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Phase I MD > Pharmacology > Flashcards

Pharmacology Flashcards

1
Q 
B-Blockers
E.g.
Used For:
MOA:
SE:
A

B1 adrenoreceptor antagonists

E.g. ‘-olols’ Propranolol (nonselective), atenolol (selective)

Used For: Angina, MI, HTN, Hyperthyroidism

MOA: Inhibit binding of Noradrenaline

SE: cold extremities, impotence, vivid dreams, fatigue

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2
Q 
SAMAs/LAMAs
E.g.
Used For:
MOA:
SE:
A

E.g. Ipatropium (SAMA) Tiotropium (LAMA)

Used For: Management of COPD > Management of Asthma

MOA: Antagonise muscarinic receptors on bronchial smooth muscle to prevent bronchoconstriction via cholonergic tone

SE: dry mouth, throat tickle

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3
Q 
SABA/LABA
E.g.
Used For:
MOA:
SE:
A

E.g. Salbutamol (SABA) Sameterol (LABA)

Used For: Treatment of Asthma, COPD

MOA: Stimulation of B2 adrenoreceptors on bronchial smooth muscle —> bronchodilation

SE: Tachycardia due to nonspecific B1 agonist, tremor, palpitations

  • Increasing use of SABA or daily use indicates worsening of asthma and requires prompt review
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4
Q 
Ca2+ Channel Blockers
E.g.
Used For:
MOA:
SE:
A

E.g. Verapamil

Used for: HTN, MI, COPD

MOA:

  • blocks Ca2+ entry to L-type Ca2+ channels therefore decreasing contractility (negative ionotropic/chronotropic effects)
  • Reduce arteriolar resistance in coronary arteries

SE: peripheral oedema, headaches, constipation

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5
Q 
Inhaled Oral Corticosteriods
E.g.
Used For:
MOA:
SE:
A

E.g. Fluticasone

Used For: Treatment of asthma, COPD

MOA: Preventative Treatment —> Reduce airway inflammation and bronchial hyper-reactivity

  • do so by preventing synthesis of chemokines by blocking Phospholipase A2 and inhibiting the action of cyclooxygenase
  • Reduce freq and severity of exacerbations

SE: oropharyngeal candidiasis, bruising

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6
Q 
Xanthines
E.g.
Used For:
MOA:
SE:
A

-

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7
Q 
PPIs
E.g.
Used For:
MOA:
SE:
A

E.g. Omeprazole

Used For: GORD, Zollinger Ellison Syndrome?

MOA: Irreversibly bind the parietal cell apical K+/H+ ATPase to prevent secretion of acid into the stomach

SE: Headache, nausea, vomiting

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8
Q 
H2 Antagonists
E.g.
Used For:
MOA:
SE:
A

E.g. Cimetidine

Used For: GORD

MOA: Competitively blocks H2-receptors on basal parietal cells reducing paracrine stimulation from ECF cells and gastric acid secretion

SE: Hypotension

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9
Q

Treatment for Hypothyroidism
Name:
MOA:
SE:

A

Name: Thyroxine

MOA:

  • Acts as exogenous T4
  • Long half life
  • Drug of choice for primary and secondary hypothyroidism

SE: similar to hyperthyroidism –> nausea, vomiting, gastric discomfort, anxiety

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10
Q 
Loop Diuretics
E.g.
Used For:
MOA:
SE:
A

-

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11
Q 
Thiazides
E.g.
Used For:
MOA:
SE:
A

Diuretic

E.g. hydrochlorothiazide

Used for: HTN

MOA: Inhibit the action of the Na+/Cl- co transporter in the proximal Distal Convoluted tubule –> decrease solute reabsorption therefore water reabsorption –> decrease blood volume

SE: Dizziness, electrolyte disturbances (Hypokalaemia, metabolic alkalosis, orthostatic hypotension

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12
Q

Oral Combined Contraceptive Pill
Used For:
MOA:
SE:

A

-

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13
Q

HRT
Used For:
MOA:
SE:

A

-

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14
Q 
ARBs
E.g.
Used For:
MOA:
SE:
A

ARBs

E.g. ‘sartans’ Valsartan

Used For: Alternative for ACEi, HTN, Diabetes

MOA: Block Angiotensin Receptor II Class I receptors to prevent vasoconstriction via Ang II

SE: Less incidence of cough

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15
Q

Therapy for TB

A

RIPE:

- Rifampicin, isonizid, pyrazinaminde, ethambutol

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16
Q

Triple Whammy
What Drugs
MOA

A

Combination of ACEi or ARB, Diuretic + NSIAD

MOA:
- NSAID inhibit COX –> inhibition of conversion of Arachodonic acid to Thromboxane A2 and Prostaglandins —> Inhibit afferent arteriole dilation —> decreased GFR

  • ACEi/ARB —> inhibit efferent arterial constriction —> decreased GFR
  • Diuretics: decrease blood volume –> decreases renal blood flow
  • Overall –> depress kidney function —> acute renal failure
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17
Q 
A2 agonist
E.g.
Used For:
MOA:
SE:
A

E.g. Clonidine, methyldopa

Used for: HTN, Pre-eclampsia (ACEi contraindicated)

MOA: centrally acting - inhibits the release of catecholamines by reducing sympathetic tone to the adrenal medulla

SE: sedation, dizziness, headaches, headache

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18
Q

Sulfonylureas
Used For:
MOA:
SE:

A

Used For: Treatment of Type II DM where ptx still has insulin production

MOA: Inhibits the B-cell Na+/K+ ATPase, increases the resting membrane potential of the B-cell and decreases the stimulation required to elicit insulin secretion

SE: hypoglycaemia

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19
Q 
Sulphonamides
E.g.
Used For:
MOA:
SE:
A

E.g. Sulfilmethazole

Used For: Bacterial Infection

MOA: Inhibit folate production essential for bacterial growth

SE: nausea, vomiting, diarrhoea

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20
Q 
Aminoglycosides
E.g.
Used For:
MOA:
SE:
A

E.g. Gentamicin

Used For: Bacterial Infection

MOA: Irreversibly bind to 30S ribosomal subunit causing cell membrane damage

SE: Nephrotoxic, ototoxic

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21
Q 
Biguanides
E.g.
Used For:
MOA:
SE:
A

E.g. Metformin

Used For: Diabetes Mellitus

MOA: decrease carbohydrate absorbtion in the GIT, decrease hepatic output of glucose

SE: diarrhoea, weight loss

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22
Q 
B-Lactams
E.g.
Used For:
MOA:
SE:
A

Penicillins
E.g. amoxicillin, ampicillin, flucloxacillin

Used For: Treatment of bacterial infection

MOA:

  • Interfere with bacterial wall peptidoglycan synthesis
  • bactericidal –> lead to cell death

SE:

  • Diarrhoea
  • Nausea
  • allergy
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23
Q 
Spirinolactone
E.g.
Used For:
MOA:
SE:
A

Used for: Hyperaldosteronism (Conns Syndrome)

MOA: Inhibits binding of Aldosterone to principal cells of the DCT and CD —> Inhibits Na+ reabsorbtion from Na+ channel and activity of the Na/K ATPase. Results in secondary decrease in K secretion

SE: Hyperkalaemia

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24
Q

Asprin
Used For:
MOA:
SE:

A

-

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25
Q

Clopidogrel
Used For:
MOA:
SE:

A

Used for: antiplatelet therapy

MOA: Binds ADP receptor on platelet to prevent aggregation

SE: Increased risk of bleeding

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26
Q

Warfarin
Used For:
MOA:
SE:

A

Anticoagulant

Used for: HTN, Angina

MOA: Inhibits metabolism of vitamin K and therefore long term synthesis of Vitamin K dependant clotting factors (2,7,9,10)

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27
Q

Heparin
Used For:
MOA:
SE:

A

Anticoagulant therapy
MOA: inhibit formation of Xa
Se: bleeding

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28
Q

Progesterone only Contraceptive Pill
Used For:
MOA:
SE:

A

Used For: Contraception, Pre-HRT

MOA: Negative feedback of GnRH, FSH, LH —> inhibit ovulation

SE: weight gain

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29
Q

Insulin
Used For:
MOA:
SE:

A

-

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30
Q

Management of Incontinence
Drugs Used:
MOA:
SE:

A

-

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31
Q 
Streptokinase
Drug class:
Used For:
MOA:
SE:
A

-

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32
Q

Management of Cholesterol / Cholesterol Lowering:
Drug
MOA

A

HMG CoA Reductase Inhibitors - Statins

E.g. Atorvastatin

MOA: Prevents synthesis of endogenous Cholesterol production by blocking HMG-CoA reductase (rate limiting step in Endogenous Cholesterol Production)

SE: Myalgia

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33
Q

Digoxin
Used For:
MOA:
SE:

A

-

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34
Q 
Leukotriene Receptor Antagonist
E.g.
Used For:
MOA:
SE:
A

E.g. Moteleukast

Used for: Prevention of asthma exacerbation

MOA: Antagonise Leukotriene receptors to prevent leukotriene mediated bronchoconstriction

SE: hyperactivity, behavioural changes, headache, abdo pain

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35
Q

Nitrates (Sublingual glyceral trinitrates)
Used For:
MOA:
SE:

A

Used For: Angina, MI

MOA:
Dilation of venules and arteries:
Metabolised to NO —> binds to 2nd messenger system —> Increase cGMP —> relaxation of SM

Effect: venule dilation: decrease preload, decrease cardiac work

arteriole dilation: decrease afterload and increase blood flow to coronary arteries

SE:

- Headache
- Postural Hypotension
36
Q

Fibrinolytics
Used For:
MOA:
SE:

A

Used for: MI, Stroke, PE

MOA: Convert plasminogen to plasmin which then breaks down fibrin

SE/Contraindications: Risk of bleeding, Contraindicated in Pregnancy

37
Q 
ACE inhibitors
E.g. 
Used For:
MOA:
SE:
A

E.g. ‘-prils’ Captopril, Perindopril

Used For: 1st line CKD, Diabetes, CHR, Angina, HTN,

MOA: Inhibits Conversion of Ang I to active Ang II

  • Decreases constriction of kidney eff arteriole
  • Decreases systemic vasoconstriction –> decrease TPR —> decrease MAP
  • Decrease Aldosterone —> decrease Na+ reabsorption in Kidneys —> decrease Blood volume

SE: Cough due to inhibition of ACE preventing breakdown of bradykinin in the lungs

38
Q 
a1 adrenoreceptor Blockers 
E.g. 
Used For:
MOA:
SE:
A

E.g. prazosin

Used for: HTN

MOA: Weak diuretic
- Arterial and venous dilation due to blockage of a1 adrenoreceptors on vascular SM

SE: Orthorstatic hypotension, dizziness, weakness

39
Q 
Loop Diuretic
E.g. 
Used For:
MOA:
SE:
A

E.g. Furosemide

Used for: Diabetes, HTN,

MOA:

  • Inhibit the Na+/K+/2Cl- transporter
  • Inhibits K+ Na+ and Cl- movement into the blood
  • Inhibits H2O following down its osmotic gradient

SE:

  • hypokalaemia
  • metabolic alkalosis due to H loss
  • depletion of Ca2+ and Mg2+
  • hypotension
40
Q 
Potassium Sparing Diuretics
E.g. 
Used For:
MOA:
SE:
A

E.g. Amiloride

Used for:

MOA: Weak diuretic

  • inhibit sodium reabsorbtion in DCT by blocking Na+ channels
  • Reduce urinary K+ exchange

SE:

  • Hyperkalaemia, hyponatraemia, hypochloraemia
  • Weakness, headache
  • nausea, vomiting
41
Q

Treatment for Hyperthyroidism

  • 2 Drug Names
  • 2 MOA
  • SEs
A

Drug 1: Carbimazole
- MOA: Inhibition of thyroperoxidase (Iodide –> Iodine conversion)

Drug 2: Polythyrouracil
MOA: At high doses inhibits deiodinase for conversion of T4 to active T3

  • SE: Itching, rash, nausea, vomiting, gastric discomfort
42
Q 
Cephalosporins
E.g.
Used For:
MOA:
SE:
A

E.g. Cephalexin

Used For: Treatment of bacterial infection

MOA: interfere with bacterial cell wall peptidoglycan synthesis leading to cell death (bacteriocidal)

SE:
- Diarrhoea, nausea, vomiting

43
Q 
Glycopeptides
E.g.
Used For:
MOA:
SE:
A

E.g. Vancomycin

Used For: Bacterial infection

MOA: Prevent formation of glycoprotein polymers

SE: Nephrotoxic

44
Q 
Tetracyclines
E.g.
Used For:
MOA:
SE:
A

E.g. Doxycycline

Used For: Bacterial Infection

MOA: Bacteriostatic, inhibit bacterial protein synthesis by reversibly binding to 30S subunit

SE: nausea, vomiting, diarrhoea

45
Q

Outline which diuretics cause hypokalaemia, which cause hyperkalaemia?

A

-

46
Q

Outline which bacterial classes inhibit the following

  • Bacterial cell wall
  • Protein synthesis
  • Bacterial metabolism
  • Bacterial DNA synthesis
A
  • Bacterial cell wall: Penicillins, B-Lactams, Glycopeptides
  • Protein synthesis: Tetracycline, Macrolides
  • Bacterial metabolism: Sulfonamides
  • Bacterial DNA synthesis: Quinolones
47
Q 
Macrolides
E.g.
Used For:
MOA:
SE:
A

E.g. Clarythromycin

Used For: Bacterial infection

MOA: Bacteriostatic, bind to 50S subunit of ribosome to inhibit protein synthesis

SE: Nausea, vomiting, diarrhoea

48
Q

Which Antibiotics are Bacteriocidal? Which are bacteriostatic?

A

Bacteriocidal: Quinolones, Penicillins, Glycopeptides
Bacteriostatic: Sulfonamides, Tetracyclines, Macrolides

49
Q 
Quinolones
E.g. 
Used for
MOA:
SE:
A

E.g. Ciprofloxacin

Used for: Bacterial Infection

MOA: Inhibit bacterial DNA synthesis by blocking topoisomerase

SE: Nausea, vomiting, diarrhoea

50
Q

Treatment for H. Pylori

A

Omeprazole, amoxicillin, clarithromycin

51
Q

Cromones
Used for
MOA
SE

A

Used for: add on therapy as prophylaxis for asthma, esp exercise induced. No use in COPD

MOA: Chloride channel blockers –> stabilise mast cell and prevent degranulation

SE: hard to use?

52
Q 
Anti-epileptics: Phenytoin
Class:
Used for: 
MOA
SE
A

Class: Na+ Channel Blocker

Used for: Partial and generalised seizures (not effective in absence seizures)

MOA: Bind to Na+ Channels preferably in inactive state –> prolong inactivation and preventing return to active state –> reduce the # of active sodium channels
* Bind preferentially to Na+ channels with a high firing frequency (those that occur w seizures)

SE: Nausea + vomiting, agitation, sedation, dizziness, blurred vision, vertigo
*Narrow therapeutic range + metabolised by liver therefore other drugs metabolised by liver will affect kinetics

Used as a second line treatment

53
Q 
Anti-epileptics: Carbamazapine
Class:
Used for: 
MOA
SE
A

Class: Na+ channel blockers

Used for: generalised and focal seizures

MOA: Bind to Na+ Channels preferably in inactive state –> prolong inactivation and preventing return to active state –> reduce the # of active sodium channels
* Bind preferentially to Na+ channels with a high firing frequency (those that occur w seizures)

SE: Drowsiness, ataxia, dizziness, blurred vision, diplopia, headache, rash
* Induces liver P450 enzymes –> increase metabolism of drugs metabolised by liver e.g. phenytoin

Used as first line treatment for focal seizures

54
Q 
Anti-epileptics: Lamotrigine
Class:
Used for: 
MOA
SE
A

Class: Na+ channel blockers

Used for: Generalised and focal seizures, can be used in absence seizures

MOA: Bind to Na+ Channels preferably in inactive state –> prolong inactivation and preventing return to active state –> reduce the # of active sodium channels
* Bind preferentially to Na+ channels with a high firing frequency (those that occur w seizures)

SE: Diplopia, blurred vision, dizziness, ataxia, headache, somnolence, hyperkinesia, nausea, vomiting, severe skin rashes (Steven-Johnsons Syndrome) occurs in 0.8% of children and 0.3% adults

  • newer drug, wider therapeutic index
55
Q 
Anti-epileptics: Valproate
Class:
Used for: 
MOA
SE
A

Class: Na+ channel blocker; weak inhibitor of GABA transaminase

Used for: Infantile seizures, adolescent seizures, absence seizures (1st line), myoclonic + tonic clonic (1st line)
*particularly useful due to lack of sedative properties

MOA:

  • Bind to Na+ Channels preferably in inactive state –> prolong inactivation and preventing return to active state –> reduce the # of active sodium channels
  • Bind preferentially to Na+ channels with a high firing frequency (those that occur w seizures)
  • Weak inhibitor of GABA transaminase –> increase GABA levels

SE: teratogenic, Nausea, vomiting, increased appetite, weight gain, tremor

56
Q 
Anti-epileptics: Ethosuximide
Class:
Used for: 
MOA
SE
A

Class: T-type Ca2+ channel inhibitor

Used for: absence seizures

MOA: Blocks T-type calcium channels pacemaker current that underlies the thalamic rhythm in spikes & waves seen in absence seizures

SE: Anorexia, nausea, vomiting, epigastric pain, weight loss, hiccup, drowsiness, dizziness, ataxia, headache, euphoria

57
Q 
Anti-epileptics: Gabapentin/Pregabalin
Class:
Used for: 
MOA
SE
A

Class: Voltage gated T type Ca2+ channel blocker

Used for: Partial seizures

MOA: Blocks voltage-gated calcium channels Ca2+ entry into neurons inhibit neurotransmitter (including glutamate & substance P) release
**Structurally similar to GABA but do not affect GABA levels

SE: sedation, fatigue, dizziness, drowsiness, confusion

58
Q 
Anti-epileptics: Benzodiazapenes
Class:
Used for: 
MOA
SE
A

Class: GABA receptor agonist

Used for: 2nd line in generalised, focal and absence seizures, status epilepticus

MOA: Bind to GABAa receptors, prolong frequency of opening –> influx of Cl- —> hyper-polarises cell and prolongs effect of GABA

SE: drowsiness, sedation, confusion, lightheadedness
* typically not used in continuous treatment bc tolerance develops after 6mo

59
Q 
Anti-epileptics: Phenobarbitol
Class:
Used for: 
MOA
SE
A

Class: GABA receptor agonist

Used for: 2nd line for generalised, focal and absence seizures

MOA: Bind to GABAa receptors, prolong duration of opening –> influx of Cl- —> hyper-polarises cell and prolongs effect of GABA

SE: Sedation, confusion, depression, cognitive impairment, altered mood and behaviour

60
Q 
Anti-epileptics: Vigabatrin + Valproate
Class:
Used for: 
MOA
SE
A

Class: GABA transaminase inhibitor

Used for: 2nd line generalised, focal and absence seizures (Valproate 1st line for absence, myoclonic and tonic clonic)

MOA: Inhibit GABA transaminase metabolism of GABA GABA

SE: Visual field defect in 20-40%, diplopia, fatigue, sedation

61
Q 
Anti-epileptics: Topiramate
Class:
Used for: 
MOA
SE
A

Class: Glutamate receptor agonists

Used for: 2nd line generalised and focal seizures

MOA: blocks glutaminergic receptors (NMDA/AMPA receptors) —> decrease release of glutamate —> decrease excitation of neurons

SE: sedation?

62
Q

Bisphosphonates
Used for:
MOA:
Se:

A

Bisphosphonates
Used for: Osteoporosis
MOA: inhibit osteoclasts
Se: oesophagitis, osteonecrosis of the jaw, must be given before breakfast sitting up

63
Q

Explain how estrogen therapy is used for the treatment of osteoporosis? What are some drawbacks of estrogen therapy

A

Oestrogen upregulates the expression of OPG which binds RANK-L preventing activation of osteoclasts, oestrogen also modulates the expression of cytokines such as IL-1, IL-6, TNFa which stimulate osteoblasts to activate osteoclasts, and downregulates M-CSF

Drawbacks: not recommended for use 5 years post menopause due to increased breast ca risk, increases blood coaguability

64
Q

Denosumab
Used for:
MOA:
Se:

A

Denosumab
Used for: Osteoporosis
MOA: monoclonal antibody that binds RANKL similar to OPG, inhibits osteoclast function and survival
SE: fatigue, headache

65
Q 
SERMS
e.g.
Used for:
MOA:
SE
A 
Selective estrogen receptor modulators
E.g. raloxifene
Used for: Osteoporosis
MOA: acts as a estrogen receptor agonist at the bone osteoblasts but as an antagonist at the mammary gland, therefore decreases risk of both osteoporosis and breast cancer
SE: increased risk thromboembolism
66
Q

Calcitriol
Used for:
MOA:
SE:

A

Calcitriol
Used for: osteoporosis esp in CKD patients where final conversion to active vit D by 1a hydroxylase cannot be achieved
MOA: Vit D is synthesised from the skin from cholesterol in the presence of UV light, it is then hydroxylated in the liver and finally in the kidneys by 1ahydroxylase to its active form. Vit D acts at the intestine to increase Ca2+ absorption by generating the synthesis of calcibindin an IC protein that binds 4 Ca2+ ions, it also acts in the kidneys to increase HPO4 reabsorbtion and Ca2+ absorbtion, and in bone to lead to resorption and reformation

67
Q 
DMARDs: Antimalarials
E.g.
Used for:
MOA:
SE:
A

E.g. Hydroxychloroquine
Used for: RA, SLE
MOA: anti-inflammatory, immunosuppressive, interefere T cell proliferation, IL production
SE: corneal opacity (require yearly eye check), rash, dermatitis

TAKE 3MO BEFORE ONSET

Others: Sulfalazine, Lefolimide
SE: sulfalazine myelosuppression, leflunomide teretogenic

68
Q

DMARDS: Methotrexate
Used for:
MOA:
SE:

A

Used for: RA, Chemotherapy for haem malignancy
MOA: Immunosuppressive, folate antagonist, reduces production of ILs
SE: N+V, stomatitis, myelosuppression, alopecia, liver toxicity,

TAKE 3MO BEFORE ONSET

69
Q

bDMARDS
E.g.
MOA
SE

A

E.g. Infliximab (cytokine production - TNFa), Rituximab (, Abatacept
MOA: inhibit TNFa (Infliximab), B-cells (Rituximab), T cells (Abatacept)
SE: myelosuppression,

GENERALLY FAST ACTING BUT ONLY USED IN CONJUNCTION WITH MTX

70
Q

Alteplase rtPA
Indication:
MOA:
SE:

A

Class: thrombolytic
Indication: Stroke re-perfusion
MOA: recombinant tissue plasminogen activator –> binds fibrin and converts plasminogen to plasmin –> clot degradation
SE: increased bleeding risk

71
Q

Antipsychotics - typical
E.g.
MOA
SE

A

E.g. Halopiridol, Chloropromazine
MOA: Inhibit D2 receptors with >80% affinity –> decrease mesolimbic pathway (positive ssx),
SE: also bind Histamine receptors (sedation), alpha receptors (hypotension), and effect the other dopaminergic pathways (tubuloinfundibular - prolactinaemia; nigrostriatal - basal ganlia - EPSE)

EPSEs may be relieved by anticholinergic co administration - e.g. cogentin

72
Q

Antipsychotics - atypical
E.g.
MOA
SE

A

E.g. Clozapine, respiridone
MOA: inhibit D2 receptors with less affinity –> decrease EPSE
SE: sedation, hyperglycaemia, cholesterol and lipid abnormalities, EPSE

EPSEs may be relieved by anticholinergic co administration - e.g. cogentin

73
Q

Antidepressants - SSRIs
E.g.
MOA
SE

A

E.g. Sertraline, Fluoxitene
MOA: inhibit 5HT reuptake from the post synaptic cleft
SE: N+V, diarrhoea, insomnia

74
Q

Antidepressants - SNRIs
E.g.
MOA
SE

A

E.g. Duloxitine
MOA: inhibit the reuptake of 5HT and NE at the post synpatic cleft
SE: N+V, hypertension

75
Q

Antidepressants - NRIs
E.g.
MOA
SE

A

E.g. Buproprion
MOA: inhibit reuptake of NE at post synaptic cleft
SE: headache, dry mouth

76
Q

Antidepressants - MAOIs
E.g.
MOA
SE

A

E.g. Phenelzine
MOA: inhibit the breakdown of monoamines by MAO-A and MAO-B
SE: interact with tyramine containing foods –> malignant hypertension (tyramine is a sympathomimetic broken down by MAOs)

77
Q 
Antidepressants - TCAs
Indications:
E.g.
MOA
SE
A

E.g. Amytriptaline
Indications: depression, tension headaches
MOA: inhibit reuptake of 5HT and NA
SE: Sedation, anticholinergic effects

78
Q

Benzodiazepines
Indications
MOA
SE:

A

Indications: management of acute psychosis, intense agitation, high risk of immediate danger, status epilepticus
MOA: increase the affinity of GABA receptors for GABA –> increase Cl- influx into the neuron –> inhibtion
SE: addictive, respiratory depression, muscle weakness

79
Q

Analgesics: Opioids
E.g.
MOA
SE

A

E.g. Morphine
MOA: act preferentially on mu receptors to provide supraspinal analgesia, inhibit Ca2+ entry and increase K+ efflux, inhibiting AC and cAMP –> inhibit pain perception
SE: arteriodilation and venodilation, sedation, gi motility + constipation, addiction

80
Q 
Muscle relaxants - Depolarising agents
Indications
E.g.
MOA
SE
A

E.g. Succinylcholine
Indications: orthopeadic surgery - allow for intubation, surgical anaesthetics for manipulation
MOA: competitive agonists for nicotinic ACh receptors - similar structure to ACh –> cause prolonged depolarisation leading to closure of the inactivation gate and prevention of further muscle APs
SE: muscle soreness, rapidly hydrolysed by plasma butrylcholinesterase
Progression: muscle fasisculations over chest –> rapid paralysis

81
Q 
Muscle relaxants - Non-depolarising
Indications
E.g.
MOA
SE
A

E.g. Rocuronium
Indications: Surgery
MOA: Competitive antagonist for Ach receptors –> prevent muscular depolarisation
Progression –> small fasiculations –> small muscle paralysis –> larger muscle paralysis –> reversal from large to small

82
Q 
Anticholinesterases
Indications
E.g.
MOA
SE
A

E.g. Neostigmine
Indications: myasthenia gravis, reversal of muscle relaxants
MOA: inhibit the breakdown of ACh in the post synaptic cleft –> increase avaliability
SE: hypotension, bradycardia, N+V

83
Q

Dantrium
Indication
MOA

A

Indication: treatment for malignant hyperthermia, severe spasticity in non ambulatory ptx
MOA: blocks the release of Ca2+ from SR

84
Q

Propofol
Indication
MOA
SE:

A

Indication: induction anaesthesia, maintainence anaesthesia, status epilepticus
MOA: binds GABAa receptors in prefrontal cortex and hippocampus
SE: amnesia (hippocampus), N+V, depression of airway reflexes, decrease in BP

85
Q

Ketamine
Indication:
MOA:
SE

A

Indication: induction/maintenance anaesthesia, neuropathic pain
MOA: NMDA receptor antagonist in thalamus and limbic system. Some analgesia
SE: sympathetic NS activation –> increase HR, BP, CO

86
Q

Tranaxemia Acid
Indications:
MOA
SE

A

Indications: surgery, bleeding disorder
MOA: inhibits the formation of plasmin therefore increasing time for fibrinolysis
SE: increased clotting propensity

Phase I MD (7 decks)

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