Cardiovascular 1 Flashcards

Question

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?

Answer 1

ANTICOAGULATION THERAPY for 3 weeks BEFORE cardioversion AND continue for 4 weeks AFTER

Answer 2

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

Answer 3

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

Answer 4

- 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

Answer 5

Patient needs SPECIALISED MANAGEMENT Refer within 4 WEEKS

Answer 6

Beta blockers (not sotalol) Rate limiting CCB Digoxin (monotherapy- dual therapy- rhythm control)

Answer 7

Block calcium channels in the heart Reduce electrical conduction through atrioventricular node Slows down heart rate (The AV node helps regulate heart rhythm)

Answer 8

Block adrenaline from binding to beta- adrenergic receptors in the heart Reduce hearts response to adrenaline This results in a slower heart rate

Answer 9

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

Answer 10

< 48 hours Rate or rhythm control (for rhythm control use electrical or amiodarone/ flecainide) >48 hours Rate control (Verapamil, beta- blocker)

Answer 11

FIRST LINE IS RATE CONTROL: Beta blockers (NO SOTALOL) Rate limiting CCB Digoxin (monotherapy- dual therapy- rhythm control)

Answer 12

SECOND LINE IS RHYTHM CONTROL Beta blockers OR oral anti- arrhythmic drug (SOTALOL, OR amiodarone, flecainide, propafenone, dronedarone)

Answer 13

The second line treatment for maintenance drug treatment for atrial fibrillation is RHYTHM CONTROL SO GIVE THIS!

Answer 14

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

Answer 15

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)

Answer 16

if the risk of thromboembolic stroke > the risk of bleeding

Answer 17

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)

Answer 18

If score is 2 OR MORE

Answer 19

Male= 0 Females= 1

Answer 20

Parenteral anticoagulation

Answer 21

warfarin or NOAC

Answer 22

new oral anticoagulants

Answer 23

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

Answer 24

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

Answer 25

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)

Answer 26

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

Answer 27

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

Answer 28

As they can increase the risks of falls/ trauma Therefore, CONTRIBUTE to BLEEDING COMPLICATIONS

Answer 29

- pulseless ventricular tachycardia - unstable sustained ventricular tachycardia - stable sustained ventricular tachycardia - non- sustained ventricular tachycardia

Answer 30

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.

Answer 31

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.

Answer 32

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.

Answer 33

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.

Answer 34

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.

Answer 35

direct current cardioversion If this fails give IV amiodarone and repeat direct current

Answer 36

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.

Answer 37

IV anti- arrhythmic drug (amiodarone preferred)

Answer 38

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.

Answer 39

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

Answer 40

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

Answer 41

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.

Answer 42

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)

Answer 43

sotalol and other drugs that prolong QT interval hypOkalaemia bradycardia

Answer 44

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

Answer 45

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.

Answer 46

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

Answer 47

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).

Answer 48

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

Answer 49

direct current cardioversion

Answer 50

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

Answer 51

a class III anti- arrhythmic drug

Answer 52

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

Answer 53

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

Answer 54

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.

Answer 55

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.

Answer 56

Peripheral neuropathy PATIENT COUNSELLING: to look out for numbness, tingling hand, and feet's, tremors may involve direct drug toxicity to nerves and muscles

Answer 57

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.

Answer 58

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.

Answer 59

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

Answer 60

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

Answer 61

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

Answer 62

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.

Answer 63

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

Answer 64

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

Answer 65

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.

Answer 66

Quinolones Macrolides TCAs SSRIs Lithium Quinine Hydroxychloroquine Anti- malarials (chloroquine, mefloquine) Antipsychotics (especially sulpiride, primozide, amisulpride)

Answer 67

1-2mcg/L Cardiac glycoside High risk drug

Answer 68

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

Answer 69

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

Answer 70

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.

Answer 71

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)

Answer 72

NO unless toxicity suspected or in renal impairment (as digoxin is cleared renally)

Answer 73

As it has a long half life

Answer 74

125- 250 mcg

Answer 75

62.5- 125 mcg

Answer 76

ELIXIR= 75% TABLET= 90% IV= 100%

Answer 77

risk of toxicity in hypO K+ hypo Mg2+ hyper Ca2+ hypoxia and renal impairment

Answer 78

"SLOW AND SICK" - bradycardia/ heart block - nausea, vomiting and diarrhoea, abdominal pain - blurred or yellow vision - confusion, delirium - rash

Answer 79

Withdraw: correct electrolyte imbalances Using digoxin- specific antibody for life- threatening ventricular arrhythmias unresponsive to Atropine

Answer 80

Diuretics (loop/ thiazide) B2 agonist Steroids Theophylline (If K+ <4.5mmol/L: give K+ supplements or K+ sparing diuretic (preferred))

Answer 81

Amiodarone (give half digoxin dose) rate limiting CCBs. macrolides, ciclosporin (enzyme inhibitors)

Answer 82

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

Answer 83

NSAIDs, ACE inhibitors/ ARBs Digoxin is renally excreted therefore drugs that decrease renal excretion= increase digoxin plasma conc

Answer 84

- 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

Answer 85

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

Answer 86

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

Answer 87

60mg ONCE daily HOWEVER, 30mg ONCE daily if: on current treatment with ' DECK' Dronedarone Erythromycin Ciclosporin Ketoconazole OR if body weight < 61 kg

Answer 88

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

Answer 89

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

Answer 90

dabigatran, rivaroxaban, apixaban, and edoxaban

Answer 91

ACEi or ARB (if not tolerated then beta- blocker)

Answer 92

ACEi or ARB (if not tolerated then beta- blocker)

Answer 93

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

Answer 94

Give CCB or thiazide like diuretic

Answer 95

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

Answer 96

Give ACEi or ARB or thiazide like diuretic *if patient is African/ Carribean, ARB is preferred in their second line treatment

Answer 97

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

Answer 98

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

Answer 99

both drugs cause hypoglycaemia

Answer 100

calcium channel blocker

Answer 101

thiazide like diuretic

Answer 102

Ace inhibitor

Answer 103

Angiotensin II receptor blocker

Answer 104

120/ 80 mmHg

Answer 105

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

Answer 106

ALL patients with such a blood pressure SHOULD be treated

Answer 107

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

Answer 108

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

Answer 109

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)

Answer 110

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.)

Answer 111

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.

Answer 112

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.

Answer 113

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

Answer 114

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

Answer 115

IF CKD, Diabetes, proteinuria > 1g in 24 hours: < 130/ 80 (consider ACEi/ ARB if proteinuria present) FOR EVERYONE ELSE: <140/90

Answer 116

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!)

Answer 117

CHRONIC HYPERTENSION <140/90 CHRONIC HYPERTENSION & if target organ damage or have already given birth <140/90

Answer 118

Labetalol (this drug is hepatotoxic- remember that Other drugs include: methyldopa (stop 2 days after birth) nifedipine MR (unlicensed)

Answer 119

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.

Answer 120

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

Answer 121

CATOPRIL should be taken BD

Answer 122

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

Answer 123

Azilsartan CANDERSARTAN eprosartan Irbersartan LOSARTAN Olmesartan Telmisartan VALSARTAN

Answer 124

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

Answer 125

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)

Answer 126

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

Answer 127

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.

Answer 128

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.

Answer 129

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.

Answer 130

if liver transamines 3x normal or jaundice occurs

Answer 131

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)

Answer 132

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)

Answer 133

- 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.

Answer 134

drowsiness (so can affect driving)

Answer 135

- 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.

Answer 136

fluid retention tachycardia

Answer 137

tachycardia fluid retention & increase cardiac output

Answer 138

prazosin terazosin indoramin

Answer 139

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.

Answer 140

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.

Answer 141

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

Answer 142

hypertension in PERIO OPERATIVE period has short half life

Answer 143

labetalol but this is HEPATOXIC

Answer 144

class 3 anti- arrhythmic side effect: torsade de pointes

Answer 145

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)

Answer 146

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

Answer 147

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

Answer 148

well- controlled asthma under a specialist if no other choice Examples are (B A MAN) Bisoprolol Atenolol Metoprolol Acebutol Nebivolol

Answer 149

once daily dosing intrinsically long duration of action Examples are (BACN) Bisoprolol Atenolol Celiprolol Nadolol

Answer 150

bradycardia, hypotension hypErglycaemia OR hypOglycaemia (beta- blockers mask symptoms of hypOglycaemia e.g. tachycardia)

Answer 151

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.

Answer 152

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.

Answer 153

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.

Answer 154

DIHYDROPYRIDINE CBBS RATE LIMITING CCB

Answer 155

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.

Answer 156

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.

Answer 157

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

Answer 158

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

Answer 159

headaches (common) ankle swelling flushing

Answer 160

those with heart failure

Answer 161

constipation

Answer 162

GRAPEFRUIT JUICE is an enzyme inhibitor- leads to increased CCB concentration

Answer 163

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.

Answer 164

beta blocker + alpha- blocker (phenoxybenzamine) *refer to BNF*

Answer 165

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

Answer 166

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

Answer 167

Their risk of developing a VTE versus their risk of bleeding

Answer 168

- 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

Answer 169

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

Answer 170

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

Answer 171

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

Answer 172

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.

Answer 173

compression stockings exert pressure on the leg vein | Improving Blood Flow: Compression stockings are specially designed to pr

Answer 174

For pts scheduled for surgery Compressions stockings are continued for these pts until they are sufficently mobile

Answer 175

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)

Answer 176

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

Answer 177

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

Answer 178

5-7 days or until sufficient mobility

Answer 179

extended duration

Answer 180

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

Answer 181

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

Answer 182

antithrombin

Answer 183

standard heparin SHORTER duration of action Preferred choice if: - high risk of bleeding - renal impairment Monitor: APTT

Answer 184

TINZEPARIN ENOXAPARIN DALTEPARIN

Answer 185

Longer duration of action Generally preferred choice as HAS LOWER RISK OF: - osteoporosis - heparin induced thrombocytopenia USED IN PREGNANCY!

Answer 186

Haemorrhage Hyperkalaemia: as heparin inhibits aldosterone secretion which means, potassium cant be excreted and is built up Osteoporosis Heparin- induced thrombocytopoenia

Answer 187

withdraw heparin if rapid reversal required= antidote protamine

Answer 188

KNOW that this risk is higher in diabetes mellitus and chronic kidney disease monitor POTASSIUM levels before treatment AND if treatment lasts >7 days

Answer 189

occurs 5-10 days after treatment CLINICAL SIGNS: - 30% reduction in platelets - skin allergy -thrombosis MONITORING: before treatment and if > 4 days use

Answer 190

heparinoid argatroban hirudin heparin flushes epoprostenol fondaparinux

Answer 191

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

Answer 192

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

Answer 193

INR every 3 months once stable

Answer 194

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

Answer 195

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.

Answer 196

at least 3 months/ long- term

Answer 197

2.5 AF, MI, cardioversion, bioprosthetic, mitral valve

Answer 198

3.5 for recurrent VTE in patients receiving anticoagulant and INR>2

Answer 199

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)

Answer 200

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

Answer 201

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

Answer 202

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

Answer 203

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

Answer 204

omit warfarin give IV vitamin K repeat if INR still high after 24 hours restart warfarin when INR <5.0

Answer 205

omit warfarin oral vitamin K repeat i INR is still high after 24 hours restart warfarin when INR< 5

Answer 206

omit warfarin IV vitamin K repeat if INR still high after 24 hours Restart warfarin when INR <5.0

Answer 207

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

Answer 208

If surgery can be delayed: delay 6-12 hours If cant be delayed give IV vitamin K and dried prothrombin complex

Answer 209

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

Answer 210

start LMWH 48 hours after surgery

Answer 211

inhibits specific clotting factors ie thrombin or factor Xa

Answer 212

direct thrombin inhibitor

Answer 213

Special container 4 month expiry

Answer 214

apixaban edoxaban rivaroxaban

Answer 215

rarely causes bleeding and no monitoring reqiored

Answer 216

blood clot obstructs blood supply

Answer 217

weak blood vessel in brain bursts (intracerebral haemorrhage)

Answer 218

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

Answer 219

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

Answer 220

Avoid aspirin, statin and anticoagulants (increases risk of bleeding, only give if essential Treat hypertension and take care to avoid hypoperfusion

Answer 221

decrease platelet aggregation and inhibit thrombus formation in the arterial circulation

Answer 222

low dose apsirin: 75mg daily

Answer 223

following acute coronary syndromes or PCI)

Answer 224

secondary prevention of strokes

Answer 225

take tablets 30-60 mins before food

Answer 226

persantin retard capsules - special container, 6 weeks expiry

Answer 227

- 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.

Answer 228

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

Answer 229

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.

Answer 230

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.

Answer 231

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

Answer 232

carbamazepine st johns wort rifampicin phenytoin

Answer 233

clotting Urea and electrolytes Liver Function Tests Full Blood Count

Answer 234

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

Answer 235

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

Answer 236

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

Answer 237

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

Answer 238

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

Answer 239

reduced perfusion to vital organs e.g. kidneys

Answer 240

- 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

Answer 241

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

Answer 242

candersartan and valsartan

Answer 243

bisoprolol, cardevilol

Answer 244

hydralazine + isosorbide dinitrate (specialist use)

Answer 245

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)

Answer 246

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)

Answer 247

ACEi/ ARB + B blocker alternatives: hydralazine + isosorbide dinitrate = specialist use

Answer 248

add on loop diuretic add on thiazide diuretics in mild heart failure (thiazides are ineffective in RENAL failure eGFR <30mL/min/1.73m2

Answer 249

high blood levels of cholesterol, triglycerides or both

Answer 250

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

Answer 251

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.

Answer 252

- 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)

Answer 253

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

Answer 254

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

Answer 255

6mmol/L total cholestrol

Answer 256

≤ 5mmol/ L

Answer 257

≤ 4 mmol/L

Answer 258

≤ 3 mmol/L

Answer 259

≤ 2 mmol/L

Answer 260

> 1 mmol/L ('good' cholesterol- higher the better!)

Answer 261

<1.7 mmol/L

Answer 262

DRUGS and CONDITIONS

Answer 263

- antipsychotics - immunosuppressants - corticosteroids - antiretrovirals (HIV drugs)

Answer 264

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

Answer 265

statins bile acid sequestrants fibrates nicotinic acid group ezetimibe lomitapide alirocumab

Answer 266

atorvastatin fluvastatin pravastatin rosuvastatin simvastatin

Answer 267

colesevelam colestipol colestyramine

Answer 268

bezafibrates ciprofibrate fenofibrate gemfibrozil

Answer 269

acipimox nicotinic acid omega- 3 fatty acid

Answer 270

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.

Answer 271

All of them except Atorvastatin, rosuvastatin? (cholesterol synthesis greater at night; more effective)

Answer 272

- atorvastatin 20mg- 80mg - rosuvastatin 10mg -simvastatin 80mg

Answer 273

atorvastatin

Answer 274

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

Answer 275

atorvastatin rosuvastatin simvastatin

Answer 276

statin first choice

Answer 277

high intensity statin If statin not tolerated or contra- indicated= ezetimibe

Answer 278

high intensity statin if statin not tolerated or contra- indicated = fibrate

Answer 279

add on ezetimibe (under specialist supervision)

Answer 280

add fibrate or nicotinic acid (also lowers LDL)

Answer 281

- hypothyroidism - uncontrolled diabetes mellitus - nephrotic syndrome (albuminuria) - liver disease e.g. alcoholic cirrhosis

Answer 282

myopathy myositis rhabdomyolysis patient counselling: report tender, weak and painful muscles

Answer 283

- personal or family history of muscle disorder - high alcohol intake - renal impairment - hypothyroidism (treat before starting statin)

Answer 284

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

Answer 285

report short breath, cough, weight loss

Answer 286

statins can raise HbA1c or blood glucose levels

Answer 287

baseline lipid profile renal function thyroid function HbA1c if high risk of developing diabetes

Answer 288

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)

Answer 289

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)

Answer 290

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

Answer 291

Max. 10mg with ciclosporin

Answer 292

Initially 5mg Max. 20mg with clopidogrel

Answer 293

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

Answer 294

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.

Answer 295

statins as can cause myopathy= rhabdomyolysis

Answer 296

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

Answer 297

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

Answer 298

statins (myopathy, renal impairment)

Answer 299

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

Answer 300

colesevelam colestipol colesytramine

Answer 301

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

Answer 302

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

Answer 303

specialist use use limited by flushing (prostaglandin- mediated)

Answer 304

short- acting nitrates long- acting nitrates

Answer 305

acute angina attacks

Answer 306

long term prophylaxis of angina

Answer 307

glyceryl trinitrate isosorbide dinitrate (S/L)

Answer 308

MR Isosorbide dinitrate isosorbide mononitrate beta- blockers calcium channel blocker ivabradine ranolazine nicorandil

Answer 309

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

Answer 310

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

Answer 311

effects last 20-30 minutes if using more than twice a week- long term prophylaxis

Answer 312

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

Answer 313

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

Answer 314

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

Answer 315

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

Answer 316

BD unless MR preparation: OD

Answer 317

BD (also active sublingually; alternative to glyceryl trinitrate)

Answer 318

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

Answer 319

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

Answer 320

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

Answer 321

worsens angina

Answer 322

GTN OR intravenous dinitrate -> IV diamorphine/ morphine with metoclopramide

Answer 323

Aspirin 300mg + clopidogrel 300mg PCI or thrombolytic (altepase within 4.5 hours, streptokinase within 12 hours- avoid 4 days)

Answer 324

parenteral anticoagulant

Answer 325

SAAB statin ace- inhibitor aspirin indefinitely beta- blocker clopidogrel (4 weeks= stemi, 12 months= NSTEMI/ unstable angina)

Answer 326

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

Answer 327

glycoprotein IIb/ IIa inhibitor

Answer 328

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

Answer 329

dispersible/ chewable aspirin 300mg STAT + Note GTN as required sublingually (0.3- 1mg) or spray (1-2)

Answer 330

dispersible/ chewable aspirin 300mg STAT + Note GTN as required sublingually (0.3- 1mg) or spray (1-2) ADD on: IV diamorphine/ morphine + metoclopramide

Answer 331

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

Answer 332

in the morning to avoid sleep disruption

Answer 333

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

Answer 334

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

Answer 335

bendroflumethazide cyclopenthiazide

Answer 336

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

Answer 337

amiloride triamterene (blue urine in some lights)

Answer 338

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

Answer 339

mannitol (use in cerebral oedema)

Answer 340

acetazolamide (use in glaucoma)

Answer 341

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

Answer 342

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

Answer 343

onset: 1 hour duration: 6 hours

Answer 344

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+

Answer 345

BD Take last dose at 4 pm 20mg- 40mg OM- furosemide doses

Answer 346

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

Answer 347

inhibits Na+/ Cl- transporter in distal convulated tubule

Answer 348

1-2 hour onset 12- 24 hour duration

Answer 349

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

Answer 350

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)

Answer 351

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

Answer 352

preferred over potassium supplements in counteracting hypOkalaemia

Answer 353

hyperkalaemia

Answer 354

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

Cardiovascular 1 Flashcards

(391 cards)