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MP323 > L18 - L25 > Flashcards

L18 - L25 Flashcards

1
Q

Beta Blockers Action in Heart

A
  1. BB block B1 receptors in heart. meaning NA/A have less effect to increase heart rate.
  2. slows SA node, slowing heart rate allowing LV to fill completely before contraction. easing workload
  3. vascular smooth muscle has B2 receptors which increase cAMP in lungs leading to dilation. blocking B2 leads to constriction of airways which is why BB is contra in asthma patients
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2
Q

B1 Adrenergic Receptor as a Target

-interactions between NA and B1

A

interactions between NA and B1 receptor include:

  • charged amine (+) forms ionic bond with aspartic acid at terminal 3
  • aromatic ring binds phenylalanine at terminal 6 in pi bond
  • hydrogen bonding at catacholhydroxyls & serene amino acids at TM1
  • alkyl groups between wedge OH & amine promote alpha selectivity
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3
Q

Beta Blocker Development

  • Propranolol (non-selective BB causes dizziness)
A
  1. developed by increasing chain link from benzene to amine
  2. reduced the lipophilicity to reduce CNS side effects
  3. it forms a hydrogen bond at specific site absent from B2 to increase B1 selectivity
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4
Q

Practolol & Bisoprolol

  • most selective beta blocker
A

Proctolol - serious liver damage
- separated amide from aromatic ring giving increased selectivity

Bisoprolol
very selective yet still binds to B2 sometimes
- ratio of 1/70
- occupies lipophilic pocket in B1 which isnt in B2

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5
Q

Selectivity of Steroid Hormones

  • Adrenaline / Noradrenaline / Isoprenaline
A

All more selective to Beta adrenoreceptors.
- NA more useful at B1 than iso

Catechol Group = aromatic ring with 2 hydroxyls next to each other

  • wedged OH R config is more potent than S. amide can also gain charge
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6
Q

IV Injection vs Infusion

A

Injection
- 1mm or less
- rapid increase in drug plasma concentration

Infusion
- up to a few litres
- generates steady state

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7
Q

Areas for IV Administration

  • Central line
  • Intra-arterial
A

Central Line
- for high toxicity drugs (anti-cancer drugs)
- rapid dilution in large volume of drug

Intra-arterial
- much greater risk

Intracardiac
- greatest risk only done in life-threatening situations

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8
Q

Injection types

  • Intra-dermal
  • Subcutaneous
  • Intramuscular
  • Intra-articular
A

ID - skin
- volume up to 0.2ml, slow absorption, long delivery
- typically used for vaccines

SC - injected to fatty tissue
- 1ml volume of aqueous solution/suspension
- faster absorption because well vascularised

IM - buttocks/thighs/shoulders
- up to 4ml
- slower systemic absorption than SC

IA - aqueous solution/suspension
- synovial fluid of joint cavities
- anti-inflammatory drugs to treat arthritic conditions

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9
Q

Injection Types

  • Intraspinal
A

Intrathecal - up to 10ml
- only aqueous solutions
- potential to avoid BBB

Epidural
- injection into epidural space
- requires anaesthesia

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10
Q

Chronotropic Control
Sympathetic & Parasympathetic Fibre Action

  • NA
  • ACh
A

Sympathetic
- NA activates B1 in heart, increasing permeability of nodal cell plasma membrane to NA2+ & Ca2+

Parasympathetic
- ACh activates M2 muscarinic receptors , to increase permeability to K+ and decreasing permeability to Na2+ and Ca2+

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11
Q

Vagal Nerve

  • stimulates ACh release
A
  • ACh and parasymp innervation stimulates opening of K+ channels
  • allowing efflux of potassium to lower membrane potential and slow the upstroke
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12
Q

Mechanisms For Heart Arrythmia

  • absolute refractory period - 250ms in myocytes
A
  1. abnormal impulse conduction
  2. abnormal automaticity
  3. re-entry arrythmia
  • Arrythmia is when heart beats irregularly because of abnormal electrical activity
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13
Q

Use for CCB and SCB

A

CCB Use
- SA and AV node are slow conductors , using calcium channels for action potential upstroke
- blocked by CCB
- CCB in vessels stops calcium entering cells , reducing contraction

SCB Use
- atrium and ventricular cells are fast conductors , using sodium channels for ap upstroke
- blocked by sodium channel blockers SCB

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14
Q

Ventricular Cells Action Potential Phases

  • resting at -90mV
A

Phase 0 Depolarisation
- at -70mV voltage gated sodium channels open, resulting in influx and fast rise

Phase 1 Repolarisation
- Na+ channels close & voltage gated K+ channels open, K+ leaves a little to decrease membrane potential

Phase 2 Plateau
- voltage gated L-type calcium channels open due to depolarisation & balances out K+ efflux (causes contraction )

Phase 3
- Ca2+ channels close & K+ efflux dominates, reducing potential to baseline (large efflux)

Phase 4 Return to Resting
- negatic intracellular (90mV) at rest

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15
Q

Action Potential of Nodal Cells

  • phase 4 , phase 0 , phase 3
A

Phase 4 Slow Depolarisation
- Na+ enters at -60mV. at -50mV, T-type Ca2+ opens causing gradual depolarisation

Phase 0 Depolarisation
- depolarisation of Ca2+ influx through voltage gated L-type channels

Phase 3 Repolarisation
- L-type Ca2+ channels close , voltage gated K+ channels open and efflux of K+ is priorities

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16
Q

Classification Of Anti-Arrhythmic Drugs

  • Class I (rhythm control)
A

affect upstroke of action potential by slowing depolarisation - affects phase 0

  • Sodium Channel Blockers
  • targets Phase 0 depolarisation in Ventricular cells or Nodal cells

IC - flecainide.
- majorly inhibits membrane responsiveness to electrical impulses, slowing rate

17
Q

Classification of Anti-Arrhythmic Drugs

  • Class II (rate control)
A

Blocks effects of catecholamines at B1 receptors , reducing Ca2+ influx

  • decreasing SA & AV node conduction & contractility
  • NA opens sodium + Ca2+ channels, BB block this
  • decreases sinus rate
  • Beta Blockers (metoprolol, propranolol)
  • affects Phase 4
18
Q

Classification Of Anti-Arrhythmic Drugs

  • Class III (Rhythm Control)
A

Amiodarone & Sotalol

  • Potassium Channel Blocker, delaying repolarisation
  • has slight Na & Ca channel inhibition effects and blocks beta & alpha receptor selectivity
  • blocks potassium channels in phase 3 repolarisation
  • very long half life 42days
  • works primarily on phase 3 but has effects on phase 0, 1 & 2
19
Q

Classification of Anti-Arrhythmic Drugs

  • Class IV (rate control)
A

Targets AV/SA node conduction & affects contractility so prolongs upstroke. blocks Ca2+ channels phase 4

  • CCBs’ (verapamil, diltiazem)

Verapamil: slows nodal depolarisation at phase 4 (first stage for nodal cells AP)
- decreases contraction force too

20
Q

Digoxin Treatment

  • digoxin increases Ca2+ stimulating K+ channels to shorten action potential and refractory period
A
  1. digoxin exerts positive inotropy effect by binding & inhibiting Na/K ATPase in myocyte membrane
  2. causes increase in intracellular Na+ and Ca2+ due to Na/Ca antiport : stronger contraction
    - Na/Ca pump takes sodium out, bringing Ca2+ in
  • only used in Heart Failure with Arrhythmia
21
Q

Atropine

A
  • reduces effect of excessive vagal activation on heart
  • negative inotropic effect
  • reduces rate of firing
  • reduced conduction velocity
22
Q

Atrial Fibrillation

  • Definition
  • Risk Factors
A

AF is supraventricular tachycardia characterised by disorganised electrical activity
- no significant atrial depolarisation - no P-wave

Risk Factors
- HTN, ACS, CAD, hyperthyroidism, lung diseases, viral infections

Symptoms
- dyspnoae, dizziness, palpitations, tiredness, chest discomfort
- need to confirm with ECG (lack of Pwave)

23
Q

Diagnosing AF

A
  • ECG
  • Holter monitor
  • Loop recorder (records arrhythmic function

Blood results to rule out underlying conditions
- diabetes, hyperthyroidism, anaemia

24
Q

Thromboembolic Risk Assessment

  • CHADSVAS score
    >/= 2 should be offered ac DOAC
A
  • measures need for anticoagulation

C - chronic heart failure 1p
H - hypertension 1p
A - age >65 1p, >75 2p
D - diabetes 1p
S - stroke/TIA 2p
Va - vascular disease 1p
S - gender female 1p

25
Q

Apixaban vs Edoxaban

  • Factor Xa inhibitors
A

Apixaban
- 5mg BD standard
- 2.5mg BD if 2 of following apply:
age > 80 , weight <60kg , creatinine <133mcm/L

Edoxaban
- 60mg OD standard
- 30mg OD if CrCl is 15-50ml/min

if CrCl lower than 15ml/min use warfarin

26
Q

New Onset AF

  • AF onset within 48hrs with haemodynamic instability
A
  • give direct current cardioversion within 48hrs to avoid stroke risk

If Stable
- give flecanide if heart is normal and no past CVD/MI/HF/angina

Unstable - give amiodarone (requires counselling)

27
Q

Rate Control for AF Management

  • controls ventricular rate by using AV nodal blocking drugs
  • BB, CCB, digoxin
A

BB
- antagonises beta receptor, reducing NA binding and less stimulation on AV node, reduces HR

CCB Verapamil
- antagonises voltage Ca2+ channels decreasing intracellular calcium, reducing LV contractility

Digoxin
- only reduces ventricular rate at rest

28
Q

Rhythm Control for AF Management

A

Class IA - quinidine, procainamide

Class IC - flecainide
- contra with MI history because increases risk of pro-arrhythmia

Class III - amiodarone , sotalol
- preferred for patients with HF and blocks potassium channels
- can lead to T4 & T3 inhibition and causes grey skin

29
Q

Amiodarone Counselling

A
  • can inhibit T3 & T4 causing hypothyroidism (weight gain)
  • need to wear sunscreen
  • long half life so S/E will stay for over a month
  • can cause grey skin
  • avoid grapefruit
  • give warning card
30
Q

Anticoagulants

  • warfarin
  • DOACs
  • S/E : bleeding, interactions with antibiotics
A

works on the blood coagulation pathway

Warfarin - vitamin K antagonist. vitamin K releases clotting factor and warfarin stops this
- vitK deficiency, liver/kidney damage
- works more broadly (patients with valve disease)

DOAC’s (apixiban , edoxiban)
- inhibit the factor Xa in the coagulation pathway
- liver/kidney damage, GI upset

31
Q

Antiplatelets

  • prevent activation of platelets
  • aspirin, clopidogrel, ticagrelor
A

Aspirin
- COX-1 inhibitor and cox release platelet activator thromboxane A2. aspirin blocks this

Clopidogrel
- ADP platelet activator release from P2Y12 and clopidogrel irreversibly inhibits this

Ticagrelor
- same as clopidogrel but reversibly inhibits

32
Q

Stroke Subtypes

  • ischemic
A
  • blood clot blocking flow to brain causing complete occlusion
  • do thrombectomy surgery to remove blood clot from
  • can become haemorrhagic if blood clot causes rupture

Long-Term
- mobility (weakness on one side of body)
- ataxia lack of co-ordination
- sensory loss + vision issues
- chronic pain

33
Q

Stroke Subtypes

  • Haemorrhagic
  • usually due to HTN
A
  • internal bleeding in brain due to loss of structure/vessel damage
  • usually in small capillaries in brain due to malignant HTN

Long-Term
- mobility (weakness on one side of body)
- ataxia lack of co-ordination
- sensory loss + vision issues
- chronic pain

34
Q

Stroke Subtypes

  • Transient (TIA)
A
  • brief stoppage of blood to brain causing neurological dysfunction
  • lasts less than 24hrs classes as TIA

Short-Term
- cerebral oedema , seizures , inc. infection risk

35
Q

Primary Stroke Prevention
- A-E

A

A - antiplatelet / anticoagulant
- aspirin 300mg stat on admission (avoided for 24hrs post thrombolysis)
- then aspirin 300mg daily 14days then clopidogrel 75mg daily

  • AF patients this antiplatelet started 10-14days after

B - Blood pressure under 130/80
- If under 55 years old –an ACE inhibitor or anangiotensin receptor blocker (ARB).
- If 55 or older or African – Caribbean origin of any age – a calcium channel blocker

C - cholesterol
- atorvastatin 40-80mg 1st line
- not used in haemorrhagic stroke

D - diabetes
- sliding scale insulin and glucose to keep tight control on blood sugar

E - Exercise
- counselling and lifestyle advice to reduce chance of stroke in future

36
Q

Acute Stroke Care

A
  1. hospitilisation + ASPIRIN 300mg stat
  2. CT scan (quicker than MRI) rules out haemorrhagic stroke
  3. Thrombolysis (alteplase)
    - within 4.5hrs of onset
    - 0.9mg/kg max 90mg dose
    - 10% given bolus 2-3min and 90% given over 6hrs
  4. stop ALL anticoagulants, antiplatelets, NSAID’s or HTN meds because you dont want to limit blood flow

MP323 (4 decks)

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