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Pharmacology > Week 3 & 4 > Flashcards

Week 3 & 4 Flashcards

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1
Q

Why is there both a vasoconstrictor and vasodilatory effect within the Sympathetic nervous System

A

constriction in areas where blood flow needs to be diverted e.g. GIT and dilation in areas where more blood is needed e.g. Skeletal Mm.

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2
Q

A1 receptor locations and function

A

Blood vessels
Bladder (int. sphincter)
GIT (sphincters)
Iris Dilator Mm.
Arrector pili.

CONSTRICT

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3
Q

A2 receptor location and function

A

Presynaptic neurons .

act to inhibit noradrenaline release and cause negative feedback

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4
Q

Location and function of B1 receptors

A

Heart (PM and myocardium)
kidney (glomerulus)

constriction.

can also increase HR & force of Heart contraction.

Releases renin in renal system.

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5
Q

Location and function of B2 receptors

A

Bronchioles -> dilates.
Uterine smooth mm. -> relax
blood vessels -> dilate
bladder (detrusor mm.) -> relax
liver (glycogenesis)
Eye - ciliary mm. -> lense is relaxed for distance vision

DILATE/RELAX

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6
Q

Location and function of B3 receptors

A

Fat cells -> lipolysis (extra E for skeletal Mm.)

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7
Q

What is the main difference between using a higher dose of adrenaline and a lower dose ?

A

higher: a1 stim (constricts)

lower: b2 stim (dilates)

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8
Q

Why is adrenaline used to overcome anaphylaxis ?

A

we need to reverse the effects of HISTAMINE released by the body.

A&B stim will cause vasoconstriction and bronchodilation.

(Histamine causes the opposite, vasodilation and bronchoconstriction).

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9
Q

Side effects of A1 agonists

A

HTension
May precipitate angina
Rebound congestion through the use of decongestants (body becomes less sensitive to A agonists)

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10
Q

Main use of B agonists

A

Asthma & delaying pregnancy

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11
Q

Main uses for B blockers?

A

Protection from cardiac arrhythmia
Angina
Htension
Migraine prophylaxis (= prevention)
Glaucoma

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12
Q

How do B - blockers help prevent cardiac arrythmia ?

A

Cardiac mm. is irritable post - MI and has increased risk of arrhythmia.

Cardioselective B - blockers can be used to stop the stimulatory effect of adrenaline on the heart.

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13
Q

What effect does B - blockers have on BP and what is their main danger?

A

Lower BP by causing vasodilation and decreasing force of contraction but can cause reflex vasoconstriciton and therefore SHOULDNT BE USED ACUTELY.

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14
Q

Why are B - blockers useful for migraine prevention?

A

Vasoconstriction causes less blood to reach the brain and therefore reduces intracranial pressure.

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15
Q

What part do B blockers play in glaucoma treatment?

A

block B receptors that typically cause aqeuous humour production.

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16
Q

why cant B - blockers be used acutely?

A

Chance of rebound vasoconstriction

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17
Q

muscarinic agonists(drugs) to constrict pupil

A

carbachol, pilocarpine

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18
Q

Drugs that increase Aqueous humour drainage

A

Prostaglandin F2 agonists (latanaprost, bimaraprost)

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19
Q

Contrainindications to B blockers

A

Asthma
COPD
Cardiogenic shcok
Bradycardia
Hypotension

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20
Q

B blockers adverse affects

A

Hypotension
Bronchospasm
Cold hands and feet (due to poor circulation)
Dizziness and fatigue
Reduce response / signs to hypoglycaemia
Decrease HDL
Insomnia
Nightmares

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21
Q

2 types of cholinergic receptors and where they are found

A

Nicotinic (smooth mm, brain and PNS) and muscarinic (organs, glands - involved in parasymp response and brain).

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22
Q

Main use of muscarinic agonists

A

Glaucoma

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23
Q

Main use of muscarinic antagonists

A

Asthma
Anti-spasmodics
Diarrhoea
Motion sickness

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24
Q

Ipratropium use

A

Bronchodilation (muscarinic antagonist)

Can be used with a B blocker to increase effects

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25
What do cardiac glycosides do?
control Calcium levels in heart
26
resting BPM for bradyarrhythmia?
60 or below
27
resting BPM for tachyarrhythmia
above 100
28
TypesofSupraventricular T- Arrhytmia
Paroxysmal Supravntricular Tacchycardias Atrial fib
29
typesVentricular T-arryhtmia
Prem. vent. contractions Vent. tachycardia vent. fib.
30
Who is typically at risk of SVT
More common in younger ppl.
31
acute treatment for SVT
valsalva and anti-arrhyth- drugs (Adenosine IV)
32
Long term treatment for SVT
Catheter ablation anti-arrhyth- drugs.
33
Bradycardia ECG
Large break between next PQRST wave
34
Sick sinus syndrome is?
SA node not producing electrical activity fast enough (bradycardia/arrythmia)
35
Heart block degrees on ECG
1st: slow signal that gets through - Elongated PR 2nd: Some signals get through, others do not. - skipped beats 3rd: no signals getting through. - atria and vent. operate independently.
36
what level of heart block often get treated with Pmaker?
2nd and 3rd. sometimes 1st but not often
37
which anti-arrythm- drugs mainly act on vent. cells?
Flecainide (blocks Na+ fast channels) - blocks initial action potential Lignocaine (blocks Na+ fast channels) Amiodarone. (blocks outwards K+ current) - blocks repolarisation
38
Adenosine main use for arrythmias?
SVT in acute care.
39
Why can Adenosine only really be used in acute care for arrythmia?
short 1/2 life.
40
Drugs best used for long term treatment of SVT?
Dilitiazem and verapamil (Calcium channel blockers)
41
Dilitiazem and verapamil can be used to treat for Ventricular Tachcardia but are often not, why?
chance of sudden death (yikes)
42
What arrythmic condition is digoxin mainly used for?
Atrial fib.
43
main risk of digoxin?
narrow TI
44
How do Flecainide and lignocaine work?
blocks FAST NA+ channels & have greater effect of ventricular cells although have shown proarrhythmia.
45
What are often preferred over Flecainide and lignocaine?
Ablation or implanted devices.
46
What is Amiodarone effective against?
VT, SVT (best at these two) and AF (but only used if other treatments arent effective).
47
main draw backs of amiodarone?
Bound in tissues - Requires loading dose and days/ weeks for actions to develop. Side effects : phlebitis (if Periph. I.V.), photosensitive skin rashes, blue skin discolouration, thyroid abnormalities, pulm. fibrosis.
48
SVT treatments acute
Sometimes solve themselves Vagotonic manoeuvres (avoid carotid massage in elderly). Adenosine IV.
49
SVT treatments Long term
Catheter ablation of abnormal pathways. Verapamil or B blocker.
50
AF treatment pathway
Anti-coags (warfarin) to control stroke risk. Bring vent. rate down to below 110BPM. (B blockrt, dilitiazem or verapamil -> digoxin on elderly). Cardioversion -> (DC or drug induced)
51
VT Treatment (acutely)
DC cardioversion Lignocaine Flecainide Amiodarone
52
VT Treatment (Long term)
Ablation Implantation of devices
53
main risk of using drugs for arrhytmias?
always a risk of worsening arrhythmia
54
Causes of heart failure
mainly Left Vent damage. CHD Previous MI HyperTen. Cardiomyopathy (disease to heart muscle). Failure of mitral valve - retrograde blood flow to L. Atria,
55
Main events leading to CONGESTIVE heart failure
1. Failure of L vent.: reduced musc contraction, reduced blood flow and blood pressure (systemically). Blood pools and flows retrograde , back into pulm Aa. .. Increassed pressure on right side of heart, -> R vent failure... back up increased blood pressure into venous system. 2. kidneys detect lowered blood pressure (flowing to it) RAAS activated. Sodium and h20 retention occurs. blood volume increases. further pressure in body and veins. adema in feet and ankles + pulm odema.
56
How does RAAS work?
Renin (enzyme) is released and converts Angiotensin into Angiotensin 1. AGT 1 goes to lungs and is converted into AGT 2 using AngioConverting Enzyme (ACE). AGT 2 releases aldosterone and causes retention of sodium and water. + AGT2 causes vasoconstriction.
57
Signs and symptoms of heart failure
-Pulm. oedema. -Sympathetic response. -Infarct. -Pale skin -Splenic and hepatic damage -venous pressure -> peritoneal cavity. -> nausea and vomitting. -Jug. vein distension. Decreased urine output.
58
Pathway to treat heart failure
remove excess fluid and sodium counteract RAAS Restore contraction strength of cardic muscle.
59
How to remove excess fluid and sodium during heart failure?
Diuretics
60
How to counteract RAAS in heart failure
ACE inhibs or Anti-AGT2
61
How to increase heart muscle strength and reduce tachycardia?
Cardiac Glycosides (increase contraction) B-blockers (reduce tachycardia).
62
Example of a cardiac glycoside?
Digoxin.
63
Dangers of Digoxin?
Arrythmias, GIT upsets, Confusion, Delirium, mm. weakness.
64
How do cardiac glycosides work?
inhibs sodium potassium pump. buildup of sodium in cell. Cell counteracts by inhibit the transport of any more sodium in cell and therefore inhbits the movement of calcium out of cell. increase calcium increase strength of contraction and movement of calcium ions accross cell meaning muscle contraction lasts longer.
65
What is Pre load?
Filling of the heart chambers prior to contraction
66
what does an increased preload cause?
increases strength of contraction and workload of heart (workload increases as more powerful contractions cause blood to return to heart faster)
67
What is after load?
resistance that the vent. have to pump against. determined by the pressure in arterial system.
68
what does increased afterload cause?
cardiac workrate.
69
both afterload and pre load require increased energy to increase. but which is the most costly interms of required energy?
Afterload
70
Which coronary artery is often blocked?
LAD
71
what is MI?
Myocardia infarction . clotting resulting in death of cardiac tissue / mm.
72
What drugs can be used to reduce workrate of heart after MI
Cardioselective B blockers or Calcium channel blockers if pt. has airway pathologies Nictotinic agents in some cases.
73
other than decreaseing cardiac workload, whatother effect do calcium channel blockers have?
vasodilatory effect of blood vessels.
74
what is coagulation?
formation of fibrin on top of platelets
75
main anti-coags?
Warfirin (apirin if warfirin is contrainindicated) Heparin
76
risk of warfirin?
narrow TI
77
Can Heparin be used acutely
Yes but is often used for venous thrombi and during surgery to reduce risk of clots.
78
which acts quicker warfirin or heparin?
heparin.
79
Why is warfarin more common than heparin?
warfarin can be ingested orally. Heparin requires subCutaneously or IV
80
what do clot busting drugs activate?
plasminogen
81
types of plaminogen activators?
streptokinase urokinase recumbent human tPA

Pharmacology (6 decks)

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