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WEEK 20:
Renin-angiotensin-aldosterone system:
| Question | Answer |
|---|---|
| kidney functions | Regulate pH (H+ and HCO3-) Remove metabolic waste product Produce hormones (erythropoeitin) Activate vitamin D Regulation of osmolarity (control of solute concentrations) Regulation of salt concentrations Regulation of extracellular fluid volume |
| functional unit of kidney | nephron |
| renal corpuscle contains (2) | glomerulus and bowmans capsule |
| juxtaglomerular apparatus (JGA) | structure where afferent arterioles makes contact with DCT, involved in blood pressure regulation and found at vascular pole of each renal corpuscle |
| juxtaglomerular apparatus is made of (3) | macula densa (DCT), juxtaglomerular cells, and extraglomerular mesangial cells |
| macula densa are made of | accumulation of columnar cells within DCT |
| function of macula densa | monitor Na+ concentration in forming of urine, regulate glomerular filtration rate (GFR), and release of renin from juxtaglomerular cells |
| GFR affected by | sympathetic nerves directly innervating juxtaglomerular cells |
| renin | proteolytic enzyme synthesised by granular cells (juxtaglomerular cells) in the wall of glomerular afferent arterioles |
| renin function | cleaves angiotensinogen to angiotensin I (to raise BP via other mediators) |
| when is renin released (3) | in response to decreased arterial pressure, decrease in sodium load to distal tubule, and direct stimulation by sympathetic nervous system |
| why is renin released in response to decreased arterial pressure | body acts like low BP is caused by fluid loss and there are baroreceptors in afferent arteriole |
| why is renin released when there is a decrease in sodium load to distal tubule | macula densa responds to sodium concentration |
| why is renin released in response to direct stimulation by sympathetic nervous system | being stressed raises BP which is mediated through B1 adrenergic receptors |
| ACE conversion largely occurs during | transit through the lungs |
| ACE inhibitors | stop the production of angiotensin II |
| angiotensin II (ANGII) | constricts resistance vessels, stimulates ADH release from the posterior pituitary, stimulates thirst, and promotes aldosterone release from adrenal cortex |
| zona glomerulosa releases | mineralocorticoids eg aldosterone |
| zone fasciculata releases | glucocortocoids eg cortisol |
| zona reticularis releases | gonadocorticoids eg oestrogens |
| medulla releases | adrenaline, noradrenaline (chromaffin cells) |
| aldosterone targets | mostly principal cells in renal tubule distal segments with multiple actions (which promote recovery of Na+ and osmotically obligated water from tubule) taking 48 hours to work |
| antidiuretic hormone (ADH) aka arginine vasopressin is released from | posterior pituitary when tissue osmolality rises of blood volume decreases |
| if circulating levels of ADH is high | it can vasoconstrict too eg in haemorrhage |
| high RAA can occur in what conditions | both chronically and acutely in response to decrease in blood flow to kidney |
| hypertension (HTN) | abnormal elevation of systolic and or diastolic blood pressure, generally asymptomatic for many years |
| secondary hypertension | occurs when specific cause for HTN found (hence secondary to underlying disease process) eg renal disease and primary hyperaldosteronism (too much also) aka Conn's syndrome |
| primary (Essential) hypertension | cause unknown in 95% of cases, can be benign (slowly progressive) or malignant (rapid onset and above 180/110) |
| benign primary (essential) hypertension | slowly progressive |
| malignant primary (essential) hypertension | rapid onset and above 180/110 |
| describe the RAAS system | key hormonal regulator of blood pressure where its activation promotes vasoconstriction through angiotensin II and sodium and water retention through aldosterone |
| which demographic/ epidemiology of people have elevated blood renin concentrations | in hypertensive patients who are white and aged less than 55 |
| hypertensive shock | condition in which blood pressure is below autoregulatory range for maintenance of cerebral and renal perfusion so consciousness is lost and vital organ perfusion is critically impaired |
| shock | reduced perfusion of tissue which results in impaired oxygenation of tissue |
| types of shock | cardiogenic, hypovolaemic, distributive, and obstructive |
| obstructive shock | cardiac tamponade and tension pneumothorax |
| why does hypovolaemic shock occur | due to excessive loss of sodium containing fluid (Eg blood, sweat) causing hypotension and multiorgan failure and decreases CO |
| range for loss of blood volume leading to hypovolaemic shock | >20% (1000mL) |
| common causes of hypovolaemic shock occur | penetrating trauma, gastrointestinal bleeding, trauma to solid organ (eg liver), and a ruptured abdominal aortic aneurysm |
| BP formula | BP = CO X total peripheral resistance |
| low BP can be due to | low CO and or peripheral vasodilation |
| explain decreased left ventricular end diastolic pressure (LVEDP) | lowered by a lower volume of blood entering the heart |
| increase in vascular peripheral resistance (PVR) is due to (3) | catecholamines (cause vasoconstriction), ADH (can also cause vasoconstriction) and ANGII (vasoconstriction) |
| what causes vasoconstriction (2) | ANGII and ADH |
| all effects of shock lead to | decrease in oxygen delivery to tissues leading to SHOCK |
| what can you investigate in clinical findings | pulse (rate, rhythm and character), BP (symptoms), skin colour and character, urine output, and blood tests |
Created by:
kablooey
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