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PHAR2002 > Term 1 > Flashcards

Term 1 Flashcards

1
Q

What actions do muscarinic antagonists have on the peripheral NS?
5 actions

A
  1. Block of secretions: saliva, tears, bronchial secretion , sweating
  2. Tachycardia – by blocking the vagal inhibition of heart (no change in blood pressure because most of blood vessels have no parasympathetic innervation)
  3. Pupillary dilation (myadriasis) – blocks parasympathetic influence on sphincter pupillae. Myadriasis interferes with drainage via canal of Schlem → raises intraocular pressure. Cyclopegia – ciliary muscle paralysis → paralysis of accommodation
  4. Inhibition of motility and secretion of GI tract
  5. Other smooth muscle is also relaxed (bronchi, bladder)
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2
Q

What actions do muscarinic antagonists (atropine, hyoscine and atropine-like drugs) have on the central NS?
3 actions

A

Atropine – in high doeses causes stimulation, reustign in restlessness, disorientationand hallucinations
More subtle effects – attention and memory – can appear at low doses in the elderly

Hyoscine – powerful CNS depressant, sleep and amnesia
Anti – emetic action (anti-seasickness pills)

Atropine-like drugs – supress the tremor of Parkinson’s – probably by blocking cholinergic transmission in the basal ganglia

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3
Q

the mechanism for smooth muscle contraction?

A
  1. rise in intracellular calcium
  2. calcium bind to calmodulin
  3. ca-calmodulin activated Myosin light chain kinase
  4. MLCK phosphorylated MLC
  5. cross-bridge formation between myosin heads and actin filaments
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4
Q

how is smooth muscle contraction regulated?

A

intracellular calcium

increase in conc:

  • calcium is released from SR storage sites
  • calium enters the cell

decrease in calcium:

  • calcium is taken back into the storage sites via ATP-calcium pump
  • calcium leaves the cell via ATP-dependent ca pump or the Na/ca exchanger
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5
Q

What are the primary blood vessels for resistance?

how is the smooth muscle of these controlled?

A

arterioles

  • control mean arterial blood pressure
  • control blood flow to specific tissues

VSM controlled by sympathetic nervous system and local factors

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6
Q

what are the main capacitance vessels and how are they regulated?

A
  • systemic veins and venules
  • have 50% of total blood volume
  • systemic and humoral regulation of these vessels -> changed venous return (preload) and fluid exchange in the capillary beds
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7
Q

What can intimate contraction of vascular smooth muscles

A
  1. passive stretching - originates from the smooth muscle = myogenic response
  2. electrical depolarisation - opening of voltage-gated calcium channels (L-type calcium) -> increased intracellular calcium concentration
  3. chemical stimuli
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8
Q

what chemical stimuli can contract VSM?

what are their receptors?

A 
noradrenaline (alpha1 adrenoreceptor)
angiotensin II
endothelin (Eta, ETb2) 
vasopressin (V1 receptor)
ergot alkaloids (ergotamine)
5-hydroxytryptamine (5-HT2)
ACh (M3)
prostaglandins (DP, EP, FP)
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9
Q

how does endothelin cause muscle contraction?

A 
endothelia binds to GPCR
Gq exchanges GTP forGDP
PLC: PL - InsP3
activated calcium channel on SR
increase in intracellular calcium 
calcium binds to calmodulin
ca-calmodulin activates MLCK
cross bridges - contraction
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10
Q

How does NA cause VSM contraction?

A 
released from sympathetic nerves 
binds to alpha1-adrenoreceptors
coupled to Gq
PLC and InsP3 (inositol triphosphate) production
IP3 causes release of Ca from SR
contraction of smooth muscle
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11
Q

what are cotransmitters of NA in VSM contraction?

A
  1. ATP - activation of P2x, non selective cation channel
  2. Gq couples receptors to PLC (e.g. P2Y)
  3. neuropeptide Y - can potentiate action of NA
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12
Q

alpha1 - adrenoreceptor antagonists, action and examples

A

vasodilators -> cause falling blood pressure
prazosin
indoramine

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13
Q

how does cocaine affect VSM contraction?

A

blocks uptake of NA into nerve terminal -> vasocontriction

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14
Q

what are indirect vasoconstrictors that cause NA release from nerve terminals?

A

amphetamine
tyramine (the cheese reaction)
ephedrine

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15
Q

what does angiotensin II do?
how is it formed?
what inhibits it?

A

vasoconstrictor:

  1. AII activated AT1 receptors
  2. coupled to Gq to PLC
  3. IP3 production

angiotensin converting enzyme (ACE) expressed on nonvascular endothelial cells converts angiotensin I (inactive) to angiotensin II (active)

inhibited by captopril, an anti-hypertensic drug

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16
Q

Endothlin:
receptor and mechanism?
synthesis?
antagonists?

A

rececptor ETA-R, ETB2-R
-> coupled by Gq to PLC -> IP3 production -> ca released from SR

synthesised by endothelium

antagonists: BQ-123 (cyclic pentapeptide), BMS 182874 (sulphanomide derivative)

17
Q

vascular actions of vasopressin (VP)?

analogue?

A

V1 receptors -> Gq -> PLC -> IP3
(also works on GI tract and uterine smooth muscle)

analogue: fleypressin (V1 receptor selective) -> used as vasoconstrictor with local anaesthetics

18
Q

migraine treatments?

A

migraine = contraction/dilation of cerebral blood vessels

treated with:
1. ergotamine - causes vasoconstriction

  1. sumatriptan - HT1d-like receptor agonist
    - > sumatriptan acts on nerves from trigeminal nucleus - nerves innervate cerebral blood vessels
  2. methysergide - some selectivity as an antagonist for 5-HT2 receptors
19
Q

mechanisms for VSM relaxation

A

G-PROTEIN:

  1. Gs coupled to adenylyl cyclase
  2. increased production of cAMP
  3. inhibition of MLCK
  4. decrease in MLC phosphorylation
  5. decrease interactions between myosin and actin

drugs that increase cAMP and therefore cause vasodilation:
beta2-adrenoreceptor agonists (e.g. epinephrine, isoproterenol)
phosphoidesterase inhibitors

NITRIC OXIDE - cGMP:

  1. increase in NO
  2. activation of guanylyl cyclase
  3. increased formation of cGMP
  4. cGMP activates cGMP-dependent protein kinase
  5. inhibits ca entry into VSM
  6. activated potassium channels
  7. decrease IP3
  8. vasodilation
20
Q

how is action potential generated and conducted in excitable cell membranes?

A
  1. depolarisation: Na influx
  2. repolarisation: K+ efflux - Na channels inactivate, K channels activate
    - voltage-dependent channels
    - Na conc is low inside
    - K conc is high inside
    - depolarisation past threshold will cause AP:
    threshold is when more sodium enters the cell than potassium is leaving the cell -> membrane potential becomes more positive
21
Q

mechanism for local anaesthetic block of voltage-dependent sodium channels

A
  • LA are weak bases
  • after administration the base is liberated by relatively alkaline pH of tissue fluids
  • they exist as equilibrium of charged and unchnarged form
  • the uncharged form diffuses across the nerve sheath and neuronal membrane
  • it partially ionises inside the axoplasm
  • when the sodium channels opens, the ionised BH+ enters the Na+ channel
  • BH+ combines with a specific channel subunit resulting in channel block
22
Q

methods of LA administration

A
  • administered as water soluble hydrochlorides (base HCl)
  1. surface anaesthesia
    - applied directly to mucous membrane
    - cornea, pharynx, bronchial tree, uretha, bladder
    - lidocaine
    - benzocaine - poorly soluble, sued as powder for prolonged burns
    - EMLA = eutectci mixture of LA = lidocrain + prilocaine in crystalline mixture - applied directly to skin
  2. infiltration anaestheisa
    - injected directly into tissue to anaestheise nerve endings
    - wound stitching, minor surgery, vasectomy
    - need large amounts - danger of toxicity
    - danger of intravascular injection
    - lidocaine, prilocaine
    - use with vasoconstrictors when not in extremities
  3. nerve block anaesthesia
    - drug injected close to nerve trunk
    - anaesthetises whole area of distribution of nerve
    - e.g. block of mandibular nerve in dentistry, block of brachial plexus for hand surgery
  4. spinal anaesthesia
    - injected into subarachnoid space of spine
    - between 2nd and 5th lumbar vertebrae -> below conus modularise to avoid injury
    - major surgery use - rectal surgery, caesarian
    - procaine, tetracaine, cinchocaine
    - combined with glucose, adjusts density - can control anaesthesia by titling the patient
    - danger of reportery paralysis, paralysis vomitting, visceral pain because afferent not blocked
  5. epidural anaesthesia
    - injected into epidural space
    - diffuses to block nerve roots
    - cannot spread to brain as epidural spaces end at foreman magnum
    - similar to spinal anaesthesia, sam drugs used but large amounts needed
    - used in obstetrics
  6. intravenous regional anaesthesia
    - injected i.v. distal to cuff on the limb
    - diffuses retrogradely into tissue
    - danger of toxicity if cuff is prematurely released
23
Q

three examples of LA and their uses

A

x

24
Q

generation and conduction of cardiac action potential

A

phase 0 - rising phase: fast inward Na+ current
phase 1 - initial depolarisation: voltage gated- Na+ channel inactivation
phase 2 - slow inwards Ca2+ current
phase 3 - ca current inactivation, outwad K current
phase 4 - potassium channel closing
refractory period - Na channel inactivate, no cardiac AP can be elicited

25
Q

possible mechanism that may generate cardiac dysrhythmias

A

caused by disruption in electrical conductance of the heart

  1. delayed after-depolarisation
  2. disordered conduction pattern
  3. abnormal pacemaker activity
  4. heart block
26
Q

classification of anti-dysrhythmic drugs and example of each class

A

x

27
Q

structure of LAs?

A

aromatic group - intermediate chain (ester or amide) - tertiary or secondary amide group

28
Q

why does LA channel block develop faster and is greater when the nerve is conducting an action potential?

A
  1. the nerve is depolarised more often making the inside of the nerve more positive -> drives LA into the Na+ channel
  2. inactive form os Na+ channel has a higher affinity for LAs than the resting form of the Na+ channel
29
Q

what are the physiological characters of LA action?

A
  • small fibres are blocked before large fibres

- > small fibres carry pain sensation and so this disappears before temperature, then touch and pressure

30
Q

why is vasopressin, Adrenaline or NA added to LA solutions?

and more recently felypressin?

A
  • vasoconstriction
  • delayes absorption of anaestethic from site of injection
  • > prolong its action
  • > reduces the danger of systemic toxicity
31
Q

how are LA metabolised?

A
  • ester types (procaine, tetracaine, benzocaine) hydrolysed rapidly by cholinesterase’s
  • amide types (lidocaine, prilocaine) are catabolised more slowly in the liver
32
Q

toxic effects and side effects of LAs

A
  1. local tissue injury with infiltration and spinal anaesthesia
  2. effect on CNS
    - stimulation with hyperactivity and mani behaviour - convulsions followed by coma
    - barbiturates protect against these effects but aggravate the eventual depression
  3. cardiovascular system:
    - vasodilator action
    - depression of myocardium and cardiac slowing -> hypertension (except with cocaine)
  4. allergic reaction - rare but very dangerous
33
Q

what are cardiac dysrythmias?

A

alteration in beat of heart, often abnormal

34
Q

delayed after-depolarisation cause dysrhythmia?

A
  • the after depolarisation immediately follows the action potential
  • when Ca2+ increases above normal
  • result of a net inward current known as the transient inward (TI) current, possibly carried by the Na/Ca exchanger
35
Q

disorded patter conduction - dysrythmia

A

x

PHAR2002 (1 decks)

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