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71 Cards in this Set
- Front
- Back
electrolytes regulated by kidneys |
Sodium, chloride, potassium, calcium, phosphate,magnesium, |
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Regulation of acid‐base balance: |
Hydrogen ions (pH) |
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Excreted of metabolic waste products |
• Nitrogen (urea, ammonia, uric acid, creatinine)• Toxins, drugs, pesticides, food additives |
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Secretion of hormones: |
• Renin ‐ controls the formation of angiotensin, • Erythropoietin – stimulates red blood cell production, • 1,25‐dihydroxyvitamin D – active form of vitamin D,influences calcium homeostasis |
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Gluconeogenesis: |
Synthesis of glucose from amino acids |
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Major cation and anion in extracellular fluids is |
Na+, Cl‐ |
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Major cation and anion in intracellular fluid is |
K+, PO43‐ |
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Two forces determine thismovement between compartments |
Hydrostatic and osmotic pressure |
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Hydrostatic pressure (P) |
pressure forcing fluids across capillarywalls – generated by pumping of the heart |
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Colloid Osmotic pressure (π) |
generated by osmotic proteins in fluidthat cannot cross the semi‐permeablemembrane |
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Compartment 1 : compartment 2 Net Driving Pressure = |
(P1 – π1) – (P2 – π2) |
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Changes in ECF volume & composition are mainlydetected through: |
-Low pressure baroreceptors (jugular, R atrium), -Osmoreceptors (hypothalamus), -Renal “baroreceptors”(gives rise to renin release & angiotensin formation), -Adrenal cortex (zona glomerulosa cells, monitor K+),leading to aldosterone secretion |
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renal corpuscle: |
(filtering component) consisting ofglomerulus and Bowman’s capsule |
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Renal cortex: |
Site of glomerularfiltration & convolutedtubules |
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Renal medulla: |
Location of longerloops of Henle &drainage of collectingducts into renal pelvis& ureter |
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Urine formation |
Filtration, Reabsorption, Secretion, Excretion. |
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Glomerular filtration |
passive process, Hydrostatic pressure forces fluids & solutesfrom glomerular capillaries into Bowman’sspace |
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Tubular reabsorption |
Active & passive processes, Movement of substances from the filtrate intubules into the peritubular capillaries, Fluid taken back into body |
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Tubular secretion |
Movement of substances from peritubularcapillaries to the tubules, Remove fluid from body. |
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Excretion |
Reabsorption of water through aldosterone mediated aquaporins, Concentration of urine. |
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3 layeredglomerular filtration barrier: |
– fenestrated (pores)endothelium of glomerularcapillaries, – Basement membrane (-ve charge), – Foot processes of podocytes &slit diaphragm. |
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Course of Filtrate along tubule: |
cortex –medulla ‐ cortex – medulla – renal pelvis |
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Filterability of solutes |
Size: (<7Da freely up to 70kDa), Charge: (-ve charged molecules repelled by -ve charged membrane). |
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pressure natriuresis |
Urine flow rate is proportional to arterialpressure |
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2 mechanisms of Renal autoregulation |
1. Myogenic mechanism, 2. Tubuloglomerular feedback mechanism |
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Myogenic mechanism: |
vascular smooth muscle Contracts when stretched (high bp) and Relaxes when not stretched (bp drop). |
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Tubuloglomerular feedback mechanism: |
macular densa cells of thejuxtaglomerular complex: Senses Na+ content in distal tubule, (when Na+ low, increased Renin --> increased GFR). |
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Biochemical tests of renal function: |
Urinalysis, Measurement of GFR, Tubular function tests |
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Renal clearance (of a substance) |
Urine Flow Rate (ml/min) x [Urine] (mg/ml) / [Plasma] (mg/ml) |
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Measurement of GFR |
Inulin:– Small, polysaccharide (5200 MW), => clearance of inulin = GRF |
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Tubular secretion |
Eliminating undesirable substances or end productsthat have been reabsorbed by passive processes, Eliminating excess K+ from the body, regulating pH. |
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Tubular reabsorption |
Highly selective: glucose, aminoacids, some ions; process may be active orpassive: |
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Active reabsorption: |
ATP required (directly: primary;indirectly secondary), pinocytosis(small proteins) |
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Passive reabsorption: |
No ATP required. Diffusion,facilitated diffusion & osmosis downelectrochemical gradients |
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Na+ reabsorption in proximal tubule |
1. Na+ diffuses across luminal (apical) membraneinto cell, 2. Primary active transport of Na+ by Na+/K+ATPase across basolateral membrane, 3. Passive absorption of Na+, waterfrom interstitial fluid into peritubular capillaryby ultrafiltration |
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Glucose reabsorption (Secondary active transport) |
Sodium‐glucose co‐transporters (SGLT) on thebrush border of proximal tubular cells carryglucose into the cell, secondary active transport,against a concentration gradient. Electrochemical gradient caused by Na+/K+ ATPase in the basolateralmembrane |
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Proximal tubules |
High capacity for active & passive reabsorption– ~65% Na+, H20, 50% Cl‐, 90% HCO3‐, >90% K+– Most of glucose, lactose, amino acids |
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Specialisations of proximal tubule epithelialcells |
large number of mitochondria (active transport), – brush border (high surface area), – Rapid transport of Na+ and other substances, – Highly water permeable |
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Transporters on the proximal tubule |
Lumenal: Na+/Gluc symporter, Na+/H+ antiporter, Interstitial: Na+/K+ ATPase |
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3 sections of Loop of Henle |
Thin descending segment, thin ascending segmentand thick ascending segment |
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Thin descending limb: |
Highly permeable to water,10% reabsorbed– Water absorbed due to medullaryinterstitial Na+ concentration gradient. |
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Thin Ascending limb |
– Virtually impermeable to water, – low reabsorptive capacity |
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Thick Ascending limb |
– Na+/K+ ATPases in the basolateralmembranes– Low intracellular Na+ provides gradientfor driving a protein carrier that alsodrives the reabsorption of K + and Cl‐:the 1 Na+ , 2Cl‐, 1K+ cotransporter |
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Early distal tubule |
First section forms the macula densa – partof the juxtaglomerular apparatus |
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Late distal tubule |
aldosterone-dependant Na+ resorption, Na+/K+ ATPases– Reabsorbed with Cl‐ symporter. |
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Collecting Duct |
ADH /vasopressin– Dependent: aquaporins are mobilised tomembrane of cells and facilitate movement ofwater out of tubules by osmosis |
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Two cell types of late distal tubule &collecting duct |
1. Principal cells 2. Intercalated cells |
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Principal cells |
reabsorb Na+ & secrete K+, |
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Intercalated cells |
secrete H+ & reabsorb HCO3‐ & K+(important for acid‐base balance) |
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Four areas where ECF is monitored |
Hypothalamus, Adrenal cortex, Peripheral Baroreceptors, Renal baroreceptors. |
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Hypothalamus: Osmoreceptors |
increased osmolarity →osmoreceptor cells in theanterior hypothalamus toshrink → Shrinkage of cells causes actionpotentials → posteriorpituitary → ADH released → water resorption. |
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Adrenal cortex: zonaglomerulosa |
↑plasma K+ or angiotensin II → Aldosterone released → reabsorptionof Na+ |
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Peripheral Baroreceptors: |
aortic and carotid sinuses: ↑ in volume →Na + excretion, ↓ in volume → inhibits Na + excretion (=> ↑ECFvolume) |
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Renal Baroreceptors: Control renin release |
Granular cells, Sympathetic nerves and Macula Densa |
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Granular cells in arteriolar walls sensepressure |
↑BP → ↓renin release; ↓ BP → ↑ renin release => increase salt &water reabsorption by kidney |
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Sympathetic nerves |
Increased activity causes renin release & viceversa |
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Macula densa cells: Chemoreceptors |
Drop in flow rate leads to increased reabsorptionof NaCl in ascending loop of Henle, reducingconcentration of NaCl at macula densa →increases renin release |
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Extrinsic Mechanisms of renal output |
1. Sympathetic nerves (short term)• Arterioles, proximal tubule, granular cells, 2. Hormones (medium ‐ long term)• AngII, aldosterone, ADH, atrial natriuretic peptide (ANP) |
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Intrinsic Mechanisms of renal output |
1. Pressure natriuresis/diuresis, autoregulation• Myogenic mechanism, tubulo‐glomerular feedback (TGF), 2. Local factors• Nitric oxide (vasodilator), prostaglandins (vasodilators),endothelin (vasoconstrictor) |
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Produced by adrenal cortex & stimulates sodiumreabsorption in the collecting ducts, Increases Na+/K+ ATPases inbasolateral membrane of epithelial cells of collectingduct, sodium reabsorption |
Aldosterone |
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Activation results inincreased waterreabsorption by insertion ofaquaporins into luminalsurface of tubular epithelialcells |
Anti‐diuretic hormone |
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Activation results in decreased water and sodiumreabsorption (i.e. Increased water & sodiumexcretion), inhibits secretion of renin and aldosterone |
Atrial natriuretic peptide (ANP) |
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Effect of Dehydration |
cells shrink signalling to posteriorpituitary to release ADH → insertion of ready made aquaporinsinto luminal membrane of collecting duct →↑water reabsorption. |
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Effect of Haemorrhage |
drop in arterial pressure → reduces GFR → ↑ Na reabsorption → Increased renin release → ↑ AngII → ↑aldosterone → ↑ Na and water retention. |
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Effect of Congestive heart failure |
Reduced CO → reduced atrial pressure → reduced GFR → ↑ [Na+] → ↑ renin release → ↑ AngII → ↑aldosterone → ↑ Na and water retention. |
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3 layers of the bladder |
1. outer serosal layer, 2. thick muscular (smooth muscle)layer, 3. Internal transitionalepithelium. |
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Bladder filling |
Sympathetic NS relaxes bladder &contracts internal sphincter &inhibits PSNS ganglionic transmission, somatic motor neurons contractexternal sphincter |
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Bladder emptying |
micturition centre in braininhibit SNS nerves & therefore removesSNS inhibition of PSN ganglionic transmission, internal sphincter relaxes, bladder contracts, somatic motor neurons inhibited to relaxexternal sphincter. |
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damage to sensory nerve fibres, Micturition reflex impaired, Bladder fills to capacity and overflows a few drops at a time. |
Overflow incontinence |
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involuntary loss of urine arising from increasedintra‐abdominal pressure e.g. coughing, sneezing,bending down, lifting |
Stress incontinence |
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Result of lesions between the pontine storage & micturition centresand the lower spinal cord, No voluntary control over external urethral sphincter, involuntary voiding, Bladder never emptied completely |
Automatic bladder |