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91 Cards in this Set
- Front
- Back
Inner mucosal lining of transitional epithelial cells in the bladder is a
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barrier to prevent the passage of water between the bladder contents & blood
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Bladder structure
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-outer serosal layer
-detrusor muscle -submucosal layer of loss connective tissue -inner mucosal lining of transitional epithelial cells |
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Motor Control of bladder function
Detrusor Muscle |
Muscle of micturition
PNS-Contracts >> urine expelled from bladder SNS relaxes |
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Motor Control of Bladder Function
Abdominal Muscles |
Contraction >> increase in abdominal pressure >> increase bladder pressure
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Motor Control of Bladder Function
Internal Sphincter |
-Circular muscle in neck; cont. of detrusor. Bladder relaxed, fibers are closed, act as sphincter. When detrusor contracts, sphincter is pulled open by change in bladder shape. PNS relaxes. SNS contracts
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Motor control of Bladder Function
External Spincter |
Circular muscle surrounds urethra, acts as a reserve mechanism to stop micturition, maintain continence despite increase in bladder pressure
Under voluntary control- somatic NS |
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Micturition
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As bladder filling occurs, ascending spinal fibers relay info to center, which also receives input from forebrain about behavior cues for bladder emptying.
Coordination of micturition reflex occurs in pontine micturition center, facilitated by input from forebrain & SC reflexes. Center coordinates activity of detrusor & external sphincter. Descending pathways from center produce coordinated inhibition of somatic systems, relaxation of both sphincters. The onset of urinary flow through the urethra causes reflex contraction of the bladder. |
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Bladder fills >> _________ receptor stimulated >> pelvic nerve carries impulses to _____________ >> ____________ center stimulated >> _______________ motor neurons send impulses to detrusor muscle through the ___________ nerve >> ____________ muscle contracts >> urination
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bladder fills, stretch receptors stimulated, pelvic nerve carries impulses to sacral region of spinal cord, micturition center stimulated, parasympathetics motor neurons send impulses to detrusor muscle through the pelvic nerve, detrusor muscle contracts, urination
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At what age does a child become conscious of the urge to urinate
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2-3
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As child achieve continence, micturition is
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voluntary
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What medications do you give to spastic bladder?
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-anticholinergics
-sympathetic agonists -stent, botox |
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Neurogenic Bladder disorders
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failure to store urine= spastic bladder
failure to empty urine= flaccid bladder |
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Neurogenic bladder:
Spastic Bladder Results From: |
from neurogenic lesions above the level of the sacral cord that allow neurons in the micturition center in SC to function reflexively without the control of higher CNS centers
Bladder dysfunction that occurs with spinal cord injury, stroke, herniated discs, tumors of the spinal cord |
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Failure to empty bladder =
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flaccid bladder
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Neurogenic Bladder
Flaccid Bladder results from |
-neurologic disorders affecting motor neurons in DC or peripheral nerves that control detrusor muscle contraction and bladder emptying
-injury to cauda equina, trauma, tumors, MS, spina bifida |
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Flaccid bladder emptying can be achieved by
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-increase intraabdominal pressure
-manual suprapubic pressure |
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Treat flaccid bladder
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-catheters or pressure on bladder
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Stress incontinence
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Involuntary loss of urine associated with activities (coughing) >> increase IAP
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Overactive urinary incontinence
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Urgency, frequency assoc with hyperactivity of detrusor, may/may not involve involuntary loss of urine
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Overflow urinary incontinence
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Involuntary loss of urine when bladder pressure > urethral pressure in absence of detrusor activity
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Stress incontinence in women caused by
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-loss of posterior urethrovesical angle
-aging, childbirth, surgery -loss of pelvic floor tonus |
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Stress incontinence in women is caused by the loss of
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the angle between the bladder and the uretherovesical junction
-angle should be 90 degrees |
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Overactive/urge incontinence is caused by
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involuntary bladder contractions
-overactive bladder can occur without incontinence |
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Overactive/urge incontinence is clinical syndrome of
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incontinence, increased frequency, dysuria, nocturia
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Overflow incontinence
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retention of urine due to neural disorders or obstruction
-hypertrophy of kidney then dilate >> no muscle >> muscle substitute with fibrotic tissue >> urine in bladder >> badder pressure increases >> high enough >> sphincter, pressure decreases and sphincter closes, urinary retention |
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Overflow incontinence is when the bladder does not
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contract
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Treat overactive/urge incontinence
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-anticholinergics
-beta 2 agonists |
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Overflow incontinence
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Involuntary loss of urine that occurs when intravesicular pressure exceeds the maximal urethral pressure because of bladder distention in absence of detrusor activity
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Factors that contribute to incontinence in the elderly
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-decrease in overall bladder capacity
-urethral closing pressure decreases -detrusor closing pressure decreases -detrusor muscle function decreases -restricted mobility -medications |
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If damage glomeruli, damage to
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filtration
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Podocytes form windows that form a fenestrated epithelial cell that allowed for
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rapid filtration of substances
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Normal filtration intro bowman's capsule
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sodium, water, AA, calcium, small molecules, filtered easily, smaller than the pores
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If albumin in glomerular basement membrane this means
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-something is wrong with the membrane
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Glomerular injury, primary vs secondary
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1. autoimmune
2. DM, HTN |
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Two immune mechanisms that damage Glomerular basement membrane
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1.Antiglomerular antibodies leave circulation, react with antigens present in BM of glomerulus.
2. Antigen-antibody complexes circulating in blood become trapped as they are filtered in glomerulus. |
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Acute Nephritic Syndrome
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-acute glomerular inflammation
-sudden onset with decreased GFR, hematuria, oliguria, fluid and waste accumulation |
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Acute Postinfectious Glomerulonephritis follows infections caused by
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strains of group A Beta hemolytic streptococi
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Treatment of Postinfectious glomerulonephritis
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-antibiotics
-supportive care |
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Acute PostInfectious Glomerulonephritis causes an inflammatory response from circulating complexes that
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become entrapped in glomerular BM >> oliguria, hematuria, proteinuria > increase cap membrane permeability > increase na and water retention >> edema, HTN
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Glomerulonephritis is ___ cause of ESRD in the US
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3rd
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Nephrotic Syndrome is characterized by
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massive proteinuria
hypoalbuminemia salt and water accumulation edema HLD |
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Main disease that causes nephrotic syndrome
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-membranous glomerulonephritis: LUPUS
-deposition of immune complexes, thickening of membrane |
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Test for Lupus
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check anti DNA antibodies
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Nephrotic syndrome complications
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-pulmonary edema
-ascites -loss of globulins -thrombotic complications |
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Diabetic Glomerulosclerosis is the major cause of ___________ and ____________ and is caused by
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-CKD
-ESRD -type I and type II DM |
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Diabetic glomerulosclerosis damages the membrane by
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widespread thickening and sclerosis of glomerular basement membrane and mesangial cells
-filter does not work -mesangial cells become hypertrophic -form nodules -destory membrane |
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Manifestations of diabetic glomerulosclerosis
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microalbuminuria < 300 mg/day
-filter is starting to be malfunctioned |
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In diabetic glomerulosclerosis there is an ______ in GFR and an ______in capillary pressure
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increase in GFR
increase in capillary pressure increase in Angiotensin II >> constrict the efferent arteriole (gets blood out from glomeruli) >> open more pores >> albumin and water go into filtrate and cells work harder |
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Can diabetic glomerulosclerosis be reversed?
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-stop smoking
-control HTN |
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best meds to decrease diabetic nephropathy
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-ACEI and ARBs
-decrease pressure in efferent arteriole |
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HTN glomerular disease
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-HTN cause and effect of kidney disease
-change in kidney structure and function -sclerosis and atrophy of arterioles -2nd leading cause of ESRD |
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Acute kidney injury
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kidneys fail to remove metabolic end products from the blood and regulate the fluid, electrolyte, and pH balance of the extracellular fluids
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Chronic kidney disease
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end result of irreparable damage to the kidneys, develops over course of years
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Acute kidney injury
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abrupt, reversible with early txt
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Acute kidney injury manifestations
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azotemia
decrease GFR >> decrease urine excretion of wastes >> increase BUN >> increase creatinine |
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Azotemia
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-accumulation of nitrogenous waste products in blood
-urea, BUN, creatinine |
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Acute Kidney injury BUN and Creat?
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increase BUn
Increase Creat |
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Acute Kidney injury phases
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1. pre renal
2. intra renal 3. post renal |
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Pre renal injury
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-decrease in renal blood flow >> increase in GFR >> decrease filtration of substances >> decrease urine output >> increase BUN (urea)/Cr ratio
20/1 (normal) increases to 40/1 -pre RENAL -GFR low=less fluid in TUBULES-more BUN absorbed |
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MAP < 60
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no blood flow to the kidneys
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The kidneys receive approximately ___ of CO to filter blood regulate fluid and electrolyte balance
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20%
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Pre renal-quickly restore blood volume
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kidneys will get better
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Post renal injury
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-obstruction of urine outflow from kidneys
-ureters-calculi -urethra-BPH -bladder-tumors |
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Intrinsic Renal Injury
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-damage to structure of kidneys including: glomerular, interstitium, tubular
-injury to tubular structure-ATN : ischemia, toxic insult, intratubular obstruction |
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Ischemic ATN
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-destruction of tubular cells with acute renal failure
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Causes of ischemic ATN
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-major sx
-severe hypovolemia -overwhelming sepsis -major trauma -burns |
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Does GFR improve with RBF restoration in ischemic ATN?
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No
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Nephrotoxic ATN
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-nephrotoxic drugs or other agents
-main is contrast |
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Tubular Obstruction ATN
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-myoglobin
-Hgb -uric acid |
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Myoglobin in tubular obstruction ATN
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-skeletal m breakdown from trauma, exertion, hyperthermia, prolonged sz, sepsis
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Hgb tubular obstruction ATN
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-blood transfusion reactions
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Uric acid and myeloma light chains-tubular obstruction ATN
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--chemo and radiation
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Three phases of ATN
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1. onset/initiating phase
2. maintenance phase 3. recovery phase |
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Onset phase ATN
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hours/days from onset to insul
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Maintenance phase of ATN
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decrease GFR, retention of metabolites (urea, K, sulfate, Cr), decrease serum Na, generalized edema, pulmonary edema, metabolic acidosis
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Recovery phase of ATN
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Repair of renal tissues, gradual improvement in U/O, BUN & Cr
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1st phase of recovery in ATN is
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hyperuria
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As glomerular filtration rate decreases chronic kidney disease _____
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worsens
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At watch stage of CKD does one require dialysis
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GFR < 15, stage 5
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Why is CKD not evident until the disease is advanced?
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-2 kidneys and many nephrons
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Causes of chronic kidney disease
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-DM, HTN, glomerulonephritis
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CKD is ___________, ___________, _____________ of the nephrons
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progressive, irreversible, destruction
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CrCl=
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(140-age) x (wt(kg)) / (72 x serum Cr)
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What is the best measurement of overall kidney function
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GFR
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GFR < 60 =
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loss of > 1/2 normal kidney function
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CKD Manifestations
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-HTN
-HF -Uremia -Increase uric acid -pericarditis -coagulopathies -acidosis -anemia -low Vit D (give Vit D3-active form) |
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CKD children causes
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congenital, inherited disorders, metabolic syndromes
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CKD younger than 5 years old
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-renal dysplasia
-obstructive uropathy ***congenital MAIN disease |
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CKD greater than 5 years old
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-acquired, inherited, i.e. STREP
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CKD children manifestations
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-problems with growth and development
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CKD elderly
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decrease in GFR*
-more susceptible to nephrotoxic drugs -not associated with increase in Cr (end product of m. metabolism-they do not have m. to begin with) |