Pharmacology for chiros
Home > Flashcards > Print Preview
The flashcards below were created by user
on FreezingBlue Flashcards
. What would you like to do?
IM ketoralac and valium. What do
you have to ask about?
GORD, bleeding tendency, driving machinery.
Which pathological states result in hyperkalemia?
diet, CRF/ARF(SLE, DM),NSAID use potassium supplements, diuretics eg: spironolactone. ACE-i.
Definition - Pain?
an unpleasant sensory or emotional experience associated with actual or potential tissue damage, or described in terms of such damage.
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.
What controls pain?
higher cortical areas; at a minimum the thalamic areas.
Pain mechanisms: Inflammation
What is the cellular component?
This occurs at the microscopic level where damage occurs, starting a cascade of events
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
What are the key features of inflammation?
Redness, Swelling, Heat, Pain and loss of function.
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
What is COX?
COX - Prostaglandins (PGE2, PGI2 (prostacyclin)), thromboxanes(TXA2)
What is LOX?
How many isoforms does COX have?
Two - COX1 and COX2
What is COX1?
Present in normal cell homeostasis (kidney, gastric mucosa, airways and platlets)
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Is supposed to be more pro-inflammatory and selective COX2 inhibitors like Celebrex and Vioxx (withdrawn) were supposed to have less COX1 effects.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.
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.
Prostaglandin is needed for gastric mucosa secretion and NSAIDs stop this. What does this result in?
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.
What are the consequences of PGE/PGI?
- Arteriolar smooth muscle vasodilation
- GIT smooth muscle contraction-coliky pain
- Inhibition of platelets
- Induction of labour, Dysmenorrhoea
- Maintains Patent ductus arteriosus in utero
- Increases GFR / Gastric mucosal secretion
What are the consequences of TXA2?
Promotes thrombosis, greatly increases platelet adhesion
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
Stimulation of nociceptors result in transmission to the CNS via?
A-delta and C-fibres
What is gating?
Stimulation of A-beta fibres resulting in inhibition at the subs gelatinosa
Activity of the C-fibres may be up-regualted peripherally by what in the damaged tissues?
Serotonin, prostaglandins, thromboxane and leucotrienes
What is Hyperalgesia?
Increased sensitivity of normal pain fibres
The A-beta fibres now respond to stimuli that activate the nociceptive pathway at the CNS level. What is this called?
Central sensitisation occurs as a result of what?
As sensitivity increases....
Threshold for firing decreases. NMDA and AMPA receptors are added to cell membranes at subs gelatinosa. Glutamate (excitatory) is released.
Convergance allows for other areas to be regarded as painful
What is Long term potentiation?
Synthesis of new proteins which inhances synaptic transmission
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
Analgesics - List 5 Opiates
Morphine, Pethidine, Oxynorm, Oxycodone, Fentanyl
Analgesics - List 7 steroids
(Fucking Hot People Bite The Dust Majorly)
Fludrocortisone, Hydrocortisone, prednisolone, betamethasone, triamcinolone, dexamethasone, methylprednisone
Analgesics - List 2 opiate-like meds
Analgesics - List 3 combinations
(Pretty Pink Makeup)
Panadeine, pandadeine forte, mersyndol
Analgesics - List 6 NSAIDS
Voltaren, Ponstan, aspirin, nurofen, indocid, colchicine
Analgesics - List 1 Simple
Asthma is a polygenetic disease linked with which disorders?
Eczema, hay fever. Prelevance of 1/4
With asthma, sensitivity to certain allergens which result in bronchospasm. Is this reversible?
Yes reversibility is a key component.
What are some common triggers of asthma?
Common triggers: EIA, Infective, Stress, Cold etc.
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.
How is COPD characterized?
Characterised on spirometry or forced expiration time >7sec.
True or false: COPD commonly has genetic links?
Rarely genetic links. Usually with a history of smoking
What is a common example of COPD?
Emphysema is the classic example
What does Paracetamol do?
Inhibits COX pathway but lacks the anti-inflammatory effects of NSAIDs
How is paracetamol best given (max dose)?
Regualarly, max dose of 4 grams daily
How many grams of paracetamol can be taken before it is toxic or fatal?
- Toxic: 8 grams
- Fatal: >15 grams
Is paracetamol safe during pregnancy?
What sub groups of patients need to be careful when taking paracetamol?
- CLF: Hepatitis B/C, Haemochromatosis, biliary cirrhosis,alcoholics.
- CRF: Diabetics, Elderly
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.
Other than as an analgesic what is aspirin used for?
- Thinning blood in cardic and stroke patients.
- Good for viral illnesses
How long does it take for platelets to regenerate?
What are the signs and symptoms of Reye's syndrome?
Neurological disturbance (ataxia, lethargy, nystagmus, fits), diarrhoea +/- vomiting, hypoglycaemia, elevated LFT’s.
What does fish oil do?
Decreases synthesis of TXA2 anti-inflammatory effects and mild anti-platelet effect
What id the appropriate dose of fish oil?
2.7 grams/day (14 tablets!)
Why should you avoid cod liver oil?
Increased cholesterol and Vit A toxicity
What are the potential side effects of fish oil?
Bad in gall bladder removal, flatulence, stincky breath, farts, reflux, bleeding
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)
What are NSAIDS used for?
Acute inflammation, injury, dysmenorrhoea, headaches
Who should you NEVER give NSAIDs to?
3rd trimester pregnant women!!!
What is a side effect of NSAIDs?
Mild blood thinning effect and GORD can be severe if long term
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)
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.
What does GCS inhibit?
NF-kB, PhospholipaseA2, COX pathway and stops the inflammatory process on a number of levels
What is the Physiologic effects of GCS?
- Suppresses TSH/FSH.
- Increases GH.
- Increases insulin (d/t BSL).
- Net effect weight gain centrally.
What are the metabolic effects of GCS?
Increases BSL's (gluconeogenesis) by breaking fat, protein and carbs down.
What are the Catabolic effects of GCS?
- Connective tissue (eg skin), decrease muscle mass, osteoporosis.
- Reduction in growth in kids despite GH.
What are the Anti-inflammatory effects of GCS?
- Decreased PG, leukotiene.
- Short term increase in neuts but impotent.
- Decreased healing.
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
What is addisonian crisis?
Hypotension, vomiting, nausea, fatigue, dizziness, muscle weakness, anxiety, diarrhoea
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.
What causes neuropathic pain?
Usually occurs after a significant insult to the nervous system.
Is neuopathic pain normally acute or chronic?
What symptoms are associated with neuropathic pain?
Parethesias, radiculopathy, dull aching
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
What are the preventative drugs for migraine?
- Anti HTN - mechanism unknown
- TCA's - Reinforces serotonin dysfunction theory
- Pizotifen - 5-HT Antagonist
- Botulinum toxin - BOTOX to neck muscles
What are the abortive drugs for migraine?
What is Chvosteks sign?
Tapping the facial nerve - twitching
What are some types of muscle relaxants?
- GABA agonist
- Side effects - risk of falls, memory affected, drowsy
If the problems with muscle spasm are with sleep initiation or acute anxiety should you use short of long acting benzo?
What is Baclofen?
GABA agonist - works by hyperpolarising the cell membranes. Casues much less sedation than benzos
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
What is novel therapy for muscle spasms?
BOTOX injections - inhibits muscle completely
List 5 seronegative arthropathies
List 6 seropositive arthropathies
- Antiphospholipid syndrome
- Sjogrens syndrome
List 2 non-articular rheumatic diseases
- Polymyalgia Rheumatica
List 2 crystal induced arthropathies
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
What is the result of rheumatic diseases?
Chronic pain, loss of function, systemic decline/impairment, finacial burden, social burden, genetic repercussions, SE of meds
What is the symptomatic management of Rheumatic diseases?
- Chiropractic! and the like
- Fish oil
What do DMARDS do?
Reduce synovial inflammation and prevent joint damage - lots of SE!
eg. Methotrexate, hydroxychloroquine, leflunomide, azathioprine, cyclophosphamide, sulphasalazine
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
What should you avoid when taking methotrexate?
Alcohol abuse, hepatitis, pregnancy
What are the side effects of methotrexate?
Nausea, mouth ulcers, pancytopenia, fibrosis and cirrhosis of the liver
What does leflunomide do?
Blocks synthesis of pyridoxines and inhibits activated lymphocytes
What are the side effects of leflunomide and when should it not be used?
Liver dysfunction, diarrhoea, alopecia, rash
In pregnant women - teratogenic
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
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
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
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
What needs to be monitored during treatment?
- Clinical monitoring: Pain, function, synovitis
- Lab monitoring: CRP, ESR, antibody titre eg. rheumatic factor, ANA titre
How is gout treated?
NSAIDS esp - colchicine - inhibits mirotubule formation and decreases phagocytosis. Prednisolone can me used
Prevention is dependant on cause
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
List some examples of Microbes:
Prions, Viruses, Bacteria, Fungi, Parasites
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
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
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.
- 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
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
What can bacteria be classified in?
- Gram stain: either gram + or gram –
- Then they are mainly cocci or rods. Some are strange eg. spirochetes
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.
List some G+ bacterial Rods.
- 1)Clostridium eg. Clostridium tetani, Clostridium perfringens – gas gangarene.
- 2) Bacillus Anthracis - Anthrax
- 3) Cornybacterium Diptheriae
List some G- Cocci bacteria.
Neisseria Meningitidis, Neisseria Gonorrhea
List some G- bacterial Rods
E coli, Salmonella Typhi, Shigella, Legionella, Helicobacter Pylori, Pseudomonas, Vibrio cholera
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
What are Cephalosporins used to treat?
Bacteria. eg keflex. Usually given when allergic to penicillin's. 10% cross over reactivity. Better G- cover
What is Clavulanic acid used for?
Bacteria. usually combined with penicillin to give augmentin which overcomes beta-lactamase.
What are Macrolides used to treat?
Bacteria. Erythromycin (rulide) - covers atypical resp infx eg Legionella, mycoplasma.
What are Trimethoprim / Sulphonamides used for?
Bacteria. Affects folic acid synthesis.
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
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.
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.
List some common parasitic infections.
Malaria, Worms (helminths), scabies (mites), lice (pediculosis)
- 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
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
Summary of PTH:
- Renal: Decreases Ca and Phos excretion
- Bone: Increases Ca and Phos resorption
- Serum: Increases Ca, decreases Phos
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
- From parafollicular cells in thyroid
- Inhibits osteoclasts - blocks bone resorption
- Useful in Paget's, hypercalaemia and osteoporosis
- Blocks collagen synthesis
- Increases PTH stimulation
- Increases renal Ca excretion
- Can be used for hypercalaemia
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
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
What are the drugs used to treat osteoporosis?
- Ca supplements
- Vit D supplements
- Strontium Ranelate
- E2 supplements
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
What is ACS?
Plaque rupture and thrombosis leading to acute myocardinal infarction
What is Angina?
Demand ischaemia due to stenosis of coronary arteries. No death of tissue.
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
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
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
What are the SE of beta-blockers?
Asthma, postural hypotension, cold limbs, erectile dysfunction, lethargy
What are the SE of Calcium Channel Blockers?
What are the SE of Nitrates?
headaches, light headed, oedema
What are the anatomical sphincters associated with GORD?
- Gastro-oesophageal jx
- Oesophageal-diaphragm jx
- natural innate tone (LES)
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
What is the main cause of gastric ulcers?
Helicobacter Pylori infection- 80-90% of ulcers
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
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
What are some obstructive symptoms not to miss when assessing for GORD?
Jaundice, regurgitation…bad signs
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
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
The bad stuff. High concentration of cholesterol. Transported away from liver to cells which uptake via endocytosis through a LDL-receptor.
Describe HMG-CoA Reductase.
It is the enzyme involved in a rate controlling step in formation of cholesterol. Mild anti-inflammatory action.
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.
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
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.
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.
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
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
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
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
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
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
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)
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,
- 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
What are the contraindications for clot busters?
Elderly, pregnancy, retinal disease, recent surgery or stroke
Sensitivity of a drug is affected by the following factors
c)Age of the patient
e)All of the above.
Renal Excretion capability may be compromised in the following situations:
c)Long term NSAID use
d)Polycystic kidney disease
e)All of the above.
Significant factors affecting absorption with oral administration include
a)Autoimmune disease eg. Crohn’s disease
d)Lack of co-factors for absorption
e)All of the above
Which of the following is incorrect regarding routes of administration
a)IV is the quickest and most direct route
b)Oral administration is the slowest route
c)Rectal absorption is the slowest route
d)Topical applications by-pass 1st pass metabolism
e)Sublingual applications by pass 1st pass metabolism
Which of the following is incorrect in regards to pain medication:
a)Paracetamol should be given regularly for maximum effect
b)NSAIDS are a good choice in pregnancy related back pain
c)Laxatives should be prescribed in conjunction with long term opiate use
d)Short term use of opiates rarely leads to addiction
e)Morphine causes dysphoria in certain cases
Glucocorticoids have the following side effects & actions
b)Predisposes to vertebral compression fractures
c)Increase insulin activity
d)A & B are correct
e)Only B is correct
Colchicine (NSAID) is used to treat gout but may have the following side-effects except:
d)Increase in platelet activity
Short term Benzodiazepines may be indicated in the following cases
a)Patients with emphysema with cyanosis on minimal exertion with difficulty sleeping
b)Insomnia from the loss of a loved one
c)A patient with a headache after a concussion
d)Narcolepsy (sudden/unpredictable sleep onset)
e)Patients operating heavy machinery
Current treatment for Osteoporosis include the following except:
a)Bright light therapy
b)Adequete supplementary calcium and Vit D intake
d)Regular weight bearing exercise
Regarding Bisphosphonates (eg Fosamax) in the treatment of osteoporosis
a)They may be prescribed on suspicion of osteoporosis in a patient
b)Can cause oesophagitis
c)All patients need a dental review prior to commencement of therapy
d)Needs to be taken on an empty stomach immediately before sleep for maximum absorption
e)A & D are incorrect
Which of the following is incorrect in regards to Glyceryl Trinitrate sprays,
a)Repetitive use (after 3 attempts without relief) is an indication for urgent medical assessment
b)Is safest used sitting or lying down
c)Takes approximately 15 mins to work d)Causes veno-dilatation predominantly
e)May cause a headache
Statins (Atorvastatin / Lipitor) work by
a)Decreasing Low density lipo-proteins (LDL’s)
b)Stabilisation of the athersclerotic plaque
c) Inhibiting HMG Co-A reductase
d) All of the above are correct
Oral anti-hyperglycaemic agents should be started immediately on a patient who has impaired glucose tolerance
Good control in a px with impaired glucose tolerance requires:
a)Patient education & compliance
c)An insulin pump
d)Combinations of oral hyperglycaemic agents
e)Only a & b are correct
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
Cardiac Risk factors for Ischaemic Heart Disease include the following except
a)Type 1 Diabetes Mellitus
d)Obstructive Sleep Apnea
Antibiotics affecting folate metabolism such as trimethoprim are safe and appropriate in the following except:
a)Patients with Cancer
c)High performance Athlete
d)Patients with Macrocytic Anaemia
e)B & D only
In regards to Aspirin, which of the following is false?
a)It binds reversibly with platelets
b)It has a strong effect on Thromboxane A2
c)It may cause a malena (blood in stool)
d)Works by inhibiting the COX pathway e)Low dose may be used in pregnancy with patients who have SLE and recurrent miscarriages
Anti-epileptic drugs like gabapentin may be useful in the treatment of
a)Tonic-clonic seizure activity
c)Phantom limb pain
e)A, b and c are correct
Appropriate therapy in a healthy young individual with an acute prolapsed disc causing SEVERE pain includes the following:
a) Paracetamol, Voltaren (NSAID)
B) gabapentin (anti-epileptic)
C) Paracetamol, Voltaren, oxynorm (opiate), diazepam (gaba-agonist)
D) TENS and heat therapy only
E) Oxynorm and gabapentin only
An elderly patient on warfarin presenting with headaches should be screened for:
A) Temporal arteritis
B) Subdural Haemorrhage
C) Raised intracranial pressure
D) all the above are correct
E) only a and c are correct
Osteoporosis is associated with which of the following:
A) Femoral neck fracture
B) Greenstick fracture
C) Colle’s fracture
D) sternal fracture
E) A and C are correct
Risk factors for osteoporosis does not include:
A) Nursing home residents
B) Using the oral contraceptive pill
C) Menopause at 42 years old
D) Bilateral Oophrectomy (ovary removal) during adolescence
E) Use of prednisolone for long term control of eczema
Beta blockers should be used with caution in which of the following situations:
A) Severe asthmatics
B) Peripheral Vascular disease
C) Diabetic patients on insulin
D) Patients with low blood pressure
E) All of the above
Anti- viral therapy includes the following
A) Neuro-aminidase inhibitors
C) Erythromycin (macrolide)
D) A & C are correct
E) A & B are correct
In regards to HIV therapy:
A) monitoring CD4 counts and viral loads are indicative of viral activity
B) HIV has a long latent period
C) Monotherapy with a single agent is the best option
D) A & B are correct
E) B is the only correct option
Which of the following in regards to asthma is incorrect
A) It is linked with hayfever, eczema and other allergies
B) Beta blockers are the mainstay of treatment
C) Steroids should be used if initial therapy is not adequete
D) Flares are more common in winter months
E) It is a bronchospasm involving small airways
Severe asthma attacks may require treatment with
C) Invasive ventilation
D) Ipratropium bromide (parasympathetic antagonist)
E) All of the above
Tricyclic Anti-depressants may cause the following side effects
A) cardiac arrythmias
B) dry mouth
C) Urinary retention
D) dry eyes
E) All of the above
What would you like to do?
Home > Flashcards > Print Preview