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PHAR Flashcards

1
Q

What pharmacologically relevant parameter is represented by AUC of a drug concentration/time curve?

A

Drug exposure over time

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2
Q

Which products of arachydonic acid metabolism have antithrombotic effects?

A

PGI2 PGD2

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3
Q

What inflammatory responses are caused by the production of leucotrienes from phospholipids?

A

Increased vascular permeabilityVasodilationBronchoconstriction

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4
Q

Which product of AA metabolism is a pyrogen?

A

PGE2

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5
Q

What inflammatory mediator is produced from acylPAF and what is its effect within the body?

A

Platelet Activating Factor Chemotaxis, increased vascular permeabilit, vasodilation, bronchoconstriction

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6
Q

Which of the COX enzymes is represented by this diagram? How do you know? What type of cells is it present on?

A

COX-2

The characteristic “side pocket”

Found on activated inflammatory cells

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7
Q

What are the side effects of NSAID use? Explain

A

Reduced clotting ability - downregulation of PG and platlets

Gastric ulceration - downregulation of PG causing increased H+ secretion on mucosal surfaces

Hepatic damage

Altered renal blood flow

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8
Q

Why does lack of selctivity of COX enzymes by NSAIDs have systemic side effects on the body?

A

COX1 enzymes are present in most cells and are involved in homeostasis, their widespread distribution therefore leads to widespread effects if activated

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9
Q

What are the metabolic side effects of steroid use?

How can the systemic effects be decreased?

A
  1. Decreased glucose uptake - hyperglycemia
  2. Increased gluconeogenesis - hyperglycemia
  3. Increase protein catabolism
  4. Increased osteoclast activity
  5. Na+K+H2O excretion

Use of topical steroids (local effects only)

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10
Q

This class of drugs acts to increase cAMP therefore causing relaxation of smooth muscle causing bronchodilation.

Identify a drug from this class.

A

Methyxanthines

Theophylline

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11
Q

“Drugs which act by altering transcription, they act upon the HPA axis and are endogenously secreted by the adrenal gland”

A

Steroids

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12
Q

How do NSAIDs work?

A

They inhibit cyclooxygenase (COX) (enzyme for synthesis of PGs) which then inhibits prostaglandins (as PGs are pyretic (fever), pro inflammatory & hyperalgesic (increased sensitivity to pain)).

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13
Q

What does COX inhibition lead to?

A

PGs mainly increase blood flow and enhance swelling & pain, also increase body temperature. Therefore inhibition leads to:

  • Decreased vasodilation
  • Decreased swelling
  • Little effect on cellular changes in inflammation
  • Analgesia (treats pain)
  • Decreased fever

[Will not reduce heat, stress or exercise induced hyperthermia as these are not mediated by PGs]

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14
Q

What are contra indications of NSAIDs?

A
  • Do not use an NSAID with (or within 24hr use of) another NSAID - avoids confusion & potential overdose
  • Avoid use of NSAIDs in dehydrated, hypovolaemic or hypotensive animals - increases risk of renal toxicity
  • Animals with pre-existing gastric ulcers - inhibition of PGs can make this worse
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15
Q

Identify three beta2 agonists which are used to treat asthma.

What biological effect do they have on the body?

A

Terbutaline

Albuterol

Clenbuterol

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16
Q

This drug acts as a respiratory stimulant by acting on the respiratory centre of the brain.

Useful with recusitation of neonates.

A

Doxapram

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17
Q

This class of drug acts as a gastric irritant and increases vagal tone.

What effect does increased vagal tone have on the respiratory system?

A

Expectorants

Increased mucocilliary escalator, increased mucus production

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18
Q

This mucolytic is ineffective in the presence of protein from infection or inflammation.

A

Bromhexine HCl

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19
Q

Describe the mode of action of N-acetyl cysteine.

What class of drug is it from?

A

Mucolytic

Breaks disulphide bonds between mucous molecules.

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20
Q

How do opioid antitussive drugs work?

A

They inhibit kappa and lambda opioid receptors and therefore reduced the animals response to irritants.

They directly inhibit the cough

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21
Q

Bronchodilation can also be achieved by antagonism of the parasympathetic nervous system, what class of drug is used for this?

Name a PNS anatagonist.

A

Cholinergics - increase smooth muscle relaxation

Bethanechol

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22
Q

This parasympathetic antagonist increases the drainage angle of the eye by causing pupil miosis. It is therefore used to treat which painful eye condition?

A

Pilocarpine is used to treat glaucoma

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23
Q
  1. Identify the class of renal drug which inhibits the NA+K+Cl- contransporter of the nephron.
  2. What does their inhibition cause?
  3. Name a drug from this class.
A
  1. Loop diuretics
  2. Inhibition reduces th hyperosmotic environment of the renal medulla therefore reducing H2O reabsorption causing diuresis.
  3. Frusomide
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24
Q
  1. This class of diuretic counteracts the negative effects of loop diuretics or thiazines.
  2. What side effect does it counteract? And how?
  3. Name a drug from this class.
A
  1. Potassium-sparing diuretics
  2. Hyperkalaemia. They prevent the reabsorption of sodium in the distal tubule therefore causing K+ to remain in the blood.
  3. Spironolactone
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25
Q

This drug is used in the treatment of struvite uroliths.

What effect does it have on the urine?

A

Methionine

Acidifies urine

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26
Q

Name four types of uroliths and state whether they are acidic or alkaline.

A
  1. Acidic
    1. Ca oxalate
    2. Urate
    3. Cystine
  2. Alkaline
    1. Struvate
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27
Q
  1. Identify two carbonic anhydrase inhibitors.
  2. What effect do they have on the body?
A
  1. Acetylxolamide & Dichlorofenamine
  2. Inhibit the transport of bicarbonate out of the proximal convoluted tubule into the interstitium, which leads to less sodium reabsorption at this site and therefore greater sodium, bicarbonate and water loss in the urine.
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28
Q

How do osmotic diuretics work?

(2x MOA)

A
  1. These are chemicals which are readily filtered into the nephron tubules and therefore alter the osmolarity of tubular fluid, reduing water reabsorbtion by the body and also pulling water back into the tubules.
  2. Or they increase blood flow to the kidney therefore reducing concentration gradient between tubular fluid and blood
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29
Q
  1. Outline the mode of action of thiazine diuretics.
  2. What side effects might their action have?
A
  1. Inhibit Na+Cl- contransporter of the distal tubule therefore causing excretion of Na+, Cl-, K+, Mg2+ and H2O
  2. Hypokalaemia, hyperglycaemia
  3. Decreased K+ and Cl- in the ECF
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30
Q

Outline the pathological changes which occur with skin disease and the clinical signs commonly presented.

Can you related each pathophysiology to the clinical sign?

A
  • Disturbance of skin homeostasis -> inflammatory mediators / cytokines in epidermis / dermis
  • Keratinocytes -> epidermal hyperplasia
  • Resistance to microbes leads to proliferation on surface / in follicles
  • Penetrate skin barrier -> ulceration / furunculosis

Clinical signs:

  • Pruritis
  • Scaling - epidermal hyperplasia
  • Greasiness - increased sebum secretion
  • Odor - microbial proliferation
  • Allopecia - self inflicted vs hair follicle path
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31
Q

How can topical agents be formulated?

A
  • Shampoos
    • For treatment of large areas of skin disease
    • Practicalities
  • Creams
    • Smaller areas / localised lesions
  • Ear drops
    • External ear -protected, moist environment
    • Should not use if tympanic membrane ruptured
  • Systemic treatment - AB, AP, AF
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32
Q

What is an anti-seborrheic agent?

A

Those which are used to treat seborrheic dermatitis.

Seborrheic dermatitis is a chronic, relapsing and usually mild dermatitis which usually affects areas rich in sebaceous glands.

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33
Q

Name four anti-seborrheic agents.

A
  1. Sulphur
  2. Tar
  3. Salicyclic acid
  4. Selenium sulphide
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34
Q

This anti-sebhorreic agent combines with water to form hydrogen sulphide. What effect does this have on the skin? What other pharmacological actions does this drug have?

A

Sulphur

  • Keratolytic
    • Hydrogen sulphide (pentathionic acid) damage corneocytes softening stratum corneum leading to shedding
  • Keratoplastic
    • Cytostatic on basal cell layer of epidermis
    • Slows down epidermal cell proliferation
  • Also antibacterial / antifungal
  • Not good degreasing agent
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35
Q

This anti-seborrheic agent is often combined with sulphur, why?

Outline its other pharmacological properties.

A
  • Sulphur + salicyclic acid = synergism
  • Keratolytic
    • Lowers pH of skin
    • Hydrates keratin and causes swelling of corneocytes
    • Stabilises inter-cellular cement in stratum corneum = desquamation
  • No effect on mitotic rate of basal keratinocytes
  • Mildly anti-pruritic and anti-inflammatory
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36
Q

This anti-seborrheic agent is derived from either coal or plants.

Which species is it NOT used in?

A

Tar

  • Keratoplastic
  • Keratolytic
  • Anti-pruritic
  • Degreasing
  • Vasoconstricting
  • Suppresses epidermal growth & DNA synthesis
  • Toxic to cats
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37
Q

If a seborrheic dermatitis case is not responsive to sulphur, salicyclic acid or tar which agent would be your next point of call?

Outline its action and disadvantages for its use.

A

Selenium sulphide

  • Keratolytic
    • Inteferes with hydrogen-bond formation in keratin
    • Depresses epidermal growth
    • Fungicidal at higher concentrations
  • Causes skin drying
  • Stains coat
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38
Q

Name seven anti-microbials used to treat skin conditions. (Hint: BCEITMM)

A
  • Benzoyl Peroxide
  • Chlorohexidine
  • Ethyl lactate
  • Iodine
  • Triclosan
  • Miconazole
  • Mupriocin
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39
Q

How does Benzoyl Peroxide work pharmacoloically?

How long does its action persist?

Where should care be taken with this product?

A
  • Metabolised in epidermis to benzoic acid and oxygen Free radicals
    • Lowers skin pH
    • Disrupts microbial cell membranes
  • Keratoplastic
    • Inhibits epidermal metabolism & DNA synthesis
  • Activity persists for 48 hours
  • Care should be taken with patients with dry skin - its is a degreasing product
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40
Q

What active ingredient can be found in Hibiscrub?

What type of bacteria is it active against and how does it work?

A
  • Chlorohexidine
  • Staphylococcus
  • Less effective against yeast / dermatophytes
  • Cationic surfactant - Disrupts microbial cell membranes and coagulates cytoplasmic proteins
41
Q

Outline one characteristic by which chlorohexidine and iodine differ.

A

Chlorohexidine does work in the presence of organic material whereas iodine is inhibited in the presence of this type of material.

42
Q

Ethyl lactate is metabolised to what substances and by what when applied to the skin?

What action does this have?

A
  • Metabolised to ethanol & lactic acid by bacterial lipases in hair follicles & sebaceous glands
    • Solubilises lipids
    • Lowers skin pH
43
Q

This anti-microbial is an excellent bacteriocide / fungicide / virucide / sporicide, BUT it is known to badly stain the animals coat.

It is often complexed with what molecule to produce Povidone Iodine.

How does it work

A
  • Iodine
  • Pyrrolidone nitrogen
    • Augments sustained release / dispersion / penetration
    • Mildly degreasing
44
Q

This anti-microbial is used to treat infectious sebhorrea caused mainly by gram positive bacteria.

What organisms is it reported to be effective against?

A
  • Triclosan
  • Bisphenol disinfectant
  • Methicillin-resistance stahphylococcus (MRSA)
45
Q

This antifungal agent works by inhibiting synthesis of ergosterol. What is ergosterol

What other agent is it often combined with? Which fungi is it targetting in this combo?

A
  • Miconazole
  • A componant of fungal cell walls
  • Combined with chlorhexidine to treat Malassezia infections
46
Q

Mupriocin is effective against which organisms?

How does it work?

A
  • Gram positive aerobes e.g. staphylococci and malassezia
  • It inhibits bacterial protein synthesis by binding to tRNA synthetase
47
Q

These agents soften and protect skin by forming a thin film of oil on the stratum corneum decreasing water look.

What types of substances are classified in this way?

A

Emolients

  • fats
  • hydrocarbons
  • humectants
  • oils
48
Q

Name the five types of moisturiser used in veterinary practice. (Hint: UGPgEfaCo)

A
  • Urea
  • Glycerin
  • Propylene glycol
  • Essential fatty acids
  • Colloidal oatmeal
49
Q

How does urea work as a keratolytic agent?

A

It causes proteolytic digestion of fibrin.

50
Q

Which layer of the epidermis do essential fatty acids work on?

A

Stratum corneum

51
Q

Which anti-pruritic agents are commonly used in veterinary practice?

Which one requires special care due to its potential long term effects?

A
  • Hydrocortisone
  • Anti-histamines
  • Aloe vera - inhibits cyclo-oxygenase and migration of neutrophils
52
Q

Tacrolimus is used in the treatment of what kind of skin diseases?

How does it work?

A
  • Treatment of immune-mediated skin disease
  • Macrolide immuno-modulator
    • Similar action to cylocsporin
    • Inhibits lymphocytes / dendritic cells / mast cells / eosinophils
53
Q

This pharmacological agent is highly effective at penetrating the skin and is often used as a carrier molecule for other substances such as corticosteroids.

What other properties does it have?

A

Dimethyl Sulphoxide - DMSO

Also has analgesic / anti-pruritic / anti-inflammatory properties

54
Q

What special consideration must be remembered when treating painful ears?

A

You can cause ototoxicity if you put antibacterials down an ear with a ruptured tympanic membrane.

55
Q

What main classes of drugs are found in ear drops used to treat otitis externa?

A
  • Anti-inflammatories
  • Anti-bacterials
  • Anti-fungals
  • Anti-parasitics
56
Q

Name six glucocorticoids which can often be found in ear drops used to treat otitis externa.

(Hint: BFTDHP)

A
  • Betamethasone valerate
  • Fluocinolone acetonide
  • Triamcinolone acetonide
  • Dexamethasone
  • Hydrocortisone
  • Prenisolone
57
Q

What is the bioavailability of topically administrated occular drugs, how much of the drug can reach the anterior chamber?

How can this be improved?

A

Intraocular bioavailability relatively poor o 1-10% of instilled drug reaches the anterior chamber.

Increasing retention time on ocular surface, optimising ability of drug to penetrate the cornea.

58
Q

Identify whether these layers of the eye surface are classified as lipid or aqueous layers.

  • Corneal epithelium
  • Stroma
  • Corneal endothelium
A
  • Epithelium - lipid
  • Stroma - aqueous
  • Endothelium - lipid
59
Q

How does formulation of occular drugs affect its persistance?

A
  • Solution - similar to tears
  • Suspension - increased particle size increased retention (but increased irritation)
  • Ointment - oil based, sits in conjunctival sac and is released as it melts
  • Viscous fluid/gel - hyaluronic acid holds it in the eye
  • Solid delivery - eg contact lenses
60
Q

Which layers of the eye do lipid and water soluble agents cross easily?

A

Lipid soluble agents cross epithelium with ease

Water soluble agents cross stroma with ease

61
Q

Describe how weak acids/ bases cross the cornea.

A

Remember equilibrium

62
Q

Which areas of the eye are highly vascularised and therefore important to consider for systemic application?

A

Conjunctiva

Nasolacrimal duct

Nasopharynx

63
Q

Outline how drugs distribute once they penetrate the cornea

A

Once a drug penetrates the cornea it moves into the aqueous and to the iris and ciliary body, achieving similar levels in aqueous and anterior uvea. The lens and vitreous receive considerably lower levels of corneally absorbed drugs, and hence an alternative route may be more appropriate for treatment of the posterior segment.

64
Q

How does inflammation affect drug bind?

A

Many drugs can bind to protein in the tear film, rendering them unavailable. In cases with inflammation, there will be increased protein in the tear film and hence potentially reduced drug penetration.

65
Q

How do drug molecules penetrate the eye at non-corneal areas?

A

Large, hydrophilic molecules - conjunctiva and sclera

From the conjunctiva drug penetrates the eye via the sclera (the sclera is up to 10 times as permeable as the cornea!) and enter the posterior segment or enter the scleral vessels and end up in the ciliary body.

66
Q

Which types of eye infection each of these steroids useful for?

  • Betamethasone sodium phosphate 0.1%
  • Dexamethasone acetate 0.1% in hypromellose
  • Prednisolone acetate 1%
  • Prednisolone sodium phosphate 0.5%
A

Betamethasone sodium phosphate 0.1% Superficial

Dexamethasone acetate 0.1% in hypromellose Anterior uveitis

Prednisolone acetate 1% Anterior uveitis

Prednisolone sodium phosphate 0.5% Superficial

67
Q

Name the layer between the bloodstream and intraocular space.

A

blood:ocular barrier (BOB), consisting of the blood:aqueous (BAB) and blood:retinal barriers (BRB), between the bloodstream and the intraocular space.

68
Q

What makes up the blood-aqueous barrier and blood-retinal barrier?

Which layer is leakier and what effect does this have?

A

BAB - ciliary body non-pigmented epithelium, the posterior iris epithelium, capillary endothelium of iris vessels and the endothelium of the aqueous plexus.

BRB- RPE and the retinal capillary endothelium.

The BAB is leakier than the BRB, so systemic agents can cross into the anterior segment more readily than the posterior.

69
Q

Which type of drugs penetrate the BOB better?

A

Hydrophilic drugs penetrate the BOB poorly, while lipophilic drugs penetrate more readily.

70
Q

Which types of drugs can be used to dilate the pupil?

How does each act?

A

Parasympatholytics - relax the iris sphincter muscle

Sympathomimetics - contract the dilator muscle

71
Q

Describe an alternative consequence of action taken by drugs which dilate the pupil.

Why is this useful?

A

Relaxation of the muscle in the ciliary body (cycloplegia), to relieve painful spasm in cases of anterior uveitis.

72
Q

Describe two ways in which sympathomemetics are used in diagnostics.

A

Horner’s syndrome. They cause rapid pupil dilation (via α1 receptor) in cases with post-ganglionic lesions.

Differentiate between conjunctival and episcleral vessel congestion, causing rapid conjunctival vessel constriction but slower constriction of episcleral vessels.

73
Q

Atropine

Characteristics, use and side effects.

A

Relatively slow onset,

Long duration

Parasympatholytic - useful for uveitis since, once dilation & relaxation have been achieved (which is after about 1 hour in the normal eye but variable in the inflamed eye), the effect can last up to 120 hours.

Bitter tasting and induces salivation, and can cause undesirable systemic antimuscarinic effects which can be particularly problematic in the horse (colic).

74
Q

Tropicamide

Characteristics and uses.

A

Fast onset (within 30 minutes)

Shorter acting (8-12 hours)

Antimuscarinic drug

Useful for dilation of the pupil for examination purposes

75
Q

Phenyephrine.

Which receptors is it used at?

Onset of action.

Why is it used in favour of adrenaline? Why?

A

Phenylephrine is a fairly α1-selective adrenergic drug

Acts within 10 minutes of application

Adrenaline is not useful as a topical agent due to poor corneal penetration

76
Q

What is the function of the tear film?

A

Preocular tear film is essential to maintaining corneal health and clarity.

77
Q

Name two drugs which actively increase tear production

A

Parasympathomimetic pilocarpine and the immunosuppressant drug cyclosporine

78
Q

How do tear substitutes work?

(x3)

A

They mimic parts of the tear film:

  • Aqueous - lost quickly from the ocular surface.
  • Mucin - Carbomer gel or hyaluronic acid drops
  • Lipid - increase retention of tear substitute
79
Q

Why are hyaluronic-acid containing tear drops considered to be highly effective?

A

Increased visco-elastic properties

80
Q

Classes of drugs which are used in treatment of glaucoma.

(x5)

Give an example of each.

A
  1. Osmotic diuretics - Mannitol
  2. Carbonic acid inhibitors - Brinzolamide, Dorzolamide
  3. Prostaglandin analogues - Latanoprost
  4. Beta-blockers - Betaxolol
  5. Parasympathomimetics - Pilocarpine
81
Q

Osmotic diuretics

Outline their mechanism of action as glaucoma treatments.

What are the potential risks?

A

Osmotic diuretics

Increased in blood tonicity causes water to be drawn out of the aqueous and vitreous.

Relies on an intact BOB.

These drugs are short acting and cannot be safely used repeatedly due to the risk of hypovolaemia; they are for emergency intervention only

82
Q

Carbonic Anhydrase inhibitors.

Mechanism of action, names of commonly used drugs, how are they applied and why?

A

Carbonic anhydrase catalyses the reversible hydration of CO2 to form HCO3 - and H+ in the non-pigmented ciliary body epithelium. Bicarbonate ions produced in this reaction move ions into the aqueous, thus drawing water into the aqueous so inhibition of this will reduce aqueous production.

Brinzolamide and dorzolamide

Readily penetrate the eye - topical

83
Q

Prostaglandin analogues

Mechanism of action.

Drug example, metabolism.

Side effects

A

Increasing uveoscleral outflow of aqueous, due to alteration in the ultrastructure of the outflow tract. Assist with vision preservation - increase perfusion of the optic nerve head by vasodilation of vessels.

Latanoprost, metabolised to its active form during passage through the corneal epithelium.

Can be irritating, causing blepharospasm, epiphora and conjunctival hyperaemia, long term changes such as darkening of the iris and periocular skin.

84
Q

Beta-blockers

Mechanisms of action.

Drug example - selectivity.

Side effects.

A

Beta-blockers act to reduce aqueous formation - theories including blockade of β receptors in the ciliary body, inhibition of Na/K ATPase and vasoactive actions.

A topical β1 selective agent betaxolol, which has also been shown to be neuroprotective due to its effect on ion channels.

85
Q

Parasympathomimetics

Mechanism of action and effects.

When are they not effective?

Drug example

A

Contraction of the ciliary body and constriction of the pupil - widens drainage angle and increases outflow of aqueous.

Effective if the drainage apparatus is intact.

Pilocarpine, direct. Acetylcholinesterase inhibitors, indirect.

86
Q

What four groups of drugs are used in non-specific pain management of GI conditions?

Briefly describe how each works.

Name a drug from each class.

A
  • Opiates e.g. morphine, butorphanol
    • Inhibit nociception at spinal or CNS level
  • NSAIDS e.g. flunixin meglumine, dipyrone, phenylbutazone
  • Sedatives e.g. xylazine, detomidine
    • Sedation and alleviation of visceral pain in colic
  • Anti-spasmodics e.g. hyoscine
    • Inhibits M1 muscarinic acetylcholine receptors in GI tract resulting in smooth muscle relaxation
87
Q

By which three mechanisms can antacids work?

A
  • Reduce acid secretion
    • Histamine2 blocker e.g. cimetidine, ranitidine and proton pump inhibitor e.g. omeprazole
  • Locally acting
    • eg Al/Mg salts - Neutralise luminal acid and inhibit pepsin cleavage, protects mucosa, acts as adsorbent and stimulate prostaglandins
  • Gastric Protectives
    • eg Sucralfate - Viscous gel at pH < 4 – binds to ulcerated protein protecting from acid / pepsin
88
Q

How can the vomiting centre of the brain be triggered? (x3 ways.

Name a centrally and peripherally acting emetic and briefly describe how they work.

A
  1. Chemoreceptor trigger zone via dopaminergic input
  2. Gastro-intestinal tract via vagal / sympathetic afferent pathways
  3. Vestibular apparatus via cholinergic / histaminergic afferent pathways
  • Centrally acting - Apomorphine
    • Stimulates chemoreceptor trigger zone
  • Peripherally acting - NaCl or Bicarbonate of soda
    • Stimulate sympathetic / vagal afferent receptors in pharynx / stomach
89
Q

How can anti-emesis be achieved?

(x3 ways)

Name and example of a drug from each method.

A
  1. Anti-histamines - diphenhydramine, promethazine
    1. Block histaminergic and cholinergic afferent pathways from vestibular organs to vomiting centre.
  2. Anti-cholinergics - propantheline
    1. Block cholinergic afferent pathways from GI tract to vomiting centre
  3. Antidopaminergic agents
    1. Phenothiazines e.g. acepromazine, prochlorperazine - blocks D2 at the CTZ and vomitting centre
    2. Metoclopramide - blocks D2 at CTZ and stimulates peristalsis of duodenum and stomach
90
Q

How do osmotic cathartics work?

Name examples of drugs from this class.

A

lactulose, magnesium sulphate (Epsom salts), sodium sulphate (Glauber’s salts), polyetheylene glycol electrolyte solutions
They are non-absorbable therefore osmotically retain water in intestinal lumen. Also lactulose is metabolised by colonic bacteria into organic acids (lactic, formic, acetic) – increase osmotic pressure.

91
Q

Name four classes of cathartics and explain how they work, giving an example for each.

A
  • Irritant cathartics e.g. castor oil
    • Stimulate peristalsis & reduce fluid absorption
  • Bulk laxatives e.g. ispaghula, sterculia
    • Contain hydrophillic colloids that absorb water and increase ingesta bulk to stimulate peristalsis
  • Lubricants e.g. liquid paraffin
    • Lubricate and soften faeces
  • Surfactants e.g. docusate
    • Anionic sufactant that acts in large bowel by hydrating and softening faeces by an emulsifying action
92
Q

Adsorb toxins and provide protective coating to inflamed mucosa.

This definition is indicative of which class of drug? What are they used to treat?

Give egs.

A

Protectants / Adsorbents

kaolin-pectin, bismuth salts
Bismuth salts also stimulate mucosal prostaglandin & bicarbonate secretion

93
Q

How do opiates work to prevent diarrhoea?

A

Diphenoxylate, loperamide, codeine
Inhibit acetylcholine release – increased segmental contractions and decreased peristalsis slow transit time and increase water absorption.
Directly stimulate absorption of fluid and electrolytes via mu-opiate receptors in CNS and intestinal mucosa.

94
Q

How do anti-cholinergics work to reduce diarrhoea?

A

Inhibit propulsive and non-propulsive GI motility
Also inhibit cholinergic-mediated basal secretions of GI tract

95
Q

Inhibition of the satiety centre causes what effect?

Name and describe the MOA of two drug types which are able to do this.

A

Appetite stimulation

  1. Benzodiazapines e.g. diazepam, oxazepam
    1. Increases GABA = anti-serotonergic effect depresses satiety centre
  2. Cyproheptadine
    1. Serotonin and histamine (H1) antagonist – supresses satiety centre

Also glucocorticoids

96
Q

What is the difference between pro and prebiotics?

A 
Probiotics = sample of normal intestinal microbes
Prebiotics = substrates that promote normal intestinal microbes
97
Q

How is Sulfasalazine metabolised in the gut to produce an anti-inflammatory substance?

Which drug counters the side effects of this class and how?

A

Sulfasalazine = sulfapyridine + 5-aminosalicylic acid

This reaction is catalysed by intestinal bacteria
Olsalazine does not produce sulfapyridine which can cause keratoconjunctivitis sicca.

98
Q

Anti bacterials/ anti-protozoans which are used in bowel inflammation?

A

Tylosin (macrolide antibiotic) and metronidazole (anti bact/ prot)

NSF (14 decks)

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