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mpharm year 3 sem 1 > MP322 week 7 > Flashcards

MP322 week 7 Flashcards

1
Q

diarrhoea

A

increased liquidity of still and or increased loose/ liquidity stool frequency

classification
- acute 14 days or less
- persistent more than 14 days
- chronic more than 30 days

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2
Q

2 main pathophysiological categories of diarrhoea

A

inflammatory and non inflammatory

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3
Q

inflammatory diarrhoea

A
  • presence of an inflammatory process (can be due to viral, bacteria or parasitic infection), radiation injury, or inflammatory bowel disease
  • mucoid and bloody stool, temesmus, fever, cramps abdominal pain
  • small, frequent bowel movements
  • histology of GI tract is abnormal
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4
Q

non-inflammatory diarrhoea

A
  • watery, large-volume, frequent stool (10, 20 per day)
  • volume depletion is possible die to high volume and frequency of bowel movements
  • no tenesmus, blood in the stool, fever, or faecal leucocytes
  • histology of GI tract is preserved
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5
Q

non inflammatory: osmotic diarrhoea

A
  • presence of unabsorbed or poorly absorbed slate (eg Mg2+, mannitol)
  • stool volume is small (compared to secretory diarrhoea)
  • stops or improves with fasting
  • due to maldigestion or malabsorption
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6
Q

non inflammatory: secretory diarrhoea

A
  • altered transport of ions across the mucosa
  • increased secretion and decreased absorption of fluids
  • doesn’t improve with fasting
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7
Q

aetiology: infectious

A
  • most common cause of acute diarrhoea
  • bacteria
    – E.coli, campylobacter, salmonella, clostridium difficle, listeria, vibrio cholerae
  • viruses
    – rotavirus, noravirus, adenovirus, astrovirus
  • parasites/ protozoa
    – entamoeba hisolitca, girardia lablia, cryptosporidium
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8
Q

aetiology: non infectious

A
  • most common cause is medication
  • cardiovascular drugs
    – digoxin, quinidine, propranolol, ACE inhibitors
  • GI drugs
    – antacids (magnesium salts), laxatives, H2 antagonists
  • endocrine system drugs
    – oral hypoglycaemic agents, thyroxine

-antibacterials
– amoxicillin, cephalosporins, erythromycin

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9
Q

physiology of diarrhoea

A

water follows the movement of electrolytes (Na+, K+, cl-, water) and glucose

due to different concentrations of solutes and water, the water is moved by osmosis

epithelial cells are polarised- meaning the membrane on one side of the cell has different transport systems than the other

membrane that faces GI lumen, is the apical membrane and membrane that faces interstitial side is called basolateral membrane

therefore the reabsorption of water requires prior movement of solute to create an osmotic gradient (water will always follow movement of electrolytes for this reason)

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10
Q

mechanisms causing diarrhoea

A
  • increased secretion of liquid in the GI tract
  • decreased absorption into the blood

absorption of water is passive and is secondary to the absorption of solutes

  • increased cl- secretion
  • reduced Na+ absorption
  • increased paracellular permeability
  • reduced Cl- absorption
  • reduced H2O absorption
  • reduced Na+ and glucose absorption
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11
Q

Cl- transport in the intestine

A
  • secreted Cl- is provided by the Na+/K=/2Cl- co-transporter
  • activity is driven by low intracellular Na+
  • Cl- is secreted through Cl- channels
  • Na+ and water enter lumen by paracellular transport (also transcellular for water)
  • paraceullular- diffusion between epithelial cells
  • this is limited by tight junctions between epithelial cells
  • water can use aquaporins to pass into the cell and then pass out again to the other side
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12
Q

infection - vibrio cholerae

A
  • cholera toxin from vibrio cholerae enter cells
  • activates G protein, which is coupled to and activates adenylyl cyclase (enzyme which converts ATP to cyclic AMP)
  • increases cellular cAMP and activation of protein kinase A (PKA)
  • phosphorylation of Cl- channel
  • increased efflux of Cl- (and water)
  • water and sodium ions are drawn into the lumen
  • diarrhoea
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13
Q

use of antibacterials (in diarrhoea)

A
  • disruption of normal intestinal microflora
  • proliferation of opportunistic pathogens ( eg C. diff- produced 2 toxins)
  • impaired fermentation of poorly absorbed carbohydrate and/ or reduced production of short chain fatty acids
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14
Q

increased motility

A
  • reduction in intestinal transit time will result in inadequate absorption
  • drugs with cholinergic activity (eg pilocarpine- for dry mouth)
  • drugs with anti cholinesterase activity (eg donepezil for Alzheimer’s disease)
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15
Q

drug treatment of diarrhoea

A
  • anti motility drugs
  • prolong the duration of intestinal transit
  • uncomplicated acute diarrhoea in adults
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16
Q

diphenoxylate

A
  • u (mu) opioid receptors on neuronal varicosities
  • myenteric plexus
  • activation pf opioid receptors decreases ACh release
  • peristaltic activity is decreased
  • increased segmental contraction
  • diphenoxylate is usually provided as a mixture with atropine (co-phenotrope)
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17
Q

codeine phosphate

A
  • symptomatic relief of chronic diarrhoea
  • POM
  • mechanism of action similar to that of diphenoxylate
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18
Q

adverse effects of opiates

A
  • rebound constipation
  • higher doses can have CNS effects
  • prolonged use can lead to opioid dependence
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19
Q

racecadotril

A
  • activation of delta opioid receptors decreases the cellular cAMP level
  • decreased secretion of Cl-
  • decreased water secretion
  • enkephalins are the endogenous activator of delta opioid receptors
  • racecadotril (pro-drug) metabolised to thiorphan
  • thiorphan is an enkephalinase inhbitor (prevents the breakdown of enkephalins)
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20
Q

constipation

A
  • heterogeneous disorder
  • patietnts report one or more of these symptoms
    – fewer than 3 bowel movements per week
    – straining
    – lumpy or hard stools
    – sensation of anorectal obstruction
    – sensation of incomplete defaecation
    – manual manoeuvring required to defaecate
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21
Q

common causes of constipation

A

primary
- normal - transit constipation
- slow transit constipation (colonic inertia)
- pelvic floor dysfunction
- irritable bowel syndrome with constipation

secondary
- medications
- metabolic disorders
- endocrine disorders
- psychiatric (anxiety, depression)

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22
Q

mechanisms of drug- induced constipation

A
  • drugs with anticholinergic activity (eg antidepressants, antihistamines, antimuscarinics, antipsychotics, antiparkinsonian agents)
  • opioids
  • drugs affecting electrolytes
  • laxative misuse (leads to atonic colon)
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23
Q

treatment of constipation

A

laxatives
- osmotic
- stimulant
- bulk-forming
- faecal softeners

drug treatment
- predominantly used in constipation associated with IBS and chronic idiopathic constipation

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24
Q

linaclotide

A
  • 14 amino acid synthetic peptide
  • linaclotide activates guanylate cyclase C (GC-C)
  • increases cellular cGMP and activation of protein kinase G (PKG)
  • phosphorylation of Cl- channel
  • increased efflux of Cl- and water
  • restricted use (SMC)
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25
Q

lubiprostone

A
  • member of a class of agents called prostones
  • derived from functional fatty acids that occur naturally
  • lubiprisone directly activates a Cl- channel (CIC-2)
  • increase efflux of Cl- and water
  • may restore mucosal barrier function
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26
Q

adverse effects of linaclotide and lubiprostone

A
  • generally well tolerated
  • diarrhoea
  • nausea
  • vomiting
  • abdominal pain
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27
Q

treatment of GIT inflammation

A
  • carboxylic acids are converted to sodium salts
  • the di-sodium salt is more water soluble and therefore dissolves faster
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28
Q

mechanism of action of salfalazine

A
  • its a pro drug
  • breakdown to the active 5-aminosalisilic acid (5-ASA)
  • site of action is the colon
  • mechanism of action is not clear but possibly inhibits prostaglandin and leukotriene biosynthesis amongst others
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29
Q

delivery and absorption of sulfalazine in the colon

A
  • delivery and absorption is mainly at the colon
  • due to bacterial induced cleavage of sulfalazine to the active 5-ASA
  • the resulting sulfapryidine has no anti-inflammation effect
  • but some side effects arise from sulfapyridine hence why balsalazide and olsalazine designed
  • the colonic microflora contain many species of bacteria
  • low in oxygen and pH (6-7)
  • gives rise to reductive environment
  • bacterial ago-reductases cleave sulfalazine ago bond to give 5-ASA (more lipophilic)
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30
Q

administration and formulation

A
  • structure and environment of colon dictate its use
  • administration as oral coated tablet disintegrating at pH 7 in the intestine or suspension
  • administration by rectum in suppositories or enema
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31
Q

pKa rule of 2

A

for base
- pH 2 above pKa =100% ionised
- pH 2 below pKa = 100% unionised

for acid
- pH 2 above pKa= 100% unionised
- pH 2 below pKa= 100% ionised

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32
Q

absorption of sulfalazine

A
  • log P = 3, OH, COOH and SO2NH are not ionised
  • pyridine is fully ionised at pH in stomach
  • log D=0, no absorption across stomach membrane
  • the drug travels to the small intestine
  • sulphonamides are weakly acidic
  • SO2NH dissociation and OH and pyridine no ionised
  • COOH is fully ionised and so molecule not absorbed
  • molecule is large and so it passes through to the colon where it gets cleaved to 5-ASA
  • OH, SO2NH, pyridine not fully ionised
  • COOH is fully ionised at pH=7 and it not absorbed passively
  • but the molecule is then cleaved by gut flora to 5-ASA
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33
Q

absorption of mesalazine

A
  • OH and NH2 not ionised
  • COOH if fully ionised at pH 7 so no passive diffusion
  • but it may absorb through aqueous gaps in between epithelial cells as it is a small, polar molecule
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34
Q

delivery of drugs to the colon

A

delivery is directed to the colon via MR tablets/ capsules, granules, suspensions or foam, suppository or enema

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35
Q

active form of sulfalazine

A

active form is 5-ASA or mesalazine (hydrophilic)
breakdown to the active form is done by gut flora

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36
Q

what are steroids

A
  • hormone molecules which control many biological events
  • sex hormones, inflammation, immunomodulation, stress
  • they are all derived from lanosterol in animals
  • produced in adrenal glands
  • glucorticosteroids (corticosteroids) are important in controlling inflammation
  • all share same 4 membered ring structure backbone
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37
Q

steroid backbone structure

A
  • organic 4 ring containing compounds
  • A, B, C = 6 membered ring
  • D= 5 membered ring
  • with hydroxyl groups known as sterols
  • no aromatic
  • aliphatic- is what gives 3D space
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38
Q

hydrocortisone (cortisol)

A
  • hydroxyl groups - aliphatic
  • carbonyl groups
  • won’t go into dissociation equilibrium at physiological pH
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39
Q

beclometasone

A
  • extra bond on A ring
  • added chlorine (will increase lipophilicity)
  • extra methyl group
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40
Q

budesonide

A
  • long carbon tail - increases lipophilicity
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41
Q

prednisolone

A
  • double bond in A ring
42
Q

lipinski ‘rule of 5’

A
  • molecular weight less than 500
  • no more than 5 H bond donor groups
  • no more than 10 H bond acceptor groups
  • calculated log P of less than +5

orally absorbed drugs normally observe these rules
not true for all molecules but good rule of thumb

43
Q

how do steroids work

A
  • act at the glucocorticoid receptor
  • regulates genes controlling inflammation
  • also regulates genes that control development, metabolism
  • expressed in every cell in the body in different forms
    -has many different effects in the body
  • difficulty in selectivity with steroid drugs
44
Q

administration and formulation of steroids

A
  • administered orally or rectally
  • GR or MR formulations or enemas and foams
  • due to chemical functionality ie non ionised and log P values between 0.5 and 1.2
  • absorption therefore in stomach or in colon

environment doesn’t affect them, log p = log d - doesn’t ionise

45
Q

omeprazole MOA

A
  • Further improvement achieved by increasing the pka of the pyridine ring by placing electron donating groups on it
  • This allows om to diffuse through the fatty secretary canals of the parietal cells
  • Causes om to be completely ionised
  • Quaternary salt- always charged – now not in equilibrium
  • Sulphenamide- active form of om
  • In this form om cannot diffuse back out of cell – known as ion trapping
  • Results in a build up in concentration of om
  • Chemical conversion then occurs
  • Sulphenamide reacts with thiol groups in H+, K+ - ATPase enzyme which forms a stable disulphide complex
  • No more acid is produced until a new enzyme is made which results in log duration of inhibition of gastric acid production
  • H+, K+-ATPase enzyme catalyses the final step of acid (H+) production hence why om is known as ppi
  • At ph 8 (small intestine) has a log d of 1.6 = will absorb
  • at ph 2 (stomach) has log d of -4.3 = wont absorb
  • Maximal conversion to sulphenamide – due to steep proton gradient caused by H+, K+-ATPase enzyme
  • There is ion trapping of both om and the sulphenamide (as permanently charged quaternary ammonium salt)
  • This is why it specifically acts in parietal cells
46
Q

why is an enteric coating required on omeprazole

A
  • Enteric coating- protects from acidic environment in stomach
  • At low ph, the basic functional group will be ionised
  • When its ionised a chemical conversion- into active sulphenamide
  • Other functional group is also ionised-changed into quaternary salt now this is positively charged – now cannot go into dissociation – all pi bonds- not hydrogen- can never be unionised
  • If we have conversion in the stomach it cannot cross the membrane and be absorbed- its stuck in the stomach
  • Sulphenamide reacts with thiol groups in H+ K+-ATPase enzyme which forms a stable disulphide complex
  • No more acid is produced until new enzyme s made which results in long duration on inhibition of gastric acid production
47
Q

why can’t we just give active form of omeprazole right away

A
  • Pro drug is omeprazole
  • It is then changed into sulphenamide
  • Cant just give sulphenamide- it will be bind to food etc and wouldn’t be absorbed
48
Q

why is particle size so important

A

particle size can affect
- drug bioavailability
- settling rate (suspensions)
- possibility of obtaining homogenous mixtures and maintaining it
- flowability
- other properties important for the transformation of powders into tablets, capsules
- tolerability of some dosage forms (ocular delivery)

49
Q

particle size reduction and selection

A

mechanical methods (more common)
- step 1- milling (size reduction)
- step 2 sieving (to select powders of desired size)

50
Q

cutting methods

A

principle- the material is cut by one or more blades

51
Q

compression methods

A

principle- a pressure is applied
traditionally mortar and pestle
roller mill

52
Q

impact methods

A

principle 1- particles are hit by a moving surface
2- moving particles hit a surface
hammer mill

53
Q

attrition methods

A

principle - pressure and friction
rollers rotate at different speeds

54
Q

combined impact and attrition methods

A

if too slow- balls move up the side then just slide back down- don’t hit particles
if too fast centrifugal force means balls are at outside of mill

55
Q

selection of appropriate mill

A
  • particle size to obtain
  • characteristics of the material
    – cutter mills are excellent for elastic, fibrous materials like roots and woods
    – attrition methods are used for ointments, solid in suspensions and pastes
    – impact methods are sued for brittle materials
  • other factors (cost, time, stability of ingredients)
56
Q

statistical diameters

A

dependent on orientation and shape. These are statistical diameters so many measurements are taken to derive average.

ferret’s (DF)
martin’s (DM)

Feret is diameter is the mean distance between two parallel tangents of the projected outline of a particle.

Martin mean chord length – i.e. boundry separating equal particle areas.

57
Q

size analysis

A

particle size
approx. particles are spheres

projected area diameter (DA)
protected perimeter diameter (DP)

58
Q

methods to analyse particle size

A

direct
- sieving
- microscopy

indirect (determine a parameter correlated with size)
- sedimentation rate
- permeability

59
Q

particle size distribution

A

monosized distribution
Normal distribution
positively skewed distribution
bimodal distribution

60
Q

microscopy methods

A

light miroscopy
- size range 1- 1000 um
- images are 2D

electron microscopy
- size range as low as 0.001 um
- adv- gives 3D images, info on shape
- disadvantage- expensive, need skills to do, slow

61
Q

Coulter counter

A

measures the volume of particles 0.1 to 1000 um

62
Q

laser light scattering methods

A

principle- laser light interacts with particles

light is diffracted by particles by an angle that is inversely proportional to the volume of the particles

a detector analyses the radiation diffracted by the particles

He and Ne laser are the most widely used

63
Q

sieve methods

A
  • sieves are classified based on the sieve aperture diameter (expressed in um)
64
Q

size separartion

A

size separation aim- select a specific size range
1- by sieving
2- by sedimentation
– larger particles travel further

65
Q

sedimentation methods

A

the diameter of particles is estimated based on their sedimentation rate

D2 is the most important part of the equation

66
Q

cyclone separation

A

centrifugal elutriation process or centrifugal sedimentation process

particles suspended in medium (air) are introduced at high fluid velocity

coarser particles separate from build stream and fall out the bottom

67
Q

elutriation methods

A

fluid direction is opposite to sedimentation direction

68
Q

mesalzine MR tablets counselling

A
  • split doses evenly throughout the day
  • don’t chew- these have an enteric coating to protect them
  • take with water of juice, before or after a meal
  • side effects- nausea, vomitting, muscle/joint pain
69
Q

mixing

A

aim- obtain a homogenous distribution of 2 or more components (without physical or chemical changes occurring)
- opposite of mixing is segregation
- mixing is a particularly key factor when very active drugs are employed
- positive mixtures- materials that mix spontaneously and irreversibly
- negative mixtures - the components tend to separate (suspensions)
- neutral mixtures- components neither tend to separate nor to mix

70
Q

general observations- particles

A

the more particles are present in a dose, the more likely it is that the content will mirror the ratio in the mixture
- implication - what will happen if we decrease particle size

the lower the proportion of a component in a mixture, the more difficult it is to achieve the same (correct) amount in each sample

71
Q

parameters that affect mixing

A
  • particle size
  • particle shape
  • density
  • flowability
  • ratio between different components
  • mixing time
  • electrostatic interactions
  • total volume of powders being mixed
  • friability of the material
  • humidity
72
Q

granulation

A
  • is the process inn which homogenous mixtures of primary powder particles form larger, still homogenous particles called granules
  • improve powder flow
  • prevent segregation
  • improve compaction
73
Q

wet granulation

A
  • the powders are mixed with a granulating fluid
  • the mass is forced though a sieve
  • adhesion and cohesion forces in immobile films
  • interfacial forces in mobile liquid films
  • solid bridges (hardening binders or crystallisation of dissolved substances)
  • attractive forces between particles
74
Q

dry granulation

A
  • a pressure is applied
  • the intermediate product is broken
  • sieving

granulation mechanisms
- attractive forced between solid particles
- solid bridges (by particle melting)

mechanisms of granule formulation
- applied pressure
- formation of a sheet
- milling and sieving
- granules

advantages
- cheap
- easy to scale up

75
Q

list 5 different milling methods

A

cut
compression
impact
attrition
combination of impact and attrition

76
Q

name one mill based on compression

A

roller mill

77
Q

name one mill based on impact

A

hammer mill

78
Q

in a ball mill, do you have a better size reduction at the critical angular velocity or at 2/3 of the critical angular velocity?

A

2/3 of the critical angular velocity

79
Q

what type of mill would you use if you ha dot reduce a root to coarse particles

A

a cutter mill

80
Q

define the projected area diameter

A

it is the diameter of a circle whose area is equivalent to that of the projected particle

81
Q

if I take a sieve number 500, what is its aperture in mm?

A

0.5mm

82
Q

What characteristics of a particle do you detect if you use a Coulter counter?

A

the volume

83
Q

For what types of drugs is mixing particularly important?

A

very potent drugs
drugs with small therapeutic index

84
Q

Name three factors that are responsible for segregation?

A

density, shape and size

85
Q

Name the three main reasons for granulation.

A

Improve powder flow, prevent segregation and improve compaction

86
Q

There are 2 main types of granulation, name them

A

Wet granulation and dry granulation

87
Q

Formation of solid bridges is one of the possible granulation mechanisms in wet granulation how does it occur?

A

Hardening of binders or crystallisation of dissolved substances

88
Q

Formation of solid bridges is one of the possible granulation mechanisms in dry granulation how does it occur?

A

by particle melting

89
Q

List the 3 main mechanisms of ball growth responsible for granule formation in wet granulation

A

Coalescence, breakage and abrasion transfer.

90
Q

List the 3 main mechanisms of ball growth responsible for granule formation in wet granulation

A

Coalescence, breakage and abrasion transfer.

91
Q

What is the role of the chopper in high-speed mixer/granulators?

A

To break up the wet mass and produce granular material

92
Q

What is the main difference between a fluidised-bed drier and a fluidised-bed granulator?

A

The fluidised bed granulator is equipped with a nozzle to spray granulating liquid inside
the chamber

93
Q

DNA bases

A

DNA has A,T,C,G
mRNA has A,U,C,G

94
Q

mRNA

A
  • gene transcription produces mRNA
  • mRNA is spliced to remove the 5’ and 3’ ends as well as introns - leaving just
  • translation of mRNA produces a protein
  • mRNA determines the amino acid sequence of proteins
  • codon- every 3 nucleotides
  • stop codons tell the ribosome to stop translating the mRNA into the protein
95
Q

single nucleotide polymorphisms (SNPs)

A
  • polymorphism is any difference in the nucleotide sequence between individuals
  • SNPs are the most common type of polymorphism
  • polymorphisms may or may not have phenotypic effects
  • we refer to the specific nucleotide present at a SNP as an allele (ie T allele)
  • can occur in both coding and noncoding DNA regions
96
Q

classification of SNPs

A

coding SNPs
- occur in exons
- synonymous: do not change the encoded amino cid
- non-synonymous: change the encoded amino acid

non coding SNPs
- can influence gene expression

non coding silent SNPs

97
Q

azathioprine

A

immunosuppressant used in treatment of IBD

changed into 6-MP (6- mercaptopurine)
then into thiopurine methyltransferase (TPMT)

98
Q

how could SNPs occurring outside the coding regions of TPMT gene affect the encoded enzyme?

A

won’t affect which protein is produced as it is spliced out
however the transcription factor binds to the 5’ end- if there is changes to this sequence it may not be recognised
so won’t affect the protein produced but could affect the amount of the protein produced

99
Q

other than genetic screening, how could we examine TPMT activity in patients going on to azathioprine treatment

A

enzyme assay

100
Q

Consider these two scenarios: a patient with a 50% decreases in TPMT activity and a patient with a 99% loss of activity. What do you think would be sensible treatment options in these cases?

A

50%- give a lower dose
99%- change treatment

mpharm year 3 sem 1 (10 decks)

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