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HANA Pre- Reg > Cardiovascular 1 > Flashcards

Cardiovascular 1 Flashcards

1
Q

What is arrhythmia?

A

A general term for any irregularity in the RHYTHM or RATE of the heartbeat

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2
Q

Can you name some specific types of arrhythmias?

A
  • Ectopic beats
  • Atrial fibrillation
  • Atrial flutter
  • Bradycardia
  • Tachycardia
  • Ventricular Tachycardia
  • Ventricular Fibrillation
  • Supraventricular Fibrillation
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3
Q

What are ectopic beats?

A
  • abnormal heartbeat
  • occurs outside the normal rhythm of the heart and
    DOES NOT ORIGINATE from the hearts NATURAL PACEMAKER (the sinoatrial node)
  • INSTEAD originates in other areas of the heart such as the ATRIA/ VENTRICILES
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4
Q

What is atrial fibrillation?

A

RAPID and IRREGULAR electrical impulses fired in the ATRIA (upper chambers of the heart)

Cause ATRIA to FIBRILLATE (quiver)

leading to an IRREGULAR and often RAPID heartbeat

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5
Q

What is tachycardia?

A

a FAST heart rate

Often exceeding >100beats/ min in ADULTS

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6
Q

What is bradycardia?

A

a SLOW heart rate (heart beats slower than normal)

Typically fewer than <60 beats/ min in ADULTS

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7
Q

What is atrial flutter?

A

Rapid contractions of atria

SIMILAR to atrial fibrillation

But occurs in a MORE ORGANIZED and MORE REGULAR PATTERN

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8
Q

What is ventricular tachycardia?

A

a type of tachycardia that ORIGINATES in VENTRICLES (lower chambers of the heart)

a FAST heart rate

CAN be LIFE- THREATENING and MAY REQUIRE immediate MEDICAL ATTENTION

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9
Q

What is ventricular fibrillation?

A

a MEDICAL EMERGENCY
can lead to CARDIAC ARREST

It is:

a chaotic and extremely rapid heartbeat in ventricles

results in ventricles quivering instead of contracting#

this means that the heart cannot pump blood effectively

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10
Q

What is supraventricular tachycardia?

A

A type of tachycardia that originates in a space ABOVE ventricles

This space is NOT the atria by the way!

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11
Q

What is one way to diagnose what arrhythmia a patient is presenting?

A

ECG

This records the electrical activity of the heart over a period of time

Different arrhythmia= different patterns on ECG

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12
Q

How can we treat spontaneous ectopic heart beats in a patient who otherwise has a normal heart rate?

A

In these cases, treatment is rarely required. Just reassure the patient

However, if they are troubling the patient:

BETA BLOCKERS

( sometimes effective +may be safer than other suppressant drugs)

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13
Q

What are SYMPTOMS of atrial fibrillation?

A

HEART PALPITATIONS (pounding/ fluttering)

also:
- dizziness
- shortness of breath
- tiredness

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14
Q

What are COMPLICATIONS of atrial fibrillation?

A

STROKE

HEART FAILURE

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15
Q

Why would we want to treat atrial fibrillation?

A

To REDUCE SYMPTOMS

To PREVENT complications (i.e. stroke & heart failure)

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16
Q

What are the 3 different types of atrial fibrillation?

A

PAROXYSMAL AF

PERSISTENT AF

PERMENANT AF

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17
Q

Define PAROXYSMAL AF

A

episodes STOP WITHIN 48 hours WITHOUT TREATMENT

smal= small worry

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18
Q

Define PERSISTENT AF

A

episodes LAST > 7 days

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19
Q

What is PERMENANT AF

A

AF is present ALL THE TIME

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20
Q

What are the two general ways we treat atrial fibrillation?

A

Either by

CONTROLLING THE RHYTHM
or

CONTROLLING THE RATE

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21
Q

How is RHYTHM CONTROL achieved?

A

By CARDIOVERSION

There are TWO types of cardioversion:
- electrical
- pharmacological

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22
Q

What is electrical cardioversion?

A

Electrodes are placed on the chest

They send electric signals to your heart

To restore and maintain the rhythm of your heart

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23
Q

What is pharmacological cardioversion

A

Anti- arrhythmic drugs are used to restore and maintain the rhythm of your heart

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24
Q

When can we NOT use cardioversion?

A
  • if symptoms > 48 hours as there is an INCREASED risk of stroke

(basically cause atrial fibrillation can cause blood to pool and clots to form- so longer patient has had symptoms- the higher the chances that a clot has formed)

  • if have to do cardioversion tho even tho symptoms > 48 hours, ELECTRICAl IS preferred
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25
Q

What type of therapy should a patient be on BEFORE any cardioversion therapy?

Should this therapy be continued after their cardioversion and if so, HOW LONG FOR AFTER?

A

ANTICOAGULATION THERAPY for 3 weeks BEFORE cardioversion

AND continue for 4 weeks AFTER

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26
Q

How should patients be anticoagulated before cardioversion therapy?

A

As arial fibrillation INCREASES the likelihood of clot formation

Therefore, must anticoagulated the patient to get rid of potential clots that may have formed AND also REDUCE risk of clots forming

If we do cardioversion straight away without anticoagulation
- patient may have a clot
- the cardioversion can dislodge this clot and cause it to travel to the brain causing a stroke

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27
Q

What is does ‘haemodynamically unstable’ mean?

A

A medical condition where the cardiovascular system PARTICULARLY the hearts ability to pump blood is compromised

to the extent that it cannot adequately meet the body’s demands for oxygen and nutritions

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28
Q

How do we treat a patient with ATRIAL FIBRILLATION who is HAEMODYNAMICALLY unstable?

A
  • we must first rule OUT left atrial thrombus (a blood clot forming within the left atrium of the heart)

if patient does not have LEFT ATRIAL THROMBUS

begin ELECTRICAL CARDIOVERSION
AND
PARENTERAL ANTICOAGULANT

(the reason we rule out left atrial thrombus is again so that there isn’t the risk of that clot dislodging during the cardioversion and moving to the brain)

depending on whether its life threatening or not, and also its been <48 hours >48 hours; treatment can vary. Cards coming up on this dw

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29
Q

IF a patients atrial fibrillation TREATMENT FAILS to CONTROL their symptoms OR SYMPTOMS reoccur AFTER CARDIOVERSION; what must be done?

A

Patient needs SPECIALISED MANAGEMENT

Refer within 4 WEEKS

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30
Q

What pharmacological therapies can we use to CONTROL the HEART RATE in ATRIAL FIBRILLATION?

A

Beta blockers (not sotalol)

Rate limiting CCB

Digoxin

(monotherapy- dual therapy- rhythm control)

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31
Q

How do rate limiting CBB help CONTROL HEART RATE?

A

Block calcium channels in the heart

Reduce electrical conduction through atrioventricular node

Slows down heart rate

(The AV node helps regulate heart rhythm)

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32
Q

How do BETA BLOCKERS help CONTROL HEART RATE?

A

Block adrenaline from binding to beta- adrenergic receptors in the heart

Reduce hearts response to adrenaline

This results in a slower heart rate

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33
Q

How do we treat LIFE- THREATENING HAEMODYANMIC INSTABILITY atrial fibrillation?

A

Electrical cardioversion

(in reference to previous card, make sure to rule out left atrial thrombus before doing this procedure)

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34
Q

How do we treat NON-LIFE THREATNING haemodynamic instability atrial fibrillation?

A

< 48 hours
Rate or rhythm control
(for rhythm control use electrical or amiodarone/ flecainide)

> 48 hours
Rate control
(Verapamil, beta- blocker)

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35
Q

What is the first line treatment for MAINTENANCE DRUG TREATMENT for atrial fibrillation?

A

FIRST LINE IS RATE CONTROL:

Beta blockers (NO SOTALOL)

Rate limiting CCB

Digoxin

(monotherapy- dual therapy- rhythm control)

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36
Q

What is the second line treatment for MAINTENACE DRUG TREATMENT for atrial fibrillation?

A

SECOND LINE IS RHYTHM CONTROL

Beta blockers OR oral anti- arrhythmic drug

(SOTALOL, OR amiodarone, flecainide, propafenone, dronedarone)

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37
Q

If post- cardioversion therapy; a patient still requires RHYTHM control what treatment do we give?

A

The second line treatment for maintenance drug treatment for atrial fibrillation is RHYTHM CONTROL

SO GIVE THIS!

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38
Q

How do we treat paroxysmal and symptomatic atrial fibrillation?

(so if symptoms stop within 48 hours without treatment and if they got symptoms of their AFib)

A

VENTRICULAR CONTROL or RHYTHM CONTROL
- standard beta blocker or oral anti- arrhythmic drug

‘PILL IN POCKET’ if infrequent episodes (self treatment)

  • flecainide or propafenone restores sinus rhythm if episode occurs
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39
Q

How do we TREAT ATRIAL FLUTTER?

A

similar treatment to atrial fibrillation BUT
CATHETER ABLATION = MORE SUITABLE

(ablation creates controlled tissue lesions in the atria- so im guessing it gets rid of the tissues that were generating the abnormal electrical signals)

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40
Q

When do we give anticoagulants?

A

if the risk of thromboembolic stroke > the risk of bleeding

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41
Q

How is the risk of stroke calculated?

A

CHA2- DS2- VASc tool

C= chronic heart failure or left ventricular dysfunction

H= hypertension

A2= Age 75+

D= Diabetes Mellitus

S2= stroke/ transient ischaemic attack/ venous thromboembolism history

V= vascular disease

A= 65- 74 years

Sc= Sex category (male/ female)

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42
Q

What score of CHA2- DS2- VAsc tool suggest patient NEEDS ANTICOAGULANT therapy?

A

If score is 2 OR MORE

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43
Q

What score of CHA2- DS2- VAsc tool suggest patient DOES NOT NEED ANTICOAGULANT therapy?

A

Male= 0

Females= 1

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44
Q

What anticoagulant do we give FOR NEW ONSET ATRIAL FIBRILLATION?

A

Parenteral anticoagulation

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45
Q

What anticoagulant do we give for DIAGNOSED ATRIAL FIBRILLATION?

A

warfarin or NOAC

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46
Q

What are NOAC?

A

new oral anticoagulants

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47
Q

When do we give NOACs?

A

in NON VALVULAR Afib

with ≥ 1 risk factors which are: 75+, heart failure, hypertension, diabetes mellitus, previous stroke or TIA

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48
Q

What is TIA?

A

Transient ischemic attack

A mini stroke

It is the temporary disruption of blood flow to a aprt of the brain

It is a WARNING sign of INCREASED RISK of FUTURE stroke

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49
Q

what is the HAS- BLED tool?

A

a risk assessment to estimate the risk of bleeding

It helps to evaluate the POTENTIAL BENEFITS of anticoagulation vs POTENTIAL RISKS

(use in conjunction with CHA2- DS2- VASc tool)

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50
Q

What does the HAS- BLED tool stand for?

A

H= hypertension
A= abnormal renal/ liver function
S= stroke history

B= bleeding history or predisposition
L= Labile international normalized ratio
E= elderly (age>65 years)
D= drug or alcohol use

The higher the score (it is out of 9 in total), the higher the risk of bleeding complications

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51
Q

what is labile INR?

A

labile INR means fluctuations in values of INR.
Suggests difficulty in maintain consistent anticoagulation levels= increasing risk of bleeding

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52
Q

Why do drugs and alcohol increase risk of bleeding?

A

As they can increase the risks of falls/ trauma

Therefore, CONTRIBUTE to BLEEDING COMPLICATIONS

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53
Q

What are the different types of VENTRICULAR TACHYCARDIA?

A
  • pulseless ventricular tachycardia
  • unstable sustained ventricular tachycardia
  • stable sustained ventricular tachycardia
  • non- sustained ventricular tachycardia
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54
Q

what is PULSELESS ventricular FIBRILLATION?

A

LIFE- THREATENING

In VF, the heart’s electrical signals become chaotic and disorganized.

the ventricles (the lower chambers of the heart) quiver or fibrillate instead of contracting effectively.

the heart is unable to pump blood to the body.

The absence of a pulse indicates that the heart is not generating enough blood flow to maintain organ function.

VF is a medical emergency

immediate intervention with CPR (cardiopulmonary resuscitation) and defibrillation (shocking the heart) is required to restore normal heart rhythm and save the person’s life.

PULSE is NOT PRESENT
Patients with pulseless VF are in cardiac arrest. They are unresponsive, not breathing normally, and have no palpable pulse.

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55
Q

What is pulseless ventricular TACHYCARDIA?

A

LIFE- THREATENING

a rapid heart rhythm that originates in the ventricles.
In VT, the heart beats at a very fast rate, but the contractions may not be coordinated or effective.

The heart may still be beating fast enough to generate a pulse, but in “pulseless VT,” there is no detectable pulse.

Pulseless VT is a medical emergency, as it indicates inadequate circulation.

Treatment for pulseless VT includes CPR and immediate defibrillation, similar to VF.

PULSE is NOT PRESENT
Patients with pulseless VT are in cardiac arrest. They are unresponsive, not breathing normally, and have no palpable pulse.

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56
Q

What is defibrillation?

A

Defibrillation is a medical procedure that involves the use of an electrical shock to restore the normal rhythm of the heart in cases of life-threatening cardiac arrhythmias, particularly ventricular fibrillation (VF) and pulseless ventricular tachycardia (VT).

The goal of defibrillation is to “reset” the heart’s electrical activity, allowing it to resume a coordinated and effective pumping action.

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57
Q

In such cases where defibrillation has not been successful in restoring a normal heart rhythm and pulse, what must be done?

A

Iv amiodarone is given refractory to defibrillation

Amiodarone is a potent antiarrhythmic drug that can be administered intravenously. It works by affecting the electrical properties of the heart and can help stabilize the rhythm.

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58
Q

What is UNSTABLE sustained ventricular tachycardia?

A

a serious cardiac arrhythmia characterized by a rapid and abnormal heart rhythm originating in the ventricles, the lower chambers of the heart.

In this context, “unstable” refers to the fact that the patient’s condition is deteriorating or at risk of deteriorating due to the arrhythmia. It is a medical emergency that requires immediate attention and intervention.

PULSE is present

have symptoms of haemodynamic instability: such as severe chest pain, palpitations, shortness of breath, dizziness, or altered consciousness.

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59
Q

How is unstable sustained ventricular tachycardia treated?

A

direct current cardioversion

If this fails give IV amiodarone and repeat direct current

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60
Q

What is stable sustained ventricular tachycardia?

A

Stable sustained ventricular tachycardia (VT) is a cardiac arrhythmia characterized by a rapid and regular heart rhythm originating in the ventricles, the lower chambers of the heart.

In this context, “stable” means that the patient is not experiencing severe symptoms or hemodynamic instability, and they are conscious and alert despite the abnormal rhythm.

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61
Q

How do we treat stable sustained ventricular tachycardia?

A

IV anti- arrhythmic drug (amiodarone preferred)

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62
Q

What is non- sustained ventricular tachycardia?

A

Non-sustained ventricular tachycardia (NSVT) is a cardiac arrhythmia characterized by episodes of rapid heartbeats originating in the ventricles (the lower chambers of the heart) that last for a brief duration, typically less than 30 seconds.

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63
Q

How do we treat non- sustained ventricular tachycardia?

A

beta- blocker

can slow down the heart rate by blocking the effects of adrenaline (epinephrine) on the heart

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64
Q

What is the maintenance treatment for patients at high risk of cardiac arrest?

A

MOST PATIENTS: cardioverter defibrillator implant

SOME PATIENTS also require a drug: sotalol, beta- blocker alone or beta- blocker with amiodarone

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65
Q

What is TORSADE DE POINTES (prolonged QT interval)?

A

a specific type of ventricular tachycardia, a rapid and abnormal heart rhythm originating in the ventricles, the lower chambers of the heart.

often associated with a prolonged QT interval on the ECG. The QT interval represents the time it takes for the ventricles to repolarize (reset) after each heartbeat. A prolonged QT interval can lead to a susceptibility to TdP.

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66
Q

How is TORSADE de POINTES treated?

A

magnesium sulphate

because it addresses one of the underlying factors that can trigger this specific type of ventricular tachycardia—namely, electrolyte imbalances, particularly hypomagnesemia (low levels of magnesium in the blood)

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67
Q

What are the CAUSES of TORSADE de POINTES

A

sotalol and other drugs that prolong QT interval

hypOkalaemia

bradycardia

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68
Q

why can sotalol prolong QT interval?

A

It can prolong the QT interval on an electrocardiogram (ECG) due to its action on potassium channels in the heart.

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69
Q

What is paroxysmal supraventricular tachycardia? PSVT

A

is a type of cardiac arrhythmia characterized by sudden and intermittent episodes of abnormally fast heart rate.

This rapid heart rate originates above the ventricles, usually in the atria or atrioventricular (AV) node, which are the upper chambers of the heart.

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70
Q

How is paroxysmal supraventricular tachycardia treated?

A

Terminates spontaneously or with reflex vagal nerve stimulation e.g. Valsalva manoeuvre, carotid sinus massage or immersing face in ice cold water

/
IV adenosine (BUT contra- indicated in COPD/ asthma)

/
Iv Verapmil

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71
Q

What is reflex vagal nerve stimulation

A

stimulating the vagus nerve (cranial nerve X), leads to various physiological responses, including changes in heart rate, blood pressure

this nerve can be stimulated by e.g. Valsalva manoeuvre, carotid sinus massage or immersing face in ice cold water

Valsalva maneuver involves forceful exhalation against a closed airway (like trying to exhale against a closed mouth and nose). This increases pressure within the chest and can stimulate the vagus nerve.

Carotid sinus massage involves gently massaging the carotid sinus, a small area near the carotid artery in the neck. This stimulation can lead to activation of the vagus nerve and result in a slowing of the heart rate

Plunging the face into ice-cold water or applying cold stimuli to the face can stimulate the trigeminal nerve, which is closely connected to the vagus nerve. This can lead to a vagal response, including bradycardia (slowing of the heart rate).

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72
Q

How does adenosine help treat PSVT?

A

It works by briefly blocking electrical signals in the heart’s AV node, which can interrupt the abnormal rhythm causing PSVT and restore a normal heart rate

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73
Q

How do we treat haemodynamically unstable PSVT?

A

direct current cardioversion

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74
Q

How do we treat recurrent episodes of PSVT?

A

catheter ablation OR drugs (verapamil, diltiazem, beta- blockers, flecainide or propafenone)

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75
Q

What is amiodarone?

A

a class III anti- arrhythmic drug

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76
Q

what is the initial loading dose of amiodarone?

A

200mg TDS for 7 days
200mg BD for 7 days and then
200mg OD as maintenance

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77
Q

Where can pts experience side effects of amiodarone?

A

EYES, SKIN, NERVES, LUNGS, LIVER, THYROID DYSFUNCTION

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78
Q

What are the EYE side effects of amiodarone?

How will you counsel patients?

A

1) Corneal micro- deposits

PATIENT COUNSELLING: night time glares when driving

2) Optic neuropathy/ neuritis (blindness)

PATIENT COUNSELLING: STOP if impaired vision

Amiodarone contains iodine, which can deposit in various tissues, including the cornea of the eye.

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79
Q

What are the SKIN side effects of amiodarone?

How will you counsel patients?

A

1) Phototoxicity (burning, erythema)

2) Slate - grey skin on light exposed areas

PATIENT COUNSELLING: shield skin from light during treatment. Use wide spectrum, high SPF sunscreen for months after stopping

(Phototoxicity (photoirritation) is defined as a toxic response that is elicited after the initial exposure of skin to certain chemicals and subsequent exposure to light)

The skin reactions are thought to be related to the drug’s accumulation in the skin and its effects on pigmentation.

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80
Q

What are the NERVE side effects of amiodarone?

How will you COUNSEL patients?

A

Peripheral neuropathy

PATIENT COUNSELLING: to look out for numbness, tingling hand, and feet’s, tremors

may involve direct drug toxicity to nerves and muscles

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81
Q

What are the LUNG side effects of amiodarone?

How will you COUNSEL patients?

A

Pneumonitis, pulmonary fibrosis

PATIENT COUNSELLING: shortness of breath, dry cough

The exact mechanism of amiodarone-induced lung toxicity is not fully understood, but it is thought to involve inflammation and fibrosis in the lung tissue.

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82
Q

What are the LIVER side effects of amiodarone?

How will you COUNSEL patients?

A

Hepatoxicity

PATIENT COUNSELLING: patients must REPORT jaundice, nausea, vomiting, malaise, itching, bruising, abdominal pain, 3x raised liver transaminases

The precise cause of amiodarone-induced liver toxicity is not well understood, but it may involve direct toxicity to liver cells.

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83
Q

What are the THYROID side effects of amiodarone?

A

Amiodarone contains iodine, which can disrupt the normal regulation of thyroid hormones. It may also cause inflammation of the thyroid gland

Can cause THYRPOD DYSFUNCTION - Can cause hypo and hyperthyroidism

Hyperthyroidism e.g. weight loss, heat intolerance, tachycardia. Give carbimazole if necessary. Withdraw amiodarone

Hypothyroidism e.g. weight gain, cold intolerance, bradycardia. Start levothyroxine without withdrawing amiodarone if essential

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84
Q

How can we monitor patients on amiodarone?

A

EYES: annual eye test

LUNGS: chest x- ray before treatment

LIVER: liver function tests every 6 months

THYROID: monitor TSH, T3, T4 before treatments and every 6 months

as can also cause HYPOTENSION and BRADYCHARDIA: monitor blood pressure and do ECGs

amiodarone causes HypOkalaemia, this enhances arrhythmogenic effects of amiodarone. MONITOR SERUM POTASSIUM

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85
Q

Why are there danger of interactions with AMIODARINE several months AFTER STOPPING?

A

Amiodarone has an EXTREMELY LONG HALF-LIFE (around 50 days)

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86
Q

Why should you avoid grapefruit juice whilst taking amiodarine?

A

grapefruit juice REDUCES amiodarone metabolism

leads to INCREASED plasma amiodarone concentration

the concentration of amiodarone in your bloodstream can increase significantly. Higher amiodarone levels can increase the risk of side effects and toxicity associated with the medication.

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87
Q

Why does amiodarine interact with warfarin, phenytoin and digoxin (half)?

A

amiodarine is a is a potent inhibitor of enzymes that are responsible for metabolising for these drugs

increasing their levels in the blood + increase risk of side effects

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88
Q

Why does amiodarine interact with statins?

A

like statins, amiodarone is associated with an increased risk of myopathy, which is a condition characterized by muscle pain, weakness, or inflammation.

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89
Q

Why does amiodarone interact with BETA BLOCKERS and RATE LIMITING CCBs?

A

Basically all these drugs SLOW DOWN HEART RATE

When amiodarone is used in combination with beta blockers or rate-limiting CCBs, the cumulative effect of all these medications can result in significant bradycardia. This means the heart rate can become dangerously slow.

Therefore can lead to BRADYCARDIA, AV BLOCK and MYOCARDIAL DEPRESSION

Atrioventricular (AV) block is a type of heart block that occurs when there is a disruption or delay in the transmission of electrical signals between the atria (the upper chambers of the heart) and the ventricles (the lower chambers of the heart).

Myocardial depression refers to a condition where the heart muscle (myocardium) becomes weakened and less able to pump blood effectively.

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90
Q

Amiodarone is known to interact with a variety of MEDICATIONS, potentially leading to a prolongation of the QT interval on an electrocardiogram (ECG)

This increases risk of ventricular arrhythmia

Give examples of such MEDICATIONS

A

Quinolones

Macrolides

TCAs

SSRIs

Lithium

Quinine

Hydroxychloroquine

Anti- malarials (chloroquine, mefloquine)

Antipsychotics (especially sulpiride, primozide, amisulpride)

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91
Q

What is digoxin?

A

1-2mcg/L

Cardiac glycoside

High risk drug

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92
Q

What is a positive inotrope?

A

A positive inotrope is a substance or medication that increases the force of contraction of the heart muscle, improving its ability to pump blood.

e.g digoxin

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93
Q

What is a negative inotrope?

A

A negative inotrope is a substance or medication that decreases the force of contraction of the heart muscle, reducing its ability to pump blood

e.g. beta blockers, calcium channel blockers

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94
Q

What is the mechanism of action of digoxin?

A

It enhances myocardial contractility by inhibiting the sodium-potassium pump (Na+/K+ pump) in heart muscle cells. This inhibition leads to an increase in intracellular calcium levels, which improves the force of cardiac muscle contraction.

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95
Q

What are the therapeutic levels of digoxin?

A

Therapeutic levels of digoxin refer to the range of blood concentrations at which the medication is effective in treating specific heart conditions while minimizing the risk of toxicity.

1-2 mcg/ L (Cp 6 hours after dose)

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96
Q

Is regular monitoring required for digoxin maintenance therapy?

A

NO

unless toxicity suspected or in renal impairment (as digoxin is cleared renally)

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97
Q

Why are loading doses required for digoxin?

A

As it has a long half life

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98
Q

What is the maintenance once daily dose of DIGOXIN for ATRIAL FLUTTER and NON- PAROXYSMAL AF in sedentary patients?

A

125- 250 mcg

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99
Q

What is the maintenance once daily dose of DIGOXIN for WORSENING OR SEVERE HEART FAILURE (in sinus rhythm)?

A

62.5- 125 mcg

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100
Q

What are the bioavailability’s of digoxin when it is in the following different dosage forms?

ELIXIR

TABLET

IV

A

ELIXIR= 75%

TABLET= 90%

IV= 100%

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101
Q

When is there a risk of digoxin toxity?

A

risk of toxicity in hypO K+

hypo Mg2+

hyper Ca2+

hypoxia and renal impairment

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102
Q

What are signs of toxicity?

A

“SLOW AND SICK”

  • bradycardia/ heart block
  • nausea, vomiting and diarrhoea, abdominal pain
  • blurred or yellow vision
  • confusion, delirium
  • rash
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103
Q

What is the treatment for digoxin toxicity?

A

Withdraw: correct electrolyte imbalances

Using digoxin- specific antibody for life- threatening ventricular arrhythmias unresponsive to Atropine

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104
Q

HypOkalaemia predisposes to digoxin toxicity.

What drugs cause this?

A

Diuretics (loop/ thiazide)
B2 agonist
Steroids
Theophylline

(If K+ <4.5mmol/L: give K+ supplements or K+ sparing diuretic (preferred))

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105
Q

What drugs INCREASE plasma digoxin concentration?

A

Amiodarone (give half digoxin dose)

rate limiting CCBs. macrolides, ciclosporin (enzyme inhibitors)

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106
Q

What drugs decrease plasma digoxin concentration

A

St Johns wart, rifampicin (enzyme inducers- speed
up metabolism of digoxin)

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107
Q

What drugs decrease renal excretion?

Why can this cause digoxin toxicity?

A

NSAIDs, ACE inhibitors/ ARBs

Digoxin is renally excreted therefore drugs that decrease renal excretion= increase digoxin plasma conc

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108
Q

What drugs does digoxin interact with

A
  • drugs that cause hypokalaemia e.g. diuretics, b2 agonists etc
  • drugs that are enzyme inhibitors and INCREASE plasma digoxin conc e.g. amiodarone, rate limiting CBBs
  • drugs that are enzyme inducers and DECREASE plasma digoxin conc e.g. st johns wart
  • drugs that reduce renal excretion and INCREASE plasma digoxin conc as digoxin is renally excreted e.g. NSAIDs, ACE inhibitors/ ARBs
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109
Q

“CRASED” is an acronym for digoxin interations.

Write out this acronym

A

C= calcium channel blockers (verapamil)
R= rifampicin
A= amiodarone
S= St johns wart
E= erythromycin
D= diuretics

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110
Q

Digoxin is said to have a narrow therapeutic index. What does this mean?

A

means the difference between a therapeutic and toxic dose is relatively small.

Therefore, careful monitoring of blood levels and clinical symptoms is essential when using these medications

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111
Q

what is the usual dose of edoxaban for prophylaxis of stroke in atrial fibrillation?

A

60mg ONCE daily

HOWEVER,
30mg ONCE daily if:
on current treatment with ‘ DECK’

Dronedarone
Erythromycin
Ciclosporin
Ketoconazole

OR

if body weight < 61 kg

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112
Q

Why do we use DOACs in atrial fibrillation?

A

to reduce the risk of stroke and systemic embolism

as atrial fibrillation can lead to the formation of blood clots within the atria. If these clots dislodge and travel to the brain, they can cause a stroke

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113
Q

why are DOACs preferred over Warfarin?

A

Predictable pharmacokinetics: Unlike warfarin, which requires regular monitoring of INR and dose adjustments, DOACs have more predictable pharmacokinetics and do not require routine monitoring, making them more convenient for patients.

Fewer drug and food interactions: DOACs have fewer interactions with other drugs and foods compared to warfarin, simplifying their use in clinical practice.

Lower risk of bleeding: DOACs have a lower risk of causing major bleeding, such as intracranial hemorrhage, compared to warfarin.

Rapid onset and offset of action: DOACs have a rapid onset of action, providing anticoagulation more quickly than warfarin, and their effects diminish rapidly once the medication is stopped, reducing the risk of bleeding complications during surgical procedures or emergencies.

However, the choice of anticoagulant therapy should be individualized based on the patient’s specific clinical characteristics, including their risk of stroke and bleeding, renal function, and other comorbidities. Regular follow-up and monitoring are necessary to ensure the safety and efficacy of DOAC therapy

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114
Q

give examples of DOACs

A

dabigatran, rivaroxaban, apixaban, and edoxaban

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115
Q

What is the Step 1 treatment for HYPERTENSION WITH TYPE 2 DIABETES

A

ACEi or ARB

(if not tolerated then beta- blocker)

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116
Q

What is the Step 1 treatment for HYPERTENSION WITHOUT TYPE 2 DIABETES
Age <55 and not of black African or African- Caribbean family origin?

A

ACEi or ARB

(if not tolerated then beta- blocker)

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117
Q

What is the Step 1 treatment for HYPERTENSION WITHOUT TYPE 2 DIABETES
Age 55 or over

A

CCB

if high risk of heart failure or CBB not tolerated: give thiazaide like diuretc TLD

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118
Q

What is the Step 2 treatment for a patient already recieving ACEi or ARB?

A

Give CCB or thiazide like diuretic

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119
Q

What is the Step 1 treatment for HYPERTENSION WITHOUT TYPE 2 DIABETES
Black African or African- Carribean family origin

A

CCB

if high risk of heart failure or CBB not tolerated: give thiazaide like diuretc TLD

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120
Q

What is the Step 2 treatment for a patient already recieving CCB?

A

Give ACEi or ARB or thiazide like diuretic

*if patient is African/ Carribean, ARB is preferred in their second line treatment

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121
Q

What is the Step 3 treatment for someone who needs antihypertensive drug

A

ACEi or ARB
+CCB
+ thiazide like diuretic

(give a low dose spironaloctone as the TLD. However, you can give a higher dose TLD if their K+ levels > 4.5)

If other diuretics are ineffective. ADD ALPHA or BETA- BLOCKER

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122
Q

What is the Step 4 treatment for someone who needs antihypertensive drug

A

confirm resistant hypertension
confirm elevated BP with ABPM or HBPM
check for postural hypotension and discuss adherence

Consider seeking expert advice or adding a:
- low dose spironolactone if blood potassium level is ≤4.5mmol/L
- alpha blocker or beta blocker if blood potassium level is >4.5mmol/L

seek expert advice if BP is uncontrolled on optimal tolerated doses of 4 drugs

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123
Q

Why should you avoid TLD and beta- blocker together ESPECIALLY in diabetes or high risk of diabetes?

A

both drugs cause hypoglycaemia

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124
Q

CCB

A

calcium channel blocker

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125
Q

TLD

A

thiazide like diuretic

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126
Q

ACEi

A

Ace inhibitor

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127
Q

ARB

A

Angiotensin II receptor blocker

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128
Q

What is normal hypertension

A

120/ 80 mmHg

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129
Q

What should you do if a patient has blood pressure of 140/90?

When would you treat such a patient?

A

OFFER LIFESTYLE ADVICE

ONLY TREAT IF UNDER 80 with:
- target organ damage (left ventricular hypertrophy, CKD, retinopathy)#
- CVD or 10 year CVD risk >20%, renal disease, diabetes

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130
Q

What should you do if a patient has a blood pressure of 160/90?

A

ALL patients with such a blood pressure SHOULD be treated

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131
Q

What should you do if a patient has a blood pressure of >180 as their SYSTOLIC and >110 as their DIASTOLIC?

A

This is a HYPERTENSIVE CRISES.
It can be either a HYPERTENSIVE EMERGENCY or a HYPERTENSIVE URGENCY

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132
Q

What is hypertensive emergency

A

HYPERTENSIVE EMERGENCY:
- in a hypertensive emergency, the blood pressure is so high that it is causing immediate and severe damage to one or more critical organs. This is a life-threatening situation that requires rapid medical intervention, typically in a hospital setting, to lower the blood pressure and prevent further organ damage or complications.
-Treatment involves IV medications to lower blood pressure rapidly. Otherwise can have: reduced organ perfusion= blindess, MI, cerebral infarcation and severe renal impairment

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133
Q

What is hypertensive urgency

A

blood pressure is significantly elevated but does not currently exhibit acute or immediate target organ damage. Unlike a hypertensive emergency, where there is evidence of acute organ damage, hypertensive urgency is characterized by the high blood pressure itself without other acute symptoms or complications.

Treatment: Oral medications to reduce blood pressure slowly over 24- 48 hours.

(gradually and safely lower the blood pressure over a period of hours to days to reduce the risk of complications over the long term)

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134
Q

what is reduced organ perfusion

A

inadequate perfusion (blood flow) to vital organs

can result in organ damage

hypertensive emergency can cause reduced organ perfusion

(Chronic high blood pressure can cause the arteries and arterioles (smaller blood vessels) to constrict or narrow. When blood vessels narrow, it increases resistance to blood flow, making it harder for blood to move through these vessels. As a result, blood flow to organs and tissues can be compromised, reducing perfusion.)

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135
Q

why can high blood pressure lead to retinopathy?

A

Extremely high blood pressure can damage the blood vessels in the eyes, leading to retinopathy. Rapid reduction of blood pressure can help prevent or minimize this eye damage and reduce the risk of blindness.

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136
Q

why can severe high blood pressure lead to myocardial infarction (heart attack)

A

Severe hypertension can place excessive strain on the heart, increasing the risk of a heart attack (myocardial infarction). Lowering blood pressure quickly can reduce this strain and minimize the risk of cardiac events.

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137
Q

why can high blood pressure cause kidney damage?

A

reduced organ perfusion

Impaired blood flow to the kidneys can lead to kidney dysfunction or failure.

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138
Q

What are clinical blood pressure targets in: UNDER 80 YEARS?

A

IF they have atherosclerotic CVD* or diabetes with kidney, eye or cerebrovascular disease**
130/80

For EVERYONE ELSE
<140/90

  • a condition in which fatty deposits (plaques) build up on the inner walls of arteries.

** a group of medical conditions that affect the blood vessels and blood supply to the brain

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139
Q

What are clinical blood pressure targets in: OVER 80 YEARS?

A

<150 /90

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140
Q

What are clinical blood pressure targets in: pts with RENAL DISEASE

A

IF CKD, Diabetes, proteinuria > 1g in 24 hours:

< 130/ 80

(consider ACEi/ ARB if proteinuria present)

FOR EVERYONE ELSE:
<140/90

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141
Q

what are clinical blood pressure targets in: pts with DIABETES?

A

IF have complications with their diabetes such as: EYE, KIDNEY or CEREBROVASCULAR DISEASE
<130/80

FOR EVERYONE ELSE
<140/80

(THIS IS NOT A TYPO, IT ACTUALLY IS 80 AND NOT 90!)

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142
Q

What are clinical blood pressure targets in: pregnant pts?

A

CHRONIC HYPERTENSION
<140/90

CHRONIC HYPERTENSION & if target organ damage or have already given birth

<140/90

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143
Q

What drug is widely used as first choice in gestational hypertension?

A

Labetalol

(this drug is hepatotoxic- remember that

Other drugs include:
methyldopa (stop 2 days after birth)

nifedipine MR (unlicensed)

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144
Q

What is the mechanism of action of angiotensin- converting enzyme inhibitors?

A

Inhibits the conversion of angiotensin I to angiotensin II

Angiotensin II is a potent vasoconstrictor, meaning it narrows blood vessels, leading to increased blood pressure. It also stimulates the release of aldosterone, which promotes sodium and water retention by the kidneys, further raising blood pressure.

Therefore ACEi inhibiting the conversion of angiotensin I to angiotensin II, ACE inhibitors cause blood vessels to dilate or relax. This dilation reduces peripheral vascular resistance, which is the resistance that the heart must overcome to pump blood through the circulatory system. As a result, blood pressure decreases, and the workload on the heart is reduced.

ACE inhibitors also lead to a decrease in the production of aldosterone, a hormone that acts on the kidneys to increase the reabsorption of sodium and water. By reducing aldosterone levels, ACE inhibitors promote the excretion of sodium and water by the kidneys, which helps lower blood pressure and reduce fluid retention.

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145
Q

Give examples of ACE inhibitors?

A

Captopril (BD)
ENALAPRIL
Fosinopril
Imidapril
LISINOPRIL
Moexipril
PERINDROPIL (30- 60 minutes before food)
Quinapril
RAMPIRIL
Trandolapril

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146
Q

All ACEi inhibitors should be done once a take except for one of them. What is this and what is its dosing?

A

CATOPRIL

should be taken BD

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147
Q

When should a patient take their first dose of ACEi

A

At bedtime

(could be to mitigate side effects, as individuals may sleep through the initial period when side effects are most likely to occur)

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148
Q

What are examples of Angiotensin II receptor blockers (ARB)?

A

Azilsartan
CANDERSARTAN
eprosartan
Irbersartan
LOSARTAN
Olmesartan
Telmisartan
VALSARTAN

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149
Q

What are side effects of ACEi?

A

persistent dry cough: give ARB as alternative

hyperkalaemia: higher risk in renal impairment and diabetes mellitus

anaphylactoid reactions* e.g. angioedema**

OTHER SIDE EFEFCTS:
oral ulcer, taste disturbance and hypOglycaemia

*non-allergic anaphylaxis but are not caused by the immune system’s production of IgE antibodies.

**condition characterized by the sudden and often rapid swelling of deeper layers of the skin, usually in areas such as the face, lips, tongue, throat

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150
Q

What is anaphylaxis

A

a severe and potentially life-threatening allergic reaction that can occur rapidly and affect multiple organ systems in the body. It is characterized by a sudden and systemic release of chemical mediators, including histamines, that lead to a wide range of symptoms.

Allergic Anaphylaxis: This type of anaphylaxis occurs when the immune system recognizes a specific allergen as harmful and mounts an exaggerated immune response. The immune system produces IgE antibodies in response to the allergen, and upon re-exposure, these antibodies trigger the release of histamines and other chemicals

Non- allergic anaphylaxis: does not involve IgE-mediated immune responses. Instead, non-allergic anaphylaxis occurs when certain substances, such as some medications (e.g., radiocontrast dye, certain opioids), directly trigger the release of histamines and other mediators, leading to similar severe symptoms. The key difference is that non-allergic anaphylaxis does not involve the production of IgE antibodies or prior sensitization to an allergen.

(basically in allergic its the IgE antibodies that stimulate the release of the histamines BUT in non-allergic the thing thats irritating is releasing the histamine all by itself)

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151
Q

Out of ACEi and ARBs, which one is renoprotective in renal disease such as CKD?

A

ARB

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152
Q

Some drugs are NEPHROTOXIC and should be avoided in AKI. DAMN is the acronym to describe these drugs.

Spell out the DAMN acronym

A

D= diuretics
A= ace inhibitors/ arbs
M= metformin
N= Nsaids

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153
Q

Why should ARBs be avoided in renovascular disease?

A

reduces eGFR via efferent arteriole dilation

May give in unilateral renal artery stenosis* BUT not severe bilateral stenosis

*Unilateral renal artery stenosis is a medical condition characterized by the narrowing or constriction of one of the renal arteries, which are the blood vessels that supply blood to the kidneys. “Unilateral” means that only one of the renal arteries is affected, while the other remains normal.

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154
Q

What is renovascular disease

A

Renovascular disease refers to conditions that affect the blood vessels supplying the kidneys. It often involves the narrowing or blockage of these blood vessels, which can reduce blood flow to the kidneys and potentially lead to high blood pressure and kidney dysfunction.

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155
Q

What are the hepatic effects of ARBs?

A

cholestatic jaundice

hepatic failure

*s a type of jaundice that occurs when there is an interruption in the normal flow of bile from the liver to the small intestine.

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156
Q

In relation the the hepatic effects of ARBs, when must we stop ARBs?

A

if liver transamines 3x normal

or

jaundice occurs

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157
Q

What is the advice for ACEi and pregnancy?

A

AVOID

158
Q

What are drug interactions of ACEi?

A

HYPERKALAEMIA if given with: aliskeren, ARB, K+ sparing diuretics/ aldosterone antagonists

Nephrotoxicity and reduced eGFR if given with: NSAIDs (afferent arteriole constriction)

HYPOTENSION: if given with diuretics (volume depletion= low blood pressure)

RENAL IMPAIRMENT, HYPERKALAEMIA and HYPOTENSION if given with renin- angiotensin system drugs i.e ACEi/ ARB, renin inhibitor

(avoid concomitant ACEi + ARB in diabetic neuropathy)

159
Q

Why are angiotensin- II receptor blockers an alternative to an ace inhibitor if a persistent dry cough occurs?

A

they do not inhibit the breakdown of bradykinin

(ACE inhibitors work by inhibiting the enzyme ACE, which is responsible for breaking down bradykinin. When ACE is inhibited, bradykinin levels in the body increase= It’s thought that the accumulation of bradykinin in the respiratory tract may stimulate the cough reflex= lead to dry cough)

160
Q

What are examples of centrally acting anti- hypertensives?

A
  • methyldopa
  • clonidine
  • moxonidine

“Centrally acting hypertensive” typically refers to a class of antihypertensive medications that work in the central nervous system (CNS) to lower blood pressure. These drugs act on specific receptors or pathways in the brain to reduce the signals that cause blood vessels to constrict, ultimately leading to a decrease in blood pressure.

161
Q

What is a side effect of methyldopa

A

drowsiness (so can affect driving)

162
Q

What is a side effect of clonidine

A

flushing

163
Q

what are examples of vasodilator antihypertensives?

A
  • hydralazine
  • minoxidil

a type of medication or substance that causes blood vessels to relax and dilate (widen). When blood vessels dilate, their diameter increases, allowing blood to flow more easily and reducing blood pressure.

164
Q

what are the side effects of hydralazine

A

fluid retention
tachycardia

165
Q

what are the side effects of minoxidil

A

tachycardia
fluid retention
& increase cardiac output

166
Q

what are examples of alpha- blockers?

A

prazosin
terazosin
indoramin

167
Q

what is the mechanism of action of alpha blockers

A

Alpha-1 receptors are found in the smooth muscle of blood vessels, particularly in the walls of arteries and arterioles. When these receptors are stimulated by the neurotransmitter norepinephrine, they cause the smooth muscle to contract, leading to vasoconstriction (narrowing of blood vessels). This vasoconstriction increases blood pressure.

Alpha blockers are antagonists of alpha-1 adrenergic receptors. This means that they bind to these receptors and prevent norepinephrine from activating them. By doing so, alpha blockers inhibit the vasoconstrictive effect of norepinephrine.

When alpha-1 receptors are blocked by alpha blockers, the smooth muscle in the blood vessel walls relaxes, leading to vasodilation (widening of blood vessels). This dilation reduces the resistance to blood flow, which, in turn, decreases blood pressure.

The net result of alpha blockade is a reduction in systemic vascular resistance and a decrease in blood pressure. By reducing the work the heart has to do to pump blood against high resistance, alpha blockers can help lower blood pressure and improve blood flow to various organs and tissues.

168
Q

What is the mechanism of action of beta- adrenoreceptor blockers (BETA- BLOCKERS)

A

In the body, there are beta-adreceptors located in various tissues, including the heart, blood vessels, and lungs. These receptors are activated by the stress hormones adrenaline and norepinephrine, which are released by the adrenal glands in response to stress or other stimuli.

When adrenaline or norepinephrine binds to beta-adreceptors, it triggers various physiological responses, including increased heart rate, increased force of heart contraction, and vasoconstriction (narrowing of blood vessels). These responses can result in increased blood pressure and a faster heart rate.

Beta-blockers work by binding to and blocking beta-adreceptors. By doing so, they prevent the binding of adrenaline and norepinephrine to these receptors, effectively reducing or blocking their stimulatory effects.

Cardiovascular Effects:

Heart Rate Reduction: By blocking beta-1 receptors primarily found in the heart, beta-blockers slow down the heart rate (negative chronotropic effect).

Decreased Force of Contraction: Beta-blockers also reduce the force of contraction of the heart muscle (negative inotropic effect), which can help lower blood pressure and reduce the heart’s workload.

Vasodilation: Some beta-blockers have additional effects on blood vessels. They can lead to vasodilation (widening of blood vessels), which reduces peripheral vascular resistance, helping to lower blood pressure.

169
Q

What are examples of beta- adrenoreceptor blockers (BETA- BLOCKERS)

A

acebutol
atenolol
bisoprolol
carvedilol
esmolol
labetalol
metoprolol
nadolol
nebivolol
oxprenolol
pindolol
propranolol
sotalol
timolol

170
Q

What is esmolol used to treat?

A

hypertension in PERIO OPERATIVE period

has short half life

171
Q

which betablocker is used for hypertension in pregnancy

A

labetalol

but this is HEPATOXIC

172
Q

what class is sotalol and what is a side effect

A

class 3 anti- arrhythmic

side effect: torsade de pointes

173
Q

what are the four different types of beta blockers and their acronyms?

A

Intrinsic sympathomimetic activity (ice PACO)

Water soluble, less likely to cross blood- brain barrier ( water CANS)

Cardio selective= less bronchospasm (Be A MAN)

Once daily dosing (BACoN)

174
Q

Describe ice PACO

‘intrinsic sympathomimetic activity’ beta blockers

A

intrinsic sympathomimetic activity: Intrinsic sympathomimetic activity (ISA) is a characteristic of some beta-blockers, particularly selective ones. Beta-blockers with ISA have a unique property in that they not only block beta-receptors but also have partial agonist activity at these receptors. In other words, they partially stimulate or activate the beta-receptors even as they are blocking them.

these beta blockers HAVE:
- less bradycardia
- less coldness of extremities

EXAMPLES (PACO):

  • pindolol
  • acebutolol
  • celiprolol
  • oxprenolol
175
Q

Describe water CANS beta blockers

‘water- soluble, less likely to cross- blood- brain barrier’

A

as they are less- likely to cross the blood- brain barrier

means LESS nightmares and sleep disturbances

make sure to REDUCE their dose though in renal impairment as these beta blockers are RENALLY CLEARED

Examples are (CANS):
- celiprolol
- atenolol
- nadolol
- sotalol

176
Q

Describe Be A MAN beta blockers

‘cardio- selective= less bronchospasm’

A

well- controlled asthma under a specialist if no other choice

Examples are (B A MAN)

Bisoprolol

Atenolol

Metoprolol
Acebutol
Nebivolol

177
Q

Describe BACoN beta blockers?

A

once daily dosing

intrinsically long duration of action

Examples are (BACN)

Bisoprolol
Atenolol
Celiprolol
Nadolol

178
Q

What are side effects of beta- blockers?

A

bradycardia, hypotension

hypErglycaemia OR hypOglycaemia

(beta- blockers mask symptoms of hypOglycaemia e.g. tachycardia)

179
Q

What are contra- indications of beta- blockers?

A

ASTHMA
(as beta- blockers cause bronchospasm. This includes B blocker eye drops e.g. timolol)

WORSENING UNSTABLE HEART FAILURE

SECOND/ THIRD DEGREE HEART BLOCK*

SEVERE HYPOTENSION AND BRADYCARDIA

*heart rhythm disturbances that occur when the electrical signals in the heart don’t flow properly.

180
Q

What are some interactions of beta- blockers

A

VERAPAMIL* INJECTION
(asystole** and hypotension)

THIAZIDE- LIKE DIURETIC
(causes hyperglycaemia: avoid in diabetes, high risk of diabetes)

*type of CCB
**Asystole is when your heart’s electrical system fails entirely, which causes your heart to stop pumping.

181
Q

what is the mechanism of action of calcium channel blockers?

A

Calcium channels are proteins on the cell membranes of these muscle cells and neurons that control the entry of calcium ions into the cells when activated.

Voltage-gated calcium channels open in response to changes in the electrical membrane potential (voltage) of the cell. When they open, calcium ions flow into the cell.

In cardiac muscle cells, calcium ions are essential for the generation of an action potential—the electrical signal that triggers muscle contraction. Calcium influx during the action potential allows the heart to contract and pump blood effectively.

In smooth muscle cells found in the walls of blood vessels, calcium ions also play a crucial role in muscle contraction. An increase in calcium levels in these cells leads to vasoconstriction (narrowing of blood vessels), which can increase blood pressure.

Calcium channel blockers work by binding to and blocking the voltage-gated calcium channels on the cell membranes of cardiac and smooth muscle cells.

By blocking these channels, calcium channel blockers prevent or reduce the entry of calcium ions into the cells. This leads to the following effects:

Cardiac Effects: In the heart, CCBs reduce the influx of calcium ions during the action potential, resulting in a decreased force of contraction (negative inotropic effect) and a slower heart rate (negative chronotropic effect). This helps reduce the heart’s workload and oxygen demand.

Vasodilation: In smooth muscle cells of blood vessels, CCBs inhibit calcium entry, leading to relaxation and dilation of the blood vessels. This reduces peripheral vascular resistance and lowers blood pressure.

The combined effects of reduced cardiac contractility and vasodilation make calcium channel blockers effective in lowering blood pressure and relieving angina by decreasing the heart’s workload and improving blood flow to the heart muscle.

182
Q

What are the two different types of calcium channel blockers?

A

DIHYDROPYRIDINE CBBS

RATE LIMITING CCB

183
Q

what are dihydropyridine CCBS?

A

Dihydropyridine CCBs primarily target the L-type calcium channels in vascular SMOOTH MUSCLE CELLS By blocking these channels, they inhibit calcium influx, leading to vasodilation (widening of blood vessels). This results in reduced peripheral vascular resistance and lower blood pressure.

184
Q

what are rate limiting CCBs

A

Rate-limiting CCBs, also known as non-dihydropyridine CCBs, primarily target the L-type calcium channels in the HEART, particularly in the atrioventricular (AV) node. By blocking these channels, they slow down the conduction of electrical impulses through the AV node, which results in a reduction in heart rate and a decrease in the force of atrial contraction.

185
Q

What are examples of dihydropyridine CCBs?

A

AMLODIPINE
FELODIPINE
Lacidipine
Lercanidipine
Nifedipine (maintain the same modified release brand)

186
Q

What are examples of rate- limiting CCBs?

A

verapamil and diltiazem

note: if pt. is on diltiazem make sure to maintain on same brand when doses > 60mg

187
Q

what are side effects of calcium channel blockers?

A

headaches (common)
ankle swelling flushing

188
Q

who should rate- limiting CCBs be avoided in?

A

those with heart failure

189
Q

what can verapamil cause

A

constipation

190
Q

what is the only CCB licensed for arrhythmia?

A

verapamil

191
Q

what is an interaction of CCBs?

A

GRAPEFRUIT JUICE

is an enzyme inhibitor- leads to increased CCB concentration

192
Q

What is a phaechromocytoma and why can it cause high blood pressure?

A

A phaeochromocytoma is a rare tumour of the adrenal glands, which sit above the kidneys.

A phaeochromocytoma can cause the adrenal glands to produce too much adrenaline and noradrenaline which often results in problems such as heart palpitations and high blood pressure.

193
Q

How to treat phaechromocytoma induced hypertension?

A

beta blocker + alpha- blocker (phenoxybenzamine)

refer to BNF

194
Q

What is deep vein thrombosis? DVT

A

A blood clot occurs in a deep vein, usually in calf of one leg

195
Q

What is pulmonary embolism? PE

A

The detachment of a blood clot which travels to the lungs and blocks the pulmonary artery

196
Q

For all patients admitted to hospital what two risks must we compare?

A

Their risk of developing a VTE versus their risk of bleeding

197
Q

What are some factors that increase the risk of VTE?

A
  • immobility
  • obesity, BMI >30
  • malignant disease
  • 60+ years
  • personal history of VTE
  • thrombophilic disorders (means have disorder which means have increased tendency of developing blood clots)
  • a first degree relative of theirs has VTE
  • HRT/ combined contraceptive (due to their effect on the body’s clotting factors and blood flow
  • pregnancy
  • varicose veins with phlebitis (enlarged veins that have become inflamed and painful.
  • pregnancy
  • critical care
  • significant co- morbidities
198
Q

What is VTE?

A

Venous thromboembolism is a broader term that encompasses two related conditions: deep vein thrombosis (DVT) and pulmonary embolism (PE).

199
Q

What factors increase the RISK OF BLEEDING in a patient?

A
  • thrombocytopenia (low platelet)
  • acute stroke
  • bleeding disorders
  • Acquired: liver failure
  • Inherited: haemophilia, von willebrands disease
  • anticoagulants
  • systolic hypertension
200
Q

What is haemophilia

A

Hemophilia is a rare genetic bleeding disorder characterized by a deficiency or dysfunction of specific clotting proteins called clotting factors

201
Q

What is von willebrands disease?

A

von Willebrand disease (vWD) is a genetic bleeding disorder characterized by a deficiency or dysfunction of von Willebrand factor (vWF), a protein that plays a crucial role in blood clotting.

202
Q

What is an example of mechanical VTE prophylaxis?

A

compression stockings

exert pressure on the leg vein

Improving Blood Flow: Compression stockings are specially designed to pr

203
Q

When do we use mechanical VTE prophylaxis

A

For pts scheduled for surgery

Compressions stockings are continued for these pts until they are sufficently mobile

204
Q

When do we provide pharmacological VTE prophylaxis to patients?

A

For HIGH RISK VTE patients undergoing general/ orthopaedic surgery OR admitted to hospital as general medication patients

If contraindicated offer mechanical prophylaxis

(orthopaedic= bones, joints, ligaments, tendons and muscles)

205
Q

What are parenteral anticoagulants we can give as pharmacological VTE prophylaxis?

A

Low molecular weight heparin
or
unfractionated heparin in renal failure
or
fondaparinux

206
Q

When do we give NOACs?

A

prophylaxis after knee/ hip replacement surgery
edoxaban: treatment and prevention of recurrent VTE

207
Q

What is the duration of VTE prophylaxis for GENERAL SURGERY?

A

5-7 days or until sufficient mobility

208
Q

What is the duration of VTE prophylaxis for MAJOR CANCER SURGERY in ABDOMEN or PELVIS?

A

28 days

209
Q

What is the duration of VTE prophylaxis for KNEE/ HIP surgery?

A

extended duration

210
Q

How do we treat VTE?

A

LMHW
(or unfractionated heparin in renal failure- but make sure to monitor *APTT if unfractionated heparin given)

For at least 5 days
AND
until INR at 2 or more for at least 24 hours

AND AT THE SAME TIME start an oral anticoagulant, usually warfarin

*Activated Partial Thromboplastin Time (aPTT) monitoring is a laboratory test used to assess the clotting ability of a patient’s blood

211
Q

How do we treat VTE in pregnancy?

A

LMHW is the preferred choice

as lower risk of osteoporosis and heparin- induced thrombocytopenia

Stop at labour- onset. Seek specialist advice on continuing after birth

212
Q

What does unfractionated heparin activate?

A

antithrombin

213
Q

What does low molecular weight heparin INACTIVE?

A

factor Xa

214
Q

What is unfractionated heparin?

A

standard heparin

SHORTER duration of action

Preferred choice if:
- high risk of bleeding
- renal impairment

Monitor: APTT

215
Q

What are examples of low molecular weight heparin

A

TINZEPARIN

ENOXAPARIN

DALTEPARIN

216
Q

What is low molecular weight heparin?

A

Longer duration of action

Generally preferred choice as HAS LOWER RISK OF:
- osteoporosis
- heparin induced thrombocytopenia

USED IN PREGNANCY!

217
Q

What are the side effects of heparin?

A

Haemorrhage

Hyperkalaemia: as heparin inhibits aldosterone secretion which means, potassium cant be excreted and is built up

Osteoporosis

Heparin- induced thrombocytopoenia

218
Q

What to do if a patient on heparin develops the side effect: HAEMORRHAGE?

A

withdraw heparin

if rapid reversal required= antidote protamine

219
Q

how to prevent pt on heparin developing HYPERKALAEMIA

A

KNOW that this risk is higher in diabetes mellitus and chronic kidney disease

monitor POTASSIUM levels before treatment AND if treatment lasts >7 days

220
Q

When does heparin- induced thrombocytopenia occur and what are the clinical signs? And how do we monitor

A

occurs 5-10 days after treatment

CLINICAL SIGNS:

  • 30% reduction in platelets
  • skin allergy
    -thrombosis

MONITORING:
before treatment and if > 4 days use

221
Q

What are examples of other parenteral anticoagulants?

A

heparinoid
argatroban
hirudin
heparin flushes
epoprostenol
fondaparinux

222
Q

What is warfarin?

A

an ORAL anticoagulant
a HIGH risk drug

It antagonises actions of vitamin K in blood clotting
Takes 48 to 72 hours to work

strengths: 0.5, 1mg, 3mg, 5mg

Warfarin acts as a vitamin K antagonist. It inhibits an enzyme called vitamin K epoxide reductase (VKOR), which is responsible for recycling and regenerating active vitamin K in the body. By inhibiting VKOR, warfarin reduces the availability of active vitamin K. With reduced active vitamin K available, the liver is less able to produce functional clotting factor

223
Q

What is the dose of warfarin?

A

5mg initially and monitor every 1-2 days
maintenance dose: 3-9mg at same time each day

224
Q

how is warfarin monitored?

A

INR every 3 months once stable

225
Q

how long does duration of treatment last for: ISOLATED CALF DVT?

A

6 weeks

Isolated calf deep vein thrombosis (DVT) refers to the development of a blood clot (thrombus) within the deep veins of the calf muscle, without involvement of the more proximal veins in the thigh or pelvis

226
Q

how long does duration of treatment last for: PROVOKED VTE (COCs, pregnancy, leg plaster cast)

COCs - combined oral contraceptives

A

3 months

Provoked venous thromboembolism (VTE) refers to the development of a blood clot (thrombus) in the deep veins of the body in response to a specific triggering event or provoking factor.

227
Q

how long does duration of treatment last for: UNRPOVOKED VTE (e.g. atrial fibrillation)

A

at least 3 months/ long- term

228
Q

what is target INR in VTE (within 0.5 units)?

A

2.5

AF, MI, cardioversion, bioprosthetic, mitral valve

229
Q

what is target INR in recurrent VTE (within 0.5 units)?

A

3.5

for recurrent VTE in patients receiving anticoagulant and INR>2

230
Q

How do you counsel patients on warfarin?

A

yellow treatment booklet: explains treatment. also a section for you to write down and keep a record of your warfarin dose.

anticoagulant alert card: patient safety card (also known as an alert card) which provides appropriate details of their treatment.

Tell patient to STOP and SEEK immediate medical attention if any sign of bleeding e.g. nose bleeds or blood in urine. Also pts told to report painful skin rash (calciphylaxis)

231
Q

What are some interactions of wafarin?

A

DIRECT ACTING antivirals to treat chronic hepaptitis

  • Risk of interaction with vitamin k antagonists and can cause changes in INR. Affects efficacy of warfarin. CLOSELY monitor INR

OVER THE COUNTER ORAL MICONAZOLE GEL

  • closely monitor patient if miconazole is prescribe. Miconazole is a POTENT ENZYME INHIBITOR. It increases anticoagulant effect of warfarin. Increases the INR- increased risk of bleeding
232
Q

what are some side effects of warfarin?

A

BLEEDING e.g. nose bleeds >10 minutes, bleeding gums, bruising. The ANTIDOTE is VITAMIN K

CALCIPHYLAXIS (risk factor for this side effect is end- stage renal disease)
Patients should be counselled to report painful skin rash. Consider stopping warfarin if calciphylaxis diagnosed

233
Q

What to do when patient on warfarin has MAJOR bleeding?

A

STOP warfarin
IV Vitamin K
Dried prothrombin complex or fresh frozen plasma

234
Q

What to do if pt is on wafarin and has INR 5-8 AND NO BLEEDING

A

withold 1-2 dose
reduce maintenance dose
measure INR after 2-3 days

235
Q

what to do if pt INR is 5-8 AND MINOR BLEEDING

A

omit warfarin

give IV vitamin K

repeat if INR still high after 24 hours

restart warfarin when INR <5.0

236
Q

what to do if pt INR is <8.0 and NO BLEEDING

A

omit warfarin

oral vitamin K

repeat i INR is still high after 24 hours

restart warfarin when INR< 5

237
Q

what to do if pt INR is >8 and minor bleeding

A

omit warfarin

IV vitamin K

repeat if INR still high after 24 hours

Restart warfarin when INR <5.0

238
Q

What to do with pt who takes warfarin BEFORE they have elective surgery?

A

make sure their warfarin is stopped 5 days before elective surgery

give oral vitamin K for one day if INR >1.5

restart warfarin on evening OR next day

239
Q

What to do with pt who takes warfarin before EMERGENCY surgery?

A

If surgery can be delayed: delay 6-12 hours

If cant be delayed give IV vitamin K and dried prothrombin complex

240
Q

If a patient on warfarin has HIGH RISK OF VTE and is about to have surgery?

A

bridge with LMWH (treatment dose) and stop 24 hours before surgery

A pt is thought to be at high risk of VTE if:
- VTE in last 2 months
- AF with previous stroke/ TIA
- mechanical valve

241
Q

if patient on warfarin has high risk of bleeding and is about to have surgery?

A

start LMWH 48 hours after surgery

242
Q

How do novel oral anticoagulant drugs work?

A

inhibits specific clotting factors ie thrombin or factor Xa

243
Q

What is the mechanism of action of dabigatran?

A

direct thrombin inhibitor

244
Q

How is dabigatran packaged and what is its expiry?

A

Special container

4 month expiry

245
Q

What are examples of drugs that are direct factor Xa inhibitors?

A

apixaban
edoxaban
rivaroxaban

246
Q

what are advantages of NOACs in comparison to warfarin?

A

rarely causes bleeding and no monitoring reqiored

247
Q

what does ischaemic mean

A

blood clot obstructs blood supply

248
Q

what does haemorrhagic mean?

A

weak blood vessel in brain bursts (intracerebral haemorrhage)

249
Q

How is transient ischaemic attack managed?

A

MR dypridamole and aspirin

give statins irrespective of serum cholestrol
treat hypertension, not with beta- blockers unless indicated for another condition

250
Q

how is ischaemic stroke managed?

A

clopidogrel

(in atrial fibrillation- related stroke, review for anticoagulant)’give statins irrespective of serum cholestrol
treat hypertension, not with beta- blockers unless indicated for another condition

251
Q

What do we avoid in a intracerebral haemorrhage?

A

Avoid aspirin, statin and anticoagulants (increases risk of bleeding, only give if essential

Treat hypertension and take care to avoid hypoperfusion

252
Q

What are antiplatelet drugs?

A

decrease platelet aggregation and inhibit thrombus formation in the arterial circulation

253
Q

how do we have secondary prevention of CVD/ event?

A

low dose apsirin: 75mg daily

254
Q

when do we give clopidogrel?

A

following acute coronary syndromes or PCI)

255
Q

when do we give dipyridamole?

A

secondary prevention of strokes

256
Q

when do we take dipyridamole?

A

take tablets 30-60 mins before food

257
Q

when is the expiry date for dyspirdamole?

A

persantin retard capsules - special container, 6 weeks expiry

258
Q

what is the mechanism of action of edoxaban?

A
  • belongs to a class of drugs known as factor Xa inhibitors

ability to selectively and reversibly bind to factor Xa, which is a serine protease involved in the coagulation cascade. By binding to factor Xa, edoxaban inhibits its activity, thereby preventing the conversion of prothrombin to thrombin. Thrombin is a key enzyme in the coagulation cascade that converts fibrinogen to fibrin, leading to the formation of blood clots. By inhibiting factor Xa, edoxaban ultimately prevents the formation of blood clots, thereby reducing the risk of thromboembolic events such as stroke, DVT, and PE.

259
Q

why is it good that edoxoban is a reversible inhibitor?

A

Being a reversible inhibitor means that its anticoagulant effect can be reversed when necessary, which is particularly important in emergency situations where rapid reversal of anticoagulation may be required to control or prevent life-threatening bleeding events.

e.g.
- emergency surgery
- severe bleeding
- overdose
- emergency situations

260
Q

is warfarin considered a reversible anticoagulant?

A

It acts as a vitamin K antagonist, inhibiting the synthesis of vitamin K-dependent clotting factors (factors II, VII, IX, and X) in the liver. While its effects on clotting factors are long-lasting, the anticoagulant effect of warfarin can be reversed with the administration of vitamin K or other specific reversal agents, such as prothrombin complex concentrate (PCC) or fresh frozen plasma (FFP), depending on the clinical situation.

261
Q

what determines what reversible anticoagulant we give to patients?

A

The choice of reversal agent depends on various factors, including the patient’s clinical condition, the urgency of the situation, and the availability of specific reversal agents.

262
Q

what are contraindications of edoxaban?

A

CrCl < 15mL/ min
antiphospholipid syndrome
prosthetic heart valve
uncontrolled severe hypertension

263
Q

what does edoxoban have a reduced effect with?

A

carbamazepine
st johns wort
rifampicin
phenytoin

264
Q

what should we MONITOR in a patient BEFORE commencing EDOXOBAN?

A

clotting

Urea and electrolytes

Liver Function Tests

Full Blood Count

265
Q

If we were switching from warfarin to edoxoban, what considerations must be made?

A

The time it takes to make the switch depends on the patients INR

If
INR < 2 START EDOXOBAN

INR 2 - 2.5 START EDOXABAN THE NEXT DAY (i guess u stop the warfarn for one day and then start edoxaban, helps avoid overlapping the two medications, which could potentially increase the risk of bleeding complication)

INR > 2,5 wait until INR < 2

266
Q

what does a high INR mean

A

A high INR indicates that the blood has a reduced ability to clot, which may put the individual at an increased risk of bleeding.

267
Q

what does a low INR mean?

A

low INR suggests that the blood has an increased tendency to clot

268
Q

What is the mechanism of action of vasoconstrictor sympathomimetics?

A

medications or substances that mimic the effects of the sympathetic nervous system’s neurotransmitters, particularly norepinephrine and epinephrine (adrenaline). These drugs work by activating adrenergic receptors in the body, leading to vasoconstriction (narrowing of blood vessels) and an increase in blood pressure

269
Q

What are examples of vasoconstrictor sympathomimetics?

A

noradrenaline
phenylephrine (longer- acting: prolonged rise in blood pressure)

270
Q

what are side effects of vasoconstrictor sympathomimetics?

A

reduced perfusion to vital organs e.g. kidneys

271
Q

What are symptoms of heart failure?

A
  • dyspnoea* during an activity or at rest
  • exercise intolerance**/ fatigue
  • oedema
    (pulmonary oedema= breathlessness
    peripheral oedema***= swollen ankles, legs)

difficulty or discomfort in breathing.
** describe a person’s reduced ability or capacity to engage in physical activity or exercise compared to what is expected based on their age, fitness level, and overall health
**swelling caused by the retention of fluid in legs, ankles, feet and even sometimes in the arms and hands

272
Q

What are the NICE GUIDANCE steps for treating chronic heart failure in adults

A
  1. ACEi/ ARB+ B- Blocker
  2. Add spironolactone (or eplerenone after acute MI with LVSD or mild heart failure)
  3. add ivrabadine or add digoxin
273
Q

Which ARBs are licensed in heart failure?

A

candersartan and valsartan

274
Q

what is the first line beta- blocker treatment for mild- mod stable heart failure and 70+?

A

nebivolol

275
Q

what is the first line treatment for ALL GRADES of patients with heart failure with LVSD (Left ventricular systolic dysfunction)

A

bisoprolol, cardevilol

276
Q

if ACEi/ ARB + B- blocker are not suitable for 1st line, what other first line treatment is available for heart failure?

A

hydralazine + isosorbide dinitrate (specialist use)

277
Q

what is the step 2 treatment for heart failure?

A

add spironolactone or EPLERENONE after acute MI with LVSD or mild heart failure

Alternatives:
- hydralazine + isosorbide dinitrate (esp in African/ Carribean)
- ARB (only give with ACEi if no other option)
- Sacubutril valsartan ( LVEF <30% and taking stable dose of ACEi/ ARB)

278
Q

what is the step 3 treatment for heart failure?

A

ADD IVARABADINE
(add to standard therapy if patient in sinus rhythm and heart rate > 75bpm)

OR

ADD DIGOXIN
(worsening or severe heart failure- does not reduce mortality)

279
Q

what is the step 1 treatment for heart failure?

A

ACEi/ ARB + B blocker

alternatives:
hydralazine + isosorbide dinitrate = specialist use

280
Q

how would you treat patients with fluid overload?

A

add on loop diuretic

add on thiazide diuretics in mild heart failure

(thiazides are ineffective in RENAL failure eGFR <30mL/min/1.73m2

281
Q

What is hyperlipidaemia?

A

high blood levels of cholesterol, triglycerides or both

282
Q

what can hyperlipidaemia lead to?

A

cardiovascular disease

hyperlipidaemia causes atherosclerosis and in turn:
- coronary heart disease (angina, myocardial infarctions)
- strokes and transient ischaemic attacks (TIA)
- peripheral arterial disease

283
Q

What is the difference between primary and secondary prevention of cardiovascular event?

A

In summary, primary prevention aims to prevent the initial occurrence of cardiovascular disease, while secondary prevention focuses on preventing recurrent events and managing established heart disease.

284
Q

Who needs primary prevention of cardiovascular disease?

A
  • type 1 diabetes mellitus
  • type 2 diabetes mellitus only if CVD risk > 10%
  • if risk calculators e.g. QRISK 2: 10 year CVD risk > 10%
  • chronic kidney disease or albuminuria
  • familial hypercholesterolaemia
  • 85 years and above (reduce risk of non- fatal myocardial infarction)
285
Q

who needs secondary prevention of cardiovascular disease?

A

those with established CVD

coronary heart disease (angina, MI)
cerebrovascular disease (stroke/ transient ischaemic attack)
peripheral arterial disease

286
Q

who can we NOT use the QRISK2 tool for?

A

patients at high cardiovascular risk as their score will be underestimated

this includes:
- type 1 diabetes mellitus
- established cardiovascular disease
- over 85 years
- chronic kidney disease (eGFR <60mL/min/1.73m2)
- familial hypercholesterolemia

287
Q

how is hyperlipidaemia diagnosed?

A

6mmol/L total cholestrol

288
Q

What are TOTAL cholesterol targets for HEALTHY ADULTS?

A

≤ 5mmol/ L

289
Q

What are TOTAL cholesterol targets for HIGH RISK ADULTS?

A

≤ 4 mmol/L

290
Q

what are LDL cholesterol targets for HEALTHY ADULTS?

A

≤ 3 mmol/L

291
Q

What are LDL cholesterol targets for HGIH RISK ADULTS?

A

≤ 2 mmol/L

292
Q

What should HDL levels be?

A

> 1 mmol/L

(‘good’ cholesterol- higher the better!)

293
Q

What should Triglycerides levels be?

A

<1.7 mmol/L

294
Q

What are causes of hyperlipidaemia?

A

DRUGS and CONDITIONS

295
Q

What drugs can cause hyperlipidaemia?

A
  • antipsychotics
  • immunosuppressants
  • corticosteroids
  • antiretrovirals (HIV drugs)
296
Q

What conditions can cause hyperlipidaemia?

A
  • hypOthyroidism
  • liver or kidney disease
  • diabetes mellitus
  • family history of high cholesterol
  • lifestyle factors: smoking, excess alcohol consumption, obesity and a poor fatty diet
297
Q

What are examples of hyperlipidaemia drugs?

A

statins
bile acid sequestrants
fibrates
nicotinic acid group
ezetimibe
lomitapide
alirocumab

298
Q

What are examples of statins?

A

atorvastatin
fluvastatin
pravastatin
rosuvastatin
simvastatin

299
Q

What are examples of bile acid sequestrants?

A

colesevelam
colestipol
colestyramine

300
Q

What are examples of fibrates?

A

bezafibrates
ciprofibrate
fenofibrate
gemfibrozil

301
Q

What are examples of nicotinic acid group?

A

acipimox
nicotinic acid
omega- 3 fatty acid

302
Q

what is the mechanism of action of statins?

A

Statins work by inhibiting an enzyme called HMG-CoA reductase. This enzyme is involved in the liver’s production of cholesterol, a key component of lipoproteins (such as LDL, low-density lipoprotein) in the blood.

Lowers LDL cholesterol synthesis by the liver via inhibition of HMG- CoA reductase

By inhibiting HMG-CoA reductase, statins reduce the production of cholesterol within liver cells. This leads to a decrease in the intracellular levels of cholesterol.

Also, As a response to reduced intracellular cholesterol levels, liver cells increase the number of LDL receptors on their surface. These receptors are responsible for capturing LDL cholesterol particles circulating in the blood.

This process helps lower the levels of LDL cholesterol circulating in the blood.

303
Q

Which statins must be taken at night?

A

All of them except Atorvastatin, rosuvastatin?

(cholesterol synthesis greater at night; more effective)

304
Q

What are examples of high- intensity statins?

A
  • atorvastatin 20mg- 80mg
  • rosuvastatin 10mg
    -simvastatin 80mg
305
Q

What statin is high intensity statin choice for prevention of cardiovascular prevention?

A

atorvastatin

306
Q

what is atorvastatin dose for PRIMARY PREVENTION?

A

20mg OD

307
Q

what is atorvastatin dose for SECONDAY PREVENTION?

A

80mg OD

308
Q

What is MHRA warning for simvastatin 80mg?

A

high risk of myopathy

give only if high risk of cardiovascular complications or severe hypercholesterolaemia and treatment goals not achieved at lower dose

309
Q

which high- intensity statins are used to prevent cardiovascular disease?

A

atorvastatin
rosuvastatin
simvastatin

310
Q

how is hyperlipidaemia treated?

A

statin first choice

311
Q

how is primary hypercholesterolaemia and familial hypercholesterolaemia treated?

A

high intensity statin

If statin not tolerated or contra- indicated= ezetimibe

312
Q

how is moderate hypertriglyceridemia treated?

A

high intensity statin

if statin not tolerated or contra- indicated
= fibrate

313
Q

how is severe hyperlipidaemia treated?

A

add on ezetimibe

(under specialist supervision)

314
Q

if a persons triglycerides are still high after LDL reduced?

A

add fibrate or nicotinic acid (also lowers LDL)

315
Q

Before starting statins, we MUST address any secondary causes of dyslipidaemia. What may these be?

A
  • hypothyroidism
  • uncontrolled diabetes mellitus
  • nephrotic syndrome (albuminuria)
  • liver disease e.g. alcoholic cirrhosis
316
Q

What are side effects of statins?

A

myopathy
myositis
rhabdomyolysis

patient counselling: report tender, weak and painful muscles

317
Q

Who has a higher risk of muscle toxicity?

A
  • personal or family history of muscle disorder
  • high alcohol intake
  • renal impairment
  • hypothyroidism (treat before starting statin)
318
Q

When is there an increased risk of myopathy?

A
  • concomitant ezetimibe or fibrates, especially gemfibrozil
  • concomitant fusidic acid: restart statin 7 days after last dose (increased risk of rhabdomyolysis)
319
Q

How should we counsel patients who have interstitial lung disease and are taking statins?

A

report short breath, cough, weight loss

320
Q

why should we take caution when giving statins to diabetics or those at high risk of diabetes?

A

statins can raise HbA1c or blood glucose levels

321
Q

How can we monitor those on statins?

A

baseline lipid profile

renal function

thyroid function

HbA1c if high risk of developing diabetes

322
Q

When should we discontinue statins for a patient?

A

If
- severe muscle symptoms
- if creatinine kinase levels are 5 x normal*
- if liver transaminases 3x normal (liver function)

*if level returns to normal and muscle symptoms resolve a statin can be reintroduced at a lower dose and monitor)

323
Q

What drugs interact with statins?

A

drugs that increase statin levels as = increased myopathy risk

macrolide antibiotic e.g. clarithromycin
(patient counselling: stop taking statin until antibiotic course completed. There is no need to contact the prescriber)

ezetimibe/ fibrates especially gemfibrozil : AVOID!

fusidic acid
(restart statin 7 days after last ORAL fusidic acid dose)

324
Q

What are statin dose adjustment’s due to interactions for: SIMVASTATIN

A

Max. 10mg with fibrate
Max. 20mg with amiodarone, amlodipine, diltiazem, verapamil

325
Q

What are statin dose adjustment’s due to interactions for: ATORVASTATIN

A

Max. 10mg with ciclosporin

326
Q

What are statin dose adjustment’s due to interactions for: ROSUVASTATIN

A

Initially 5mg

Max. 20mg with clopidogrel

327
Q

Can you take statins whilst being pregnant?

A

NO as TERATOGENIC

Effective contraception must be used DURING AND 1 month after stopping

Stop taking the statin 3 months before conceiving and restart after breastfeeding finished

328
Q

What is the mechanism of action of ezitimibe?

A

TO DO WITH CHOLESTROL ABSORPTION!

Cholesterol absorption occurs through specialized transporters in the intestinal cells, including the NPC1L1 (Niemann-Pick C1-Like 1) protein.

Ezetimibe acts as a cholesterol absorption inhibitor by selectively blocking the NPC1L1 protein in the small intestine. This protein plays a key role in cholesterol uptake from the digestive tract.

Ezetimibe inhibits NPC1L1, reducing the absorption of cholesterol from the diet. As a result, less dietary cholesterol enters the bloodstream.

leads to a decrease in the concentration of LDL cholesterol in the bloodstream over time, as the liver compensates by removing LDL cholesterol from circulation.

329
Q

What is an alternative to statin in familial and primary hypercholesterolaemia?

A

ezitimibe

330
Q

what are interactions of ezitimibe?

A

statins

as can cause myopathy= rhabdomyolysis

331
Q

what is the mechanism of action of fibrates

A

fibrates lower blood triglyceride levels

by reducing the livers production of VLDL (the triglyceride- carrying particle that circulates in the blood)

and by speeding up the removal of triglycerides from the blood

332
Q

how can we treat those with severe hypertriglyceridaemia > 10mmol/L or in those who cannot tolerate a statin (specialist)

A
  • bezafibrate
  • fenofibrate
  • ciprofibrate
  • gemfibrozil (do not use with statin as high risk of myopathy - rhabdomyolysis)
333
Q

What are interactions of fibrates?

A

statins
(myopathy, renal impairment)

334
Q

What is the mechanism of action of bile acid sequestrants?

A

they bind and sequesters bile acids
the liver then produces more bile acids to replace those that have been lost
The body uses cholestrol to make bile acids
This reduces the amount of LDL cholestrol ciruclating in the blood

335
Q

what are examples of bile acid sequestrants?

A

colesevelam
colestipol
colesytramine

336
Q

what are interactions of bile acid sequestrants?

A

impair absorption of fat- souble vitamins ADEK and other drugs

pt counselling: take other drugs 1 hour BEFORE (4 hours for colevesalm) OR 4 hours AFTER bile acid sequestrant

337
Q

when are omega- 3 fatty acids used in hyperlipidaemia?

A

no evidence for use
used an adjunct to statins and diet to lower triglycerides

338
Q

when are nicotinic acid groups used in hyperlipidaemia?

A

specialist use
use limited by flushing (prostaglandin- mediated)

339
Q

what are the two different categories of nitrates?

A

short- acting nitrates
long- acting nitrates

340
Q

What are short- acting nitrates used to treat?

A

acute angina attacks

341
Q

What are long- acting nitrates used to treat?

A

long term prophylaxis of angina

342
Q

what are examples of short- acting nitrates?

A

glyceryl trinitrate
isosorbide dinitrate (S/L)

343
Q

What are examples of long- acting nitrates?

A

MR Isosorbide dinitrate
isosorbide mononitrate

beta- blockers
calcium channel blocker
ivabradine
ranolazine
nicorandil

344
Q

what is the mechanism of action of glyceryl trinitrate?

A

converted to nitric oxide which is a short acting vasodilator; improves blood supply

345
Q

what are the formulations of glyceryl trinitrate?

A

sublingual tablet*/ spray

*special container for sublingual tablets. Expires 8 weeks after opening. Foil- lined container with no cotton wadding

346
Q

How long do the effects of glyceryl trinitrate last for?

A

effects last 20-30 minutes

if using more than twice a week- long term prophylaxis

347
Q

When should glyceryl trinitrate be taken?

A

when required OR before angina- inducing activities e.g. exercise

348
Q

How should glyceryl trinitrate be taken?

A

the patient should SIT down as otherwise dizziness can occur

Take 1st dose under tongue and wait 5 minutes
Take 2nd dose under tongue and wait 5 minutes
Take 3rd dose under tongue and wait 5 minutes

(dose is either 1 tablet OR 1-2 sprays)

If pain is still present after 3 doses call 999

349
Q

What is used for angina prophylaxis?

A

B- Blocker or CCB e.g. diltiazem

B- Blocker + dihydropyridine CCB (amlodipine, MR nifedipine, felodipine. Max 2 drugs. —> if one or both is contraindicated add/use vasodilator

Vasodilator:
- long acting nitrate
- ivabradine (only in normal sinus rhythm)
- ranolazine
- nicorandil in adults only (K- channel activator)*

*MHRA/ CHM warning (Jan 2016): now given second line as risk of ulcer complications, mouth, skin, eye, gastrointestinal.
ALSO not drive until it is estabilished performance is not impaired

350
Q

What are nitrates?

A

nitrates are potent coronary vasodilators and reduce venous return and cardiac output

351
Q

how is isosorbide mononitrate taken?

A

BD
unless MR preparation: OD

352
Q

how is MR isosorbide dinitrate taken?

A

BD

(also active sublingually; alternative to glyceryl trinitrate)

353
Q

How can we ensure patients dont develop tolerance to nitrates?

A

need to use long acting preparations or transdermal patches
maintain effectiveness by reducing blood nitrate concentrations to low levels for 4 to 12 hours a day

Can do this by either

  1. leave patches off for 8-12 hours (overnight) in a day
    OR
  2. take second dose after 8 hours not 12 hours for MR isosorbide dinitrate (BD) and isosorbide mononitrate (BD)
    OR
  3. take MR isosorbide mononitrate as this is taken OD and therefore does not produce tolerance
354
Q

what are side effects of nitrates?

A

vasodilation, flushing, throbbing, headache, dizziness, postural hypotension, tachycardia, dyspepsia, heartburn

355
Q

what are site effects of injection (GTN and isosorbide dinitrate in MI)

A

severe hypotension, sweating, apprehension, restlessness, muscle twitching, retrosternal discomfort and palpitations

356
Q

why should we avoid abrupt withdrawal of nitrates and CCB?

A

worsens angina

357
Q

What to give if theres hypoxia?

A

O2

358
Q

What to give for ischaemic pain?

A

GTN OR intravenous dinitrate

-> IV diamorphine/ morphine with metoclopramide

359
Q

What to give for reperfusion?

A

Aspirin 300mg + clopidogrel 300mg

PCI or thrombolytic (altepase within 4.5 hours, streptokinase within 12 hours- avoid 4 days)

360
Q

What to give to prevent re-occlusion systemic and embolisation?

A

parenteral anticoagulant

361
Q

what to give for long term management for myocardial ischaemia?

A

SAAB

statin
ace- inhibitor
aspirin indefinitely
beta- blocker

clopidogrel (4 weeks= stemi, 12 months= NSTEMI/ unstable angina)

362
Q

what is Percutaneous coronary intervention (PCI)

A

s a non-surgical, invasive procedure with a goal to relieve the narrowing or occlusion of the coronary artery and improve blood supply to the ischemic tissue

363
Q

what can pecutaneous coronary intervention be given with?

A

glycoprotein IIb/ IIa inhibitor

364
Q

What is dual antiplatelet therapy?

(to do with pecutaneous coronary intervention?)

A

Dual antiplatelet therapy (DAPT) with PCI (percutaneous coronary intervention) is a medical treatment strategy commonly used in patients who have undergone coronary artery stent placement, particularly drug-eluting stents. It involves the use of two different antiplatelet medications to reduce the risk of blood clots forming within the stent, which could lead to complications like stent thrombosis or restenosis

aspirin (forever)
+

clopidrogrel

elective= one month*
bare metal stent= 12 months
drug- eluting stent= 12 months+

  • a medical procedure used to treat coronary artery disease (CAD) in a planned and non-emergent manne
365
Q

how to treat unstable angina and NSTEMI?

A

dispersible/ chewable aspirin 300mg STAT + Note

GTN as required sublingually (0.3- 1mg) or spray (1-2)

366
Q

how to treat STEMI?

A

dispersible/ chewable aspirin 300mg STAT + Note

GTN as required sublingually (0.3- 1mg) or spray (1-2)

ADD on: IV diamorphine/ morphine + metoclopramide

367
Q

how to treat cardiac arrest?

A

cardipulmonary resuscitation:
30 compressions: 2 breaths ~ 100 compressions/ min

IV adrenaline
1in in 1000 every 3-5 min
(sympathomimetic ionotropic used in cardiogenic shock)

if ventricular fibrillation present: Iv amiodarone

368
Q

when should drugs to treat oedema be taken?

A

in the morning to avoid sleep disruption

369
Q

what are examples of drugs to treat oedema?

A

loops
thiazides
thiazide like diuretic
potassium sparing diuretic
aldosterone antagonists
osmotic diuretic
carbonic anhydrase inhibitors

370
Q

what are examples of LOOPS?

A

bumetanide (most potent)
furosemide (gout)
torasemide (musculoskeletal pain)

371
Q

what are examples of thiazides?

A

bendroflumethazide
cyclopenthiazide

372
Q

what are examples of thiazide related diuretics?

A

chlortalidone (long half life)
indapamide (less aggravation of diabetes)
metolazone (still works in severe renal failure)
xipamide

373
Q

what are examples of potassium- sparing diuretics?

A

amiloride
triamterene (blue urine in some lights)

374
Q

what are examples of aldosterone antagonists?

A

spironolactone (ascites liver failure)
eplerenone (use in post- acute myocardial infarction)

375
Q

what is an example of an osmotic diuretic?

A

mannitol (use in cerebral oedema)

376
Q

what is an example of carbonic anhydrase inhibitor?

A

acetazolamide (use in glaucoma)

377
Q

how do diuretics work?

A

diuretics increase urine output by the kidneys i.e promotes diuresis by inhibiting sodium reabsorption at different parts of the renal tubular system (nephron)

378
Q

what is the mechanism of action of loops?

A

inhibits Na+/ K+/ Cl- co transporter in ascending limb of loop of henle

379
Q

what is the onset and duration like for loops?

A

onset: 1 hour
duration: 6 hours

380
Q

what are the side effects of loops?

A

ototoxicity (tinnitus, deafness)
acute urinary retention= too rapid diuresis, caution in benign prostatic hyperplasia

hyperglycaemia (diabetes)

hyperuricaemia (gout- furosemide)

Hypo K+ Na+ Cl- Mg2+ (alcoholic cirrhosis)
Hypo Ca2+

381
Q

how should those with heart failure take furosemide?

A

BD
Take last dose at 4 pm

20mg- 40mg OM- furosemide doses

382
Q

How should resistant hypertension be treated with loops?

A

bumetanide (most potent)
torasemide (musculoskeletal pain)
furosemide (gout)

383
Q

what is the mechanism of action of thiazides and related?

A

inhibits Na+/ Cl- transporter in distal convulated tubule

384
Q

what is the onset and duration of thiazides and related like?

A

1-2 hour onset
12- 24 hour duration

385
Q

what are side effects of thiazides and related?

A

GI disturbances
impotence
high LDL/ triglycerides

hyperglycaemia (diabetes)
hyperuricaemia (gout)

Hypo K+ Na+ Cl- Mg2+ (alcoholic cirrhosis)
Hyper Ca2+

INEFFECTIVE IF eGFR<30mL/ min except metolazone

386
Q

what is the dose of thiazides and related in HEART FAILURE?

A

OM 5mg

387
Q

what is the dose of thiazides and related in HYPERTENSION?

A

OM 2.5mg
- Bendroflumethiazide doses

indapamide (less diabetes)
metolazone (use in severe renal failure)

chlortalidone (long half life, given on alternative days if acute retention is a problem or dislikes frequent urination)

388
Q

What is the mechanism of action of potassium sparing diuretics?

A

promotes urination (diuresis)
without the loss of potassium
by inhibiting sodium channels in the distal convoluted tubule

they are weak diuretics used as an adjunct to loop and thiazide diuretics

389
Q

when are potassium sparing diuretics used?

A

preferred over potassium supplements in counteracting hypOkalaemia

390
Q

what are side effects of potassium sparing diuretics?

A

hyperkalaemia

391
Q

what are interactions of potassium sparing diuretics

A

AVOID concomitant ACEi/ ARB, K+ supplements, aldosterone antagonist
as can lead to hypERkalaemia.

HANA Pre- Reg (10 decks)

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