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STUDY FOR BARRIERS > Pharmacology 😎 > Flashcards

Pharmacology 😎 Flashcards

1
Q

Chemotherapy following surgery is

A

Adjuvant

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2
Q

Chemo prior to surgery is

A

Neoadjuvant

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3
Q

Cytotoxic chemo - 6 key features?

A

Cell kill

Kill mechanism - cell cycle specific or not

Administer cyclically

Give as combinations

Resistance

Dose intensity / toxicity

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4
Q

In a medium size tumour what percentage of cells are actively dividing?

A

5%

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5
Q

Why is chemo given in cycles?

A

Drug target and injury rapidly dividing cells but are not cancer specific (normal cells also affected)

Rest periods allow normal cells to recover and body to regain strength

Cancer don’t repair so easily

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6
Q

Why is chemo given in combination?

A

To enhance cell kill and decrease chance of resistance without additive toxicity

Use drugs active to tumour type and with different mechanisms and with non-overlapping dost-limiting toxicities and used at optimum stages

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7
Q

Resistance to chemotherapy drugs can occur due to

A

In-built protecting to toxins (genetic resistance)

Spontaneously

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8
Q

Mechanisms of cytotoxic resistance :

A 
Reduced accumulation in cells 
Decreased uptake in cell and increase intracellular breakdown
Bypass biochemical pathways 
Utilise alternative gene amplification 
Overproduction of blocked enzyme 
Rapid repair to damaged DNA
Genetic mutations
Genetic resistance
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9
Q

Main possible side effects of chemotherapy

A 
Anaemia 
Infection
Nausea and vomiting 
Neutropenia
Skin reactions 
Thrombocytopenia
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10
Q

Alkylating agents

A

Cisplatin
Interfere with DNA base pairing, leading to strand breaks and arresting replication
Attach alkyl group to guanine base
Effects manifest during S phase –> block at g2 and apoptotic cell death

Toxicity:
Myelosuppression
N&V
Haemorrhagic cysts (due to bladder fibrosis and pulmonary fibrosis )

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11
Q

Antimetabolites

A 
Gemcitabine
Methotrexate (Lower dose as dMARD) 
Either direct inhibition of enzymes needed for dna replication or repair OR incorporation of an Antimetabolite directly into dna (disrupts structure and function)
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12
Q

5-fluorouracil

A

Antimetabolite
Pyramidine antagonist

Given with folic acid

Binds to thymidylate synthetase

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13
Q

Anthracyclines

A

-rubicin
Epirubicin
Cell cycle non specific
Inhibit dna replication and therefore cell division

Inhibit Dna and rna synthesis by intercalating between base pairs

Inhibit topoisomerase II preventing relaxing of recoiled dna blocking transcription and replication

Produced reactive free radicals

Toxicity:
Cumulative cardiotoxicity
The usual

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14
Q

Antimicrotubule agents

Taxanes

A

Bind to tubulin
Interfere with microtubules
Blocks cell growth by stopping mitosis

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15
Q

P glycoprotein is

A

An inbuilt mechanism for multi-drug resistance

Responsible for decreased drug accumulation in multi drug resistant cells and often mediates the development of resistance to anticancer drugs

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16
Q

Targeted cancer therapy includes

A

Monoclonal antibodies
Small molecule drugs
Angiogenesis inhibitors
Drugs targeting apoptosis

Combines with chemo

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17
Q

Monoclonal antibodies

A

Not cytotoxic
Target on cell surface of target extra cellular components

The more mouse the more chance of hypersensitivity reaction
Premedication- antihistamine and corticosteroids

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18
Q

EGFR antagonists

A

Epidermal growth factor
Cutaneous reactions

Cancer

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19
Q

Main antiemetic options

A

Serotonin antagonists
Dopamine antagonists
NK1 blocker
Anticholinergics

Corticosteroids

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20
Q

Dopamine antagonists

A

Metaclopramide
D2 antag with 5HT3 and 5HT4 agonist activity

Central - blocks d2 in CTZ
Peripheral - blocks 5ht3 (blocks vagus nerve going to CTZ) and agnostic 5ht4 (increased gastric emptying)

AEs: extrapyrimidal symptoms, galactorrhea

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21
Q

5HT3 antagonist

A

Ondansetron
Selective
Blocks in cns and periphery
Potent

AEs: QT prolongation

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22
Q

Aprepitant

A

Oral NK-1 antagonist
Selective
Can penetrate brain - used in brain tumours

Usually combined with ondansetron/dexamethasone a steroid to help brain penetration

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23
Q

Treatment for mucositis

A 
Oral hygiene: 
Salt mouthwash
Chlorhexidine (antiseptic) 
NSAIDs (for pain and other areas)
Palifermin - recombinant human keratinocyte growth factor, binds to KGF receptor

Common in patients on 5-flurouraciln

Lignocaine - local anaesthetic to reduce pain - blocks na channels

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24
Q

Management of diarrhoea

A

Opioids - mu receptor agonists

  1. Codeine (cns and periphery )
  2. Diphenoxylate or loperamide (Imodium) - peripheral only

Somatostatin

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25
Q

Octreotide

A

Somatostatin
Octreotide acetate

Decreases GIT transit time and endogenous fluid secretion in jejunum
Stimulates intestinal absorption of water and electrolytes

Treatment of diarrhoea and radiation-induced colitis

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26
Q

G-CSF

A

Filgrastem/peg-filgrastem

Decreased risk of febrile neutropenia in myelosuppressive chemo

Autometabolised by neutrophils

AEs: bone pain
Given only in FN risk 20% or more

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27
Q

Darbopoietin alpha

A

Acts on RBCs

Indication - chronic myelosuppression post chemo

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28
Q

Treatment for recurrent oral thrush

A

Nystatin oral drops (antifungal)

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29
Q

-ciclovir

A

Aciclovir
Valaciclovir
Famciclovir

DNA polymerase inhibitors

Antivirals

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30
Q

Tumour lysis syndrome can lead to

A

Hyperuricemia

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31
Q

Treatment for hyperuricemia

A

Xanthine oxidase inhibitor - allopurinol

Urate oxidase - rasburicase (Uric acid –> allantoin

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32
Q

Anti platelet agents act on

A

Primary haemostasis

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33
Q

Anticoagulant acts on

A

Secondary haemostasis

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34
Q

Antimalarial used to prevent relapse

A

Primaquine

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35
Q

Main antimalarials

A

Chloroquine

Quinine

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36
Q

Aspirin

A

Antiplatelet
Inhibits prostaglandin
Inhibits prostacyclin and thromboxane a2 but more txa
Inhibits platelet activation and

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37
Q

Dipyridamole

A

Anti platelet

Inhibits PDE in platelets and in vessels

Vasodilation and

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38
Q

Mode of action to COC:

A

Oestrogen inhibits fsh via neg feedback –> suppresses development of ovarian follicle
Progesten inhibit release of LH –> prevent ovulation and thicken cervical mucus
Both together –> alter endometrium to discourage implantation

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39
Q

Progesten only pill acts on

A

Mainly the cervical mucus

Maybe some effect on endometrium and motility and secretions of Fallopian tube

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40
Q

Postcoital (emergency) contraception treatment with

A

Levonorgestrel
Within 72 hr
Repeated 12hr later
Or IUD - affective for up to 5 days

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41
Q

What is the dose of oestrogen needed to be effective in contraceptive pills?

A

At least 20 micrograms
No more than 50

Standard dose is 30-35

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42
Q

Contraceptive pills

Monophasic formulation?

A

Fixed dose of oestrogen and progestogen for 21 days

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43
Q

Contraceptive pill

Triphasic formulation?

A

3 phases with progesterone “step up” in phase 3

More closely mimics hormone changes during menstrual cycle
Reduce breakthrough bleeding

44
Q

Contraceptive pills

Quadriphasic formulation?

A

4 phases of oestrogen step down , progestogen step up regimen

45
Q

P2Y12 receptor blockers

A

Clopidogrel - irreversible inactivates receptor

Ticagrelor - reversible ADP receptor p2y12 inhibitor
Rapid onset action (2-4hrz)

46
Q

Glycoprotein IIb/IIIa blockers

A

Blocks platelet aggregation
Abciximab
Very expensive

47
Q

Warfarin

A

Vitamin k antagonist
Low therapeutic index but reversible with vitamin k
Target INR = 2-3
Need monitoring

Anticoagulant

48
Q

Heparins

A

Anticoagulant

Indirect thrombin inhibitors
Reversibly inhibit

Basically inactivates all factors except 13 lol

49
Q

Unfractionated vs LMW heparin

A 
LMW:
works more on factor Xa 
Doesn't inhibit platelet function
Renal elimination 
Monitoring generally not needed but Xa assay can be done which is difficult 
Unfractionated: 
Inhibits platelet function 
Equally anti Xa and IIa 
Renal and hepatic elimination
Monitored with APTT frequently 
Rapid onset and clearance
50
Q

Direct thrombin inhibitor

A

Dabigatran
Oral
No antidote
Renal elimination

51
Q

Factor Xa inhibitors

A 
Rivaroxaban
Apixaban 
Oral 
Directly factor Xa inhibitors 
Can get away with lower renal function than dabigatran and won't accumulate
52
Q

NOACs

A

Novel oral anticoagulants
Dabigatran
Rivaroxaban

53
Q

Fibrinolytic agents

A

T-PA eg alteplase
Tenecteplase

Dissolves existing thrombus
Activates plasminogen
Used when clot already formed in patient

Within 3 hrs of stroke

AEs: works too well

54
Q

Beta lactams mechanism of action

A

Penicillins and cephalosporins

Amoxicillin (+clavulanic acid)

Bactericidal

Interfere will cell wall peptidoglycan synthesis (inhibits the enzyme that cross links the peptide chains

55
Q

Penicillins

A 
Narrow spectrum: 
Active against gram +ve 
Haemophilus influenzae 
Otitis media 
Inactivated by beta lactamses produced by staphylococci 
Benzylpenicillin

Anti staphylococcal:
Methicillin
Flucloxacillin
Methicillin resistant staph aureus - resistant to all beta-lactams

Broad spectrum: 
Greater activity against gram -Ve 
E. coli, h influenzae 
Destroyed by beta lactamases producing strains 
Amoxycillin, ampicillin

Anti-pseudomonal:
Pseudomonas aeruginosa
Piperacillin, ticarcillin

56
Q

Beta lactamase inhibitors

A

Clavulanic acid
Tazobactam

Inhibit enzymes prod by staph aureus, bacteroides fragillis, and E. coli

57
Q

Cephalosporins

A

First generation:
Cephalexin
Active against penicillinase prod staph, and gram -ve s like E. coli and klebsiella (enteric rods)

Not active against some gram negative anaerobes like bacteroides fragillis and some enterobacter or pseudomonas spp

2nd generation:
Cephamandole, cefoxitin
More stable to gram neg beta lactamase a

3rd gen:
Ceftazidime, cefpirome
Cover majority of gram negative rods
Able to enter CSF

58
Q

Tetracyclines

A

Reversibly bind to 30s subunit of microbial ribosomes and blocks attachment of transfer-RNA to the A site on ribosome, prevents introduction of new amino acids to peptide chain

Doxycycline
Tetracycline

Bacteriostatic
Broad spectrum

Most commonly used in skin infections

59
Q

Amino glycosides

A

Gentamicin
Conc-related bacteriocidal effect

Inhibit protein synthesis by promoting misreading of DNA

Gram negative spectrum including pseudomonas aureginosa

Monitor for nephrotoxicity and ototoxicity

60
Q

Sulfonamides

A

Analogues of PABA
Compete for enzyme dihydropteroate synthetase (needed for folic acid synthesis in bacteria)

Bacteriostatic

Sulphamethoxazole

(Comb with trimethoprim- dihydrofolate reductase inhibitor)

61
Q

Trimethoprim

A

Folate antagonist
Bacteriostatic

Dihydrofolate reductase inhibitor

Usually:
PABA –> folate –> tetrahydrofolate and then DNA

62
Q

Quinolones

A

Ciprofloxacin
Norfloxacin

Analogues of nalidixic acid

Bactericidal
Inhibits nucleic acid synthesis
Inhibitor of DNA gyrase (coils DNA) and topoisomerase

Broad spec 
Basically - Gram negatives
Pseudomonas aureginosa 
H influenzae 
Poor activity against streptococci

AEs. Achilles tendinitis

63
Q

Macrolides

A

Erythromycin
Azithromycin
Clarithromycin

Broad spec
Gram pos and neg cocci and anaerobes but not gram negative rods

Maybe cidal or static depending on conc

Inhibits protein synthesis by binding to 50s ribosome

Nausea
(Erythromycin Resembles motilin )

64
Q

Nitroimidazoles

A

Metronidazole

Cidal
Gram negative anaerobes such as bacteroides fragillis
Protozoa
And some gram pos

Significant interaction with alcohol

65
Q

Glycopeptides

A

Vancomycin

Cidal
Inhibit cell wall synthesis

Narrow spec
Gram pos aerobic and anaerobic organisms

Used in MRSA

66
Q

Centrally acting sympatholytics (CV drugs)

A

Clonidine (presynaptic a2 agonist)
Alpha- methyldopa
(Inhibits dopa decarboxylase to decrease dopamine prod and stimulates presynaptic a2 adrenoceptors

67
Q

Beta blockers

A

Propranolol - nonselective beta 1 and 2

Metoprolol - b1 antagonist (will give less bronchoconstriction)

68
Q

Alpha1 blockers

A

Prazosin (alpha1 adrenoceptor antagonist)
–> vasoconstriction to NA

Arterial and venous dilation (decreased TPR and venous return (decreased contractility and CO and therefore, BP)

69
Q

Non selective alpha blocker causes

A

Reflex tachy

As blocking a2 stops the negative feedback loop and increases NA which acts on b1 on heart muscle as a1 (vascular smooth muscle) is also blocked

70
Q

Loop diuretics

A

Frusemide

Acts on ascending loop
Inhibit na/k/Cl carrier
Prevent transport of nacl from tubule

Potent, 4-6hrs

71
Q

Thiazide diuretics

A

Hydrochlorothiazide
Act on DCT
Inhibit na/Cl transport system

Short term - decrease plasma volume
Long term- direct vascular effects by action on K channels

Most commonly used for HT and mild heart failure

AE: can worsen diabetes (hyperglycaemia)

72
Q

Potassium sparing diuretics

A
  1. Amiloride
    Block na channels on last part of DCT and collecting tubules
    Therefore, decreased K+ excretion
  2. Spironolactone
    Same thing by antagonising aldosterone
    Can affect other steroid receptors –> menstrual disturbances

Used in comb with K losing agents

Both cause limited diuresis

73
Q

ACE inhibitors

A

Perindopril
Inhibit A2 mediated vasoconstriction and release of aldosterone

AEs: dry cough

74
Q

AT receptor blockers

A

Irbesartan
Block AT1 receptor subtype

AEs: less cough and hypotension

75
Q

Drugs to produce peripheral vasodilation

A

Calcium antagonists:
Depress contractility directly

Nitric oxide donators:
Induce dilation

76
Q

Calcium channel antagonists

A

Dihydropyridines:
Amilodipine, nifedipine
More effective on vascular muscle –>peripheral vasodilation
Indications : hypertension
AEs: flushing, headache, ankle swelling, palpitations (reflex tachy) (increased SNS activity)

Non-dihydropyridines:
Verapamil, diltiazem
More effective on heart (dilate coronary arteries, inhibit AV node conduction, reduce cardiac contractility)
Indications: angina
Contraindications: HF as can cause heart block and negative inotropy

77
Q

The 5 main classes of drugs used to treat hypertension

A 
Calcium channel blocker
Ace inhibitors 
ARBs 
Beta blockers
Diuretics

Usually start with beta blocker and thiazide diuretic
Complementary comb therapy eg ace inhibitor and diuretic

78
Q

Atropine is used in

A

Sinus bradycardia

To dilate pupils

79
Q

Adrenalin is administered in which cardiac event

A

Cardiac arrest

80
Q

Isoprenaline is used in which cardiac problem

A

Heart block

81
Q

Digoxin is used for

A

Rapid atrial fibrillation

82
Q

What do you administer for ventricular tachycardia due to hyperkalaemia

A

Calcium chloride

83
Q

What is used for VF and digoxin toxicity?

A

MgCl2/MgSO4

84
Q

Class 1 antyarrythmics

A

Na channel blockers
Reduce rate of depol during phase 0
Inhibit AP in excitable cells –> decreased conductivity and contractility
Dependent channel block (use dependence) - bind most when channels in open or refractory state

85
Q

1A antiarrythmic

A

Quinidine
Procainamide

Slow phase 0
Lenghten AP
Prolong refractory period
Prolong QT

Use: ventricular arrhythmias (eg VT)

AEs incl mild anticholinergic effects

86
Q

1B antiarrythmic

A

Lignocaine

Use dependence
Shortened depol
Decrease AP duration

Use: severe ventricular arrhythmias

Precautions - HF, bradycardia (weak inotropes)

87
Q

1C antiarrythmic

A

Flecainide

High affinity for open channel and very slow dissociation
No effect on AP duration
Reduce automacity, reduce AV conduction and contractility

AEs : QT prolongation

Negative inotrope

88
Q

Class 2 antiarrythmic

A

Beta blockers
Metoprolol, atenolol

Block catecholamines activations of beta receptors AND depress phase 4 depol of pacemaker cells

Inhibit SNS activation and cause indirect Ca2+ inhibition (on phase 2)
Decrease HR
Prolong PR interval (atrial depol)
Increase RO and prolong AP by decrease conduction through AV node

Use: prevent tachys
Eg SVT and paroxysmal AF
Provoked by SNS eg AMI and exercise

89
Q

Class 3 antiarrythmic

A

Sotalol
Amiodarone

Block K+ channel
Substantially extend AP and RP without affecting phase 0
Prolong RP and QT& PR intervals

Use: supraventricular and ventricular tachys

90
Q

Sotalol

A

Non selective beta blocker and k channel blocker

Prolongs AP and QT and RP

Use: SVT, AF, VA

Contraindications: asthma, sinus bradycardia, prolongs QT, sever HF
Accumulates in renal impairment

91
Q

Amiodarone

A

Class 1, 2, 3 and 4 effect

Prolong QT!
Long half life

Many side effects!
Incl photosensitivity, pulmonary fibrosis!, corneal deposits, N&V, blue grey discolouration of skin

92
Q

Class 4 antiarrythmic

A

Calcium channel blockers
Verepamil and diltiazem

Slow AV conduction and increase RP
Suppress premature ectopic beats

L type channels
Negative inotrope and chronotrope
Also decrease BP

Contraindications -
Bradycardia 
HF
Oedema
Constipation (verapamil) 
Headache and dizziness and fatigue

Use: predominantly for SVTs and angina but now prefer IV adenosine for acute episodes

93
Q

All antiarrythmics should be avoided in sever heart failure except

A

Amiodarone

Digoxin

94
Q

Drugs for atrial fibrillation

A

DC shock or drugs:
Use drugs that increase block at AV node

Acute -
Sotalol or amiodarone
Maintainers: beta blocker or amiodarone

Normal LVF:
Beta blockers or calcium channel blockers

LV dysfunction:
Digoxin (often ineffective) or amiodarone

95
Q

Digoxin

A

Cardiac glycoside
Narrow therapeutic range
Renal clearance
Long half life

Useful in LV dysfunction, HF

Cardiac slowing
Increase RP - reduces ventricular rate
Slowing rate of conduction through AV

96
Q

Drug therapy for SVT

A

Adenosine (slows AV conduction and also produces peripheral and coronary vasodilation) (*can precipitate bronchospasm)
If fails –> verapamil

Prevention:
Choose drug that blocks at AV node
Verapamil, digoxin, beta blocker
Sotalol, amiodarone

97
Q

NO donors

A 
Relax smooth muscles via cGMP mediated activation of PKG 
Dilate peripheral arteries and veins 
Decrease venous return 
Decrease preload and after load 
Reduce demand on heart

Short acting - glyceryl trinitrate
Activated by mitochondrial aldehyde dehydrogenase-2 at low conc

Long acting - isosorbine dinitrate or mononitrate
High concentrations –> high potency
Low potency activated by p450 enzymes

Reflex tachycardia evoked
(Stop with beta blocker?)
Tolerance and “pseudotolerance”

98
Q

Treatment for reducing CVS risk

A
  1. NO donor
  2. Aspirin/anti platelet
  3. Statins
    3.
99
Q

Adverse affects of statins

A

Myopathy:
Myalgia + increased CK

Rhabdomyolysis:
Severe muscle pain assoc with serum CK > 40 times upper limit
Rare but potentially fatal

Skin rashes

GIT: 
Cramps 
Constipation 
Diarrhoea
Heartburn

drug interactions
Warfarin
Higher incidence of myopathy with CYP inhibitors

100
Q

Fibrates

A 
Activate PPAR (peroxisome proliferator- activated receptors) (modulate carb and fat metabolism) 
Increase activity of lipoprotein lipase and decrease synthesis of apoC-III together enhance clearance of circulating TG-rich lipoproteins

Gemfibrozil or fenofibrate
Decrease TG by 40%
Increase HDL by 10-20%

AEs:
Myopathy
Increase gallstone risk and increased cholesterol in bile
Blood dyscrasias
Photosensitivity
Drug interaction (increased bleeding risk with warfarin

101
Q

Adenosine diphosphate is

A

Released from platelet dense granules and injured cells

Bing to P2Y1 (platelet aggregation) and P2Y12 (platelet activation)
Induces activation of GP2b/3a receptor and platelet aggregation
Inhibited by clopidogrel

102
Q

Acute uncomplicated UTI/cystitis

A 
Trimethoprim 3d
Cephalexin 
Amoxicillin/ clavulanic acid 
Nitrofurantoin 
5d 
Men - 7d

Pyelo - increase duration 10-14 d or frequency

If ESBL producing:
Meropenem

103
Q

Prophylaxis of recurrent UTI

A

Ph modifiers
Acidifiers- ascorbic acid (vit c) or Cranberry juice (contains proanthocyanidines (inhibit adhesion of fimbriae) and fructose)
Alkalinisers - citric acid or tartaric acid or sodium bicarbonate (relieves discomfort on urination but not prophylaxis benefit)

Continuous

Intermittent self treatment

104
Q

Urinary antiseptics

A

Require acidic urine for activity
H examine hippurate
Hexamine mandelate

105
Q

Which drugs would cover e.coli or staph sap uti ?

A

Trimethoprim

Cephalexin

STUDY FOR BARRIERS (11 decks)

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