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Pharmacy 201 > GI > Flashcards

GI Flashcards

1
Q

what are protecting groups?

A
  • chem. modification functional group
  • chemoselectivity in reaction/synthesis
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2
Q

what are the advantages of protecting groups?

A
  • reaction guided to happen only at desired part
  • prevent unwanted products
  • protect parts from destruction
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3
Q

what is to be considered for choosing PGs?

A
  • inexpensive
  • commercially available
  • introduction = easy & efficient
  • stable & efficient removal
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4
Q

what must PGs do?

A
  • react & removed selectively
  • provide good yield
  • no additional functionality = side reactions
  • no additional stereocentres = uncontrolled stereocentres = major concern pharmaceutical chem.
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5
Q

what are some functional groups commonly protected?

A
  • alcohols
  • carbonyls = aldehydes, ketones & carboxylic acids
  • amines
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6
Q

what are some PGs used for alcohols?

A
  • silyl ethers
  • benzyl ethers
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7
Q

what are some PGs used for aldehydes & ketones?

A
  • acetals
  • ketals
  • thioketals
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8
Q

how is a carboxylic acid protected from further reaction?

A

turn into less reactive ester = allyl esters

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9
Q

why is amine group most susceptible to side reactions & needing protection in synthesis?

A
  • vulnerable acid & basic conditions
  • primary & secondary = prone oxidation
  • N-H bond = metallation on exposure organolithium & Grignard reagents
  • amino group = lone pair = react w/ electrophiles
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10
Q

what are some amine PGs?

A
  • amides
  • carbamates
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11
Q

what are some amide drugs and their uses?

A
  • frovatriptan = anti-migraine
  • brivaracetam = anti-epileptic
  • axitinib = anti-cancer
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12
Q

what are the uses of prodrugs?

A
  • increase solubility & stability
  • improve taste & reduce toxicity
  • modify the time of duration of action
  • deliver drugs to specific site in the body
  • alleviate pain when administered by injection
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13
Q

what are the 2 main classes of prodrugs?

A
  • bioprecursor
  • carrier
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14
Q

what is a bioprecursor prodrug?

A
  • molecule needs modification = active compound
  • rely on metabolic or chemical modification
  • can involve one step/series of steps; like oxidation or reduction
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15
Q

what is a carrier prodrug?

A
  • combi. active drug & carrier species = lipophilic carrier transport drug across membrane
  • link between carrier & active species = group easily metabolised = ester/amide
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16
Q

what are some spec. uses of carrier prodrugs?

A
  • site-specificity = hydrophilic drugs & lipophilic carrier = dihydropyridine
  • minimise SE = aspirin & salicylic acid
  • improve drug stability = avoid 1st pass metabolism
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17
Q

what are some example of drug alliances?

A
  • sentry drugs = clavulanic acid & penicillins
  • localising area of activity = adrenaline & procaine
  • increasing absorption = metoclopramide & analgesics
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18
Q

what are antacids and what are they used for?

A
  • treat heartburn; indigestion & upset stomach
  • neutralise stomach acid
  • Magnesium OH or aluminium OH
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19
Q

what are H2 receptor antagonists and what are they used for?

A
  • acid-peptic disease
  • block action of histamine at H2 receptors of parietal cells in stomach
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20
Q

what are promotility agents and what are they used for?

A
  • treat slow movement of matter thru digestive system = gastroparesis & constipation
  • enhance effect ACh
  • block effect inhibitory neurotransmitter
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21
Q

what are laxatives and what are they used for?

A
  • constipation & limited movement conditions
  • accelerate fecal passage/decrease consistency
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22
Q

what is the mechanism of action of laxatives?

A
  • increase fluid retention by hydrophilic/osmotic mechanisms
  • decrease fluid absorption = manipulation electrolyte transport
  • stimulation propulsive contractions/inhibition of non-propulsive contractions
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23
Q

what are the 2 main types of antidiarrheal drugs?

A
  • antimotility agents = loperamide & codeine
  • anticholinergic agents = atropine & scopolamine)
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24
Q

what are PPIs and how do they work?

A
  • gastric ulcer treatment = omeprazole
  • racemic prodrug = active metabolite in parietal cells
  • inhibits gastric acid secretion by inhibiting H+, K+ -ATPase
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25
Q

how is PPI activated?

A
  • PPI = weak base = pKa 4.0
  • ionised strongly acidic environments
  • cross parietal cell membrane when unionised
  • too polar to cross back because protonation
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26
Q

what are immunosuppressive drugs and what are they used for?

A
  • thiopurines 1st line & methotrexate 2nd line
  • maintain remission if ICS needed after 2 or more exacerbations in 12-months
  • only if aminosalicylates = not effective
  • increase risk non-melanoma skin cancer
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27
Q

what are the 2 main classifications of antispasmodics?

A
  • antimuscarinics
  • smooth muscle relaxants
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28
Q

what are aminosalicylates used for?

A
  • specialist treatment = ulcerative colitis
  • consider mild-moderate proctitis & proctosigmoiditis
  • topically = suppository or enema
  • oral use if no remission in 4 weeks
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29
Q

what is the mechanisms of aminosalicylates?

A
  • activate class nuclear receptors = control inflammation, cell proliferation, apoptosis &
    metabolic function
  • highly express colon epithelial cells
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30
Q

why is oral administration ineffective with aminosalicylates?

A
  • absorbed in small bowel = slow transit time
  • effective conc. don’t make it to distal gut
  • use prodrugs w/ enzyme azoreductase break down in azo cleavage reaction
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31
Q

which vitamins are absorbed where?

A
  • fat soluble = vits A, D, E & K = small intestine
  • water soluble = vits C & B; except B12 = mediated transport
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32
Q

where is vitamin B12 absorbed and why?

A
  • in the ileum because contain cobalt
  • intestinal transporter
  • only complex with intrinsic factor secreted by parietal cells
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33
Q

what does the rate of drug absorption depend on?

A
  • vascularisation of the site of absorption
  • characteristics of formulation/dosage forms
  • lipid solubility of the drug
  • pH of the site of absorption
34
Q

what is film coating made of?

A
  • polymer
  • plasticizer
  • colorant
  • solvant
35
Q

what are the symptoms of GORD?

A
  • bad breath
  • nausea & vomiting
  • acid reflux
  • heartburn
36
Q

what are the causes of GORD?

A
  • coffee
  • stress
  • pregnancy
  • NSAIDs
  • smoking
  • being overweight
37
Q

what is the treatment for GORD?

A
  • 1st line = PPI = omeprazole
  • 2nd line = H2 receptor antagonist = ranitidine
38
Q

what causes peptic ulcers?

A
  • NSAIDs
  • H. pylori
39
Q

what is the treatment for peptic ulcer caused by NSAIDs & H. pylori?

A
  • NSAIDs = stop it & PPI
  • H. pylori = amoxicillin + clarithromycin + PPIs
  • 2nd line = levofloxacin + metronidazole + PPIs
  • pen-allergic = metronidazole + clarithromycin + PPIs
40
Q

what is a side effect of quinolones?

A
  • tendon damage
  • QT-prolongation
41
Q

how do you diagnose for H. pylori?

A
  • carbon 13 urea breath test
  • stool & blood test
42
Q

what causes treatment failure?

A
  • patient compliant
  • prior use antibiotics
  • bacteria resistant
43
Q

what are the GI defenses to infections?

A
  • mucus secretion
  • lysozyme
  • acid
  • gut flora
44
Q

what are the 3 types of symbiotic relationships?

A
  • mutualistic
  • commensalism
  • parasite
45
Q

what are the functions of normal gut flora?

A
  • defense
  • metabolism = fiber fermentation, absorb minerals & sterols
  • structural = enhance epithelial barrier
46
Q

how do bacteria damage host cells?

A
  • toxins
  • enzymes
  • hypersensitivity = trigger exaggerated immune response = damage tissue
47
Q

what are the types of toxins?

A
  • exotoxins
  • endotoxins
  • cytotoxins
  • neurotoxins
  • enterotoxins = interfere GI lining
48
Q

what are the A & B enterotoxins?

A
  • cholera = diarrhoea
  • e.coli = block protein synthesis host cell
  • c. diff = diarrhoea
49
Q

what is the pathogenesis of C. diff?

A
  • flora is disrupted by antibiotics
  • ingest c. diff
  • colonisation in the colon by bacterium
  • A & B released = formation pseudomembrane
50
Q

what is the treatment for C. diff?

A
  • vancomycin
  • give hydration
51
Q

what are the causes of ceoliac disease?

A
  • immune response to gluten
  • thyroid disease
  • diabetes type 1
52
Q

what is the treatment for diverticular disease?

A
  • stop NSAIDs
  • lifestyle
  • laxatives
  • paracetamol
53
Q

what are the 2 causes of diverticular disease?

A
  • NSAIDs
  • smoking
  • obesity
  • genes
54
Q

what is the treatment for diverticulitis?

A
  • antibiotics = co-amoxiclav
    = trimethoprim & metronidazole
55
Q

what are the factors that cause vomiting?

A
  • toxic substances
  • pregnancy
  • palliative care & meds
56
Q

what are the risk factors of ulcerative colitis?

A
  • non smoker = smoking crohns
  • no appendicectomy = appendicectomy crohns
  • NSAIDs
  • family history
57
Q

what is the main complication of UC?

A
  • toxic megacolon = dilation colon
58
Q

what are the severe symptoms of UC that require hospitalisation?

A
  • bloody diarrhoea
  • fever
  • tachycardia
  • hypotension
59
Q

what is the main side effect of aminosalycilates?

A
  • blood dyscrasia = leukopenia
    = bleeding, bruising, sore throat
60
Q

what are the progressive complications of GORD?

A
  • ulcers on oesophagus = bleed & swallowing painful
  • oesophagus becoming scarred and narrowed
  • changes in the cells lining oesophagus
61
Q

what are the progressive complications of peptic ulcers?

A
  • bleeding ulcer site & stomach lining split open
  • ulcer blocking food movement through the digestive
    system = gastric obstruction
62
Q

what are the red flag symptoms of GORD?

A
  • unintentional weight loss
  • stomach pain/difficulty when swallowing
  • persistent vomiting & jaundice
63
Q

how is omeprazole converted to a prodrug?

A
  • omeprazole = sulphonamides
  • sulphonamides bind to cysteine residue on pump
  • disulphide bonds with cysteine
64
Q

how does h. pylori lead to a peptic ulcer?

A
  • h. pylori attack stomach lining w/ urease
  • make stomach acid less acidic = weaken mucosal lining
  • bacteria stick stomach lining & stim. acid secretion
65
Q

what are progressive complications of IBD?

A
  • primary sclerosing cholangitis = bile ducts inside the liver become damaged
  • risk developing bowel cancer
  • poor growth & development = children & young people
66
Q

what are the symptoms for UC & Crohn’s disease?

A
  • diarrhoea = w/ blood, mucus or pus UC
  • abdominal pain
  • empty bowel frequently = UC
  • bloody stool, fatigue & weight loss = Crohn’s
67
Q

what is the treatment for diarrhoea?

A
  • antimotility = loperamide
  • anticholinergic = atropine
68
Q

why is azathioprine a high-risk medication?

A
  • immunosuppressant
  • SE related to SNP in gene for TMPT = degradation and efficacy of AZA
  • can increase types cancer
69
Q

what are some counselling points for azathioprine?

A
  • regular blood tests = before & during treatment
  • more likely get infections
  • use sunscreen = photosensitivity
70
Q

what are the 3 phases of digestion?

A
  • cephalic
  • gastric
  • intestinal
71
Q

what is the role of TPMT in treating IBD?

A
  • direct correlation bw. TPMT gene polymorphisms & toxicity AZA
  • need TPMT genotyping
72
Q

what is cholescytokinin?

A
  • stim. release pancreatic juices from gall bladder
  • inhibit gastric emptying
  • release by I-cells
73
Q

what is gastrin?

A
  • stim. HCL secretion
  • cause growth gastric & colonic mucosa
  • release from G-cells
74
Q

what are the functions of histamine, gastric & somatostatin & secretin in HCl secretion?

A
  • somatostatin & secretin = inhibit
  • histamine & gastric = increase
75
Q

what is a filler?

A
  • increases bulk volume for compression
  • lactose
76
Q

what is a buffer?

A
  • sodium bicarbonate
  • maintains pH
77
Q

what is a disintegrant & superdisintegrants?

A
  • swell up when in contact H2O
  • friction between that and drug particles
  • starch & crospovidone
78
Q

what is a lubricant?

A
  • reduce friction
  • magnesium stearate
79
Q

what is a glidant?

A
  • improve flowability
  • colloidal sillica
80
Q

what is a binder?

A
  • improve cohesiveness
  • starch
81
Q

what is secretin?

A
  • stim. growth of exocrine pancreas
  • inhibit gastric acid secretion
  • secrete bicarbonates to small intestine = neutralise chyme from stomach
  • released S cells = duodenum
82
Q

what is GIP?

A
  • secreted from duodenum cells & proximal jejunum
  • in presence glucose = stim. secretion insulin by endocrine pancreas

Pharmacy 201 (4 decks)

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