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HYMS PPT > Cardiorespiratory > Flashcards

Cardiorespiratory Flashcards

1
Q

If you suspect pulmonary embolism, what treatment should be initiated before the results of investigations come through?

A

Low molecular weight heparin
OR
DOACs: Apixaban/ Rivaroxaban

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2
Q

What forms of anticoagulation are available in the UK for immediate coagulation?

A

LMWH
DOACs
Fondaparinux (related to LMWH)
Unfractionated heparin (less commonly used)

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3
Q

What factors influence your choice with different anticoagulants?

A

Patient preference
Side effects
Ease of use (SC/ IV/ PO)

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4
Q

What blood tests should you take before giving LMWH?

A

COAG
FBC
You want a baseline coagulation status and to ensure that platelet count is normal.

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5
Q

Why should you check that platelet count is normal before starting heparin?

A

Risk of heparin induced thrombocytopenia

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6
Q

Why do you need to continue LMWH for at least 5 days after starting a patient on warfarin?

A

Risk of a further embolism
To ensure that the patient reaches an appropriate therapeutic level of anticoagulation from warfarin which takes longer to start acting.

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7
Q

When is it safe to stop LMWH?

A

After 5 days, assuming INR has been above 2 for at least 48 hours

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8
Q

Which drugs affect the actions of warfarin?

A

Simvastatin

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9
Q

What should you tell a patient before they take warfarin?

A

What the drug is for
Bleeding risk - avoid sports/ actions that would increase chances of this
They should have bloods checked by doctor regularly
If they notice any side effects, see doctor asap.

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10
Q

What treatment would you give to a patient with a high INR?

A

Oral vitamin K

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11
Q

What advantages do NOACs/DOACs have over warfarin?

A

More predictable so no monitoring is needed (offsets drug costs)

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12
Q

What advantage does warfarin have over NOACs/DOACs?

A

More expensive drug cost
It has a reversal agent
(Dabigatran only just got one)

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13
Q

How long should patients with resolved PE be anti coagulated for?

A

3 months of warfarin

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14
Q

How do simvastatin and clarithromycin interact?

A

CYP3A4 - clarithromycin is a strong inhibitor

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15
Q

What are common causes of inappropriate ADH syndrome (SIADH?)

A

Pneumonia

Diuretics (indapamide & spironolactone)

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16
Q

How do you manage hyponatraemia in patients on diuretics?

A

Stop indamamide

Give IV fluids to correct hypovolemia

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17
Q

What IV fluids are most appropriate to give to patients?

A

0.9% NaCl

Hartmann’s solution (primarily sodium lactate)

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18
Q

Why are beta-blockers and verapamil contraindicated in combination with each other?

A

Interaction can cause serious bradycardia

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19
Q

How do you monitor indapamide?

A

Blood pressure

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20
Q

What alternatives can you provide for verapamil?

A

Dihydropyridine calcium channel blockers:
Felodipine
Amlodipine

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21
Q

What must you be careful of when swapping verapamil to a dihydropyridine calcium channel blocker?

A

Watch the dose of simvastatin

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22
Q

What medication would you consider first starting a patient with angina on?

A

Short acting nitrate

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23
Q

How do beta blockers work?

A

Stop norepinephrine binding to beta-adrenoreceptors, ultimately reduces PK-A mediated Ca2+ entry into the cell and smooth muscle contraction.

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24
Q

What are the types of nitrodilators?

A

Two types:

  1. Release NO spontaneously
  2. Require an enzymatic process to form NO
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25
Q

How do nitrates work in angina?

A

Nitric oxide activates guanylyl cyclase (GC) which forms cGMP.
The increased cGMP inhibits Ca2+ entry into the cell -> smooth muscle relaxation.

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26
Q

What are the adverse features of beta-blockers?

A 
Dizziness, fatigue
Cold hands
Impotence
Bronchoconstriction
Bradycardia, heart block
Masking hypoglycaemia
Raynaud's phenomenon
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27
Q

How do calcium channel blockers work?

A

Bind to L-type calcium channels which would ordinarily facilitate calcium influx into muscle cells and allow for smooth muscle contraction. Blocking them therefore causes relaxation.

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28
Q

What are the adverse features of calcium channel blockers?

A

Peripheral oedema
Constipation
Headache & flushing
Tachycardia

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29
Q

What are the adverse features of nitrates?

A

Tolerance - need nitrate free intervals
Postural hypotension
Headache & flushing
Tachycardia

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30
Q

What are the adverse features of aspirin?

A

GI irritation, ulceration & haemorrhage

Bronchospasm

31
Q

How does aspirin work?

A

COX-1 inhibitor - blocks thromboxane production which is needed for coagulation
COX-2 inhibitor - blocks I5R-HETE and ATL production resulting in reduced inflammation

32
Q

How do you manage a patient who has had an MI?

A

Morphine
Oxygen
Nitrates
Aspirin

Admit- repeat ECG/ troponin
Anti-thrombin therapy
Risk assessment for intervention
Cardiology referral

33
Q

Would you offer rate or rhythm control in an AF patient?

A

Offer rate control as the first-line strategy except in people who have:

  • AF with a reversible cause, heart failure secondary to AF
  • New onset AF
  • Atrial flutter which is considered suitable for ablation
  • AF who are clinically judged to be more suited for rhythm control
34
Q

What drugs are available for the treatment of AF?

A

Beta-blocker
Non-dihyrdropyridine Ca2+ blocker
Amiodarone
Digoxin

35
Q

What is amiodarone’s mechanism of action?

A

Poorly understood membrane stabiliser

Non-selective action on Na+ and Ca2+ receptors and alpha-receptors

36
Q

What is digoxin’s mechanism of action?

A

Na+/Ca2+ exchanger blocker; positive inotropic and chronotropic effect?

37
Q

Why is adrenaline used in the ‘cardiac arrest algorithm’?

A

Protects heart and brain perfusion through vasoconstriction elsewhere
Secondary direct effect on the myocardium

38
Q

What are the adverse effects of amiodarone?

A 
Arrhythmias
Hepatic disorders
Hyperthyroidism
Nausea
Respiratory disorders
Skin reactions
39
Q

When is amiodarone used in cardiac arrest?

A

Management of tachycardias (after failed cardio version in unstable wide complex tachycardias)

40
Q

How is amiodarone administered in cardiac arrest?

A

IV infusion

41
Q

What are the investigations for pulmonary embolism?

A

CTPA
2 Level Well’s score
D-dimer (where Well’s is <4)

42
Q

What is stage 1 hypertension?

A

Clinic blood pressure is 140/90 mmHg or higher.
AND
Ambulatory blood pressure is 135/85 mmHg or higher.

43
Q

What is stage 2 hypertension?

A

Clinic blood pressure is 160/100mmHg or higher
AND
ABPM is 150/95mmHg or higher

44
Q

What is severe hypertension?

A

Clinic blood pressure is 180mmHg
OR
Clinic diastolic blood pressure is 110mmHg or higher

45
Q

Which patients with hypertension need pharmacological treatment?

A

Patients <80 with stage I hypertension, evidence of end-organ damage or elevated CVD risk

46
Q

Which patients with hypertension are suitable for lifestyle advice and annual review?

A

<20% CVD risk and no evidence of end-organ damage

<40 years old - evaluation of secondary causes of HTN

47
Q

How do you assess patients with hypertension for other risk factors and end organ damage?

A
  • Urine dip - test for haematuria
  • Urine sample to lab - test for proteinurea (albumin: creatinine ratio)
  • Bloods - plasma glucose, electrolytes, creatinine, eGFR, total cholesterol & HDLs
  • 12-Lead ECG
48
Q

What drugs can be used in hypertension?

A 
ACE inhibitors - first line in under 55s
Calcium channel blockers - in >55s &amp; ACs
Angiotensin II receptor blocker
Thiazide-like diuretic 
Aldosterone antagonist (spironolactone)
49
Q

How long would you wait before evaluating the therapeutic effect of the antihypertensives?

50
Q

What are the main adverse events with ACE inhibitors?

A 
Hypotension
Dry cough
Hyperkalaemia
Renal failure exacerbation
Angioedema
Anaphylaxis
51
Q

What would you offer if a patient originally given an ACE inhibitor struggled to tolerate it?

A

Angiotensin II receptor blocker

52
Q

What is the mechanism behind dry cough caused by ACE inhibitors?

A

Increased bradykinin levels which would have been blocked by ACE.

53
Q

What precautions should you consider when using ACE inhibitors?

A 
Avoid in:
Renal artery stenosis 
Acute kidney injury
Pregnancy 
Breastfeeding
Chronic kidney disease
54
Q

What are important interactions for ACE inhibitors?

A

Potassium-elevating drugs (includes potassium supplements) - risk of hyperkalaemia
NSAIDs - increased risk of AKI

55
Q

What should you tell patients before they start ACE inhibitors?

A

Side effects - dry cough, dizziness, allergic reactions
Requirement for blood test monitoring
Avoid using OTC anti-inflammatories

56
Q

How do you monitor ACE inhibitors?

A

Efficacy - reduced symptoms, improved BP

Safety - electrolytes, eGFR for renal function

57
Q

How would you treat hypercholesterolaemia?

A
  • Lifestyle modification
  • Optimisation of modifiable cardiovascular risk factors
  • Atorvastatin 20mg for primary prevention of CVD (in people who have 10% or more 10 year risk of developing CVD)
58
Q

What non-pharmacological therapies could you recommend to a patient with hypercholesterolaemia?

A 
Cardio-protective diet
Physical activity
Weight management
Alcohol consumption
Smoking cessation
59
Q

What is the mechanism of action for statins?

A

HMG CoA reductase inhibitor, reducing cholesterol synthesis and increasing LDL receptor expression

60
Q

What are the main adverse drug events with statins?

A

Headache
GI disturbances
Aches -> myopathy, rhabdomyolysis
Increased ALT -> drug-induced hepatitis

61
Q

What precautions are to be considered when using statins?

A

Hepatic impairment - use with caution
Renal impairment - reduced dose
Avoid in pregnancy and breastfeeding

62
Q

What are important interactions for statins?

A

Cytochrome P450 inhibitors (amiodarone, diltiazem, itraxonacole, macrolides, protease inhibitors) reduce their metabolism
Grapefruit juice inhibits CYP450 3A4

63
Q

What drugs are examples of P450 inhibitors?

A 
Amiodarone
Diltiazem
Itraconazole
Macrolide antibiotics
Protease inhibitors
64
Q

What is the active chemical group that mediates the effect of grapefruit juice on cytochrome P450?

A

Furanocoumarins; potent CYP450 3A4 inhibitors

65
Q

What should you tell patients before you start them on statins?

A

Seek medical attention if they experience muscle symptoms
Repeat bloods in 3 and 12 months
Avoid consuming grapefruit juice

66
Q

How do you monitor statins in the prevention of CVD?

A

Primary - lipid profile before treatment only
Secondary - efficacy via target cholesterol levels (specified in guidelines); safety via ALT measured at baseline, 3 months and 12 months and ask patients to report muscle symptoms.

67
Q

How would you manage a rise in ALT of three times the upper limit of normal in a patient on statins?

A

Stop the statin, restart it at a lower dose when liver enzymes have returned to normal.

68
Q

Why is it better to take short acting statins at night?

A

HMG-CoA reductase is more active at night

69
Q

What is co-trimoxazole?

A

Trimethoprim & sulfamethoxazole; antibiotics indicated in lower respiratory tract infections

70
Q

What antibiotics are most commonly implicated with C diff./ MRSA/ carbopenem resistant enterococci/ ESBL?

A

Fluoroquinolones
Clindamycin
Broad spectrum penicillins
Cephalosporins

71
Q

What is the difference between compliance and concordance?

A

Compliance - patient expected to stick to regimen prescribed by doctor without question
Concordance - mutually agreed contract between doctor & patient so that patient takes medicines in a way that suits both parties

72
Q

What is the difference between intentional and unintentional adherence?

A

Intentional - not agreeing with what was decided

Unintentional - lack of understanding

73
Q

What factors could improve adherence & concordance?

A

Simplify/ rationalise therapy
Assessment: self-medication schemes, medication review service
Aids: reminder charts, medication record charts

HYMS PPT (4 decks)

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