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Clinicopathological conference: hypertension. TAKE HOME MESSAGES

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. The case.

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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

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