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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
How do nitrates work in angina?
Nitric oxide activates guanylyl cyclase (GC) which forms cGMP. The increased cGMP inhibits Ca2+ entry into the cell -> smooth muscle relaxation.
26
What are the adverse features of beta-blockers?
``` Dizziness, fatigue Cold hands Impotence Bronchoconstriction Bradycardia, heart block Masking hypoglycaemia Raynaud's phenomenon ```
27
How do calcium channel blockers work?
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.
28
What are the adverse features of calcium channel blockers?
Peripheral oedema Constipation Headache & flushing Tachycardia
29
What are the adverse features of nitrates?
Tolerance - need nitrate free intervals Postural hypotension Headache & flushing Tachycardia
30
What are the adverse features of aspirin?
GI irritation, ulceration & haemorrhage | Bronchospasm
31
How does aspirin work?
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
How do you manage a patient who has had an MI?
Morphine Oxygen Nitrates Aspirin Admit- repeat ECG/ troponin Anti-thrombin therapy Risk assessment for intervention Cardiology referral
33
Would you offer rate or rhythm control in an AF patient?
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
What drugs are available for the treatment of AF?
Beta-blocker Non-dihyrdropyridine Ca2+ blocker Amiodarone Digoxin
35
What is amiodarone's mechanism of action?
Poorly understood membrane stabiliser | Non-selective action on Na+ and Ca2+ receptors and alpha-receptors
36
What is digoxin's mechanism of action?
Na+/Ca2+ exchanger blocker; positive inotropic and chronotropic effect?
37
Why is adrenaline used in the 'cardiac arrest algorithm'?
Protects heart and brain perfusion through vasoconstriction elsewhere Secondary direct effect on the myocardium
38
What are the adverse effects of amiodarone?
``` Arrhythmias Hepatic disorders Hyperthyroidism Nausea Respiratory disorders Skin reactions ```
39
When is amiodarone used in cardiac arrest?
Management of tachycardias (after failed cardio version in unstable wide complex tachycardias)
40
How is amiodarone administered in cardiac arrest?
IV infusion
41
What are the investigations for pulmonary embolism?
CTPA 2 Level Well's score D-dimer (where Well's is <4)
42
What is stage 1 hypertension?
Clinic blood pressure is 140/90 mmHg or higher. AND Ambulatory blood pressure is 135/85 mmHg or higher.
43
What is stage 2 hypertension?
Clinic blood pressure is 160/100mmHg or higher AND ABPM is 150/95mmHg or higher
44
What is severe hypertension?
Clinic blood pressure is 180mmHg OR Clinic diastolic blood pressure is 110mmHg or higher
45
Which patients with hypertension need pharmacological treatment?
Patients <80 with stage I hypertension, evidence of end-organ damage or elevated CVD risk
46
Which patients with hypertension are suitable for lifestyle advice and annual review?
<20% CVD risk and no evidence of end-organ damage | <40 years old - evaluation of secondary causes of HTN
47
How do you assess patients with hypertension for other risk factors and end organ damage?
- 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
What drugs can be used in hypertension?
``` ACE inhibitors - first line in under 55s Calcium channel blockers - in >55s & ACs Angiotensin II receptor blocker Thiazide-like diuretic Aldosterone antagonist (spironolactone) ```
49
How long would you wait before evaluating the therapeutic effect of the antihypertensives?
1 month
50
What are the main adverse events with ACE inhibitors?
``` Hypotension Dry cough Hyperkalaemia Renal failure exacerbation Angioedema Anaphylaxis ```
51
What would you offer if a patient originally given an ACE inhibitor struggled to tolerate it?
Angiotensin II receptor blocker
52
What is the mechanism behind dry cough caused by ACE inhibitors?
Increased bradykinin levels which would have been blocked by ACE.
53
What precautions should you consider when using ACE inhibitors?
``` Avoid in: Renal artery stenosis Acute kidney injury Pregnancy Breastfeeding Chronic kidney disease ```
54
What are important interactions for ACE inhibitors?
Potassium-elevating drugs (includes potassium supplements) - risk of hyperkalaemia NSAIDs - increased risk of AKI
55
What should you tell patients before they start ACE inhibitors?
Side effects - dry cough, dizziness, allergic reactions Requirement for blood test monitoring Avoid using OTC anti-inflammatories
56
How do you monitor ACE inhibitors?
Efficacy - reduced symptoms, improved BP | Safety - electrolytes, eGFR for renal function
57
How would you treat hypercholesterolaemia?
- 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
What non-pharmacological therapies could you recommend to a patient with hypercholesterolaemia?
``` Cardio-protective diet Physical activity Weight management Alcohol consumption Smoking cessation ```
59
What is the mechanism of action for statins?
HMG CoA reductase inhibitor, reducing cholesterol synthesis and increasing LDL receptor expression
60
What are the main adverse drug events with statins?
Headache GI disturbances Aches -> myopathy, rhabdomyolysis Increased ALT -> drug-induced hepatitis
61
What precautions are to be considered when using statins?
Hepatic impairment - use with caution Renal impairment - reduced dose Avoid in pregnancy and breastfeeding
62
What are important interactions for statins?
Cytochrome P450 inhibitors (amiodarone, diltiazem, itraxonacole, macrolides, protease inhibitors) reduce their metabolism Grapefruit juice inhibits CYP450 3A4
63
What drugs are examples of P450 inhibitors?
``` Amiodarone Diltiazem Itraconazole Macrolide antibiotics Protease inhibitors ```
64
What is the active chemical group that mediates the effect of grapefruit juice on cytochrome P450?
Furanocoumarins; potent CYP450 3A4 inhibitors
65
What should you tell patients before you start them on statins?
Seek medical attention if they experience muscle symptoms Repeat bloods in 3 and 12 months Avoid consuming grapefruit juice
66
How do you monitor statins in the prevention of CVD?
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
How would you manage a rise in ALT of three times the upper limit of normal in a patient on statins?
Stop the statin, restart it at a lower dose when liver enzymes have returned to normal.
68
Why is it better to take short acting statins at night?
HMG-CoA reductase is more active at night
69
What is co-trimoxazole?
Trimethoprim & sulfamethoxazole; antibiotics indicated in lower respiratory tract infections
70
What antibiotics are most commonly implicated with C diff./ MRSA/ carbopenem resistant enterococci/ ESBL?
Fluoroquinolones Clindamycin Broad spectrum penicillins Cephalosporins
71
What is the difference between compliance and concordance?
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
What is the difference between intentional and unintentional adherence?
Intentional - not agreeing with what was decided | Unintentional - lack of understanding
73
What factors could improve adherence & concordance?
Simplify/ rationalise therapy Assessment: self-medication schemes, medication review service Aids: reminder charts, medication record charts

HYMS PPT (4 decks)

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