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M Dawes Flashcards

1
Q

Why can’t you give warfarin to pregnant women?

A

Because it will cross the placenta

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2
Q

How is warfarin metabolised?

A

By cytochrome P450 - other drugs interfere with P450

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3
Q

What are the adverse events of warfarin?

A

Haemorrhage - older age,
Teratogenic - first trimester - bone disease and haemorrhages in the brain in the last trimester.

Should be avoided in those with risk:
Pregnancy
Uncontrolled alcohol/drug abuse
Unsupervised dementia
Falls
Poor concordance/insight
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4
Q

What determines how much warfarin should be given and for how long?

A

The duration of treatment depends on the condition:
3-6 months for transient causes and 6-12 months idiopathic causes of DVT.

If the disorder is lifelong or long-term, such as cancer thrombophilia, then can give lifelong. Warfarin doesnt work for these conditions.

Give a loading dose

The INR that you are trying to achieve also depends on the condition. Huge individual variants - such as haw much vitamin K in the persons diet, liver disease, absorption issues, drugs.

Concomitant drugs

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5
Q

What are some drugs that inhibit cytochrome P450?

A 
Alcohol
Amiodarone 
Antibiotics
Anti-fungals
Antacids
Analgesics
Allopurinol
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6
Q

What drugs inhibit warfarin by activating P450?

A 
Alcohol
Barbiturates
Phenytoin
Contraceptives
Rifampicin
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7
Q

What do you do if someone is bleeding on warfarin?

A

Vitamin K - IV (slow onset)
IV prothrombin X
Withhold warfarin

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8
Q

What are the problems of warfarin?

A

Narrow therapeutic window
Lifetime risk of haemorrhage
Drug interactions
Regular INR required

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9
Q

What does dabigatran do?

A

Inhibits thrombin - oral.

Not cytochrome P450 
dependent
P-glycoprotein substrate
Half-life 12 hours
Excreted renally.

Good alternative to warfarin. for atrial fibrilation and VTE (DVT and PE)

Should not be used for metal heart valves.

Idarucizumab - antidote.

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10
Q

What are some drugs that inhibit platelet function?

A

Aspirin
Clopidogrel
Tricagrelor

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11
Q

What are the indicators for anticoagulants?

A

For arterial disease (antiplatelets + anticoagulants)

  • coronary artery disease
  • cerebrovascular disease
  • peripheral vascular disease

Thrombo-embolic disease (anti-coagulatns)

  • atrial fibrillation
  • Venous thrombo-embolism (DVT, PE)
  • Prosthetic cardiac valves
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12
Q

What is unfractionated heparin used for?

A

Has to be given intravenously.

Acute coronary syndrome (MI)
Thromboembolism
- venous (DVT, PE)
Arterial - AF
Temporary warfarin therapy - such as in pregnancy

Has to be given intravenously. But has a rapid offset. Can just stop to reduce effects.

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13
Q

How does unfractionated heparin work?

A

Binds to and increase the activity of anti-thrombin III, which inactivates thrombin and factor Xa. Also inhibits IXa, XIa and XIIa.

Requires APTT monitoring

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14
Q

What are the adverse events of unfractionated heparin?

A

Brusing/bleeding

Heparin induced thrombocytopenia - check platelets levels - it is an autoimmune antibody generated against the heparin but recognizes platelets - only treatment is to stop treatment

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15
Q

How do you reverse fractionated heparin?

A

Stop heparin - short half-life
Protamine i.v.
Monitor APTT

Protamine dissociates heparin from antithrombin
irreversible binding to heparin

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16
Q

How does low molecular weight heparin work?

A 
Binds anti-thrombin III
Inhibits factor Xa only
More predictable than unfractionated
Patients can administer it themselves
No monitoring required
Can give subcutaneously

Less thrombocytopenia than unfractionated, but can’t be monitored by APTT or reversed by protamine.

Care needs to be taken with renal failure. - excreted by kidneys

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17
Q

When is LMWH used?

A

Non-stemi
STEMI
Initial DVT/PE Rx
Warfarin alternative

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18
Q

How do you treat PE/DVT?

A

Give LMWH for arround 5 days and give warfarin. When the INR is therapeutic then stop heparin

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19
Q

When do you give warfarin?

A

Treatment of venous or arterial thrombosis.

  • DVT/PE
  • Mural thrombosis (post anterior MI to reduce the risk of embolism).

Prevention of venous or arterial thromboembolism

  • mechanical, heart valves
  • Atrial fibrilation
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20
Q

What are the main ACE inhibitors?

A

They all end in pril

Cilazapril
Captopril

Renally excreted.

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21
Q

What are the main angiotensin antagonists?

A

They all end in sartan

Candesartan
Losartan

Renally excreted.

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22
Q

What does the RAAS system do?

A

Regulates

  • blood pressure
  • intravascular volume (Na/K)
  • Fetal development
  • sympathetic system regulation

Juxta-glomerular cell produce circulating renin

Locally produced RAA - myocardium, vascular endothelium and adrenal

It is also involved in pathology:
Increased activity in heart failure and hypertension
Involved in chronic heart failure progression
- Cardiac hypertrophy
-Atherosclerosis development and plaque rupture
-Proinflammation

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23
Q

What do ACE inhibitors do?

A

Prevent the conversion of angiotensin I into angiotensin II.

Also prevents the breakdown of bradykinin and substance P, which also have beneficial vascular effects.

The excess Angiotension I then goes to angiotensin (1-9) then (1-7), which have anti-hypertensive functions

Over time, other things begin to produce Ang II in the presence of an ACE inhibitor.

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24
Q

What do angiotensin II antagonists do?

A

Inhibit angiotensin II type I receptors

Angiontensin II is still formed but can only bind AT-2,

Type II receptor stimulation is beneficial - induces tissue repair, vasodilarion, kidney development

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25
Q

What does angiotensin II do?

A

Increases aldosterone

  • Na retention
  • K loss
to cardiac myocytes:
- hypertrophy
Apoptosis
Increased O2 consumption
Impaired relaxation

Peripheral artery:
Vasoconstriction
Hypertrophy
Decreased compliance

Causes fibrosis

Coronary artery:
Vasoconstriction
Endothelial dysfunction
Atherosclerosis
Thrombosis
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26
Q

What happens when you give ACEi or AIIA?

A

Vasodilation:

  • decreased arterial and venous pressure
  • decreased preload and afterload

Decreased blood volume

  • natriuresis
  • diuresis

Decreased sympathetic activity
Decreased cardiac and vascular hypertrophy

They are vasodilators but don’t cause tachycardia.

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27
Q

When do you give ACE inhibitors?

A

Hypertension

  • monortherapy and combination therapy
  • Diuretic + ACEi (synergistic combination)

Congestive heart failure

  • as part of multiple treatments
  • ACEi (or AIIA)
  • Diuretic
  • beta blocker
  • aldosterone antagonist (spiralactalone)
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28
Q

When do you give AIIA ?

A

In patients who can’t get ACE inhibitors

  • Hypertension
  • Heart failure
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29
Q

What are the side effects of ACEi?

A

Dry cough, tickly
- because of bradykinin/substance P

Hyperkalaemia - because it reduces aldersterone
Renal function deterioration

Hypotension

Don’t give in pregnancy.

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30
Q

What are the side effects of AIIA?

A

No dry cough because of no increase in bradykinin

Hyperkalaemia - because it reduces aldersterone
Hypoension
Renal function deterioration

Don’t give in pregnancy.

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31
Q

What are the cautions with use of AIIA and ACEi?

A

Monitor potassium
Renal impairment
Volume depleted patients - because they depend on the RAAS system

Do not use in bilateral renal artery stenosis or pregnancy

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32
Q

What is bilateral renal artery stenosis?

A

Perfusion pressure in the glomerulus is reduced wehn the artery to the kidney is stenosed. Angiotensin II is produced to constrict the efferent arteriol to increase that pressure.

If you give AIIA or and ACEi then that reduces the efferent constriction and the GFR is reduced significantly

Need to monitor the creatinine.

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33
Q

Why don’t you give ACEi or AIIA in pregnancy?

A

It is important in kidney development.

ACEii/AIIA crosses placenta - only necessary in 2nd and 3rd trimester

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34
Q

What is the role of ANG II in diabetes?

A

It can promote abnormal glucose handling.

Reduces reduced insulin sensitivity.

It may prevent the development of diabetes

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35
Q

Should you give and AIIA and an ACEi?

A

No, adverse events really bad.

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36
Q

Future directions?

A

renin inhibitors

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37
Q

What are the likely causes of DVT?

A

Virchow’s triad: stasis, endothelial damage, hypercoaguability.

Stasis: flight, obese

Family history of VTE: factor V lieden, lupus anticoagulant,
Previous DVT

Tumour history: estrogen y
Drugs

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38
Q

Why is there swelling, redness and heat with a DVT?

A

Because the blockage increases the pessure in the capllaries ausing more fluid to leave the vessels at the capillaries causing oedema.

It is red and hot because of the imflammation.

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39
Q

What are the treatment options for DVT?

A

LMW Heparin (enoxaparin; clexane) - given sub cut.

Warfarin also if long term treatment. Can be given orally.

Analgesia
Elevate leg

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40
Q

What are the problems with warfarin and what else could be used?

A

Warfarin has drug interactions and the INR needs to be checked twice weekly.

Dabigatran does not need to be checked with blood tests but is required twice daily. blocks thrombin directly Given orally.

Rivaroxaban only once daily with no blood tests.

Both dabigatran and rivaroxaban are excreted renally, may need dose changes in poor kidney functionand shouldn’t be given with a GFR <30.
These are also not good for people with metal heart valves.

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41
Q

Is there an antidote for rivaroxaban?

A

No

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42
Q

What are the treatments for PE?

A

LMWH
Warfarin

You can do thrombolysis in those with severe PE with right heart impairment

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43
Q

What are the risks associated with atrial fibrillation?

A

High heart rate can cause heart failure because the high rate increases you cause ischaemia because of reduced ejection fraction that requires remodeling -> heart failure.

A thrombus can form in the left atrial appendage. This can cause a stroke. They need anticoagulation.

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44
Q

How do you treat someone with atrial fribulation?

A

Can either try and slow the heart rate or try to convert them to sinus rhythm.

Rate control:
- beta blocker
+/- diltiazem

Blood pressure control
Lipid control (cholestrol)
Anticoagulation:
- aspirin vs warfarin vs dabigatran other anticoagulant. CHAD-VAS score

Heparin is not needed. No rush for anti-coagulation.

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45
Q

When do you give warfarin with atrial failure?

A

CHADS-VAS score.

Congestive cardiac failure
Hypertension
Age >75
Diabetes
Stroke
Vascular damage
Age (>65)
Sex female

Score 2 or more = warfarin

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46
Q

How do you know the risk of haemorrhage on anti-coagulation?

A

HAS BLED score

Hypertension
Abnormal blood results - (creatinine or liver function tests)
Stroke
Bleeding previously
Labile INR
Elderly >65
Drug use (alcohol)

3 or above = no treatment because its too risky.

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47
Q

What is a alpha 1 receptor blocker?

A

Doxazosin

Causes vasodilation and hypotension by acting on the postsynaptic receptors receptors and inhibiting NA induced vasoconstriction.

Also has an effect on prostatic smooth muscle.

Used once daily. Oral.
Mainly faecal elimination. Elimination half-life 22 hours. Linear kiertic. Peak plasma level in 2-3 hours. Reversible binding.

Side effects:
Postural hypotension - take drug at night before bed or take a low does.
Urinary incontenance in women 
Feeling tired
Nasal stufiness
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48
Q

What is a alpha 2 receptor blocker?

A

Blocking increases norepinephrine release by blocking the presynaptic receptors that inhibit NA release.

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49
Q

What drug inhibits both alpha 1 and alpha 2 receptors?

A

Phenoxybenzamine
Used in phaeochromocytoma

Irreversible binding
Oral
Can cause postural hypotension, tachycardia

50
Q

What is the first line therapy for raised blood pressure?

A

Diuretic, beta blocker and ace inhibitor.

Third line could be an alpha blocker

51
Q

What are alpha blockers used for?

A

To treat hypertension, usually as an add on.

To treat prostatism, causes relaxation of the smooth muscle in the prostate that helps urination.

52
Q

What are the combined alpha and beta blockers?

A

Labetalol

  • reversible antagonist
  • hypertension in pregnancy
  • phaeochromocyoma

Carvedilol
-congestive cardiac failure

53
Q

What is a drug that is specific for the prostatic alpha receptors?

A 
Tamsulosin
- oral
-competitive antagonist
Blocks alpha 1a and d subtypes
Relaxes thebladder and prostate smooth muscle
Less postural hypertension
 Little effect on blood pressure.
54
Q

What are Ca channel blockers used for?

A

Hypertension
Angina
Arrhythmias - supraventricular tachyarrhythmias
-Atrial fibrilation/flutter (they reduce the potentials that get through the AV node and into the ventricle, i.e they don’t convert to synus rhythum but reduce ventricular rate.)
SVT termination

Vasospasm - such as Raynaud’s phenomenon or cerebral vasospasm vb bn

55
Q

How do Ca channel blockers work?

A

They block the L-type Ca channels in cardiac and smooth muscle tissues.

Decrease arteriolar smoooth muscle tone
Decrease peripheral vascular resistance
Decrease blood pressure/ decrease afterload

In cardiac cells - decrease contractility
Decrease sinus node rate and AV node transmission

56
Q

What are the different classes of Ca channel blockers?

A

Dihydropyridine (nifedipine, amlodipine)
- function on resistance vessels

Benzothiazepine (diltiazem)
- effects on both the resistance vessels an on the heart. Reduce heart rate and reduce cardiac work and vasodilation.

Phenylalkylamine (verapamil)

  • functions on the cardiac tissue to slow the heart rate, can also decrease inotropy. Don’t want to give for heart failure. because it does decrease inotropy. Used for heart rate control.
  • also can cause constipation.
57
Q

How are Ca channel blockers administered?

A

All can be oral

Diltiazem and verapamil can be given i.v., this is important to treat supraventricular tachycardia.

Formulations can also be made with the capsule to decrease the administration. Sometimes the capsules can be found in the poop.

58
Q

What is nifidepine used for?

A

hypertension
Vasospasm (raynald’s)

Oral
Renal excretion
Flushing, headache and peripheral oedema. This oedema is not helped by diuretics so need to reduce drugs.

Low half life so slow release capsules is required.

59
Q

What is diltiazem used for?

A

Angina (reduces HR and heart work)
Hypertension
Tachyarrhythmias (AF rate control) - can be used with a beta blocker here.

Oral and iv

60
Q

What is verapamil used for?

A

Tachyarrhythmias (SCT, AF- rate control)
Hypertension

Don’t use in combination with a beta blocker. - too potent and cause AV node block.

Negatively ionatropic so shouldnt use in heart failure.

Oral and iv

Inhibits cytochrome P450- 3A4
- care with statins such as simvistatin

Inhibits p-glycoproteins
- increases digoxin/cyclosporin

61
Q

What is a quick way to block Ca channels?

A

Clevidipine - broken down quickly so needs to be given i.v.
Good to treat sever hypertension in a crisis.
Dose can be easily controlled by constant infusion.

Good in intensive care.

62
Q

What would you give to an older man with asthma and stable angina?

A

Beta blockers would usually be given to treat angina but they are contraindicatd in those with asthma because of beta agonist use.

Need to give an alpha channel blocker. Diltiazem, would lower blood pressure, heart rate and heart work.

63
Q

What are the indications for beta blockers?

A

Hypertension
Angina - reduce heart and cardiac work
heart failure - metoprolol increases the expression of beta 1 receptors back to normal levels.
Post MI
Arrhythmias (atrial fribillation/flutter and SVT)

64
Q

Where are the different beta receptors?`

A

Blood vessels - alpha 1 (constriction) and beta 2 (dilation)
Heart - beta 1 (tachycardia, increased contractilty)
Bronchi - beta 2 (relaxation)
Kidneys - beta 1 and beta 2 (renin release)

65
Q

What are some beta blockers and what are their main targets?

A

Metoprolol
Binds beta 1 more than beta 2 - lipid soluble so hepatic secretion

Propranolol
beta 1 = beta 2

Labetalol - mixed alpha and beta (1 and 2) antagonist - used in hypertension and in pregnancy.

66
Q

How are beta blockers eliminated?

A

Either via the liver or kidneys.

Water soluble are excreted by the kidneys and have a long half life - need good renal function.

Lipid soluble are excreted by the liver - short half life. need a slow release capsule.

All given orally.

67
Q

What are the effects of beta blockers?

A

Blood pressure lowering

  • reduced cardiac output (decreased HR and work)
  • reset baroreceptors
  • Renin inhibition
  • cross the blood brain barrier and reduce sympathetic activity
  • reduce presynaptic norepinephrine release -> decreasing peripheral resistance

Negative chronotropic by decreasing beta 1 stimulation at the SA and AV nodes.

Inotrophic effects - negative effect short term/acute)
Positive effect (chronic/long term)
Therefore, use other medications first  and then add a small dose when stable. It is bad to use immediately in acute heart failure.

In the lungs the cause asthma attaches in those with asthma.

In diabetics - decreased glyconeogenolysis - can’t produce glucose when hypotension. Not only does it reduce the response to hypoglycaemia it reduces symptoms of it. Just warn diabetics.

68
Q

What are the side effects of beta blockers?

A

Asthma exacerbation

Hypotension
Bradycardia
acute heart failure issue
Tired
Bring on nightmares
Erectile dysfunction
Mask hypoglycaemia
Drug withdrawal occurs because of increased postsynaptic beta receptor expression. This can cause increased sympathetic response after withdrawal  -> angina. Need to gradually reduce.
69
Q

What are the drug interactions for beta blockers?

A

Verapamil (calcium channel blocker) - reduces heart rate. Together with a beta blocker can cause complete AV block.

Diltiazem - just use caution.

Other BP lowering drugs

70
Q

How do beta blockers mediate their effects?

A

Decrease cardiac sympathetic tone - decrease heart rate, increase diastolic filling, decrease oxygen consumption

Upregulation of beta receptors

Attenuate apoptosis

Improve baroreceptor function

Improve LV remodeling

71
Q

What is the value of hypertension?

A

> 140/90

72
Q

Problems with treating hypertension?

A
  • Lifelong disease
  • concurrent diseases
    perceived benefit of treatment
  • asymptomatic
  • need adherence
  • side effects
73
Q

What are the drugs used to treat hypertension?

A

ABCD

Ace inhibitors / Angiotensin II antaonists
Beta blockers
Calcium channel blockers
Diuretics - thiazide, loop, aldosterone antagonists

Alpha blockers

74
Q

What are the features of an ACEi?

A

This is the first line therapy for most people with hypertnsion.

Cilazapril

Side effects of cough, angiooedema, hyperkalemia

75
Q

What are the features of an Angiotensin II antagonist?

A

Candesartan (losartan)

Side effects of hypotension and hyperkalaemia (decreased aldosterone)

76
Q

What is the mechanism of action of beta blockers?

A

They are second or third line therapy for hypertension

Antagonis beta-adrenoreceptors

Mechanism of reducing blood pressure
- reduce cardiac output
reset baroreceptors
renin inhibition
reduce sympathetic activity
reduce norepinephrine release
77
Q

What line of treatment are Ca channel blockers for hypertension?

A

Third line.

Usually given are the vasodilators used for hypertension, such as nifidepine and amlodipine

78
Q

What are the features of thiazide diuretics?

A

Bendrofluazide

Also first line therapies. particularly the thiazides

They inhibit the Na/Cl exchange channel in the distal convoluted tubule. Weak diuretics.
Also cause vasodilation (open vascular K+ channels) -> this is the main path for blood pressure reduction.

Thiazide diureticus initially reduce the fluid volume, but this activates the RAAS system, which then returns the volume to normal. However, the BP remains reduced because of the vasodilator role.

Side effects: metabolic

  • increase glucose.
  • increase urate levels ( a problem for gout)
  • decrease potassium, Na and Mg
  • erectile dysfunction
79
Q

What are the features of loop diuretics?

A

Frusemide

  • inhibit the Na/K/Cl cotransporter in the thick ascending limb
  • potent diuretic
  • they have little anti-hypertensive effect alone because the RAAS activity that is stimulated by the diuresis counter acts that diuresis. Has a potent effect if used with ACEi (this stops the compensatory fluid return from RAAS)
  • used in heart failure
  • used in resistant hypertension

Side effects: dehydration/polyuria
Decrease in Na, K and Mg

80
Q

What is the best treatment combination for hypertension?

A

Diuretics and ACEi

81
Q

What are the features of the potassium-sparing diuretics?

A

Third line or beyond - good for people with aldesterone issues

Spironolactone (aldosterone antagonist)
- inhibits distal Na/K exchange in the collecting duct

Side effect:

  • hyperkalaemia
  • dehydration
  • gynaecomastia (oestrogen like structure)
82
Q

What are the features of alpha blockers

A

Second or third line therapy

83
Q

When should you decide to treat hypertension?

A

Persistent BP of >160/100

> 140/90 and at a high cardiovascular risk for another reason, such as

  • cerebrovascular disease
  • coronary artery disease
  • LVH
  • heart failure
  • DM
  • Proteinuria/renal impairment

Or if you have a 10 year cardiovascular risk of >20%

84
Q

What the differences in the hypertension in those <55 and those >55?

A

A (orB) then in older C or D

If need combination then add one from the other group.

Best combo is Diuretic + ACEi + vasodilator
e.g. bendrofluazide + cilazapril + felodipine

Those <55 with hypertension usually have a renin associated issues. They should be treated with an ACEi (or ARB) or a beta blocker.

Those >55 usually have less of a role of renin and should be put on a diuretic or Ca channel blocker

If one treatment doesn’t work then add the other sides drug, i.e an ACEi and a diuretic

85
Q

What is the most effective tripple therapy to lower blood pressure?

A

Diuretic + ACEi + vasodilator

e.g. bendrofluazide + cilazapril + felodipine

86
Q

What should you do in pregnancy and hypertension?

A

Maternal and fetal complications can develop

> 140/90 mmHg

Give a beta blocker (lebetalol)
a Ca antagonist - nifedipine

Don’t use ACEi/AIIA, diuretics or atenalol

87
Q

What patients do you use an inotrope for?

A

Patients in shock. - inadequate organ perfusion to meet the demand.

  • hypovolumeic - haemorrhage/dehydration
  • cardiogenic
  • distributive - sepsis or anaphylaxis
  • obstructive e.g.pulmonary embolism

have to give the ionotropes into central vessels because it would take too long in periphery vessels because of their condition.

88
Q

What are the goals of shock resuscitation

A

Restore blood pressure
Normalize systemic perfusion
Preserve organ function
Treat underlying cause

89
Q

What do you want to do in cardiogenic shock?

A

Cardiogenic shock is when there is high systemic resistance and low cardiac output

Make the patient euvolemic because this with maximize the CO.

Then use ionotropes to increase CO and therefore global perfusion. They can cause tachycardia and myocardial oxygen consumption so increased risk of myocardial ischaemia and arrhythmias.

90
Q

What are some vasopressor/inotropic agents?

A

Alpha and beta adrenoceptor agonists

  • norepinephrine
  • erpinephrine
  • dobutamine
  • dopamine

They are either alpha 1 or beta 1 agonists - opposite to hypertension medication.

alpha 1 receptors are mostly in blood vessels stimulate vasculalar smooth muscle contraction - norepinephrine

Beta 1 receptors are mostly in the heart and they stimulate heart contraction and increase heart rate - dobutamine

Most drugs vary in their alpha 1 and beta 1 receptor stimulation

91
Q

What are the features of norepinephrine?

A

First choice vasopressor (constriction)
Potent alpha 1-adrenergic agonist - vasoconstriction
Increases peripheral resistance
Increases BP

Taken into the presynaptic neuron via the uptake 1 method.

Minimal beta 1-adrenergic agonism

Short half-life - continuous intravenous infusion

92
Q

What are the features of adrenaline?

A

Mixed alpha and beta-adrenergic effects - depends on the expression of these receptors in a given organ.
Mostly alpha if given systemically

Beta 1 stimulation causes vasodilation and alpha 1 stimulation cause vasoconstriction.

Increases heart contraction and rate.

During anaphylaxis it is a vasoconstriction - Increase in BP and dilates bronchi

93
Q

What are the features of dobutamine?

A

Beta 1 agonist mostly in the heart - potent positive inotrope and variable chronotrope

half-life = 2 minutes

hepatic metabolism

94
Q

What are the features of dopamine?

A

Short T1/2

Low dose = vasodilation in the renal vessels

Moderate dose - beta 1 agonist on the heart

high dose = alpha 1 agonist

95
Q

What are the side effects of vasopressors?

A

In shock, sympathetic activity is alredy high and alpha agonism (vasoconstriction) can cause ischaemia - cardiac, limb, gut and cerebrovascular

Increased cardiac work - cardiac ischaemia and arrhythmias

96
Q

What do the phosphodiesterase inhibitors do?

A

Amrinone and milrinone

  • phosphodiseterase III inhibitor
    Prevents the break down cAMP.
  • this causes vasodilation in vessels and inotropy
  • causes increased mortality, arrhythmias
97
Q

What does levosimendan do?

A

It improves the sensitivity of troponin for Ca. causes increased inotropy

increased risk of arrhythmias and increased mortality

98
Q

What are the features of digoxin?

A

Third line to control atrial fibrilation rate control and in acute heart failure with fast atrial fibrilaiton

Used for atrial fibrillation

  • slows the heart rate
  • improves cardiac work
  • acute/ chronic heat failure

No effect on mortality
Improves symptoms

Eliminated in the kidneys
Long half life (1.5 days)
need to give a loading dose.

It functions by blocking the Na/K ATPase - this causes increase intracellular Na. This stimulates the Na/Ca exchange that then takes Ca into the cell and Na out. Ca increases contractility.

It competes with K+ at the Na/K ATPase. Thus if less extracellular K+ then there is less competition for digoxin -> more chance of toxicity.

It slows ventricular response rate by increasing vagal tone at the AV node. Slows conduction through the AV node.

Side effects: nausea/vomiting
diarrhoea
abdominal pains
Fatigue
Changes in ECG (reverse tick sign)
Arrhythmias

Digoxin interactions include - decreased K+ or Mg2+ - this increases the digoxin effect and side effects
- quinidine, amiodarone, verapamil, diltiazem, erythromycin

P-glycoprotein in the kidney excretes digoxin. Blocking can cause toxic levels of digoxin.

Can monitor digoxin levels in the plasma.

99
Q

What are the order of drugs given to treat rate control atrial fibrilation?

A

First line - beta blocker (metropolol; try as monotherapy)
then diltiazem added
Then digoxin

100
Q

What does insulin do and what counter regulates this?

A

Regulates the glucose and lipid metabolism

Stimulates glucose uptake in muscle and adipose tissue, stimulates glycolysis, glycogen synthsis, potein synthesis, and uptake of ions (K+).
It stops glucogenesis, glycogenolysis, lipolysis

Glucagon and catecholamines (adrenaline) and cortisol and growth hormone counter regulate this

101
Q

What are lipids?

A

Cholesterol
Triglycerides
Fatty acids
Phospholipids

102
Q

What is the role of LDL?

A

To transport cholesterol from the liver to the circulation and peripheral tissues.

Increases LDL increases cholesterol transport and increases the chance of athersclerosis

103
Q

What is the role of HDL?

A

Pick up cholesterol from the peripheries and deliver it to the Liver

Increased HDL levels slow athersclerosis

104
Q

Why lower cholesterol?

A

Secondary event prevention for those who have had an MI, stroke, peripheral vascular disease. Reducing LDL reduces their mortality

Less clear benefit to prevent primary disease

The impact of cholesterol has a synergistic effect with other factors, such as smoking, hypertension, diabetes

105
Q

Who do you treat with statins?

A
  • those with angina, MI, CVA, peripheral vascular disease, diabetes

Primary prevention for those with >30% risk over 10 years

106
Q

Name the lipid lowering drugs?

A

Statins - decrease total cholesterol by lowering LDL mainly. Slightly increase HDL and decrease triglycerides
- simvastatin and atorvastatin

Fibrates - bezafibrate
- decreases triglycerides 30-50% (decrease LDL and increase HDL).
Can be given in combination with statins

Ezetimibe - low efficacy as a monotherapy
Use with a statin

107
Q

How do statins work?

A

They reduce HMG CoA reductase, which inhibits the production of cholesterol in the liver.

The hepatocytes still needs cholesterol to perform its functions and so it increases the expression of the LDL receptor to acquire LDL from the blood and uses it to function.

CYP3A4 degrades statins - this is blocked by amiodearone, verapamil, diltiazem and erythromycin

108
Q

How do fibrates work and what are the side effects?

A

Bezafibrate

Reduce triglycerides

May be used in combination with statins

Is an agonist of PPARalpha.
Reduces synthesis of VLDL and increases absorption in the liver. Activates lipoprotein lipase to breakdown triglycerides.
- side effects
mylgias
GI upset
Deranged liver function tests
109
Q

What is the mechanism of action of Ezetimibe and what are the side effects?

A

Reduces LDL cholesterol absorption

Can use with statin - low efficacy as a monotherapy

Decreases intestinal absorption of cholesterol to the liver
Increase expression of hepatic LDL receptors

Side effects - abdominal pain
diarrhea

110
Q

What are some drugs that increase your blood pressure?

A

NSAIDs and the contraceptive pill, steroids, licorices

111
Q

What are do you look for if suspecting primary hypertension?

A 
Obese (cushingoid)
BMI
Blood pressure
Radial femoral delay
Abdominal bruit
Renal masses
Echo
CXR
Urine dipstick
urine glucose
Aldosterone / renin ratio
MRI checking for renal artery stenosis
112
Q

When can you use rivaroxaban?

A

VTE and AF

113
Q

What drug would you use for someone who is hypertensive and has nocturia?

A

Doxazosin -blocks the alpha channels that control the smooth muscle of the vessels and prostate

Worn about dizziness when standing

114
Q

What are the side effects of Ca channel blockers?

A

Flushing, headache and peripheral oedema.

115
Q

When are beta blockers used?

A

Angina - to reduce HR and cardiac work. They improve the ejection fraction, decrease O2 consumption.
- give metoprolol

Post MI
- decrease arrhythmias,

Heart failure

  • stable and chronic
  • meoprolol

Hypertension - 3rd line - metoprolol

116
Q

During heart failure, when should you give beta blockers?

A 
Inotrophic effects - negative effect short term/acute)
Positive effect (chronic/long term)
Therefore, use other medications first  and then add a small dose when stable. It is bad to use immediately in acute heart failure.
117
Q

What drugs are good for what illness combinations?

A

ACEi - hypertension + HF

Beta blocker - Angina/HF + hypertension

Diuretics - hypertension + HF

Alpha blockers - hypertension + prostatism

118
Q

What are drugs that you need to give for angina?

A

Anti-platelet
Decrease function (Ca of beta blocker)
Statin

119
Q

What do you need to monitor in someone you are treating for hypertension?

A

Monitor potassium

BP

HR

120
Q

What are the side effects of statins?

A

Side effects - skeletal muscle aches and pains

  • myopathy
  • rhabdomyloysis
  • shouldn’t be used during pregnancy or breast feeding
  • abnormal liver function tests

RBF (9 decks)

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