Urinary and Renal Disorders Module 6 PDF

Urinary and Renal Disorders Module 6  Overview Background Urinary Tract Obstructions Urinary Incontinence Urinary Tract Infections Glomerular Disorders Renal Failure Prostate Disorders  The Kidney Function: Maintain s...

Urinary and Renal Disorders Module 6  Overview Background Urinary Tract Obstructions Urinary Incontinence Urinary Tract Infections Glomerular Disorders Renal Failure Prostate Disorders  The Kidney Function: Maintain stable internal environment – Excrete metabolic waste – Maintain acid-base balance – Retain nutrients – Manage water, solute transport – Regulate endocrine functions Located on posterior Figure 37-1 abdominal wall  The Nephron The nephron is the Afferent arteriole fundamental unit of the kidney Efferent arteriole Consists of the glomerulus, proximal convoluted tubule, loop of Henle, distal convoluted tubule and collecting duct Three types: – cortical nephrons, midcortical nephrons and juxtamedullary nephrons  The Nephron Afferent Materials present within arteriole the blood are filtered Efferent through the glomerular arteriole capillaries and into Bowman’s capsule – Fenestrated capillaries – Associated with podocytes which regulate filtration – Endothelial cells and basement membrane are negatively charged and repel negatively charged proteins in plasma  The Nephron Fluid that enters Bowman’s Afferent arteriole capsule is known as ‘filtrate’ Efferent arteriole Once inside the nephron, filtrate passes through each tubular element of the nephron and ions, water and nutrients are reabsorbed – Pass through tubular cells and enter extracellular space where they are absorbed by peritubular capillaries  The Nephron These cells can also secrete Afferent arteriole materials into the filtrate that the body needs to get Efferent arteriole rid of The filtrate is sent through the collecting duct to the renal papillae, which then drain into the minor calyces, the major calyces and renal pelvis before entering the ureter Ureters bring urine to bladder  Gross Anatomy of Kidney Surrounded by fibrous capsule Renal cortex – Glomeruli of all nephrons, tubular elements of cortical nephrons and some tubular elements of juxtamedullary nephrons Renal medulla – Proximal and distal tubules – Collecting ducts – Renal papillae Figure 37-2 Figure 37-11  The Bladder Stores urine produced by the kidneys until voiding can occur Can expand to accommodate urine The bladder contains a thick layer of smooth muscle cells known as the detrusor muscle Contraction of the detrusor causes micturition Urine is expelled from the body via the urethra – Contains internal and external sphincters that regulate micturition The Bladder  Tests of Renal Function Urinalysis evaluates: – Color, turbidity, protein, pH, specific gravity, sediment, and supernatant Normal urine: clear straw-colored liquid – Has slight odor, contains some crystals, small number of cells that line the bladder, and transparent (hyaline) casts – Does NOT contain sugars, yeast cells, protein, ketones, bacteria, or parasitic organisms. – Acidity: the pH of normal urine is 4.5-8.0 – Specific gravity (a measure of solute concentration) is 1.0005-1.035  Tests of Renal Function Urine Sediment – Examined microscopically – Red Blood Cells: Few or no RBCs normally Hematuria – large number of RBCs present – Casts: accumulations of cellular precipitates Red Cell Casts: Bleeding in tubules White Cell Casts: Inflammation Epithelial Cell Casts: Degradation or necrosis – Crystals – White Blood Cells  The Aging Kidney Decrease in kidney size Decrease in renal blood flow and GFR Number of nephrons decrease – Oxidative stress and inflammation – Renal blood flow and glomerular filtration rate decline Tubular transport and reabsorption decrease with age – Response to acid-base changes and reabsorption of glucose are delayed Neurogenic and myogenic changes in the bladder may lead to symptoms of urgency, frequency, nocturia Urinary Tract Obstruction  Urinary Tract Obstruction An interference with urine flow at any site along the urinary tract Can be anatomical or functional Causes backup of urine/filtrate upstream of blockage site Can lead to dilation/damage of urinary structures – Leads to fibrosis Figure 38-1  Urinary Tract Obstruction Increases pressure within Bowman’s capsule – Decreases renal filtration Urinary stasis increases likelihood of infection Severity determined by – Location – Involvement of one or both upper urinary tracks If unilateral, unaffected kidney can partially compensate – Completeness – Duration – Cause Figure 38-1  Upper Urinary Tract Obstruction Nephrolithiasis Characterized by the formation of masses of crystals, protein, or other substances within the kidneys or ureters – AKA kidney stones, calculi, renal stones – Classified according to composition of primary minerals (salts): Calcium oxalate Calcium phosphate Struvite Uric acid  Upper Urinary Tract Obstruction Nephrolithiasis Risk factors include: – Age, gender, race, geographic location, seasonal factors, fluid intake, diet, occupation, genetic predisposition Stone formation requires – Supersaturation of one or more salts – Precipitation of salt(s) from liquid to solid state Temperature- and pH-dependent – Growth via crystallization or aggregation Size of stone determines likelihood that it will pass through the urinary tract and be excreted  Upper Urinary Tract Obstruction Kidney Stones Clinical manifestations include – Renal colic – Nausea – Vomiting – Hematuria – Urgency – Frequent voiding ***Watch clinical integration video on kidney stones  Lower Urinary Tract Obstruction Primarily related to the bladder – Urine storage or emptying Anatomical obstructions causing resistance to urine flow include: – Prostate enlargement – Urethral stricture – Severe pelvic organ prolapse – Low bladder wall compliance  Lower Urinary Tract Obstruction Neurogenic alterations can also lead to lower urinary tract obstructions Lesions of spinal cord between C2 and S1 result in impaired co-ordination between bladder and external urethral sphincter – Both contract at same time Lesions of the sacral spinal cord (below S1) or sacral peripheral nerves result in an impaired ability of bladder to contract when full Neurogenic Bladder Figure 38-3 Lower Urinary Tract Obstruction Clinical manifestations include: – Frequent daytime voiding – Nocturia – Poor force of stream – Intermittency of stream – Urgency – Hesitancy – Feelings of incomplete bladder emptying Urinary Tract Infections  Urinary Tract Infections (UTIs) Infection occurring anywhere within the urinary tract from urethra to kidney that leads to inflammation of urinary epithelium Most commonly caused by E. coli Inciting micro-organism travels in retrograde fashion through urethra to bladder and must overcome defense mechanisms of urinary tract Classified by location affected: – Cystitis: Infection/inflammation of bladder – Pyelonephritis: Infection/inflammation of upper urinary tract Also classified based on presence or absence of complications  UTI: Acute Cystitis Inflammation of the bladder Can cause redness, pus formation, suppurative exudates, sloughing leading to ulcer formation, necrosis Most common site of UTIs – More common in females than males Manifestations – Frequency, dysuria, urgency, and lower abdominal and/or suprapubic pain  UTI: Acute Pyelonephritis Infection and inflammation of one or both upper urinary tracts – Renal pelvis, calyces and/or nephrons Infection either spreads up the ureters from the bladder (more common) or enters from bloodstream Often preceded by symptoms of cystitis Acute pyelonephritis causes systemic signs of inflammation – Fever, chills, nausea, vomiting Also characterized by back pain  UTI: Chronic Pyelonephritis Persistent or recurring episodes of acute pyelonephritis Risk increases with recurrent renal infections and obstructive pathologic conditions Can cause irreversible scarring within the kidneys, atrophy of nephrons and destruction of glomeruli Can lead to chronic kidney failure Figure 38-6 Glomerular Disorders  Glomerular Disorders Glomerular disorders affect the glomerulus and change the filtration properties of the kidney http://robbwolf.com/2011/06/16/clearing-up-k idney-confusion-part-deux/  Glomerulonephritis Inflammation of the glomerulus caused by glomerular injury Significant cause of chronic kidney disease and end-stage renal failure Primary glomerulonephritis can be due to: – Immunological responses – Ischemia – Free radicals – Medications – Toxins – Vascular disorders – Infections Secondary glomerulonephritis is caused by systemic disease, such as diabetes mellitus  Acute Glomerulonephritis Typically results from immune-mediated tissue damage Antigen-antibody complexes can get deposited in intricate glomerular capillary networks (Type III hypersensitivity) – Acute post-streptococcal glomerulonephritis Antibodies can bind to antigens that have been embedded in glomerulus (Type II hypersensitivity) Antibodies can target glomerular tissues Cell-mediated injuries can also occur (Type IV hypersensitivity)  Acute Glomerulonephritis Regardless of the underlying mechanism, antibodies embedded within the glomerulus can activate complement proteins Activation of complement causes cell lysis and recruits additional immune cells This damages glomerular endothelial cells, the basement membrane and podocytes Leads to increased permeability of the renal corpuscle Get red blood cell casts (hematuria) and proteins (proteinuria) in urine Scar tissue formation and epithelial cell proliferation can increase pressure inside of Bowman’s capsule, thereby decreasing glomerular filtration rate  Acute Glomerulonephritis Clinical Manifestations Vary depending upon the underlying cause of the disease – Onset can be sudden or insidious – Can range from mild to severe Hematuria results in brown-tinged urine and red blood cell casts Proteinuria accompanies hematuria Nephrotic or nephritic syndrome Severe cases can result in oliguria, hypertension and renal failure Chronic glomerulonephritis can lead to end-stage kidney failure  Nephrotic vs. Nephritic Syndrome Glomerulonephritis can lead to either nephrotic syndrome or nephritic syndrome Nephrotic syndrome: Nephritic syndrome: 1. Massive proteinuria 1. Hematuria 2. Hypoalbuminemia 2. Oliguria 3. Edema 3. Decreased GFR 4. Hyperlipidemia/ 4. Hypertension hyperlipiduria Renal Failure Classification of Kidney Dysfunction Acute or chronic; reversible or irreversible Renal insufficiency – Decline of renal function to approximately 25% of normal Renal failure – Significant loss of renal function End-stage renal failure – Less than 10% of renal function remains  Acute Kidney Injury Sudden decline in kidney function with a decrease in glomerular filtration and accumulation of nitrogenous waste products in the blood Increase in serum creatinine and blood urea nitrogen Classification – RIFLE: Risk; Injury; Failure; Loss; End-stage disease Criteria to guide the diagnosis of renal injury  Acute Kidney Injury Three categories/types: 1. Prerenal: most common; caused by renal hypoperfusion (i.e. low blood pressure) 2. Intrarenal: caused by damage to the kidney (i.e. glomerulonephritis, acute tubular necrosis, and acute interstitial nephritis) 3. Postrenal: rare; consequences of urinary tract obstruction  Chronic Kidney Disease Progressive loss of renal function associated with systemic diseases Kidney damage: GFR less than 60 mL/min/1.73 m2 for 3 months or more, irrespective of cause Clinical manifestations: Do not occur until renal function declines to less than 25% of normal  Chronic Kidney Disease Theory – Intact nephron hypothesis Loss of nephron mass with progressive kidney damage causes the surviving nephrons to sustain normal kidney function. Factors that advance disease – Proteinuria Contributes to tubulointerstitial injury by promoting inflammation and progressive fibrosis. – Angiotensin II Promotes glomerular hypertension, and participates in tubulointerstitial fibrosis and scarring.  Chronic Kidney Disease Factors that contribute to progression of disease – Glomerular hypertension – Hyperfiltration – Tubulointerstitial inflammation – Fibrosis  Chronic Kidney Disease Processes Figure 38-12  Chronic Kidney Disease Clinical manifestations – Affects every body system – Uremic syndrome Proinflammatory state with the accumulation of urea and other nitrogenous compounds Toxins Alterations in fluid and electrolyte and acid-base balance Figure 38-13 Urinary Incontinence  What is Urinary Incontinence? Involuntary leakage of urine – different types: Stress UI: Associated with a sudden increase in intra-abdominal pressure (i.e. laugh, cough, sneeze, exercise) Urge UI: Loss of urine with a strong, unstoppable urge to urinate (can be neurologic or non-neurologic) Overflow UI: overdistention of bladder leading to involuntary urine loss (may be Mixed UI: a combination of stress and urge incontinence Functional UI: involuntary loss of urine due to dementia or immobility See Table 38-1 Watch clinical integration video on urinary incontinence