Denver School of Nursing BIO 206 & 308 – Week 9 CH28 & 29 Renal Phys & Path

 Anatomy of the Urinary System  Ureter  Urinary bladder  Urethra  Kidney  Physiology of the Urinary System:  Renal function ▪ Filtration ▪ Reabsorption ▪ Secretion  Regulation of Urine Volume

Image from: Lets start with the basics 

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Image from:  What is the medical term for where the kidney is located??

Image from:  What is the medical term for where the kidney is located = Retroperitoneal

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 1.2 million nephrons per kidney  Functional unit of the kidney  Cortical nephrons  Juxtamedullary nephrons

 Renal corpuscle  Glomerulus  Bowman capsule  Mesangial cells  Bowman space

Nephron

 Glomerular filtration membrane  Inner capillary endothelium  Basement membrane  Outer capillary epithelium ▪Also referred to as podocytes or visceral epithelium ▪Filtration slits  Filtrate passes through the three layers and forms the primary urine

 Juxtaglomerular apparatus  Juxtaglomerular cells  Macula densa

 Renal tubules  Proximal tubule  Loop of Henle  Distal tubule  Collecting duct  Principal cells : water & ECV…reabsorb NA+  Intercalated cells : acid-base…reabsorb K+ & HCO3-,secrete H+

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This is really the critical testable material  Physiology of the Urinary System:  Renal function ▪ Filtration ▪ Reabsorption ▪ Secretion  Regulation of Urine Volume ▪ Renin Aldosterone Angiotensin system (RAAS)

Filtration = the movement of water and protein- free solutes from the blood plasma of the arteries in the glomerulus, across the glomerular capsular membrane, into the capsular space of the Bowman’s capsule.

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Filtration = the movement of water and protein- free solutes from the blood plasma of the arteries in the glomerulus, across the glomerular capsular membrane, into the capsular space of the Bowman’s capsule. As the filtrate moves through the renal tubule, the osmolarity of the filtrate changes. As it moves deeper into the medulla, the osmolarity increases, and when it ascends the loop of Henle, it decreases, then once again increases while going down the collecting duct. Why does the kidney have this roller coaster of osmolarity?!?!?

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26 Why is it important to maintain fluid balance?

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EFP = Effective Filtration Pressure The EFP is regulated and controlled by the exact same mechanism that regulated all ion movement in the body  the concentration gradient. The EFP is determined by the 4 different concentration gradients / pressures that exist in the kidney: 1) Glomerular Hydrostatic pressure (Systemic blood pressure and the resistance to blood flow in the glomerular capillaries) 2) Glomerular Osmotic pressure 3) Capsular Hydrostatic Pressure (2 & 3 are the forces that move fluid back into the Glomerulus) 4) Capsular Osmotic Pressure = negligible amount The Net EFP equals Glomerular HP – (Glomerular OP + Capsular HP) GFR = Glomerular Filtration Rate GFR is the rate of movement of fluid out of the glomerulus and into the capsular space. GFR is directly proportional to the EFP but can also be changed by: 1) Vasodilation / vasoconstriction of the afferent and efferent arterioles 2) Changes in the systemic Blood Pressure

Image from: Southwest University: EFP = Glomerular HP – (Glomerular OP + Capsular HP) These two on left are the same. If these increase then filtration will increase (and vis versa) These two on right will decrease filtration if they increase in pressure. (and vis versa)

Reabsorption = the tubular reabsorption is the movement of ions (electrolytes) out of various segments of the tubule back into the blood. These ions enter the “peritubular blood vessels.” Image from: Southwest University:

Image from: It is this hyperosmotic condition in the medulla that allows passive transport to occur.

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Image from: Crazy Micah Style notes…

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 Urea  Aldosterone  Antidiuretic hormone (ADH)  Atrial natriuretic peptide  Diuretics

 Hydrogen excretion Ammonia excretion

 Urodilatin (natriuretic peptide)  Inhibits sodium and water reabsorption  Vitamin D  Necessary for the absorption of calcium and phosphate  Erythropoietin  Released when decreased oxygen to the kidney

 Clearance and glomerular filtration rate  Inulin  Creatinine  Clearance and renal blood flow  Blood tests  Plasma creatinine concentration  Blood urea nitrogen (BUN)

 Urodynamic tests  Cystometry, uroflowmetry, postvoid residual, electromyography, video urodynamics  Direct visualization tests  Cystoscopy, ureteroscopy

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 Urinary tract obstruction is an interference with the flow of urine at any site along the urinary tract  The obstruction can be caused by an anatomic or functional defect ▪Obstructive uropathy

 Severity based on:  Location  Completeness  Involvement of one or both upper urinary tracts  Duration  Cause

 Hydroureter  Hydronephrosis

Structures of the Kidney

 Compensatory hypertrophy  Obligatory growth  Compensatory growth  Post-obstructive diuresis

 Kidney stones  Calculi or urinary stones ▪Masses of crystals, protein, or other substances that form within and may obstruct the urinary tract  Risk factors ▪Gender, race, geographic location, seasonal factors, fluid intake, diet, and occupation  Kidney stones are classified according to the minerals comprising the stones

 Supersaturation of one or more salts  Presence of a salt in a higher concentration than the volume able to dissolve the salt  Precipitation of a salt from liquid to solid state  Temperature and pH  Growth into a stone via crystallization or aggregation

 Other factors affecting stone formation  Crystal growth-inhibiting substances  Particle retention  Matrix  Stones  Calcium oxalate or calcium phosphate  Struvite stones  Uric acid stones  Cystine stones

 Manifestation  Renal colic  Evaluation  Stone and urine analysis  Intravenous pyelogram (IVP) or kidney, ureter, bladder x-ray (KUB)  Spiral abdominal CT

 Treatment  High fluid intake, decreasing dietary intake of stone-forming substances, stone removal

 Neurogenic bladder  Dyssynergia ▪Detrusor hyperreflexia ▪Detrusor areflexia  Obstruction  Low bladder wall compliance

 Renal tumors  Renal adenomas  Renal cell carcinoma (RCC)  Bladder tumors  Transitional cell carcinoma  Gross, painless hematuria  Most common in males older than 60 years

 UTI is inflammation of the urinary epithelium caused by bacteria  Acute cystitis  Noninfectious cystitis  Interstitial cystitis  Acute and chronic pyelonephritis

 Most common pathogens  Escherichia coli  Virulence of uropathogens  Host defense mechanisms

 Acute cystitis  Cystitis is an inflammation of the bladder  Manifestations ▪Frequency, dysuria, urgency, and lower abdominal and/or suprapubic pain  Treatment ▪Antimicrobial therapy, increased fluid intake, avoidance of bladder irritants, and urinary analgesics

 Pyelonephritis  Acute pyelonephritis ▪Acute infection of the renal pelvis interstitium ▪Vesicoureteral reflux, E. coli, Proteus, Pseudomonas  Chronic pyelonephritis ▪Persistent or recurring episodes of acute pyelonephritis that leads to scarring ▪Risk of chronic pyelonephritis increases in individuals with renal infections and some type of obstructive pathologic condition

Structures of the Kidney

 The glomerulopathies are disorders that directly affect the glomerulus  Urinary sediment changes  Nephrotic sediment  Nephritic sediment  Sediment of chronic glomerular disease “ Proteinuria”

 Glomerular disease demonstrates a sudden or insidious onset of hypertension, edema, and an elevated blood urea nitrogen & creatinine (BUN/Cr)  Decreased glomerular filtration rate  Elevated plasma creatinine, urea, and reduced creatinine clearance

 Glomerular damage causes a decreased glomerular membrane surface area, glomerular capillary blood flow, and blood hydrostatic pressure

 Increased glomerular capillary permeability and loss of negative ionic charge barrier result in passage of plasma proteins into the urine  Resulting hypoalbuminemia encourages plasma fluid to move into the interstitial spaces  Edema

Nephron Function

 Glomerulonephritis  Inflammation of the glomerulus ▪Immunologic abnormalities (most common) ▪Drugs or toxins ▪Vascular disorders ▪Systemic diseases ▪Viral causes  Most common cause of end-stage renal failure

 Mechanisms of injury  Deposition of circulating soluble antigen- antibody complexes, often with complement fragments: Type III  Formation of antibodies against the glomerular basement membrane: Type II  Streptococcal release of neuramidase

 Acute poststreptococcal glomerulonephritis  Rapidly progressing glomerulonephritis  Antiglomerular basement membrane disease (Goodpasture syndrome)  Chronic glomerulonephritis

 Excretion of 3.5 g or more of protein in the urine per day  The protein excretion is caused by glomerular injury  Findings  Hypoalbuminemia, edema, hyperlipidemia, and lipiduria, and vitamin D deficiency

 Membranous glomerulonephritis  Focal glomerulosclerosis  Minimal change disease (lipoid nephrosis)

 Prerenal acute renal failure  Most common cause of ARF  Caused by impaired renal blood flow  GFR declines because of the decrease in filtration pressure

 Chronic renal failure is the irreversible loss of renal function that affects nearly all organ systems  Stages  Chronic renal insufficiency  Chronic renal failure  End-stage renal failure

 Proteinuria and uremia  Creatinine and urea clearance  Fluid and electrolyte balance  Sodium and water balance  Phosphate and calcium balance  Potassium balance  Acid-base balance

 Alterations seen in following systems:  Musculoskeletal  Cardiovascular and pulmonary  Hematologic  Immune  Neurologic