Brainscape's Knowledge GenomeTM


Top Flashcards (Certified)
All Flashcards

Pharmacy 201 > GI > Flashcards

GI Flashcards

1
Q

what are protecting groups?

A
  • chem. modification functional group
  • chemoselectivity in reaction/synthesis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

what is to be considered for choosing PGs?

A
  • inexpensive
  • commercially available
  • introduction = easy & efficient
  • stable & efficient removal
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

what are some functional groups commonly protected?

A
  • alcohols
  • carbonyls = aldehydes, ketones & carboxylic acids
  • amines
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

what are some PGs used for alcohols?

A
  • silyl ethers
  • benzyl ethers
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

what are some PGs used for aldehydes & ketones?

A
  • acetals
  • ketals
  • thioketals
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

how is a carboxylic acid protected from further reaction?

A

turn into less reactive ester = allyl esters

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

what are some amine PGs?

A
  • amides
  • carbamates
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

what are some amide drugs and their uses?

A
  • frovatriptan = anti-migraine
  • brivaracetam = anti-epileptic
  • axitinib = anti-cancer
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

what are the 2 main classes of prodrugs?

A
  • bioprecursor
  • carrier
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

what are laxatives and what are they used for?

A
  • constipation & limited movement conditions
  • accelerate fecal passage/decrease consistency
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

what are the 2 main types of antidiarrheal drugs?

A
  • antimotility agents = loperamide & codeine
  • anticholinergic agents = atropine & scopolamine)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
how is PPI activated?
- PPI = weak base = pKa 4.0 - ionised strongly acidic environments - cross parietal cell membrane when unionised - too polar to cross back because protonation
26
what are immunosuppressive drugs and what are they used for?
- 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
27
what are the 2 main classifications of antispasmodics?
- antimuscarinics - smooth muscle relaxants
28
what are aminosalicylates used for?
- specialist treatment = ulcerative colitis - consider mild-moderate proctitis & proctosigmoiditis - topically = suppository or enema - oral use if no remission in 4 weeks
29
what is the mechanisms of aminosalicylates?
- activate class nuclear receptors = control inflammation, cell proliferation, apoptosis & metabolic function - highly express colon epithelial cells
30
why is oral administration ineffective with aminosalicylates?
- 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
31
which vitamins are absorbed where?
- fat soluble = vits A, D, E & K = small intestine - water soluble = vits C & B; except B12 = mediated transport
32
where is vitamin B12 absorbed and why?
- in the ileum because contain cobalt - intestinal transporter - only complex with intrinsic factor secreted by parietal cells
33
what does the rate of drug absorption depend on?
- vascularisation of the site of absorption - characteristics of formulation/dosage forms - lipid solubility of the drug - pH of the site of absorption
34
what is film coating made of?
- polymer - plasticizer - colorant - solvant
35
what are the symptoms of GORD?
- bad breath - nausea & vomiting - acid reflux - heartburn
36
what are the causes of GORD?
- coffee - stress - pregnancy - NSAIDs - smoking - being overweight
37
what is the treatment for GORD?
- 1st line = PPI = omeprazole - 2nd line = H2 receptor antagonist = ranitidine
38
what causes peptic ulcers?
- NSAIDs - H. pylori
39
what is the treatment for peptic ulcer caused by NSAIDs & H. pylori?
- NSAIDs = stop it & PPI - H. pylori = amoxicillin + clarithromycin + PPIs - 2nd line = levofloxacin + metronidazole + PPIs - pen-allergic = metronidazole + clarithromycin + PPIs
40
what is a side effect of quinolones?
- tendon damage - QT-prolongation
41
how do you diagnose for H. pylori?
- carbon 13 urea breath test - stool & blood test
42
what causes treatment failure?
- patient compliant - prior use antibiotics - bacteria resistant
43
what are the GI defenses to infections?
- mucus secretion - lysozyme - acid - gut flora
44
what are the 3 types of symbiotic relationships?
- mutualistic - commensalism - parasite
45
what are the functions of normal gut flora?
- defense - metabolism = fiber fermentation, absorb minerals & sterols - structural = enhance epithelial barrier
46
how do bacteria damage host cells?
- toxins - enzymes - hypersensitivity = trigger exaggerated immune response = damage tissue
47
what are the types of toxins?
- exotoxins - endotoxins - cytotoxins - neurotoxins - enterotoxins = interfere GI lining
48
what are the A & B enterotoxins?
- cholera = diarrhoea - e.coli = block protein synthesis host cell - c. diff = diarrhoea
49
what is the pathogenesis of C. diff?
- flora is disrupted by antibiotics - ingest c. diff - colonisation in the colon by bacterium - A & B released = formation pseudomembrane
50
what is the treatment for C. diff?
- vancomycin - give hydration
51
what are the causes of ceoliac disease?
- immune response to gluten - thyroid disease - diabetes type 1
52
what is the treatment for diverticular disease?
- stop NSAIDs - lifestyle - laxatives - paracetamol
53
what are the 2 causes of diverticular disease?
- NSAIDs - smoking - obesity - genes
54
what is the treatment for diverticulitis?
- antibiotics = co-amoxiclav = trimethoprim & metronidazole
55
what are the factors that cause vomiting?
- toxic substances - pregnancy - palliative care & meds
56
what are the risk factors of ulcerative colitis?
- non smoker = smoking crohns - no appendicectomy = appendicectomy crohns - NSAIDs - family history
57
what is the main complication of UC?
- toxic megacolon = dilation colon
58
what are the severe symptoms of UC that require hospitalisation?
- bloody diarrhoea - fever - tachycardia - hypotension
59
what is the main side effect of aminosalycilates?
- blood dyscrasia = leukopenia = bleeding, bruising, sore throat
60
what are the progressive complications of GORD?
- ulcers on oesophagus = bleed & swallowing painful - oesophagus becoming scarred and narrowed - changes in the cells lining oesophagus
61
what are the progressive complications of peptic ulcers?
- bleeding ulcer site & stomach lining split open - ulcer blocking food movement through the digestive system = gastric obstruction
62
what are the red flag symptoms of GORD?
- unintentional weight loss - stomach pain/difficulty when swallowing - persistent vomiting & jaundice
63
how is omeprazole converted to a prodrug?
- omeprazole = sulphonamides - sulphonamides bind to cysteine residue on pump - disulphide bonds with cysteine
64
how does h. pylori lead to a peptic ulcer?
- h. pylori attack stomach lining w/ urease - make stomach acid less acidic = weaken mucosal lining - bacteria stick stomach lining & stim. acid secretion
65
what are progressive complications of IBD?
- primary sclerosing cholangitis = bile ducts inside the liver become damaged - risk developing bowel cancer - poor growth & development = children & young people
66
what are the symptoms for UC & Crohn's disease?
- diarrhoea = w/ blood, mucus or pus UC - abdominal pain - empty bowel frequently = UC - bloody stool, fatigue & weight loss = Crohn's
67
what is the treatment for diarrhoea?
- antimotility = loperamide - anticholinergic = atropine
68
why is azathioprine a high-risk medication?
- immunosuppressant - SE related to SNP in gene for TMPT = degradation and efficacy of AZA - can increase types cancer
69
what are some counselling points for azathioprine?
- regular blood tests = before & during treatment - more likely get infections - use sunscreen = photosensitivity
70
what are the 3 phases of digestion?
- cephalic - gastric - intestinal
71
what is the role of TPMT in treating IBD?
- direct correlation bw. TPMT gene polymorphisms & toxicity AZA - need TPMT genotyping
72
what is cholescytokinin?
- stim. release pancreatic juices from gall bladder - inhibit gastric emptying - release by I-cells
73
what is gastrin?
- stim. HCL secretion - cause growth gastric & colonic mucosa - release from G-cells
74
what are the functions of histamine, gastric & somatostatin & secretin in HCl secretion?
- somatostatin & secretin = inhibit - histamine & gastric = increase
75
what is a filler?
- increases bulk volume for compression - lactose
76
what is a buffer?
- sodium bicarbonate - maintains pH
77
what is a disintegrant & superdisintegrants?
- swell up when in contact H2O - friction between that and drug particles - starch & crospovidone
78
what is a lubricant?
- reduce friction - magnesium stearate
79
what is a glidant?
- improve flowability - colloidal sillica
80
what is a binder?
- improve cohesiveness - starch
81
what is secretin?
- stim. growth of exocrine pancreas - inhibit gastric acid secretion - secrete bicarbonates to small intestine = neutralise chyme from stomach - released S cells = duodenum
82
what is GIP?
- secreted from duodenum cells & proximal jejunum - in presence glucose = stim. secretion insulin by endocrine pancreas

Pharmacy 201 (4 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2025 Bold Learning Solutions. Terms and Conditions