BIG THREE Flashcards

1
Q

Non-urgent endoscopy referral criteria

A

-Patients with haematemesis
-Patients aged >= 55 years who’ve got:
treatment-resistant dyspepsia or
-upper abdominal pain with low haemoglobin levels or
raised platelet count with any of the following: nausea, vomiting, weight loss, reflux, dyspepsia, upper abdominal pain
nausea or vomiting with any of the following: weight loss, reflux, dyspepsia, upper abdominal pain

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2
Q

Urgent endoscopy referral criteria

A

-All patients who’ve got dysphagia
-All patients who’ve got an upper abdominal mass consistent with stomach cancer
-Patients aged >= 55 years who’ve got weight loss, AND any of the following:
upper abdominal pain
reflux
dyspepsia

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3
Q

Managing patients who do not meet referral criteria (‘undiagnosed dyspepsia’)

A

This can be summarised at a step-wise approach
1. Review medications for possible causes of dyspepsia
2. Lifestyle advice
3. Trial of full-dose proton pump inhibitor for one month OR a ‘test and treat’ approach for H. pylori
if symptoms persist after either of the above approaches then the alternative approach should be tried

Testing for H. pylori infection
initial diagnosis: NICE recommend using a carbon-13 urea breath test or a stool antigen test, or laboratory-based serology ‘where its performance has been locally validated’
test of cure:
there is no need to check for H. pylori eradication if symptoms have resolved following test and treat
however, if repeat testing is required then a carbon-13 urea breath test should be used

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4
Q

Atrial fibrillation: rate control

A

Rate control should be offered as the first‑line treatment strategy for atrial fibrillation except in people:
whose atrial fibrillation has a reversible cause
who have heart failure thought to be primarily caused by atrial fibrillation
with new‑onset atrial fibrillation (< 48 hours)
with atrial flutter whose condition is considered suitable for an ablation strategy to restore sinus rhythm
for whom a rhythm‑control strategy would be more suitable based on clinical judgement

Medications

Agents used to control rate in patients with atrial fibrillation
beta-blockers
a common contraindication for beta-blockers is asthma
calcium channel blockers
digoxin
Digoxin is not considered first-line anymore as they are less effective at controlling the heart rate during exercise
should only be considered if the person does no or very little physical exercise or other rate‑limiting drug options are ruled out because of comorbidities
may have a role if there is coexistent heart failure

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5
Q

Atrial fibrillation: rhythm control

A

Agents used to maintain sinus rhythm in patients with a history of atrial fibrillation

  • beta-blockers
  • dronedarone: second-line in patients following cardioversion
  • amiodarone: particularly if coexisting heart failure
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6
Q

Atrial fibrillation: catheter ablation

A

NICE recommends the use of catheter ablation for those with AF who have not responded to or wish to avoid, antiarrhythmic medication.

Technical aspects
the aim is to ablate the faulty electrical pathways that are resulting in atrial fibrillation. This is typically due to aberrant electrical activity between the pulmonary veins and left atrium
the procedure is performed percutaneously, typically via the groin
both radiofrequency (uses heat generated from medium frequency alternating current) and cryotherapy can be used to ablate the tissue

Anticoagulation
should be used 4 weeks before and during the procedure
it should be remember that catheter ablation controls the rhythm but does not reduce the stroke risk, even if patients remain in sinus rhythm. Therefore, patients still require anticoagulation as per their CHA2DS2-VASc score
if score = 0: 2 months anticoagulation recommended
if score > 1: longterm anticoagulation recommended

Outcome
-notable complications include
cardiac tamponade
stroke
pulmonary vein stenosis
-success rate
around 50% of patients experience an early recurrence (within 3 months) of AF that often resolves spontaneously
longer term, after 3 years, around 55% of patients who've had a single procedure remain in sinus rhythm. Of patients who've undergone multiple procedures around 80% are in sinus rhythm
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7
Q

Patient on Mesalazine (Ulcerative colitis) feeling unwell. Most important 1st test and why

A

FBC - as mesalazine (an aminosalicylate) causes many haematological adverse effects, including agranulocytosis

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8
Q

1st line treatment of C difficile

A

Oral vancomycin

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9
Q

1st line treatment of life-threatening C.difficile

A

Oral vancomycin + IV metronidazole

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10
Q

Treatment of recurrent C. difficile

A

Prescribe oral fidaxomicin - recommended if the patient presents with a recurrent episode of C.difficile within 12 weeks of symptoms resolution. Recurrence of C.difficile infection within 12 weeks may indicate that the organism is resistant and thus requires fidaxomicin.
Should this fail provide oral vancomycin + IV metronidazole

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11
Q

Pulses: pulsus paradoxus

A

greater than the normal (10 mmHg) fall in systolic blood pressure during inspiration → faint or absent pulse in inspiration
severe asthma, cardiac tamponade

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12
Q

Pulses: slow rising/plateau

A

aortic stenosis

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13
Q

Pulses: collapsing

A

aortic regurgitation
patent ductus arteriosus
hyperkinetic states (anaemia, thyrotoxic, fever, exercise/pregnancy)

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14
Q

Pulses: Pulsus arternans

A

regular alternation of the force of the arterial pulse

severe LVF

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15
Q

Pulses: bisferiens pulse

A

‘double pulse’ - two systolic peaks

mixed aortic valve disease, HOCM

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16
Q

Aortic dissection - investigation of choice

A
CT angiography: pelvis/chest/abdomen (depending on stability of patient) 
Transoesophageal echocardiography (TOE)
more suitable for unstable patients who are too risky to take to CT scanner
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17
Q

Budd-chiari syndrome classic triad

A

The features are classically a triad of:
abdominal pain: sudden onset, severe
ascites → abdominal distension
tender hepatomegaly

Budd-Chiari syndrome is a condition characterized by obstruction to hepatic venous outflow. It usually occurs in a patient with a hypercoagulative state (e.g. antiphospholipid syndrome) but can also occur as a result of physical obstruction (e.g. tumour). The venous congestion can cause hepatomegaly and portal hypertension which can can also result in splenomegaly and ascites.

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18
Q

Severe exacerbation of asthma

A

The features of acute severe asthma are: PEFR 33-50% best or predicted, inability to complete full sentences, RR >25/min and pulse >110 bpm

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19
Q

Moderate exacerbation of asthma

A

PEFR 50-75% best or predicted
Speech normal
RR < 25 / min
Pulse < 110 bpm

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20
Q

Life-threatening asthma

A
PEFR < 33% best or predicted
Oxygen sats < 92%
'Normal' pC02 (4.6-6.0 kPa)
Silent chest, cyanosis or feeble respiratory effort
Bradycardia, dysrhythmia or hypotension
Exhaustion, confusion or coma
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21
Q

Indicator of HOCM

A

Ventricle thickening
Tall R waves in V4-6
Deep q waves common

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22
Q

HOCM management (ABCDE)

A
A- Amioderone
B- Beta-blockers or verapamil for symptoms
C- Cardiac defibrillation 
D- Dual chamber pacemaker
E- Endocarditis prophylaxis
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23
Q

HOCM - Drugs to avoid

A

Nitrates
Ace-inhibitors
Inotropes

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24
Q

Why transferrin saturation, total ferritin is high but total iron-binding capacity is low in Haemochromatosis

A

Haemochromatosis is an iron storage disorder therefore binding capacity in the blood is unaffected

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25
Q

HOCM ECG findings

A

T wave inversion
LVH - tall r waves
Deep ST depression

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26
Q

VIT C deficiency signs/symptoms

A

involved in connective tissue (collagen) synthesis thus associated with poor wound healing
involved with iron absorption thus can have iron deficiency anaemia (pale, pale conjunctiva,bleeding gums,fatigued)

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27
Q

Klebsiella pneumonia A’s

A

Alcoholism, Aspiration pneumonia (affects upper lungs) and Abscesses (empyema)
Also presents with red jelly-like sputum
also more common with diabetics

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28
Q

Asbestos & Asbestosis

A
  • Commonly affects lower lobes (typically)
  • Length of exposure can relate to the severity
  • Crocidolite (blue) asbestos is the most dangerous form.
  • Causes pleural thickening
  • Causes pleural plaques (benign and do not undergo malignant change).
  • Can cause mesothelioma.
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29
Q

New onset Atrial fibrillation: Pharmacological conversion

A

Agents with proven efficacy in the pharmacological cardioversion of atrial fibrillation:
amiodarone
flecainide (if no structural heart disease)
others (less commonly used in the UK): quinidine, dofetilide, ibutilide, propafenone

Less effective agents
beta-blockers (including sotalol)
calcium channel blockers
digoxin (used in non-paroxysmal AF only if sedimentary)
disopyramide
procainamide
30
Q

STEMI ECG CRITERIA

A
≥ 2 contiguous leads of:
2.5 mm (i.e ≥ 2.5 small squares) ST elevation in leads V2-3 in men < 40 years, or ≥ 2.0 mm ST elevation in leads V2-3 in men > 40 years
1.5 mm ST elevation in V2-3 in women
1 mm ST elevation in other leads
new LBBB
31
Q

COPD: stable management - First line problems

A

Bronchodilator therapy
a short-acting beta2-agonist (SABA) or short-acting muscarinic antagonist (SAMA) is the first-line treatment
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’

32
Q

COPD: stable management - second-line therapy (non-asthmatic features/ features suggesting steroid responsiveness)

A

add a long-acting beta2-agonist (LABA) + long-acting muscarinic antagonist (LAMA)
if already taking a SAMA, discontinue and switch to a SABA

33
Q

COPD: stable management - second-line therapy (asthmatic symptoms/features suggesting steroid responsiveness)

A

Asthmatic features/features suggesting steroid responsiveness
LABA + inhaled corticosteroid (ICS)
if patients remain breathless or have exacerbations offer triple therapy i.e. LAMA + LABA + ICS
if already taking a SAMA, discontinue and switch to a SABA
NICE recommend the use of combined inhalers where possible

34
Q

main ECG findings with hypercalcaemia

A

Shortened QT interval

35
Q

Features of hypercalcaemia

A
  • ‘bones, stones, groans and psychic moans’
  • corneal calcification
  • shortened QT interval on ECG
  • hypertension
36
Q

Prevention of acute mountain syndrome (altitude-related disorders)

A
  • the risk of AMS may actually be positively correlated to physical fitness
    -gain altitude at no more than 500 m per day
    -acetazolamide (a carbonic anhydrase inhibitor) is widely used to prevent AMS and has a supporting evidence base
    it causes a primary metabolic acidosis and compensatory respiratory alkalosis which increases respiratory rate and improves oxygenation
    -treatment: descent
37
Q

Management of high altitude cerebral oedema (HACE/O)

A

descent

dexamethasone

38
Q

Presentation of high altitude cerebral oedema (HACE/O)

A

papilloedema
headache
ataxia

39
Q

Presentations of high altitude pulmonary oedema (HAPE)

A

-Dyspnoea (SOB particularly on exertion)
-coughing (may produce pink frothy sputum)
-Feeling of choking/drowning when horizontal.
-Wheezing
ETC.

40
Q

Management of HAPE

A
  • Descent
  • Nifedipine, dexamethasone, acetazolamide, phosphodiesterase type V inhibitors*
  • Oxygen if available
41
Q

Treatment of Wilson’s Disease

A
  • Penicillamine - chelates copper

- Trientine hydrochloride is an alternative chelating agent

42
Q

Torsades de pointes - Treatment

A

IV magnesium sulphate

43
Q

DUKE criteria for bacterial endocarditis

(either pathological criteria positive, or
2 major criteria, or
1 major and 3 minor criteria, or
5 minor criteria)

A

-Presence of pathological findings: Positive histology or microbiology of pathological material
- Major criteria:
Positive blood cultures
~two positive blood cultures showing typical organisms consistent with infective endocarditis, such as Streptococcus viridans and the HACEK group, or
~persistent bacteraemia from two blood cultures taken > 12 hours apart or three or more positive blood cultures where the pathogen is less specific such as Staph aureus and Staph epidermidis, or
~positive serology for Coxiella burnetii, Bartonella species or Chlamydia psittaci, or
positive molecular assays for specific gene targets

Evidence of endocardial involvement
~positive echocardiogram (oscillating structures, abscess formation, new valvular regurgitation or dehiscence of prosthetic valves), or
~new valvular regurgitation

Minor:
predisposing heart condition or intravenous drug use
microbiological evidence does not meet major criteria
fever > 38ºC
vascular phenomena: major emboli, splenomegaly, clubbing, splinter haemorrhages, Janeway lesions, petechiae or purpura
immunological phenomena: glomerulonephritis, Osler’s nodes, Roth spots

44
Q

Signs of wilsons disease

A
Copper ring deposits (green/brown) around iris (Kayser-fleisher) 
Jaundice / liver cirrhosis
Arthritis
Blue nails
Cardiomyopathy
renal tubule dysfunction 
Neurological/cognitive impairment
45
Q

-gatran drug suffix

A
Thrombin inhibitors (argatroban type)	e.g efegatran
Can be used in AF
46
Q

-pine drug suffix

A

Calcium channel blockers - e.g amilodipine

Lowers BP

47
Q

What drug to use if bleeding on antithrombin dabigatran

A

Idracizumab - is a humanised monoclonal antibody fragment that binds specifically to dabigatran and its metabolites, thereby reversing the anticoagulant effect.

48
Q

Drugs to reverse Heparin

A

Protamine sulphate

49
Q

Drug to reverse warfarin

A

Phytomenadione (vitamin K)

50
Q

2nd line warfarin reversal treatment if Vit K insufficient

A

Prothrombin complex - This is used to treat major bleeding on warfarin despite treatment with phytomenadione.

51
Q

ECG territories and arteries

A

Anteroseptal - V1->V4 - LAD

Inferior - II, III and aVF - Right coronary/RCA

Anterolateral - V4-V6, I and aVL - LAD or Left Circumflex

Lateral - I, aVL, +/- V5-V6 - Left circumflex

Posterior - Tall R waves V1-V2 - Usually left circumflex, also right coronary

52
Q

Adverse effects of Adenosine

A
chest pain
bronchospasm
transient flushing
can enhance conduction down accessory pathways, resulting in increased ventricular rate (e.g. WPW syndrome)
Heart-block
53
Q

Adverse effects Beta-blockers

A
Side-effects
bronchospasm
cold peripheries
fatigue
sleep disturbances, including nightmares
erectile dysfunction
54
Q

Contraindications of Beta blockers

A
  • uncontrolled heart failure
  • asthma
  • sick sinus syndrome
  • concurrent verapamil use: may precipitate severe bradycardia
55
Q

Side/Adverse effects of ACEi

A

~cough - occurs in around 15% of patients and may occur up to a year after starting treatment, thought to be due to increased bradykinin levels
~angioedema: may occur up to a year after starting treatment
~hyperkalaemia
~first-dose hypotension: more common in patients taking diuretics

56
Q

Contraindications of ACEi

A

~Pregnancy and breastfeeding - avoid
~renovascular disease - may result in renal impairment
~aortic stenosis - may result in hypotension
~hereditary of idiopathic angioedema
~specialist advice should be sought before starting ACE inhibitors in patients with a potassium >= 5.0 mmol/L

57
Q

Causes of ST depression

A
secondary to abnormal QRS (LVH, LBBB, RBBB)
ischaemia
digoxin
hypokalaemia
syndrome X
58
Q

Adverse effects of amioderone

A
thyroid dysfunction: both hypothyroidism and hyper-thyroidism
corneal deposits
pulmonary fibrosis/pneumonitis
liver fibrosis/hepatitis
peripheral neuropathy, myopathy
photosensitivity
'slate-grey' appearance
thrombophlebitis and injection site reactions
bradycardia
lengths QT interval
59
Q

Wolf-parkinson- white syndrome ECG findings

A

Wolff-Parkinson-White syndrome (left-sided accessory pathway)
a short PR interval
delta waves
right axis deviation

60
Q

What is Dressler’s Syndrome

A

Dressler’s syndrome tends to occur around 2-6 weeks following a MI. The underlying pathophysiology is thought to be an autoimmune reaction against antigenic proteins formed as the myocardium recovers. It is characterised by a combination of fever, pleuritic pain, pericardial effusion and a raised ESR. It is treated with NSAIDs.

61
Q

Causes of LBBB

A

myocardial infarction
diagnosing a myocardial infarction for patients with existing LBBB is difficult
rhe Sgarbossa criteria can help with this
hypertension
aortic stenosis
cardiomyopathy
rare: idiopathic fibrosis, digoxin toxicity, hyperkalaemia

62
Q

Loop-diuretics adverse effects

A
hypotension
hyponatraemia
hypokalaemia, hypomagnesaemia
hypochloraemic alkalosis
ototoxicity
hypocalcaemia
renal impairment (from dehydration + direct toxic effect)
hyperglycaemia (less common than with thiazides)
gout
63
Q

PE ECG changes

A

Pulmonary embolism
inverted T waves
right bundle branch block
right axis deviation

64
Q

Wolff-Parkinson-White syndrome (left-sided accessory pathway) ECG Changes

A

a short PR interval
delta waves
right axis deviation

65
Q

T Wave inversion causes

A
myocardial ischaemia
digoxin toxicity
subarachnoid haemorrhage
arrhythmogenic right ventricular cardiomyopathy
pulmonary embolism ('S1Q3T3')
Brugada syndrome
66
Q

Peaked T wave ECG causes

A

hyperkalaemia

myocardial ischaemia

67
Q

Causes of RBBB

A

normal variant - more common with increasing age
right ventricular hypertrophy
chronically increased right ventricular pressure - e.g. cor pulmonale
pulmonary embolism
myocardial infarction/ischaemia
atrial septal defect (ostium secundum)
cardiomyopathy or myocarditis

68
Q

Aortic dissection Features

A

severe tearing chest pain, unequal BP in arms
widened mediastinum on chest x-ray
false lumen on CT angiography

69
Q

Pneumonia : caused by legionella pneumphillia

A

dry cough and atypical chest signs, hyponatraemia and lymphopenia

70
Q

Pneumonia: Pneumocystis jiroveci

A

a history of HIV, dry cough, exercise-induced desaturations and the absence of chest signs