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MPharm Year 3 > MP322 - Management of GastroIntestinal and Endocrine systems > Flashcards

MP322 - Management of GastroIntestinal and Endocrine systems Flashcards

1
Q

Dyspepsia occurs in how many % of the population?

A

Around 40%, and leads to primary care consults in 5% and endoscopy in 1%

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2
Q

What findings are identified after a patient undergoes endoscopy?

A
  1. 40% - non-ulcer (functional dyspepsia)
  2. 40% - GORD confirmed
  3. 13% - ulcer disease
  4. 2% - Gastric Cancer
  5. 1% - oesophageal cancer
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3
Q

How is the lining of the somach protected?

A

The upper mucosal layer releases alkaline mucus, keeping the layer safe from exposure to the stomach acid

There are tight junctions between epithelial cells

Damaged cells usually get replaced every few days

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4
Q

What factors cause/ contribute to Peptic Ulcer Disease?

A
  1. H.Pylori bacteria
  2. Smoking, alcohol, genetics, and stress raise the likelihood of developing ulcers
  3. Use of NSAID’s reduce the production of protective prostaglandins, again, rendering it more likely
  4. Hypersecretory states (but these are uncommon)
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5
Q

What are the symptoms of a Peptic Ulcer?

A
  1. Abdominal pain, discomfort and/or nausea
  2. Pain in the epigastrum and usually not radiating
  3. Burning, gnawing, and hunger pains?
  4. Gastric ulcer pain are aggravated by food, but duodenal ulcers are relieved upon food consumption
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6
Q

How is a peptic ulcer definitely diagnosed?

A

Usually GP’s likely to refer for endoscopy, those are cameras sent through the oesaphagus, to view stomach and duodenal area, to examine for ulcers.

Other methods are possible via lab work if believed to be caused by H.Pylori

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7
Q

What is H.Pylori and how is it related to peptic ulcers?

A

40% of individuals are believed to be infected with H.Pylori.

H.Pylori is a gram-negative bacterium responsible for 95% of gastric ulcer patients and 80% of dudodenal ulcer patients

Dr Marshall and Warren won Nobel Prize in 2005 for role in identifying H.Pylori in gastritis.

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8
Q

Where does H.Pylori target?

A

Lower part of the stomach, H.Pylori causes inflammation of gastric mucosa (leading to gastritis)

It can pass the mucus layer of the stomach and raise pH, causing mucin to de-gel.

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9
Q

Where H.Pylori is suspected, how can this be diagnosed?

A

Can do serologic evaluation for presence of H.Pylori antibodies but this may not be reliable as these can be present due to a previous infection

Urea Breath Test can be done based on the idea that H.Pylori contains large amount of the enzyme urease, which converts urea to NH3 and CO2 (carbon 13).

Can also use stool antigen test designed to detect an antigen released by organisms present in the stomach - this will prove an active infection.

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10
Q

If H.Pylori is not eradicated, what happens?

A

80% of H.Pylori infection-related ulcers can re-occur within a year.

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11
Q

What does the stomach body secrete?

A

Mucus via mucous cells - secrete bicarbonate

Parietal Cells - release stomach acid (HCl), and intrinsic factor

Enterochromaffin-Like cells (ECL), release histamine

Chief cells - Secrete pepsinogen

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12
Q

What different components act on the parietal cells?

A
  1. Acetylcholine acts on M3 receptors - promotes acid secretio
  2. Histamine acts on H2 receptors - promotes gastric acid secretion
  3. Gastrin acts on CCK receptors on parietal cells, which also promotes secretio of acid.
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13
Q

How is HCl produced for the stomach?

A

Carbonic anhydrase converts to Bicarbonate and Hydrogen ions

Bicarbonate is exchanged for Chloride ions and said chloride ions diffuse into the stomach lumen

Hydrogen ions are then pumped into the lumen by the Hydrogen/Potassium/ ATPase

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14
Q

How are peptic ulcers treated?

A

Antacids are used. These are antisecretory agents.

They can raise pH above 3 for few hours/ day and this promotes healing.

Duration of acid suppression determines how quickly stomach will heal

Rapid healing requires suppression for 18-20 hours a day.

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15
Q

What are H2 receptor antagonists?

A

These are products such as cimetidine, ranitidine, nizatidine, and famotidine

Act competitively on H2 Receptors on gastric acid parietal cells

Reduce basal acid secretion and prevent the increase that occurs in response to secretory stimuli.

This can reduce secretion by around 60%

Can be used for ulcers but relapse is common after treatment stops.

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16
Q

Side effects of H2 antagonists?

A

Diarrheoa,
Headache,
Confusion in elderly,
Gynaecomastia with Cimetidine (because of anti-androgen effect)
Cimetidine inhibits cytochrome P450 system (interacts with warfarin, phenytoin, and theophylline)

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17
Q

What are proton pump inhibitors?

A

Products such as Omeprazole, lansoprazole, pantoprazole, and esomeprazole

These inhibit the pump - almost completely block acid secretion

Proton Pump Inhibitors are irreversible, and acid secretion can only return with synthesis of new enzymes (H+, k+ ATPase)

Acid secretion inhibited by 90% for 24 hours with single dose

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18
Q

Adverse effects of PPI’s?

A

GI upset (discomfort, nausea, diarrheoa)

Headache

Skin Rashes

Omeprazole has both stimuatory and inhibitory effects on cytochrome p450

Long term use may cause Gastric Atrophy

Osteoprosis

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19
Q

Treatment regimen to eradicate H.Pylori infection

A

Triple therapy:
PPI
Amoxicillin
Clarithromycin OR metronidazole

For patients allergic to penicillin:
PPI
Clarithromycin
Metronidazole

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20
Q

Example of cytoprotective agents which can reduce acid secretion?

A

Misoprostol - it’s a metyl analogue of prostaglandin E1, and enhances duodenal bicarb secretion

Weakly inhibits gastric secretion by activating prostaglandin receptor on parietal cells.

Causes increased blood flow

Must NOT be used in pregnancy, as it can cause intrauterine contractions to be induced, which can lead to abortions etc.

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21
Q

What is Zollinger- Ellison Syndrome?

A

Rare disorder which can cause gastric or duodenal ulcers (usually multiple), as well as in the jejunum

Massive gastric acid hypersecretion
Due to gastrin secreting tumour in the pancreas or duodenum (gastrinoma), that stimulates acid secretion in stomach

Patient likely to have intractable ulcer disease

Treatment must control the hypersecretion and the gastrinoma

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22
Q

What is the situation with GORD?

A

Amount of acid secretion

Functionally incompetent LOWER oesophageal sphincter

Allows reflux of gastric contents (containing acid and pepsin into oesophagus

Symptoms - restrosternal burning

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23
Q

What medications can assist with GORD?

A

Antacids and antacid/alginate combinations

Drugs which inhibit gastric acid secretion (H2 receptor antagonists and proton pump inhibitors)

Drugs which act on Oesaphageal and/or gastric motility.

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24
Q

What is Barrett’s Oesaphagus?

A

This is commonly diagnosed in patients with long term GORD

Caused by the replacement of normal stratified squamous epithelium by columnar epithelium with goblet cells

Can lead to oesophageal adenocarcinoma (>85% mortality)

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25
Q

What is Inflammatory Bowel Disease?

A

This is a broad term consisting of 2 diseases - Ulcerative Colitis and Crohn’s disease

Both are characterised by inflammation, swelling, and ulceration of intestinal tissue - chronic periods of remission

Symptoms include stomach pain, weight loss, diarrheoa (blood/ mucus), and tiredness

Can also cause joint pain, inflamed eyes and rashes.

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26
Q

What is the main difference between Crohn’s and Ulcerative Colitis?

A

UC only affects the large bowel and inflammation is on the inner lining.

Crohn’s can affect any area of the GI system and all layers of tissue can be inflamed.

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27
Q

How is IBD diagnosed?

A

Symptoms presented in Primary care,

Blood tests conducted for anaemia, vitamin deficiencies, and inflammatory markers

Can also get an X-Ray or MRI

Sigmoidoscopy and Colonoscopy

For Chron’s disease, small bowel enema and small capsule endoscopy can be used.

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28
Q

Causes of IBD?

A

Genetics,
Autoimmune Disease
Environmental
Previous infection

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29
Q

Prevalence of IBD?

A

Most common in late teens or early 20’s, more common with white ethnic folk, is slightly more common in women than men,
can affect 1 in 350 in the UK.

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30
Q

What is the main aim of treatment?

A

Induce and maintain remission
Reduce symptoms and improve quality of life
Reduce inflammation - steroid, aminosalicylates, and cytokine modulators
Reduce autoimmune response - immunosuppressant drugs

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31
Q

How are Corticosteroids administered and examples?

A

Administered Orally and rectally - should use GR/ MR forms or enemas and foams etc.

Hydrocortisone
Beclomethasone
Budesonide
Prednisolone

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32
Q

How does Steroids work in terms of their pharmacology?

A

Reduce inflammatory mediators directly, and also have effects on expression of genes associated with inflammatory and anti-inflammatory proteins

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33
Q

What are the cautions of Corticosteriods?

A

Avoid in congestive heart failure, hypothyroidism, osteoprosis, and untreated infection

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34
Q

Side effects of Corticosteroids?

A

Insomnia, dyspepsia, Cushing’s syndrome, impaired healing, adrenal suppression with long term use.

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35
Q

Interactions of corticosteroids?

A

Grapefruit juice increases plasma concentration or oral budesonide, corticosteroids antagonise diuretic effect.

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36
Q

Examples of Aminosalicylates and how they’re administered?

A

Administered orally or rectally - Can be MR tabs/ caps/ granules, suspensions, or foam, suppository, enema’s

Balsalazide
Mesalazine
Olsalazine
Sulfalazine

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37
Q

Side effects of Aminosalicylates?

A

Blood disorders - unexplained bleeding, brusing, purpura, sore throat, fever, or malaise during treatment?

Renal function should be checked before starting oral therapy then 3 months later, then annually

Salicylate sensitivity?

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38
Q

If you are diagnosed with Ulcerative colitis….

A

Aminosalicylates are likely to be recommended:

  • As an initial treatment for people who have mild to moderate flare-ups of Colitis.
  • To maintain a period of recovery (remission), and help prevent flare-ups of colitis in longer term
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39
Q

If you are diagnosed with Crohn’s…

A

Aminosalicylates are not commonly prescribed unless:

  • To get your symptoms under control, if your symptoms are mild, and you cannot, or decide against usage of steroids
  • If it is not clear whether you have Crohn’s or colitis?
  • To help maintain remission if you have had surgery for Crohn’s
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40
Q

What are the predominant interactions and side effects of Sulfasalazine?

A

Urine and contact lenses are coloured orange - hence contact lenses may be discouraged

Sulfasalazine decreases concentration of digoxin (moderate) and absorption of folates (moderate).

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41
Q

What is the function of cytokine modulators?

A

These are monoclonal antibodies which inhibit pro-inflammatory cytokine, tumour necrosis factor alpha (TNF-a)

Administered subcutaneously

Examples - infliximab, adalimumab, golimumab, vedolizumab

These stop the expansion of activated T-cells by interrupting the calmodulin-calcineruin cascade.

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42
Q

How does immunosuppressants work in the treatment of IBD?

A

Mainly T-cell effects, administered orally or by injection, care required when handling in pharmacy

Azathioprine, Ciclosporin, mercaptopurine
Methotrexate

Anticancer drugs with blood toxicity and liver toxicity so require regular monitoring of blood counts and organ function for safe use

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43
Q

How is methotrexate administered?

A

Weekly dosage, usually orally but can be done via subcutaneous and intramuscular injection

2.5mg tablets normally used

Can get sore throats, bleeding, bruising, and mouth ulcers.

Regular monitoring - FBC, renal and liver

Keep safety card

High risk drug for MCR

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44
Q

In what manner are IBD drugs used?

A

In mild cases of disease in rectum and rectosigmoid is treated via local steroid or aminosalicylate

Diffuse or unresponsive IBD is treated orally as above

Parenteral administration is used in severe cases (steroid, immunosuppression and antibody therapy)

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45
Q

Non-drug treatment for IBD?

A

Smoking cessation

Attention to diet
- low residue diet
- trigger foods?

Surgery
- Stoma operations
- resection operations

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46
Q

Examples of alginates?

A

Peptac, gaviscon (rafting agents)

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47
Q

Examples of antacids?

A

Co-magaldrox, magnesium trisilicate

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48
Q

Examples of PPI’s and strengths?

A

Omeprazole - 10, 20, 40mg
Lansoprazole - 15, 30mg
Esomeprazole - 20, 40 mg
Rabeprazole - 10, 20mg

49
Q

Examples of PPI dosage forms?

A

Tabs, caps, granules - gastro-resistant

Dispersible, oro-dispersible tabs

Oral Liquids/ suspensions from specials

Injections

50
Q

What are the cautions associated with PPI use?

A

Increased risk of bone fracture on prolonged use in susceptible patients

Increase of C.dif infection

Masks symptoms of cancer

Rebound hyper secretion of acid on cessation

51
Q

What common interactions occur with PPI’s?

A

Esomeprazole and Omeprazole reduce the antiplatlet effect of clopidigrel

Pantoprazole may increase anticoagulant effect of warfarin.

52
Q

Examples of side effects of PPI’s?

A

Abdominal Pain, headaches - common

Arthralgia, parasthesia - uncommon

Confusion, gynaecomastia - Rare

53
Q

Examples of H2-receptor antagonists?

A

Ranitidine (150, 300mg)
Cimetidine (200, 400, 800mg)
Famotidine (20mg, 40mg)
Nizatidine (150, 300mg)

54
Q

Side effects of H2R antagonists?

A
  1. Masks symptoms of cancer
  2. Diarrheoa, dizziness (common)
  3. erythema - multiform (uncommon)
  4. Hepatitis, confusion (rare).
55
Q

Interactions of H2R antagonists?

A

Cimetidine increases blood conc of erythromycin

Famotine and ranitidine reduce plasma conc or atazanavir

56
Q

What other drugs can be used in disorders of gastric acid and ulceration?

A

Chelates and complexes:
Sucralfate - 1000mg
Tripotassium dicitratobismuthate (120mg)

Prostaglandin analogue:
Misoprostol (200 mcg)

Pro-kinetic drugs:
Domperidone, metoclopramide

57
Q

How should drugs like antacids and PPI’s be used?

A

Should use lowest effective dose for shortest period, move from treatment doses to maintenance dose after period of time dependent upon the indication

Can be used in combination with antibacterials for H.Pylori eradication

58
Q

What is Omeprazole’s mechanism of action?

A

Omeprazole is usually in gastro-resistant form when administered - hence, it passes the stomach and evades being ionised at this point - it enters the bloodstream once absorbed in the small intestine, and then, once going through the bloodstream, it reaches the parietal cells and diffuses through the fatty secretory canals of the parietal cells.

The pH of the parietal cells is very low (approx 1)

Because of this, and the presence of the pyridinic groups, becomes ionised, and is thereafter trapped in the parietal cells as it cannot diffuse back out

This results in a build up of omeprazole and causes chemical conversion

Omeprazole converts to sulphenic acid and then sulphenamide (Which is omeprazole’s active form). There is maximal conversion to sulphenamide due to steep proton gradient due to the proton pump enzyme

Omeprazole and Sulphenamide are ion-trapped (sulphenamide is a permanently charged quarternary ammonium salt

Sulphenamide reacts with thiol groups in the proton pump enzyme, which forms a stable disulphide complex.

No more acid is produced until new enzyme is made, which results in long term inhibition of gastric acid production.

59
Q

How is Omeprazole designed fairly well?

A
  • formulated in hard gelatine capsules - prevents conversion to sulphenamide in stomach

-if sulphenamide was formed, it would react with thiols in food and gastric mucus and be charged, rendering it unavailable.

60
Q

How well does Omeprazole work?

A

High doses (80mg) are able to eliminate gastric acid production for atleast 4 hours

Single 40mg does can still affect acid secretion 72 hours later with effects taking 3-5 days to disappear.

Patients are given 20mg doses daily for 2-4 weeks (duodenal ulcer) or upto 8 weeks (gastric ulcer)

61
Q

What is noted about Omeprazole and how it can be further improved?

A

Improvement was sought but omeprazole is effective as a chiral molecule

R-enantiomer was noted to give 15% gastric acid inhibition whereas the S-enantiomer gives 90% inhibition.

Hence, Esomeprazole is now manufactured which is simply omeprazole but only the s-enantiomer form.

62
Q

How do H2 receptor antagonists work?

A

Ranitidine has a tertiary aliphatic amine, and 2 x Secondary alipathic amine, a thio-ether and nitro group.

The sulfur can be converted to suloxides etc.

There is likely complementary binding with the receptor and the antagonists, preventing the binding of other agonists etc. and therefore, inhibiting the activation of H2 receptors.

63
Q

What is the name of the group of drugs which are typically used for treating GIT inflammation?

A

Aminosalicylates

64
Q

What is the drug which is also referred as 5-Aminosalicylic acid?

A

Mesalazine

65
Q

How are balsalazide and Olsalazine formulated?

A

Typically formulated as sodium salts due to the presence of carboxylic acids - the di-sodium salt makes the molecule more water soluble for formulation

66
Q

What is sulfalazine?

A

It is a pro-drug, which is responsible for breaking down to the active 5-aminosalisilic acid (Mesalazine)

67
Q

Where is the site of action for mesalazine?

A

The colon

68
Q

What is the mechanism of action for aminosalicylates?

A

Not completely clear but believed to inhibit prostaglandin and leukotriene biosynthesis amongst others.

69
Q

How is sulfalazine broken down?

A

Broken due to bacterial cleavage. The resulting sulfapyridine has no anti-inflammatory effect but can possibly give side effects hence balsalazide and olsalazine are designed.

70
Q

Describe the colon environment?

A

Colonic microflora contains many species of bacteria

It is low in oxygen and pH is between 6-7

Gives rise to reductive environment

Hence bacterial azo-reductases cleave the sulfalzaine azo bond

71
Q

How is aminosalicylates formulated?

A

They typically are formed as oral coated tablets which disintegrate at pH 7 in the intestine or suspension

Administered by the rectum in suppository and enemae form

72
Q

How to work out fraction unionised for an acid?

A

1/(1+10^Ph-pka)

73
Q

How to work out fraction unionised for a base?

A

1/(1+10^pka-ph)

74
Q

In the stomach, describe how each functional group of aminosalicylates would act?

A

Carboxylic acid has pka 2.5
Aromatic hydroxyl (phenol) has pka 11.5 and is acidic.
Azo group acts fairly neutral in all circumstances
Sulphonamide group has pka 6.5 and is also acidic
Pyridine has pka of 4 and is basic so will be ionised.

Because pH of stomach is roughly 2, carboxylic acid, phenol and sulphonamide will remain unionised.

But pyridine will be fully ionised hence wouldn’t absorb across stomach membrane. Log D = 0

75
Q

In the ileum, describe how each functional group of aminosalicylates would act?

A

In ileum, pH is roughly 7-8.

Pyridine won’t be ionised as it’s pka is 4 and it’s a base

Sulphonamide will be dissociated as it has a pka of 6.5

Carboxylic acid will be ionised fully (pka 2.5)

Phenol not ionised as it acts as acid and pka is 11.5.

Furthermore, due to molecule size, it’s able to pass through to colon where it is cleaved to 5-ASA

76
Q

In the colon, describe how each functional group of aminosalicylates would act? N.B colon pH 5.5-7.8

A

Carboxylic acid will be ionised fully (pka 2.5) and therefore can’t passively absorb.

Sulphonamide will be dissociated as it has a pka of 6.5 and therefore not fully ionised. Pyridine also may be partially ionised as it’s pka is 4.

Phenol not ionised as it acts as acid and pka is 11.5.

Hence still has inability to passively be absorbed.

BUT, is broken down to 5-ASA

77
Q

How does 5-ASA get absorbed in the colon?

A

With 5-ASA, the carboxylic acid is still fully ionised, and Aromatic amine and hydroxyl are not ionised, hence would still not passively absorb, but, because of the size of molecule being smaller, it is able to absorb through aqeuous gaps in between epithelial cells as it is a small molecule.

78
Q

What is the advantage of using Olsalazine and Balasalazide ?

A

It does cleave but does not cause sulfa pyridyl toxicity.

79
Q

What things can particle size affect?

A

Bioavailability
Settling rate
Possibility of obtaining homogenous mixtrues (and maintaining it)
Flowability
Other properties important for transformation of powders into tablets, capsules

80
Q

How can particle size be increased?

A

Granulation

81
Q

How can particle size be reduced?

A

Milling
Attrition

82
Q

Examples of mills used and purpose?

A

Pin and ball mills - combined impact and attrition methods

vibration mills and hammer mills - Impact methods

End runners mills roller mills - compression methods

83
Q

Cutting methods

A

Cutter mill can be used so the material is cut by one or more blade

84
Q

Compression methods

A

Designed to apply pressure -

can use Mortar and Pestle or use Roller mills

85
Q

Impact methods

A

designed to cause particles to be hit by a moving surface and Moving particles to hit a surface

86
Q

Attrition methods

A

pressure and fiction principle
can use Roller mills, but ones which rotate at different speeds.

87
Q

What is important for a ball mill?

A

The speed of rotation

Need to use 2/3 of the angular velocity where centrifugal force occurs to ensure that the balls are lifted on the rising side of the drum, until their dynamic angel of repose is exceeded. At this point, they fall back or roll back and cascade back to base of drum - rendering most effective size reduction

88
Q

How to select appropriate form of mill?

A

consider Particle size to obtain

Consider characteristics of the material:
1 - Cutter mills for elastic, fibrous, materials like roots and woods.
2 - Attrition methods are used for ointments, solid in suspensions and pastes
3. impact methods used for brittle materials

Other factors such as cost,time, product stability should be considered.

89
Q

What is the area diameter?

A

The diameter of the area of space taken by particle surface, assuming it is fully circular

90
Q

What is the perimeter diameter?

A

The diameter of of the complete area of space taken by particle, regardless of circularity or lack thereof.

91
Q

What is feret’s diameter?

A

The mean distance between 2 parallel tangents of the projected outline of a particle

92
Q

How to analyse particle size??

A

Direct methods are sieving and microscopy

Indirect methods include sedimentation rate and permeability

93
Q

What is the size range for using light microscopy?

A

1-1000 micrometers for particles - provides 2D images and very diluted suspension used.

94
Q

What is the size range for using electron microscopy?

A

Size as low as 0.001 micrometers
Can give 3D images, and info on shapes
Disadvantages would be - expensive, high level of operator exercise.

95
Q

How does Coulter Counter work?

A

Measure the volume of particles 0.1 to 1000 micrometres.

The aperture creates a sensing zone. As the particle moves through the aperture there is a change in impedance and the change can be correlated to the volume of the particle.

96
Q

How does laser light scattering work?

A

Laser lights react with particles

Light is diffracted by particles by an angle which is inversely proportional to the volume of the actual particle

Detector analyses the radiation diffracted by the laser.

He and Ne laser are more widely used laser.

97
Q

How does Sieve methods work?

A

Sieve’s seaparate varying sizes of particles, they are classified based on the sieve aperture diameter (expressed in Micrometres).

Sieve 1000 means the sieve aperture diameter is 1000 micrometer (1mm).

Sieve aperture diameter - distance between 2 consecutive wires.

98
Q

What is sedimentation methods?

A

It is another method of particle seperation and the idea is the diameter of particles are estimated based on their sedimentation rate.

Stokes equation is also used for this.

99
Q

What is cyclone separation?

A

This is where particles suspended in medium are introduced at high fluid velocity.

This results in vortex drawing them down due to fluid flow (gravity interactions are relatively minor).

A tip of cyclone fluid flow is above the critical velocity where it can escape through narrow opening.

This forms in inner vortex that travels up the cyclon and out of the outlet.

coarser particles separate from fluid stream and fall out.

100
Q

What is elutriation and how does this work?

A

This is where fluid direction is opposite to sedimentation direction.

Separatiom is dependent on veolcity of fluid flow

Vectors are velocities

If settling velocity is less than the fluid flow velocity particles get moved into direction of fluid flow.

101
Q

What is mixing?

A

Where two or more components are mixed together with the aim to obtain a homogenous distribution (without physical or chemical changes occurring).

102
Q

What is a positive mixture?

A

Materials that mix sponteneously and irreversibly.

103
Q

What is a negative mixture?

A

The components tend to separate

104
Q

What is a neutral mixture?

A

Components neither tend to separate nor mix.

105
Q

What is the definition of a random mixture?

A

Where the probability of selecting a particular type of particle is the same at all positions in the mix and is equal to the proportion of such particles in the total mix.

106
Q

Observation about particles?

A

The more particles are present in a dose, ther more likely it is that the content will mirror the ratio in the mixture.

Lower the proportion of a component in the mixture, the more difficult it is to achieve the same correct amount in each sample.

107
Q

What other parameters affect mixing?

A

Particle size
Shape
Density
Flowability
Ratio between different components
Mixing time
Electrostatic interactions
Total volume of powders being mixed
Friability of material
Humidity

108
Q

What is segregation?

A

The opposite process of mixing (i.e. de-mixing)

Due to powders having different densities, shapes, and sizes

109
Q

Equipment used for mixing?

A

Tumbling mixers (mixing franuels and free flowing powders - at correct speed, tumbling action and powder bed dilates, resulting in shear mixing).

Agitator mixers (motion of blade or paddle due to convection),

mixer- granulators (impeller blade at high speed forces material up before it drops. Overall high shear forces and good mixing. Once mixed, granulation liquid can be added, chopper blade to break down products.

110
Q

What are the practical considerations for mixing?

A
  1. Initially mixing active ingredients with equal amount of diluent. Mix and then add more diluent
  2. Not overflow mixing unit.
111
Q

What is granulation?

A

The process in which homogenous mixtures of primary powder particles form larger, still homogenous particles called granules.

112
Q

What does granulation do?

A

Improve powder flow,

Patient segregation

improve compaction

113
Q

What is wet granulation?

A

The powders are mixed with granulating fluid, and the mass is then forced through a sieve.

114
Q

Mechanism of wet granulation?

A
  1. adheshion and cohesion forces in immobile films
  2. Interfacial forces in mobile liquid films.
  3. Solid bridges (hardening binders or crystallization of dissolved substances).
  4. Attractive forces between particles.
115
Q

What machines can you use for wet granulation?

A

High speed mixer/ granulator - mixing, massing, and granulation all in one piece of equipment.

OR

fluidized - bed granulator - all granulation processes done in one equipment, but requires optimisation.

116
Q

How does dry granulation work?

A

This is where a pressure is applied,

intermediate product is broken,

Sieving.

117
Q

Dry granulation mechanisms?

A
  • use of attractive forces between solid particles
  • solid bridges (by partial melting)

Granules formed via applied pressure, formation of sheet, milling and sieving etc.

118
Q

What form of compaction can dry granulation utilise?

A

Roller compaction.

119
Q
A

MPharm Year 3 (1 decks)

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