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61 Cards in this Set
- Front
- Back
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Renal physiology
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receive 22% of CO, 1200 mL/min
GFR 125 mL/min or 180 L/day autoreg of GFR btwn 80-180, GFR ceases MAP<40-50 innervation from T4-T12, B1, alpha, dopamine receptors |
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Nephron
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a million functioning nephrons
2 types: cortical and juxtamedullary |
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Cortical nephrons
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short L of H
more of these 7:1 get 80% of the CO lack a thick ascending limb |
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Juxtamedullary nephrons
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long L of H--dips down into medulla with peritubular capillary network--vasa recta
has thick ascending limb get 20% of CO these do a higher degree of O2 extraction so they are prone to damage during an ischemic event or when GFR drops "workhorses of kidney" |
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Afferent arteriole
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ulfiltered blood to the glomerulus
its tone is indirectly related to GFR--if it's constricted (inc tone) then less blood to glomerulus specifically affected by prostaglandins--NSAIDS can be an issue |
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Glomerulus
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large SA for filtration
have 3 types of cells that for a tight cell matrix: endothelial cells basement membranes podocytes These 3 layers work together to keep things out of urine that we need such as albumin Creates a negative charge that keeps proteins away mesangial cells--vasoactive cells that are affected by chemicals allowing them to contract and dec GFR or relax and inc GR Hydrostatic Pressure is 60mmHg |
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Bowman's Capsule
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receives filtered fluid
has its own HP--18mmHg fluid looks like plasma minus proteins |
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Efferent arteriole
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carries blood away from glomerulus
forms extensive peritubular cap network--vasa recta imp in countercurrent multiplier system its tone is DIRECTLY related to GFR |
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Determinants of Glomerular Filtration
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Net Filtration Pressure (10) = Glomerular HP (60) - Bowman's capsule HP (18) - Glomerular Oncotic Pressure (32)
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Proximal Tubule
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gets fluid from Bowman's capsule
60-70% reabsorbed Na and 90% of our HCO3 Renal pts can't buffer acids bc they can't reabsorb HCO3 if you give ASA or XR dye (organic subst) this is how it's secreted |
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Descending Loop of Henle
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start of countercurrent multiplier system--allows us to fine tune what we keep and give away
highly permeable to water--water gets in |
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Ascending Loop
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part of CMS
impermeable to water--water stays in and not going to blood thick segment actively reabsorbs solutes--Na, K, Ca, HCO3 fluid here is pretty dilute |
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Distal tubule
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Ca reabsorbtion here in response to PTH and Vit D
small amount of aldosterone activ here--allows body to keep Na and H2O |
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Cortical collecting tubule
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fine tuning
2 imp cells: principal and intercalated principal cells--where aldosterone primarily works to reabs Na and water and secrete K intercalated--aic/base regulation, secreting or keeping H ions |
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Medullary collecting tubule
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Aquaporin-2 channels--ADH works here
Aq 2 ch close--no more water into collecting tubules body acidifies urine here by releasing H ions |
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Collecting duct
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99% of all filtered fluid is reabsorbed
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Juxtaglomerular Complex
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Contains 2 cell types: Macula densa and juxtaglomerular cells
Macula densa: epith cells in distal tubule next to AA senses changes in volume and decreased Cl flow, which occurs with BP and GFR stimulates AA dilation releases prostaglandins which trigger JCs to release renin Juxtaglomerular cells: located in afferent arteriole release renin into blood require beta 1 stim or increased AA tone or prostaglandin release |
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Renin
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low Arterial BP-->INC renin-->Ang I-->ACE-->Ang II-->Renal retention of Na and water + vasoconstriction-->INC BP
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Hormones
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Renin--see above
Adrenal catecholamines--INC AA tone to decrease GFR Prostaglandins--protective fxn under periods of stress of low perfusion states, help dilate AA and preserve GFR Atrial natriuretic peptide--released from atrial myocytes in resp to stretch. Smooth muscle dilator, dilates AA, relaxes mesangial cells of glomerulus all to maintain GFR. Also provides negative feedback to kidneys to release less renin |
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Summary of Renal Functions
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Reg of body fluid composition/volume/ electrolytes
Elim of toxins: metabolic by products & foreign chemicals Reg of acid/base balance Reg of BP Secretion, metab, and excretion of certain hormones |
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Systemic Manifestations of Broken Beans
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Metabolic--Pt can no longer concentrate or dilute urine properly
Water retention Na retention, however most pts are hyponatremic sec to above hyperkalemia--cardiac effects hyperphosphatemia--usually benign hypermagnesemia--usually benign |
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Hypokalemia EKG
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prominent U waves
hyperpolarizes resting membrane delayed repolarization in heart actually makes myocardium excited so reentrant arrythmias more common |
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Hyperkalemia EKG
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peaked T waves, short QT, wide QRS, prolonged PR, loss of p wave, ST depression, then sine wave
prolonged depolarization and inactiv of Na ch Hypocalcemia, hyponatremia and acidosis can enhance this effect |
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Hypocalcemia
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sec to dec intestinal abs d/t no 1,25 dihyroxycholecalciferol
inc phosphates encourage deposit into bone in response to body releases more PTH but pts are resistant likely to develop hyperparathyroidism |
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More metabolic manifestations
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hypoalbuminemia--lose albumin affecting plasma oncotic pressure leading to pulm edema
metabolic acidosis--normal and high anion gap possible--Oxy-hgb curve shifts to the RIGHT--dissociates more readily brittle bone dx |
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Hematological manifestations of broken beans
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Anemia (Hgb 6-8) d/t DEC E-poetin=DEC RBC production and d/t DEC RBC survival from acidotic envir
INC 2,3 DPG (product of glycolysis that inc in times of stress) production in response to anemia Oxy-hgb shift to right--consider recent dialysis and risk for residual heparin WBC dysfxn--INC risk for infxn Platelet dysfxn--uremic pts Chronic anemia--leads to osteomalacia as we deplete our bones of calcium continually as bones demineralize hyperphosphatemia worsens d/t dec GFR when phosphate is free in the serum it binds to calcium so our ionized calcium will be lower |
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Cardiac Manifestations of Broken Beans
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Most common comorbidity
mortality 10x greater 44x higher when ESRD and DM DM pts have hard time discerning angina CO INCREASED--DEC O2 carrying capacity, gotta work harder to keep up Systemic HTN: Renin-angiotensin hyperactivity ECF volume expansion leeads to CHF--both concentric and eccentric pericarditis 2 to uremia or dialysis--risk of tamponade 20% accelerated vessel dx--PVD and CAD Arrythmias Hypotension--common intraop d/t dialysis |
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Essential HTN and ESRD
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90-95% of renal pts have this form
arterial BP inc 40-60% above baseline etiology--stress, obesity, and genetic changes impaired reg of BP leads to INC PVR, overactiv of renin-angiotensin system leads to sodium and water retention Chronically elevated BP-->nephrosclerosis |
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Renal disease and Secondary HTN
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5-10% of HTN falls into this category
2 causes: renal parencymal dx and renal artery stenosis (RAS) RAS: caused by atherosclerosis 90% of time narrow lumen leads to decreases in perfusion and renal vessel damage has to corrected soon to prevent damage Decreased perfusion causes overactiv of renin-angio ultimately causing INC PVR |
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Pulmonary manifestations
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chronic metabolic acidosis leads to central hyperventilation
hypoalbuminemia leads to leaky capillaries, inc A-a gradient (nml is 8) inc incidence of pulmonary edema |
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Endocrine manifestations
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mostly with chronic renal failure
Insulin resistance=poor glucose control secondary hyperparathyroidism hypertriglycerides--contributes to atherosclerosis and vessel dx thought to be due to abn lipid metab increased circ of some hormones--insulin, glucagon, PTH, LH, GH, prolactin |
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GI manifestation
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azotemia (accum of nitrogenous wastes): anorexia, n/v, and adynamic ileus
INC secretion of gastric acids INC risk of GI bleed (ulcers and plt dysfxn) autonomic neuropathies common leads to delayed gatric emptying INCREASED RISK FOR ASPIRATION |
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Neurological manifestations
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Uremic encephaolopathy--can lead to asterixis, lethargy, confusion, seizures, and possibly coma
Autonomic neuropathies comon-pts will likely have numbness, tingling extremities--makes positioning and padding all the more imp |
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ACUTE RENAL FAILURE
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sudden decrease in renal fxn that results in the accum of nitrogenous wastes (azotemia)
mortality <10% 3 types: pre-renal--DEC blood flow to kidneys intra-renal or intrinsic--ischemia, toxins, or dx of renal parenchyma post-renal--obstruction in the urinary collection system |
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ARF: Oliguric vs nonoliguric
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OLIGURIC--defined as UO < 400mL/day
worse prognosis 2 to causative insults and likelihood of interstitial damage NONOLIGURIC: UOP>400mL/day better prognosis 20-60% of pts with ARF require dialysis |
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Pre-renal causes
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volume depletion: trauma, burns, severe diarrhea, vomiting
cardia: MI, CHF, valve probs renal vasc dx: renal artery stenosis, embolism, blockade of prostaglandin synthesis (possibly caused by NSAIDS) peripheral dilation: sepsis, shock, anesthesia positioning: dec blood flow to kidneys |
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Symptoms of Pre-renal ARF
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dec GFR noted by increases in creatinine
Oliguria (< 0.5 mL/kg/hr) or anuria electrolyte abnormalities--hyperk and hyponat precipitating event |
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Pre-renal considerations
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REVERSIBLE as long as blood flow does not fall below 20% of normal
treatment is to correct underlying cause beforep ermanent renal damage occurs nephrons most susceptible are the juxtamedullary nephrons |
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Intra-renal ARF causes
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Glomerular Small vessel damage: vasculitis, cholesterol emboli, MH, acute glomerulonephritis
Tubular injury: ATN 2 to ishemia (usually a pre-renal event usually) or ATN 2 to toxins (heavy metals or poisons) interstitial injury: acute pyelonephritis, acute allergic interstitial nephritis |
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ATN
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definition--prolonged hypoperfusion or toxins lead to damage to the tubular epith cells. the cells then slough off and block filtration at the glomerulus. The blockage at the nephrons can continue when perfusion improves
most common etiology of ARF in surgical pts pts with multi organ failure and ATN have 90% mortality rates |
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Common nephrotoxins
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Abx--aminoglycosides, cephalosporins, amph B, sulfonamides, tetracyclines, vanc
anesthetic agents--methoxyflurane, enflurane, sevoflurane NSAIDS--reversible, ASA-irreversible Chemo Contrast media Calcium, uric acid, myoglobin, hemoglobin, bilirubin, paraproteins, oxalate crystals |
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Glomerulonephritis
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Intrinsic failure that occurs after Group A beta strep infxns (1-3 wks later)
damage to the glomerulus occurs bc antibody-antigen rxns lead to insoluble complexes that clog the glomerulus blockage causes an inflammatory rxn within glom that causes blockage with WBCs acute phase resolves within 2 wks, dec fxn up to a few months rarely leads to chronic renal failure |
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Post-renal Causes
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Pressure increases and transmits back to glomerulus decreasing GFR
least common cause, < 5% of cases REVERSIBLE if underlying cause is corrected promptly |
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Nephrotic syndrome
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Renal Disease Process occuring as a result of an underlying renal dx
leads to damage of the glom is such a way that proteins pass into the tubules |
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Manifestations of nephrotic syndrom
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Hypoalbuminemia--conc <3.5
Hypovolemia Inc Infxns Hypercoag-loss of coag proteins C & S Edema--loss of plasma oncotic pressure Proteinuria Hypercholesterolemia |
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Causes of Nephrotic Syndrome
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Chronic Glomerulonephritis
Amyloidosis--abn proteins are deposited into basement memb of vessels leading to damage Minimal Change Nephrotic Syndrome--a pediatric condition, ages 2-6, these patients have a loss of negative charges within the basement memb and therefore low molecular weight proteins pass such as albumin |
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Chronic Renal Failure
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Definition: a loss of at least 70% of fxning nephrons resulting in GFR <25% of nml and the inability to meet physiologic demands
IRREVERSIBLE Renal insufficiency-25-40% nml Decreased renal reserve 60-75% of nml |
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ESRD--etiology
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Initial reaction to periods of stress within the kidneys is adaptation to increase GFR and preserve UOP
Over time further damage occurs to remianing nephrons possibly d/t chronically inc pressures Ultimately vessels become slerosed and no further adaptation can occur. Requires transplant or dialysis |
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Symptoms of Chronic Renal Failure
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systemic manifestations are same as for ARF
manifestation of these symptoms in pts with ESRD is called uremia ESRD classified as GFR < 25mL/min ESRD pts are dialysis dependent which is effective in the mgmt of uremia |
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Dialysis Complications
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HYPOTENSION: dialysate solution with acetate which causes vasodilation
Neutropenia: 2 to reaction between WBCs and dialysis membranes Disequilibrium: 2 to rapid osmolarity changes |
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Lab assessment of renal function: BUN
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BUN: byproduct of protein catabolism in liver. Amino acids broken down to ammonias then to ureas
Nml value: 10-20 Inversely related to GFR Directly related to protein catabolism--not a constant rate of protein catabolism 40-50% of filtered ureas are reabsorbed Liver dysfxn or starvation can cause decreases So it is not a reliable indicator of GFR TAKE HOME MESSAGE: BUN GREATER THAN 50 IS ASSOCIATED WITH RENAL IMPAIRMENT |
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Lab assessment of renal function: Creatinine
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by product of muscle breakdown
production typically constant for any given person but will vary upon muscle mass Men: 20-25 mg/kg Women: 15-20 mg/kg Almost all creatinine fully filtered |
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Creatinine
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Serum creatinine directly related to muscle mass, inversely related to GFR
Can be altered by high meat diets, cimetidine, and states of ketoacidosis Value requires 48-72 hrs to reflect any acute renal changes NML: Men 0.8-1.3 Women 0.6-1 TAKE HOME: Serum creatinine GENERALLY a reliable indicator of GFR |
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Creatinine
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be careful with this value in the ELDERLY
less muscle mass GFR declines 5% per decade after age 20 A small change in creatinine in this population is SIGNIFICANT |
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BUN/Creatinine Ratio
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Decreased renal perfusion will lead to an increase in this ratio
with decreases in tubular flow BUN (ureas) are reabsorbed more...leading to increases above normal ratio nml ratio is 10:1 Can see increases in ratio with: hypvolemia, heart failure, cirrhosis, and nephrotic syndrome |
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Creatinine Clearance
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MOST ACCURATE METHOD FOR ESTIMATING GFR
10-20% overestimation of GFR 2 to small amount of secretion from tubules Nml GFR--125mL/min Usually collected over 24hrs but can be collected over 2 hrs with reasonable accuracy Mild impairment: 40-60mL/min Moderate: 25-40 Severe (failure): <25 mL |
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Equation for Creatinine Clearance
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(140 - AGE) X lean body weight / 72 X plasma creatinine
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Urinalysis
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not useful in eval renal fxn
pH--only helpful if you know serum pH. urinary alkalosis in the presence of systemic acidosis indicates renal tubular acidosis specific gravity: helps know if kidneys are concentrating properly Low spec grav < 1.01 in the setting of hyperosmolality of plasma is indicative of DI Glycosuria: nml glucose threshold is 180, could reflect hyperglycemia proteinuria: conc > 150 are considered signif, could indicate tubular dysfxn (nephrotic syndrome) RBCs and WBCs |
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Excretion of Filtered Sodium: FEF Na
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helps to distinguish pre-renal from renal failure
Ratio of urine to plasma conc of sodium and urine to plasma conc of creatinine Pre-renal failure: < 0.01 LOW renal Failure: > 0.01 HIGH TAKE HOME MESSAGE: PRE-RENAL--GFR and RBF are decreased but tubes working so lots of Na reabsorption. Excretion of Na is small RENAL FAILURE: Tubes not working. Na reabsorption is decreased and Excretion is of Filtered Na is Large |
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Urinalysis
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not useful in eval renal fxn
pH--only helpful if you know serum pH. urinary alkalosis in the presence of systemic acidosis indicates renal tubular acidosis specific gravity: helps know if kidneys are concentrating properly Low spec grav < 1.01 in the setting of hyperosmolality of plasma is indicative of DI Glycosuria: nml glucose threshold is 180, could reflect hyperglycemia proteinuria: conc > 150 are considered signif, could indicate tubular dysfxn (nephrotic syndrome) RBCs and WBCs |
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Excretion of Filtered Sodium: FEF Na
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helps to distinguish pre-renal from renal failure
Ratio of urine to plasma conc of sodium and urine to plasma conc of creatinine Pre-renal failure: < 0.01 LOW renal Failure: > 0.01 HIGH TAKE HOME MESSAGE: PRE-RENAL--GFR and RBF are decreased but tubes working so lots of Na reabsorption. Excretion of Na is small RENAL FAILURE: Tubes not working. Na reabsorption is decreased and Excretion is of Filtered Na is Large |
