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4/9/08 Urinary System Chapter 24 – Day 2
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4/9/08 Review Nephron Structure Network with blood vessels Two types of nephrons ♦Cortical Nephrons – loop of Henle does not extend below cortex ♦Juxtamedullary nephrons – loop of Henle extends into medulla ♦Vasa recta – feature of jextamedullary nephrons ♦85% are cortical nephrons Majority of process is done here ♦15% are juxtamedullary Important role in concentrating urine Conserving water in the body
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4/9/08 Renal corpuscle Renal arteries branch into afferent arterioles in the cortex One afferent arteriole enters the renal corpuscle Wall of the renal corpuscle is the Bowman’s capsule Afferent arteriole branches into capillary network ♦Glomerulus, inside the corpuscle within the bowman’s capsule A second efferent arteriole connects to the glomerulus – brings blood out of the renal corpuscle ♦(Efferent arteriole is thinner than afferent) Efferent arteriole branches around nephron as peritubular capillaries and vasa recta Eventually the efferent arteriole connects to venules – carries blood to renal veins and out of the kidney
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4/9/08 Nephrons & blood supply Fig. 24.7
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4/9/08 Kidneys – Blood supply Fig. 24.5
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4/9/08 Glomerulus Surrounded by 2 layers ♦Bowman’s capsule: Visceral epithelium Parietal epithelium ♦Separated by capsular space Blood in the glomerulus is bounded by 2 walls ♦Endothelial cells of the blood vessels ♦Visceral layer of the bowman’s capsule Fig. 24.8
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4/9/08 Glomerulus Endothelial cells of blood vessels ♦Have large diameter pores: Fenestrations Basement membrane Visceral Layer of the Bowman’s capsule ♦Special basement membrane = lamina densa ♦Special cells = podocytes These have special feet like structures called pedicels Spaces between pedicels = filtration slit/slit pore Special structures of the endothelial cells and visceral layer restrict the passage of particles according to size (analogous to the filter paper) Capsular space = place where filtrate is released
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4/9/08 Glomerulus - barriers Fig. 24.8
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4/9/08 Glomerulus blood boundaries Fig. 24.8c
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4/9/08 Filtration in the Glomerulus Blood rushes into glomerulus via the afferent arteriole Difference in diameter between afferent & efferent arterioles results in High Blood Pressure inside the Glomerulus ♦= Effective Filtration Pressure (EFP) This pushes blood against the endothelial cells ♦Filtration takes place ♦Fenestrated capillaries – stops blood cells from passing through, but all other contents go through ♦Basement membrane – stops large proteins ♦Pedicels/filtration slits – stops medium-sized proteins from leaving blood
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4/9/08 Glomerular Filtration Fig. 24.10
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4/9/08 Filtrate Remaining contents end up in the capsular space and are called filtrate Contents of filtrate: ♦Water ♦Small proteins ♦Glucose ♦Amino acids ♦Vitamins ♦Citric acid ♦Ions: Na +, Cl -, K +, HCO 3 ♦ ammonia ♦Urea ♦Bilirubin ♦Neurotransmitter ♦Hormones
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4/9/08 Filtrate - PCT Filtrate passes to proximal convoluted tubule (PCT) ♦PCT walls = simple cuboidal epithelium ♦Outside fluid = peritubular fluid ♦Then peritubular capillaries PCT – reabsorption begins ♦99% of the reabsorption is of organic materials Glucose, amino acids, vitamins, citric acid ♦Facilitated diffusion ♦Transport of Ions = active transport & passive ♦Water reabsorption = osmosis Enters peritubular fluid, then to capillaries
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4/9/08 Filtrate – Loop of Henle Tubular fluid with remaining contents flows into Loop of Henle ♦Descending & Ascending Limbs Juxtamedullary nephrons – in contact with the vasa recta Reabsorption of water & solutes ♦(specifically Na + & Cl - ) Descending & Ascending limbs have different properties – very important in concentrating urine
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4/9/08 Loop of Henle Descending limb = thin ♦Permeable to H 2 O ♦Mostly impermeable to salts (Na +,Cl -) Ascending limb = thick ♦Impermeable to H 2 O and solutes ♦Prevents diffusion by concentration gradient ♦Allows selective permeability ♦Only Na + & Cl - can leave via active transport while wastes stay in ♦Salts (Na +,Cl - ) are pumped out by active transport = reabsorption of Na + & Cl - into blood Fig. 24.13
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4/9/08 Loop of Henle As tubular fluid moves up, salts enter peritubular fluid via active transport into vasa recta Results in a high solute concentration of peritubular fluid Know: ♦Direction of H 2 O? Direction of salts? ♦From which limb? ♦What is the significance/importance? ♦How does the countercurrent work? Fig. 24.13
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4/9/08 Loop of Henle Countercurrent flow drives reabsorption ♦Osmotic concentration is constantly maintained ♦Allows reabsorption of H 2 O into blood b/c osmotic concentration is high in the peritubular fluid (due to high salts) ♦= contercurrent multiplication (exchange increases) Loss of H 2 O from descending limb concentrates solutes in urine Tubular fluid containing mostly wastes & some ions enters distal convoluted tubule (DCT)
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4/9/08 Filtrate – Distal Convoluted Tubule Further reabsorption of salts (Na + & Cl - ) ♦Active and Passive Presence of aldosterone alters rate of Na + reabsorption Ca 2+ may be reabsorbed depending on calcitriol Secretion also occurs in DCT Wastes are not reabsorbed – moves forward to collecting tube Fig. 24.15
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4/9/08 Filtrate – Distal Convoluted Tubule Further reabsorption of salts (Na + & Cl - ) ♦Active and Passive Presence of aldosterone alters rate of Na + reabsorption Ca 2+ may be reabsorbed depending on calcitriol Secretion also occurs in DCT Wastes are not reabsorbed – moves forward to collecting tube Fig. 24.15
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4/9/08 Urinary System Chapter 24 – Day 3
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4/9/08 Nephron - Secretion Reabsorption & secretion take place in the DCT Secretion: ♦Other wastes that did not enter the nephron during filtration ♦Transported later by secretion ♦Peritubular capillaries → nephron ♦PCT & DCT are involved in secretion ♦K + and H + ions – depends on blood levels/blood conditions Example: H + ions increase from CO 2 conversion, they are secreted to maintain balance Diabetes: ketones are released = acidic, so more H + is secreted ♦NH 4 + ions (comes from removal of NH 3 group from amino acids) ♦Other secreted compounds = drugs, creatinine, neurotransmitters
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4/9/08 Filtrate – Collecting Duct Urine moves into the collecting tubule (urine) ♦Some reabsorption: Na + ions HCO 3 - ions Some urea reabsorption (helps to maintain high salt concentration in peritubular fluid) Concentration gradient is very important to keep the flow of things moving properly ♦Ions & H 2 O enter peritubular fluid, then go to vasa recta Keeps a constant concentration gradient of high salt levels in the peritubular fluid H 2 O reabsorption in kidney = very important process ♦Helps to keep H 2 O balanced in the body ♦Depends on solute concentration
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4/9/08 Urine - hydration If the body is well hydrated H 2 O absorption occurs only in the descending limb of Loop of Henle Solute concentration gradient in Loop of Henle & Collecting Tubule** Fig. 24.13
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4/9/08 Urine - hydration Dilute urine = large volume because high amounts of water are retained Only ions are reabsorbed heavily If the body is dehydrated – activates pituitary gland to produce antidiuretic hormone (ADH) ♦Body conserves H 2 O in the kidney & thirst response for more H 2 O intake ♦Special H 2 O channels open in collecting tubule ♦H 2 O is reabsorbed from collecting tubule ♦Driven by diffusion because salt concentration is already high outside ♦Yields concentrated urine – small volume (conc. urea) Diuretics like caffeine: ♦Prevent H 2 O reabsorption in collecting tubule, force H 2 O out of cells ♦Leads to dilute urine but reduces blood volume ♦Are also used to alter blood pressure
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4/9/08 REVIEW & LEARN Fig. 24.16
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4/9/08 REVIEW & GET THE “GIST” Fig. 24.17
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4/9/08 Urine Collection and Reabsorption After filtration, reabsorption & secretion – urine is produced From the papillary duct it enters the minor calyx There it joins with other to form the major calyx Then it joins the renal pelvis Fig. 24.7, 24.4
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4/9/08 Urine Collection and Reabsorption Urine collects in the renal pelvis Urine is then delivered & eliminated through the urinary tract: ♦Ureters Transport ♦Urinary bladder Storage ♦Urethra Elimination Fig. 24.1
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4/9/08 Ureters Ureters are 30cm long, muscular tubes Ureters are attached to the posterior wall of the abdomen Ureters are arranged differently in men & women because the placement of the bladder is different in men and women Fig. 24.19
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4/9/08 Urinary Bladder The urinary bladder is a highly muscular organ Inside layer = transitional epithelium ♦This permits stretching of the bladder without damage to the surface cells The urinary bladder is held in place with the help of ligaments The region near the neck ♦= Inner urethral sphincter ♦Under involuntary control The neck leads to the urethra Fig. 24.19c
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4/9/08 Urethra The urethra is placed in different places in males and females ♦Males – from bladder to penis ♦Females – short urethra, located at the front of the vagina Fig. 24.19
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4/9/08 Urethra At the end of the urethra is the external urethral sphincter ♦This is a muscular sphincter ~ valve ♦Voluntary control As pressure builds up against pressure – sensitive receptors in bladder The external sphincter relaxes – this opens the internal sphincter & urine is eliminated Fig. 24.19c
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4/9/08 Urethra At the end of the urethra is the external urethral sphincter ♦This is a muscular sphincter ~ valve ♦Voluntary control As pressure builds up against pressure – sensitive receptors in bladder The external sphincter relaxes – this opens the internal sphincter & urine is eliminated Fig. 24.19c
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4/9/08 Urine Elimination – Neural Control Fig. 24.21
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4/9/08 Kidney Problems Glomerular Nephritis Caused by inflammation of the glomerulus How does that inflammation occur? ♦Allergic reaction, bacterial infection, other pathogens lead to an inflamed, swollen glomerulus Filtration is affected ♦There is less of a “block” to the permeability of endothelial cells and capsular membrane ♦More RBCs and proteins end up in the filtrate Degree of affliction: acute to minimal
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4/9/08 Acute Glomerular Nephritis Typical cause: ♦Strep. infection elsewhere in the body ♦Glomerulus produced inflammatory response due to antibody/antigen complex ♦Most common in children and young adults Symptoms ♦Fever, chills, nausea, edema, urinary failure ♦Can result in kidney failure Treatment: ♦Drugs to eliminate antibody/antigen complex ♦Steroids to reduce inflamation ♦Rest Glomerular lesions already present will not heal
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4/9/08 Urinary Tract Infection Very common, especially in females Cystitis = infection in urinary bladder Urethritis = infection in urethra Pyelonephritis = infection in the kidney Symptoms: ♦Back pain, fever, nausea, discharge ♦Urgency to urinate ♦Frequent urination Causes: ♦Bacterial infection (entered at urethra) Treatment ♦Antibiotics
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4/9/08 Incontinence Lack of bladder control Urinary sphincters cannot control passage of urine May be psychological or physiological Incontinence ♦Causes: muscle damage to sphincter Nerve damage (surgery or tumor) Medications &/or stress ♦Treatments (adult patients) Kegel exercises to improve sphincter muscle tone Electrical stimulations to suppress bladder contractions May just need absorptive pads Read about urine retention p749 for developmental stages - Enuresis (bed wetting )
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4/9/08 Kidney Problems – Kidney Stones Kidney stones = renal caliculi Salt exchange happens in the kidney, thus crystals can be formed Normally, protein acts as a crystal growth inhibitor If abnormal conditions exist: ♦Crystal growth is not prevented – growth in renal pelvis Mostly kidney stones are precipitated Ca 2+ salts like CaPO 4 These can get trapped in the ureter and this causes severe pain
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4/9/08 Kidney Problems – Kidney Stones Causes of Kidney Stones: ♦No inhibition ♦Dehydration ♦Excess Ca 2+ intake ♦“Hard” water ♦Oaxalates Treatment ♦Observe kidney stones on pyelogram (use dye for urinary tract) ♦Pass the stone? ♦Vibration to break apart crystals ♦Extracorporeal shock wave lithotripsy http://www.webmd.com/kidney-stones/extracorporeal-shock-wave-lithotripsy-eswl-for-kidney-stones
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4/9/08 Renal Failure Acute & Chronic Hemodialysis Read about it 745-746
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4/9/08 Fig. 24.6
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4/9/08 Kidneys – Blood supply Fig. 24.7
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4/9/08 Kidneys – Blood supply Fig. 24.8
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4/9/08 Kidneys – Blood supply Fig. 24.5
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4/9/08 Kidneys – Blood supply Fig. 24.5
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