Pharmacology for chiros

  1. IM ketoralac and valium. What do
    you have to ask about?
    GORD, bleeding tendency, driving machinery.
  2. Which pathological states result in hyperkalemia?
    diet, CRF/ARF(SLE, DM),NSAID use potassium supplements, diuretics eg: spironolactone. ACE-i.
  3. Definition - Pain?
    an unpleasant sensory or emotional experience associated with actual or potential tissue damage, or described in terms of such damage.
  4. Types of pain:
    • -Acute pain: usually has a trigger, lasts for a short duration approx up to 3/52 (variable). Inflammation is the causative process.
    • -Chronic pain: present after injury has healed, usually assoc with an emotional aspect (depression, anxiety, hopelessness) and physical compensatory effects (hypertonicity, LOE, LOA).
    • -Neuropathic pain: complex, usually seen with diseases that damage neurological systems eg MS, shingles, phantom limb etc. Can be intense shooting, burning, P&N.
  5. What controls pain?
    higher cortical areas; at a minimum the thalamic areas.
  6. Pain mechanisms: Inflammation

    What is the cellular component?
    This occurs at the microscopic level where damage occurs, starting a cascade of events
  7. Pain Mechanisms: Inflammation

    What is the neurological level?
    The pathways that lead finally to processing of pain signals at the cortical level. Invloves the spinothalamic tracts, somato-sensory area (S1) and its projections to the amygdala, hippocampal, frontal areas of the brain which result in the experimental component of pain and suffering. Chemical changes at each juncture
  8. What are the key features of inflammation?
    Redness, Swelling, Heat, Pain and loss of function.
  9. What does cell membrane damage lead to?
    • Phospholipids realease Arachidonic acid (Aa) via Phospholipase C and A2
    • Increase in intracellular Aa
    • Free Aa the undergoes metabolism by 2 pathways - COX & LOX
  10. What is COX?

    COX - Prostaglandins (PGE2, PGI2 (prostacyclin)), thromboxanes(TXA2)
  11. What is LOX?
  12. How many isoforms does COX have?
    Two - COX1 and COX2
  13. What is COX1?
    Present in normal cell homeostasis (kidney, gastric mucosa, airways and platlets)
  14. What is COX2?
    Is supposed to be more pro-inflammatory and selective COX2 inhibitors like Celebrex and Vioxx (withdrawn) were supposed to have less COX1 effects. Vioxx was PRO-thrombotic and gastric SE were not much different in either.
  15. What does LOX do?
    End up with formation of LTB4 & LTE4. High concentrations in mast cells, marcophages, neuts etc. Seem to be involved in asthma.
  16. Prostaglandin is needed for gastric mucosa secretion and NSAIDs stop this. What does this result in?
  17. Prostaglandin increases GFR in the kidneys. In the elderly what needs to be monitored?
    The use of NSAIDs as they decrease GFR and in the elderly this is already decreased.
  18. What are the consequences of PGE/PGI?
    • Arteriolar smooth muscle vasodilation
    • GIT smooth muscle contraction-coliky pain
    • Inhibition of platelets
    • Induction of labour, Dysmenorrhoea
    • Pyrexia
    • Maintains Patent ductus arteriosus in utero
    • Increases GFR / Gastric mucosal secretion
  19. What are the consequences of TXA2?
    Promotes thrombosis, greatly increases platelet adhesion
  20. Pain receptors in the skin are stimulated by injury due to the release of various chemicals by the damaged cells. What are the chemicals?
    Histamine, substance P, serotonin, bradykinin and prostaglandins
  21. Stimulation of nociceptors result in transmission to the CNS via?
    A-delta and C-fibres
  22. What is gating?
    Stimulation of A-beta fibres resulting in inhibition at the subs gelatinosa
  23. Activity of the C-fibres may be up-regualted peripherally by what in the damaged tissues?
    Serotonin, prostaglandins, thromboxane and leucotrienes
  24. What is Hyperalgesia?
    Increased sensitivity of normal pain fibres
  25. Peripheral sensitisation
    The A-beta fibres now respond to stimuli that activate the nociceptive pathway at the CNS level. What is this called?
  26. Central sensitisation occurs as a result of what?
  27. Central sensitisation
    As sensitivity increases....
    Threshold for firing decreases. NMDA and AMPA receptors are added to cell membranes at subs gelatinosa. Glutamate (excitatory) is released.
  28. Dendritic Growth....
    Convergance allows for other areas to be regarded as painful
  29. What is Long term potentiation?
    Synthesis of new proteins which inhances synaptic transmission
  30. How do you deal with pain?
    • Identify the type - acute, chronic, neuropathic
    • Treat accordingly, early and individually
    • Watch for side effects of both OTC and prescribed meds
  31. Analgesics - List 5 Opiates
    Morphine, Pethidine, Oxynorm, Oxycodone, Fentanyl
  32. Analgesics - List 7 steroids
    (Fucking Hot People Bite The Dust Majorly)
    Fludrocortisone, Hydrocortisone, prednisolone, betamethasone, triamcinolone, dexamethasone, methylprednisone
  33. Analgesics - List 2 opiate-like meds
    (Too Cool)
    Tramadol, codeine
  34. Analgesics - List 3 combinations
    (Pretty Pink Makeup)
    Panadeine, pandadeine forte, mersyndol
  35. Analgesics - List 6 NSAIDS
    (Vast PANIC)
    Voltaren, Ponstan, aspirin, nurofen, indocid, colchicine
  36. Analgesics - List 1 Simple
    Paracetamol (panadol)
  37. Asthma is a polygenetic disease linked with which disorders?
    Eczema, hay fever. Prelevance of 1/4
  38. With asthma, sensitivity to certain allergens which result in bronchospasm. Is this reversible?
    Yes reversibility is a key component.
  39. What are some common triggers of asthma?
    Common triggers: EIA, Infective, Stress, Cold etc.
  40. Some drug treatments available for asthma are:
    • Beta-agonists: Salbutamol/Ventolin/terbutaline, salmeterol - Activates beta 2 receptors on smooth muscles - bronchodilation.
    • Steroids: Prednisolone , Inhaled Steroids: beclomethasone (becotide), fluticasone (flixotide)
    • Other therapies for Asthma include: Montelukast – leukotriene receptor antagonist. Useful in EIA but still hardly used.
    • Ipratropium. Anticholinergic. Mainly used as nebs in COPD.
  41. How is COPD characterized?
    Characterised on spirometry or forced expiration time >7sec.
  42. True or false: COPD commonly has genetic links?
    Rarely genetic links. Usually with a history of smoking
  43. What is a common example of COPD?
    Emphysema is the classic example
  44. What does Paracetamol do?
    Inhibits COX pathway but lacks the anti-inflammatory effects of NSAIDs
  45. How is paracetamol best given (max dose)?
    Regualarly, max dose of 4 grams daily
  46. How many grams of paracetamol can be taken before it is toxic or fatal?
    • Toxic: 8 grams
    • Fatal: >15 grams
  47. Is paracetamol safe during pregnancy?
  48. What sub groups of patients need to be careful when taking paracetamol?
    • CLF: Hepatitis B/C, Haemochromatosis, biliary cirrhosis,alcoholics.
    • CRF: Diabetics, Elderly
  49. What does Aspirin do?
    • Inhibits COX pathway - decreases PG synthesis
    • Strongly inhibits TXA2 in platelets and increases clotting time after 1/52 dosing. Irreversible till platelets regenerate.
  50. Other than as an analgesic what is aspirin used for?
    • Thinning blood in cardic and stroke patients.
    • Good for viral illnesses
  51. How long does it take for platelets to regenerate?
    8 Days
  52. What are the signs and symptoms of Reye's syndrome?
    Neurological disturbance (ataxia, lethargy, nystagmus, fits), diarrhoea +/- vomiting, hypoglycaemia, elevated LFT’s.
  53. What does fish oil do?
    Decreases synthesis of TXA2 anti-inflammatory effects and mild anti-platelet effect
  54. What id the appropriate dose of fish oil?
    2.7 grams/day (14 tablets!)
  55. Why should you avoid cod liver oil?
    Increased cholesterol and Vit A toxicity
  56. What are the potential side effects of fish oil?
    Bad in gall bladder removal, flatulence, stincky breath, farts, reflux, bleeding
  57. What is the two glass technique for taking bottled fish oil?
    Float oil on 30ml of juice. Drink quickly avoid lips, then follow with another 30ml of juice. Take before meals (with no liquid during meal)
  58. What are NSAIDS used for?
    Acute inflammation, injury, dysmenorrhoea, headaches
  59. Who should you NEVER give NSAIDs to?
    3rd trimester pregnant women!!!
  60. What is a side effect of NSAIDs?
    Mild blood thinning effect and GORD can be severe if long term
  61. What are steroids (Glucocorticoids) used for?
    Treatment of various inflammatory and allergic conditions such as gout, RA, OA, COPD, Asthma, SLE, Eczema, ALL and premature fetal lung development (surfactant)
  62. What is the mechanism of action of GCS?
    • Transported into cytoplasm and bound to a protein complex which enters nucleus.
    • Causes gene up-regulation and down-regulation for others. Depends on tissue type.
  63. What does GCS inhibit?
    NF-kB, PhospholipaseA2, COX pathway and stops the inflammatory process on a number of levels
  64. What is the Physiologic effects of GCS?
    • Suppresses TSH/FSH.
    • Increases GH.
    • Increases insulin (d/t BSL).
    • Net effect weight gain centrally.
  65. What are the metabolic effects of GCS?
    Increases BSL's (gluconeogenesis) by breaking fat, protein and carbs down.
  66. What are the Catabolic effects of GCS?
    • Connective tissue (eg skin), decrease muscle mass, osteoporosis.
    • Reduction in growth in kids despite GH.
  67. What are the Anti-inflammatory effects of GCS?
    • Decreased PG, leukotiene.
    • Short term increase in neuts but impotent.
    • Decreased healing.
  68. What are the effects of long term GCS use?
    • Euphoria, sometimes depression or psychotic symptoms.
    • Buffalo hump, Hypertension, Thinning of skin, Cataracts, Moon Face, Increased abdominal fat, Easy bruising, Poor wound healing, thin arms and legs due to muscle wasting, osteoporosis, hyperglycaemia, increased appetite and obesity
  69. What is addisonian crisis?
    Hypotension, vomiting, nausea, fatigue, dizziness, muscle weakness, anxiety, diarrhoea
  70. What are the side effects of opiates?
    Euphoria, dysphoria (10%), restlessness, skin itch, constipation (no tolerance), sedation, resp. depression, cough suppression, Miosis (no tolerance), N/V, urinary retention.
  71. What causes neuropathic pain?
    Usually occurs after a significant insult to the nervous system.
  72. Is neuopathic pain normally acute or chronic?
  73. What symptoms are associated with neuropathic pain?
    Parethesias, radiculopathy, dull aching
  74. What are the medications used to treat neuopathic pain?
    • Tricyclics - Amitriptline. Given at low doses. Can be quite effective.
    • SSRI's - Prozac, lexapro. Not as bad with side effects
    • Opiates - Fentanyl patch, oxynorm for break through. Oxycontin for long acting effect.
    • AED's - Sodium valproate, gabapentin. Stabilises nerve membranes. SE -dizzy, drowsy, oedema
  75. What are the preventative drugs for migraine?
    • Anti HTN - mechanism unknown
    • TCA's - Reinforces serotonin dysfunction theory
    • Pizotifen - 5-HT Antagonist
    • AEDs
    • Botulinum toxin - BOTOX to neck muscles
  76. What are the abortive drugs for migraine?
    • NSAIDS
    • Triptan
    • Ergots
    • Opiates
  77. What is Chvosteks sign?
    Tapping the facial nerve - twitching
  78. What are some types of muscle relaxants?
    • GABA agonist
    • Benzodiazepines
    • Valium
    • Side effects - risk of falls, memory affected, drowsy
  79. If the problems with muscle spasm are with sleep initiation or acute anxiety should you use short of long acting benzo?
  80. What is Baclofen?
    GABA agonist - works by hyperpolarising the cell membranes. Casues much less sedation than benzos
  81. What does Dantrolene do?
    • Interferes with excitation-contraction coupling of muscle fibres by inhibiting the release of Ca from the sarcoplasmic reticulum.
    • Causes generalised muscle stiffness and sedation
  82. What is novel therapy for muscle spasms?
    BOTOX injections - inhibits muscle completely
  83. List 5 seronegative arthropathies
    • AS
    • RS
    • EA
    • OA
    • PA
  84. List 6 seropositive arthropathies
    • RA
    • SLE
    • Antiphospholipid syndrome
    • Scleroderma
    • Polymyositis
    • Sjogrens syndrome
  85. List 2 non-articular rheumatic diseases
    • Fibromyalgia
    • Polymyalgia Rheumatica
  86. List 2 crystal induced arthropathies
    • Gout
    • CPPD
  87. What is the pathophysiology of rheumatic diseases?
    • Inflammation and auto-immunity
    • Failure of T-supressor cells - production of auto-antibodies by B-lymphocytes
    • Antibodies attach to antigens - cell death or immune complex deposits
  88. What is the result of rheumatic diseases?
    Chronic pain, loss of function, systemic decline/impairment, finacial burden, social burden, genetic repercussions, SE of meds
  89. What is the symptomatic management of Rheumatic diseases?
    • Chiropractic! and the like
    • Analgesics
    • Fish oil
    • Steroids
  90. Rheumatic diseases

    What do DMARDS do?
    Reduce synovial inflammation and prevent joint damage - lots of SE!

    eg. Methotrexate, hydroxychloroquine, leflunomide, azathioprine, cyclophosphamide, sulphasalazine
  91. Rheumatic diseases

    What is methotrexate?
    • Folic acid analogue - antagonises it and reduces available amount. Folic acid needed for DNA synthesis - impairs cell division
    • Mechanism - increases adenosine - decreases inflammation cell activation and cytokine release
  92. Rheumatic diseases

    What should you avoid when taking methotrexate?
    Alcohol abuse, hepatitis, pregnancy
  93. Rheumatic diseases

    What are the side effects of methotrexate?
    Nausea, mouth ulcers, pancytopenia, fibrosis and cirrhosis of the liver
  94. Rheumatic diseases

    What does leflunomide do?
    Blocks synthesis of pyridoxines and inhibits activated lymphocytes
  95. Rheumatic diseases

    What are the side effects of leflunomide and when should it not be used?
    Liver dysfunction, diarrhoea, alopecia, rash

    In pregnant women - teratogenic
  96. Rheumatic diseases

    What do gold salts (sodium aurothiomalate) do and what are their side effects?
    Inhibits T-cells and phagocytes

    SE: Itch, eczema, gold deposits, aplastic anaemia
  97. Rheumatic diseases

    What is hydroxychloroquine, what was it previously used for and what are it's side effects
    • Supresses inflammatory response
    • Used previously to treat malaria
    • Nausea, rash, dizziness
  98. Rheumatic diseases

    What are cyclophosphamide and Cyclosporin and what is a common side effect?
    Immune suppressants. Used in post-transplant patients or with sever rheumatologic disease

    Renal toxicity is common
  99. Rheumatic diseases

    What do biologic DMARDS do, what are the SE and how much does it cost?
    • Tumour Necrosis Factor is released in inflammation. TNF inhibitors like etanercept and infliximab are monoclonal antibodies which bind and inactivate it
    • SE: Hypersensitivity and infections
    • Cost: $847 per infusion
  100. Rheumatic diseases

    What needs to be monitored during treatment?
    • Clinical monitoring: Pain, function, synovitis
    • Lab monitoring: CRP, ESR, antibody titre eg. rheumatic factor, ANA titre
    • SE
  101. How is gout treated?
    NSAIDS esp - colchicine - inhibits mirotubule formation and decreases phagocytosis. Prednisolone can me used

    Prevention is dependant on cause
  102. How does PTH increase serum Ca?
    • Increasing bone turn over
    • Reabsorbing renal and GIT
    • Ca at the expense of Phos
    • Increases Vit D activation to 1,25 dihydroxy-vitamin D
  103. List some examples of Microbes:
    Prions, Viruses, Bacteria, Fungi, Parasites
  104. What is Creutzfeldt-Jakob Disease?
    A prion . Human variant of mad cow disease aka Bovine Spongiform encephalopathy which causes neuro-degenerative disease in the brain and spinal cord. No known cure
  105. What is a virus? Give some examples
    • Consists of nucleic acid (RNA or DNA) surrounded by a protective protein coat (capsid). It attaches itself to the cell wall and inserts its nucleic acid which incorporates into the host DNA to form more virions.
    • Rhinovirus, to the exotic viruses like Herpes Simplex or HIV
  106. List the 5 steps of virus replication:
    • 1) Absorption and penetration of host cell
    • 2) Synthesis of early non structural proteins. Eg. nucleic acid polymerases.
    • 3) Synthesis of RNA or DNA.
    • 4) Synthesis of late structural proteins.
    • 5) Assembly and maturation with release of virions.
  107. Describe HIV.
    • Retrovirus with long incubation period. RNA is converted to DNA by reverse transcriptase. High genetic variability due to high replication rate with new variants of protein structure- which allow evasion from host immune system.
    • Infects CD4 T-helper cells- loss of cell-mediated immunity & subsequent rise in opportunistic infections
  108. In HAART, What are the three anti viral drugs used in conjunction to traet HIV?
    • NARTI’s – nucleoside analogue reverse transcriptase inhibitors, Protease inhibitors
    • NNRTI’s- non nucleoside reverse transcriptase inhibitors
  109. What can bacteria be classified in?
    • Gram stain: either gram + or gram –
    • Then they are mainly cocci or rods. Some are strange eg. spirochetes
  110. In bacterial infections, what are the two types of G+ cocci?
    • Staphylo-coccus or Strepto-coccus
    • Staphylococcus Aureus: causes cellulitis, toxic shock syndrome…golden staph?
    • Staphylococcus Epidermidis: commensal on skin but can cause endocarditis in susceptible individuals.
    • Streptococcus Pyogenes: strep sore throat, pneumonia or necrotising fascitis.
  111. List some G+ bacterial Rods.
    • 1)Clostridium eg. Clostridium tetani, Clostridium perfringens – gas gangarene.
    • 2) Bacillus Anthracis - Anthrax
    • 3) Cornybacterium Diptheriae
  112. List some G- Cocci bacteria.
    Neisseria Meningitidis, Neisseria Gonorrhea
  113. List some G- bacterial Rods
    E coli, Salmonella Typhi, Shigella, Legionella, Helicobacter Pylori, Pseudomonas, Vibrio cholera
  114. What is penecillin used for?
    Bactera. good for strep's, most staphs have resistance. Not bad for certain G- like E-coli. Beta lactamase breaks Abx down- resistance
  115. What are Cephalosporins used to treat?
    Bacteria. eg keflex. Usually given when allergic to penicillin's. 10% cross over reactivity. Better G- cover
  116. What is Clavulanic acid used for?
    Bacteria. usually combined with penicillin to give augmentin which overcomes beta-lactamase.
  117. What are Macrolides used to treat?
    Bacteria. Erythromycin (rulide) - covers atypical resp infx eg Legionella, mycoplasma.
  118. What are Trimethoprim / Sulphonamides used for?
    Bacteria. Affects folic acid synthesis.
  119. List reasons why antibiotics don’t work:
    • Wrong diagnosis: could be a viral infection.
    • Antibiotic resistance- more common esp in community as opposed to classically nosocomial
    • Delayed Initiation
    • Inability to get to target site eg: abscess Co-morbidities: DM, steroid use, HIV, oedema, poor oxygenation or vascular supply etc
  120. List some common fungi.
    • Candida Albicans: causes vaginal thrush, oral thrush.
    • Tinea: affects different areas.itchy. easily managed
    • Pneumocystis Jiroveci: found mostly in HIV patients. Can cause fatal pneumonia. Difficult to treat.
  121. List some anti-fungal pharmaceuticals:
    • The –azoles: eg clotrimazole,, ketoconazole. Blocks synthesis of fungal biolipids
    • Nystatin: binds to ergosterol and disturbs membrane permeability.
    • Amphotericin-B: mother of all anti-fungals… binds to ergosterol and increases permeability of membranes.
  122. List some common parasitic infections.
    Malaria, Worms (helminths), scabies (mites), lice (pediculosis)
  123. Describe Malaria.
    • A number of life cycle stages. Parasites reside in RBC’s and cause haemolysis.
    • Biggest issue is increasing drug resistance. Recommended treatment includes prophylaxis and preventative measures
  124. What are some drugs used to treat malaria?
    • Chloroquine: Now not used due to drug resistance.
    • Mefloquine: very effective. Needs to be trialed 1 month before leaving for potential SE - neuro-psychiatric disturbance inc epilepsy.
    • Primaquine: active against late stages. Good at terminating attacks.
    • Proguanil: folic acid antagonist. Good for primary stage. Combined with
    • Atovaquone: to give good prophylaxis against falciparum
  125. Summary of PTH:
    • Renal: Decreases Ca and Phos excretion
    • Bone: Increases Ca and Phos resorption
    • Serum: Increases Ca, decreases Phos
  126. Summary of Vit D
    • GIT: Increases absorption of Ca and Phos
    • Renal: Decreases Ca and Phos excretion
    • Bone:Increases resorption of Ca and Phos
    • Serum: Increases Ca and Phos
  127. Describe Calcitonin
    • From parafollicular cells in thyroid
    • Inhibits osteoclasts - blocks bone resorption
    • Useful in Paget's, hypercalaemia and osteoporosis
  128. Describe Glucocorticoids
    • Blocks collagen synthesis
    • Increases PTH stimulation
    • Increases renal Ca excretion
    • Can be used for hypercalaemia
  129. HRT can help decrease bone loss in menopausal women but is mainly used to treat the symptoms. What are the symptoms?
    Vaginal dryness, itchy. prolapse. Hot flushes and sweats, decreased concentration, memory loss, fatigue and mood liability
  130. What are some metabolic bone diseases?
    • Hypercalaemia: can be a medical emergency - cancer, hyperparathyroidism and Vit D overdose
    • Hypocalaemia: Tetany, paresthesias, muscle cramps, convulsions - causes - Hypoparathyroidism, vit D deficiency, renal failure and malabsorption
    • Vit D deficiency: Cultural predispositions, lack in diet
  131. What are the drugs used to treat osteoporosis?
    • Ca supplements
    • Vit D supplements
    • Bisphosphonates
    • Strontium Ranelate
    • E2 supplements
    • SERMs
  132. What are the biochemical markers for heart attack?
    • Troponin is th primary marker
    • Blood test: FBE, UEC, CMP, TFT's, glucose, lipids
    • Triple screen: History, Troponin, ECG
  133. What is ACS?
    Plaque rupture and thrombosis leading to acute myocardinal infarction
  134. What is Angina?
    Demand ischaemia due to stenosis of coronary arteries. No death of tissue.
  135. What is the treatment of ACS and Angina?
    • 1) stabilisation of plaque
    • 2) restoring blood flow to critical organs
    • 3) Decrease myocardial demand
    • 4) Prevention of complications
    • 5) Decrease long term complications and recurrence
    • 6) Minimise systemic illness esp respiratory
  136. How to reduce O2 demand?
    • Slow the heart
    • Decrease load on the heart
    • Decrease force of pump/contractility
    • Fix oxygenation issues eg anaemia
    • Fix plumbing - stent vs bypass
    • Minimise risk factors
  137. What therapy is used for heart conditions?
    • Beta blockers: slow the heart down. Anti-arrythmia. Decreases contractility. Also has a role in preventing pathological re-modelling of the heart
    • Calcium Channel blockers: Same mechanism as above but less chronotropicity
    • Nitrates: acute treatment
    • Nicorandil: opens K+ channels
    • ACE-i: decreases BP
  138. What are the SE of beta-blockers?
    Asthma, postural hypotension, cold limbs, erectile dysfunction, lethargy
  139. What are the SE of Calcium Channel Blockers?
    SOA, oedema
  140. What are the SE of Nitrates?
    headaches, light headed, oedema
  141. What are the anatomical sphincters associated with GORD?
    • Gastro-oesophageal jx
    • Oesophageal-diaphragm jx
    • natural innate tone (LES)
  142. What are the local gastric factors assosciated with GORD?
    mucus, acid production (ZES), blood supply, smoking, regenerative capability, dietary factors eg caffeine, chocolates, alcohol, NSAIDS, onions, high fat, stomach motility
  143. What is the main cause of gastric ulcers?
    Helicobacter Pylori infection- 80-90% of ulcers
  144. Describe some treatments for GORD:
    • Diet modification: reduce caffeine, fatty foods
    • Weight Loss
    • Decrease Smoking
    • Avoid supine or lifting after meals
    • Drug Rationalisation: decrease NSAIDs, anticholinergics, calcium channel blockers ( nifedipine, verapamil), Bisphosphonates, doxycycline, progesterone (pregnancy/ pill)
    • Decrease alcohol intake
    • H. Pylori eradication
  145. Drug therapy for GORD.
    • 1st line- Antacids: Mylanta, Gaviscon
    • 2nd line- Proton Pump Inhibitors (PPI’s) eg somac, nexium.
    • Excellent response. Good protection. Minimal SE: headache, diarrhoea, nausea, constipation.
    • 3rd line- H2 receptor antagonist eg: zantac, ranitidine SE- liver toxicity, blood dyscrasias,skin rashes etc Motility agents eg domperidone increase rate of stomach emptying. Surgical therapy- vagotomy, Nissen fundoplication
  146. What are some obstructive symptoms not to miss when assessing for GORD?
    Jaundice, regurgitation…bad signs
  147. What is Cholesterol and what are its subtypes?
    Cholesterol is a sterol derived mainly from organic diet. precursor of steroid hormones. Transported as a lipo-protein eg: HDL, LDL, VLDL, chylomicrons
  148. Describe HDL.
    the good stuff. High density of protein to lipid. Found in fish oil. Helps to remove cholesterol from periphery back to liver for excretion via bile acids
  149. Describe LDL.
    The bad stuff. High concentration of cholesterol. Transported away from liver to cells which uptake via endocytosis through a LDL-receptor.
  150. Describe HMG-CoA Reductase.
    It is the enzyme involved in a rate controlling step in formation of cholesterol. Mild anti-inflammatory action.
  151. What is the management for high cholesterol levels?
    • Treat reversible causes of dyslidaemia: hypothyroidism, nephrotic syndrome, cholestasis, NIDDM, obesity, alcohol use, oestrogen use.
    • Diet Modification: decrease saturated fat, increase unsaturated fat, increase fibre, decrease salt, increase plant sterols
    • Risk factor modification eg: OSA , HTN, Smoking, Obesity, NIDDM.
  152. Describe the drug therapy for increased cholesterol levels:
    • 1st line- statins- inhibit HMG-CoA reductase. SE- myalgias, myositis,
    • 2nd line- Ezetimibe- decreases absorption of chol from intestines. SE: diarrhoea, myalgias.
    • Bile-acid resins- cholestyramine binds bile salts in the GIT-> decreasing available acids which trick liver to produce more bile acids->utilising cholesterol in the process. SE- nausea, GORD.
    • Nicotinic acid- SE: flushing, itch, hypotension, myositis, hepatic toxicity
    • Fibrates- Fenofibrate and Gemfibrozil enhance triglyceride clearance. SE: increase risk of gall stones. Phototoxic in some cases. Myositis
  153. Some facts regarding diabetes:
    • 275 new cases / day.
    • Estimated 1.7 million patients but only ½ diagnosed
    • In 20 years, 3.3 million will have DM
    • Cost to the health care system is $10.3 billion
    • Australia’s fastest growing chronic disease
    • 60% are preventable with good lifestyle choices
    • 10-15% of DM are Type 1 in nature.
  154. What is type 1 Diabetes (DM/IDDM)?
    • Absolute lack of insulin either through physical destruction of pancreas or autoimmune destruction of beta cells
    • Usually occurs < 30 y.o., Symptoms include thirst, polyuria, weight loss.
  155. What is the treatment to type 1 diabetes?
    • Treatment requires lifelong insulin replacement and monitoring for complications
    • Combination of long acting and short acting insulin to give basal levels eg: Novomix 30/70
    • Note increased requirements in times of stress, illness etc
  156. What is type 2 Diabetes (DM/NIDDM)?
    • Genetic predispositions. RF include: fam hx, HTN, > 55 y.o. , overweight, Aboriginal / Torres Strait, Pacific Islander, Chinese, Indian, PCOS & gestational DM.
    • Characterised by insulin RESISTANCE or relative decreased insulin production
  157. What is the treatment for type 2 diabetes?
    • Treatment is both conservative initially and with medications if poor glycaemic control
    • Insulin may be needed as a last resort
  158. What are the basic management treatments for T2 Diabetes?
    • Weight loss via Diet and Exercise: decrease fat = decrease IL-1, IL-6, FFA’s , adiponectin, leptin -> decreased insulin resistance.
    • Correction of other risk factors: HTN, Smoking, Renal failure, Foot care, Eye care, Prevention of PVD.
    • Drug Therapy - Glycaemic Control: BSL’s, HbA1c
  159. List the four lines of treatment for type 2 diabetes.
    • 1st line. Insulin sensitizers - Biguanide (Metformin) and Glitazones (Thiazolidinediones/ TZD)
    • 2nd line. Insulin Secretogogues-Sulfonylurea's & Glitinides
    • 3rd line. Acarbose- inhibits alpha-glucosidase (breaks down complex carb’s).
    • 30% of NIDDM’s will go onto requiring insulin. Usually after 10-15 years of oral therapy
  160. Discuss Virchow’s Triad.
    • - Hypercoagulability: composition of blood, Anti-thrombin III deficiency, polycythaemia, thrombocytosis, leukaemia, Protein C deficiency, Factor V Leiden mutation.
    • - Quality of vessel wall: endothelial cell wall injury – plaques, stents,
    • - Nature of Blood Flow: Turbulence, stagnation
  161. List some anti-platelet drugs:
    • Aspirin: inhibits COX pathway which decreases TXA2. prevents platelet binding. Platelet regeneration in 10/7.
    • Adenosine Diphosphate Receptor inhibitors: Clopidogrel (Plavix). The “dog” of surgeons, irreversible for 7 days.
    • Glycoprotein IIB/IIIA inhibitors: Abciximab, Tirofiban
    • Adenosine Re-uptake inhibitors: Dipyrimidole (Persantin)
  162. List some anti-clotting drugs.
    • Heparin: binds to Anti thrombin (IIa) and increases potency by x 1000.
    • Derivatives like enoxaparin (clexane) inhibit anti-Factor Xa activity.
    • SE: osteoporosis, thrombocytopaenia, haemorrhage,
  163. Discuss warfarin.
    • Commonly used for Atrial Fibrillation and DVT prevention.
    • Impairs utilisation of Vit K and stops formation of F2,7,9,10 (TV channels)
    • Needs to be monitored with INR INR easily affected by other drugs eg amiodarone, panadol etc
    • Signs of overdose: Haematemesis/malena, haemoptysis, spont nose bleeds, gum bleeds, bruising
  164. What are the contraindications for clot busters?
    Elderly, pregnancy, retinal disease, recent surgery or stroke
  165. Sensitivity of a drug is affected by the following factors

  166. Renal Excretion capability may be compromised in the following situations:

  167. Significant factors affecting absorption with oral administration include

  168. Which of the following is incorrect regarding routes of administration

  169. Which of the following is incorrect in regards to pain medication:

  170. Glucocorticoids have the following side effects & actions

  171. Colchicine (NSAID) is used to treat gout but may have the following side-effects except:

  172. Short term Benzodiazepines may be indicated in the following cases

  173. Current treatment for Osteoporosis include the following except:

  174. Regarding Bisphosphonates (eg Fosamax) in the treatment of osteoporosis

  175. Which of the following is incorrect in regards to Glyceryl Trinitrate sprays,

    e)May cause a headache
  176. Statins (Atorvastatin / Lipitor) work by

  177. Oral anti-hyperglycaemic agents should be started immediately on a patient who has impaired glucose tolerance
    A) True
    B) False
  178. Good control in a px with impaired glucose tolerance requires:

  179. History taking of a NIDDM patient on oral hyperglycaemics (OHG) include the following:
    a)Time of diagnosis and OHG initiation b)Use of beta blockers
    c)Increasing Oedema, fatigue and nocturia
    d)Recognition of hypoglycaemic effects e)All of the above are correct
  180. Cardiac Risk factors for Ischaemic Heart Disease include the following except

  181. Antibiotics affecting folate metabolism such as trimethoprim are safe and appropriate in the following except:

  182. In regards to Aspirin, which of the following is false?

  183. Anti-epileptic drugs like gabapentin may be useful in the treatment of

  184. Appropriate therapy in a healthy young individual with an acute prolapsed disc causing SEVERE pain includes the following:

  185. An elderly patient on warfarin presenting with headaches should be screened for:

  186. Osteoporosis is associated with which of the following:

  187. Risk factors for osteoporosis does not include:

  188. Beta blockers should be used with caution in which of the following situations:

  189. Anti- viral therapy includes the following

  190. In regards to HIV therapy:

  191. Which of the following in regards to asthma is incorrect

  192. Severe asthma attacks may require treatment with

  193. Tricyclic Anti-depressants may cause the following side effects

Card Set
Pharmacology for chiros
Pharm for chiros