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42 Cards in this Set
- Front
- Back
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A patient was found to have a BP of 153/88
How would you classify this case of hypertension? |
Isolated systolic.
SBP>140, DBP<90 |
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Briefly describe the 7 types of hypertension:
Essential, White Coat, Isolated systolic, Secondary, Complicated, Accelerated, Malignant |
Essential: no cause/multifactorial pathogenesis
White Coat: only when examined by a health professional Isolated Systolic: SBP>140, DBP<90 Secondary: identifiable cause Complicated: HTN + CV damage consequent to it (stroke, CCF etc) Accelerated: markedly elevated BP + retinopathy Malignant: diastolic >140 + papilloedema |
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What is the protocol for diagnosing high BP?
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The average of 2-4 measurements on at least 2 separate clinic visits is higher than normal.
When systolic and diastolic measurements fall into different categories, the higher applies. |
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What are some suggested lifestyle modifications that can be recommended to patients with hypertension?
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Smoking cessation
Sleep apnoea correction Weight reduction Diet - reduce salt and fat, and increase fruit and vegetables Aerobic exercise at least 30 minutes per day Limit alcohol consumption to 1 or 2 drinks per day for women and men respectively. Remember SNAP! (smoking, nutrition, alcohol, physical activity) |
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What are the contraindications to ACE inhibitor use?
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renal artery stenosis (bilateral, or unilateral if single kidney)
renal failure hyperkalaemia angioedema pregnancy |
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What are some drug interactions important for the thiazides?
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ACEis: increase risk of severe first dose hypotension
Digoxin: can cause diuretic-induced hypokalaemia Lithium: decrease lithium clearance NSAIDs/COX-2 inhibitors: decreased natriuresis and decreased antihypertensive effect; increased risk of nephrotoxicity Binding resins cholestyramine/colestipol: decreased thiazide absorption Amphotericin: increased potassium depletion |
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What are the causes of secondary hyperlipidaemia?
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Hypothyroidism
nephrotic syndrome renal failure diabetic dyslipidaemia drug induced - protease inhibitors, glucocorticoids, isotretinoin |
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What are the four conventional classes of drugs used to treat dyslipidaemias?
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HMG-CoA reductase inhibitors
fibrates resins absorption inhibitors |
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Name risk factors for developing atherosclerosis
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Increased cholesterol in LDL, VLDL and IDL
Low levels of HDL Diabetes mellitus Cigarette smoking Obesity Hypertension |
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What are some drugs that can cause hypertension?
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NSAIDs, Oral contraceptives, corticosteroids, erythopoietin, ergotamine, liquorice-containing substances
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Silent ischaemia - what other medical condition do many patients with this type of angina have?
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Diabetes - pain is not transmitted very well due to nerve damage.
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What kind of symptoms are considered "anginal equivalents" and what does this term mean?
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dyspnea (difficulty breathing)
profound fatigue weakness syncope (fainting) diaphoresis (profuse sweating) pain in the back, neck or arm These are all symptoms that a person may experience during an episode of angina or ACS and are needed to diagnose the condition, if no typical chest discomfort is experienced. |
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In stable angina, what are some symptoms other than physical exertion that can precipitate an attack?
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cold weather
smoking a cigarette eating a big meal emotional distress |
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What investigations would a person undergo if stable angina was suspected?
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Blood pressure
Chest X-ray Blood tests: complete blood examination, lipids, glucose, thyroid function, electrolytes and creatinine ECG - stress testing Coronary angiogram |
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What are the directions for taking GTN spray in an acute attack of angina?
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Spray 400 mcg subingual
Repeat after 5 minutes if pain hasn't been relieved If pain still present 5 minutes after second spray, dial 000 |
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What are the first and second line drugs for treatment of stable angina?
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First line:
aspirin beta-blocker Second line: clopidogrel calcium channel blocker nitrates nicorandil |
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Give some practice points for perhexiline.
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Give a large loading dose and measure trough levels after 3 days to identify slow metabolisers.
Monitor peripheral neuropathy, hepatotoxicity, blood glucose (in diabetics) and weight throughout duration of therapy. |
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How should GTN tablets be used in an acute attack?
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- 0.5-1 tablet sublingual
- repeat every 3-5 minutes if pain persists, to a maximum of 3 tablets - if pain still persisting after a few minutes, dial 000! |
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What are the contraindications to GPIIb/IIIa Inhibitors?
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recent stroke (<1 month ago)
uncontrolled hypertension bleeding disorders & thrombocytopenia recent thrombolytic |
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What parameters do we need to monitor when a patient starts an HMG-CoA Reductase Inhibitor?
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Cholesterol
LFTs Creatine kinase - elevation could indicate rhabdomyolysis |
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What are the ADRs of nicotinic acid?
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GIT - epigastric distress, activation of peptic ulcer, activation of chronic bowel disease
Skin - flushing, itching, skin rash, acanthosis nigricans (rare) Other - hepatotoxicity, glucose intolerance, hypotension, hyperuricaemia, cardiac arrhythmias |
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What complementary therapies can help in cholesterol control?
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Policosanol, fish oil and plant sterols
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Why would we need to conduct a chest x-ray to diagnose heart failure?
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As the heart begins to compensate, it hypertrophies and becomes enlarged (cardiomegaly). Over time, the ventricles decrease force of contraction and have difficulty relaxing (incr. afterload).
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What are some lifestyle modifications in relation to diet that will help with CHF?
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- decrease salt intake
- high fibre, low fat - fluid restrictions (if severe) |
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We find that our ACEi dose for CHF is ineffective: should we increase the dose or introduce a beta-blocker?
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The combination of ACEi + beta-blocker is preferred (otherwise we risk hypotension if we increase the dose, then add the beta-blocker later on)
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What are some medications that we should be aware of when initiating ACEi therapy for CHF?
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- avoid NSAIDs/COX2s (renal failure)
- cease amiloride/K+ supplements (hyperkalaemia) - review spironolactone dose (<= 50mg - hyperkalaemia) |
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You find case notes on a patient about to start CHF drug therapy:
Frusemide 20mg daily Will this be sufficient for the patient? |
Loop diuretics should not be used as monotherapy (no compensatory blocking, no decr. mortality). Add to background ACEi or with thiazide (risk dehydration though).
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Which of these isn't used for CHF: a) carvedilol b) metoprolol c) bisoprolol
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Technically, metoprolol is only used as a sustained-release formulation (less evidence for immed-release). Remember to increase dose slowly from very low initial dose - do not stop suddenly
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Which ACE inhibitor has the least likelihood of causing first-dose hypotension?
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Perindopril.
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What is the non-sulfa alternative to frusemide and bumetanide, only used in sulfur allergy?
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Ethacrynic acid
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What is a likely reason for resistant hypokalaemia?
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Underlying hypomagnesaemia
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Which beta-blockers are used in hypertension?
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Atenolol and metoprolol
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How should we go about stopping a beta-blocker in coronary artery disease?
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Discontinue over 1-2 weeks, and advise patient to limit physical activity. Abrupt cessation can lead to severe exacerbation of angina, and MI and ventricular arrhythmias without warning.
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How is Tirofiban used?
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GPIIb/IIIa Inhibitor: used for NSTEACS, high risk patients in conjunction with aspirin and clopidogrel
Administered IV |
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Describe the pathophysiology of Acute Coronary Syndrome (ACS), as experienced in a case of Myocardial Infarction
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Sudden rupture of atherosclerotic plaque and subsequent release of prothrombotic and platelet activating factors lead to thrombus formation. This may lead to partial or full occlusion, causing muscle death (not necessarily in partial).
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How many hours after a MI does PCI (percutaneous coronary intervention) overtake fibrinolytics in reducing mortality?
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3-12 hours - late presentation: PCI is superior
<1 hour - very early presentation: 50% reduction in mortality with thrombolytics 1-3 hours - early presentation: both PCI and fibrinolysis are effective |
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Which is worse: ST elevation myocardial infarction (STEMI) or non-ST EMI?
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STEMI is worse: ST elevation refers to the raised ST segment on ECG, which indicates the full thickness of the heart has died.
NSTEMI have ischaemias limited only to the subendothelium |
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We can diagnose an episode of Acute Coronary Syndrome via blood testing for biomarkers - in particular, certain cardiac enzymes. What are two of these?
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Troponin T/I, Creatine Kinase (CK-MB in heart muscle).
An advantage of CK-MB is we can test again to determine if a subsequent MI occurred (levels normalise in 2 days, cf 10-14d for troponin) |
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What are examples of risk factors for Venous Thromboembolism? (think Virchow's Triad)
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- Venous stasis: major illness/surgery (>30mins) paralysis, immobility
- Vascular injury: multiple trauma, indwelling venous catheters, external compression (tumours etc.) - Hypercoagulable states: protein C/S deficiency, drugs (oestrogens, cigarettes, heparin) - Age: incidence doubles each decade once >40yrs |
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What is the oral dose for unfractionated heparin for prevention of Venous Thromboembolism?
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Oral dosing with UFH is not preferred, due to unreliable absorption (very large molecule). SC or IV infusion only, with dose correlating to weight (except with obese patients).
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How do we manage overanticoagulation with UFH, LMWH and warfarin?
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- UFH: depends on APTT, severity/site of bleeding, time. Protamine +- infusion
- LMWH: depends on bleeding. Protamine (60% reversal) (<12hrs) +- transfusion - Warfarin: depends on INR, bleeding. Vitamin K (not immediate) +- transfusion (fresh frozen plasma +- clotting factor concentrates) Remember: protamine (highly +ve) binds to heparin (highly -ve), while warfarin inhibits vitamin K epoxide reductase |
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How can we monitor the efficacy of Unfractionated Heparins?
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- Activated partial thromboplastin time (aPTT) - baseline, 6hrs after initiation/dose adjustment
- Activated clotting time (ACT): best for high heparin doses - Anti-factor Xa: recommended for heparin resistance LMWHs have predictable response, so no routine monitoring necessary |
