1. Boris Hlebec

2. Contents  What is it ?  Who gets it ?  What causes it ?  What are the symptoms ?  How is it diagnosed ?  What is the treatment ?  How can you prevent it ? ( C an you ?)

3. What is it ?  Hypertension  Mean arterial pressure consistently > 110 mmHg  (Dia >90 ; Sys >140)  Secondary hypertension:  identifiable cause  Renovascular:  hardening and stenosis of the renal artery

4. Who gets it ?  6 out of 100,000 people  Age of onset depends upon cause  Men: >45 years => Atherosclerosis  Women : Fibromuscular dysplasia  10% of children with fibromuscular dysplasia

5. Some risk factors  Smoking  High salt intake  Obesity  Stress  Heavy metals (not music)

6. What causes it ?  Renal ischemia !  Atherosclerosis  Fibromuscular dysplasia  Injury  Tumour  Clots  Whatever that might narrow the renal artery

8. How does that affect blood pressure ?

9. Kidney – a selfish bastard

10. RAAS A – Renal corpuscle B – Proximal tubule C – Distal convoluted tb. D – Juxtaglomerular app. 1. Basal lamina 2. Bowman's capsule – parietal layer 3. Bowman's capsule – visceral layer 3a. Pedicels (podocytes) 3b. Podocyte 4. Bowman's space 5a. Mesangium – iIntraglomerular cell 5b. Mesangium – extraglomerular cell 6. Juxtaglomerular cells 7. Macula densa 8. Myocytes 9. Afferent arteriole 10. Glomerulus Capillaries 11. Efferent arteriole

11. 3 main stimuli for renin release:  sympathetic nerve  β 1 -adrenoceptors  renal artery hypotension  systemic hypotension or renal artery stenosis  juxtaglomerular apparatus  decreased sodium delivery to the distal tubules  macula densa

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13. Angiotensin II  Constricts resistance vessels (via AII [AT 1 ] receptors) thereby increasing systemic vascular resistanceAII [AT 1 ] receptors  Adrenal cortex releases aldosterone => increase sodium and fluid retentionaldosterone  Release of vasopressin (ADH) from the posterior pituitary = water retentionvasopressin  Stimulates thirst centers within the brain  Facilitates noradrenaline release from sympathetic nerve endings and inhibits norepinephrine re-uptake by nerve endings, thereby acting as a sympathomimetic agentnoradrenalinesympathetic nerve  Stimulates cardiac hypertrophy and vascular hypertrophycardiac hypertrophy

14. Symptoms  High blood pressure ( Sherlock)  all the following complications:  Headache  Fatigue  Nausea and vomiting  Chest pain  Vision problems, confusion, anxiety  Excessive perspiration, pale or reddened skin  Sudden pain in the side and bloody urine – CLOT!  No symptoms at all

15. Diagnosis  Severely high blood pressure that is difficult to control  Vascular murmur over left or right lumbar and/or periumbilical regions of abdomen  bruit  Ultrasound  Angiography  Levels of renin production

16. Fibromuscular dysplasia (DSA)

17. Treatment  Lifestyle changes  Medication  ACE inhibitors !!!!!  ATII-R blockers !!!!!  Beta blockers  Ca antagonists  Catheterisation (baloon) - MOVIEMOVIE  Surgery  Bypass  Renectomy

19. Literature  Pathophysiology: Kovač, Marušić, Gamulin (2005)  Guyton’s physiology (2004)  Wikipedia  http://www.hmc.psu.edu/healthinfo/r/renova scularhypertension.htm http://www.hmc.psu.edu/healthinfo/r/renova scularhypertension.htm Mentor: A. Žmegač Horvat