rasburicase

129
Q

What is the stereotypical history for mycoplasmia pneumonia?

A

Worsening flu-like symptoms and a dry cough, with erythema multiforme on examination

130
Q

What kind of haemolytic anaemia do you get with a mycoplasma pneumonia?

A

Cold AIHA

131
Q

How is mycoplasma pneumonia diagnosed?

A

Serology

132
Q

How is legionella pneumonia diagnosed?

A

Urinary antigens

133
Q

What neuro conditions can you get due to mycoplasma?

A

Encephalitis and GBS

134
Q

What heart conditions can you get due to mycoplasma?

A

Pericarditis/myocarditis

135
Q

What is the gold standard investigation for diagnosis of degenerative cervical myelopathy?

A

MRI cervical spine

136
Q

What are some symptoms of degenerative cervical myelopathy?

A
  1. Pain (neck, upper/lower limbs)
  2. Loss of motor function
  3. Loss of sensation
  4. Loss of autonomic function (faecal/urinary incompetence and impotence)
  5. Hoffman’s sign
137
Q

What is Hoffman’s sign?

A

A reflex test to assess for cervical myelopathy. It is performed by gently flicking one finger on a patient’s hand. A positive test results in reflex twitching of the other fingers on the same hand in response to the flick.

138
Q

What may an MRI C-spine show in degenerative cervical myelopathy?

A

Disc degeneration and ligament hypertrophy, with accompanying cord signal change

139
Q

What is the only effective treatment for degenerative cervical myelopathy?

A

Decompressive surgery

140
Q

What are the 3 components of hyperkalaemia management?

A
  1. Stabilisation of the cardiac membrane
  2. Short-term shift in potassium from extracellular to intracellular fluid compartment
  3. Removal of potassium from the body
141
Q

What drug is given for stabilisation of the cardiac membrane?

A

IV calcium gluconate

142
Q

What is given for short-term shift in potassium from extracellular to intracellular fluid compartment?

A
  1. Combined insulin/dextrose infusion

2. Nebulised salbutamol

143
Q

What is given for removal of potassium from the body?

A
  1. Calcium resonium
  2. Loop diuretics
  3. Dialysis
144
Q

Why are calcium resonium enemas more effective than oral potassium?

A

As potassium is secreted by the rectum

145
Q

What is the most likely cause of right sided tenderness on a PR exam?

A

Appendicitis

146
Q

What may you see on FBC with appendicitis?

A

A neutrophil-predominant leucocytosis

147
Q

What is a dermatological complication of warfarin?

A

Skin necrosis. 3F:1M, typically occurs within 10 days of warfarin administration

148
Q

How does skin necrosis with warfarin present?

A

A large red patch progressing to purpura/ecchymosis with an INR still in the therapeutic range

149
Q

What is the MOA of warfarin?

A

Vitamin K epoxide reductase inhibitor, prevents the reduction of Vitamin K to its active hydroquinone form, which in turn acts as a cofator in the carboxylation of clotting factor 2,7,9,10 and Protein C

150
Q

What are 3 indications for warfarin?

A
  1. VTE
  2. AF
  3. Mechanical heart valves
151
Q

What is the target INR when giving warfarin for VTE?

A

2.5, if recurrent 3.5

152
Q

What is the target INR when giving warfarin for AF?

A

2.5

153
Q

What is the target INR when giving warfarin for mechanical heart valves?

A

Depends on type of valve and location, mitral valves generally require a higher INR than aortic valves

154
Q

What are 4 side effects of warfarin?

A
  1. Haemorrhage
  2. Teratogenic
  3. Skin necrosis
  4. Purple toes
155
Q

What are some factors that may potentiate warfarin?

A
  1. Liver disease
  2. P450 enzyme inhibitors e.g. amiodarone, ciprofloxacin
  3. Cranberry juice
  4. Drugs that displace warfarin from plasma albumin e.g. NSAIDs
  5. Inhibit plt function e.g. NSAIDs
156
Q

What kind of virus is parvovirus B19?

A

DNA virus

157
Q

What is the MOA of sulfnylureas?

A

Bind to an ATP-dependent K+(KATP) channel on the cell membrane of pancreatic beta cell. They increase pancreatic insulin secretion and hence are only effective if functional B-cells are present

158
Q

What are 3 side effects of sulfonylureas?

A

Hypoglycaemic episodes
Weight gain
Peripheral neuropathy

159
Q

What causes Wilson’s disease?

A

A defect in the ATP7B gene located on chromosome 13, leading to increased copper absorption from the small intestine and decreased hepatic copper excretion.

160
Q

When does Wilson’s disease present?

A

10-25 years old

161
Q

How does Wilson’s typically present?

A 
Liver = hepatitis/cirrhosis
Neurological = basal ganglia degeneration, speech, behavioural and psychiatric problems
162
Q

How is Wilson’s diagnosed?

A
  1. Reduced serum caerulopasmin
  2. Reduced serum copper (as 95% of plasma copper is carried by caeruloplasmin)
  3. Increased 24hr urinary copper excretion
163
Q

How is Wilson’s diagnosed?

A
  1. Penicillamine (chelates copper)

2. Trientine hydrochloride (another chelating agent for the future)

164
Q

What can precipitate renal failure in pts with multiple myeloma and should therefore be avoided?

A

NSAIDS

165
Q

What are the X-ray findings of the skull in multiple myeloma?

A

‘Rain-drop’ skull

166
Q

What causes hypercalcaemia in myeloma?

A

Increased osteoclastic bone resorption causes by local cytokines (IL1, TNF) released by myeloma cells

167
Q

Where do cancers below the pectinate line spread to?

A

The superficial inguinal nodes

168
Q

Where do cancers above the pectinate line spread to?

A

Internal iliac lymph nodes

169
Q

What do the pararectal lymph nodes drain?

A

Upper part of the rectum and parts of the colon

170
Q

What lymph nodes do the testes and the ovaries drain to?

A

Para-aortic lymph nodes

171
Q

What drains into the superficial inguinal lymph nodes?

A
  1. Anal canal below pectinate line
  2. Perineum
  3. Skin of the thigh
  4. Penis
  5. Scrotum
  6. Vagin
172
Q

What drains into the deep inguinanl lymph nodes?

A

Glans penis

173
Q

What drains into the para-aortic lymph nodes?

A
  1. Testes, ovaries
  2. Kidneys
  3. Adrenal gland
174
Q

What drains into the axillary lymph nodes?

A
  1. Lateral breast

2. Upper limb

175
Q

What drains into the internal iliac lymph nodes?

A
  1. Anal canal above the pectinate line
  2. Lower part of the rectum
  3. Pelvic structures, including cervix and inferior part of uterus
176
Q

What drains into the superior mesenteric lymph nodes?

A

The duodenum and jejenum

177
Q

What drains into the inferior mesenteric lymph nodes?

A

The descending colon, sigmoid colon and upper part of the rectum

178
Q

What drains into the coeliac lymph nodes?

A

Stomach

179
Q

When do you refer pts for a 2wk lung cancer appointment?

A
  1. CXR with findings that suggest lung cancer

2. >40y/o with unexplained haemoptysis

180
Q

What is the first line treatment for treating agitation and confusion in a palliative setting?

A

Oral Haloperidol

181
Q

What is the best treatment for treating agitation and confusion in the terminal phase of an illness?

A

Subcutaneous midazolam

182
Q

What is the finding on ABG for an Addisonian crisis?

A

A hyponatraemic, hyperkalaemic metabolic acidosis

183
Q

Why can an Addisonian crisis occur during and after pregnancy?

A

Due to immune-regulatory changes

184
Q

What are 3 situations where an Addisonian crisis is common?

A
  1. Sepsis/surgery causing an acute exacerbation of chronic insufficiency (Addison’s, Hypopituitarism)
  2. Adrenal haemorrhage (Waterhouse-Friderichsen syndrome due to fulminant meningococcaemia)
  3. Steroid withdrawal
185
Q

What is the management of an Addisonian crisis?

A
  1. Hydrocortisone 100mg IM/IV (continue 6hrly until pt stable)
  2. 1L 0.9% saline infused over 30-60mins/with dextrose if hypoglycaemic
186
Q

What is a pharyngeal pouch?

A

A posteromedial herniation between thyropharyngeus and cricopharyngeus muscles

187
Q

How can you classify the causes of dysphagia?

A
  1. Extramural
  2. Mural
  3. Intramural
  4. Neurological
188
Q

What are the extramural causes of dysphagia?

A
  1. Mediastinal masses

2. Cervical spondylosis

189
Q

What are the mural causes of dysphagia?

A
  1. Achalasia
  2. Oesophageal spasm
  3. Hypertensive lower oesophageal sphincter
190
Q

What are the intramural causes of dysphagia?

A
  1. Tumours
  2. Strictures
  3. Infection (candidiasis)
  4. Oesophageal web
  5. Schatzki rings
191
Q

What are some neurological causes of dysphagia?

A
  1. CVA
  2. Parkinsons
  3. MS
  4. Brainstem pathology
  5. Myasthenia gravis
192
Q

Why might an SGLT2 inhibitor cause worsening of thrush?

A

Prevents the reabsorption of glucose from the proximal renal tubule, resulting in more glucose being secreted in the urine

193
Q

What is an example of an SGLT2 inhibitor?

A

Empagliflozin

194
Q

What are 3 important adverse effects of SGLT2 inhibitors?

A
  1. Urinary and genital infection
  2. Normoglycaemic ketoacodisis
  3. Risk of lower limb amputation
195
Q

How does rhabdomyolysis cause AKI?

A

Myoglobin causes tubular cell necrosis

196
Q

What is the most common cause of secondary hyperparathyroidism?

A

CKD

197
Q

What is an obese, young female with headaches/blurred vision (and papilloedema) most likely to have?

A

Idiopathic intracranial hypertension

198
Q

What is the management of idiopathic intracranial hypertension?

A
  1. Weight loss
  2. Diuretics e.g. acetozolamide
  3. Repeated LP
  4. Surgery = optic nerve sheath decompression and fenestration to prevent damage to the optic nerve
  5. Surgery = VP/lumboperitoneal shunt
199
Q

What are the differentials for hypertension with low potassium?

A
  1. Conn’s
  2. Cushing’s
  3. RAS
  4. Liddle’s
200
Q

How do you differentiate between the causes of hypertension with low potassium?

A

Check renin and aldosterone levels

  1. High A + Low R = Cushings and Conns
  2. High A + High R = RAS
  3. Low A + Low R = Liddle’s
201
Q

What is Liddle’s syndrome?

A

Rare hereditary disorder due to increased activity of ENaC, causing hypernatraemia, hypokalaemia and hypertension (and thus also a metabolic alkalosis)

202
Q

What organism causes Lyme disease?

A

Borrelia Burgdorferi

203
Q

What are the features of Lyme disease?

A
  1. Systemic = fever, arthralgia
  2. Cardiovascular = heart block, myositis
  3. Neuro = facial nerve palsy, meningitis
  4. Derm = erythema chronicum migrans
204
Q

What is the first line test for diagnosis of Lyme disease?

A

ELISA for Borrelia Burgdorferi

205
Q

What is the management for Lyme disease?

A
  1. Doxycycline if early disease
  2. Amoxicllin if doxy c/i (e.g. pregnancy)
  3. Ceftriaxone if disseminated disease
206
Q

What is the Jarisch-Herxeimher reaction?

A

A reaction to endotoxin-like products (e.g. lipoproteins) being released by the death of microorganisms during antibiotic treatment.

207
Q

What infections when treated most commonly lead to a Jarisch-Herxeimher reaction?

A
  1. Syphilis
  2. Spirochetes = Lyme, Leptospirosis
  3. Tropical = Q fever, bartonella, trypanosomiasis
208
Q

What is the CHA2DS2-VASc scoring system used for?

A

Used to determine the need to anticoagulate a patient in atrial fibrillation

209
Q

ABCD2 score?

A

Prognostic score for risk stratifying patients who’ve had a suspected TIA

210
Q

NYHA score?

A

Heart failure severity scale

211
Q

DAS28 score?

A

Measure of disease activity in rheumatoid arthritis

212
Q

Child-Pugh classification?

A

A scoring system used to assess the severity of liver cirrhosis

213
Q

Wells score?

A

Helps estimate the risk of a patient having a deep vein thrombosis

214
Q

MMSE?

A

Mini-mental state examination - used to assess cognitive impairment

215
Q

HAD scale?

A

Hospital Anxiety and Depression (HAD) scale - assesses severity of anxiety and depression symptoms

216
Q

PHQ-9?

A

Patient Health Questionnaire - assesses severity of depression symptoms

217
Q

GAD-7?

A

Used as a screening tool and severity measure for generalised anxiety disorder

218
Q

SCOFF?

A

Questionnaire used to detect eating disorders and aid treatment

219
Q

What are 3 alcohol screening tools?

A

AUDIT, CAGE and FAST

220
Q

CURB-65?

A

Used to assess the prognosis of a patient with pneumonia

221
Q

Epworth Sleepiness Scale?

A

Used in the assessment of suspected obstructive sleep apnoea

222
Q

IPSS?

A

International prostate symptom score

223
Q

Gleason score?

A

Indicates prognosis in prostate cancer

224
Q

Waterlow score?

A

Assesses the risk of a patient developing a pressure sore

225
Q

FRAX?

A

Risk assessment tool developed by WHO which calculates a patients 10-year risk of developing an osteoporosis related fracture

226
Q

Ranson criteria?

A

Acute pancreatitis

227
Q

MUST

A

Malnutrition

228
Q

What are the two categories for results of a Wells score?

A
  1. DVT likely = 2 points or more

2. DVT unlikely = 1 point or less

229
Q

What investigations are indicated if Wells score shows DVT likely?

A
  1. A proximal leg vein ultrasound scan should be carried out within 4 hours and, if the result is negative, a D-dimer test
  2. If a proximal leg vein ultrasound scan cannot be carried out within 4 hours a D-dimer test should be performed and low-molecular weight heparin administered whilst waiting for the proximal leg vein ultrasound scan (which should be performed within 24 hours)
230
Q

What investigations are indicated if Wells score shows DVT unlikely?

A
  1. Perform a D-dimer test and if it is positive arrange:
  2. A proximal leg vein ultrasound scan within 4 hours
  3. If a proximal leg vein ultrasound scan cannot be carried out within 4 hours low-molecular weight heparin should be administered whilst waiting for the proximal leg vein ultrasound scan (which should be performed within 24 hours)
231
Q

What is the management of a DVT?

A
  1. Low molecular weight heparin (LMWH) or fondaparinux should be given initially after a DVT is diagnosed.
  2. Warfarin should be given within 24 hours of the diagnosis
  3. LMWH or fondaparinux should be continued for at least 5 days or until the international normalised ratio (INR) is 2.0 or above for at least 24 hours, whichever is longer
  4. Warfarin should be continued for at least 3 months. At 3 months, NICE advise that clinicians should ‘assess the risks and benefits of extending treatment’
  5. NICE add ‘consider extending warfarin beyond 3 months (usually 6 months) for patients with unprovoked proximal DVT if their risk of VTE recurrence is high and there is no additional risk of major bleeding’
232
Q

How can you classify the different types of stroke?

A

The Oxford Stroke classification (a.k.a. Bamford stroke classification). It classifies strokes based on the initial symptoms

233
Q

Which criteria should be assessed as part of the Bamford stroke classification?

A
  1. Unilateral hemiparesis and/or hemisensory loss of the face, arm and leg
  2. Homonymous hemianopia
  3. High cognitive dysfunction e.g. dysphasia
234
Q

What are the 4 possible classifications of stroke as per the Bamford stroke classification system?

A
  1. TACS = total anterior circulation stroke (15%)
  2. PACS = partial anterior circulation stroke (25%)
  3. LACS = lacunar stroke (25%)
  4. POCS = posterior circulation stroke (25%)
235
Q

What causes a TACS and which bamford criteria are present?

A
  1. Involves middle and anterior cerebral arteries

2. All 3 criteria present

236
Q

What causes a PACS and which bamford criteria are present?

A
  1. Involves smaller arteries or anterior circulation e.g. upper or lower division of middle cerebral artery
  2. 2 criteria present
237
Q

What causes a LACS and which bamford criteria are present?

A
  1. Involves perforating arteries around the internal capsule, thalamus and basal ganglia
  2. Presents with 1 of the following
    a. unilateral weakness (and/or sensory deficit) of face and arm, arm and leg or all three.
    b. pure sensory stroke.
    c. ataxic hemiparesis
238
Q

What causes a POCS and which bamford criteria are present?

A
  1. Involves vertebrobasilar arteries
  2. Presents with 1 of the following
    a. cerebellar or brainstem syndromes
    b. loss of consciousness
    c. isolated homonymous hemianopia
239
Q

What causes lateral medullary syndrome and what is it also known as?

A

Blockage of posterior inferior cerebellar artery, and a.k.a. Wallenberg’s syndrome

240
Q

What are the features of lateral medullary syndrome?

A
  1. Ipsilateral: ataxia, nystagmus, dysphagia, facial numbness, cranial nerve palsy e.g. Horner’s
  2. Contralateral limb sensory loss
241
Q

What is Weber’s syndrome?

A

A midbrain stroke syndrome that involves fascicles of the oculomotor nerve resulting in an ipsilateral CN III palsy and contralateral hemiplegia or hemiparesis

242
Q

What is titubation?

A

Head tremor

243
Q

What is the most common cause of titubation?

A

Benign essential tremor

244
Q

What are 3 features of benign essential tremor?

A
  1. Postural tremor
  2. Improved by alcohol and rest
  3. Most common cause of titubation
245
Q

What is the management of benign essential tremor?

A
  1. Propranolol is 1st line

2. Primidone is sometimes used

246
Q

What causes haemolytic uraemic syndrome?

A

E. coli 0157

247
Q

What is the triad of HUS?

A

MAHA
Thrombocytopenia
AKI

248
Q

What are the types of Hodgkin’s lymphoma?

A
  1. Classical HL

2. Nodular lymphocyte-predominant HL

249
Q

What are the types of Classical HL?

A
  1. Nodular sclerosing
  2. Mixed cellularity
  3. Lymphocyte-rich
  4. Lymphocyte-depleted
250
Q

What implies poor prognosis in Hodgkin’s lymphoma?

A

B symptoms

  1. Weight loss >10% in last 6m
  2. Fever >38C
  3. Night sweats
251
Q

What is the best way to assess response to Hep C treatment?

A

Viral load

252
Q

What kind of virus is Hep C?

A

RNA flavivirus

253
Q

What is the incubation period of Hep C?

A

6-9 weeks

254
Q

What is the investigation of choice to diagnose acute Hep C infection?

A

HCV RNA

255
Q

What is the prognosis of Hep C?

A

Around 15-45% will clear the virus after an acute infection, and hence the majority (55-85%) will develop chronic Hep C§

256
Q

What is the definition for chronic Hep C?

A

The persistence of HCV RNA in the blood for 6m

257
Q

What are some complications of Hep C?

A
  1. Rheum = arthralgia, arthritis
  2. Eye = sjogrens
  3. Hepatic = cirrhosis, HCC
  4. Type II cryoglobulinaemia
  5. PCT
  6. Membranoproliferative glomerulonephritis
258
Q

What is the aim of Hep C treatment?

A

A sustained virologic response (SVR) defined as undetectable serum HCV RNA 6m after the end of therapy

259
Q

What is the treatment of Hep C?

A

A combination of protease inhibitors +/- ribavarin

260
Q

What are complications of ribavarin?

A
  1. Haemolytic anaemia
  2. Cough
  3. Teratogenic (women cant become pregnant within 6m)
261
Q

What is the treatment of genital warts?

A
  1. Multiple non-keratinised warts = topical podophyllum

2. Solitary, keratinised warts = cryotherapy

262
Q

What are genital warts also called and what are they caused by?

A

Condylomata accuminata

HPV 6&11

263
Q

What is a contraindication to triptans?

A

A history of (or risk factors for) ischaemic heart disease or cerebrovascular disease

264
Q

What are 4 first line treatments for neuropathic pain?

A
  1. Amitryptiline
  2. Gabapentin
  3. Pregabalin
  4. Duloxetine
265
Q

What is neuropathic pain?

A

Pain which arises following damage or disruption of the nervous system

266
Q

What are 4 causes of neuropathic pain?

A
  1. Diabetic neuropathy
  2. Post-herpetic neuralgia
  3. Trigeminal neuralgia
  4. Prolapsed intervertebral disc
267
Q

What may be used for localised neuropathic pain?

A

Topical capsaicin

268
Q

What is vitamin C also known as?

A

Ascorbic acid

269
Q

What are 4 functions of Vitamin C?

A
  1. Antioxidant
  2. Cofactor for collagen synthesis
  3. Facilitates iron absorption
  4. Cofactor for NA synthesis
270
Q

What are some features of Vitamin C deficiency?

A
  1. Gingivitis, loose teeth
  2. Poor wound healing
  3. Bleeding from gums, haematuria, epistaxis
  4. General malaise
271
Q

What are 5HT3 antagonists used for and what are some examples?

A

Anti-emetics used mainly in the management of chemo-related nausea, they mainly act in the CTZ area of the medulla oblongata
E.g. ondansetron and granisetron

272
Q

Which drugs have been shown to improve mortality in pts with chronic HF and what trials proved this?

A
  1. ACEi (SAVE, SOLVD, CONSENSUS)
  2. Spironolactone (RALES)
  3. BBs (CIBIS)
  4. Hydralazine w/ nitrates (VHEFT-1)
273
Q

What other options are available for tx of chronic HF once triple therapy has failed?

A

CRT, digoxin, and Entresto

274
Q

Renal transplant + infection?

A

CMV

275
Q

What percentage of renal transplant pts have a significant infection w/in the first 12m of having a renal transplant?

A

50%

276
Q

What is the appearance of CMV-infected cells>

A

‘Owl’s eye’ appearance due to intranuclear inclusion bodies

277
Q

What causes red man syndrome?

A

Rapid IV infusion of vancomycin leading to redness, pruritis and a burning sensation predominantly in the upper body. Due to vancomycin-related activation of mast cells with release of histamine

278
Q

What is the management of red man syndrome?

A

Cessation of vancomycin infusion, and when symptoms have resolved, recommencement at a slower rate

279
Q

What are some adverse effects of vancomycin?

A
  1. Nephrotoxicity
  2. Ototoxicity
  3. Thrombophlebitis
  4. Red man syndrome
280
Q

What is the HbA1c target in T2DM?

A
  1. Lifestyle = 48mmol/mol (6.5%)
  2. Lifestyle + metformin = 48mmol/mol (6.5%)
  3. Lifestyle + any drug which might cause hypo = 53mmol/mol (7.0%)
281
Q

How often should HbA1c levels be checked in T2DM?

A

Every 3-6m until stable, then 6 monthly

Medicine and Surgery Mushkies (52 decks)

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