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CPT to learn Flashcards

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1
Q

general treatment for sickness

A

ondasteron (5HT3 inhibitor)
Cylizine (H2 receptor antagonist)

dexamethasone (corticosteroid)

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2
Q

general treatment for sickness in pregnancy caused by hCG (hyperemesis gravidarum)

A

promethazine

metoclopramide

ondansetron

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3
Q
A
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4
Q

patients who use metformin need

A

good renal function

DDI

  • ACEi (drugs which impair renal function)
  • Diuretics (drugs which impair renal function)
  • NSAIDs (drugs which impair renal function)
  • Loop and thiazide like diuretics which increase glucose so can reduce metformin action
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5
Q

types of B cell lymphoma

A

Diffuse large B-cell lymphoma (DLBCL)

Follicular lymphoma

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6
Q

difference between X-rays in RA and OA

A

RA

  • reduced joint space
  • juxta artciular osteolytic lesions
  • soft tissue damage
  • deformity

OA

  • osteophytes
  • reduced joint space
  • sclerotic lesions
  • bony spurs
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7
Q

how to diagnose lupus with acronymn

A

A RASH POINTS

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8
Q

name the antiplatelet classes

A

Cyclo-oxygenase inhibitors

ADP receptor antagonists

Phosphodiesterase inhibitors

glycoprotein IIb/IIIa inhibitors

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9
Q

active form of aspirin

A

hepatic hydrolysis to salicylic acid (active form)

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10
Q
A
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11
Q

MOA of ADP receptor antagonist prasrugel

A
  • ADP receptor antagonist- inhibits binding of ADP to P2Y12 receptor
  • Inhibiting activation of GPIIb/IIIa receptors (independent of COX pathway)
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12
Q

CYP inhibitors

A

omeprazole (PPI)

ciprofloxacin (abx)

erythromycin (abx)

some SSRIs e.g. fluoxetine

grapefruit juie

amiodarone

disulfarim

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13
Q

CYP inducers

A

phenytoin

carbamazepine

rifampicin

smoking

barbituates

sulphyureas

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14
Q

Mode of action: Dipyridamole

A
  • Inhibits cellular reuptake of adenosine–> increased plasma [adenosine] –> inhibits platelet aggregation via adenosine (A2) receptors
  • Also acts as a phosphodiesterase inhibitor which prevents cAMP degradation –> inhibits expression of GP IIb/IIIa
  • inhibits activation of platelets
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15
Q

abcximab MOA

A
  • Blocks binding of fibrinogen and von Willebrand factor (vWF)Abciximab= antibody- blocks GPIIb/IIIa receptors >80% reduction in aggregation – bleeding risk
  • IV admin
  • Target final common pathway- more complete platelet aggregation
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16
Q

classes of lipid lowering drugs

A

statins

fibric acid derivatives (fibrates)

cholesterol absorption inhibitors

PCSK9 inhibitors

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17
Q

Drug-drug interaction: Fenofibrate

A

warfarin- can increase the effects - bleeding

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18
Q

Mode of action: Fenofibrate (fibric acid dervivative)

A

Activation of nuclear TF such as PPARα (peroxisome proliferation-activated receptor)

PPARα regulates expression of genes that control lipoprotein metabolism- increase production of lipoprotein lipase

  • increase TAG from lipoprotein in plasma (lipolysis)
  • increase fatty acid uptake by the liver
  • increase HDL levels
  • increase LDL affinity for receptor
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19
Q

mode of action of cholesterol absoprtion inhibitors (Ezetimibe)

A
  • inhibits NPC1L1 transporter at brush border
  • reducing absorption of cholesterol by gut by 50%
  • hepatic LDL receptor expression increase
  • decrease in total cholesterol
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20
Q

PCSK9 inhibitors mode of action

A
  1. LDLR on the liver cell surface binds to LDL and the LDLR–LDL complex is then internalized, after which the LDLR is normally recycled back to the cell surface
  2. PCSK9 binds to the LDLR on the surface of the hepatocyte, leading to the internalization and degradation of the LDLR in the lysosomes, and reducing the number of LDLRs on the cell surface.
  3. Inhibition of secreted PCSK9 by PCSK9 inhibitors therefore increases the number of available LDLRs on the cell surface and increase uptake of LDL‐C into the cell.
  4. lowering LDL in plasma
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21
Q

main hypertension medication with example drug

A

ACEi (ramipril)

ARB (losartan and candesartan)

CCB

  • dihydropyridine (nifedipine and amlodopine
  • non dihydropyridine
    • phenylalkaline (veramapil)
    • benzothiazepine (diltiazem)

Thiazide (bendroflumethiazide)and thiazide like diuretics (indapamide)

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22
Q

which antihypertensives should never be prescribed together

A

B blocker and Non-dihydropyridine CCBs

(verapamil and diltiazem- asystole!!)

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23
Q

name a drug under the drug class CA inhibitors

A

Acetazolamide

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24
Q

Diuretic delivery to renal tubule and disease: liver disease

A
  • Gut oedema- reduces absorption or oral diuretic
  • Reduced albumin- furosemide needs to be bound to albumin to be delivered to the kidneys
  • Bound to albumin so not filtered
  • Actively transported into PCT lumen via Organic Anion Transporter with albumin
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25
Q

Bartter’s syndrome

A
  • Genetic defects which cause cotransporter not to work
  • 100% blockage of the Na+/K+/2Cl- channel
  • Like giving someone extreme furosemide
  • Common symptoms include:
    • muscle weakness, cramping and spasms
    • fatigue
    • excessive thirst (polydipsia)
    • excessive urination (polyuria)
    • nocturia
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26
Q

Gitelmans syndrome

A
  • Genetic defects which cause cotransporter not to work
  • 100% blockage of Sodium chloride channel
  • Like giving extreme thiazide
  • Symptoms
    • painful muscle spasms (tetany), muscle weakness or cramping,
    • dizziness, and
    • salt craving
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27
Q

Liddles sydrome

A
  • eNac channels permanently turned on (dont need aldosterone) therefore excessive excretion of potassium and excessive reabsorption of sodium
    • hypernatremia
    • hypertension
    • symptoms
    • weakness
    • fatigue
    • palpitations
    • muscular weakness
    • shortness of breath
    • constipation/abdominal distention
    • exercise intolerance
    • long-standing hypertension could become symptomatic.
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28
Q

DDI of loop diuretic

A

aminglycosides

  • ototoxicity
  • nephrotoxicity
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29
Q

NSAIDs and protein binding

A

NSAIDs displace other protein bound drugs- increasing free drug conc of other drugsParticularly high protein bound drugs

  • MOA= competitive displacement
  • Likely dose adjustment needed and increase monitoring

e.g.

  • sulfonylureas- hypoglycaemia
  • methotrexate – accumulation and hepatotoxicity
  • warfarin- increased risk of bleeding
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30
Q

why does paracetamol have very little anti-inflammatory action

A

Related to peroxidases

Peroxide is important for the activity of paracetamol

In peripheral inflammation there is high levels of peroxidases which break down peroxide- therefore cant help with inflammation in peripheral tissue

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31
Q

renal considerations and NSAIDS

A
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32
Q

general MOA of corticosteroids

A

reduce transcription of IL-1 and IL-6

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33
Q

MOA of azathioprine

A
  1. Azathiprine is cleaved to 6-MP
  2. 6-MP is metabolised by TPMT to various molecules e.g. TIMP
  3. TIMP further metapolises to 6-MeMPN (antimetabolite)
  4. which inhibits purine synthesis
  5. DNA and RNA need purines to be made
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34
Q

Mode of action Mycophenolate mofetil

A

Inhibits inosine monophosphate dehydrogenase (required for guanosine synthesis)

Impairs B and T cell proliferation

Spares other rapidly dividing cells (due to guanosine salvage pathways in other cells)

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35
Q

what to remember with methotrexate

A

GIVEN WEEKLY

Methotrexate competitively and reversibly inhibits dihydrofolate reductase (DHFR)

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36
Q

adverse drug response Anti-TNFa

A

TB reactivation is a risk

TNFa released by macrophages in response to M TB infection

TNFa is essential for development and maintenance of granulomata

Need to screen for latent TB before anti-TNF treatment

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37
Q

rituximab depletes

A

B cells by bidning to CD20 receptor on B cells

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38
Q

Q

How is acid produced by parietal cells

A
  1. Carbonic anhydrase produces H2CO3 from water and carbon dioxide
  2. This dissociates to form HCO3- and H+
  3. H+ is pumped out of the cell on the apical membrane in exchange for potassium which comes into the cell
  4. Potassium conc of the lumen is replenished by the K+ transporter
  5. The chloride channel allows Cl- to move out of the cell into the lumen and combine with H+ à HCL
  6. Meanwhile the Cl- conc of the cell is maintained by the HCO3-/Cl- antiport on the basal membrane
  7. Influx of HCO3- into bloodstream= ALKALINE TIDE
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39
Q

confirmation of H.pylori infection

A
  • Urea breath test
    • Gastric urea= C12 isotopes (99%) and C13 isotopes= 1%
    • Pts ingest urea with enriched C13
    • H. pyrloi should convert this to ammonia and CO2
    • Can detect C13 in exhaled CO2
  • Stool antigen test
  • Endoscopy with biopsy
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40
Q

H. pylori treatment

A

One week triple therapy

PPI + two antibacterial agents

  • Lansoprazole + clarithromycin + amoxicillin OR
  • Lansoprazole + clarithromycin + metronidazole (where allergic to amoxicillin )

Some evidence of local metronidazole resistance

Compliance with full course important for effectiveness and minimise risk of bacterial resistance

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41
Q

mesalazine first line treatment for

A

UC

Release of 5-aminosalsylic acid

Topical anti-inflammatory action at the colon (enteric coated tablets limit gastric breakdown)

Mesalazine has no role in rheumatoid arthritis (no systemic effect)

Sulfasalazine has more side effects so used infrequently for UC but sulfa group good for rheumatoid arthritis

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42
Q

Adverse drug response ICS

A

If taken correctly very few significant ADRS

Local immunosuppressive action e.g. candidiasis, horse voice (in pharynx)

Wash mouth out after

Pneumonia risk at high doses

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43
Q

Mode of action B agonists

A
  • Bind to B2 receptors (GPCR)
  • Increase cAMP
  • Increase PKA
  • Cause airway smooth muscle to relax
  • Also increase mucus clearance by action of cilia
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44
Q

B agonist should alwyas be prescribed with

A

ICS

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45
Q

MOA of LTRA

A

Inhibit leukotrienes released by mast cells/eosinophils by blocking CysLT1 receptor

Reducing bronchoconstriction

Reducing mucus

Reducing oedema

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46
Q

define features of acute severe asthma

A

Unable to complete sentences

Peak flow 33-50% best or predicted

Respiratory rate ≥ 25/min

Heart rate ≥ 110/min

Plus any of the following considered life-threatening:

Peak flow < 33% best or predicted (if recordable)

Arterial oxygen saturation (SpO2) < 92%

Partial arterial pressure of oxygen (PaO2) < 8 kPa

Normal partial arterial pressure of carbon dioxide (PaCO2) (4.6–6.0 kPa)

Silent chest, Cyanosis, Poor respiratory effort, Arrhythmia, Exhaustion, Altered conscious level, Hypotension

treatment

Q

treatment of acute severe and life threatening asthma

A

Oxygen!!

Increase to 94-98%

High dose (nebulised) B2 agonist- continuous if necessary

Driven in with oxygen

Oral steroid (prednisolone) should be prescribed for minimum 5 days (IV if not oral- preferably oral)

Continuous IC alongside

Nebulised ipratropium bromide (ipratropium) – short acting muscarinic antagonist (SAMA) alongside b2 agonist if poor response alone

Ipratropium less selective for M3 receptors compared to tiotropium, M2 activity too

Consider IV aminophylline if life threatening/near fatal and no success with above

Caution with taking PO theophylline

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47
Q

how do sodium channel blockers work in epilepsy

A
  • Blocking of Na channels in central neurones
  • This slows recovery of neurones from inactive to closed state
  • Reduces neuronal transmission
48
Q

Adverse drug response of Phenytoin

A

Exhibit zero order kinetics- care when adjusting doses

  • Bone marrow suppression
  • Hypotension
  • Arrythmias (IV use)
49
Q

levetiracetam

A

Option for focal seizures and generalised seizures

Anecdotally being used more frequently, easy dosing and well tolerated

Safe in pregnancy

MOA

  • Novel mechanism of action
  • Synaptic vesicle glycoprotein binder.
  • Stops the release of neurotransmitters into synapse and reduces neuronal activity
50
Q

inhibitors vs inducers

A
51
Q

safest anti-epileptic for women of childbearing age

A

Lamotrigine and particularly Levetiracetam are the safest

52
Q

what converts L-DOPA to dopamine

A

dopamine decarboxylase

53
Q

parkinsons treatment

A

levodopa (LDOPA)

dopamine receptor agonists

MAOI type B inhibitors

COMT inhibitors

anticholinergics

54
Q

LDOPA given with

A

peripheral DOPA decarboxylase inhibitor e.g. carbidopa or benserazide

–> prevents conversion of L-DOPA to dopamine in the periphery= unpleasant side effects

55
Q

dopamine is broken down by

A

COMT and MAOb

56
Q

treatment with LDOPA requires

A

there to be enough substantia nigra cells left to convert LDOPA to dopamine

57
Q

DDI LDOPA

A

Pyridoxine (vitamin B6) increases peripheral breakdown of L-DOPA

MAOIs risk hypertensive crisis

(not MOABIs at normal dose-lose specificity at high dose)

Many antipsychotic drugs block dopamine receptors and parkinsonism is a side effect (newer, ‘atypical’ antipsychotics less so)

58
Q

name a dopamine receptor agonist

A

rotigone

59
Q

name a MAOb inhibitor

A

selegiline

Inhibits monoamine oxidase B to decrease metabolism of dopamine and therefore increase amount found in synaptic cleft

prolong effect of LDOPA

60
Q

COMT inhibitors

A

entacapone

No therapeutic effect alone (can use combination tablets COMT inhibitors and L-DOPA and peripheral dopa decarboxylase inhibitor- e.g. carbidopa

Sinemet (carbidopa-levodopa) and Stalevo (carbidopa, levodopa, and entacapone)

61
Q

Drugs affecting neuromuscular transmission – exacerbate myasthenia gravis

A

Aminoglycosides

Beta-blockers, CCBs, quinidine, procainamide

ACE inhibitors

62
Q

pharmacokinetics of Nitrofurantoin

A

Up to 50% of an oral dose Nitrofurantoin is excreted in the urine in unchanged form

This allows Nitrofurantoin to concentrate within urine, leading to more effective levels within the bladder than in other tissue compartments

This makes it one of the first-line agents in treating Urinary Tract Infections

63
Q

quinolones e.g. cipro target

A

DNA gyrase (topoisomerase II)

64
Q

side effects of quinolones

A

Tendinitis +/- rupture

Aortic dissection

Central nervous system effects (inc. Convulsions)

65
Q

trimethoprim targets

A

folate synthesis ( inhibitor of dihydrofolate reductase,)

66
Q

outline how opioid GPCR receptors decrease pai felt

A
  • Agonist (opioid) binds to GPCR e.g. MOP receptor
  • Leads to decrease in cAMP
  • Efflux of potassium
  • Hyperpolarisation of membrane
  • Decreases substance P and GABA release
  • Increases dopamine release
  • Reveal Answer
67
Q

Compared to morphine…fentanyl is

A

100x potency

Higher affinity for U (MOP) receptor

Less histamine release, sedation and constipation

68
Q

Q

Contraindication buprenorphine

A

A

Hepatitis

Liver problems

Alcohol intoxication

Biliary and gall bladder problems

Drug-drug interactions (many) buprenorphine

  • amiodarone
  • amplodopine
69
Q

Mode of action naloxone

A

Competitive antagonism of opioid – MU or MOP receptor

Blocks effect of other opioids e.g. morphine

Therefore increase in cAMP, increase pain, less of a high

Reveal Answer

70
Q

opiod tolerance

A
  1. phosphorylation and ucnoupling (think arrestin bidnin to U receptor due to chronic phosphorylation- GPCR unbinds)
    • reduced decrease in cAMP
  2. cAMP production
    • when opioid stopped massive rebound of cAMP- withdrawal symptoms
71
Q

factor Xa activates

A

prothrombin (II)–> thrombin (IIa)

72
Q

thrombin actiates

A

fibrinogen to fibrin —> fibrin clot

fibrin clot interacts with platelets

73
Q

name some low molecular weight heparins (LMWH)

A

dalteparin, enoxaparin, fondaparinux

74
Q

unfractionated heparin vs LMWH

A

both large negatively charged drugs which have poor GI absorption

  • IV or Sc
75
Q

Heparin induce thrombocytopenia (HIT)

A

Autoimmune response 2-14 days after initiation of heparin

  • Antibodies to heparin platelet factor 4 complex produced
  • Depletion of platelets
  • but paradoxically can lead to thrombosis as more platelets activated by damaged endothelium
76
Q

Heparin monitoring and reversal

A
  • (activated) partial thomboplastin time (aPTT) when using therapeutic i.v. doses of UFH required – dose titrated/adjusted against this value
  • LMWH much more predictable in its action so normally requires little monitoring
77
Q

heparin reversal

A

Protamine sulphate forms inactive complex with heparin – given i.v. dissociates heparin from ATIII, irreversible binding amount given guided by heparin dose

Paradoxically can cause bleeding!?

Much greater effect with UFH than LMWH, no affect on fondaparinux

78
Q

warfarin vs heparin

A
  • Generally used in longer term anticoagulation compared to heparins
  • Slow onset of action likely to require heparin cover (see later slides) if anticoagulation needed immediately
  • Good GI absorption and taken orally ~95+% bioavailability
79
Q

hepatic synthesis of which clotting factors requires vitamin K

A

clotting factors II, VII, IX and X (2,7, 9 and 10) requires vitamin K as cofactor for activation

warfarin is a vitamin K epoxide reductase inhibitor

80
Q

can heparin or warfarin be used in pregnancy

A

heparin- yes

warfarin - no passes placenta

81
Q

drug drug interaction warfarin

A
  • Vitamin K intake e.g. fluctuating amount of green vegetable e.g. broccoli, cucumber
  • Changes to gut bacteria e.g. cephalosporin antibiotic (reduces vitamin K)
  • Alcohol
  • Inhibition of CYP29C9 e.g. clopidogrel, alcohol, amiodarone
    • Likely increase INR (more anticoagulated)
  • Accelerated warfarin metabolism by inducers e.g. barbiturates, phenytoin, rifampicin, St Johns Wort
    • Decrease INR- less anticoagulation
82
Q

INR -international normalised ratio

A
  • Factor VII most sensitive to vitamin K deficiency so used in prothrombin time - standardised against control plasma
  • clotting time against a standard
  • Allows for standard corrected value comparable across all laboratories

aiming for an INR of 2.5

DVT

PE

AF

83
Q

aiming for an INR of 3.0 - 3.5

A

Recurrent DVT or PE in patients currently receiving anticoagulation

higher INR= more anticoagulated e..g takes 3.5x longer than average to clot

84
Q

DOAC admin

A

oral

85
Q

name three alkylating agent

A
  • Carmustine (BCNU)

Alkylating compounds under the class Platinum compounds:

  • Cisplatin
  • Oxaliplatin
86
Q

name 2 spinal poisons

A

A

Vinca alkaloids

Taxanes

87
Q

name 2 antimetabolites

A

methotrexate

5-flourouracil

88
Q

MOA of 5-fluorouracil

A
  • 5-FU is converted to fluorodeoxyuridine monophosphate (FdUMP)
  • FdUMP forms a stable complex with thymidylate synthase (TS), and thus inhibits deoxythymidine mono-phosphate (dTMP) production.
  • dTMP is essential for DNA replication and repair and its depletion therefore causes cytotoxicity
89
Q

methotrexate MOA

A
  1. methotrexate competitively inhibits dihydrofolate reductase (DHFR), an enzyme that participates in the tetrahydrofolate synthesis.
  2. The affinity of methotrexate for DHFR is about 1000-fold that of folate. DHFR catalyses the conversion of dihydrofolate to the active tetrahydrofolate.
  3. Folic acid is needed for the de novo synthesis of the nucleoside thymidine, required for DNA synthesis.
  4. Also, folate is essential for purine and pyrimidine base biosynthesis, so synthesis will be inhibited.
  5. Methotrexate, therefore, inhibits the synthesis of DNA, RNA, thymidylates, and proteins
90
Q

The fractional kill hypothesis states

A

that a defined chemotherapy concentration, applied for a defined time period, will kill a constant fraction of the cells in a population, independent of the absolute number of cells

91
Q

chemotherapy adverse reactions

A
92
Q

Q

Drug-drug interaction of COCP

A
  • Oral contraceptive efficacy is reduced by enzyme (CYP450) inducing drugs- increasing the production of CYP450- therefore reduced plasma drug
    • Antiepileptics such as carbamazepine or phenytoin
    • Antibiotics e.g. rifampicin and rifabutin
    • St Johns Wort
  • Soya protein products enhance oestrogen absorption and reduce its storage in adipose and muscle so reduce half-life from 15 to 7 hours
93
Q

menopause results in

A

high FSH

94
Q

name a hormone replacement therapy

A

medroxyprogesterone acetate

95
Q

adverse effects of POP

A

Spontaneous fetal abortion

Ectopic pregnancy

Headache

Breast tenderness

GI issues

96
Q

bisphosphonates e.g. alendronic acid absopriton

A

must be taken on an empty stomach- absorption effected by contents of stomach

MOA

  • Reduce bone turnover by reducing osteoclast activity
97
Q

ADR of bisphosphonates

A
  • Upper GI effects
    • Oesophagitis (must stay seated or standing 30 mins after taking)
  • Hypocalcaemia
    • Check calcium and Vit D levels prior to initiating treatment
98
Q

name a drug under the class of RU486

A

Mifepristone- abortion

Progesterone and glucocorticoid receptor antagonist

Therefore = anti-progesterone

  • Sensitising the myometrium to prostaglandin- induced contractions
99
Q

examples of drugs under the class SERM- selective oestrogen receptor modulator

A

Tamoxifen (breast cancer), Clomiphene (anovulation)

100
Q

clomiphene MOA

A

Competes with oestrogen for ER binding

Leads to ovulation induction through increased production of anterior pituitary hormones (LH)

101
Q

tamoxifen

A

Acts as a SERMconverse effects in breast and endometrial tissue

in endometrium = ER agonist

in breast = ER antagonist

cell cycle arrest

102
Q

name a drug under the class Selective progesterone receptors modulators

A

Ulipristal acetate (e.g. ellaOne) - emergency contraception

103
Q

define confounding factor

A
104
Q

aim of placebo effect

A

Cancel out any placebo effect that may exist in the active treatment

105
Q

Cytochrome P450 (CYPs)

A

Oxidation reaction most important

Found abundantly in smooth ER in hepatocytes

Numerous genes that encode these enzymes, CYP families 1-4 deals with most reaction

106
Q

hydrophobic same as

A

lipophillic

107
Q

to be eliminated drugs must be

A

hydrophillic

therefore hydrophobic drugs must be made more ionic by CYP450

108
Q

age/hepatic disease and CYP

A

reduce activity of CYP- higher conc in blood

109
Q

example of self induced metabolism of CYP

A

E.g. carbamazepine induces CYP3A4 and is also a substrate for CYP3A4

–> reduce conc of carbamazepine

110
Q

CYP 2D6

A

(substrates inc B-blockers, many SSRs and some opioids)

Missing in 7% of Caucasians

  • Drug toxicity
  • Cant metabolise drug
  • Hyperactive in 30% east Africans
  • Hard to get to therapeutic level of drugs
  • E.g. wont feel effect of opioids

CYP 2D6 also inhibited by SSRIs, other antiarrhythmic agents and other antidepressants

111
Q

ecretion of drugs

A

low weight- kidneys (OAT)

high molecular weight- liver - conjugated with glucoronic acid- excreted in faeces

112
Q

loading dose equation

A
113
Q

steady state

A
114
Q

A new antiepileptic drug GSK7890 is undergoing phase II clinical trials. The average Vd has been reported as 70L and the overall clearance was 35 ml min-1 .

12) What is the t1/2 in hours for this new drug?

A

convert 35ml to 0.0351

0693 x 70/0.0351= 1,386

in hours

1,386/60= 23 hours

115
Q

If clearance remains unchanged during the course of long term treatment and 10mg of drug is eliminated per day, what daily dose is required?

A

10mg of drug/day

clearance= administration

ESA1-4 revision sessions (17 decks)

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