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Medicine Sem 4 > Drugs > Flashcards

Drugs Flashcards

1
Q

what is co-amoxiclav?

A

Amoxicillin (β-lactam antibiotic)
+
clavulanic acid (β-lactamase inhibitor)
(it can overcome antibiotic resistance in bacteria that secrete β-lactamase, which otherwise inactivates most penicillins)

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2
Q

what is the mechanism of action for co-amoxiclav?

A
  • Amoxicillin inhibits formation of peptidoglycan cross links in bacterial cell wall.
  • Clavulanic acid prevents the survival of β-lactamase enzyme which is produced by the bacteria.
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3
Q

what is botulinum toxin used for?

A

achalasia

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4
Q

how does botulinum work?

A
  • Inhibits the calcium dependent release of ACh from the presynaptic neurones.
  • This relaxes the Lower Oesophgeal Sphincter.
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5
Q

what are antacids? what used for? contraindications? side effects?

A
  • magnesium/aluminium salts
  • dyspepsia (indigestion)
  • Contraindicated for patients with renal insufficiency.
  • Magnesium = laxative
  • Aluminium = constipation
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6
Q

what is the mechanism of action for antacids?

A

Direct neutralisation of gastric acid inside the duodenum.

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7
Q

what are examples of PPIs?

A
  • Omeprazole/ Lansoprazole, Pantoprazole, Rabeprazole sodium
  • Esomeprazole (Nexium) - second generation PPI (S-isomer only)
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8
Q

what are PPIs used for?

A
  • Gastritis
  • Gastric Ulcers
  • Peptic Ulcers
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9
Q

what do PPIs do?

A

Block the action of the H+,K+ -ATPase pump permanently in the gastric parietal cell by binding to its sulphydryl group.

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10
Q

what are examples of histamine-2 (H2) receptor antagonist?

A

Ranitidine/ Cimetidine

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11
Q

what are H2 receptor antagonists used to treat?

A
  • Gastritis
  • Gastric Ulcers
  • Peptic Ulcers
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12
Q

what is H. pylori triple therapy?

- standard and modern

A

Standard Triple Therapy (2 antibiotics +PPI)
e.g “CAP” – Clarithromycin, Amoxicillin, PPI (e,g, Omeprazole)
Metronidazole can be used instead of Amoxicillin.

Modern Bismuth-Based Regimens (2 antibiotics + Bismuth compound)
e.g. “CAB” - Clarithromycin, Amoxicillin, Ranitidine Bismuth Citrate
Metronidazole can be used instead of Amoxicillin.

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13
Q

what is mechanism of action of omeprazole? what activated by? what is MAO of clarithromycin? what is MAO of ranitidine bismuth citrate?

A

Omeprazole - irreversible H+/K+ proton pump inhibitor (PPI). Activated by acidity, specific to canaliculi of parietal cells.

Clarithromycin – inhibits translation during bacterial DNA synthesis.

The H2 antagonist ranitidine combined with a bismuth compound both coat the gastric mucosa and help reduce HCl secretion.

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14
Q

what is used for patients allergic to penicillin?

A

metronidazole

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15
Q

what is pancreatin? what used for? other name? what enhanced by?

A
  • Mixture of enzymes produced by exocrine pancreas e.g. amylase, lipase and trypsin.
  • Chronic pancreatitis
  • Cystic fibrosis
  • Creon (pancrelipase)
  • PPI
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16
Q

what is fluorouracil (5-FU)? what used for?

A
  • Pyrimidine analog
  • Thymidylate synthase inhibitor
  • Anti-metabolite
  • CRC
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17
Q

what is the MAO of 5-FU?

A
  • Prevents pyrimidine from incorporating into DNA during ‘S’ phase.
  • Drug is converted to a ‘fraudulent’ nucleotide called FDUMP and inhibits thymidylate synthase preventing the conversion of 2’-deoxyuridylate (DUMP) to 2’-deoxythymidylate (DTMP) resulting in ↓DNA synthesis = cell death.
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18
Q

what is folinic acid also caused? what molecule?

A

leucovorin

- calcium/sodium folinate

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19
Q

what is folinic acid used for?

A
  • Enhance effect of 5FU (stabilise bond of 5-fdUMP to thymidylate synthetase)
  • Counteract cytotoxic drug methotrexate (which is a folic acid antagonist)
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20
Q

what is the MAO of folinic acid?

A
  • ↑Tetrahydrofolate for 5FU to bind with and ↑ stability of 5FU-thymidylate synthase complex = ↑cytotoxicity.
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21
Q

what is PEG-interferon alpha2A?

A

antiviral

  • Chronic Hep B
  • Chronic Hep C
  • Acute Hep C (works in 85% of cases)
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22
Q

what is MAO of PEG-interferon alpha2A? how administered? why PEG?

A
  • Binds to cell surface receptors on virally infected cells and interferes with the viral mRNA translation.
  • Proteins that interfere with viral replication and activate other immune cells.
  • Given as injection.
  • Can be pegylated to ↑ half-life.
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23
Q

what is another old drug used for chronic hep C?

A

ribavirin

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24
Q

what is the MAO of ribavirin?

A
  • Inhibits viral RNA dependent RNA polymerase enzyme, therefore inhibiting viral replication.
  • RNA mutagen, giving a defective HCV.
  • Given as an oral tablet.
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25
Q

what are the different types of insulin? how long does each last?

A 
6	Insulin	Rapid-Acting (lispro) 
Short-Acting (regular) 
Intermediate-Acting (NPH)
Long-Acting (glargine/detemir)
Pre-mixed (short + intermediate)

RA – 3-5 hrs (covers meal with injection)
SA – 5-8 hrs (covers meals within 30-60 minutes)
IA – 18-24 hrs (half a day/full night, used with RA/SA)
LA – up to 24 hrs (full day with RA/SA)
Pre-mixed – taken 2/3 times a day before meals.

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26
Q

what type of drug is metformin what for? what does it do?

A
  • Biguanide
  • Insulin sensitisers
  • First line DRUG for Type II diabetes.
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27
Q

what is the MAO of metformin?

A
  • Activates AMP kinase which is involved in GLUT4 metabolism.
  • ↓gluconeogenesis in liver
  • ↑ peripheral glucose uptake (GLUT4)
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28
Q

what is example of sulfonylureas? what do they do?

A
  • Gliclazide (X-amide/X-azide)

- (increased insulin secretion)

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29
Q

what is the MAO of Gliclazide?

A
  • Activates sulfonylurea receptors which inhibits ATP-sensitive K+ channels -> ↑intracellular K+ -> depolarisation and Ca2+ influx -> insulin release
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30
Q

what are examples of thiazolidinediones? what also called? what are they?

A
  • (Rosiglitazone,) pioglitazone etc.
  • Glitazones
  • (insulin sensitisers) = increase sensitivity of cells to insulin
  • PPARgamma agonists
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31
Q

what is the MAO of thiazolidinediones? side effects?

A
  • Interaction with peroxisome proliferator-activated receptor-gamma (PPAR-gamma), mainly found on adipose cells. This increases adipogenesis and glucose uptake.
  • May lower free fatty acids promoting glucose uptake by muscles.
  • Lower blood glucose but do not return to normal.
  • Weight gain of 5-6kg
  • Oedema
  • Hypoglycaemia
  • Redistribution of fat from central adiposity to peripherals.
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32
Q

what are DDP-4 inhibitors used in? what example?

A

type II diabetes
- Sitagliptin
(X-gliptin)

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33
Q

what is the MAO of DDP-4 inhibitors?

A

The DPP-4 enzyme degrades incretins such as GLP-1, thus reducing insulin secretion. Hence DDP-4 inhibitors increase the action of incretins, thereby increasing insulin secretion and reducing glucagon secretion.

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34
Q

what are two of the most important incretins?

A

glucagon-like peptide-1 (GLP-1) and glucose-dependent insulinotropic polypeptide (GIP).

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35
Q

what is X-tide an example of?

A

GLP-1 Receptor Agonists

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36
Q

what do GLP-1 receptor agonists do?

A

Acts as a functional analog of GLP-1, thus increasing insulin and reducing glucagon secretion.

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37
Q

what are SGLT2 inhibitors used for? what is an example?

A
  • type II diabetes and diabetic kidney disease

- X-gliflozin

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38
Q

what is the MAO of SGLT2?

A

Reduction of glucose reabsorption in the kidney, reducing blood glucose levels.
Inhibition of SGLT2 (Sodium/Glucose cotransporter in the proximal tubule), preventing glucose reabsorption, allowing glucose to be passed out in the urine

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39
Q

what are alpha-glucosidase inhibitors? what used for?

A
  • Miglitol, Acarbose, Voglibose, Deoxynojirimycin

- type II diabetes

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40
Q

what is MAO of alpha-glucosidase inhibitors? side effects?

A

Prevent digestion of carbohydrates into monosaccharides, preventing food from increasing blood glucose levels.
Competitive inhibitor of alpha-glucosidase enzymes found in the small intestinal brush border, slowing carbohydrate digestion.

  • Flatulence and diarrhoea (bacterial digestion of carbohydrates)
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41
Q

what is an example of an osmotic diuretic? what indication for use?

A

mannitol

  • ↑ICP/cerebral oedema
  • ↑intraocular pressure
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42
Q

what is the MAO of osmotic diuretics?

A
  • Act on parts of nephron freely permeable to water e.g. proximal tubule, descending limb and collecting duct.
  • Inert substance which ↑osmolarity of the filtrate and reduces passive reabsorption of water.
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43
Q

what are examples of loop diuretics? what indication for use?

A

Furosemide, bumetanide

  • Oedema
  • Resistant hypertension
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44
Q

what is the MAO of loop diuretics? what is to note about these?

A
  • Act on thick ascending loop of Henle.
  • Inhibit the Na+/Cl-/K+ transporter by attaching to the Cl- binding site.
  • These ions can therefore not be reabsorbed, as a result a hypotonic renal medulla is not formed and water remains in collecting duct.
  • Mg2+ and Ca2+ reabsorption is dependent upon the reabsorption of the other ions these are also lost in urine.
  • ↑ potassium intake should be encouraged.
  • Most powerful diuretic.
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45
Q

what example of thiazide diuretic? what indication for use?

A

Bendroflumethiazide

  • Mild/moderate heart failure.
  • Hypertension
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46
Q

what is the MAO of thiazide diuretics?

A
  • Act on distal convoluted tubule.
  • Block Na+/Cl- symporter by attaching to Cl- site, hence preventing their reabsorption.
  • Also ↑ reabsorption of Ca2+ by increasing activity of Na+/Ca2+ antiport.
  • K+ and H+ are lost due to activation of RAAS.
  • ↑ potassium intake should be encouraged.
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47
Q

what are examples of K+ sparing? when used?

A
  • Triamterene, amiloride
  • oedema
  • heart failure
  • adjunct with loop/thiazide
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48
Q

what is the MAO of K+ sparing?

A
  • Act on collecting ducts and tubules.

- Inhibit Na+ reabsorption by blocking lumenal channels and ↓K+ excretion.

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49
Q

what are examples of aldosterone antagonists? what are these also called? what used for? what do they act on?

A
  • spironolactone, eplerenone
    = potassium-sparing diuretics (increase risk of hyperkalaemia)
  • on principal and alpha-intercalated cells
  • oedema/ascites
  • heart failure
  • primary hyperaldosteronism
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50
Q

what are finasteride and dutasteride examples of? what used for?

A

5α-reductase inhibitor
(finasteride is selective for type II, dutasteride for I and II)
= anti-androgens

  • BPH
  • Male-pattern baldness
51
Q

what is MAO of 5alpha-reductase inhibitors? side effects? effect on PSA?

A
  • block enzyme 5alpha-reductase type 2
  • prevents metabolism of testosterone into dihydrotestosterone which is indicated in causing prostate enlargement.
  • decrease growth of stromal and epithelial prostate cells
  • increase apoptosis
  • decrease PSA (to do with hormone stuff)
  • maintain improvement of symptoms
  • Impotence
  • ↓libido
  • Ejaculation disorders
52
Q

what are alpha-1 blockers also? what are alpha-1 blocker examples? what for? effect on PSA?

A
  • alpha1-andrenergic antagonists
  • Tamsulosin, alfuzosin, doxazosin, terozasin (Tamsulosin selective for alpha-1a subtype (and alpha-1b?) specific to bladder neck/prostate/urethra)
  • BPH
  • Kidney stones
  • no effect on PSA
53
Q

what is the MAO of tamsulosin?

A
  • Inhibit the alpha 1/1a receptors resulting in relaxation muscles of bladder neck = ↑ urinary flow and ↓pain.
54
Q

what are examples of thyroid hormone inhibitors? what used for?

A

Carbimzaole/ Methimazole/ Propylthyiouracil (PTU) = THIOUREYLENES

  • Pro-drug for methimazole
  • Thyroid hormone inhibitor
  • Mild immunosuppressant
  • for hyperthyroidism
55
Q

what are the MAO of methimazole and PTU?

A
  • Prevents thyroid peroxidase from iodinating and coupling tyrosine, therefore reducing hormone production.
  • Partly blocks coupling of two iodinated tyrosines
  • PTU: reduces the conversion of T4 to T3 in the peripheral tissue.

Quickly reduces hormone production however takes 10-20 days for clinical benefit due to high half lives of existing T4/T3. Hence β-blocker can be used for rapid symptom control.

56
Q

what other medications used for hyperthyroidism?

A
  • thyiocyanate ions
  • iodide ions
  • radioiodine I-131 (first-line treatment for hyperthyroidism)
57
Q

what is the MAO of thyiocyanate ions?

A
  • Reduces iodide trapping by competitive inhibition of the Na+/I- symporter
58
Q

what is the MAO of iodide ions?

A
  • Given in high concentrations
  • Reduces thyroid function.
  • with KI
59
Q

what is the MAO of radioiodine I131?

A
  • Absorbed by thyroid.
  • Emits beta and gamma radiation.
  • Beta radiation kills thyroid follicle cells.
60
Q

what is propranolol? what used for? MAO? what is to note?

A
  • Non-selective β-blocker
  • treat side effects of hyperthyroidism (used while thioureylenes or radioiodine takes effect)
  • Hypertension
  • Anxiety
  • Blocks adrenaline and noradrenaline at β1 and β2 adrenergic receptors.
  • Crosses BBB therefore may have psychological effects e.g. vivid dreams, psychoses
61
Q

what used to treat hypothyroidism? what is it?

A
  • Levothyroxine

- Synthetic hormone to replaces deficient T4 .

62
Q

what are examples of antibiotics?

A
  • tetracycline
  • clarithromycin
  • amoxicillin
  • metronidazole
  • fluoroquinolone
  • sulphonamides
63
Q

what is misoprostol?

A

prostaglandin analogue

64
Q

what are examples of antacids?

A
  • ranitidine bismuth citrate
  • bismuth citrate
  • bismuth subsalicylate
  • sodium carbonate
  • calcium carbonate
65
Q

what is the weight-loss drug?

A

orlistat - blocks gastric and pancreatic lipase

66
Q

what are P-CABs?

A

potassium competitive acid blockers

67
Q

what do bismuth compounds and P-CABs do?

A
  • Potassium competitive acid blockers (P-CABs) in development (& use in the Far East)
    =faster onset and longer lasting but more reversible
  • It’s all to do with pH!
  • H. pylori tolerates very acid pH but only grows/divides at less acid pH (>5.5)
  • Clarithromycin, amoxicillin & tetracycline all work best in dividing cells
  • PPIs reduce acidity, enhancing antibiotic action (new P-CABs may give a longer lasting high pH)
  • Bismuth blocks H+ influx into H. pylori so enhance antibiotic action even as the effects of PPIs are diminishing with time
68
Q

what is ezetimibe?

A
  • inhibits endocytosis of cholesterol

- lowers cholesterol levels

69
Q

what is levamisole?

A

used with fluorouracil

70
Q

what is methotrexate?

A

folic acid antagonist (chemotherapy agent)

71
Q

what is avastin (bevacizumab)?

A

VEGF-inhibitor - treat angiogenesis

72
Q

what is pembrolizumab? what does it do?

A
  • antibody used in cancer immunotherapy

- blocks PD-1

73
Q

what are 5-HT3 antagonists?

A

anti-emetics (chemotherapy)

74
Q

what is naloxone?

A

opioid receptor antagonist -> increase motility and secretion

75
Q

what is an opioid receptor agonist? what used for?

A

imodium/loperamide = decrease frequency of diarrhoea

76
Q

what is lomotil? what used for?

A
  • used to treat acute and chronic diarrhoea
  • diphenoxylate (opioid) and atropine (muscarinic agonist)
  • decrease peristalsis, decrease gastric emptying
77
Q

what are enkephalinase inhibitors?

A

substances that enhacne action of enkephalins

78
Q

what is oxaliplatin? what used with? how work?

A

chemotherapy drug

  • often used with 5-FU and folinic acid
  • interferes with development of DNA
79
Q

what class of antivirals used for hep B? what also used for?

A

nucleoside (analogue) reverse transcriptase inhibitors (NRTIs)
- also for used for HIV

80
Q

what are examples of NRTIs?

A
  • lamivudine (3TC)
  • adefovir
  • entecavir
  • tenofovir
81
Q

what is the new treatment for hep C?

A

DAAs (direct-acting antivirals) (four classes)

82
Q

what is a commonly used DAA? how does it work?

A

sofosbuvir = nucleoside & nucleotide NS5B polymerase inhibitor
They directly target the hep C virus to stop it from making copies of itself in the liver. They attach themselves onto the genetic information, called RNA, to block the virus from multiplying.

83
Q

what is another class of DAA?

A 
NS3/4A Protease Inhibitors (PIs)
- Telaprevir 
- Boceprevir 
(these were first DAA that were approved) 
- Simeprevir
84
Q

what is old treatment for hep C?

A
  • PEG-INF
  • ribavirin = not used with PEG-INF anymore (still used with Sofosbuvir)
    = ribavirin = antiviral nucleoside analogue
  • Ribavirin is phosphorylated to ribavirin triphosphate and is a substrate for many viral RNA-directed RNA polymerases (RdRps)
85
Q

what does interferon do in hep B?

A

get rid of cccDNA

86
Q

what is the treatment for hep D?

A
  • PEG-INF > 48 weeks

- not antiviral drugs for this

87
Q

what is viagra?

A

phosphodiesterase 5 inhibitor (PDE5i) -> relax blood vessels

88
Q

what used to treat an overactive bladder?

A

anticholinergic

89
Q

what used to treat polycystic kidney disease?

A

vasopressin receptor antagonist

90
Q

what is ADT treatment? what included in it?

A

androgen deprivation therapy

  • GnRH agonists (e.g. Leuprolide and Goserelin) - pre-treatment with anti-androgen
  • GnRH antagonist (e.g. Degarelix) - initial treatment then transfer to agonist
91
Q

what is used for metastatic prostate cancer?

A
  • chemotherapy -> docetaxel, cabazitaxel

- hormone therapy -> abiraterone

92
Q

what does abiraterone do?

A

CYP17 inhibitor

93
Q

what is used to treat bone cancer?

A

radium 223

94
Q

what are the anti-thyroid substances?

A
  • thiocyanate ions
  • thioureylenes
  • iodide
  • radioiodine I-131
95
Q

what is the treatment for hypoadrenalism?

A

(Addison’s disease)

  • hydrocortisone
  • fludrocortisone (mineralocorticoid replacement)
96
Q

what medication used for Cushing’s syndrome?

A

cortisol production inhibitors:

  • metyrapone
  • ketoconazole
  • mitotane
97
Q

what used to treat phaeochromocytoma?

A
  • alpha-blocker (phenoxybenzoamine)

- beta-blocker (propranolol)

98
Q

what used to treat diabetic nephropathy?

A

blood pressure

  • ACE inhibitors
  • Losartan - angiotensin-2 receptor blockers
  • Aliskeren - renin-inhibitors
99
Q

what is salicylate? what effect?

A

aspirin - reverse insulin resistance

100
Q

what is the treatment intensification for hypertension in diabetes?

A

ACD
A = ACE inhibitors
C = calcium channel blockers
D = diuretics

101
Q

what’s en example of an ACE inhibitor?

A

ramipril

102
Q

examples of NSAIDs

A

apirin, diclofenac, ibuprofen

103
Q

what are the different insulin secretagogues?

A
  • sulfonylureas
  • meglitidines
  • DPP4 inhibitors
  • GLP-1 receptor agonists
104
Q

what are the insulin sensitisers?

A
  • thiazolidinediones

- biguanides

105
Q

what are the other drugs for diabetes?

A
  • insulin
  • alpha-glucosidase inhibitors
  • SGLT2i
106
Q

what do biguanides do?

A
  • decrease hepatic glucose production

- increase muscle cell sensitivity to insulin

107
Q

benefits side effects of biguanides?

A
  • no hypoglycaemia
  • no weight gain
  • vitamin B12 deficiency
108
Q

what do sulfonylureas do?

A

increase insulin secretion

109
Q

what are side effects of sulphonylureas?

A
  • hypoglycaemia

- weight gain

110
Q

what do thiazolidinediones do?

A

increase insulin sensitivity

111
Q

what are advantages and side effects of thiazolidinediones?

A
  • no hypoglycaemia

- weight gain

112
Q

what do DPP-4 inhibitors do? example

A
  • increase insulin secretion (glucose-dependent)
  • decrease glucagon secretion (glucose dependent)
  • gliclazide
113
Q

what is advantage of DPP-4 inhibitors?

A
  • no hypoglycaemia
114
Q

what do GLP-1 receptor agonists do? example?

A
  • increase insulin secretion (glucose-dependent)
  • decrease glucagon secretion (glucose dependent)
  • slows gastric emptying
  • increase satiety
  • exenatide, lixisenatide, liraglutide)
115
Q

what are advantages of GLP-1 receptor agonists?

A
  • no hypoglycaemia

- weight reduction

116
Q

what does insulin do?

A
  • increase glucose disposal

- decrease hepatic glucose production

117
Q

what are side effects of insulin?

A
  • hypoglycaemia

- weight gain

118
Q

what do meglitinides (glinides) do?

A

increase insulin secretion

119
Q

what are side effects of meglitinides?

A
  • hypoglycaemia
  • weight gain
  • not very population – because very short acting drugs – they act similar to sulfonylureas
120
Q

what do alfa-glucosidases inhibitors do?

A
  • slow intestinal carbohydrate digestion/absorption

- blocks the amylases and carbohydase enzymes

121
Q

advantages and side effects of alfa-glucosidase inhibitors?

A
  • no hypoglycaemia

- GI side effects = not very popular

122
Q

SGLT2i what do they do?

A
  • increase glucose excretion from kidneys

- lower threshold for glucose urine secretion

123
Q

advantages and side effects of SGLT2i?

A
  • insulin independent mechanism
  • diuretic effect
  • thrush

Medicine Sem 4 (23 decks)

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