Patho 11/ 7 - Lecture notes 19 PDF

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Chapter 25 & 26: Renal Failure...

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CHAPTER 25/26 When Kidneys Fail ● Bless waste is removed more waste remains in blood ○ If BUN and creatinine and GFR levels are not normal, waste is remaining in blood ● Unable to regulate fluids, electrolyte and pH balance ● Acute kidney injury (acute renal failure) ● Chronic kidney injury (chronic renal failure) ● Nitrogenous compounds builds up in the blood ○ BUN ■ Blood urea nitrogen ○ Creatinine ■ Renal function approximated by initial creatinine level divided by current creatinine level ■ A breakdown product of creatine which is constantly produces that is used in your muscles which has to be broken down and put out to the blood and goes through the kidneys and gets rid of creatinine Acute Kidney Injury ● Rapid deterioration in renal function characterized by progressive azotemia ● Azotemia ○ High blood concentration of nitrogen waste products ■ Urea, nitrogen uric acid and creatinine ● GFR is reduced ○ Reduced excretion of nitrogenous waste and fluid electrolyte imbalances ○ Because kidneys are failing the GFR is reduced because the nephrons are losing function ● Often asymptomatic ● Classification based on where the injury occurs ○ Prerenal ■ Obstructed renal blood flow = ischemia ■ Always a restriction of blood flow ■ Results from marked decrease in renal blood flow ■ Most common form of acute renal failure ■ Etiologies ● Profound loss of circulation vascular vommes ○ Hemorrhage, shock ■ Clinical manifestations ● Ischemic changes seen when renal blood flow is 25% of normal → Acute Tubular Necrosis which then causes an internal problem ● Sharp decrease in urine osmotic pressure due to less Na being filtered ○ Early sign ● Disproportionate elevation in the ratio of BUN to serum creatinine

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to greater than 20:1 ○ Normal is 10:1 ■ Normal GFR can be maintained despite a broad range of renal blood flow ○ Intrarenal ■ Damage to structures within the kidney ■ Results from condition that causes damage to glomerular, tubular or interstitial structures within the kidney ■ Acute tubular necrosis ● Most often ischemic or toxic in origin and can be post surgical ■ Etiologies ● Ischemia associated with prerenal failure damages structures in the kidney ● Glomerulonephritis ● Acute pyelonephritis ○ Inflammation that moves from the pelvis through the calyces and backs up all the way into the tubules ○ Postrenal ■ Obstructed urine outflow ■ Results from obstruction of urine outflow from the kidneys ● Least common ■ Obstruction may occur in the ● Ureter ○ Stones or strictures ● Bladder ○ Tumors or neurogenic bladder ● Urethra ○ Most commo ○ Prostatic hyperplasia ■ Both ureters must be occluded to pdorce renal failure except in persian with only one functioning kidney ■ Goal of treatment ● Removal of the underlying of obstruction prior to permanent nephron damage Clinical Course ○ Onset ■ Hours to days ■ Time from onset of the precipitating event ● Ischemia toxin or exposure until tubular injury occurs ○ Characterized by marked decrease in GFR resulting in sudden retention of urea, K SO4 and creatinine ■ Urine output at lowest point (oliguria) ■ Fluid retention gives rise to endeam, water intoxication and pulmonary congestion ○ Recovery

■ Respai of renal tissue Acute Tubular Necrosis ● Destruction of tubular epithelial cells with acute suppression of renal function ● Most common cause of intrinsic intrarenal failure ● Frequently reversibel ● High risk groups ○ Major sx ○ Severe hypovolemia ○ Overwhelming sepsis ○ Trauma ○ Burns ● GFR does not improve with restoration of renal blood flow The renal tubules filter blood by selectively reabsorbing the items the body needs for survival ● Water only moves out if there is a higher concentration of solutes into which it can move ● Most reabsorption happens in the proximal tubules ● Fine tuning occurs in the distal tubules and collecting duct ○ ADH and aldosterone ● Lasix blocks the NKCC transporter which prevents water and solutes to be reabsorbed so fluid levels fall and urine volume increase Chronic Kidney Disease ● Progressive and irreversible destruction of kidney structures ● Deterioration of GFR tubular reabsorptive capacity and endocrine function of the kidney ● Etiologies include condition that cause permanent loss of nephrons ○ Diabetes, hypertension, glomerulonephritis, polycystic kidney disease ● Symptoms occur gradually and not evident until disease is far advanced ● Each kidney contains about 1 million tiny nephrons ● A proportional relation exist between the number of nephrons affected by disease and the resulting GFR ● Mechanisms and manifestations ○ Na and Water balance ■ Hypertension ● Heart failure ■ Increased vascular volume ● Heart failure ○ K balances ■ Hyperkalemia ○ Elimination of nitrogenous wastes ■ Uremia ● Coagulopathies ○ Bleeding ● Pericarditis ● Impaired immune function ● Skin disorders

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● GI manifestations ● Neurologic manifestation ● Sexual dysfunction Erythropoietin production ■ Anemia Acid base balance ■ Acidosis ■ Skeletal buffering ● Osteodystrophies Activation of vitamin D ■ Hypokalemia ● Hyperparathyroidism ■ Osteodystrophies PO4 elimination ■ Hypocalcemia ● Hyperparathyroidism ○ Osteodystrophies

CHAPTER 27 Male v. Female Urethra ● Female ○ Shorter ○ More prone to incontinence and bladder infections ○ Allows urine to pass more freely ● Male ○ Longer ○ Passes through prostate ○ More prone to difficulty voiding Lower UT disorders ● Obstruction ○ Retentio or stasis of urine ● Urinary incontinence ○ Involuntary loss of urine Evaluation of bladder function ● Indications of outflow obstruction ○ Frequency ○ Hesitancy ○ Straining to urinate ○ Weak or interrupted urine stream ○ Post void residual urine volume (PVR) can be estimated by palpation or percussion ■ Catheterization or ultrasound can obtain specific measurements ● Causes ○ Benign prostatic hypertrophy

○ Meatal stenosis Compensatory and Compensatory changes ● Mechanisms to prevent urine retention ○ Compensatory stage ■ Detrusor muscle hypertrophy ■ Diminished ability to suppress urination ● Often to the point of incontinence ■ Diverticula start to form from excess pressure ● Urine gets stuck in those pockets and cna get infected ■ Not failing at this point ○ Decompensatory stage ■ Failure of compensation ■ Increased frequency with a weak small stream ■ Urine remains in the bladder, increasing the risk of infection, burning on urination and cloudy urine ■ Severe overstretching decreases ability to contract Micturition Reflex ● Beings when the bladder contains 150 to 250 mL of urine ● Urine produced in the kidneys → ureters → the bladder fills with urine ● Stretching of the bladder sends a ANS signal to the spinal cord ○ Parasympathetic ● Spinal cord sends a signal back to the detrusor muscle telling the bladder to contract ● A signal also goes to the pons to tell you it's time to go ● You can override this reflex ● When you are ready to urinate, you can relax the external urethral sphincter muscle and detrusor muscle contracts pushing out urine Autonomic Disruption ● Neuronal damage can lead to problems with autonomic nervous system function ● Parasympathetic ○ Rest and digest ■ Note that PNS originate in brain stem and sacral regions ● Sympathetic ○ Fight or flight ○ Note that upper thoracic neurons control heath and lungs ○ Lower thoracic control GI and adrenal gland ○ Lumbar controls bladder Neurogenic Bladder Disorders ● Neuronal function can be interrupted at ay level ● Spastic bladder dysfunction ○ Overactive bladder ■ Failure to store urine ■ Higher control mechanisms ● Lesions above sacral level of spinal cord ■ Sympathetic

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Neurogenic reflex bladder ○ Failure to contorant and empty ○ Neurological disorders affecting the motor neurons in the sacral cord or peripheral nerves that control detrusor motor construction and bladder emptying ○ Parasympathetic ● Causes ○ Stoke, parkinson disease, spinal cord injury, injury to sacral cord or spinal roots, herniated discs, diabetic neuropathies and MS Urinary Incontinence ● Involuntary loss or leakage of urine that is sufficient to be a problem ● Four main types ○ Stress incontinence ■ Involuntary loss of urine associated with activities that increased intraabdominal pressure ● Coughing ,sneezing laughing nd lifting ● More common in women because of weakened pelvic floor muscles or damaged nerves from pregnancy ○ Overactive or urge incontinence ■ Urgency and frequency ■ May or may not involve involuntary loss of urine ○ Overflow incontinence ■ Intravesical pressure exceeds maximal urethral pressure ● Bladder distension ○ Other incontinence ■ Decreased bladder compliance and distensibility UTI ● Inflammation of the urinary epithelium caused by bacteria ● Acute cystitis is inflammation of bladder ● Acute and chronic pyelonephritis ● Most common is E. coli ● Second most common type of bacterial infections ○ Involve both lower and upper urinary tract structures because of their ability to cause renal damage, upper UTI ares considered more serious ○ Upper UTI ■ Acute inflammation of kidney pelvis with marked systemic manifestations of infection ■ Chills, fever, back pain ● Lower UTI ○ Pathogens tend to propagate in the urine and cause irritation symptoms with voiding ○ Frequency, burning, cloudy urine and minimal system signs of infection Acute Cystitis ● Inflammation of the bladder ● Manifestations

○ Frequency, dysuria, urgeny and lwoer abdominal and or suprapubin pain Treatment ○ Antimicrobial therapy, increases fluid intake, avoidance of bladder irritant and urinary analgesic Cancer of the bladder ● 90% divided form transitional cells that line the bladder ● More common in whites ● Early detection ○ Good prognosis ● Etiology unknown ○ Highly associated with cigarette smoking ● S/S ○ Painless hematuria is most common ○ Occasionally frequency urgency and dysuria ●...