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Pharmacology (Dan) Flashcards

1
Q

What are the 2 major divisions in the peripheral nervous system?

A
  • Efferent neurons
  • Afferent neurons
    > seonsory neurons that carry info to CNS from sensory receptors
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2
Q

What are the 2 types of efferent neuron and what does each do?

A

1) Somatic motor neurons: project to skeletal muscle and control posture and movement (voluntary)
2) Autonomic neurons: efferent neurons that innervate smooth and cardiac muscle (involuntary)

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3
Q

Describe the anatomy of the somatic motor pathway

A
  • Cell bodies of somatic neuron in ventral horn of spinal cord
  • myelinated axon runs to skeletal muscle
  • May branch and innvervate more than 1 muscle cell (motor units)
  • Neurotransmitter = ACH
  • Acts on ACH receptors
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4
Q

Describe the anatomy of the sympathetic pathway

A
  • Neurons originate in the thoracic and lumbar regions of spinal cord
  • Consists of 2 efferent neurons:
    > Preganglionic: from CNS to autonomic ganglion (short)
    Uses ACH and nicotinic ACH receptor
    > Postganglionic: from ganglion to target organ (long)
    Uses noradrenaline and adrenergic receptor
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5
Q

Describe the anatomy of the parasympathetic pathway

A 
- Neurons originate in brain stem or sacral regions of spinal cord
Consists of 2 efferent neurons:
> Preganglionic (long)
Uses ACH and nicotinic ACH receptor
> Postganglionic (short)
Uses ACH and muscarinic ACH receptor
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6
Q

Describe the transmission of a signal at the neuromuscular junction

A
  • choline acetyltransferase transfers acetyl group form acetyl-CoA to choline to make ACH
  • Packaged into vesicles
  • Action potential arrives - depolarises nerve terminal
  • Causes voltage gated Ca2+ channels - calcium influx
  • Ca2+ causes vesicles containing ACH to fuse with the presynaptic nerve terminal membrane
  • ACH released into synaptic cleft (regulated exocytosis)
  • ACH binds to alpha subunit of ACH receptors
  • Triggers the opening of ion channels in post synaptic membrane
  • Na+ influx causes depolarisation (end plate potential (EPP))
  • If large enough, will cause action potential
  • ACH hydrolysed by acetylcholinesterase into choline and acetic acid
  • Reuptake of choline by membrane choline carrier into nerve terminal to make more ACH
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7
Q

What is vesamicol and how does it work?

A
  • Cholinergic antagonist
  • Causes a reversible, non competitive block to vesicular acetylcholine transporter (VAChT)
  • VAChT responsible for transporting newly sysntesised ACH to vesicles for packaging
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8
Q

What is Botulinum toxin and how does it work?

A
  • A drug that inhibits acetylcholine release
  • Prevents acetylcholine release by enzymatically cleaving the proteins (e.g synaptobrevin) required for docking of vesicles to the presynaptic membrane
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9
Q

How is botulinum toxin type A administered and what is it used to treat?

A

Used to treat certain dystonias (abnormalities of muscle tone resulting in spasm) such as blepharospasm (spasmodic eye closure)

  • Injected into muscle to cause paralysis for ~12 weeks
  • Can also be used as a treatment for incontinence
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10
Q

How do competitive neurotransmitter blocking drugs work, why are they used clinically and what are the 5 main drugs?

A
  • Bind to nicotinic ACH receptors and block the entry binding of ACH
  • Used as anesthetic as they cause paralysis
    5 main:
  • Pancuronium
  • Vecuronium
  • Atracurium
  • Cisatracurium
  • Rocuronium
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11
Q

What are the common side effects of competitive neurotransmitter blocking drugs?

A
  • Histamine release
  • Vagal blockage (vagal nerve blokade - vagal nerve assists in loweing heart rate)
  • ganglion blockade
  • sympathomimetic actions
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12
Q

What is the duration and side effects of Pancuronium?

A
  • Relatively long duration
  • Does not block ganglion
  • Does not cause histamine release
  • Can cause tachycardia (abnormally high heart rate)
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13
Q

What is the duration and side effects of Vecuronium?

A
  • Commonly used
  • Recovery after 20-30 minutes - attractive for short procedures
  • No cardiovascular effects
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14
Q

What is the duration and side effects of Atracurium?

A
  • Duration of action of 15-30 minutes
  • Only stable at low pH and kept cold
  • In body pH and temp, decomposes in plasma so does not depend on renal or hepatic excretion
  • Therefore used in renal and hepatic disease
  • Can cause histamine release
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15
Q

What is the duration and side effects of Cisatracurium?

A
  • Isomer of atracurium

- does not cause histamine release

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16
Q

What is Suxamethonium and how does it work?

A
  • Depolarizing neuromuscular blocking drug
  • Works in 2 phases:
    1) Depolarising phase Suxamethonium binds to nicotinic ACH receptors and causes them to open - end plate depolarisation
  • Last longer than ACH
  • Usually rapidly degraded by plasma pseudocholinesterase, but in some people (1 in 3000) they inherit atypical form of enzyme so block may last hours
  • Prolonged receptor activation - continuous action potentials - muscle twitches
    2) Desensitizing phase
  • Inactivation of voltage gated Na+ channels in surrounding mucle fibre membranes - no action potentials
  • Transformation of activated receptors to desensitized state
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17
Q

What type of disease is Myasthenia Gravis (MG), what causes it and how is it treated?

A
  • Autoimmune disease
  • Circulating heterogeneous IgG antibodies cause loss of nicotinic acetylcholine receptor function
  • Choice of drugs are acetylcholinesterase inhibitors:
    > Neostigmine or Physostigmine
  • Less ACH degradation, higher chance it will stimulate receptor
    Also, immunological treatments:
    > Azathioprine - interferes with IgG antibody production
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18
Q

What are the differences between the autonomic and somatic nervous systems?

A

A controls involuntary actions
S controls voluntary actions

A - primary transmitters - ACH and NA
S - Primary transmitters ACH

A interacts with nicotinic and muscarinic receptors
S interacts with nicotinic only

A innervates tissue via 2 neurons connected by ganglion
S innervates skeletal muscle via single motor neuron

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19
Q

What are the different types of adrenoreceptors and are they pharmacologically distinct?

A 
Alpha 1, Beta 1, Alpha 2 and Beta 2 adrenoreceptors
Pharmacologically distinct (targets for different drugs)
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20
Q

What are the different types of muscirinic ACH receptors and are they pharmacologically distinct?

A
  • G protein coupled receptors, subtypes M1 - M3
  • M1 in brain, M2 in heart and M3 in smooth muscle and glands
  • Pharmacologically indistinct
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21
Q

What are the main drug types used to treat autonomic diseases?

A
  • Muscarinic agonists and antagonists
  • a1, B1, a2 and B2 agonists and antagonists
  • Nicotinic agonists (ganglionic stimulants) and blockers
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22
Q

What is the main muscarinic agonist and what is it used to treat?

A

Pilocarpine (choline ester)

- Used to treat glucoma; reduces intraocular pressure by contraction of ciliary muscles, increasing aqueous outflow

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23
Q

What is the main muscarinic antagonist and what is it used to treat?

A

Atropine
Used in anaesthetic; prevents slowing of heart and bronchial secretion/reflex contraction
- Another mACH antagonist is hyoscine (causes more drowsiness and amnesia than atropine)

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24
Q

What other drug type might be used in the parasympathetic nervous system?

A

Acetylcholinesterases

- common is Physostigmine

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25
Q

What is released in a sympathetic nervous response?

A

Noradrenaline from sympathetic nerve terminal

- in some forms of stress, adrenaline also released from adrenal medulla

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26
Q

What is a sympathomimetic drug?

A

A drug that partially or completely mimics the actions of normal sympathetic agonists (nor and adrenaline)

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27
Q

What is phenylephrine and what does it cause?

A

alpha 1 agonist

- used in decongestant prep - reduction if bronchial secretions, also in eye drops to dilate pupils

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28
Q

What is clonidine and what does it do?

A

alpha 2 agonist

- centrally acting hypotensive drugs (lowers blood pressure)

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29
Q

What is Prazosin and what does it cause?

A

alpha 1 antagonist
- used to treat benign prostatic hyperplasia (BPH) in men and high blood pressure
also called alpha blockers

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30
Q

What are beta blockers and what are they used to treat? Give an example drug

A

Beta 1 antagonists
- used to treat blood pressure and angina; decreased cardiac output
most common is Atenolol

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31
Q

What is salbutamol and what is it used to treat?

A

Beta 2 agonist

- Treatment of acute asthma, causes bronchial dilation

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32
Q

What are the main pathologies affecting the cardiovascular system?

A
  • Hypertension
  • Hypotension
  • Angina pectoralis
  • Heart failure
  • Cardiac arrythmia
  • Atherosclerosis
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33
Q

What is hypertention and what is it measured in?

A

Hypertension is high blood pressure

  • Measured in mmHg at systolic and diastolic
  • Hypertension indicated at pressure reading og 160mmHg/100mmHg
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34
Q

What are the risk factors of hypertension?

A 
Smoking
Obesity
Dietary influence
Diabetes
- Lifestyle changes should be considered before therapeutic intervention
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35
Q

What 3 drug types can be used to treat hypertension?

A
  • Thiazide diuretics
  • Beta blockers (beta 1 adrenoreceptor antagonists)
  • Angiotensin converting enzyme (ACE) inhibitors
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36
Q

Where do thiazide diuretics act and what do they cause?

A
  • Site of action is the distal region of the kidney
  • Act upon specific transporter proteins that allow reabsorption of salts from the tubule to the blood
  • Transport process is electrically neutral
  • Regulation of salt excretion also regulates water excretion by osmosis
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37
Q

What is the thiazide diuretic mechanism of action?

A
  • Bind to the chloride-binding site of the sodium chloride co-transport system, located on luminal side of tubule
  • Co- transport of sodium and chloride ions inhibited so prevents salt re absorption into the blood
  • Retention of osmotic balance keeps water in distal tubule
  • Water excreted in urine
  • Reduction in blood volume
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38
Q

What region of the thiazide diuretic interacts with the binding site on the co-transport protein?

A

The thiazide region

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39
Q

What are the side effects of thiazide drugs?

A
  • Increased frequency of urination
  • Erectile dysfunction
  • Increased LDL in blood
  • Gout
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40
Q

What are the advantaged of thiazide drugs?

A
  • Low cost
  • Low dose
  • Synergistic activity with other drugs
41
Q

Where are beta adrenoreceptors mainly found?

A
  • Cell membranes of cardiac, intestinal, bronchial and vascular smooth muscle
42
Q

What is the usual effect of Beta-1 adrenoreceptor activation?

A

Increases heart rate and force of contraction

43
Q

Give 2 examples of beta blockers

A

Atenolol (B1-selective)

Propanolol (blocks B1 and B2 equally)

44
Q

What is the normal Beta-1 adrenoreceptor mode of action?

A
  • Release of noradrenaline from post ganglionic nerve terminal
  • Interaction with G protein coupled receptor (GPCR) on cardiac cell
  • Activation of GPCR mediated pathway via Gs and adenylyl cylase pathway (increase in cAMP)
  • Increase of cAMP phosphorylates alpha-1 subunit of calcium ion channels on cardiac cell membrane by protein kinase A, calcium channels open
  • More intracellular calcium ions results in increased rate and force of contractions
45
Q

How do beta-1 adrenoreceptor antagnoists interrupt this system?

A

Competitive antagnoism of beta 1 adrenoreceptors

46
Q

What is the problem with using non selective beta blockers?

A

Can cause bronchoconstriction

  • Problem for asthmatics
  • wouldnt use propanolol (B1 and B2), just athenolol (Just B1, not in brochioles)
47
Q

What is the purpose of the renin-angiotensin system?

A

To regulate blood pressure

48
Q

How does the renin-angiotensin system work?

A
  • Decrease in renal perfusion (reduced blood flow to kidney) causes juxtaglomerular apparatus to produce renin (enzyme)into the blood
  • Renin converts angiotensinogen (produced by the liver) into angiotensin I
  • Angiotensin I converted to angiotensin II by ACE
  • Angiotensin II binds to AT1 receptors and causes many effects:
    > Increase in sympathetic activity (vasoconstriction)
    > Tubular Na+ reabsorption by aldosterone action
    > ADH secretion, reabsorption of water from collecting duct
    > Increases blood pressure - negative feedback on juxtaglomerular apparatus
49
Q

How do both renin and ACE act to convert their substrates?

A
  • Renin is proteolytic enzyme
  • Removes 10 AAs from N terminus to angiotensinogen to form angiotensin I
  • ACE cleaves 2 AAs from C-terminus of angiotensin I to form angiotensin II
50
Q

What are the names of some ACE inhibitor drugs?

A

Captopril and Lisinopril

51
Q

What are a new type of drugs used to inhibit angiontensin II activity and give an example?

A

AT1 receptor antagonists e.g Losartan

52
Q

Where are mast cells found?

A

In aerated tissue e.g lings, skin, mucosa of GI tract

Also in stomach

53
Q

Explain what occurs upon first exposure of an allergen

A

Stimulates binding of IgE antibodies to specific receptors on mast cells

54
Q

Explain what occurs upon second exposure of an allergen

A

Histamine stored in granules, bound to heparin and ATP
- Renewed exposure to allergens results in increase in intracellular cAMP, entry of calcium ions through channels, and degranulation and release of histamine and other mediators

55
Q

Why is histamine released?

A

To mediate inflammatory and allergic reaction

56
Q

How is histamine synthesised?

A

Precursor amino acid histidine is converted to histamine by histadine decarboxylase

57
Q

What sort of spread does a histamine response have?

A

Histamine is a local transmitter which leads to a highly localised response

58
Q

What are the physiological effects mediated by histamine and what receptor is involved?

A

1) Vasodilation in vasculature (H1)
- leads to fall in peripheral resistance, venous return and cardiac output
2) Increased permeability in microcirculation (H1)
- Allows white blood cells to infiltrate regions of potential pathogen insult; also leads to water loss and therefore local oedema (swelling)
3) Stimulation of sensory nerve endings (H1)
- Leads to local pain perception
4) Contraction of bronchial smooth muscle

5) Stimulation of gastric acid secretion (H2)

59
Q

How does histamine cause acid secretions?

A
  • Released from mast cells
  • Binds to H2 receptors on parietal cells of the gastric glands
  • Causes parietal cell proton pump (H+/K+ ATPase) to secrete hydrochloric acid (H+ out for K+ in) into the stomach lumen
60
Q

What drugs can be given to prevent gastric acid secretions as a result of histamine? Give an example

A 
H2 receptor antagonists
- prevent binding of histamine
e.g Cimetidine (Zantac)
Can also use proton pump inhibitors
- e.g  omeprazole
61
Q

H2 receptor antagonists and proton pump inhibitors are commonly used to treat what disorder?

A

Peptic ulcers

- An ulcer in an area in which the mucosa is bethed in HCl and pepsin of gastric juice

62
Q

What are H1 antagonists used for?

A

Used to treat symptoms of hayfever e.g Loratidine (Clarityn) or Terfenadine (Triludan)

63
Q

What are the 4 relevant physiological areas of the bronchioles?

A

1) Smooth muscle that contracts and relaxes under autonomic control
2) Mast cells that respond to invasion by spasmogens
3) Inflammatory cells that infiltrate areas of perceived invasion
4) Epithelial lining that protects basement membrane

64
Q

What are the physiological effects of bronchial asthma?

A
  • Smooth muscle contraction
  • Oedema through microvascular deposition of water in surrounding tissue
  • Excess mucus production
  • Desquamation of epithelial lining
    All lead to constriction and hypersensitivity of the airways
65
Q

Give a summary of the 2 phases of bronchial asthma

A

Early phase: Bronchospasm
- Rapid onset after allergen exposure and short duration
Late phase: Inflammation and hypersensitivity
- Later onset and longer duration

66
Q

Describe what occurs in the early phase of bronchial asthma

A
  • Allergens promote degranulation of mast cells that release smasmogens
  • Spasmogens include:
    > Histamine
    > Prostoglandins
    > Cysteinyl leukotrienes (cysLTs) (LTC4 and LTD4)
    Results in bronchoconstriction and bronchospasms
  • Also release chemotaxins and chemokines
67
Q

Describe what occurs in the late phase of bronchial asthma

A
  • Chemotaxins and chemokines from early phase cause:
    > Infiltration of cytokine releasing Th2 cells and monocytes
    > Activation of inflammatory cells, particularly eosinophils
  • More pro-inflammatory mediators produced (e.g cysLTs)
  • Eosinophils produce toxic peptides (eosinophil major basic protein (EMBP) and eosinophil cationic protein (ECP)) leading to epithelial desquamation
  • Resulting airway inflammation and hyper sensitivity causes bronchospasms, wheezing and coughing
68
Q

What drugs are used to treat early phase asthma?

A

Bronchodilators

  • Beta-2 adrenoreceptor agonists cause relaxation of bronchial smooth muscle
  • Most common is salbutamol (ventolin)
69
Q

How does salbutamol act to cause bronchial smooth muscle relaxation

A
  • Salbutamol binds to B2 adrenoreceptors
  • Interaction with G protein coupled receptor (GPCR)
  • Activation of GPCR mediated pathway via Gs and adenylyl cylase pathway (increase in cAMP)
  • Increase of cAMP causes phosphorylation and deactivation of myosin light chain kinase by protein kinase A
70
Q

What is a common side effect of beta-2-agonists

A

Oral administration can have activity on cardiac muscle beta-1-receptors, leading to elevated cardiac output

71
Q

What drugs are prescribed to treat late phase asthma, and when is this appropriate to do?

A
  • Glucocorticoids

- Prescribed when beta-2-agonists do not improve asthma

72
Q

What are glucocorticoids, what do they bind to and what do they cause?

A
  • Steroid hormones
  • Bind to cytoplasmic glucocorticoid receptors
  • Act in nucleus to reduce transcription of genes involved in pro-inflammatory response
73
Q

What are common side effects of glucocorticoids?

A
  • Oral administration leads to wide range of effects as glucocorticoids also affect glucose and protein metabolism (hyperglycemia, rounded face, skeletal muscle wastage and weakness)
  • Prolonged therapy can lead to unwanted immunosuppression
  • Inhaled administration can lead to oral infections
74
Q

What are some emerging therapies for bronchial asthma?

A
  • cystLT receptor antagonists

- Phosphodiesterase 4 inhibitors (inhibit breakdown of cAMP/cGMP second messengers

75
Q

What is the difference between the paracrine and endocrine system?

A

Endocrine system allows hormones to act on effector tissue some distance from site of release by plasma transport
Paracrine system hormones diffuse locally through extracellular fluid to local cells

76
Q

Describe some disorders that are associated with loss of endocrine function

A
  • Growth retardation (acromegly, gigantism)
  • Infertility (problems with GnRH, LH, FSH, oestrogen etc)
  • Hypothyroidism
  • Graves disease
  • Diabetes (insulin)
77
Q

What are the main 2 classes of steroid hormone released by the adrenal cortex?

A

1) Mineralocorticoids
- Mainly aldosterone
- Salt retaining activity
2) Glucocorticoids
- Mainly cortisol
- affect carbohydrate and protein metabolism
- also on imflammation

78
Q

Describe the regulation of adrenal hormones

A
  • Hypothalamus releases corticotrophin releasing hormone (CRH)
  • CRH acts upon the anterior pituitary, which in turn releases adenocorticotrophic hormone (ACTH)
  • ACTH activates GPCRs on the adrenal cortex, activating adenylyl cyclase and stimulating secretion of corticosteroids (glucocorticoids and mineralocorticoids)
  • ACTH (short feedback loop) and glucocorticoids (long feedback loop) both have negative feedback on CRH secretion from hypothalamus
79
Q

What are the metabolic effects of glucocorticoids?

A
  • Decrease uptake/usage of glucose
  • Increase gluconeogenesis
  • Increase glycogen storage
  • Decrease in protein synthesis
  • Increase in protein degradation to AAs
80
Q

What are the immune effects of glucocorticoids?

A
  • Inhibits early and late stage inflammation
  • Decreases movement of neutrophils out of blood vessels by decreasing microvascular permiability
  • Decreases proliferation of T cells
  • Decreases inflammatory mediators
81
Q

What is the major clinical use of glucocorticoids and what are the main symptoms?

A 
Major clinical use:
- Chronic asthma
- Inflammatory diseases e.g arthritis
Side effects:
- Unwanted immunosuppression
- Fluid retention (rounded face)
- Metabolic imbalance (hyperglycemia, weak muscles)
82
Q

What is the action of glucocorticoids?

A
  • Act upon steroid hormone receptors that affect transcription of specific genes via hormone response elements?
83
Q

What are the names of the 4 mechanisms by which glucocorticoids can alter transcription?

A

1) Basic transactivation mechanism
2) Basic transrepression mechanism
3) Fos/Jun mechanism
4) Nuclear factor kB mechanism

84
Q

Describe the basic transactivation mechanism

A
  • Transcriptional machinery (TM) is presumed to be operating at a low level
  • The liganded glucocorticoid receptor (GR) dimer binds to one or more ‘positive’ glucocorticoid response element (GREs) wihin the promoter sequence and up regulated transcription
85
Q

Describe the basic transrepression mechanism

A
  • TM is constitutively driven by transcription factors (TFs)

- In binding to the negative GRE (nGRE), the receptor complex displaces these factors and expression falls

86
Q

Describe the Fos/Jun mechanism

A
  • Transcription is driven at high level by Fos/Jun transcription factors binding to their AP-1 regulatory sites
  • This effect is reduced in the presence of the liganded glucocorticoid receptor (GR)
87
Q

Describe the Nuclear factor kB mechanism

A
  • Transcription factor P65 and P50 bind to the NFkB site, promoting gene expression
  • This is prevented by the presence of the GR, which binds the transcription factors, preventing their action
88
Q

Which 2 mechanisms contribute to a reduction in an inflammatory response and why?

A

Fos/Jun and Nuclear factor kB mechanisms
- Glucocorticoids repress AP-1 and NFkB that would usually cause transcription of cyxlooxygenase 2 and a number of cytokines, thus beneficial in asthma treatment

89
Q

What do the basic transactivation and basic transrepression mechanisms cause?

A

Result in induction or repression of other genes that mediate metabolic effects (side effects)

90
Q

What are the 2 types of contraceptive pill?

A

Combination pill

Progesterone only pill

91
Q

What do combination pills contain and when should they be taken?

A
  • Contain oestrogen derivative (usually ethinyl estradiol) (20-50µg) plus synthetic progesterone derivative (0.1-1mg) and variable through a 28 day cycle to mimic cyclical progesterone levels
  • Taken for 20-21 days then not taken for 6-7 days to allow menstruation to occur
92
Q

What do progesterone only pills contain and when should they be taken?

A

Contain low dose of progesterone

Taken continuously

93
Q

What is the mechanism of action of the combination pill?

A
  • Oestrogens have negative feedback on LH secretion
  • Progesterone negative feedback on GnRH and LH
    Prevents ovulation
    > Also cause endometrium changes so unreceptive to implantation
    > Alter fallopian tube motility
    > Change composition of cervical mucus
    Latter effects also produced by progesterone only pill
94
Q

What are some side effects of contraceptive pills?

A
  • Breakthrough bleeding
  • weight gain
  • libido changes
  • breast soreness
  • headaches
  • nausea
95
Q

How do pro-fertility drugs work and give examples

A

Inhibit normal negative feedback by oestrogen
- promotes ovulation
Include selective estrogen receptor modulators (SERMs) e.g clomiphene, taxoxifen

96
Q

Give an example of an emergency contraceptive pill (morning after pill)

A
  • Levonorgestrel (Brand name: Plan B)
  • Prescribed to females 17 years or younger
  • Up to 3 days after unprotected intercourse
97
Q

Why is hormone replacement therapy (HRT) used for post-menopausal women?

A
  • Used to counter decreased ovarian function and consequent reduction of oestrogen
  • Improves common side effects: hot flushes, vaginal dryness, osteoporosis
98
Q

Why do post-menopausal women get these symptoms?

A

Emerge due to reduced oestrogen activity on oestrogen receptors, found in many different tissues (breast, bone, uterus, pituitary, vasculature)

99
Q

What is the risk of HRT?

A

Million women trial identified enhanced risk of breast cancer in HRT users

Biomed (18 decks)

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