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Renal system - Coggle Diagram

- - - - acellular
      - collagen and glycoproteins discourage filtration of small proteins since glycoproteins are negatively charged
      - albumin (smallest plasma protein) can pass if the maintain is strectched due to high blood pressure byut generally won't because of repelling
      - if proteins pass it can indicate nephritis
      - high intenesity exercise can cause transient barrier disruption and cause albumin to be led into urine
    - - Molecules move through podocytes
      - filtrate enters lumen of Bowmen's capsule
      - fluid is now the filtrate and is modified to the point of urine
  - - - if blood pressure at afferent arteriole end increases the rate remains the same because of autoregulation
      - the afferent is not under neural control but rather an intrinsic control in response to pressure change, the sympathetic control comes at arcuate arterial end so there is some nervous control but none at afferent
      - if pressure increases the filtration rate increases then processes allow vasodilation of afferent to restrict blood pressure to reduce it back to normal adn vasoconstriction of efferent and incrase in holes of Bowman's tubule
- - - - Renin-angiotensin-aldosteron esystem controls aldosterone secretion
      - no aldosterone is secerted when Na+ load is high
      - liver secretes angiotension and kidneys secrete renin to angiotensin 1 (inactive) which is then converted to angiotensin 2 (catalysed by enzyme from lungs) (active)
      - angiotensin 2 acts on adrenyl cortex to release aldosterone
  - - - controlled by aldosterone
      - Nautriuretic peptides
        
        these inhibit Na+ in distal regions of nephron
        
        they inhibit renin secretion by kidney adn aldosterone from aldosterone secretion
        
        if sodium is retained then blood pressure increases so the heart stretches more, this degree of stretch control their release- atria release ANP and ventricle release BNP (ANP more effective than BNP)
        
        overall effect is reduced blood pressure since reduced Na+ load and thus reduced fluid load, it also reduce peripheral vascular resistnace by inhibiting sympathetic NS to heart and blood vessels
    - - symport carries Na and glucose cotransporter allows passive Na+ across luminal membrane and basolateral pump moves Na+ into lateral space
      - this pulls glucose through SGLT against concentration gradient
      - passive diffusion down concentration gradient across basolateral membrane into plasma through faculative carrier glucose transporter
    - - water passively moves through tubule becasue of movement of Na+
      - absorbed in proximal tubule (65%) and descending limb of LoH (15%)
      - aquaporins
        
        aquaporin 1 is always open
        
        hypertonicity in lateral space
        
        AQP2 is in distal part of nephron under vasorepression
      - water can either move between cells or through water channels
      - more 75% of fluid that intiially enters the nephron is reabsorbed but the overall osmolarity does not change so it is isomotic reabsorption
    - - urea concentration in filtrate=plasma urea concentration so no net movement of urea
      - extensive reabsorption of water reduces volume so increase concentration by end of proximal tubule, which creates concentration gradient between filtrate
      - tubule walls are not fully permeable so 50% reabsorbed but usually adequate removal
- - - - bicarbonate is made in the cells and secreted into the bloodstream where it acts as a buffer
      - H+ is then secreted out of Type A I cells through a channel into the filtrate (combines with a phosphate) and reabsorb bicarbonate
      - H+ can then be excreted as ammonium ion when combined with amino acid
      - H+ comes from carbonic anhydrase (which is important as otherwise it would rely soley on natural diffusion)
    - - Type B I cells excretes bicarbonate and reabsorbs H+
      - Type B have ATPase on basolateral surface which means potassium is now excreted
  - - - increased breathing, more CO2 loss
      - cannot generate enough bicarbonate so kidneys massively reabsorb bicarbonate (in Type A I cells)
    - - hypoventilation means CO2 is retained adn H+ and bicarbonate levels are elevated
      - this creates an acidic pH
      - commonly seen with alcohol, drug use, asthma, lung disease
    - - diets increase H+ input or lactic acid builds up or ketoacidosis (excessice breakdown of fats or certain amino acids)
      - H+ increases so pH and bicarbonate decrease
    - - Hyperventilation means less CO2
      - this causes low H+ so pH rises
      - kidney uses Type B to excrete bicarbonate
      - rebreathing CO2 can reintroduce CO2 into the bloodstream
    - - excessive vomiting of stomach acid or excessiveingestion of bicarbonate antacids reduces H+ and CO2 and increases bicarbonate
      - the body tries to compensate with hypoventilation and by excreting bicarbonate and reabsorbing H+
- - - - there is 25% Na+ and K+ erabsorption in ascending limb
      - the luminal side contains ion symporters which pulls in Na+, then K+ and Cl- follow. The Basolateral side has a Na-K ATPase to pump Na out and K+ and Cl- leaky channels
      - The NKCC symporter uses energy stored in Na+ concentration gradient to transport Na+ K+ 2Cl- from lumen to epithelial cell
      - NKCC mediated transport can be inhibited by loop diuretics Furosemide
  - - - V2 receptor (in blood vessel) and V1 (on basolateral surface) to exert vasoconstrictor effect
      - binding of ADH stimulates mechanism
      - aquaporins are stored in vesicles ready for release and type 2 are inserted in luminal side
      - osmoreceptors are stretch sensitive neurones that increase fire rate as osmolaroty increase, so high salt concentration increase vasopressin release
      - need a 4% change in plasma osmolarity to stimulate a need to drink
      - cells shrink and nonspecific cartionic channles linked to actin filaments open which depolarises the cell but are only activated above 280mOsm
    - - lots of vasopressin is released to produce concentrated urine in mourning
      - nocturnal enuresis is reduced vasopressin secretion and results in bed wetting
    - - water deficit
        
        water moves by osmosis into interstial fluid
        
        0.5L of urine produced per day, concentrated (0.3ml/min)
      - water excess
        
        hyptonic tubular fluid entering distal and collecting duct
        
        no vasopressin and no reabsorption
        
        large dilute urine produced (25ml/min)
- - - - innervated by sympathetic NS so when activated it constricts and reduces blood supply
      - blood moves into the kidney s and divides into interlobular arteries
    - - interlobular veins brings blood back to renal veins
      - renal vein feeds into vena cava
    - - near Bowman's capsule
      - arteries give rise to afferent arteriole then glomerulus then efferent arteriole
    - - ball of capillaries
      - exits into efferent arteriole then into loop of Henley and collecting duct
      - after efferent arteriole is the peritubular
    - - these capillaries surround the proximal and distal convoluted tubules
      - some peritubular capillaries run into medulla parallel to LoH forming vasa recta
  - - - mainnly in cortex
      - called proximal because near glomerulus
      - goes down into medulla and then into loop of Henley
    - - separated into ascending and descending
      - ascending has a thick and thin segment
      - macular densa are short segments of specialised epithelia cells that produce renin which is needed to converts angiotensinogen to angiotensin (regulates blood pressure)
      - some nephrons have londer LoH than others which is an adaptation to concentrate urine
    - - short segment between macula densa and collecting duct
    - - Cortical nephron
        
        Glomeruli in cortex
        
        Short loops of Henley
        
        long efferent arteriole
      - Juxtamedullary nephron
        
        Bowman capsule on cortex-medulla border
        
        LoH is deep in medulla
        
        Long efferent arterioles
        
        specialised peritubular capillaries to produce concentrated urine
- - - - Plasma clearance is less than GFR
        
        glucose plasma clearnace should be 0 since all filtered glucose is reabsorbed with the rest of the returning filtrate
        
        urea is partially reabsorbed so only part of the filtered plasma is cleared, 50% filtered urea is passively reabsorbed so 62.5ml/min is cleared
        
        this is when a substance is freely filtered and reabsorbed but not secreted
      - Plasma clearance is greater than GFR
        
        this is when a substance is filtered and secreted but not reabsorbed
        
        only about 20% of plasma entering the kidney is filtered so rest is cleared using secretion
        
        H+ filtered plasma is cleared of non reabsorbable H+ but the plasma from which H+ is secreted is also cleared of H+, so clearance rate for H+ is 150ml/min so 125ml of plasma loses H+ through filtration (with no reabsorption) and 25ml through secretion each minute
- - - - there is active absorption of K+ without regulation and then goes straight into blood stream since ECF has relatively small K+ concentration as 98% of K+ is in intracellular fluid
      - filtered K+ is almost completely reabsorbed in prosimal tubule meaning any K+ in urine comes from secretion
    - - a Na-K pump establishes a gradient so that potassium diffuses out of the blood into the interstitial fluid
      - The ATP channel then pumps K into the principal cell and the presence of leaky channels means K moves into the lumen
      - when K+ levels are low the secretion is low since electrochemical gradient needs to be maintained
      - when K+ levels are high the secretion in distal nephron is increased so just enough is added to filtrated to reduce plasma K+ to normal
      - mechanism
        
        Mechanism Na+ is transported to lateral space from principal cell and K+ moves into principal cell from lateral space (Na-K pump)
        
        the high intracellular concentration of K+ favours net movement into the tubule lumen with passive diffusion through K+ leaky channels
        
        the interstitial fluid concentrations of K+ is low so passive movement out of peritubular capilalry plasma nad basolateral pump actively induecs net secretion of K+ from peritubular capillary into tubular lumen
    - - Aldosterone increases K+ secretion since it promotes insertion of Na channels in distal and collecting tubule
      - aldosterone is stimualted by rise in plasma K+ level which promotes tubular secretion so more K+ in urine
      - Low Na+ triggers renin angiotensin system to produce aldosterone (drinking lots of water can lower Na+ concentration so more K+ is excreted)