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Year 2 > Drugs > Flashcards

Drugs Flashcards

1
Q

What drug would you use for acute gout, MSK disorders or pain and inflammation in acute/chronic conditions

A

Diclofenac - non steroidal anti inflam

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2
Q

Diclofenac

A
  • Anti- inflammatory
  • Analgesic
  • Antipyrexia

Competitive inhibitor of COX1 and COX2
Inhibition of cyclo-oxygenase 2 (COX2), suppresses prostaglandin synthesis from arachidonic acid in inflammatory cells.
Decreased prostaglandins synthesis:
i. Decreases vasodilation and swelling (anti-inflammatory)
ii. decreases sensitisation of nociceptive nerve endings to pain (analgesic).
iii. decreases ability for acute phase proteins to cause prostaglandins to shift temperature set point in the hypothalamus (antipyretic).

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3
Q 
What drug would you use for •	Pain and inflammation in acute or chronic conditions
•	Musculoskeletal disorders
•	Dysmenorrhea
•	Migraine 
•	Dental pain
A

Ibruprofen - analgesiac, NSAID

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4
Q

Mechanism action ibuprofen

A

Mechanism of action
• Competitive inhibitor of COX1 and COX2
• Inhibition of cyclo-oxygenase 2 (COX2), suppresses prostaglandin synthesis from arachidonic acid in inflammatory cells.
• Decreased prostaglandins synthesis:
i. Decreases vasodilation and swelling (anti-inflammatory)
ii. decreases sensitisation of nociceptive nerve endings to pain (analgesic).
iii. decreases ability for acute phase proteins to cause prostaglandins to shift temperature set point in the hypothalamus (antipyretic).

Contradiction
•	Allergic disorders e.g. asthma
•	Coagulation disorders
•	gastro-intestinal ulceration or bleeding
•	Ischaemic heart disease
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5
Q

Colcichene

A

Acute gout - • Inhibits polymerization of α/β tubulin dimers preventing formation of microtubules.
• Leads to:
i. decreased endocytosis of urate crystals
ii. decreased synthesis and secretion of chemotactic factors (particularly LTB4)
iii. decreased adhesion and migration of neutrophils

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6
Q

Allopurinol

A

Prophylaxis gout, uric acid + calcium oxalate renal stones.
• It is a substrate for xanthine oxidase
• Forms oxypurinol (alloxanthine), which competitively inhibits the xanthine oxidase
• Inhibiting formation of uric acid from purines

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7
Q

Sulfasalazine

A

Anti inflam -> RA IBD
• A pro-drug converted to 5-aminosalicylic acid and sulfapyridine
• May involve scavenging of oxygen free radicals
• Suppression of leukocyte chemotaxis

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8
Q

Methotrexate

A

DMARD, Anti inflam
RA IBD

• Methotrexate inhibits dihydrofolate reductase!!!!!

preventing the formation of tetrahydrofolate from dihydrofolate.

  • It has immunosuppressive and antiproliferative effects.
  • It decreases cell proliferation and increases T cell apoptosis.
  • It increases endogenous adenosine release (which suppresses the inflammatory functions of neutrophils, macrophages, monocyes, dendritic cells and lymphocytes in the pathogenesis of joint inflammation)
  • Methotrexate also influences cytokine production, humoral responses and has effects on bone formation.
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9
Q

When is trimethoprim indicated

A

UTI
Bronchitis
Pneumocystitis pneumonia

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10
Q

Trimethoprim mechanism

A

AB + folic acid inhibiton

Inhibits bacterial dihydrofolate reductase, preventing the formation of tetrahydrofolate from dihydrofolate.

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11
Q

Prednisolone indications and classifications

A

Anti inflam, glucocorticosteroid (mimics cortisol)
Ulcertive colits
Crohns

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12
Q

Predisalone mechanism action

A

• The steroid binds with the intracellular glucocorticoid receptor.
• The receptors dimerize, produce conformational changes that expose the DNA-binding domain on the receptor and migrate to the nucleus.
• The receptor complex can
a) Bind to the glucocorticoid- response elements (GRE) on the DNA within the nucleus and bring about basic transactivation of anti-inflammatory genes or..
b) transrepression of inflammatory genes
c) steroid receptors can also interact at promoter regions of other pro-inflammatory genes preventing them interacting with their response elements and producing inflammation e.g. NFkB and AP1

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13
Q

Immunosupressive affects glucocorticosteroids

A

i. Inhibition of the leukocyte adhesion molecules preventing adherence of neutrophils and monocyte-macrophages to the capillary endothelial cells in the inflamed area
ii. decreased activation of plasminogen to plasmin
iii. Inhibition of COX2 activity thereby preventing the formation of prostanoids
iv. Sequestration of lymphocytes from the blood

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14
Q

Anti inflam effects glucocorticoids

A

i. Gene expression of annexin 1 which inhibits phospholipase A2 (preventing production of arachidonic acid from cell membrane phospholipids)
ii. Gene expression of IL-10

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15
Q

Ferrous sulphate type and indication

A

ANTI ANEMIC -> IRON DEFICIENCY ANEMIA

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16
Q

Ferrous sulphate mechanism

A

• Ferrous sulphate replaces iron, an essential component in the formation of haemoglobin.
• It is absorbed from the entire length of the GI tract, but primary absorption sites are the duodenum and proximal jejunum (see PBL Case 6 q2 for details on iron absorption).
risk GI irritation

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17
Q

Alpha calcidol class and indications

A

Vit d hormone analogue
Conditions with a disturbance of calcium metabolism due to impaired 1-α hydroxylation such as when there is reduced renal function

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18
Q

Alpha calcidol Mechanism

A
  • Administered as 1 α-vitamin D
  • Precursor of the active calcitriol
  • It does not require renal 1α-hydroxylation but does require 25-hydroxylation in the liver.
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19
Q

Simvastatin class and indications

A

Antihyperlipid - HMG-CoA reductase inhibitor

Hyperlipediemia + prevention cardiovascular events in patients diabeties

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20
Q

Simvastatin mechanism

A
  • A prodrug that is hydrolyzed to active metaboloite that structurally similar to HMG-CoA.
  • This metabolite competes with HMG-CoA for HMG-CoA reductase (the rate limiting enzyme in cholesterol biosynthesis).
  • Interferance with the activity of this enzyme reduces the quantity of mevalonic acid; a precursoer to cholesterol
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21
Q

Ramipril class and indications

A

Antihyertensive - Angiotension converting enzyme (ACE) inhibitor

  • Diabetic nephropathy
  • Hypertension
  • Cardiac failure
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22
Q

Ramipril Mechanism

A
  • Inhibits conversion of angiotensin I to angiotensin II
  • Prevents angiotensin receptor (AT1) mediated constriction of arterioles and to a lesser extent veins.
  • It also prevents angiotensin receptor (AT1) mediated stimulation of aldosterone secretion from the adrenal cortex.
  • Prevents angiotensin AT2 mediated hypertrophy of the left ventricle and arteries
  • It blocks the breakdown of bradykinin, a potent vasodilator.

-> dry cough due accumulation bradykinin lungs

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23
Q

Sulfonylureas class and indication

A

hypoglyceamic - type 2 DM

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24
Q

Sulfonylureas mechanism

A
  • Sulfunylurea’s bind to the SUR subunit of the Potassium-ATP channel on pancreatic beta cells.
  • This causes the channel to close.
  • Closing of the channel depolarizes the cell.
  • Depolarisation of the cell increases Ca2+ influx into the cell via voltage dependant calcium channels.
  • This increases endocytosis of insulin vesicles and insulin release form the pancreatic beta cell.
25
Q

Metformin class and indications

A

anti hyperglyceamic - biguanide, Type 2 DM PCO

26
Q

Metformin mechanism

A
  • Reduces blood glucose by improving hepatic and peripheral tissue sensitivity to insulin (without affecting insulin secretion)
  • Reduces hepatic glucose production (gluconeogenesis)
  • Increase glucose uptake and utilisation in skeletal muscle (reduces insulin resistance)
  • Increase fatty acid oxidation (through AMPK)
27
Q

Levothyroxine class and indications

A

Synthetic T4, hypothyroidosis

28
Q

Levothyroxine mechanism of action

A
  • increases basal metabolic rate,
  • increases utilization and mobilization of glycogen stores,
  • promotes gluconeogenesis; involved in growth development and stimulates protein synthesis
29
Q

Propranolol class and indications

A

Anti-anginal, anti hypertensive, Beta adrenergic blocker

30
Q

Propranolol mechanism of action

A

It blocks the β1 receptors that mediate sympathetically evoked increases in heart rate and force of contraction, making the heart beat more slowly and reducing cardiac output
• Competes with neurotransmitters such as catecholamines in the heart, inhibiting sympathetic stimulation.

31
Q

Carbimazloe class and indication

A

Anti- thyroid, hyperthyroidism

32
Q

Carbimazole mechanism

A
  • Carbimazole, a thionamide, is a pro-drug which undergoes metabolism to thiamazole.
  • inhibits the organification of iodide and the
  • coupling of iodothyronine residues which in turn suppress the synthesis of thyroid hormones.
33
Q

Paracetamol

A
  • inhibition of cyclooxygenase (COX), with a predominant effect on COX-2.
  • Inhibition of COX enzymes prevents the metabolism of arachidonic acid to prostaglandins.
  • In the CNS, inhibition of COX enzymes reduces concentrations of prostaglandin E2, which lowers the hypothalamic set-point to reduce fever, and activates of descending inhibitory serotonergic pathways to produce analgesia.
34
Q

Morphine class and indications

A

Narcotic, anagelsiac, opioid. Acute pain and terminal conditions

35
Q

Morphine mechanism

A
  • Mu-Opiod receptor agonist
  • Opiod receptors are G protein coupled receptors present on the surface of neurones. They act to inhibit adenylate cyclase and reduce cAMP content within cells.
  • This promotes K+ ion channels opening and inhibits Ca2+ ion channels opening which reduces neuronal excitability and reduces neurotransmitter release, which reduces the sensation of pain.
  • Induces respiratory depression, and sedation
  • Suppresses cough by acting centrally in medulla.
36
Q 
Orlistat class and 
indications
A

Anti obesity - lipase inhibitor

37
Q

Orlistat mechanism

A

Inhibits pancreatic lipase and prevents lipid absorption as the undigested triglycerides cant cross the enterocyte membrane.

38
Q

Metaclopromide class and indications

A

Antiemetic - dopamine receptor antagonist

treatment nausea + vomiting

39
Q

Metaclopromide mechanism

A
  • It blocks dopamine receptors, preventing dopamine from stimulating the chemoreceptor trigger zone and thereby preventing nausea and vomiting.
  • It has gastroprokinetic activity in the oesophagus, stomach and intestine.
  • Increases the tone of oesophageal sphincter to prevent reflux of stomach contents.
40
Q

Lactulose class and indictation

A

Laxative - osmotic

  • Constipation
  • Hepatic encephalopathy (portal systemic encephalopathy)
41
Q

Lactulose mechanism of action

A
  • Lactulose is broken down primarily to lactic acid by colonic bacteria causing acidification of bowel contents.
  • It produces an osmotic gradient causing water to remain in the lumen of the bowel.
  • In the case of liver disease, the liver cannot metabolise ammonia and so it is essential that it leaves the body.
  • The acid favours the conversion of ammonia to ammonium, trapping it in the colon and not allowing reabsorption into the blood.
42
Q

Spironolactone class and indication

A

Potassium sparing diuretic
Inhibitor aldosterone

  • Oedema
  • Ascites from cirrhosis of -the liver
43
Q

Spironolactone mechanism

A

• Aldosterone is a steroid hormone that binds to the mineralocorticoid receptor where it works through nuclear transcription factors to induce the expression of the:
I. H+ ATPase
II. Epithelial Sodium Channel (ENAC): which allows Na+ to be taken up more efficiently at the DCT
III. Na+/Na+ ATPase: which pumps more sodium into the interstitium
IV. K+ Channel to prevent hyperkalaemia

  • Spironolactone inhibits the binding of aldosterone to the renal mineralocorticoid receptor in the distal convoluted tubule
  • Increases sodium and thus water excretion
  • By inhibiting sodium transport, spironolactones decrease the transepithelial potential difference. This reduces the driving force for potassium movement into the tubular lumen and thus decreases potassium excretion.
44
Q

Aspirin mechanism

A

Irreversibly Inhibits both COX 1 and COX 2 (acetylates serine residue)
Enzyme invovled in prostaglandin synthesis via the arachidonic acid pathway
Phospholipids to AA via Phospholipase A2 and Lipocortins. AA via COX to Endoperoxides.
Endoperoxides can make Prostaglandins, Prostacyclin, Thrombox-A2.
Decreases the synthesis of prostaglandins involved in mediating inflammation, sensitizing nociceptors involved in transmitting pain, fever and swelling
Decrease in TXA2 so lack of platelet activation, adherence, aggregation
Inhibit thrombus formation
No significant anti-inflammatory action-mild analgesic
Effective against nociceptive inflammatory pain
Ineffective against Visceral severe pain
Little effect on neuropathic pain

45
Q

Ibuprofen type and indications

A

NSAID

Gout
Chronic back pain

46
Q

Ibuprofen mechanism

A

Non-selective inhibitor of cyclooxygenase (mainly COX 2), an enzyme invovled in prostaglandin synthesis via the arachidonic acid pathway
Enzyme invovled in prostaglandin synthesis via the arachidonic acid pathway
Phospholipids to AA via Phospholipase A2 and Lipocortins. AA via COX to Endoperoxides.
Endoperoxides can make Prostaglandins, Prostacyclin, Thrombox-A2.
Decreases the synthesis of prostaglandins involved in mediating inflammation, sensitizing nociceptors involved in transmitting pain, fever and swelling
Decrease in TXA2 so lack of platelet activation, adherence, aggregation
Inhibit thrombus formation
No significant anti-inflammatory action-mild analgesic
Effective against nociceptive inflammatory pain
Ineffective against Visceral severe pain
Little effect on neuropathic pain
Inhibition of COX-1 is thought to cause some of the side effects of ibuprofen including GI ulceration

47
Q

Colchicine mechanism

A

Interupts cycle monosodium urate crystal depositation.

BINDS ALPHA/BETA tubulin in leukocytes * prevents polymerization into microtubules.

Inhibits phagocytic activity + migration leukocytes to areas uric acid depositation.

Decreases leukocyte chemotaxis + phagocytosis.

48
Q

Colchicine side effects

A

Nausea
Vomitting
Abdo pain
Renal damage

49
Q

Allopurinol mechanism

A

Allopurinol + active metabolite oxypurinol inhibits enzyme Xanthine oxidase * blocks conversion
hypoxanthine -> xanthine -> uric acid

Facilitates incoporation hypoxanthine/ xanthine into DNA/RNA * inhibition de novo synthesis -> decrease serum uric acid concentrations.

Lower urate levels prevent formation new crystals + slowly break down crystals already there.

50
Q

DMARDS side effects

A 
Severe myelosupression
Sore throat
Fever
Unexpected bleeding
fatigue
51
Q

DMARDS mechanism

A

Inhibits DNA synthesis, inhibits folic acid reductase. Prevent proliferation of T lymphocytes - binds cyclophilin decreased IL-2.
Prevent activates B cells - prevent AB production.
Inhibits enzymes destroy cartilage - inhibit inflammation * bone erosion.

52
Q

Gold injections mechanism

A

Sodium aurothiomalate
suppress disease process
inhibits the following enzymes: Acid phosphatise, Beta-glucuronidase, Elastase, Cathepsin G, Thrombin
Inhibits the synthesis of prostaglandins
Modulates phagocytic cells and inhibits Class II major histocompatibility complex-peptide interactions.
inhibit IL-1 and TNF Alpha

53
Q

Infliximab

A

RA
Block TNF/ TNF receptors
Soluble form of the p75 TNF receptor that can bind to two TNF molecules
Thereby effectively removing them from circulation
Prevent adhesion expression on endothelial cells, so prevention of recruitment of leukocytes, depress inflammatory response. Turn down synthesis of SAA Acute Phase protein in Liver

54
Q

Side effects of infliximab

A

Septicaemia
Hypersensitivity
AB formation

55
Q

When is belimumab indicated and what are its side effects

A

Lupus
Nausea
Fever
Immunosupression

56
Q

Belimumab mechanism and how this links to SLE

A

SLE caused caused autoimmune B cells proliferate + survival factors protect them from cell suicide. BAFF required required dev + survival B cells. SLE BAFF is over expressed. Belimumab human AB that binds to BAFF * BAFF not free to bind to B cells. Without BAFF b cells commit suicide * reduced autoimmune response.

57
Q

Diclofenac

A

NSAID
Reversible
lower affinity

Ibuprofen also reversible

58
Q

Rituximab

A

IgG1 kappa immunoglobin Against CD20 antigen found surface normal/ malignant B lymphocytes * selective killing B cells.
reduces B-cell survival and so B-Cell mediated immunity and the autoimmune response.

59
Q

Eteplirsen

A

Removes exon 51 DMD * no longer codes stop codon

Year 2 (12 decks)

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