Renal.pdf

Osmosis — movement of H2O down concentration gradient Osmolality — concentration of molecules per weight of H2O Normal 275-295 295 = dehydrated Osmotic Forces — amount of hydrostatic pressure required to oppose the osmotic movement of H20 Na most abundant ion in ECF — responsible for osmotic balance...

Osmosis — movement of H2O down concentration gradient Osmolality — concentration of molecules per weight of H2O Normal 275-295 295 = dehydrated Osmotic Forces — amount of hydrostatic pressure required to oppose the osmotic movement of H20 Na most abundant ion in ECF — responsible for osmotic balance of ECF K most abundant ion in ICF — maintains osmotic balance of ICF FOUND IN ICF: K+ P organic ions (-) FOUND IN ECF: Na+ Cl- — follows Na & varies inversely with HCO3 HCO3- Mediated by aldosterone secreted when Na levels are depressed K levels increases, or renal perfusion is decreased leads to Na & H2O reabsoption back into circulation & K & H secretion to be lost in urine Filtration — movement of fluid from capillary into interstitial space Reabsorption — movement of fluid from interstitial space into capillary 4 forces: capillary hydrostatic pressure (blood pressure) — facilitates outward movement of H20 from capillary to interstitial space capillary (plasma) oncotic pressure — attracts H20 from interstitial space back into capillary osmotically interstitial hydrostatic pressure — facilitates inward movement of H2O from interstitial space into capillary interstitial oncotic pressure — attracts H2O from capillary into interstitial space osmotically forces favoring filtration or opposing reabsorption — capillary hydrostatic pressure (BP) & interstitial oncotic pressure (H2O pulling) forces opposing filtration or favoring reabsorption — capillary (plasma) oncotic pressure (H20 pulling) & interstitial hydrostatic pressure major forces for filtration & reabsorption are those within the capillary = capillary hydrostatic pressure (filtration) & capillary oncotic pressure (reabsorption) Accumulation of fluid in interstitial spaces Patho = increase in forces favoring fluid filtration from capillaries or lymphatic channels into tissues localized = limited to site of trauma or specific organ system generalized = dependent edema ANP — produced in atria BNP — produced in ventricles natural antagonist to RAAS — decreases BP & increases Na & H2O excretion released when there is increased atrial pressure (increased volume); ex) CHF decrease in BP decrease atrial pressure therefore inhibiting release of ANP & BNP antidiuretic hormone released when there is an increase in plasma osmolality, decrease in BP which all result in decrease atrial pressure & ultimately secretion of ADH increases water reabsorption interacts with Ca low serum levels cause renal conservation HYPERMAGNESEMIA causes — renal failure manifestations — skeletal muscle depression, muscle wkness, hypotension, respiratory depression, bradycardia HYPOMAGNESEMIA causes — from malabsorption; associated with hypocalcemia & hypokalemia manifestations — neuromuscular irritability, tetany/ convulsions, increased reflexes isotonic alterations = no change in concentration isotonic volume depletion = hypovolemia isotonic volume excess = hypervolumia hypertonic alterations — hypernatremia, hypercloremia, water deficit hypotonic alterations — hyponatremia (decreases ECF osmotic pressure & H2O moves into cell) HYPONATREMIA Na deficits cause plasma hypoosmolality & cellular swelling dilution hyponatremia — excess total body H2O (TBW) in relation to total body Na or shift of H2O from ICF to ECF = mannitol hypertonic hyponatremia — shift of H2O from ICF to ECF in hyperglycemia, hyperlipidemia, & hyperproteinemia hypotonic hyponatremia — TBW exceeds increase in Na although both are increased; severe CHF or ARF aldosterone, insulin, epi, & alkalosis facilitate K into cells; deficiency of these/ acidosis/strenuous exercise facilities it out hypokalemia causes — reduced K intake, increased K entry into cell, increased K loss, hyperaldosterone state, respiratory alkalosis hyperkalemia causes — increased intake, shift of K from ICF to ECF, decreased renal excretion, hypoaldosterone state, hypoxia, acidosis, insulin def., cell trauma HYPERKALEMIA mild attacks — tingling of lips & fingers, restlessness, intestinal cramping & diarrhea, peaked T waves severe attacks — muscle wkness, loss of muscle tone, flaccid paralysis, cardiac arrest renin is released by juxtaglomerular cells of kidney & stimulates release of angiotensin I (inactive) to angiotensin II (active) by ACE (angiotensin converting enzyme) in the pulmonary vessels which stimulates secretion of aldosterone HYPERPHOSPHATEMIA causes — exogenous or endogenous addition of P to ECF, long term use of P enemas or laxatives, renal failure high P levels related to low Ca levels manifestations — same as hypocalcemia with possible calcification of soft tissue HYPOPHOSPHATEMIA causes — intestinal malabsorption & renal excretion, vit D deficiency, antacid use, alcohol abuse manifestations — diminished release of O2, osteomalacia (soft bones), muscle wkness, bleeding disorders (plt impairment), leukocyte alterations if concentration of one increases the other decreases regulated by 3 hormones: parathyroid hormone (PTH) — increases plasma Ca levels via kidney reabsorption & is secreted in response to low serum Ca vit D — tat soluble steroid; increases Ca absorption from GI tract calcitonin — decreases plasma Ca levels HYPERCALCEMIA causes — hyperparathyroidism, bone metastasis, excess vit D, immobilization, acidosis manifestations — decreased neuromuscular excitability, muscle wkness, kidney stones, constipation, heart block HYPOCALCEMIA causes — inadequate intake or absorption, decreases in PTH & vit D, blood transfusion manifestations — increased neuromuscular excitability, muscle spasms, Chvostek & Trousseau signs, convulsions, tetany Causes: lactic acidosis, renal failure, DKA, starvation H+ ions move to intracellular space & K+ moves to extracellular space to maintain ion balance (both positive) pH drops below 7.35 HCO3 drops less than 24 mEg/L Manifestations: headache, lethargy, Kussmaul respirations Negative logarithm of H+ concentration. If H+ high in number, pH is low. If H+ low in number, pH is high. To maintain body's normal pH (7.35 - 7.45), H+ must be neutralized by retention of HCO3- or excreted. pH < 6.8 or > 7.8 = death pH = base/acid pH = renal regulation (slow)/ pulmonary regulation (fast) pH = metabolic acid-base function/respiratory acid-base function buffer = a chemical that can bind excessive H+ (acid) or OH- (base) without significant change in pH consists of buffering pair: weak acid & its conjugate base most important plasma buffering systems: carbonic acid-bicarbonate system & hemoglobin CARBONIC ACID—BICARBONATE BUFFERING operates in lungs & kidney must maintain ratio of bicarb & carbonic acid at 20:1 for pH to remain normal lungs can decrease carbonic acid kidneys can reabsorb or regenerate bicarb but don't act as fast as the lungs if bicarb decreases then pH decreases & can cause acidosis; pH can be returned to normal if carbonic acid also decreases — this is called compensation respiratory system compensates by increasing or decreasing ventilation; renal system compensates by producing acidic or alkaline urine RESPIRATORY & RENAL BUFFERING respiratory: acidemia causes increased ventilation; alkalosis slows respirations renal: secretion of H+ in urine & reabsorption of HCO3 normal arterial blood pH is 7.35—7.45 acidosis is pH 7.45; systemic decrease in H+ concentration or excess of base pH 7.35–7.45: based on H+ ions PaCO2 35–45mmHg: partial pressure of CO2 HCO3 (bicarb) 22–26mEq/L: calculated value of amount of bicarb in bloodstream base excess -2 to +2mEq/L: indicates amount of excess or insufficient level of bicarb SaO2 95–100%: arterial oxygen saturation 1. Respiratory acidosis — elevation of pCO2 as result of ventilation depression or alveolar hyperventilation; causes true hypercapnia 2. Respiratory alkalosis — depression of pCO2 as result of hyperventilation; causes hypocapnia 3. Metabolic acidosis — depression of HCO3 from ECF or an increase in non carbonic acids 4. Metabolic alkalosis — elevation of HCO3 usually as result of excessive loss of metabolic acids, like with vomiting, GI suctioning, excessive bicarb intake, hyperaldosterinism, & diuretic therapy Causes: prolonged vomiting, gastric suctioning, excessive bicarbonate intake, hyperaldosteronism with hypokalemia, diuretic therapy pH elevated above 7.45 HCO3 is elevated above 26mEq/L Compensation: hypoventilation (kidneys conserve H+ & eliminate bicarb) Manifestations: weakness, muscle cramps, & hyperactive reflexes with signs of hypocalcemia Causes: respiratory center depression (brainstem trauma/oversedation), respiratory muscle paralysis, disorders of chest wall (kyphoscoliosis, pickwickan syndrome, flail chest), disorders of lung parenchyma (pneumonitis, pulmonary edema, emphysemas asthmas bronchitis) pH is below 7.35 CO2 elevates (hypercapnia) >45mmhg Compensation: not as effective since kidneys take time but conserve bicarbonate & eliminate H+ Manifestations: headache, restlessness, blurred vision, apprehension, lethargy, muscle twitching, tremors, convulsions, coma Must be careful when correcting because rapid reduction of PCO2 can cause respiratory alkalosis with seizures & death Causes: high altitudes, hypermetabolic states (fever, anemia, & thyrotoxicosis), early salicylate intoxication, anxiety or panic disorder, improper use of mechanical ventilators pH above 7.45 CO2 decreased through duct of Bellini —> intro into renal papillae (projections of ducts) —> into the calyces —> collected in renal pelvis inner layer — glomerular endothelium middle layer — glomerular basement membrane (GBM) outer layer — visceral epithelium that forms inner layer of Bowman capsule glomerular endothelial cells — synthesize nitric oxide la vasodilator), synthesize endothelium-1 (a vasoconstrictor), both which regulate glomerular blood flow visceral epithelium of bowman capsule & is composed of cells called podocytes; form elaborate network of clefts called filtration slits that modulate filtration plasma nitrate from glomerulus passes through glomerular membrane into the Bowman space to form primary urine JUXTAGLOMERULAR APPARATUS (JGA) juxtaglomerular cells — located around afferent arteriole macula densa — portion of distal convoluted tubule with specialized sodium & chloride-sensing cells control of renal blood flow (RBF), glomerular filtration, & renin secretion occurs at this site long intertwining smooth muscle bundles that pass through posterior aspect of bladder peristaltic activity moves urine to bladder & mictivition compresses lower end of water to avoid urine reflux glomerular filtration rate (GFR) — directly related to perfusion pressure in glomerular capillaries if mean arterial pressure decreases or vascular resistance increases, then the renal plasma flow (RPF) decreases & so does GFR myogenic mechanism (stretch) — as systemic pressure declines, glomerular perfusion increases an increase in systemic pressure decreases glomerular perfusion tubuloglomesular feedback (NaCl content) — when Na filtration increases then GFR decreases; macula densa cells stimulate efferent arteriolar vasoconstriction neural regulation — sympathetic nervous system (vasoconstriction diminishes GFR), baroreceptor reflex (vasoconstriction of afferent arterioles decreases perfusion & GFR), exercise & change of body position (mild vasoconstriction), severe hypoxia (decreases RBF) renin-angiotensin-aldosterone system (RAAS) — increases systemic arterial pressure & increases Na reabsorption BLADDER detrusor muscle — smooth muscle in bladder trigone — smooth triangular area lying between opening of the ureters & urethra URETHRA internal sphincters — smooth muscle at junction of bladder & urethra external sphincters — striated skeletal muscle under voluntary control females 3-4 cm long; males 18-20 cm long INNERVATION parasympathetic fibers (autonomic) — bladder & internal ureter sphincter that contracts detrusor muscle sympathetic (autonomic) — allows bladder to fill skeletal muscle neurons in pudendal nerve (somatic) — external urethral sphincter PROXIMAL TUBULE active reabsorption of Na (majority) LOOP OF HENLE concentration of urine descending loop — water reabsorption (Na diffuses in) ascending loop — Na reabsorbed by active transport) GLOMERULOTUBULAR BALANCE when GFR spontaneously decreases or increases — renal tubules & primarily the proximal tubules automatically adjust their rate of reabsorption of Na & water to balance the change in GFR compensatory hypertrophy & hyperfunction relief usually followed by post-obstructive dieresis — may cause fluid & electrolyte imbalance classified according to minerals that make up stone risk factors — male, most develop before age 50, inadequate fluid intake (most prevalent), geographic location 70-80% calcium oxalate & calcium phosphate (most common), 15% struvite (Mg, ammonium, P — forms during infection like klebsiella pseudomonas), 7% uric acid temperature & pH of urine influence risk of precipitation & calculus formation — pH more important renal colic is a manifestation that indicates obstruction of renal pelvis or proximal ureter renal adenoma — benign; located at cortex of kidney & can become malignant renal transitional cell carcinoma — rare renal cell carcinoma (RCC) — most common; adenocarcinomas that arise from tubular epithelium in renal cortex; clear cell has better prognosis & most common; papillary has worse prognosis classic clinical manifestations: hematuria, dull/aching flank pain, palpable flank mass in thin pts early stages often silent excretion of 3.0g or more of protein in urine caused by increased permeability of glomerular filtration membrane RIFLE — Risk, Injury, Failure, Loss, End-stage disease UREMIA syndrome of renal failure elevated blood urea & creatinine levels fatigue, anorexia, nausea, vomiting, pruritus, & near changes retention of toxic wastes, deficiency states, electrolyte disorders, & pro-inflammatory state patio manifestation to severe azotemia AZOTEMIA increased serum urea levels & frequently increased creatinine levels renal insufficiency or renal failure, causing azotemia measured clinically but no symptoms most common urological tumor; urothelial (transitional cell) carcinoma clinical manifestations: gross painless microscopic hematuria nonbacterial; thought to be result of autoimmune reaction responsible for inflammatory response that includes mast cell activation, altered epithelial permeability, & increased sensory nerve sensitivity infection of one or both upper urinary tracts (ureter, renal pelvis, & interstitum) acute pyleo — primarily affects tubules, glomeruli usually spared NEPHROTIC SEDIMENT massive amounts of protein & lipids microscopic amount to no blood NEPHRITIC SEDIMENT blood is present in urine with red cell casts & varying degrees of protein most common cause of internal renal failure occurs most often after surgery; also associated with sepsis, obstetric complications, & severe trauma/burns described as postischemic or nephrotoxic postischemic — involves persistent HTN, hypoperfusion, hypoxemia producing ischemia/reduced ATP, & generates toxic oxygen- free radicals with loss of antioxidant protection that causes cell swelling, injury, & necrosis nephrotoxic — produced by numerous antibiotics; neomycin, gentamicin, & torbramycin are major ones