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Clinicopathological conference: hypertension. TAKE HOME MESSAGES PowerPoint Presentation
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Clinicopathological conference: hypertension. TAKE HOME MESSAGES

Clinicopathological conference: hypertension. TAKE HOME MESSAGES

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Clinicopathological conference: hypertension. TAKE HOME MESSAGES

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  1. Clinicopathological conference: hypertension.TAKE HOME MESSAGES • HBP is common and usually asymptomatic. • Vast majority of cases are primary. • Treatment is to reduce stroke (and IHD) risk. • Most patients don’t take their medicines. • See http://www.hyp.ac.uk/bhs/gl2000.htm

  2. The case. • A 45 year old man referred for investigation. • GP has started a screening programme for hypertension: • 200/100 in December • 190/96 in January • 190/102 in March • Asymptomatic

  3. What symptoms did you expect?

  4. What symptoms did you expect? • Usually none. • Relationship to headache dubious. • (Causes of HBP) • (Results of HBP)

  5. Family history

  6. Family history • Father died of stroke aged 55 • Mother has had 2 x MI • Elder brother has NIDDM

  7. Social history

  8. Social history • Unemployed ex car-worker • Married with kids at home • Smokes 20 per day • Drinks ‘a couple of pints per day’. • Likes salt • No medications • No known allergies.

  9. Review of systems: causes of HBP?

  10. Review of systems: causes of HBP? • Urinary • Dysuria? • Nocturia? • Poor stream? • (Flushing) • (Polydypsia)

  11. Review of systems: consequences of HBP?

  12. Review of systems: consequences of HBP? • Chest pain? (Angina) • Dyspnoea/orthopnoea (LVF) • Transient neurological syndromes • amaurosis fugax • transient hemiparesis • perturbation of consciousness

  13. Review of systems: conditions relevant to drugs

  14. Review of systems: conditions relevant to drugs • Airways obstruction: beta blockers • Local urinary problems (prostate in men, stress incontinence in women): loop diuretics.

  15. Examination?

  16. Examination? • The BP today. • Consequences of hypertension • Other causes of atheroma • Causes of hypertension His BP is 190/100.

  17. Consequences. • Apex beat. • Heart sounds. • Fundi. • (Signs of heart failure) CLINICAL PICTURES: fundi

  18. Other causes of atheroma.

  19. Other causes of atheroma. • Hyperliproteinaemias: • Xanthomata • Xanthalesmata • Corneal arcus CLINICAL PICTURES: xanthalesmata etc.

  20. Causes #1 • Endocrine • Phaeochromocytoma • Cushings • Acromegaly • Conn’s • Metabolic • Hypercalcaemia CLINICAL PICTURES

  21. Causes #2 • Vascular • coarctation of the aorta • renal artery stenosis • Renal • polycystic kidneys • features of chronic renal failure • features of nephrotic syndrome

  22. The case • Nil on REVIEW OF SYSTEMS • Nil on EXAMINATION (save a wheezy chest)

  23. What tests do you want? • Urinary • Blood • Imaging • ‘Special’

  24. What tests do you want?Urine tests. • Dipstick urinalysis • Blood and protein: could be a clue to renal pathology • Sugar: may be a clue to diabetes mellitus • MSSU • look for WHITE CELLS as well as organism growth All normal

  25. What tests do you want?Blood tests Assess renal function: urea and creatinine. (Assess calcium). (Assess potassium). All normal Fasting blood sugar Fasting lipids Cholesterol = 7.2 mmol/L

  26. Imaging: what do you want to know?

  27. Imaging: what do you want to know? • CXR may help you decide about cardiomegaly (but many radiologists think this unnecessary). • CXR will allow assessment of his COAD, and will exclude unsuspected cancer. • (CXR may pick up coarctation).

  28. Imaging: what do you want to know? • Renal ultrasound scan • helps exclude polycystic disease, RAS and hydronephrosis. • But, unless the biochemistry is abnormal, renal U/S is often not needed. R = 13 cm and L = 9 cm. ?RAS. WHAT NEXT?

  29. Renal isotope scan with captopril challenge • Isotope is injected IV and excreted. • Scanning allows the rate and extent of excretion of isotope to be determined for each kidney • Captopril would reduce perfusion in a kidney with RAS Our patient’s scan is normal. But, had it shown RAS, what next?

  30. Summary so far. • Young smoker with + FH. • GP has already established sustained HBP. • Tests show mild  cholesterol. • Life style • Drugs

  31. Life style • Stop smoking • Reduce saturated fat, alcohol, salt. • Increase oily fish and vegetables. • Exercise.

  32. Choice of drug • Little evidence of differences in efficacy • Patient needs to understand the aims of treatment… • …And the risks. • Aim for as few drugs as possible… • ...At as low a dose as possible.

  33. Thiazides • Bendrofluazide • Inexpensive, effective. • Increase cholesterol and sugar • May precipitate gout • May cause impotence

  34. ACE-inhibitor • Captopril, enalapril, ramipril, lisinopril • Effective but more expensive. • Well tolerated. • Contraindicated in the presence of bilateral RAS (rapid worsening of renal function).

  35. Calcium channel antagonist. • Nifedipine, verapamil, nicardipine, diltiazem • Effective, more expensive than thiazide. • Lots of symptomatic toxicity: • constipation • flushing • ankle swelling • (gum hypertrophy)

  36. Beta blocker • Atenolol • Effective and inexpensive. • Contraindicated in: • airways obstruction • PVD • Bradyarrhythmias • (Heart failure) • Symptomatic adverse effects.

  37. The case • BP remained high on two further outpatient visits. • Cholesterol was unaffected by diet (did he stick to it?) •  enalapril and simvastatin September 1998.

  38. Follow up • October 1998: still no lifestyle change. BP = 180/100. • February 1999: cholesterol now 5.0. Enalapril dose now maximal. BP 170/100. • April 1999: BP 160/96. Add thiazide. • June 1999: BP 140/92. Cholesterol 6.2. Simvastatin dose increased.

  39. Emergency admission July 1999 • 2 hours of tight retrosternal pain associated with: • sweating • dyspnoea • nausea • Pale, BP = 110/50. Fine basal crackles. What diagnosis? What tests? Briefly, what management?

  40. Tests and management. • ECG looking for ST segment changes. • Troponin-T • Chest radiograph. • Diamorphine • FOLLOW PROTOCOL for streptokinase • Monitor • Aspirin

  41. Further follow up • September 1999: no change in lifestyle. 160/94, cholesterol 5.5. • November 1999 2 episodes sudden loss vision L eye. Carotid bruit noted. • Diagnosis and investigations?

  42. Amaurosis fugax

  43. Retinal artery occlusion

  44. Tests • Carotid Doppler studies: 80% occlusion of L carotid artery. • Referred for vascular surgery opinion. • Continued on aspirin

  45. http://pathology.mc.duke.edu/neuropath/nawr/blood-set.html