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Drugs List Flashcards

Welcome to my drugs list deck. They should contain the MOA + usage & side effects that we need to know for every drug on the list. Some cards have ways to remember the drugs/picture prompts... also if there are any mistakes/any could be refined or made better please let me know and ill edit! (96 cards)

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1
Q

Antacids

A
  • Aluminium Hydroxide and Magnesium Hydroxide - Maalox
  • Calcium Carbonate and Magnesium Carbonate - Rennie

Gastric Acid Neutralisation

Uses: Reflux oesophagitis - OTC & prescribed

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2
Q

Antacids + Alginates

A
  • Sodium Alginate with Sodium Bicarbonate, Calcium Carbonate (Gaviscon)

Anionic polysaccharides - form a viscous gel raft upon binding with water, this floats to the top of the stomach reducing symptoms. Also contains antacid to neutralise excess acid

Uses: Reflux oesophagitis - OTC + prescribed

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3
Q

H2 Receptor Antagonists

A
  • Cimetidine
  • Ranitidine

Competitively inhibits gastric H2 receptors to decrease acid secretion.

OTC

Cimetidine inhibits many cytochrome P450 enzymes

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4
Q

Proton Pump Inhibitors

A
  • Omeprazole
  • Lansoprazole

Blockade of parietal cell proton transporters:

Irreversibly inhibits H+/K+-ATPase pump, terminal step in acid secretion pathway. Decreases basal and stimulated acid production.

Very specific - inative at neutral pH thus accumulate in secretory canaliculi or parietal cells and are activated in acidic environment.

Prescribed drug of choice for reflux oesophagitiss.

More effective than H2 antagonists.

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5
Q

Bulk Laxatives

A
  • Methylcellulose
  • Isphagula Husk

Polysaccharide polymers not broken down by normal digestion so retain water in the GI lumen, softening and increasing bulk load and promoting increased motility.

Act over 1-3 days.

First line for constipation & IBS

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6
Q

Stimulant Purgatives (2)

A
  • Bisacodyl

Stimulates rectal mucosa resulting in massmovements - defaecation in 15-30 mins

  • Senna

​Passes unchanges into colon where bacterial action causes direct effect on myenteric plexus to increase intestinal motility

Chronic use (>3/week for >year) can cause cathartic colon (laxative dependency + req. higher doses) can lead to serious consequences

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7
Q

Faecal Softeners

A
  • Docusate
  • Arachis oil

Anionic surfactants. Lower surface tension allowing water or fats to enter the stool, softening faeces. Stimulates water & electrolyte secretion into the intestinal lumen

Used for constipation and fissures/piles

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8
Q

Osmotic Laxatives (3)

A
  • Saline purgatives - Magnesium sulphate, Magnesium Hydroxide -

Uses: Bowel prep before procedure. Potent, rapid action (1-2hrs)

  • Macrogol Uses: Faecal impaction in children, LT management of chronic constipation

Poorly absorbed solutes that maintain increased fluid volume in GI tract by osmosis, accelerating small intestine transit - large fluid volume in colon leads to distension and purgation.

  • Lactulose

Semi-synthetic disaccharide converted to poorly absorbed monocaccharides by colonic bacteria - Fermentation ields acetic acid which acts as an osmotic laxative

Acts 1-3 days

SEs: Abdo cramp, gas, flatulence

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9
Q

Oral Rehydration Therapy

A
  • Isotonic/hypotonic solution of glucose and NaCl

​Exploits ability of glucose to enhance absorption of Na+ and so water.

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10
Q

Opioid Anti-Motility Agents

A
  • Codeine
  • Loperamide

Agonist on u-opioid receptors in the myenteric plexus. Increases tone and rhythmic contractions of the colon, but diminishes propulsive activity. Pyloric, illocaecal and anal sphincters are contracted

SEs: Chronic use = constipation. Abdo cramps, dizziness

Uses: Acute uncomplicated diarrhoea in adults

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11
Q

Carbonic Anhydrase Inhibitor

A
  • Acetazolomide

Inhibits carbonic anhydrase in PCT to stop the reapsorption of Na+ so increasing the volume of urine (osmotic balance). Weak diuretic action as only a small amount of sodium is reabsorbed this way

Also prevents H+ secretion (and HCO3- reabsorption) so can lead to metabolic acidosis

Uses: Reduce intraocular pressure in glaucoma (aqueous humour prod. req. HCO3- secretion)

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12
Q

Loop Diuretics

A
  • Furosemide

​Powerful diuretics. Act on thick ascending limb og LOH. Inhibits the Na+K+2CL- co-transporter (competes with Cl- binding). Decreased NaCl reabsorption in thick ascending loop causes decreased osmotic concentration in the medulla thus decreased ADH mediated water absorption.

Binds to plasma proteins so not filtered but secreted directly into the PCT thus effective in renal impairment.

SEs: Hypovolaemia + hypotension, hypokalaemia

Uses: peripheral oedema (chronic heart failure), acute pumonary oedema.

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13
Q

Osmotic diuretic

A
  • Mannitol

Increases the osmolarity of glomerular filtrate thus prevents water reabsorption. Acts mostly where water reabsorption occurs - PCT + descending limb of LOH)

Uses: reducing intracranial pressure + reducing intraocular pressure (glaucoma)

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14
Q

Thiazide Diuretics

A
  • Bendroflumethiazide
  • Indapamide
  • Hydrochlorothiazide
  • Chlortalidone

(BICH)

Weak/moderate diuresis. Acts on the DCT. Inhibits Na+/Cl- co-transporter (competes with Cl- binding). Slower acting bur longer lasting than loop diuretics.

SEs: Hyponatraemia/Hypokalaemia, increased plasma uric acid (gout), ED, Hyperglycaemia

Uses: Peripheral oedema (chronic heart failure), hypertension

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15
Q

Potassium Sparing Diuretics

Subclass: Aldosterone Antagonists

A
  • Spironolactone
  • Eplerenone

Weak diuretic alone. Aldosterone antagoniss, binds to and blocks mineralocorticoid (MR) receptor. Prevents synthesis of ENaC and Na+/K+ATPase activity which stops Na+ reabsorption (and water by osmosis) and reduces K+ secretion into the lumen to K+ is retained.

SEs: Hyperkalaemia, gynaecomastia

Uses: Chronic HF, Periph oedema +ascites caused by cirrhosis. Can be used in comination to prevent K+ loss from use of loop/thiazide diuretics.

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16
Q

Potassium Sparing Diuretics

Subclass: ENaC Antagonists

A
  • Amiloride

Weak diuretic alone. ENaC antagonist - blocks ENaC, competes for Na+ binding site thus decreasing luminal permeability to Na+. This causes reduced Potassium secretion into the lumen to potassium is retained

SEs: Hyperkalaemia,

Uses: Chronic heart failure; Peripheral oedema and ascites caused by cirrhosis. Can be used in combination to prevent K+ loss from use of loop/thiazide diuretics

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17
Q

Renin Inhibitor

A
  • Aliskiren

​Inhibits the action of Renin thus stopping formation of Angiotensin I so the RAAS system cannot be used to increas BP

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18
Q

Angiotensin-converting Enzyme (ACE) Inhibitor

A
  • Ramipril

Binds to ACE stopping the converstion of Ang I to Ang II so the RAAS system cannot increase BP

SEs: Dry cough (bradykinin build up as not inactivated by ACE), hypotension.

Caution in renal failure - ACE normally constricts efferent arterioles thus ACEI can lead to decreased GFR

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19
Q

Angiotensin-II receptor antagonists

A
  • Losartan

Binds to the angiotensin-II receptor, preventing it from working. RAAS cannot increase BP

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20
Q

Aldosterone Antagonist

A
  • Spironolactone

​Antagonist of aldosterone by blocking the mineralocorticoid receptor. Means RAAS cannot increase BP

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21
Q

Thyroid Hormones

A
  • Levothyroxine
  • Liothyonine

Mimics thyroid hormone by binding to incracellular alpha & beta thryoid receptors

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22
Q

Alpha-adrenergic blocker

(for urinary retention)

A
  • Doxazosin

Blocks alpha adrenoreceptors of the sympathetic autonomic nervous system, this relaxes smooth muscles around the bladder (internal and external urinary sphincters) allowing micturition.

  • Uses: Urinary retention, can be used for benign prostatic hyperplasia*
  • Doxazosin - ZO sounds like GO - makes you GO for a wee*
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23
Q

Urinary anti-spasmodic; anticholinergic

(for urinary incontinence)

A
  • Oxybutinin

competitively antagonizes the muscarinic acetylcholine receptor leading to reduction of bladder detrusor activity

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24
Q

B2-Adrenergic Agonists

A
  • Salbutamol (short acting)
  • Terbutaline (short acting)
  • Salmeterol (long acting)
  • Formoterol (long acting)

B2 agonists bind to B2-adrenergic receptors that activate adenylate cyclase. AC increases cAMP levels, activting protein kinase A (PKA). PKA phosphorylates myoin light chain kinase, deactivating it. This causes a reducation in smooth muscle contraction resulting in relaxation of smooth muscle in the airway.

SEs: Tremor, tachycardia, cardiac arrythmia

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25
**Anti-cholinergics**
* **Ipratropium (short acting)** * **Tiotropium (long acting)** Targets bronchiolar smooth muscle cells. Blocks M3 muscarinic ACh receptors. Decreases action of PLS, reducing Ca2+ release into the cytoplasm, reducing smooth muscle contraction causing bronchodilation. SEs: Dry mouth, constipation, urinary retention
26
**Methylxanthines**
* **Theophylline** * **Aminophylline** Targets bronchiolar smooth muscle cells. Blocks phosphodiesterase (PDE). This sustains cAMP levels and promotes muscle relaxation - bronchodilation. *Toxic side effects to must monitor serum - cardic arrythmias + seizures*
27
**Leukotriene Antagonists**
* **Montelukast** * **Zafirlukast** Primarily targest mast calls in the lungs. Blocks CysLT leukotriene receptors. This reduces the inflammatory response in early and late phases of asthma SEs: Abdo pain, headache
28
**Glucocorticoids**
* **Beclomethasone** * **Fluticasone** * **Prednisolone** * **Hydrocortisone** Targets immune cells of the lungs especially macrophages, T-lymps and eosinophils. Activates the glucocorticoid receptor (GR) which interacts with selected nuclear DNA sequences and influences the expression of g=key genes: - **Repression of pro-inflammatory mediators (TH2 cytokines)** **Expression of anti-inflammatory products (B2 adrenoceptors)** SEs: MANY - Moon face, weight gain, osteoporosis, hyperglycaemia
29
**Beta-adrenergic receptor antagonists** **(Beta blockers)**
* **Bisoprolol** * **Attenolol (cardioselective B1 antag.)** * **Propanolol (B1 & 2 antag.)** Competitive inhibitors of adrenaline and noradrenaline at B-adrenoceptor sites. Inhibit sympathetic stimulation of heart muscle. B1 antagonists are selective for the cardiomyocytes and contractility. Reduce workload on the heart relieving oxygen demand. **Reduces inotropy & chronotropy** SEs: Dizziness, constipation
30
**Calcium Channel Antagonists** **(for heart failure and hypertenison)**
* **Nifedipine** * **Amlodipine** Prevent opening of VGCCs. Bind to K-type calcium channels on cardiac and smooth muscle - act on BOTH the heart and vessels. Cause coronary artery dilation. Negative chronotropic effects, negative inotropic effects. SEs: Ankle swelling, palpitations, interact with B-blockers & grapefruit juice
31
**Nitrate Vasodilators**
* **Glycerol trinitrate (GTN)** * **isosorbide mononitrate (ISMN)** Metabolised to release **Nitric Oxide NO** which stimulates soluble guanylate cyclase. Increases cGMP in vasc. smooth muscle cells. Drives dephosphorylation of MLC via activation of MLCP causing **vascular smooth muscle relaxation**. Can act to dilate arteries AND veins. Venodilation decreases preload. Coronary artery dilarion increases blood and oxygen supply to the myocardium. SE: Headache
32
**Anti-cholinergic** **(for emergency bradycardia treatment)**
* **Atropine** IV. Binds to and blocks muscarinic M2 Ach receptors in the heart. Inhibits effects of cholinergic vagus nerve transmission (normally chronotropic effects). Accelerates repolarisation rate in cardiac muscle cell, so raises heart rate Uses: Sinus Bradycardia
33
**Sympathomimetics**
* **Noradrenaline (alpha)** * **Dobutamine (beta)** * **Adrenaline (alpha and beta)** Activate the sympathetic NS, stimulatinf cardiac inotropy and chronotropy Uses: Chronic Heart Failure
34
**ACE inhibitors**
* **Ramipril** Inhibits conversion of Ang I to Ang II. Reduces vasoconstriction
35
**HMG-CoA Reductase Inhibitors** **(statins)**
* **Atorvastatin** * **Simvastatin** Inhibition of malevonate metabolism in cholesterol synthesis pathway
36
**Neprilysin inhibitors** **(used with an ARB drug)**
* **Sacubitril (used with valsartan)** Inhibition of natriuretic peptide breakdown
37
**Antiplatelet Drugs (2)**
* **Aspirin** ​Inhibits synthesis of Thromboxane A2 by reversibly inactivating COX1. Less TXA2 can bind to glycoprotein receptiors on another platelet thereby preventing cross-linking of fibrinogen. * SEs: GI bleeding, gastric ulcers due to decreased prostaglandins E2 and I1* * **Clopidogrel** Binds to and blocks the platelet ADP receptor, causes decreased expression of GPIIb and GPIIIa receptors so decreased platelet aggregation as fibrinogen cannot cross link between platelets. *SEs: GI bleeding and gastric ulcers due to decreased prostaglandins E2 and I2* *_The cloppy dog has 5 limbs (2+3) GPIIb and GPIIIa_*
38
**Anticoagulants (4)**
* **Warfarin** ​Targest extrinsic pathway which inhibits vitamin K dependent synth of Ca2+ dependent clotting factors 10, 9, 7 and 2. By inhbiting vitamin K carboxylation of the factors it decreases thrombin production. **WKD TimE = _W**_arfarin inhibits vitamin _**K_, _d_**ecreasing **_T_**hrombin which is **_E_**xtrinsic pathway. _Vit K is clotting factors 1972 - 10,9,7,2._ * **Unfractioned heparins, low molecular weight heparins** Targes intrinsic pathway, activates antithrombin III which inactivates thrombin and Xa. has immediate effect as binds to products already there whereas warfarin must inactivate - Heparin used to bridge treatment for warfarin. **HAITTI - _H**_eparins activate _**A_**nti-thrombin 3, **_I_**nactivating **_T_**hrombin and **_T_**enA -**_I_**ntrisic pathway * **Dabigatran** Direct inhibition of thrombin - thrombi cannot convert fibrinogen into fibrin and formation of secondary plug is inhibited A wolf, a hippo and a big dab
39
**Thrombolytics**
* **Altepase** * **Streptokinase** * **Urokinase** Activates plasminogen to plasmin which digests fibrin and fibrinogen to restore blood flow. SEs:Arrhythmias, bleeding. Can only use streptokinase once as an immune response is generated againset the bacteria (streptococci) and memory B cells produce anti-streptokinase ABs.
40
**Dopaminergics** **(pharma basal ganglia disorders)** **LPRR**
* **Levodopa (DA precursor)** ​Levodopa converts to dopamine as dopamine does not cross BBB - restores activity in the nigrostriatal pathway. * **Pramipexole (synthetic agonist)** * **Ropinirole (synthetic agonist)** * **Rotigotine (synthetic agonist)** ​Synthetic dopamine agonists stimulate D2 receptors on striatal neurons improving dopaminergic transmission. SEs: Anorexia, drowsiness, hypomania, hypotension, sudden onset sleep, 'on-off effects'. **Use Carbidopa to maintain higher levels in CNS.** Uses: Parkinsonism
41
**Dopa-decarboxylase inhibitor**
* **Carbidopa** * **Benserazide** **​**Inhibits dopa-decarboxylase, preventing GI and peripheral metabolism of levodopa meaning more is available to the CNS Uses: Used with levodopa for Parkinsonism
42
**COMT inhibitor** **(catechol-O-methyl transferase inhibitor)**
* **Entacapone** * **Tolcapone** Inhibits COMT in the periphery (outside CNS), reducing dopamine breakdown and allowing for more in the CNS
43
**MAOIB Inhibitor** **(Monoamine oxidase inhibitors, B form inhibitor)** (The Gills)
* **Rasagiline** * **Selegiline** Inhibits MAOIB so reducing central metabolism breakdown of dopamine in the CNS Use: Adjunct with levodopa/carbidopa for Parkonsonism
44
**Anticholinergics**
* **Orphenadrine** * **Procyclidine** * **Trihexphenidyl** Muscarinic cholinergic receptor antagonist - in Parkinsons a decrease in dopamine lease to an increase in Ach concentration. Anticholinergics (antimuscarinics) readdress this balance). SEs: may reduce absorption of levodopa **_Orph**_ans becoming _**pro-cyc_**lists and **_tri_**athletes
45
**Dopamine-depleting Drugs**
* **Tetrabenazine** Inhibits VMAT within basal ganglia, preventing uptake of DA into vesicles. Depletes serotonin, noradrenaline and dopamine. Dopamine is req for fine motor movement, so inhibition is helpful for kyperkinesis. SEs: Causes depression by decreasing 5HT and NA levels *Uses: Chorea e.g. Huntington's*
46
**Weak analgesic/Antipyretic**
* **Paracetamol** Non-selective COX inhibitor, decreasing prostaglandin production. Also improves peripheral vasodilation (anti-pyretic effects). *In OD - conjugation (phase II metab.) pathway is saturated, phase I metab yields toxic metabolite NAPBQI which in high levels is toxic to hepatocytes --\> liver failure.*
47
**NSAIDs**
* **Aspirin** * **Ibuprofen** * **Diclofenac** * **Naproxen** COX inhibitors. Decreased prostaglandins so less inflammation SEs: GI side effects, risk of gastric ulcers and medication overuse headaches. Uses: Anti-inflammatory, antipyretic, anticoagulant, analgesic
48
**COX-2 selective NSAIDs**
* **Celecoxib** * **Etoricoxib** Directly inhibit COX-2 enzymes - specific for inflammation Results in decreased PG production
49
**Weak opioid analgesics**
* **Codeine** * **Dihydrocodeine** Mimic endogenous opioids acting on opioid receptors to modulate pain at all CNS levels. Hyperpolarises the neuron so it is less likely to fire when a stimulus comes through. Uses: analgesia (chronic and acute) and anaesthesia SEs: Resp depression, decreased GI motility, constipation, tolerance and dependance.
50
**Strong Opioid Analgesics**
* **Morphine** * **Diamorphine** Mimic endogenous opioids acting on opioid receptors to modulate pain at all CNS levels. Hyperpolarises the neuron so it is less likely to fire when a stimulus comes through. Uses: Coronary care and cancer care SEs: Resp depression, decr GI motility, constipation, tolerance and dependance.
51
**Partial/Mixed Agonist opioid analgesics**
* **Buprenorphrine** Same as opioids but u-agonist and k-antagonist Mimic endogenous opioids acting on opioid receptors to modulate pain at all CNS levels. hyperpolarises the neuron so that it is less likely to fire when a stimulus comes through.
52
**Opioid receptor antagonists**
* **Naloxone (short lasting)** * **Naltrexone (longer lasting)** Compete for the same binding site as opioids, particularly the u receptor so reducing the effect of opioids
53
**Drugs used to manage opioid addiction**
* **Methadone** * **Buprenorphine** Opioid receptor agonists. Methadone = Mu receptor, longer lasting. Buprenorphine = partial Mu and Kappa R agonist.
54
**Drugs to treat neuropathic pain** **+ 4 types of neuropathic pain?**
* **TCAs** * **Gabapentin (AED) - inhibits VDCC, increases GABA transmission** * **Pregabalin (AED)-Inhibits VDCC** * **Carbamazepine (AED)-Sodium channel blocker** 4 types: Phantom limb, trigeminal neuralgia, post-stroke pain, post-herpetic pain (persistent pain after shingles). **T**all **Ga**ls **Pre**fer **Carb**s
55
**Tricyclic Antidepressants**
* **Amitriptyline** * **Nortriptyline** 1. NA reuptake blocker - MAIN action 2. Serotonin reuptake inhibitor 3. a1 adrenoreceptor antagonist 4. H1 receptor antagonist 5. M1 receptor antagonist SEs: Sedation (H1 blocker), Dry mouth, constipation (M1 muscarinic blocker), cardiac dysfunction (a1 adrenoreceptor blocker)
56
**Selective Serotonin Reuptake Inhibitors (SSRIs)**
* **Sertraline** * **Citalopram** Inhibits 5HT reuptake pump so increases 5HT levels. SEs: Sickness, sleep disorders, sexual dysfunction, serotonin syndrome, slow onset. (5S's)
57
**MAOIs**
* **Moclobemide** Stops breakdown of monoamines in CNS. Increases Na and 5HT levels by inhibiting enzymatic breakdown. Reversible inhibitor of monoamine oxidase A (RIMA) SEs: Postural hypotension, restlessness, convulsions, sleep disorders *Many cross-drug reactions- dont use with SSRIs or TCAs*
58
**Atypical Antidepressants**
* **Reboxetine** - NRI, inhibits reuptake of NA, elevating mood * **Bupropion**- Inhibits NA and dopamine reuptake, elevating mood * **Buspirone -** Partial 5HT agonist, reduce activity to increase transmitter levels in the synaptic cleft * **Agomelatine -** Melatonon agonist, increases slow wave sleep patterns. * **Venlafaxine -** SNRI - Inhibits reuptake of 5HT & NA * **Mirtazapine -** a2-adrenergic antagonist
59
**2nd generation (Atypical) Antipsychotics**
* **Amisulpride** **​**5HT7 and Dopamine antagonist * **Risperidone** ​5HT2A and Dopamine antagonist * **Clozapine** ​5HT2A and domapine antagonist Also affect H1, M1 and a1 receptors + interact with reuptake mechanisms. ***Atypicals are better than classical at managing negative symptoms.*** A R C
60
**Mood Stabiliser**
* **Lithium** **MOA Unclear** Uses: Mainly bipolar disorder specturm as an adjunct to anti-depressants
61
**1st generation (classical) Anti-psychotic**
* **Chlorpromazine** * **Haloperidol** Selective dopamine receptor antagonists. - D1. Also affect H1, M1 and a1 SEs: Tardive Dyskinesia (disabling involuntary movements), Extrapyramidal symptoms (dystonias, parkinsomisms), sedation, weight gain, seizures
62
**General Anaethetic** PINKS
* **Isoflurane -** Unclear * **Propofol -** Unclear * **Nitrous Oxide -** Unclear * **Sevodlurane -** Unclear * **Ketamine -** NMDA (glutamate receptor antagonist) PINKS
63
**Local Anaesthetic**
* **Lidocaine** * **Bupivacaine** * **Levobupivacaine** Blocks voltage-gated Na+ channels, preventing neuronal transmission and stopping pain sensation. Not useful in inflamed tissue due to the acidic pH of 'inflammatory soup' reducinng effectiveness of LA
64
**Neuromuscular blockers**
* **Suxamethonium (depolarising)** * **Atracurium (non-depolarising)** * **Vecuronium (non-depolarising)** * **Neostigmine -** peripheral inhibitor of acetylcholinesterase * Depolarising* - (non-competitive, agonist) Initially depolarising and desensitising of AchR. stop further depolarisation once channel is open by overloading the system. Non-reversible. * Non-depolarising* - (competitive, agonist) compete to bind to Ach receptor to stop depolarisation or presynaptically stop Ach release
65
**Drugs used to reverse NMB block**
* **Sugammadex** Oligosaccharide that forms a complex with NMB removing them from NMJ * **Neostigmine** **​**Peripheral inhibtor of acetylcholinesterase - can reverse non-depolarising blockers by increasing Ach levels to compete with the block
66
**Muscle Relaxants/Sedatives/Anxiolytic-hypnotic**
* **Zolpidem (Z drug) -** GABA PAM (mechanistically identical to BDZ) * **Temazepam (BDZ) -** GABA PAM GABA PAMs increase the effect of GABA by making the channel open more frequently or for longer periods. However, they have no effect if GABA or another agonist is not present. * **Dexmedetomidine -** a2-adrenergic receptor agonist * **Propanolol**- B blocker * **Afentanil -** Opioid receptor agonist * **Fentanil -** Opioid receptor agonist * **Remifentanil -** Opioid receptor agonist
67
**Benzodiazepine**
* **Flumazenil** BDZ antagonist - revers bezodiazepine sedatives
68
**Anti-Epilepsy drugs (AEDs)**
* **Sodium Valporate** * **Lamotrigine** * **Carbemazepine** **​**Block sodium channels in the inactivated state Use: All types of seizures except absence seizures SEs: Cognitive impairment, visual impairment, peripheral neuropathy, skin problems * **Ethosuximide - Ca2+ blocker** **​**Targets low threshold voltage dependent T-type calcium channels Use: Absence seizures - first line
69
**Benzodiazepines for Epilepsy**
* **Midazolam -** GABA PAM (Y subunit) * **Lorazepam -** GABA PAM (Y subunit) * **Diazepam -** GABA PAM (Y subunit) GABAA PAMs increase the effect of GABA by making the channel open more frequently or for longer periods. However, they have no effect if GABA or another agonist is not present.
70
**Barbituates (Barb)**
* **Phenobarbitone-** GABA PAM (B subunit) * **Pentobarbitone-** GABA PAM (B subunit) * **Primidone-** GABA PAM (B subunit) GABA PAMs increase the effect of GABA by making the channel open more frequently or for longer periods. However, they have no effect if GABA or another agonist is not present. **Barb**ara is a **prim**a**don**na
71
**Anticholinesterases** **(for dementia)**
* **Donepezil** * **Galantamine** * **Rivastigmine** Inhibitor of acetylcholinesterase
72
**Glutamate NDMA receptor antagonists**
* **Memantine** VD blocker od NMDA receptors (NMDA NAM)
73
**Antimicrobial/Antiviral drugs for CNS infection**
* **Ceftriaxone** **​**Inhibits synthesis of cell walls in bacteria * **Acyclovir** **​**Inhibits viral DNA synthesis Use: viral encephalitis * **Amoxicillin -** **​**Induces cell lysis by blocking last stages of cell wall synthesis *USES: CNS and meningococcal infections e.g. menigitis and encephalitis*
74
**Corticosteroid**
* **Dexamethasone** Glucocorticoid receptor agonist
75
**Drugs used to treat hypercalcaemia**
* **Fluids (normal saline)** ​Volume expansion stimulates excretion of Ca2+ * **Furosemide (loop diuretic)** ​​Inhibits Na+K+2Cl- transporter keeping Na+ and K+ in the lumen hence it is excreted * **Calcitonin****​** Decreases Ca2+ and PO4 reabsorption in the kidneys, inhibits bone reabsorption by preventing osteoclast action (↓ serum Ca2+ and PO4) * **Alendronic Acid (bisphosphonates)** Prevents osteoclast bone reabsorption which could further increase serum Ca2+
76
**Drugs used in the management of hypocalcaemia**
* **IV calcium gluconate** **​**Replaces lost calcium in the body * **Vitamin D** vit D in activ form Calcitriol prevents Ca2+ and PO4 excretion from the kidney and increases reabsorption in the intestines
77
**Drugs used in the management of vitamin D deficiency**
* **Vitamin D (colecalciferol** * **Calcitriol (only in advanced CKD)** Replaces vit D - active form Calcitriol prevents Ca2+ and PO4 excretion from the kidney and increases reabsorption in the intestines.
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**Drugs used to manage osteoporosis**
* **Alendronic acid (bisphosphonates)** **​**Prevents osteoclast bone reabsorption * **Raloxifene (selective oestrogen receptor modulator, SERM)** ​Inhiibits the cytokines which recruit osteoclasts thus less bone reabsorption * **Parathyroid hormone** **​**Stimulates calcitriol production which prevents Ca2+ and PO4 ecretion from kidney and increases absorption in the intestines * **Denosumab** **​**MoAb which targest RANKL or RANK receptir so inhibits maturation of osteoclasts so less bone reabsorption * **Vitamin D**
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**Anti-proliferative agents** **(DMARDs)**
* **Methotrexate** ​Folic acid antagonist (req for DNA synth) so inhibits the S phase of the cell cycle * **Azathioprine** **​**Reduces purine synthesis and reduces DNA synthesis **Both reduce lymphocyte proliferation**
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**Aminosalicylates** **(DMARDs)**
* **Sulphasalazine****​** * **Mesalazine** **Mechanism unclear - possible COX inhibition**
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**Biologics (monoclonal antibodies)**
* **Infliximab** Anti-TNF cytokine - bind and block proinflammatory function of TNF-alpha * **Rituximab** Depletion of B-lymphocytes
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**Beta lactams - Penicillins**
* **Flucoxacillin** * **Benzylpenicillin** * **Amoxicillin/co-amoxiclav** Bactericidal - cell lysis by blocking cell wall synthesis
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**Beta lactams - Carbapenem**
* **Meropenem** Bacteriocidal - cell lysis by blocking cell wall synthesis
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**Cephalosporins**
* **Ceftriaxone** Bacteriocidal - cell lysis by blocking cell wall synthesis
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**Nitroimidazole**
* **Metronidazole** Bacteriostatic- inhibition of bacterial DNA synthesis
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**Macrolides**
* **Erythromycin** **​**Bacteriostatic - inhibition of bacterial protein synthesis
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**Lincosamides**
* **Clindamycin** Bacteriostatic - inhibition of bacterial protein synthesis
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**Tetracyclines**
* **Tetracycline** * **Doxycycline** Bacteriostatic - inhibition of bacterial protein synthesis
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**Fluoroquinolones**
* **Ciprofloxacin** Bacteriostatic- inhibition of bacterial DNA coiling
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**Oral combination pill contraceptives**
* **Oestrogen/Progesterone** Suppresses ovulation, reduces LH and FSH secretion * Benefits:* Decrease ovarian cysts/cancer, anaemia, dysmenorrhoea, PMT, endometrial cancer, ectopic * Contraindications*: undiagnosed vaginal bleeding, pregnant, breast cancer, chronic liver disease (as metabolised by liver) SEs: Progesterone causes acne, increases appetit, decreased libido. Oestrogen causes breast tenderness
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**Oral mini-pill contraceptives**
* **Progesterone only** Suppresses ovulation, alters endometrium preventing sperm/egg interaction Benefits: can be used instead of COCP when oestrogen is contraindicated SEs: slight increased risk of thrombotic events (stroke, DVT) and breast cancer
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**Implants/injectible contraceptives**
* **Long acting progesterone** Moderate/high dose progesterone causing HPO onhibition suppresses ovulation. Also has mucus/endometrial effects. SEs: Progesterone related - decreased libido, increased weight gain, irregular bleeding, amenorrhoea, cost, invasive
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**Hormone Replacement Therapy (HRT)**
* **Oestrogen alone** * **combined oestrogen and progestin** * **selective oestrogen receptor modulatoes (SERMs( - tamoxifen** Oestrogen treats symptoms of menopause- hot flushes, vaginal dryness, loss of libido and reduces risk of osteoporosis. Combined oestrogen + progesterone also reduces risk of uterine cancer SERM tamoxifen is antagonist in the breast and agonist in endometrium SEs: Risk of Breast cancer, CV event (MI), venous thromboembolism, CVA, bladder cancer, lung/ovarian cancer, demetia, endometrial cancer
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**Drugs used to induce labour** **(vaginal administration)**
* **Prostaglandin E2 (PGE2; dinoprostone)** Stimulates uterine contraction and cervical ripening
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**Drugs used to augment labour** **(IV administration)**
* **Oxytocin** Oxytocin increases uterine contractions and delivery of the placenta in 3rd stage of labour Given as an infusion

Drugs List (1 decks)

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