Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

305 drugs > 305 drugs > Flashcards

305 drugs Flashcards

1
Q

Hirudin

A
  • DTI (direct thrombin inhibitor)
  • anticoagulant, inactivates thrombin bound to fibrin
  • AT3 independent agent
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Bismuth Chelate

A

Used to treat H.Pylori, coats the ulcer base, absorbs pepsin, enhances local prostaglandin (PGI) synthesis and bicarbonate secretion

  • small amounts absorbed, most secreted in urine
  • blackens tongue and poo
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Nitroglycerin and Glyceroltrinitrate

A

Nitrates that are converted to NO, activates cGMP and PKG to relax smooth muscle and improve coronary perfusion

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

Prazosin

A

A1 (AR) antagonist, used on vascular smooth muscle to relax, Used to treat hypertension. Blocks the GPC2, inhibiting IP3 linked activation causing relaxation.
- SE: tachycardia and dizziness

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

Nitric oxide

A

Is a vasodilator - rapid diffusion into smooth muscle to activate gyanaylate cyclase to increase cGMP, and stimulation of cGMP dependent PKG inhibiting ca2+ entry, and activation of K+ channels to cause hypopolarisation and relaxation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Lithium

A

Bipolar- Stabilises the manic and depressive phases, has 2-3 week onset latency and is the only/most effective treatment. Overdose causes tremor, seizure, coma and death. It dampens the phosphoinositidemediated neurotransmission.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Sucralfate

A

to treat duodenal ulcers, complex of AlOH and sulphated sucrose. Reacts with HCl, releasing AL forming a paste. Strong negative charge attaches to ulcer to stabilise the insoluble complex. Protecting ulcer from acid, pepsin. Stimulates mucous production and bicarbonate and PHI secretion

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Phenobarbitone

A

Epilepsy - increases the duration of Cl channel opening of GABAaR (increasing inhibition)

  • grand mal and some focal
  • tolerance and rebound seizures upon withdrawl
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Mocolbemide

A

For depression - selective reversible MOAa inhibitor

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

Phenelzine

A

Depression - irreversibly inhibits MOA and increases NA, serotonin and DA
- non-selective

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

Risperidone

Olansapine

A

Used in schizophrenia treatment

- anti-psycotics

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Mylanta (anti foaming)
AlOH (slow)
MgOH (fast)

A

non systemic gastric antacids. React with excess acid to neutralise.
Mg(OH)2 + 2HCl = MgCl2 + 2H2O
However can chelate other medications, folate and iron

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

LMWH

A

Low molecular weight heparin - Acts on factor 10 stop coagulation, used in the prevention blood clots and treatment of venous thromboembolism and in the treatment of myocardial infarction. Does not bind Factor 2 so therapeutically less likely to cause the immune reaction that can cause thrombocytopenia and thrombosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Warfarin

A

Oral anticoagulant

  • inhibits activity/reduction of vitamin K, inhibiting the gamma carboxylation of factors 2, 10, 7, and 9. Blocking active coagulation
  • 5-7 day onset
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Vigabatrin

A

epilepsy - GABA potentiation, used for infantile spasms, and partial/generalised seizures

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Carbidopa (inamet)

A

PD - DDC inhibitor, stops the peripheral breakdown of L-dopa

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Pravastatin

A

Hydrophilic, requiring active transport. Lowest protein binding profile. Lowers the risk of myopathies. Decreases cholesterol

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

Clonidine

A

to threat hypertension - A2 agonist which decreases peripheral vascular resistance, lowering blood pressure, (pre sympathetic specificity), Gi linked decreases presynaptic calcium levels thus inhibiting the release of NE. The net effect is a decrease in sympathetic tone.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

Ropinirole
Bromocriptine
Pergolide

A

PD - initial treatment to prolong onset of L-dopa
R - D2/D3
B - D2 partial D1
P - D2/D1

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

Diltiazem

A

Class 4: antidysrythmia, both vascular and cardiac. Calcium channel blocker, acts on phase 2 to block Ca2+ influx, therefore decreasing contraction

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

Prednisone
Methylprednisone
Dexdmethasone
Betamethasone

A

Allergy and immune steroids - synthetic analogues of cortisol. All GR agonists bind cytosolic Gr to for GR:GCR complex that migrates to the nucleus, acting as a transcription factor binding to glucocortical receptor element and a promoter region of the target gene. Decreasing expression of Pro-inflammatory genes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

Digoxin

A

Cardiac inotrope/glycoside - inhibits the Na+/K+ atpase exchanger, indirectly affecting intracellular calcium levels. Decreases the Na+ gradient pulling more Ca2+ into the cell causing contraction. Treats congestive heart failure

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

Ipilimumab

A

Allergy - monoclonal AB. Binds CTLa4 on T cells to suppress T cell function

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

Abciximab

A

Glycoprotein IIb/IIIa antagonist - Fab fragment directed against the Gp IIb/IIIa, blocking fibrinogen binding these receptors

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

Ticlopidine

A

Antiplatlet - inhibits the ADP dependent aggregation by inhibiting the expression of Gp IIb/IIIa R - preventing aggregation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

Amlodipine

A

Blocks the Ca2+ L-type channel in the inactive state. Treating hypertension, angina and arrhythmias by vasodilation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

Isosorbide Mononitrate

A

Oral drug that converts Nitrate to NO, activating cGMP and PKG to relax smooth muscle and improving coronary perfusion

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

Mianserin

A

Atypical antidepressant - antagonist/inverse agonist of:

  • H1 Receptor
  • 5HT 1D, 2a, 2b, 2c, 3, 6, and 7
  • a1 and a2 AR’s
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

Felbamate

A

Epilepsy - partial block on NMDA glutamate channels, weak effect on Na+ channels and on GABA

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

Talcapone

Entacapone

A

PD - inhibits the COMPT enzyme breaking down l-dopa peripherally to 3-O-methyldopa

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

Venlafaxine

A

depression - non-selective re-uptake inhibitor

  • low dose: targets 5HT re-uptake
  • med dose: targets 5HT/NA re-uptake
  • high dose: targets DA re-uptake
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

Misoprostol

A

GI mucosal protective agent - analogue at PGE1. Prevention of NSAID ulcers acting on parietal cells blocking cAMP and H+ pump. At lower doses it is protective and stimulates increased mucous production and increases the mucocillary blood flow.
Can induce uterine contraction and diarrohea
- multiple daily dosing needed

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

Endothelin

A

Contractile alterations - potent long action vasoconstriction. Produced from ET-1 39aa). ET-1 binds Eta and ETb receptors (GPCRS) on adjacent vascular smooth muscle. Leading to the formation of IP3 causing ca2+ release from SR causing contraction.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

Sodium valporate

A

epilepsy - inhibition of Na+ - absence. Inhibits the T-type Ca2+ channel currents in thalamo-cortical pathway. Blocks GABA transaminase enzyme, (stops GABA breakdown) increasing inhibition by GABA.
Therapeutic concentrations may be to low to do this.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

Milnacipran

A

depression - non-selective re-uptake inhibitor

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

Dermatin Sulphate

A

AT3 independent agent. Increases the action of heparin cofactor, only inhibiting the actions of Thrombin. Stopping coagulation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

Epoprostenol

A

Glycoprotein IIb/IIIa antagonist - synthetic prostaglandin, inhibits the expression of Gp IIb/IIIa receptors –> preventing platelet aggregation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

Alirocumab
Evolocumab
Praluant

A

decrease cholesterol - PCSK9 inhibitor. For patients with inherited familial hypercholesterolemia or need additional Lipid lowering. PCSK9 is involved in LDL receptor expression/degradation. Increasing expression means more removal of cholesterol form the plasma.
Injected SC, causes sore nose and throat

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
39
Q

Gabapentin

A

Epilepsy - calcium channel blocker, partial and tonic/clonic

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
40
Q

Reboxetine

A

depression: selective norepinepherine re-uptake inhibitor

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
41
Q

Morphine

A

opioid, binds u receptor, analgesic and respiratory depressant. Releases histamine causing nausea, vomiting, and peripheral vasodilation. Slow onset (t1/2 = 16 mins)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
42
Q

Fentanyl

A

50-100x more potent than morphine. Phenyl piperidine opioid. Binds y and s, fast onset (t1/2= 4.6 mins), Used fro bolus administration of analgesic intraoperatively

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
43
Q

Ketorolac

A

NSAID –> pain, COX 1 & 2, used post operatively. Onset 30mins, duration 4-6 hours, Can cause GI bleeding. And a high dose >120mg/day may cause a delay in bone healing

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
44
Q

Paracetamol

A

NOT NSAID, lacks the anti inflammatory and anti platelet effects. Central effects on COX2 at the peroxidase site (PGI H2 synthase). Can cause hepatotoxicity = NAPQI = toxic metabolite
Immune and analgesic

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
45
Q

Progesterone

A

uterine contractility - tocolytic. Pro-pregnancy hormone, suppress pro labour genes, inhibits CAP, decreases oxytocin sensitivity, increases PGDH. Effective prophylaxis on higher risk women. Early prediction and long term treatment. Limited side effects

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
46
Q

Lamotrigine

A

epilepsy - voltage sensitive Na+ channel blocker. Inhibits the release of excitatory amino acids. For partial/Tonic/clonic seizures.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
47
Q

Alteplase
Dyteplase
Prourokinase

A

fibrinolytic agents - only activates plasminogen bound to fibrin, breaks down the thrombi and emboli.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
48
Q

Theophylline

A

Respiratory diseases - 4th line agent (100% bioavailability) Inhibits the phosphodiesterase and adenosine receptors = bronchodilation. It increases mucocillary clearance and diaphragm contractility.
Narrow therapeutic window (variable drug levels –> CYP450)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
49
Q

Ergometrine

A

promotion of contraction - ergot alkaloid, intense uterine contraction. A2 agonist. Used in the prevention and treatment of postpartum haemorrhage, in combination with syntocinin.
Side effects: hypertension, angina, headache, nausea, vomiting, diarrhoea and pain,

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
50
Q

Spironolactone

A

potassium sparing diuretic - reabsorption of K+ is NOT affected. BUT antagonised aldosterone preventing activation therefore no Na+ channels produced and no reuptake.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
51
Q

Ethacrynic acid -LOH
Furosemide -LOH
Hydrochlorothiazide - DCT

A

powerful agents that bind a subunit on CL- channels to block reabsorption, blocking Na+/K+ reabsorption and also water to maintain osmotic water balance

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
52
Q

Ethosuximide

A

Epilepsy - inhibits the Ca2+ channel, for absence seizures

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
53
Q

Atenolol

A

hypertension - B1 antagonist, works on heart and renal JG cells, Gs linked. Decreases renin release, inhibiting ANG2, causing peripheral constriction (rate limiting step), decreasing peripheral blood pressure. The heart increased inotrophy and chronotrophy, increases the AV node conduction and increasing contraction

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
54
Q

TXA2 synthetic inhibitors

A

Anti platelet - inhibit synthesis of TXA2, therefore inhibiting aggregation.

55
Q

Amitriptyline

Imapramine

A

Depression - block NA and SE re-uptake. Decrease in BAR1a. Also acts on A2 AR antagonistically to block inhibitory effects.
Side effects: antimuscurinic, only benefits 75% of people.

56
Q

TPA
Streptokinase
Urokinase

A

Fibrinolytic agents. TPA - only affective if used within 3-4 hours of stroke onset. All - interact with both free and bound plasminogen to stimulate the conversion of plasminogen to plasmin. Breaks down thrombi and emboli

57
Q

Aspirin

A

NSAID, inhibits COX1, decrease TXA2 in platelets decreasing aggregation. Increases PGI2 in endothelial cells to increase inhibition. Aspirin is used in all cardiac patients to inhibit aggregation of platelets and prevent adverse cardiac events like heart attack. Since this inhibition is irreversible, it might lead to gastrointestinal bleeding and increases the chances of strokes in the elderly.

58
Q

Topiramate

A

epilepsy - GABA potentiation, AMPA inhibition, and NA= and Ca2+ channel clocker. Increasing inhibition.

59
Q

Dinoprostone (PGE2)
Gemeprost/Misoprostol - PGE1
Carboprost - PGF2

A

Promotion of contraction - increase contraction and promote cervical ripening. Termination of pregnancy (G/M), induction of labour at term (D). treatment of PPH (M/C).
Side effects: pain, nausea, vomiting, pyrexia, bleeding

60
Q

Syntocinon (synthetic oxytocin)

A

Promotion of contraction - increase contraction and induction of labour at term and treatment of PPH.
Side effects: hyponatremia, pulmonary odema, hyperstimulation (fetal distress) hypotension and tachycardia

61
Q

Tirofiban

A

Anti-platelet, gylcoprotein IIb/IIIa antagonist. Blocks fibrinogen.

62
Q

Propranolol

A

Class 2 antidysrhythmia. BAR 1 and 2 antagonist.Either acts at phase 2 and phase 4. Tncreased sympathetic tone, lengthens phase 4 by stopping the opening of Ca2+ channels therefore decreasing contraction.

63
Q

tiagabine

A

epilepsy - GABA uptake inhibitor, increased eGABA conc. Potentiates and prolongs GABA mediated synaptic response brain.

64
Q

Alginates (gaviscon)

A

Symptomatic relief of heart burn. Forms a protective barrier to prevent acid entering oesophagus. Precipitates into a gel in presence of acid and traps CO2 (foam). Selective retention in the funds.

65
Q

Ezetimibe

A

Cholesterol absorption inhibitor. Usually used with statins. Blocks transport protein (Nieman - pick Cl like 1) NPC1L1. Specifically inhibits cholesterol absorption by 50%. Decrease in LDL by 15-20%.

66
Q

Chlorpromazine

Halperidol

A

Schizophrenia/anti-psychotics - typical.
C - tricylic, DA antagonist.
H - DA antagonist.
Both work on positive symptoms and show EPSEs caused by block D2R

67
Q

Niacin (nicotinic acid)

A

Decrease cholesterol. Adjunct therapy or if statins contradicted. At gram doses works on nicotinic receptors in liver and fatty tissue. Inhibits lipolysis = decrease substrate for VLDL = decreased LDL.

68
Q

Fluoxetine (prozac)

A

depression - selective 5HT re-uptake inhibitor.

69
Q

Heparin

A

Blood/haem - injectable first line IV or SC. binds AT3 inhibiting factors 2 & 10 (12, 11, 9). Inhibits thrombin formation, increase protease inhibits formation, decrease fibrin deposition. Needs to bind AT3 and heparin thrombin.

70
Q

Colestipol

Colesevelam

A

Decrease cholesterol - bile acids binding resins. The resins absorb acid in the intestine, prevents reabsorption and increase excretion in poo. Enhanced excretion results in increased metabolism of cholesterol into bild acids and increased number of LDL receptors and increased cholesterol into hepatocytes. Serum total and LDL concentration decrease by 15-30%. TG may increase slightly.

71
Q

SABA - salbutamol

A

Respiratory diseases - bronchodilation, local delivery, 15 min onset, B2 AR activation. 4-6 hour duration

72
Q

Gliclazide

Tolbutamate (mide)

A

Diabetes type 2 - insulin secretagogues. 2nd line treatment after metformin, oral. Increase insulin by blocking ATP sensitive K+ channel in B islet cells. Only works if B-cells can make enough insulin ( Doesn’t work in advance disease). Can cause hypoglycaemia

73
Q

Disopyramide
Lignocaine
Flecainide

A 
D - 1a intermediate dissociation
L - 1B fast dissociation
F - 1C slow dissociation
--> Class one antidysrhythmia. 
Act at phase 0 to block the voltage sensitive Na+ channels. Use dependent block, only when open or in the inactivated state (Stabilisation). Selective for the inactive state therefore selective for channels.
74
Q

Isoflurane

A

inhaled general anaesthetic. Causes unconsciousness, amnesia and immobility. Has multiple specific targets, Immobility via the glycine receptors. Mim alveolar concentration which ablates movement to noxious response in 50% of people.

75
Q

Ketamine

A

General anaesthetic, iv induction of anaesthesia. Uncompetitive antagonist of NMDAR in brain and spinal cord for pain mediation.
Effects
Cardio: stimulation of SNS ( Increased adrenaline and NA) therefore increasing HR, CO, BP and myocarudal O2 requirements.
Resp: increased rate and bronchodilation
CNS: dissociative anaesthesia on EEG, vivid dreams and hallucination
Gut: nausea and vomiting common and increased salivation

76
Q

Propofol

A

General anaesthetic, IV. GABAa to induce/maintain sedation. Distribution is quick to highly perfused lean tissue so return to consciousness is very rapid.
Effects
Cardio: Decreased systemic vascular resistance = decreased BP = bradycardia. Decreased sympathetic activity, decrease myocardial contractility.
Resp: depression leading to apnoea
CNS: excitatory effects (not true seizure)
Pain: common in small vein injection but is alleviated with the addition of Lidocaine

77
Q

Thiopental

A

General anaesthetic IV barbiturate. GABAa, blocks excitatory signals of AMPAR and kinate receptors. Sedation and hypnosis, dose dependent EEG slowing. Respiratory depression. Rapid onset due to plasma protonation (30-50s). Distribution is quick to highly perfused lean tissue so return to consciousness is very rapid, but this limits duration (5-8mins). Concentrations can saturate at high doses prolonging effects.
Infusion has a ver long recovery phase.

78
Q

Bipivacaine

A

Local anaesthetic - associated with cardio toxicity if dose is too large/fast/poorly place. Decreased conduction of purkinje fibres and myocardiocytes. Increased binding and decrease dissociation of Na channel. Direct depression of Myocardium. Bind Ca2+ channels = release of Ca2+ form SR

79
Q

Lidocaine

A

Local anaesthetic. Vasodilation (even at low concs), administration with epinephrine will prolong duration up to 50%. inhibits pro-inflammatory cytokines and has some anti-inflammatory properties. IV to achieve low concs to treat/prevent dysrhythmia after myocardial infarction. Direct neuronal toxicity shown by transient hyperalgesia/dysphesia in lower back, bum and extremities.

80
Q

Amiloride

A

potassium sparing diuretic, blocks the Na+ channel directly by aldosterone stimulation. ONLY manipulates Na+

81
Q

Torcetrapib

A

Cholesterylester transfer protein (CETP) inhibitor, which increases HDL and decreases LDL. (all treatments have failed with this so far)

82
Q

LABA (Salmeterol)

A

respiratory diseases - bronchodilation, onset 20mins, duration 12 hours. Only used in conjunction with ICS.

83
Q

Aminophylline

A

IV, used for acute life threatening asthma

84
Q

Inhaled corticosteroids

A

respiratory diseases - preventer medication targeting airway inflammation. limits the side effects of CS. Taken in combination with LABA. Can cause oral thrush, hoarse voice and skin thinning

85
Q

UltraLABA (Vilanterol)

A

respiratory diseases - bronchodilation, onset 60 mins, duration 24 hours

86
Q

Ipratropium

A

respiratory diseases - inhaled antimuscurinic, short acting, non selective antagonist. onset 15 mins, duration 6 hours

87
Q

Tiotropium (Spiriva)

A

respiratory diseases - inhaled antimuscurinic, onset 15-30 mins, duration 24 hours

88
Q

Rosuvastatin

A

Statin, hydrophyllic, active transport needed, Metabolised by CYP2C9/19, decreases cholesterol, by inhibiting HMG-COA reductase enzyme pathway

89
Q

Acetazolamide

A

Inhibits carbonic anhydrase, stopping CA formation, decreases bicarbonate and H+ formation. exchange stops transferring H+ into the lumen, Na+ exchanger reverses, No H+ into urine. Less breakdown of H2CO3 into Co2 and H2O. Water within the tubule is excreted into the lumen.

90
Q

Mamitol

A

Osmotic diuretic -indirect action on whole tubule, Alters osmotic pressure and passive H2O reabsorption is reduced. Increased osmotic pressure, decreased Na+ reabsorption. Further decrease in water reabsorption (loss)

91
Q

Fenofibrate, ciprofibrate

A

decreases cholesterol, 2nd preventativ treatment. Substantial decrease in TG and LDL and circulating VLDL. Side effects include nausea, headaches, increase in plasma creatine (possible kidney and liver damage). Gall stones due to increased cholesterol saturation in bile.

92
Q

Metoprolol

A

BAR1 antagonist acts to decrease heart rate and therefore cardiac output to lower a patient’s blood pressure. The blockage of the B1AR will inhibit sympathetic nervous system stimulation, meaning less cAMP, less PKA activation, which will decrease the probability of calcium channels opening in cardiomyocytes. The reduction in calcium will reduce the contraction of the heart and extend phase 4 in the cardiac cycle.

93
Q

Omalizimab

A

Monoclonal Anti-Ig E, Special authority, Small minority of patients. Must demonstrate a reduction in admissions , symptoms and oral steroid dose. Severe /life threatening asthma. Atopy: SPT/RAST, IgE 76-1300. Compliant on maximal inhaled therapy 1 month of steroid/12, Symptomatic, 4+ admission

94
Q

Cimetidine

A

Competitive reversible antagonists of parietal H2 (Gs). Inhibit the formation of cAMP and PKA activation. Inhibits H+/K+ ATPase pump. Decrease acid secretion by <60%. Fast onset but short duration.

95
Q

Omeprazole

A

Proton pump inhibitor. Delivered as a pro drug, weak base that passes through the blood stream to the parietal cells. Accumulates in the acidic canaliculus of the parietal cells and is activated by the decrease in pH. Irreversible covalent binding to disulphide bonds which directly inhibit the H+/K+ ATPase, reducing stomach acid secretion by <90%. Increase to pH6, short t1/2 but long duration (2-3days)

96
Q

Sodium Bicarbonate

A

Systemic. Used for symptomatic relief after meals, acts rapidly in the blood stream to neutralise acid
NaHCO3 + HCl → NaCl + H2O + CO2
Can cause metabolic alkalosis, electrolyte imbalance and belching. Not suitable for patients with hypertension.

97
Q

Montelukast

A

Leukotriene Receptor Antagonist. Special authority, limited use to wheezy preschool children and exercise-induced asthma resistant to other therapies. And during aspirin de-sensitisation.

98
Q

Pembrolizumab

A

binds PD-1 on T cells (monoclonal antibody; FDA approved 2014), PD-1 suppress/inhibit T cell function. They are inhibitory receptors. Clinically FDA approved for advanced melanoma; Clinical trials on going for many other cancer situations

99
Q

Iv Magnesium

A

Used for severe acute asthma failed first line therapy. Inhibits the Ca influx into cytosol, histamine release, ACH from cholinergic nerve endings. Increase affinity of B2 agonists for receptor (promotes SNS). SE: flushing and fatigue

100
Q

Minoxidil (active metabolite)

A

K+ channel activator. Cause relaxation indirectly by hyperpolarising the membrane. Increase K+ due to the opening of channels. Used in hypertension but the side effects include increased body hair.

101
Q

Losartan

A

ANG2 receptor subtype antagonist/ Angiotensin receptor blocker. Blocks the effects of ANG2, causing relaxation of smooth muscle, used in patients who cant tolerate ACE inhibitors.

102
Q

Dobutamine

A

Vasopressor, treats congestive heart failure. Induce vasoconstriction to increase mean arterial pressure. Mainly B1 agonist, weak B2 agonist, selective A activity. +ve isomer – B1 agonist/A1 antagonist → clinically used
Also a BAR agonist, bind the receptor on myocardial cells, increase cAMP, Pka, and increase calcium, increasing the force of contraction.

103
Q

Amantadine

A

Increases the release of DA, inhibition of DA uptake. Has a direct effect on DA receptors. Was initially used to treat influenza. Used to treat parkinsons

104
Q

NO/Realxin/progesterone

A

Phase 0 - Uterine Quiescence (Uterorelaxant). Is the main ‘propregnancy’ hormone. Inhibits CAP (contraction associated proteins). Decreases oxytocin sensitivity - so reducing Ca mobilisation, and decreases PGDH - so ↓ prostaglandin activity.

105
Q

Atosiban

A

Competitive oxytocin/vasopressin receptor antagonist. Expensive, Better side effect profile than β2 adrenergic agonists. Similar outcomes. Uterine contractility

106
Q

Isoprenaline

A

a BAR agonist, bind the receptor on myocardial cells, increase cAMP, Pka, and increase calcium, increasing the force of contraction. (B1/B2)

107
Q

Indomethacin

A

Inhibit production of PGE2 and PGF2. Reduce intracellular Ca → inhibits contractility. Also effect in membranes and cervix. Fewer maternal side effects
Fetal side effects: Renal function, ductus arteriosis, NEC, IVH. Short duration of treatment OK. Tocolytic agent, uterine contractility

108
Q

Sodium Nirtoprusside

A

IV, All convert nitrate to Nitric oxide, activate cGMP, PKG, relax smooth muscle and thus improve coronary perfusion. Powerful vasodilator, little effect on outside vasculature, has to be IV because it reacts with light to from cyanide. Used in hypertensive crisis and controlled hypertension during surgery.

109
Q

Amiodarone and sotalol

A

Class 3, Potassium channel blockers. Act on phase 3, to prolong the cardiac action potential. Blocking K+ entry, stops cell repolarisation, extending phase 2. Sotalol causes a longer cardiac action potential and a reduced phase 2. Sotalol is also a BAR antagonist

110
Q

Ibuprofen

A

NSAID non selective; fewer side effects applicable in children

111
Q

Naproxen

A

NSAID non selective

112
Q

Benztropine

A

Blocking muscarinic receptors reduces tremor and rigidity but not akinesia. Ach release strongly inhibited by DA d2 receptors. Over stimulation of the indirect pathway/ Blocks Musurininc ACH receptors, inhibits pre-synaptic inhibition on DA nerve terminal. Parkinson’s

113
Q

Carbamazepine (tegretol)

A

Inhibition of Na= channel function. Complex partial seizures, + Tonic/Clonic - but not absence. T1/2 = 30 - 50 hrs. Side-effects:- drowsiness, dry mouth, blurred vision, anticholinergic (muscarinic). Mechanism of action is unclear, but stabilises the inactive form of the Na+ channel ↓ in repetitive firing of neurons.

114
Q

Nifedipine

A

Calcium channel blockers. Inhibit voltage sensitive calcium channels. Reduce intracellular Ca → inhibits contractility. Better side effect profile than β2 adrenergic agonists. SE: hypotension, headache, nausea, vomiting

115
Q

Sidenafil (viagra)

A

Phosphodiesterase (PDE5) inhibitor combined with Nitrates causes sustained increase in cGMP, inhibition of the MLCK due to decrease in intracellular calcium, sustained relaxation, and Hypotension to the point of impaired coronary perfusion.

116
Q

Salbutamol,

A

B2 agonist, works on vascular smooth muscle/bronchi, Gs linked, causes relaxation (hypertension). Agonists at β2 receptor. Increases cAMP and PKA → inhibits contractility
Significant maternal side effects: tachycardia (+fetal), palpitations, hypotension, pulmonary oedema, hyperglycaemia and nausea/vomiting. Use limited by side effects.

117
Q

Pioglitazone

A

Thiazlolidinecliones, Targets transcription factor PPAR-y, act on improving cells, decrease insulin resistance and reduces inflammation but increases the number of adipocytes. Has cardio vascular side effects. Diabetes type 2.

118
Q

Dapagliflozin

A

SGLT2 inhibitors, Blocks glucose reuptake from the kidney via SGLT2 so excess glucose is retained in the urine and excreted so acts to reduce blood glucose levels. Diabetes type 2.

119
Q

Simvastatin

A

Most lipophilic; thus passive diffusion to many cell types. Pro-drug ; activated in gut, ↑ 1st pass metabolism (CYP3A4). Short acting. Given at night; due to C synthesis peaking when fasting. Heart – cholesterol, patients with multiple risk factors of CVD

120
Q

Atorvastatin

A

Lipophilic, potent, high 1st pass metabolism (CYP3A4), Long plasma half life. Heart – cholesterol, patients with multiple risk factors of CVD

121
Q

Phenytoin

A

Major advance, First antiepileptic lacking significant sedative effects. Used for Partial or Tonic/ Clonic seizures (not absence). Stabilizes inactive form of Na+ channel ↓ in repetitive firing. Inhibition of Na= channel function

122
Q

Captopril or Enalapril

A

ACE inhibitors. Prevent formation of ANG2 from Ang1. Decreases ANG2 levels by inhibiting the AT1 receptor coupled production of IP3. Results in vasodilation and increased urinary Na+ and water, result in cardiac remodelling. Hypertension, heart failure, heart attack and kidney disease. Side effects include a dry cough due to the increased bradykinin levels.

123
Q

Nifedipine (Relaxation - Dihydropyridines.)

A

Calcium channel blocker - Cause relaxation by directly inhibiting Ca2+ entry through voltage gated Ca2+ channels. Vascular smooth muscle selective. Relaxtaion occurs when there is reduced phosphorylation of MLC → either by decreasing calcium entry, or activation of receptors coupled to adenylated cyclase, increase cAMP and block MLC.

124
Q

Verapamil

A

Class 4 4 (Phenylalktamins) Cardioselective - Calcium channel blocker, acts on phase 2 to block the calcium influx, therefore decreasing contraction. Cardiac smooth muscle selective. Antidysrrthymia

125
Q

Amrinone or Milrinone

A

Cardiac inotropes to treat congestive heart failure. Phosphodiesterase inhibitors. Selectively inhibit PDE3, to stop the break down of cAMP, increasing Ca2+ and therefore contraction

126
Q

Diazepam

A

Status epilepticus (SE), recurrent &/or protracted seizures of > 20 min Nerve cell death death (medical emergency). i.m. Valium (diazepam) for SE (also lorazepam). USA estimated 60,000. 1/4 million cases/year of convulsive SE ↑ GABAA-receptor-mediated inhibition, ↑ frequency of Chloride channel opening

127
Q

Metformin

A

Biguanides. Acts on the liver by activating AMP kinase, helps improve insulin sensitivity in the liver. Cheap and oral, works without having to stimulate insulin secretion. However this eventually fails due to the progressive nature of the disease. Diabetes type 2.

128
Q

Clozapine

A

Atypicaleptics – reduce unwanted side effects Resurgence of use - Side-effects include agranulocytosis (white blood cell disorder characterised by a decreased number of circulating neutrophils). Clozapine does not cause EPSs perhaps due to low D2 affinity. Perhaps Therapeutic effects caused by block of D4/D3 receptors in limbic system/cortex? (Mesolimbic/cortical DA pathway).

129
Q

Levosimedan

A

K-ATP channel activator
1.Sensitisation of cardiac muscle to Ca2+ to increase the force of contraction binds troponin C in Ca2+ dependant manner but has no effect on intracellular calcium levels.
2.Acts on K-atp channels in vascular smooth muscle to cause vasodilation
3.Partially inhibits PDE2 (Increased contraction and vasodilation)
Cardiac inotropes to treat congestive heart failure

130
Q

Duloxetine

A

Non-selective re-uptake inhibitors. Increased efficacy, decreased side effects

131
Q

nomifensine

A

A-typical antidepressants,NA/DA re-uptake inhibitor, withdrawn for safety

132
Q

L-dopa

A

L-dopa is converted to DA in surviving DA terminal in the striatum and also by dopamine neurons in the substantia nigra. Because L-dopa is broken down peripherally by dopa decarboxylase (DDC) (only 1% reaches the brain), it is generally given with a peripheral DDC inhibitor (Carbidopa). Even then only approx 5-10% of the Ldopa reaches the brain. Side-effects: postural hypotension and confusion. On-Off Phenomenon:- Abrupt and unpredictable oscillations in L-dopa efficacy AFTER 5-6 years it may lose effectiveness (causes receptor desensitization? total loss of DA cells). Drug holidays may help but unclear.

133
Q

Diclofenac (Voltaren)

A

NSAID, weak preference for COX-2 + other targets. Effective for pain relief too. (trade name Voltaren) also reduces inflammation.

134
Q

Natalizumab

A

blocks leukocyte diapedesis , by binding VLA4/VCAM. Acts antagonistically, preventing this interaction.

305 drugs (1 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions