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Phase 3a > General Medicine > Flashcards

General Medicine Flashcards

1
Q

What effect does metronidazole have on INR in patient’s on Warfarin?

A

Increases INR (increased haemorrage risk)

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2
Q

What drugs decrease INR (clotting) in patients on warfarin? (3)

A

Carbamazepine (epilepsy)
Phenytoin (epilepsy)
Rifampicin (TB)

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3
Q

What is the 1st line treatment for pulmonary oedema?

A

Furosemide

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4
Q

Give 2 adverse effects of gentamicin use

A

Ototoxicity (due to auditory or vestibular nerve damage)

Nephrotoxicity (accumulates in renal failure. Toxicity is secondary to acute tubular necrosis)

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5
Q

What condition is gentamicin contraindicated?

A

Myasthenia gravis

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6
Q

At what level does the aorta terminate?

A

The aorta passes from T12 - L4

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7
Q

Give 4 functions of somatostatin

A

Inhibits growth hormone secretion

Inhibits insulin and glucagon secretion

Decreases pancreatic enzyme secretion

Stimulates gastric mucous production

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8
Q

Where is somatostatin produced?

A

Delta cells of the pancreas, pylorus and duodenum

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9
Q

Name a somatostatin analogue and 2 conditions it is used to treat

A

Octreotide

Acromegaly and Oesophageal variceal bleeds

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10
Q

Name 2 antibiotics that inhibit folate synthesis

A

Sulfadiazine (sulphonamide) and Trimethoprim

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11
Q

What class of antibiotic is Doxycycline and what is it’s MOA?

A

Tetracycline

Inhibits protein synthesis

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12
Q

What class of antibiotic is Flucloxacillin and what is it’s MOA?

A

Penicillin

Inhibits peptidoglycan crosslinking (involved in formation of bacterial cell wall)

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13
Q

What class of antibiotic is Gentamycin and what is it’s MOA?

A

Aminoglycoside

Inhibits protein synthesis

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14
Q

What class of antibiotic is Ciprofloxacin and what is it’s MOA?

A

Quinolone

Inhibits DNA synthesis

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15
Q

What class of antibiotic is Sulfadiazine and what is it’s MOA?

A

Sulphonamide

Inhibits folic acid formation

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16
Q

Define Community Acquired Pneumonia (CAP)

A

Describes an acute infection of lung tissue from the community or within 48 hours of hospital admission

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17
Q

What are the most common pathogens causing CAP? (3)

A

Streptococcus pneumoniae (most common)

Haemophilus influenzae (most common in COPD)

Mycoplasma pneumoniae

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18
Q

Define Hospital acquired pneumonia

A

Describes an acute infection of the lung that occurs in a patient >48 hours after hospital admission

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19
Q

What is the most common pathogens causing early onset and late onset HAP?

A

Early onset (<5 days after hospital admission) - Streptococcus pneumoniae

Late onset (>5 days after hospital admission) - Aerobic gram negagive enterobacteria bacilli/rods (pseudomonas aeruginosa, E.coli or Kelbsiella pneumoniae) or Staphylococcus aureus

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20
Q

What pathogen is associated with aspiration pneumonia and what name a characteristic feature.

A

Klebsiella pneumoniae

Red-Currant Jelly sputum

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21
Q

What condition may cause someone to develop aspiration pneumonia

A

Gastro-oesophageal reflux

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22
Q

What is the CURB-65 score?

A

C- Confusion
U- Urea (>7mmol/L)
R- Respiratory Rate >30
B - Blood pressure <90mmHg systolic and/or 60mmHg diastolic

65 - Age >65

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23
Q

How does the CURB-65 score measure severity?

A

0-1 Mild

2 - Moderate

> 3 severe

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24
Q

How is Mild CAP treated? (1st and 2nd line)

A

1st line - Amoxicillin

2nd Line Clarithromycin (if amoxicillin contraindicated)

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25
Q

How is Moderate CAP treated? 1st and 2nd line

A

1st line Dual - Amoxicillin + Clarithromycin

2nd line - Doxycycline if penicillin allergy

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26
Q

What should be offered instead of clarithromycin to pregnant patients with CAP?

A

Erythromycin

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27
Q

What are the 1st and 2nd line treatments for severe CAP?

A

1st line - IV co-amoxiclav and clarithromycin

(Or erythromycin if pregnant)

2nd line - Levofloxacin

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28
Q

How is aspiration pneumonia treated?

A

Co-amoxiclav

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29
Q

Name 2 organisms that cause atypical pneumonia (and name the agar they grow on)

A

Legionella pneumoniae (grows on charcoal agar)

Mycoplasma pneumoniae (eaton agar)

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30
Q

What type of pneumonia is common in patients following influenza infection?

A

Staphylococcus aureus

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31
Q

What type of pneumonia is common in HIV patients?

A

Pneumocystis jirovecii

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32
Q

What bacterium most predominantly causes TB?

A

Mycobacterium tuberculosis

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33
Q

Describe the epidemiology of TB (2)

A

Majority of cases are seen in Sub-saharan Africa and Asia

Common co-infection seen in HIV patients

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34
Q

What pathogen commonly causes pneumonia in patients with undiagnosed HIV?

A

Pneumocystis jiroveci (fungal)

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35
Q

Which white cell type is raised in viral infections?

A

Lymphocytes

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36
Q

Which white cell type is raised in bacterial infections?

A

Neutrophils

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37
Q

Where in the lungs does TB commonly localize?

A

Upper-middle portion (apex) of the lungs

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38
Q

What type of hypersensitivity reaction is seen in TB infection? What cells mediate this?

A

Type 4 hypersensitivity reaction

Mediated by T cells

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39
Q

In TB, the mycobacterium promotes recruitment of macrophages, what 2 changes do macrophages cause?

A

Formation of multinucleated giant cells (granulomas)

Formation of epithelioid cells

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40
Q

Describe the consistency of granulomas (TB) (2)

A

Caseous or cheese-like on examination.

Rich in mycolic acid, inducing granulomatous necrosis which may lead to cavitation.

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41
Q

Give 7 clinical features of TB

A

Low grade fever

Weight loss

Night sweats

Cough +/- sputum

Haemoptysis

Malaise

Clubbing (bronchiectasis)

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42
Q

Give 4 extrapulmonary features of TB

A

Lymphadenopathy

Ileocecal perforation/obstruction

Addison’s disease

Lupus vulgaris (jelly like nodules)

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43
Q

Give 2 diagnostic tests for TB

A

Ziehl-Neelsen stain (Acid fast bacilli smear)

Lowenstein-Jensen media (gold standard for mycobacterium culture)

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44
Q

What is the treatment regimen for TB? (4)

A

RIPE

Rifampicin (6 months)

Isoniazid (6 months)

Pyrazinamide (first 2 months)

Ethambutol (first 2 months)

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45
Q

Give 2 side effects of Rifampicin

A

Hepatitis

Red-orange body secretions

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46
Q

Give 2 side effects of isoniazid

A

Hepatitis

Neuropathy (tingling hands/feet)

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47
Q

What should be given in conjunction with isoniazid to prevent neuropathy?

A

Pyridoxine (vitamin B6)

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48
Q

Give 3 side effects of pyrazinamide

A

Hepatitis

Arthralgia/gout

Rash

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49
Q

Give 2 side effects of ethambutol

A

Optic neuritis

Visual impairment

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50
Q

What is the 1st line investigation for TB? What would it show?

A

Chest X-ray

Shows fibronodular opacities in the upper lobes (apices)

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51
Q

How does acute bronchitis typically present? And when?

A

Presents in autumn or winter

Presents with acute onset of;
Cough (may or may not be productive)
Sore throat
Runny nose
Wheeze

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52
Q

How is acute bronchitis managed?

A

Typically resolves in 3 weeks

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53
Q

When and which antibiotics (1st and 2nd line) are considered in acute bronchitis? (3)

A

1st line - Doxycycline (not in children/pregnant women)
2nd line - Amoxicillin

Consider if;
Patient is systemically unwell
Has pre-existing co-morbidities
Has CRP >100mg/L

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54
Q

What pathogen typically causes rheumatic fever?

A

Group A Streptococcus (Streptococcus pyogenes)

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55
Q

Describe the pathophysiology of rheumatic fever

A

Occurs due to molecular mimicry between streptococcal M protein and human cardiac myosin proteins

Similarities between the two results in antibody and T-cell activation, resulting in an immune response against both streptococcal and human proteins, resulting in tissue injury.

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56
Q

How is rheumatic fever diagnosed?

A

Requires either;

2 major criteria
or
1 major and 2 minor criteris

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57
Q

Give 5 major criteria for rheumatic fever

A

Erythema Marginatum (painless, nonpruritic pink/light red rash on trunk and limbs - face is spared)

Sydenham’s chorea (involuntary, irregular, non-repetitive movements of limbs, neck, head and/or face)

Polyarthritis

Carditis and valvitis

Subcutaneous nodules (firm and painless)

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58
Q

Give 4 minor criteria for rheumatic fever

A

Raised ESR/CRP

Pyrexia

Arthralgia

Prolonged PR interval

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59
Q

How is Rheumatic Fever managed? (2)

A

Antibiotics - Oral Penicillin V

NSAIDs

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60
Q

What cardiac condition is seen in rheumatic fever? What would be heard on auscultation?

A

Mitral stenosis (mid-late diastolic murmur)

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61
Q

How is asymptomatic mitral stenosis managed?

A

Monitor with regular echocardiography

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62
Q

What laboratory findings would confirm group A streptococcal infection in rheumatic fever (2)

A

Elevated Antistreptolysin O

Elevated Antistreptococcal DNAase B

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63
Q

What would an ECG likely show in Rheumatic Fever?

A

PR prolongation

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64
Q

How is symptomatic mitral stenosis managed? (2)

A

Percutaneous mitral balloon valvotomy

Mitral valve surgery (commissurotomy or valve replacement)

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65
Q

What medical management should be offered to patients who develop atrial fibrillation from mitral stenosis?

A

Warfarin (Moderate/Severe) or DOAC (mild)

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66
Q

Describe the location of each heart valve on auscultation

A

Aortic valve - Right 2nd intercostal space

Pulmonary valve - Left 2nd/3rd intercostal space

Tricuspid valve - Left 4th/5th intercostal space

Mitral Valve - Left 5th intercostal space

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67
Q

Is the mitral valve best heard on inspiration or expiration?

A

Expiration

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68
Q

What are the 3 main branches of the aorta?

A

Brachiocephalic artery (splits into right common and right subclavian)

Left common carotid

Left subclavian artery

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69
Q

Give 4 clinical symptoms of aortic stenosis

A

Triad of; Angina, Syncope and Heart Failure (elderly patient)

Chest pain

Exertional dyspnoea

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70
Q

What clinical signs are likely seen in aortic stenosis? (3)

A

Ejection systolic murmur

Slow rising pulse (pulsus tardus) with narrow pulse pressure

Soft/absent S2 sound

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71
Q

What may be seen on echocardiogram in aortic stenosis

A

Left ventricular hyperetrophy

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72
Q

How is aortic stenosis managed? (2)

A

TAVI - Transcatheter aortic valve implementation

Infective endocardtits prophylaxis

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73
Q

Give 1 acute and 2 chronic cause of aortic regurgitation

A

Acute - Infective endocarditis

Chronic - Bicuspid aortic valve (most common) and rheumatic fever

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74
Q

Give 3 risk factors for aortic regurgitation

A

SLE/RA

Marfan’s syndrome/Ehler’s Danlos Syndrome

Infective endocarditis

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75
Q

Marfan’s syndrome occurs due to a mutation in what protein?

A

Fibrillin 1

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76
Q

Ehler’s Danlos syndrome occurs due to a mutation in what protein?

A

COL1A2 (Type I collagen)

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77
Q

What clinical signs are seen in Aortic regurgitation? (3)

A

High pitched End Diastolic Murmur

Collapsing Pulse (waterhammer)

Wide Pulse Pressure

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78
Q

What 2 features may be seen on echocardiogram in a patient with mitral regurgitation?

A

Left atrial dilation (due to pulmonary hypertension)

Left ventricular hypertrophy

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79
Q

Give 3 clinical signs of mitral regurgitation

A

Pansystolic murmur (heard at apex, radiating to axilla)

Quiet S1

3rd heart sound

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80
Q

What is the most common cause of Mitral Stenosis?

A

Rheumatic Fever (Streptococcus pyogenes infection)

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81
Q

How may mitral stenosis present? (3)

A

Symptoms of pulmonary hypertension (dyspnoea, oedema, haemoptysis, chronic bronchitis)

Malmar flush

Atrial fibrillation

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82
Q

Give 3 clinical signs of mitral stenosis

A

Rumbling mid-diastolic murmur

Loud S1

Prominent A wave on JVP

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83
Q

What pathogen most commonly causes infective endocarditis?

A

Staphylococcus aureus

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84
Q

What pathogen commonly causes infective endocarditis in patients with poor dental hygeine?

A

Streptococcus viridans

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85
Q

What pathogen most commonly causes infective endocarditis in patients following prosthetic valve surgery?

A

Coagulase negative Staphylococci - Staphylococcus epidermidis

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86
Q

What pathogen most commonly causes infective endocarditis in patients following prosthetic valve surgery?

A

Coagulase negative Staphylococci - Staphylococcus epidermidis

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87
Q

What antibiotics are given to patients with a native valve infective endocarditis caused by staphylococci? (1st and 2nd line)

A

1st line - Flucloxacillin

2nd line - Vancomycin + Rifampicin (if penicillin allergy or MRSA)

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88
Q

What antibiotic treatment is given to patients with prosthetic valve infective endocarditis caused by staphylococci? (1st and 2nd line)

A

1st line - Flucloxacillin + Rifampicin + Low dose Gentamicin

2nd line - Vancomycin + Rifampicin + Low dose gentamicin (if penicillin allergy or MRSA)

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89
Q

What antibiotic treatment is given to patients with infective endocarditis caused by a fully sensitive streptococci (e.g viridans)? (1st and 2nd line)

A

1st line - Benzylpenicillin

2nd line - Vancomycin + low dose gentamicin

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90
Q

What is the function of the parathyroid glands? (2)

A

Regulate calcium through production of parathyroid hormone.

Secreted in response to low ionized calcium levels

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91
Q

Give 4 actions of parathyroid hormone

A

Increases osteoclast activity (releasing calcium and phosphate from bone)

Enhances distal tubular resorption of calcium

Decreases renal tubular resorption of phosphate

Increases production of 1,25 dihydroxy-vitamin D3

Net effect is to increase calcium and decrease phosphate

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92
Q

Define primary hyperparathyroidism

A

Describes overactivation of the parathyroid glands, resulting in excess release of PTH, leading to symptoms of hypercalcaemia

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93
Q

What is the most common cause of primary hyperparathyroidism?

A

Solitary adenoma

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94
Q

Give 5 clinical features of hyperparathyroidism (hypercalcemia)

A

Polydispia/Polyuria (nephrogenic Diabetes insipidus)

Bone pain

Abdominal pain

Weak, Tired, Depressed

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95
Q

What blood test results suggest primary hyperparathyroidism? (4)

A

High PTH

High Calcium

High Alkaline Phosphatase

Low Phosphate

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96
Q

How is primary hyperparathyroidism managed? (2)

A

1st line - Parathyroidectomy

2nd line - Cinacalcet (used in patients too frail for surgery)

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97
Q

What is the MOA of Cinacalcet

A

Increases sensitivity of calcium receptors on parathyroid cells, reducing PTH levels and ultimately reducing calcium levels.

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98
Q

What are the most common causes of secondary hyperparathyroidism? (2)

A

Chronic Kidney Disease

Vitamin D deficiency

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99
Q

What blood results would be seen in secondary hyperparathyroidism? (5)

A

High PTH

Low Calcium

High Alkaline phosphatase

Low Phosphate

Low Vitamin D

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100
Q

What is the MOA of dabigatran?

A

Direct thrombin inhibitor

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101
Q

What is the MOA of Rivaroxaban and Apixaban?

A

Direct factor Xa inhibitors

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102
Q

What is the MOA of heparin?

A

Activates antithrombin III

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103
Q

What is the MOA of Warfarin?

A

Inhibits Factors II, VII, IX, X (1972)

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104
Q

Define hereditary spherocytosis

A

Describes an autosomal dominant haemolytic anaemia caused by a defect in the red blood cell cytoskeleton

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105
Q

What shape red blood cells are seen in spherocytosis?

A

Sphere shaped

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106
Q

Give 4 clinical features of hereditary spherocytosis

A

Failure to thrive

Jaundice/gall stones

Splenomegaly

Aplastic crisis precipitated by parvovirus infection

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107
Q

What laboratory results would be seen in hereditary spherocytosis? (3)

A

Spherocytes (spherical red blood cells)

Raised MCHC - Mean corpuscular haemoglobin Concentration

Increase in reticulocytes

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108
Q

What test is used to diagnose hereditary spherocytosis?

A

EMA binding test

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109
Q

Give 5 common symptoms of hypercalcaemia

A

‘stones, bones, groans and psychic overtones’

Abdominal pain

Constipation

Increased confusion/lethargy

Gout

Postural hypotension

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110
Q

Hypercalcaemia is a common side effect of what drug?

A

Bendroflumethiazide

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111
Q

How is hypercalcaemia managed?

A

IV 0.9% sodium chloride

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112
Q

Give 3 common biochemical side effects of bendroflumethiazide

A

Hypercalcaemia

Hypokalaemia

Hyponatraemia

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113
Q

What is the MOA of thiazide diuretics? (bendroflumethiazide)

A

Inhibit sodium reabsorption at the distal convoluted tubule by blocking the Na/Cl symporter

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114
Q

What is the 1st and 2nd line investigations for acromegaly?

A

1st line - Serum IGF-1 levels

2nd line (if above positive) - OGTT and serial Growth hormone levels (confirms diagnosis)

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115
Q

Give 6 features of hypokalaemia in adults

A

Weakness

Constipation

Leg cramps

Cardiac arrhythmias (U waves, T wave flattening)

Rhabdomyolysis (severe)

Ascending paralysis (severe)

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116
Q

Give 4 causes of hypokalaemia

A

Drugs - (thiazides, loop diuretics), laxatives, glucocorticoids, penicillins

GI loss - Diarrhoea, vomiting, ileostomy

Salbutamol/Beta agonists

Magnesium depletion

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117
Q

How is severe (<2.5mmol/l) or symptomatic hypokalaemia managed?

A

IV KCL in 1L 0.9 saline

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118
Q

How is hypomagnesmia managed in a hypokalemia patient?

A

Initially give MgSO4 diluted with NaCL over 20 mins, then start KCL infusion

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119
Q

What ECG findings are present in hyperkalaemia? (4)

A

Tall Tented T waves

Prolonged PR interval

Absent/flat P wave

Widening QRS complex

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120
Q

What is the normal range for potassium in the blood?

A

3.5-5.0mmol/L

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121
Q

Give 4 clinical features of hyperkalaemia

A

Muscle weakness

Muscle stiffness

Fatigue

Arrhythmia (cardiac arrest)

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122
Q

What drugs can increase risk of hyperkalaemia?

A

ACEi

ARBs

Potassium sparing diuretics (spironolactone)

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123
Q

Define mild, moderate and severe hyperkalaemia

A

Mild - 5.5-5.9 mmol/L
Moderate - 6.0 -6.4 mmol/L
Severe - >6.5 mmol/L

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124
Q

How is hyperkalaemia managed (severe)? (4)

A

Stabilise cardiac membrane - IV calcium gluconate

Shift K from ECF to ICF - Insulin/dextrose infusion +/- nebulised salbutamol

Stop exacerbating drugs

IV bicarbonate if acidotic

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125
Q

What else can be used to facilitate the removal of potassium from the body in hyperkalaemia? (3)

A

Calcium resonium

Loop diuretics

Dialysis (consider in patients with AKI and persistent hyperkalaemia)

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126
Q

How may hypokalaemia present on ECG? (4)

A

Flattening T wave

Prolonged PR

QT prolongation

Prominent U waves

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127
Q

Define angina

A

Describes chest pain caused by insufficient blood supply to the heart muscle.

Myocardial oxygen demand transiently exceeds the supply, resulting in reversible myocardial ischemia

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128
Q

Name 4 types of angina

A

Stable angina

Unstable angina

Prinzmetal angina

Syndrome X

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129
Q

Describe stable angina

A

Describes chest discomfort that is worsened by exertion and relieved by rest or nitroglycein (GTN spray)

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130
Q

Describe unstable angina

A

Describes chest discomfort occurring on minimal exertion or at rest.

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131
Q

Describe prinzmetal angina. Give 4 causes

A

Describes angina that occurs at rest due to coronary vasospasm

Causes;
Cocaine
Marijuana
Amphetamine
Low magnesium

132
Q

Describe syndrome X

A

Describes angina pain + ST elevation on exercise test but with NO evidence of atherosclerosis

133
Q

How does typical angina present? (3)

A

Presents with all 3 of the following

Chest pain precipitated by physical exertion (or emotion, cold weather and heavy meals)

Constricting discomfort in the chest, neck, shoulders, jaw or arms

Relieved by rest or GTN spray

134
Q

Describe atypical angina

A

Presents with 2 features of typical angina and atypical symptoms, such as;

Gastrointestinal discomfort
Breathlessness
Nausea

135
Q

What diagnostic test is used to confirm angina?

A

CT coronary angiography

136
Q

What ECG signs may indicate previous MI or ischemia in a patient presenting with angina? (4)

A

Pathological Q waves

LBBB

ST elevation

Flat/inverted T waves

137
Q

What is the 1st and 2nd line treatment for angina?

A

1st line - GTN spray + Beta blocker/Calcium channel blocker

2nd line - Isosorbide mononitrate

138
Q

What CCB should be used in angina monotherapy?

A

Rate-limiting CCB - Verapamil/Diltiazem

139
Q

What CCB should be used in conjunction with a Beta Blocker in angina treatment?

A

Slow release dihydropyridine - Nifedipine

140
Q

What medication should not be taken with isosorbide mononitrate? and why?

A

Phosphodiesterase inhibitors (sildenafil)

Can cause excessive hypotension

141
Q

How do Beta Blockers reduce symptoms of angina?

A

Act as negative inotropes (reduce force of contraction)

142
Q

How do CCBs reduce symptoms of angina?

A

Act as primary arteriodilators

Dilate systemic arteries so reduces afterload (reducing blood pressure)

143
Q

Name 2 surgical interventions used in patients with advanced IHD (who have failed to restore coronary artery flow)

A

Percutaneous coronary intervention (PCI - Stenting)

Coronary Artery Bypass Graft (CABG)

144
Q

What artery is used in CABG?

A

Left internal mammary artery.

Used to bypass proximal stenosis in the Left Anterior Descending Artery

145
Q

How is essential hypertension defined?

A

Blood pressure >140/90mmHg

146
Q

Define malignant hypertension. Give 3 symptoms

A

Describes an acute, rapid rise in blood pressure, leading to severe vascular damage.

Presents with severe hypertension >180/120mmHg

Symptoms include;
Bilateral retinal haemorrhage +/- papilloedema
Headache
Visual disturbance

147
Q

Define Masked Hypertension

A

Describes when clinical blood pressure readings are <140/90 but ABPM/HBPM is much higher

148
Q

Describe how blood pressure is measured in a clinical setting

A

Measured using a Sphygmomanometer

Measure blood pressure in both arms

If difference between arms is >15mmHg then repeat

If difference remains >15mmHg then measure subsequent pressures form arm with higher reading

149
Q

What investigations should be offered to all patients with hypertension? (4)

A

Test for proteinuria (albumin:creatinine ratio and haematuria)

Measure HbA1c, electrolytes, creatinine, eGFR, total cholesterol and HDL cholesterol

Examine fundi (hypertensive retinopathy)

Arrange ECG

150
Q

Describe the treatment regimen for patients with hypertension who either have type 2 diabetes, are <55 or are NOT afro-carribbean (1st, 2nd and 3rd line)

A

1st line - ACEi (ramipril) or ARB (losartan)

2nd line - ACEi/ARB + Calcium Channel Blocker (nifedipine/amlodipine)

3rd line - ACEi/ARB + CCB + Thiazide like diuretic (indapamide)

151
Q

Describe the treatment regimen for patients withy hypertension who; do NOT have type 2 diabetes, are >55 or are Afro-Carribbean.

A

1st line - Calcium channel blocker (nifedipine/amlodipine)

2nd line - CCB + ACEi/ARB (ramipril/losartan)
(Consider ARB >ACEi in afrocarribbean)

3rd line - CCB + ACEi/ARB + Thiazide like diuretic (indapamide)

152
Q

Describe the 4th line treatment for hypertension. What does it depend on?

A

Depends on blood potassium levels

If blood potassium <4.5mmol/L - Spironolactone

If blood potassium >4.5mmol/L - Alpha blocker (doxasin/tamulosin) or Beta blocker

153
Q

What type of diuretic is spironolactone?

A

Aldosrterone antagonist (potassium sparing diuretic)

154
Q

Give 2 common side effects of spironolactone

A

Hyperkalaemia

Gynaecomastia

155
Q

Give 3 common side effects of ACE inhibitors

A

Dry Cough

Hyperkalaemia

May lower blood glucose in diabetics

156
Q

Give 1 common side effect of calcium channel blockers

A

Oedema

157
Q

Give 4 contraindications for calcium channel blocker use

A

Angina (stable/unstable)

Cardiogenic shock

Aortic stenosis

MI in last month

158
Q

What pulse is seen in atrial fibrillation?

A

Irregularly irregular pulse

159
Q

What pulse is seen in atrial fibrillation?

A

Irregularly irregular pulse

160
Q

Name 3 types of atrial fibrillation

A

Paroxysmal AF (self-terminating)

Persistent AF

Permanent AF

161
Q

Define paroxysmal AF (self-teminating)

A

Describes episodes lasting >30 seconds for <7 days that are self-terminating and recurrent.

162
Q

Define persistent AF

A

Describes episodes of AF lasting >30 seconds or <7 days BUT require pharmacological or electrical cardioversion

163
Q

Describe permanent AF

A

Describes AF that;

Fails to terminate following cardioversion

AF that is terminated but relapses in 24 hours

Longstanding AF (usually >1 year) in which cardioversion has not been indicated or attempted

164
Q

What are the most common complications of AF?

A

Thromboembolism > Stroke

165
Q

Give 3 common causes of AF

A

Heart Failure

Ischemic Heart Disease

Hypertension

166
Q

Give 5 symptoms of AF

A

Dyspnoea

Palpitations (irregularly irregular pulse)

Chest pain

Syncope/dizziness

Stroke/TIA

167
Q

What is used to confirm diagnosis of AF? What would it show?

A

ECG

Shows;
Absent P waves
Irregularly irregular pulse

168
Q

What risk score is used to assess stroke risk in AF?

A

CHA2DS2 VASc

169
Q

What risk score is used to assess bleeding risk in AF? When should it be used?

A

HAS-BLED/ORBIT

Used to assess bleeding risk when considering starting anti-coagulation in AF AND when reviewing patients already on anticoagulants

170
Q

How is acute atrial fibrillation managed?

A

Antiarrhythmic + Anticoagulant
Amiodarone/Flecanide + Heparin/DOAC

171
Q

Describe the moa of amiodarone. Give 1 side effect

A

Blocks potassium currents (in 3rd phase of cardiac action potential)

Contains iodine so can cause hyperthyroidism

172
Q

Describe the moa of flecainide. Who should it not be given to?

A

Prolongs depolarization by binding to fast-inward sodium channels. Also blocks potassium currents (similar to amiodarone)

Should be avoided in patients with structural heart defects, heart failure or IHD

173
Q

How is chronic AF managed? (2)

A

Rate or rhythm control

174
Q

Describe Rate Control of AF. 1st and 2nd line.

A

Involves accepting the fact that the patients pulse will be irregular but slow the rate down to avoid negative effects.

1st line - Beta blocker or RL calcium channel blocker (diltiazem/nifedipine)

Avoid CCB if patient has AF with HF

2nd line - Add digoxin

Long term anticoagulation (warfarin/DOAC)

175
Q

What is the MOA of digoxin?

A

Positive inotrope (increases contractility) + Negative chromotrope (decreases rate)

Inhibits Na/K ATPase

176
Q

When should Rhythm Control (cardioversion) be offered to patients with AF?

A

Offered to patients who continue to have symptoms after heart rate control or for whom rate control has not been successful.

177
Q

Describe 2 types of rhythm control (cardioversion) in AF.

A

Electrical cardioversion - Offered to patients whom AF has persisted for >48 hours

Pharmaceutical cardioversion - Flecainide

178
Q

Describe CHA2DS2-VASc score

A

Congestive Heart Failure
Hypertension
Age >75
Age 65-74
Diabetes
Stroke/TIA
Vascular disease
Sex (female)

179
Q

What ECG finding is present in atrial flutter?

A

Sawtooth patten of inverted flutter waves (in leads II, III and AvF)

180
Q

Define UTI. How is it characterised?

A

UTI describes an inflammatory response of the urothelium to bacterial invasion.

Characterised by;
Bacteriuria (bacteria in urine)
and
Pyuria (pus/leukocytes in urine)

181
Q

How are UTIs classified?

A

Upper - Pyelonephritis (infection of kidney/renal pelvis)

Lower - Cystitis (bladder), Prostatitis (prostate), Urethritis (ureter)

182
Q

Describe uncomplicated and complicated UTIs

A

Uncomplicated - Normal renal tract function and structure

Complicated - Structural/functional abnormality of GU tract

183
Q

Complicated UTIs include (7)

A

Pregnant women

Male

Children

Recurrent UTIs

Elderly

Abnormality in urinary tract (stones, obstruction)

Catheterisation

184
Q

What pathogen most commonly causes uncomplicated UTI

A

E.coli

185
Q

What are the 5 most common pathogens causing UTIs? (KEEPS)

A

Klebsiella (catheterisation/hospital associated)

E.coli (most common)

Enterococci

Proteus (renal stones)

Staphylococcus aureus (deep seated infection)

186
Q

Give 5 risk factors for UTIs

A

Female (due to short urethra and proximity to anus)

Sexual intercourse

Decreased urinary flow (dehydration/obstruction)

Pregnancy

Post menopause

187
Q

Give 5 classic signs of UTI

A

Bacteriuria

Pyuria (pus/leukocytes)

Dysuria (painful urination)

Cloudy urine

New nocturia

188
Q

Give 5 classic signs of UTI

A

Bacteriuria

Pyuria (pus/leukocytes)

Dysuria (painful urination)

Cloudy urine

New nocturia

189
Q

Give 6 symptoms of cystitis (bladder inflammation)

A

Dysuria (burning pain when urinating)

Frequency/urgency

Polyuria

Haematuria

Suprapubic tenderness

Foul smelling urine (streptococcus pyogenes infection)

190
Q

Give 3 symptoms of acute pyelonephritis (inflammation of kidney/renal pelvis)

A

Fever/rigors

Loin pain/tenderness

Vomiting

191
Q

Give 4 symptoms of prostatitis (prostate inflammation)

A

Dysuria

Pain (lower back, perineum, rectum, scrotum)

Fever, malaise, nausea

Swollen/tender prostate on PR

192
Q

What is the 1st line investigation for UTI in non-pregnant women?

A

Urine dipstick

193
Q

What is the 1st line investigation for UTI in pregnant women, men, children <16?

A

Urine culture and antibiotic sensitivity

194
Q

What are the 1st and 2nd line treatments for lower UTI in non-pregnant women >16?

A

1st line - Nitrofurantoin

2nd line - Pivmecillinam (penicillin) or Fosfomycin

195
Q

What are the 1st and 2nd line treatments for UTI in pregnant women >12?

A

1st line - Nitrofurantoin (don’t use in 3rd trimester)

2nd line - Amoxicllin or Cefalexin

196
Q

What is the 1st line treatment for UTI in men aged >16?

A

Trimethoprim or Nitrofurantoin (if eGFR <25ml/min)

197
Q

What is the 1st line treatment for acute pyelonephritis in non pregnant women and men >16?

A

1st line oral antibiotic - Cefalexin

1st line IV antibiotic (if vomiting or unable to take oral) - Co-amoxiclav

198
Q

What is the 1st line antibiotic treatment for acute pyelonephritis in pregnant women >12?

A

1st line oral antibiotic - Cefalexin

1st line IV antibiotic - Cefuroxime

199
Q

How is cardiac output calculated?

A

CO = Heart rate x Stroke volume

200
Q

Define stroke volume

A

Volume of blood ejected from the left ventricle during systole

201
Q

Define end diastolic volume

A

Volume of blood in the ventricles at the end of diastole

202
Q

Define heart failure

A

Describes an inefficiency of the heart as a pump. Cardiac output is inadequate for the body’s requirements.

203
Q

Name 2 types of Heart Failure

A

Heart failure with Reduced Ejection Fraction (HF-REF)

Heart failure with Preserved Ejection Fraction (HF-PEF)

204
Q

Define HF-REF. Give 3 causes

A

Describes an inability of the ventricles to contract resulting in decreased cardiac output

Causes;
IHD
MI
Cardiomyopathy

205
Q

Define HF-PEF. Give 3 causes

A

Describes an inability of the ventricles to relax and fill normally (due to abnormal thickening/stiffening of cardiac muscle) resulting in creased filling pressures

Causes;
Ventricular hypertrophy
Constrictive pericarditis
Tamponade

206
Q

Give 5 symptoms of chronic heart failure

A

Dyspnoea (on exertion, at rest or when lying flat) - May get paroxysmal nocturnal dyspnoea)

Fatigue

Peripheral oedema

Cold peripheries

Increased weight (oedema) + Cachexia (muscle wasting)

207
Q

What is used to classify heart failure?

A

New York Classification

208
Q

Describe the New York Classification of Heart Failure (4)

A

Class I - No limitation to physical activity

Class II - Slight limitation - comfortable at rest but ordinary physical exercise causes symptoms (mild HF)

Class III - Marked limitation - comfortable at rest but less than ordinary physical exercise causes symptoms

Class IV - inability to carry out physical activity without discomfort

209
Q

Describe the MRC breathlessness criteria for assessing dyspnoea (5)

A

0 - No breathlessness except with strenuous exercise

1 - SoB when hurrying on level or walking up slight hill

2 - Walks slower than people of same age due to SoB or has to stop for breath when walking at own pace

3 - Stops for breath after walking 100m or after a few minutes of walking

4- too breathless to leave the house or breathless when dressing

210
Q

What blood test result is likely raised in heart failure?

A

NT-proBNP (indicates increased wall tension)

211
Q

What would a chest X-ray likely show in heart failure? (ABCDE)

A

A- Alveolar oedema
B- Kerley B lines
C- Cardiomegaly
D- Dilated prominent upper lobe veins
E- Pleural effusions

212
Q

What is the 1st line treatment for HF-PEF?

A

Low dose loop diuretic - Furosemide

213
Q

What is the 1st and 2nd line treatment for HF-REF?

A

1st line - ACEi (ramipril) + Beta blocker (bisoprolol)

2nd line - Aldosterone antagonist (spironolactone)

214
Q

What should be offered to patients with HF-REF whom cannot tolerate ACEi/ARBs?

A

Hydralazine (vasodilator) with nitrate

215
Q

What medication should be avoided in HF-REF?

A

Calcium channel blockers

216
Q

Give 5 symptoms of acute heart failure

A

Dyspnoea, Orthopneoa, Pink frothy sputum

Cyanosis/pale

Sweaty

Tachypnoea

Pulsus alterans (alternating strong and weak pulses - indicates LV dysfunction)

217
Q

Give 1 side effect of furosemide (loop diuretic)

A

hypocalcemia

218
Q

Describe the initial management of acute heart failure (3)

A

Diamorphine

Diuretics (furosemide)

Ventilation (if resp failure or cardiogenic pulmonary oedema)

219
Q

What treatment is given once a patient with acute heart failure is stable?

A

Beta blocker + ACEi (or ARB)

220
Q

Give 5 symptoms of STEMI

A

Acute central chest pain lasting >20 minutes (may radiate to jaw, arm or back)

Nausea

Sweatiness

Palpitations

Dyspnoea

221
Q

What may be seen on an ECG in STEMI? (2) What blood test should also be performed?

A

ST elevation

Pathological Q waves

Blood test - Troponin (raised)

222
Q

Describe the immediate management of STEMI (MONA)

A

M- Morphine
O - O2 (if sats <94%)
N - Nitrates
A - Aspirin (offer ASAP) with ticagrelor

223
Q

What should be offered with aspirin in the immediate management of STEMI if the patient has a high bleeding risk?

A

Clopidogrel (P2Y12 receptor antagonist)

224
Q

Name 2 forms of reperfusion therapy used in STEMI management. When is each performed?

A

Angiography with Primary PCI - Offered if presenting within 12 hours of symptoms and PCI can be delivered in 2 hours

Fibrinolysis (streptokinase/alteplase) - Offered if presenting in 12 hours of symptoms and PCI cannot be delivered in 120 minutes

225
Q

In a patient having PCI, what medication should they be given (prior to the PCI)? (1st and 2nd line)

A

1st line - Aspirin + Prasugrel

2nd line - Aspirin + Clopidogrel (if patient is on anticoagulant)

226
Q

What is the MOA of streptokinase/alteplase

A

Thrombolytics - Activate plasminogen to form plasmin which degrades fibrin, leading to breakdown of thrombi

227
Q

Describe the secondary prevention for STEMI (prevent future MIs - ADBSA)

A

A - ACEi (ramipril) or ARB (candesartan)
D - Dual antiplatelet therapy - Clopidogrel and Aspirin
B - Beta blocker - Propranolol
S - Statin (atorvastatin)
A - Aldosterone antagonist (spironolactone)

228
Q

What would an ECG show in NSTEMI and Unstable angina? What blood test should be performed?

A

ST depression

Deep T wave inversion

No pathological Q waves

Blood test - troponin (raised)

229
Q

Describe the immediate management of NSTEMI (3)

A

Aspirin (ASAP)

Fondaparinux (antithrombin)
- Give Dalteparin or IV dose adjusted heparin where therapeutic range of anticoagulation is required (prosthetic valves, AF with thromboembolism ect)

MONA

230
Q

What can occur 2-6 weeks following MI? Describe it. How may it present? (4)

A

Dressler’s syndrome

Describes autoimmune reaction to antigenic proteins formed as myocardium recovers.

Characterised by;
Fever
Plueritic pain
Pericardial effusion
Raised ESR

231
Q

Describe the pain in pericarditis

A

Pain worse when lying down

232
Q

Define addisonian crisis

A

Describes an acute severe glucocorticoid deficiency requiring immediate emergency treatment

233
Q

Gave 3 precipitating factors for addisonian crisis

A

Stress in patients witn underlying adrenal insufficiency

Sudden discontinuation of glucocorticoids after prolonged glucocorticoid therapy

Bilateral adrenal haemorrhage or infarction (watrerhous-Friderichsen syndrome)

234
Q

Give 4 symptoms of addisonian crisis

A

Hypotension/shock

Impaired consciousness

Fever

Vomiting/diarrhoea/severe abdominal pain

235
Q

What investigation results would likely be seen in addisonian crisis? (4)

A

Hyponatremia

Hyperkalemia

Hypoglycemia

Metabolic acidosis

236
Q

How is addisonian crisis managed? (2)

A

IV hydrocortisone (1st line)

Saline + dextrose (if hypoglycemia)

237
Q

Name 2 types of gout

A

Monosodium Urate Crystals (gout)

Calcium pyrophosphate crystals (pseudogout)

238
Q

How does monosodium urate crystal gout appear histologically?

A

Needle shaped, negatively bifringent crystals under polarized light

239
Q

How does calcium pyrophosphate crystals (pseudogout) appear histologically?

A

Small rhomboid brick shaped, positively bifringent under polarised light.

Pyrophosphate crystals

240
Q

Name 4 drugs that increase the risk of gout, and why?

A

Aspirin, Indapamide, Tacrolimus (severe eczema), Pyrazinamide

Reduce urate excretion

241
Q

What diagnostic test is required to diagnose gout?

A

Joint aspiration with synovial fluid analysis

242
Q

How is gout treated? (3)

A

Stop diuretics (like indapamide) and switch to ARB (losartan promotes uric acid excretion)

Acute - NSAIDs

Recurrent;
-Allopurinol (xanthine oxidase inhibitor)
- Probenexid (uricosuric agent)
- Rasburicase (recombinant urate oxidase)

243
Q

Give 1 side effect of Probenecid

A

Kidney stones (so use is contraindicated in a patient with kidney stones)

244
Q

When should allopurinol be discontinued?

A

If patient develops a rash

245
Q

What diet can help reduce risk of developing gout?

A

High dairy diet

246
Q

How do CCBs work?

A

Act to as smooth muscle dilators, allowing for vasodilation of arteries.

Act as a negative inotrope (reduces hearts force of contractility)

247
Q

What effect does digoxin have on the heart?

A

Positive inotrope (increases force of contractility)

Negative chronotrope (decreases rate)

248
Q

Describe the typical ‘exam’ presentation of a patient with Rhabdomyolysis

A

A patient who has had a fall or prolonged epileptic seizure and is found to have an acute kidney injury on admission

249
Q

Define rhabdomyolysis

A

Describes the breakdown of skeletal muscle

250
Q

Describe the pathophysiology of rhabdomyolysis

A

Creatinine phosphokinase and serum myoglobin are released into blood > Pigment nephropathy > acute tubular necrosis > AKI

251
Q

what triad of symptoms is typically seen in rhabdomyolysis

A

Triad;
Myalgia
Generalised weakness
Darkened urine (tea coloured)

252
Q

What biochemical changes are likely seen in rhabdomyolysis (5)

A

Elevated creatinine kinase

Myoglobinuria

Hypocalcemia (myoglobin binds calcium)

Hyperphosphatemia (released from myocytes)

Metabolic acidosis

253
Q

What is Crush syndrome?

A

Rhabdomyolysis + Hypovolemia and Shock

(systemic manifestation of crush injury)

254
Q

What combination of drugs can cause rhabdomyolysis

A

Statins + Clarithromycin

255
Q

How is rhabdomyolysis managed? (1)

A

IV fluid resuscitation

Urine alkalization - Sodium bicarbonate IV promotes renal excretion
(may be required but not recommended)

256
Q

Define AKI. How is it typically characterised?

A

Describes an acute decline in kidney function resulting in a failure to maintain fluid, electrolyte and acid-base homeostasis

Typically characterised by;
- Increase in serum creatinine
- Decrease in Urine Output

257
Q

Name 3 types of AKI

A

Pre-renal (most common)

Renal (intrinsic)

Post renal (obstruction to urine outflow)

258
Q

How is Pre-renal AKI characterised? What may cause it? (3)

A

Characterised by reduced kidney perfusion (blood flow), resulting in ischemia and a reduced eGFR.

Causes;
-Hypovolemia (haemorrhage, burns, pancreatitis)
- Reduced cardiac output
- Renal vasoconstriction (ACEi, ARBs, NSAIDs, loop diuretics)

259
Q

How is renal AKI characterised? What may cause it? (4)

A

Characterised by structural damage to the kidneys.

Causes;
Toxins and drugs (antibiotics, contrast, chemo)
Vascular pathology (vasculitis, thrombosis,haemolytic uraemic syndrome)
Glomerulonephritis
Acute tubular necrosis

260
Q

How is post-renal AKI characterised? What can cause it?

A

Characterised by an acute obstruction of the outflow of urine, resulting in increased intratubular pressure and decreased GFR

Causes include;
Obstruction (renal stones, malignancy, enlarged prostate, blocked catheter)

261
Q

Give 4 complications of AKI

A

Hyperkalaemia

Metabolic acidosis

Peripheral/Pulmonary oedema

Uraemia

262
Q

Give 2 clinical features of AKI?

A

Nausea, vomiting, diarrhoea or evidence of dehydration

Confusion, fatigue or drowsiness

263
Q

Describe the stages of AKI

A

(Units - mL/Min/1.73m2)

Stage 1: >90

Stage 2 : 60-89

Stage 3A: 45-59

Stage 3B: 30-44

Stage 4: 15-29

Stage 5/ESRF: <15

264
Q

Give 4 clinical signs of AKI

A

Reduced urine output (oliguria) or changes in urine colour

Pulmonary/peripheral oedema + basal crepitations

Arrhythmias (due to hyperkalaemia)

Features of uraemia (pericarditis, encephalopathy)

265
Q

What tests should be performed in a patient with AKI? (4)

A

U and E

Urine output

Urine dipstick (ASAP)

Ultrasound (assess kidney size - Small = CKD)

266
Q

How is AKI managed? (3)

A

Pre-renal - Correct volume depletion and/or increase renal perfusion

Renal - Refer for biopsy and specialist treatment

Post-renal - Refer for catheter, nephrostomy or stenting

267
Q

What drugs should be stopped in AKI? (5)

A

ACEi

ARBs

NSAIDs

Gentamicin

Amphotericin (antifungal)

268
Q

Describe the pathology of prostate cancer

A

Majority are multifocal adenocarcinomas sarising in the peripheral zone of the prostate gland

269
Q

Where in the prostate gland does prostate cancer typically arise?

A

Peripheral zone

270
Q

What is the most common cancer that metastasizes to bone?

A

Prostate cancer

271
Q

Give 5 clinical features of prostate cancer

A

Lower back, or bone paion

Nocturia, dysuria or heritancy

Poor stream, dribbling

Weight loss

Haematuria

272
Q

How might prostate cancer feel on PR exam?

A

Hard nodular prostate

273
Q

What score is used to assess the likelihood that a patient has prostate cancer?

A

Likert Score

1- Very unlikely
2 - Unlikely
3- Difficult to tell
4- likely
5- Very likely

274
Q

What score is used to grade prostate cancer?

A

Gleason Score

275
Q

How is localised prostate cancer managed?

A

Low/intermediate risk;

Active surveillance
Radical prostatectomy
Radical radiotherapy

High risk;
Prostatectomy or radical radiotherapy

276
Q

How is metastatic prostate cancer managed? (2)

A

External beam radiotherapy

Androgen deprivation therapy (groserelin and leuprorelin)

277
Q

Give 3 adversed effects of hormone therapy in the management of prostate cancer and state how they are managed.

A

Hot flushes - Medroxyprogesterone

Sexual dysfunction - Sildenafil (phosphodiesterase inhibitors)

Osteoporosis - Bisphosphonates

278
Q

Define benign prostatic hyperplasia

A

Describes enlargement of the inner (transitional zones) of the prostate

279
Q

How may BPH be different to prostate cancer on PR examination?

A

Prostate cancer is nodular and asymmetrical

280
Q

How is BPH managed? (3)

A

Alpha blockers - Tamsulosin

5a reductase inhibitor - Dutasteride

Surgery - Transurethral resection of prostate (TURP)

281
Q

Name 1 common side effect of Tamsulosin (alpha blocker)

A

Postural hypotension (as alphablockers induce dilation of venous capacitance vessels)

282
Q

Give 1 side effect of TURP

A

Impotence

283
Q

Name 2 types of ventricular tachycardia

A

Monomorphic VT - Most commonly caused by MI

Polymorphic VT - Subtype is torsades de pointes (precipitated by prolongation of QT interval)

284
Q

What is torsades de pointes associated with?

A

Prolonged QT interval

285
Q

What can torsades de pointes degenerate into?

A

Ventricular fibrillaiton

286
Q

Give 2 congenital causes of prolonged QT interval

A

Jervell-Lange-Nielsen syndrome (inc deafness due to abnormal potassium channel)

Romano-ward syndrome (no deafness)

287
Q

Name 4 drugs that can cause QT prolongation

A

Amiodarone

Tricyclic antidepressants (fluoxetine)

Chloroquine

Erythromycin

288
Q

Name 3 electrolyte imbalances that can cause QT prolongation

A

Hypocalcaemia

Hypokalaemia

Hypomagnesaemia

289
Q

Describe the acute management of SVT (3)

A

Valsalva manoeuvre

IV adenosine (contraindicated in asthmatics, give verapamil instead)

Electrical cardioversion

290
Q

SVT management - In what patients is adenosine contraindicated? What should be given instead?

A

Asthmatics

Give Verapamil instead

291
Q

What impact can haemodynamic instability have on heart rate?

A

Can cause symptomatic bradycardia

292
Q

How may symptomatic bradycardia present? (3)

A

Recurrent episodes of syncope

Dizziness/Disorientation

Hypotension

293
Q

How is symptomatic bradycardia managed? (2)

A

1st line - Atropine/Transcutaneous pacing

2nd line - Adrenaline/Isoprenaline

294
Q

What medication is used in the management of cardiovascular failure 2nd to beta-blocker overdose?

A

Glucagon

295
Q

Give 4 indications of haemodynamic compromise

A

Shock; hypotension (systolic <90), pallor, sweating, cold

Syncope

Myocardial ischemia

Heart failure

296
Q

What 3 ECG features are present in Wolf-Parkinson-White syndrome?

A

Short PR interval

Delta waves

Prolonged QRS complex

297
Q

What congenital accessory pathway is present in WPW?

A

Bundle of Kent

298
Q

Define 1st degree heart block

A

Patients experience a slower condution velocity, resulting in prolonged PR interval

299
Q

What ECG finding may be present in a patient with a 1st degree heart block?

A

Prolonged PR interval

300
Q

Give 4 causes of 1st degree heart block

A

Inferior MI

Hyperkalaemia

AV node blocking drugs (beta blockers, calcium channel blockers, Digoxin, Amiodarone)

301
Q

Name 2 types of 2nd degree heart block

A

Type I - (Wenckebach or Mobitz I)

Type II - (Mobitz II)

302
Q

How is Wenckebach/Mobitz 1 heart block characterised on ECG?

A

Progressive prolongation of PR interval followed by blocked P wave.

(PR interval is longest before non-conducted P wave, and shortest immediately after)

303
Q

Do Mobitz I heart blocks require a pacemaker?

A

No

304
Q

Describe Mobitz II heart block

A

Describes a failure of conduction through the His-Purkinje system. May be due to structural changes/damage (fibrosis/necrosis/infarction)

305
Q

How is Mobitz II heart block characterised on ECG? (2)

A

Constant (unchanged) PR interval

Dropped (disappearing QRS complexes)

(QRS complex disappears but P wave remains)

306
Q

Do Mobitz II heart blocks require pacemaker treatment? Why?

A

Yes

Carry high risk of sudden complete AV block

307
Q

How is 3rd degree heart block characterised?

A

Characterised by complete absence of AV conduction to the ventricles. Resulting in no association between P waves and QRS complexes on ECG.

308
Q

How may a 3rd degree heart block present on ECG? (2)

A

Independent atrial (p waves) and ventricular (QRS complexes) rates. (likely more P waves than QRS complexes)

Bradycardia (as ventricular escape rhythm is slower than sinus)

309
Q

How may a left bundle branch block present on ECG?

A

WiLLiaM

Deep S waves in V1 (W)

Tall/Broad ‘Notched’ R waves (M) in V6

310
Q

How may Right Bundle Branch Block present on ECG?

A

MaRRoW

RSR pattern (M shaped) in V1

Wide Slurred S waves in V6

311
Q

Give 3 causes of RBBB

A

Pulmonary hypertension

Pulmonary embolism

Right ventircular hypertrophy/cor pulmonale

312
Q

Name 2 types of frailty scoring

A

Phenotype (Fried criteria)

Cumulative deficit model (e-FI, CFS, Rockwood criteria)

313
Q

Describe how Fried Criteria describes frailty and what criteria it uses. (5)

A

Frailty is defined as 3 or more of the following;

Unintentional weight loss

Self reported exhaustion

Weakness (grip strength)

Slow walking speed (timed up ant to go test)

Low physical activity

314
Q

What is the cut off for the Timed Up and Go Test?

A

10 seconds

315
Q

Define pre-frail (according to Fried Criteria)

A

Patients who meet only 2 of the criteria

316
Q

Describe end of life care

A

Term used to describe the last 12 months of life.

317
Q

In whom should antibiotics be offered for patients presenting with pressure ulcers? (3)

A

Clinical evidence of systemic sepsis

Spreading cellulitis

Underlying osteomyelitis

318
Q

Give 4 causes of acute liver failure

A

Paracetamol overdose

Hepatitis A

Pre-eclampsia developing into HELLP syndrome

Fructose intolerance

319
Q

What enzyme does Aspirin target?

A

COX1

320
Q

Describe the Mx of steroid responsive COPD

A

1st - SABA or SAMA

2nd - SABA + LABA + ICS (if originally on SAMA, discontinue and start SABA)

3rd - SABA + LABA + ICS + LAMA (tiotropium)

321
Q

Describe the Mx for non-steroid responsive COPD

A

1st - SABA or SAMA

2nd - SABA + LABA + LAMA (If originally on SAMA discontinue and start SABA)

322
Q

Name 1 SABA

A

Salbutamol (Beta agonist)

323
Q

Name 1 LABA

A

Salmeterol

324
Q

Name 1 SAMA (short acting muscarinic antagonist)

A

Ipratropium bromide

325
Q

Name one LAMA (long acting muscarinic antagonist)

A

Tiotropium

326
Q

Name 1 ICS (inhaled corticosteroids) used in COPD

A

Beclometasone or Fluticasone

Phase 3a (6 decks)

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