Urinary System

Chapter 25

Urinary System Organs

http://findmeacure.com/2008/03/27/hematuria-blood-in-the-urine/

• 2 Kidneys forms urine

• 2 Ureters transport urine

• Urinary bladder stores urine

• Urethra transports urine

Functions

• Primary– Filters and excretes toxins, wastes, and ions– Regulates blood volume, pressure, & composition– Maintain balance in blood (H20, salt, acids &

bases)• Supporting– Gluconeogenesis w/ fasting– Renin and EPO production– Vitamin D activation

Kidney Anatomy (external)

http://www.arizonatransplant.com/images/kidney_large_1.JPG

• Paired retroperitoneal organs – Right lower b/c liver– Renal ptosis: kidney falls w/

emaciation kinks ureters• Hydronephrosis w/ resulting urine

backup

• Adrenal glands on top• Renal hilum for vessel entry

Kidney Anatomy (internal)

http://tejatechblog.blogspot.com/2010/06/internal-struture-of-kidney.html

• Renal capsule• Renal cortex• Renal medulla

– Renal (medullary) pyramids w/ papilla

– Renal columns• Renal pelvis

– Walls are smooth muscle peristalsis

– Major and minor calyces– Pyelitis when inflamed

• Pyelonephritis all inflamed

Blood and Nerve Supply

• ¼ total CO– 90% of supply enters cortex

• Renal plexus off of celiac plexus (SNS)

Nephron

http://kvhs.nbed.nb.ca/gallant/biology/nephron_structure.html

• Forms urine from filtrate• Renal corpuscle

– Glomerulus is a fenestrated capillaries– Glomerular (Bowman’s) capsule surrounds

• Outer sim. squ. & inner podocyte

• Renal tubules – PCT: sim. cub. w/ microvilli & mitochondria (cortex)

• Increase SA for absorbing H20 & solutes and secretion

– Loop of Henle: sim. cub. sim. squ. sim. cub/col• Cortical vs juxtamedullary nephrons

– DCT: see PCT, but no microvilli (cortex)• Collecting ducts: sim. cub. (medullary pyramids)

– Intercalated cells: abundant microvill and maintain acid/base balance– Principal cells: sparse microvilli and maintain H2O and Na+ balance

Nephron Blood Supply

• Glomerulus– Afferent artery in from cortical radiate– High BP (wider too) force solute & fluid out– Produces filtrate

• Peritubular capillaries– Efferent artery out– Porous & low pressure to reabsorb filtrate (99% to

venules)– Modified as vasa recta in juxtamedullary nephrons

Juxtaglomerular (JG) Apparatus

• Regulate BP and rate of filtrate formation

• Specialized cells– Juxtaglomerular (JG) cells in

afferent arteriole• Smooth muscle w/ renin secreting

granules • Mechanoreceptors for BP

– Macula densa in renal tubule• Columnar cells• Chemoreceptors for changing

[NaCl] in filtrate

http://pclab.cataegu.ac.kr/physiology/Kidney.htm

Filtration Membrane

• B/w blood and intercapsular space• Layers– Fenestrated epi. of glomerulus

• All, but blood cells pass

– Basement membrane (b/w epi and podocytes)• All, but smallest proteins• (-) electrical charge assists repulsion of (-) proteins

– Podocyte• Filtration slits b/w feet w/additional slits prevent

macromolecule escape

Kidney Physiology (overview)

• Steps– Cell and protein free blood into tubules/collecting

duct (1)– Vasa recta reclaims needs and excretes rest• All glucose, AA’s, salt, and 99% H2O (2)

– Selective addition of other molecules (3)• Terminology– Filtrate is everything in blood, but protein– Urine is metabolic waste & excess substances

Glomerular Filtration (1)

• More efficient than other capillaries– High permeability and SA of glomerulus– Glomerular BP higher – Higher net filtration pressure (NFP)

• H2O, glucose, AA’s, & nitrogenous waste diffuse– Similar composition of filtrate & blood

• Large proteins prevented– Maintain colloid pressure– Prevent all H2O loss from blood– Proteins in blood = imbalance

Net Filtration Pressure (1)

• Review chpt 19– Hydrostatic pressure, fluid force on wall

• Filters fluids from cells and proteins

– Colloid osmotic pressure• Nondiffusible molecules encourage osmosis

• Determines filtrate formation (glomerulus)– Glomerular hydrostatic pressure pushes H2O out into

intercapsular space– Colloid osmotic pressure of glomerular blood and

capsular hydrostatic pressure opposes– NFP = HPg – (OPg + HPc)

Glomerular Filtration Rate (GFR) (1)

• Volume of filtrate made/min (~ 120 -125 ml/min)

• Regulation– SA for filtration– Filtration membrane permeability– NFP

• Directly proportional to NFP

Intrinsic Regulation of GFR (1)

• Myogenic mechanism (JG cells monitor)– Up systemic BP vasoconstrict aff. art. down flow to

glomerulus• Decreased GFR protects glomerulus

– Down systemic BP reverses• Tubuloglomerular feedback mechanism (macula

densa monitor)– GFR up = insufficent reabsorption = high NaCl

vasoconstrict aff. art. = down flow to glomerulus• NFP and GFR down to allow time for filtration

– Low NaCl reverses– Adaptable except low BP (< 80 mm Hg) = stops

Extrinsic Regulation of GFR (1)

• SNS maintain systemic BP– NE w/ stress vasoconstrict aff. art. down filtrate formation– Stimulates macula densa and JG cells

• Renin – angiotensin mechanism restores blood volume and BP– Renin converts angiotensinogen to angiotensin I

• Renin w/ down stretch, activation by macula densa, and Epi receptor stimulation

– Angiotensin I to angiotensin II • MAP up (vasoconstriction)• Increase Na+ reabsorbed by PCT• Adrenal cortex release aldosterone

Tubular Reabsorption (2)

• All glucose and AA’s• H2O and ions dependent on

hormones• Can be active or passive– Transcellular route though renal

tubule cells• Lumen and basement membrane

peritubular capillaries

– Paracellular route between renal tubule cells• Tight junctions hinder, but in PCT (Ca2+,

Mg2+, K+, & Na+)

Na+ Reabsorption(2)

• Primary cation in filtrate moved actively – 1° active transport:• Na+-K+ ATPase pumps Na+ into interstitial fluid • Low HP and high OP (undiffusible proteins) into

capillaries

– 2° active transport• From (-) electrochemical gradient primary set up

– Na+ low inside and K+ rapidly leak out– Na+ passively into cells (facilitated diffusion)

• Cotransport of glucose, AA’s, lactic acid ,and vitamins

More Reabsorption(2)

• Passive tubular transport from 1° and 2° active transport – Aquaporins

• Responsible for obligatory H2O reabsorption in PCT• Absent in collecting ducts w/o ADH

– Up [solute] in filtrate solutes diffuse out• Lipid soluble toxins and drugs also

– (-) electrochemical gradient anions diffuse out

• Transport maximum (Tm) reflects number of carriers present– Relative to need for molecule– At saturation excess molecules excreted

• Diabetes mellitus has increase [glucose] in urine

Renal Tubular Activity (2)

• PCT (previously) most active• Loop of Henle– Descending H2O in, but no ascend [aquaporins]– Solutes opposite– Role in dilute vs concentrated urine

• DCT– Depends on body needs

• ADH adds aquaporins = H2O reabsorption up• Aldosterone (renin-angiotensin) up Na+ reabsorption

– H2O follows = BP increase

• ANP encourages Na + loss– W/ high atrial pressure to drop blood volume and pressure

Diuretics (2)

• Chemicals enhancing urine output– Substances nor reabsorbed– Substances exceeding renal tubules ability to

reabsorb– Substances inhibiting Na+ reabsorption

• Alcohol inhibits ADH (H2O reabsorption) • Caffeine, drugs, and other Na+

reabsorption inhibitors• Stop obligatory H2O reabsorption

Tubular Secretion (3)

• Reabsorption in reverse– PCT mainly, but cortical collecting ducts too

• Functions– Eliminate drug bound proteins (not filtered)– Eliminate urea and uric acid (protein metabolism)– Eliminate excess K+ ions– Control blood pH• Up acidity = excess H+ in urine and HCO3

- reabsorbed

• Down acidity = HCO3- in urine and Cl- reabsorbed

Ureters

• Two tubes containing a tri-layered wall– Transitional epi. mucosa (kidney pelvis and bladder too)– Inner longitudinal & outer circular smooth muscle

• 3rd external longitudinal layer in lower 1/3

– Fibrous CT adventitia• Urine transport through peristalsis

– Stretch signal more than neural• Imbalances

– Renal calculi (kidney stones) from Ca2+, Mg2+, or uric acid salts precipitating• Bacterial infections, urine retention, high ion levels, and alkaline pH

predispose• Cranberry juice acidifies and H2O dilutes

Urinary Bladder

• Ureteral and urethral orifices form trigone– Common site of infections

• Similar tri-layer wall as ureters– Middle layer resemble lower 1/3 ureter = detrusor

muscle– Walls w/ rugae for distension

Urethra• Trans. pseudostrat. colum. strat. sqam.• Internal urethral sphincter @ junction w/ bladder

– Contraction opens• External urethral sphincter @ urogenital diphragm

– Levator ani assists• External urethral orifice• Males w/ 3 regions

– Prostatic, membranous, and spongy• Imbalances

– Dysuria (painful urination)• Indicators: up urgency, frequency, and/or presence of blood

– UTI’s from bacterial infections• Females predisposed b/c location, intercourse, wiping• Can cause urethritis, cystitis, pyelitis , inflammation of urethra, bladder, or

kidney

Urine Characteristics• Color and turbidity

– Yellow shades from urochrome, product of Hb breakdown– Higher concentration is darker yellow– Abnormal colors from foods, bile pigments, or blood– Cloudiness could indicate UTI

• Odor– Fresh is aromatic, but standing more ammonia b/c bacterial activity– Drugs, vegetables (asparagus & onions), & diseases can alter

• pH – Usually ~ 6– Down w/ acidic diet (high protein, whole wheat)– Up w/ vegetarian diet, prolonged vomiting, and infection

• Specific gravity, ratio of urine to dH2O– Higher than 1.0 b/c H2O + solutes– [solutes] determines, 1.001 – 1.035 is normal

Chemical Composition of Urine

• 95% water• 5% solutes– Nitrogenous wastes• Urea, uric acid, and creatinine (AA, nucleic acid, & CP

breakdown respectively)

– Na+, K+, Ca2+, Mg2+, HCO3- also

• Abnormal amounts, protein, or WBC presence indicates disease/imbalance

Micturition (Urination)

• Voiding of bladder• Distension of bladder walls initiates spinal reflex

– Contraction of external urethral sphincter– Inhibit detrusor muscle and internal sphincter (temporarily)

• Reflexive control till ~ 2 or 3 years of age (pons)• Incontinence when can’t control

– Laughing and coughing up abdominal pressure– Pregnancy stretches muscles

• Urinary retention when can’t go– Common after anesthesia or w/ prostate enlargement