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1 REVISION Bismillah > 4. Pharmacology - Ana Oliviera > Flashcards

4. Pharmacology - Ana Oliviera Flashcards

1
Q

Define:

  1. Pharmacokinetics

2. Pharmacodynamics

A
  1. What our body does to the drug (time course of drug from site of administration to elimination)
  2. What the drug does to our body
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2
Q

What are the 4 processes of pharmacokinetics?

A

Absorption
Distribution
Metabolism
Elimination/excretion

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3
Q

Pharmacokinetics

  1. Define absorption
  2. What factors need to be considered?
  3. Bioavailability: what is this and what is the range it is measured in?
  4. What are the 4 routes of administration?
A
  1. Process of transfer of drug from administration into general/systemic circulation
  2. Lipid solubility/disintegration/solubility/pH/molecular weight/surface area/contact time/interaction/gastric emptying rate/presence of food/alteration in intestinal motility
  3. Fraction of administered drug that reaches systemic circulation as a parent drug
    0-1
  4. Enteral
    Parenteral (IV, IM, subcutaneous)
    Mucous membrane (inhalers, sublingual, suppositories)
    Transdermal
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4
Q

Pharmacokinetics

  1. Define distribution
  2. Define volume of distribution
  3. What 2 types of drugs are mainly confined to blood and body water compartments?
  4. What 2 types of drugs are widely distributed to the tissues?
  5. What other factors effect distribution?
  6. What factors can increase the fraction of unbound drug?
A
  1. Process a compound is transferred from general circulation to other parts of body and tissues
  2. How widely a drug is distributed between various body fluids and tissues
  3. Water soluble/highly protein bound drugs
  4. Lipid soluble/extensive tissue binding drugs
  5. BBB/ plasma protein barrier
  6. Renal insufficiency/Low plasma albumin/late pregnancy
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5
Q

Pharmacokinetics

  1. Define metabolism
  2. What type of reactions are type 1 reactions?
  3. What type of reactions are type 2 reactions?
  4. What factors can affect metabolism?
A
  1. drug is chemically altered to facilitate its action or enhance its elimination
  2. Oxidation/reduction (cytochrome P450 enzymes)
  3. Conjugation/hydrolysis
  4. Race/ethnicity/age/gender/pathologies/genetics/stress/temperature/pollution/nutrition/interactions
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6
Q

Pharmacokinetics

  1. Define excretion
  2. Name 5 modes of excretion
  3. What factors effect excretion?
A
  1. Drugs/their metabolites are removed from the body
  2. Renal/biliary/respiratory/dermal/faecal
  3. Renal blood flow/renal function/glomerular filtration rate/urine flow rate and pH/concentration of drug in plasma/protein binding/size of drug complex/age
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7
Q

Pharmacokinetics

  1. What is half life?
  2. What is therapeutic drug monitoring?
A
  1. Time required to reduce plasma concentration to half its original value
  2. Individualised drug dosage by maintaining plasma or blood drug concentrations within a targeted therapeutic range.
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8
Q

Principles of medicine use in elderly
Discuss the following:
1. ADRs
2. Important aspects particular to old people

A
  1. Body changes/ Polypharmacy interactions/ compliance and concordance issues
  2. Altered physiology/ decreased homeostatic functions/ altered pharmacokinetics and pharmacodynamics/ side effects/ ADRs/ polymorbidity/ Polypharmacy/ less compliance
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9
Q

Principles of medicine use in elderly
Discuss the following:
1. Absorption
2. Distribution

A
  1. Bioavailability:
    Rate/ interactions/ surface area/ intestinal motility/ blood flow
    Swallowing difficulties
  2. Regional blood flow:
    More transport time/delayed peak concentration/ slower clearance
    Plasma protein binding:
    Less albumin levels/ less binding/ less total concentration
    Lipid solubility
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10
Q

Principles of medicine use in elderly
Discuss the following:
1. Metabolism
2. Elimination

A
  1. Less blood flow to liver=less hepatic metabolism=less clearances
    Gender/ co-morbidities/ race/ drug interactions/ frailty/ smoking/diet
  2. Renal excretion:
    Renal blood flow/ glomerular filtration rate/ urine flow rate/ pH
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11
Q

Principles of medicine use in elderly
Discuss the following:
1. Pharmacodynamics
2. Homeostatic functions

A
  1. Changes in receptor sensitivity/ receptor number/ hormone levels
  2. Less: postural control/ thermoregulation/ reserve of cognitive functions/ immune response/ response to environmental changes
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12
Q 
Principles of medicine use in elderly
Discuss the following:
1. Falls in elderly
2. Polypharmacy 
3. Compliance and concordance
A
  1. More than 4 medicines/ sedation/ hypotension/ ototoxicity/ vision disturbances
  2. Multiple diseases
    Drug interactions/ drug-disease interactions/ ADRs
  3. Poor vision/ beliefs and understanding/ impaired cognitive function/ low manual dexterity/ Polypharmacy
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13
Q

Principles of medicine use in elderly
Discuss the following:
Medication review

A 
NO TEARS
Need and indication
Open questions
Tests and monitoring
Evidence and guidelines
Adverse effects
Risk reduction/prevention
Simplifications and switches
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14
Q 
Antibiotics
Interfere with bacterial cell wall
1. Name 3 and give 2 examples of each.
2. Name 4 subtypes of one of them and give 2 examples of each
3. What is their mechanism of action?
A
  1. Beta lactams
    Glycopeptides (vancomycin and teicoplanin)
    Anti-tuberculosis drugs (pyrazinamide and ethambutol)
  2. Beta lactams:
    Penicillins (benzylpenicillin, flucloxacillin and amoxicillin)
    Carbapenems (imipenem and meropenem)
    Cephalosporins (cefadroxil and cefataroline)
    Monobactams
  3. Beta lactams: bind to and inhibit penicillin binding proteins (PBPs) = peptidoglycan cross linking effected = weakens wall = cell lysis

Glycopeptides: binds to terminal D-alanine-D alanine at the end of pentapeptide chain in growing bacterial cell wall = blocks glycosidic bonds forming = blocks formation of peptide cross links

Anti-tuberculosis drugs: interferes with cell wall of mycobacteria

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15
Q

Antibiotics
Interfere with bacterial cell wall
1. Resistance and uses for beta lactams? Caution?
2. Resistance and uses for glycopeptides? Caution?

A
  1. Beta lactams
    Beta-lactamases- hydrolyse beta lactam ring
    Carried on gene/chromosome/plasmids
    Resistance to resistor= clavulanic acid + tazobactam
    Also, dehydropeptidase is an enzyme that can degrade imipenem (a carbapenem) so you have to give it with cilastatin

Carbapenems used in serious infection resistant to other antibiotics

Caution: allergy

  1. Van A gene = inducible high level resistance to vancomycin and teicoplanin
    Van B gene = inducible high level resistance to vancomycin only

Caution: nephrotoxicity

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16
Q 
Antibiotics
Interfere with protein synthesis
1. Name the 4 and give 2 examples of each.
2. What is their mechanism of action?
3. Bacteriostatic/bactericidal? Each one
A
  1. Macrolides (erythromycin and clarithromycin)
    Tetracyclines (doxycycline and tetracyclines)
    Aminoglycosides (gentamicin and streotomycin)
    Chloramphenicol
  2. Macrolides: binds to 50s ribosome unit = blocks chain elongation

Tetracyclines: binds to 30s subunit = aminoacyl tRNA can’t enter acceptor site on ribosome = blocks chain elongation

Amino glycosides: inhibits protein synthesis in cytoplasm- binds to 30s subunit = blocks binding of formylmethionyl-tRNA to ribosome = prevents initiation complexes hence protein synthesis + misreading of mRNA codons

Chloramphenicol: binds to 50s subunit = blocks action on peptidyltransferase hence protein synthesis

Macrolides mainly bacteriostatic
Tetracyclines bacteriostatic
Aminoglycosides bactericidal
Chloramphenicol bacteriostatic

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17
Q

Antibiotics
Interfere with protein synthesis:
1. Resistance and caution for macrolides
2. Resistance and caution for tetracyclines
3. Resistance and caution for amino glycosides
4. Resistance and caution for chloramphenicol

A
  1. Macrolides
    Resistance uncommon
    Caution: interactions
  2. Tetracyclines
    Resistance: decrease in uptake or increase in extrusion/ enzymatic inactivation/ producing protein that interferes with tetracycline binding
    Caution: phototoxicity/ chelation of metal ions leading to deposition in teeth and bone growth inhibition (don’t use in children)
3. Aminoglycosides
Resistance: 1. Aminoglycoside modifying enzyme = inactivation 
2. Membrane impermeability = poor access
3. Poor action site affinity
Caution: nephrotoxicity and ototoxicity
  1. Chloramphenicol
    Resistance: chloramphenicol acetylation/ can’t bind to ribosomal target
    Caution: can effect human mitochondrial ribosomes = dose dependent toxicity to bone marrow
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18
Q

Antibiotics
Interfere with DNA replication
1. Name the 4 and give 2 examples of one of them
2. What is their mechanism of action?

A
  1. Quinolones (ciprofloxacin and ofloxacin)
    Co-trimoxazole
    Nitroimidazoles
    Rifampicin
  2. Quinolones: inhibits topoisomerase 2 and 4 = bacterial DNA can’t supercoil/ replicate/ seperate =rapid cell death

Co-trimoxazole: sulfonamides and trimethoprim (synergistic association)
Both act in following pathway: synthesis of tetrahydrofolate
Sulfonamides = structural analogues of PABA = enzyme inhibition
Trimethoprim = inhibits dihydrofolate reductase = enzyme inhibition

Nitroimidazoles: anaerobic organisms have the electron transport chain needed to reduce metronidazole to its active form = toxic to DNA = bactericidal

Rifampicin: binds to DNA dependent RNA polymerase = inhibits mRNA synthesis

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19
Q

Antibiotics
Interfere with DNA replication
1. Resistance and cautions: quinolones
2. Resistance and cautions: co-trimoxazole
3. Resistance and cautions: nitroimidazoles
4. Resistance and cautions: : rifampicin

A
  1. Quinolones
    Resistance: mutations in gene encoding subunit of DNA gyrase/ ciprofloxacin effluent in some bacteria
    Caution: interactions and caution in children
  2. Co-trimoxazole
    Resistance: DHF reductase without affinity to trimethoprim
    DHT reductase with low affinity to sulfonamides
    Caution: 1st trimester of pregnancy
  3. Nitroimidazoles
    Resistance: enzyme production = no formation of reactive metabolite
    Caution: alcohol
  4. Rifampicin
    Resistance: changes in RNA polymerases
    Caution: metabolic interactions and orange saliva, tears and sweat
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20
Q

Define agonist and state the 2 types

A

Binds and stimulates physiological regulatory effects of endogenous compounds
Full/partial

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21
Q

Define antagonist and name the 4 types

A

Bind but do not have regulatory effects and prevent binding of endogenous compounds
Competitive/non-competitive
Reversible/ irreversible

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22
Q
  1. Define drug affinity and state what it is numerically

2. Define drug efficacy and state what it is numerically

A
  1. How tightly a ligand binds to a receptor
    K(small A)
  2. Ability to produce a biological effect
    R (small max) or B (small max)
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23
Q
  1. What is drug potency?

2. What is tolerance?

A
  1. Measure of drug activity

2. Gradual decrease in responsiveness to a drug

24
Q

What are the 4 molecular mechanisms of drug action?

A
  1. Direct physiochemical effect
  2. Effect on transport systems
  3. Enzymes
  4. Interaction with a receptor
25
Q

What are the 2 types of ADR’s and define it

A
  1. On-target effects: related to pharmacological action of drug
  2. Off target effects: unrelated to main pharmacological action of drug
26
Q

What are the ABCDE types of ADR’s? Explain each one in 1 sentence

A

A= augmented reactions
Normal dose but exaggerated effect/unwanted reactions predictable from drugs pharmacology

B= bizarre reactions
Not pharmacologically predictable

C= continuing/chronic reactions
Persist for long time

D= delayed reactions
Become apparent some time after use of medicine

E= end of use reactions
Associated with withdrawal of medicine

27
Q

ADR’s

  1. Immediate reaction?
  2. First dose reaction?
  3. Early reactions?
  4. Intermediate reactions?
  5. Late reactions?
  6. Delayed reactions?
A
  1. Give slowly over 1 hour
  2. Use low first dose
  3. Introduce drug slowly
  4. Careful monitoring and dose adjustment
  5. Use short course when possible
  6. Avoid in women of child bearing age
28
Q

Treatment of lipid disorders

  1. What are the 4 drugs? Give an example of 2 of them.
  2. What is the mechanism of action of each?
A

1.resins (cholestyramine)
Ezetemibes
Fibrates (benzafibrate)
Statins

  1. Resins: bind to bile acid=more gut secretion, reducing its recirculating + reducing absorption of exogenous cholesterol
    Less bile acid so more cholesterol broken down (to try and make more bile acids)
    Less cholesterol so more LDL receptor expression so IDL removed from circulation

Ezetemibes: act in brush border of intestine = decreased absorption of biliary and dietary cholesterol
Less cholesterol so more hepatic LDL receptor expression

Fibrates: ligand for nuclear transcription factor “PPARalpha” = stimulates lipase activity
Less VLDL production by liver
Less LDL uptake by liver
Reduces TG/ LDL/VLDL

Statins: inhibits HMG-CoA in cholesterol synthesis pathway
Less cholesterol so less synthesis and secretion of lipoproteins from liver
More LDL receptor expression
Pleiotropic effects: antioxidant/ anti inflammatory and angiogenesis

29
Q

Treatment of lipid disorders

  1. ADR’s and “avoid in” for resins
  2. ADR’s and “avoid in” for ezetimibe
  3. ADR’s and “avoid in” for fibrates
  4. ADR’s and “avoid in” for statins
  5. Which one has important interactions are what are they?
A
  1. Constipation and reduced absorption of other medications
    Avoid in: bowel/biliary obstruction
  2. Rhabdomyolysis if used with statin and GI disturbance
    Avoid in: history of hypersensitivity
  3. Rhabdomyolysis if used with statin and GI side effects
    Avoid in: hepato-biliary disorders
  4. Rhabdomyolysis/GI disturbances/ insomnia/ rashes and hepato-biliary effects
    Avoid in: acute liver disease + pregnancy/breastfeeding
  5. Statins has important interactions due to CYP450
    Avoid: antibacterials/antifungals/grapefruit juice
    Interacts with anticoagulants/CCB/fibrates
30
Q

Anti platelets

  1. What are the 4 drugs? Give 2 examples for 2 of them.
  2. What is their mechanism of action?
A
  1. Aspirin
    Dipyridamole
    P2Y (ADP) receptor antagonists (clopidogrel and ticagrelor)
    GP 2b3a inhibitors (abciximab and tirofiban)
  2. Aspirin: inhibits cox-1 = inhibits TxA2 production by platelets
    Also inhibits prostacyclin synthesis

Dipyridamole: phosphodiesterase inhibitor = increases cAMP levels and may stimulate adenylyl cyclase

P2Y (ADP) receptor antagonists: blocks effect of ADP on platelets

GP 2b3a inhibitors: bind to GP 2b3a receptor = blocks binding of fibrinogen and prevents platelet aggregation

31
Q

Anti platelets

  1. Uses, 3 ADR’s and 1 “avoid in” for aspirin
  2. Uses for dipyridamole
  3. Uses for P2Y (ADP) receptor antagonists
  4. Uses and 1 route for GP 2b3a inhibitors
A
  1. Secondary prevention of MI/prevents events in PVD patients/ cerebralvascular disease
    Bleeding/ GI intolerance/ hypersensitivity
    Avoid in children (risk of Reye’s syndrome)
2. Prophylaxis of thromboembolism (with warfarin)
After TIA (with aspirin)
  1. For specific indications (with aspirin)
  2. NSTEMI/ cardiac surgery
    IV only
32
Q

Name the 4 steps of the analgesic leader, stating:
Pain level at each point
What is recommended
Some examples

Also, what is the opioid antagonist called?

A
  1. Mild pain (1-3)
    Non- opioid analgesics
    With/without adjuvant
    Paracetamol/NSAIDs
  2. Moderate pain (3-6)
    Opioids
    With/without non-opioid analgesics and adjuvant
    Codeine/tramadol + laxative
  3. Severe pain (7-10)
    Opioids
    With/without non-opioid analgesics and adjuvant
    Morphine/ diamorphine + laxative or antiemetic
  4. Interventional
    Blocks/ spinal medications/ surgical procedures

Opioid antagonist= naloxone

33
Q

Analgesic ladder
Non-opioids: NSAIDs/COXIBs
1. What kind of analgesic effect? What kind of action?
2. What is the mechanism of action?
3. What kind of agent would you give with it?
4. Give 2 examples

A
  1. Mainly peripheral
    Antipyretic and analgesic and anti-inflammatory action
  2. Competitive inhibitors of cox
    Reduces production of prostaglandins
  3. Gastroprotective agent (PPIs/misoprostol)
  4. Ibuprofen and naproxen
34
Q

Analgesic ladder
Non-opioids: paracetamol
1. What kind of analgesic effect? What kind of action?
2. What is the mechanism of action?
3. What is it extensively metabolised by?

A
  1. Mainly central
    Antipyretic and analgesic action
  2. Inhibits cox in brain
  3. Liver
35
Q

Analgesic ladder
Weak opioids:
1. What kind of analgesic effect?
2. What 3 types of receptors are involved and which G protein are they coupled to?
3. What are the 3 MOA’s?
4. Name 2 weak opioids and which one has a ceiling dose?
5. Caution in?
6. What should you definitely not do with these drugs?

A
  1. Central and peripheral
  2. Meu, delta and kappa receptors all coupled to Gi proteins
  3. Inhibit AC=less cAMP so affects phosphorylation pathway
    Inhibit voltage gated calcium channel = less NT release
    Activates potassium channels = hyperpolarises cell membrane
  4. Codeine and tramadol (codeine has ceiling dose)
  5. Renal/hepatic impairment and epilepsy
  6. Don’t “kangaroo”
36
Q 
Analgesic ladder
Strong opioids
1. Give an example of 2
2. What does the dose depend on?
3. If the pain is not relieved, what do you increase?
4. How is it excreted?
5. ADR's?
A
  1. Morphine and fentanyl
  2. Precious medications/ age/ general condition
  3. Increase dose (not frequency)
  4. Really excreted
  5. Constipation, N&V, sedation, confusion, respiratory depression, increase intrabiliary pressure, hypotension, bradycardia
37
Q

Fibrinolytics/ thrombolytics
What are the 4 drugs?
What is their mechanism of action?
Where is each one made?

A
  1. Streptokinase
    Forms 1:1 complex with plasminogen = which forms plasmin and hence dissolves the clot
    Streptococcus
  2. Alteplase
    Activates plasminogen bound to fibrin
    Recombinant human t-PA
  3. Urokinase
    Converts plasminogen to active plasmin
    Synthesised by kidney
  4. Anistreplase
    Human plasminogen + bacterial streptokinase
38
Q

Fibrinolytics/ thrombolytics

  1. What are the 4 uses
  2. What are the 2 side effects?
A
  1. Acute ischaemic stroke
    Arterial thrombosis
    Venous thrombosis
    Acute MI
  2. Bleeding
    Allergic reactions
39
Q

Diarrhoea and constipation
What are the 4 drugs?
What is their mechanism of action?

A
  1. Bulk forming laxatives
    Retain fluid within stool = increase faecal mass
    Stimulate stretch receptors and promote peristalsis
  2. Osmotic laxatives
    Draw in fluid and retain water by osmotic effect = increases volume
  3. Stool softeners
    Increased penetration of intestinal fluids into faecal mass = less surface tension
    Softens stool = promotes defaecation
  4. Stimulant laxatives
    Direct stimulation of colonic nerves = promotes propulsive motility
40
Q

Diarrhoea and constipation

  1. Time and ADR’s: bulk forming laxatives
  2. Time and high dose ADRs: osmotic laxatives
  3. What kind of action: stool softeners
  4. Time, ADR and avoid in: stimulant laxatives
A
  1. Several days
    Flatulence, bloating and abdominal distension
  2. 2-3 days
    Flatulence, bloating, diarrhoea electrolyte disturbances

3.surfactant action

  1. 8-12 hours
    Abdominal cramp
    Avoid in intestinal obstruction
41
Q

Respiratory drugs

  1. Name the 2 bronchodilators
  2. Name the bronchodilator and anti-inflammatory
  3. Name the 2 anti-inflammatorys
A
  1. Beta2 agonists and anti-cholinergics
  2. Methylxanthines
  3. Corticosteroids and leuokotrienne receptor antagonists
42
Q

Respiratory drugs - bronchodilators
Beta2 agonists
1. Which receptor is involved? Which G protein is involved? What are the next 3 compounds activated?
2. This leads to the phosphorylation of what? What is the end result?
3. Name 2
4. Caution due to?
5. ADRs?

A 
1. Beta2 receptor
Gs protein
AC, cAMP and PKA
2. MLCK
bronchodilation
3. Salbutamol and formoterol
4. Tolerance 
5. Skeletal muscle tremor/ tachycardias and arrhythmias/ metabolic response/ paradoxical hypoxaemia/hypokalaemia
43
Q

Respiratory drugs - bronchodilators
Anti-cholinergics
1. Which receptor is involved? Which G protein? What is the next compound that is activated?
2. This allows for the activation of what 2 compounds? What do both of these do? What is the final result?
3. What are anti-cholinergics also known as? So what do they do to this pathway? What does this lead to?
4. Give 2 examples
5. Caution due to?
6. ADRs?

A 
1. Muscarinic receptor 
Gq protein
PLC
2. IP3 = calcium release 
DAG = PKC activated 
Both lead to contraction 
3. Muscarinic receptor antagonists
Inhibit this pathway
Relaxation 
4. Ipratropium
Tiotropium
5. Glaucoma and prostatic Hypertrophy
6. Dry mouth/ blurred vision/ urinary retention/ paradoxical bronchoconstriction/
44
Q

Respiratory drugs - bronchodilator and anti inflammatory
Methylxanthine
1. What is its MOA that leads to bronchodilation?
2. What is its MOA that leads to anti-inflammatory effects?
3. Give 2 examples
4. Caution due to?
5. ADRs?

A
  1. Non-selectively inhibits PDE= inhibits cAMP degradation/metabolism
  2. Adenosine receptor antagonism = stops it releasing inflammatory neurotransmitter
  3. Aminophylline
    Theophylline
  4. Narrow toxicity - CP450
  5. Gastrointestinal disturbances/ CNS stimulation/ cardiovascular effects/ hypokalaemia
45
Q

Respiratory drugs - anti-inflammatory
Corticosteroids
1. It goes into what part of the cell to bind to the receptor? Where does it go to next? What does it do here?
2. It stops the conversion of phospholipids into what?
3. The end result is more of what?
Less of what?
4. Give an example of 3 and state the route of administration
5. ADRs? And with prolonged high doses?

A
  1. Cytoplasm
    Nucleus
    Alters gene transcription
  2. Arachidonic acid and therefore TXAs, LTs and PGs
  3. More anti-inflammatory molecules
    Less cytokines, inflammatory enzymes, PG and LT synthesis
  4. Inhale: beclometasone
    IV: hydrocortisone
    oral: prednisolone
  5. Oral candidiasis/dysphonia
    With prolonged high doses: osteoporosis/ suppression of response to infection/ GI upset/ hypertension/ metabolic effects (cushings syndrome)
46
Q

Respiratory drugs - anti-inflammatory
Leukotriene receptor antagonists
1. Inhibit leukotriene pathway by inhibiting what?
2. If the pathway was to go on as normal, what would the 2 effects be?
3. Give an example of 2
4. ADRs?

A
  1. Leukotriene receptor
  2. Inflammatory effects (vascular permeability and mucous production)
    Bronchoconstriction
  3. Montelukast
    Zafirlukast
  4. Headache/ gastrointestinal upset/ hypersensitivity/ dry mouth
47
Q

Anti-coagulants
Coagulation cascade
1. What are the two starting pathways called?
2. Where do they join? What is the pathway now called?
3. What are the 2 key events in the cascade?

A
  1. Intrinsic pathway and extrinsic pathway
  2. Join at factor Xa to become the common pathway
  3. Prothrombin converts to thrombin
    Fibrinogen converts to fibrin
48
Q

Anti-coagulants
1. What are the 3 drugs?
What is their MOA

A
  1. Unfractionated heparin
    Inactivated the activated clotting factors
  2. Low molecular weight heparin
    Increases action of AT3 on factor Xa
  3. Warfarin
    Acts metabolism of vitamin K
    Competitive inhibitor of vitamin k reductase
    Inhibits clotting factors 2,7,9 and 10
49
Q

Anti-coagulants

  1. Time, uses and ADRs: unfractionated heparin
  2. 1 example, what is is not neutralised by and uses: low molecular weight heparin
  3. Metabolism site, uses and ADRs (+ how to overcome this): warfarin
A
  1. Immediate action
    Thromboprophylaxis/ DVT&PE/ prevents coronary events
    Haemorrhage/ thrombocytopenia/ hyperkalaemia/ osteoporosis
  2. Enoxaparin
    Protamine
    Thromboprophylaxis/ DVT & PE/ prevent coronary events/ MI
  3. Liver (CYP450 system)
    DVT & PE/ prevents events in AF/ prevents events in mechanical heart valves
    Bleeding based on age/INR/ high BP/ peptic ulcer/ antibiotic use
    Give fresh frozen plasma/ clotting factors/ vitamin K
50
Q

Diuretics

What are the 4 drugs? Give an example of each as well as what to avoid in each case?

A
  1. Loop diuretics
    Furosemide
    Avoid: anuria
  2. Thiazide diuretics
    Hydrochlotothiazide
    Avoid: electrolyte disturbance and Addison’s disease
  3. Potassium sparing diuretics
    Amiloride
    Avoid: Avoid: electrolyte disturbance and Addison’s disease and potassium supplements
  4. Aldosterone antagonists
    Spironolactone
    Avoid: Avoid: electrolyte disturbance and Addison’s disease and potassium supplements
51
Q

Diuretics: loop diuretics

  1. Location?
  2. Time? Administration route? Dosing info?
  3. MOA: Competes with what?inhibits what?
  4. 2 uses
  5. 3 ADRs
A
  1. Thick ascending loop of henle
  2. 6 hours
    oral/ IV/ IM
    High ceiling effect
  3. Completes for chloride binding site
    Inhibits ion co-transporter for sodium/ potassium and chloride
  4. Heart failure + resistant oedema
  5. Ototoxicity/ hypokalaemia/ hyperglycaemia
52
Q

Diuretics: thiazide diuretics

  1. Location?
  2. Time? Administration route?
  3. MOA: what does it bind to? What kind of interaction is it?
  4. 2 uses? Ineffective in what?
  5. 3 ADRs
A
  1. Early distal convoluted tubule
  2. 12-24 hours
    Oral
  3. Bunds to sodium chloride symporter
    Competitive antagonism
  4. Heart failure and hypertension
    Ineffective in renal impairment
  5. Hypokalaemia/ hyperglycaemia/ hyperuricaemia
53
Q

Diuretics: potassium sparing diuretics

  1. Location?
  2. Administration route?
  3. MOA: binds to and blocks what in the luminal membrane? This increases the excretion of which 3 ions? This decreases the excretion of which ion?
  4. Use?
  5. 2 ADRs
A
  1. Late distal convoluted tubule
  2. Oral
  3. Binds to and blocks sodium channels in the luminal membrane
    Increases excretion of sodium/ chloride/ water
    Decreases excretion of potassium
  4. Preventing hypokalaemia (with other diuretics)
  5. Hyperkalaemia/ metabolic acidosis
54
Q

Diuretics: aldosterone antagonists

  1. Location?
  2. Administration route?
  3. MOA: blocks what kind of receptors? This reduces the synthesis of which 2 things? Which ion channel permeability does it also reduce?
  4. 2 uses
  5. 3 ADRs
A
  1. Late distal convoluted tubule
  2. Oral
  3. Blocks cytoplasmic receptors
    Reduces synthesis of sodium potassium ATPase and sodium channels
    Also reduces sodium channel permeability
  4. Ascites and heart failure
  5. Impotence/ menstrual disturbances/ gynaecomastia
55
Q

Cardiovascular drugs

  1. What are the 4 steps of treating someone under 55 years of age?
  2. What are the 4 steps of treating someone over 55/black person of African or Caribbean family origin?
  3. Describe the steps of the RAAS system pathway
A
  1. Ace-I
    Ace-I + CCB
    Ace-I + CCB + Th D
    Ace-I + CCB + D + alpha/beta blocker
  2. CCB
    CCB + Ace-I
    CCB + Ace-I + Th D
    CCB + Ace-I + D + alpha/beta blocker
  3. Angiotensinogen/ (renin) / angiotensin 1 / (ACE) / angiotensin 2 / angiotensin 2 receptors /
    AT 1 subtype/ aldosterone
    AT 2 subtype
56
Q

Cardiovascular drugs

  1. Name the 4 drugs and give 2 examples of each (for one of them you will need to give 3)
  2. What is their MOA?
A
  1. Ace inhibitors
    Ramipril + captopril

Angiotensin receptor antagonists
Losartan + valsartan

Calcium channel blockers
Dihydropyridines: nifedipine + amlodipine
Non-dihydropyridines: verapamil

alpha blockers
Doxazosin + indoramin

  1. ACE-I: inhibits ACE

AT receptor antagonists: block AT receptor so AT2 can’t be converted into AT 2 receptors. This effects the AT-1 subtype

CCB: binds to alpha 1 receptor on L type voltage gated calcium channel. Blocks calcium influx into heart and arterial blood vessels

Alpha blockers: binds to alpha receptor which is linked to Gq protein. So this can’t activate PLC which won’t allow activation of IP3 (so no calcium release so no contraction) and won’t allow activation of DAG (so no PKC so no contraction)

57
Q

Cardiovascular drugs

  1. Effect + ADRs + contraindications: Ace inhibitors
  2. Effects + ADRs: AT receptor antagonists
  3. Effects + uses: CCB - dihydropyridines
  4. Effects + Uses + drug interactions: CCB - non-dihydropyridines
  5. ADRs: CCB
  6. Effect + uses + ADRs: alpha blockers
A
  1. Arteriovenous vasodilation / reduced vascular resistance / reduced blood pressure
    ADRs: dry cough/ hyperkalaemia/ renal insufficiency
    Contraindications: hyperkalaemia/ renal artery stenosis/ hypersensitivity
  2. Arteriovenous vasodilation/ reduced vascular resistance/ reduced blood pressure
    ADRs: no dry cough
  3. Vasodilation (more specific for calcium channels in vascular smooth muscle)
    Hypertension + angina
  4. Vasodilation / acts on myocardium + AV node and SA node
    Hypertension + angina + supraventricular arrythmias
    Drug interaction: beta blockers
  5. Flushing / headaches/ ankle oedema
  6. Vasodilation
    Hypertension/ benign prostatic hypertrophy
    ADRs: postural hypotension/ dizziness/ fatigue

1 REVISION Bismillah (13 decks)

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