exam 3 SG SP.docx

If an adult male weighs 70kg 60% of his weight is total body water. Which is about 42L of fluid. Intracellular fluid = 2/3 of total body water. Extracellular fluid = 1/3 of total body water. Osmosis is the movement of water down a concentration gradient. Osmolality is the concentration of water mole...

If an adult male weighs 70kg 60% of his weight is total body water. Which is about 42L of fluid. Intracellular fluid = 2/3 of total body water. Extracellular fluid = 1/3 of total body water. Osmosis is the movement of water down a concentration gradient. Osmolality is the concentration of water molecules per weight of water. Osmotic forces are the amount of hydrostatic pressure required to oppose the osmotic movement of water. Sodium is most abundant in the extracellular fluid. Sodium is the primary ECF cation. Chloride is the primary EFF anion. Chloride follows sodium. Chloride varies inversely with bicarbonate. Sodium is responsible for osmotic balance of extracellular fluid. Potassium maintains osmotic balance of intracellular fluid. Filtration if the movement of fluid from the capillary into the interstitial space. Reabsorption is the movement of fluid from the interstitial space into the capillary. Capillary hydrostatic pressure is blood pressure, PUSH, it facilities outward movement of water from the capillary to the interstitial space. Plasma Capillary oncotic pressure is water pulling, it attracts water from the interstitial space back into the capillary osmotically via proteins (think albumin) PULL. Interstitial hydrostatic pressure facilitates inward movement of water from interstitial space into the capillary PUSH. Interstitial oncotic pressure PULLS water from the capillary into the interstitial space. Forces favoring filtration are Capillary hydrostatic pressure and interstitial oncotic pressure. Forces opposing filtration are plasma capillary oncotic pressure and interstitial hydrostatic pressure. Major forces for filtration and reabsorption are those within the capillary = capillary hydrostatic pressure and capillary oncotic pressure. Edema is an accumulation of fluid in the interstitial spaces. Increased capillary hydrostatic pressure causes venous obstructions which causes edema. Decreased plasma oncotic pressure from low albumin causes edema. Increased capillary permeability from inflammation causes edema. Lymph obstruction lymphedema causes edema. Sodium retention causes edema. The pathophysiology of edema is = increase in forces favoring fluid filtration from the capillaries or lymphatic channels into the tissues. Hormonal regulation of sodium is mediated by aldosterone. Aldosterone is secreted from the adrenal cortex. Aldosterone is secreted when sodium levels are low, potassium levels are high, or renal perfusion is low. Aldosterone tells the kidney to increase reabsorption of sodium and water back into circulation, potassium and hydrogen secretion to be lost in urine. Renin is released by the juxtaglomerular cells of the kidney in response to low perfusion. Renin stimulates release of Angiotensin I. Angiotensin I is converted to angiotensin II by ACE in pulmonary vessels. Angiotensin II stimulates secretion of aldosterone, increasing sodium and water reabsorption. Angiotensin II causes vasoconstriction which increases perfusion. RAAS is activated by low perfusion which stimulated release of renin from juxtaglomerular cells, renin stimulates angiotensin I which converts to angiotensin II in the pulmonary cells, angiotensin II tells the kidneys to keep water and sodium and causes vasoconstriction all of which increases perfusion. Natriuretic peptides are hormones that are a natural antagonist to the RAAS. Natriuretic peptides decrease BP and increase sodium and water excretion. Natriuretic peptides are released when there is increased atrial pressure (FVO, CHF). Natriuretic peptides are inhibited by a decrease in BP and atrial pressure. Water balance is regulated by ADH and thirst perception. Baroreceptors are stimulated by plasma depletion and causes release of ADH. ADH is released when there is an increase in plasma osmolality, decrease in circulating blood volume, or decrease BP. A decrease in atrial pressure causes secretion of ADH. Hypovolemia results in an increase of aldosterone secretion. Hypovolemia results in an increase of renin secretion. Isotonic solutions have the same osmotic pressure across membrane. Hypotonic solutions have a lower osmotic pressure. Hypertonic solutions have a higher osmotic pressure. Isotonic solutions have no change in concentration. Isotonic volume depletion is called hypovolemia. Isotonic volume excess is called hypervolemia. Hypernatremia is a hypertonic alteration where water moves from the ICF to the ECF causing intracellular dehydration. Chloride follows sodium. Hyperchloremia occurs with hypernatremia or a bicarbonate deficit. Hyponatremia decreases the ECF osmotic pressure and water moves into the cell. Hypotonic think hippo. Hypertonic hyponatremia is common in hyperglycemia because water shifts from the ICF into the ECF. Potassium is the major intracellular cation. Hypokalemia can cause decreased neuromuscular excitability, cardiac dysrhythmia. Acidosis can cause hyperkalemia. Alkalosis can cause hypokalemia. Insulin facilitates the movement of K into the cells. Calcium and phosphate are regulated by PTH, Vit D, and Calcitonin. Parathyroid hormone (PTH) increases plasma calcium levels via kidney reabsorption in response to low calcium. Calcitonin decreases plasma calcium levels. Vitamin D is a fat-soluble steroid increases calcium absorption in GI tract. Hypocalcemia can cause tetany, muscle spasms, Chvostek and Trousseaus signs. Hypercalcemia can cause weakness, kidney stones, heart block, constipation. High phosphate levels is related to low calcium levels. Chloride is an extracellular ion that is important in maintenance of fluid and electrolyte balance. Magnesium is an intracellular cation and is a co-factor in intracellular reactions, protein synthesis, nucleic acid stability, and neuromuscular excitability. As pH goes down H+ goes up Normal pH is 7.35-7.45. To maintain a normal pH hydrogen must be either retained or excreted. H+ is neutralized by the retention of bicarbonate or excreted. CO2 + H2O <-> HCO3 (carbonic acid) <-> HCO3 (bicarb) + H+ The most efficient buffering systems are hemoglobin and carbonic acid-bicarbonate system. Carbonic acid-bicarbonate buffering system takes place in the lung and kidney. The greater the pCO2 the more carbonic acid is formed. The ratio of bicarbonate to carbonic acid is 20:1 Lungs can decrease carbonic acid. Kidneys decrease bicarbonate slower than the lungs. If bicarbonate decreases then pH decreases and can cause acidosis. pH can be returned to normal if carbonic acid also decreases. The respiratory system compensates by increasing or decreasing ventilation. The renal system compensates by producing acidic or alkaline urine. In respiratory buffering, acidemia causes increased ventilation, alkalosis slows respirations. In renal buffering secretion of H+ in urine and reabsorption of HCO3- Potassium and hydrogen exchange inversely, one for the other. Normal arterial blood pH 7.35-7.45. Acidosis = pH less than 7.35. Acidosis is a systemic increase in H+ concentration or a loss of base. Alkalosis = pH greater than 7.45. Alkalosis is a systemic decrease in H+ concentration or excess of base. Normal PaCO2= 35-45 Normal HCO3- = 22-26 Normal SaO2= 95-100 Respiratory acidosis-Elevation of pCO2 as a result on ventilation depression, causes true hypercapnia. Respiratory alkalosis-depression of pCO2 as a result of hyperventilation, causes hypocapnia. Metabolic acidosis-depression of HCO3- from ECF or an increase in noncarbonic acids. Metabolic alkalosis-elevation of HCO3-, usually as a result of an excessive loss of metabolic acids from vomiting, GI suctioning, diuretic therapy, and hyperaldosteroneism, or too much bicarb intake. Metabolic Acidosis- pH<7.35 HCO3-<24. In metabolic acidosis H+ ions move into intracellular space and K+ moves to extracellular space to maintain ion balance. Metabolic acidosis can be caused by lactic acidosis, renal failure, DKA, starvation. Metabolic Alkalosis pH>7.45 HCO3->26 Metabolic alkalosis compensation-hypoventilation; kidneys H+ and eliminate bicarb. Metabolic acidosis compensation-respiratory system, low pH stimulates hyperventilation which lowers pCO2 and carbonic acid. Respiratory Acidosis caused by depression of the respiratory center, respiratory muscle paralysis, chest wall disorders (flail chest), disorders of lung parenchyma. Respiratory acidosis= pH below 7.35 CO2 >45 (hypercapnia). Respiratory acidosis compensation-not as effective since kidneys take longer, but conserve bicarb and eliminate H+. Respiratory alkalosis is caused by high altitudes, hypermetabolic states like fever anemia and thyrotoxicosis, early salicylate intox, anxiety/panic disorder, improper use of mechanical vents. Respiratory alkalosis= pH>7.45 Co2<38. Respiratory alkalosis compensation=kidneys decrease H+ excretion and bicarb absorption. Nephrons are the functional unit of the kidney. Nephrons are the urine forming unit of the kidney. The three types of nephrons are- superficial cortical nephrons, midcortical nephrons, juxtamedullary nephrons. Superficial cortical nephrons are the most abundant. Juxtamedullary nephrons secrete renin and help in urine concentration. Glomerular endothelial cells synthesize nitric oxide and endothelin-I. Nitric oxide is a vasodilator. Endothelin-I is a vasoconstrictor. Both Nitric oxide and endothelin-I regulate glomerular blood flow. Juxtaglomerular cells and macula densa make up the JGA and control renal blood flow, glomerular filtration, and renin secretion. Proximal tubules help with reabsorption. Loop of henle-transports solutes and water. Distal tubule-adjusts acid-base balance. Collecting duct-contains cells that help regulate electrolytes. Glomerular filtration rate is directly related to the perfusion pressure in the glomerular capillaries. If mean arterial pressure decreases or vascular resistance increases the renal blood flow and GFR decrease. As systemic pressure declines, glomerular perfusion increases. An increase in systemic pressure decreases glomerular perfusion. When sodium filtration increases, GFR decreases. Macula densa calls stimulate afferent arteriole vasoconstriction. GFR is the measure of how much blood passes through the kidney in a minute. \ When systemic BP increases afferent arterioles constrict to prevent an increase in filtration pressure. When systemic BP decreases, afferent arterioles dilate to allow more blood flow in to maintain GFR. Autoregulation is done to maintain sodium and water excretion despite arterial pressure changes. Sympathetic nervous system can cause vasoconstriction which diminishes GFR. Baroreceptor reflex decreases GFR. Exercise and position changes can activate renal sympathetic neurons, causing vasoconstriction. Severe hypoxia stimulates chemoreceptors decreasing RBF. The majority active reabsorption of sodium is in the proximal tubules. Loop of henle is responsible for the concentration of urine, water reabsorption, and sodium reabsorption via active transport. Agine affects renal blood flow and GFR. Aging decreases the number of nephrons. Complications of upper urinary tract obstructions include Hydroureter, hydronephrosis, and uterohydronephrosis. Compensatory hypertrophy and hyperfunction occurs when there is a loss of function in one kidney with obstructive disease which leads to an increase in function of the unaffected kidney. Post-obstructive diuresis is done after relief of an obstruction and can alter electrolytes. Kidney stones are most prevalent in young males with inadequate fluid intake. Geographic location can influence the prevalence of kidney stones. Kidney stones begin to form with an oversaturation of one or more salts. Temperature and pH of urine influence the risk calculus formation. pH is important in precipitation of a salt from a liquid to a solid. Renal colic-moderate to severe pain in the flank that radiates to the groin. Renal colic indicated obstruction of the renal pelvis of proximal ureter. Colic that radiates to the lateral flank or lower abdomen indicates obstruction in the midureter. Lower UTI symptoms arise secondary to kidney stones. Kidney stones may have nausea, vomiting, and hematuria. Lower UTI’s can arise from neurogenic bladders, dyssynergia, detrusor hyperreflexia, detrusor areflexia. Dyssynergia=overactive or hyperreflexive bladder function from loss of coordinated neuromuscular function. Detrusor areflexia-underactive, hypotonic, or atonic bladder. Sighs/symptoms of lower urinary trat obstruction-frequent daytime voiding, Nocturia, urgency, dysuria, slow stream, incomplete bladder emptying. Overactive bladder syndrome (OAB)-syndrome of detrusor overactivity, detrusor too weak to empty bladder, results in urinary retention with overflow or stress incontinence. Renal adenomas-benign tumors located near cortex of kidney, can become malignant. Renal cell carcinoma-most common, are adenocarcinomas that arise from tubular epithelium in the renal cortex. Clear cell RCC has a better prognosis than papillary RCC. Early stages of renal tumors are often silent. Renal cancer metastasizes to the lung, lymph node, liver, bone, thyroid, and CNS. Clinical manifestations of renal cancer include hematuria, dull and aching flank pain, palpable flank mass in thin people. The most common bladder tumor is urothelial carcinoma. Exposure to dyes and chemicals, smoking, arsenic, and heavy consumption of phenacetin increase risk of bladder cancer. Pyelonephritis-infection of one or both upper respiratory urinary tracts which primarily affects tubules. Pyelonephritis manifests as UTI symptoms with hypertension, fever, chills, flank and groin pain. Smoky brown-tinged urine, proteinuria are a sign of acute glomerulonephritis. Oliguria is a sign of severe glomerular disease. Nephrotic sediment contains massive amounts of protein and lipids. Nephrotic syndrome is the excretion of 3g or more of protein in urine. Kidney dysfunction can be acute or chronic. Renal insufficiency is the decline of renal function to approx 25% of normal. Renal failure is significant loss of renal function. End-stage renal failure is less than 10% of renal function remains. RIFLE is the guide to dx renal injury (RISK, INJURY, FAILURE, LOSS, END-STAGE) AKI decline in kidney function with a decrease in glomerular filtration and accumulation of nitrogenous waste products in the blood. AKI blood work will show increased creatinine and BUN. Aki is commonly from extracellular volume depletion. Prerenal AKI = inadequate perfusion. Renal AKI = cellular damage. Postrenal AKI = obstruction. Acute tubular necrosis is the most common cause of intrarenal renal failure. Chronic Kidney disease is the progressive loss of renal function. CKD = GFR < 60ml/hr for three months or more. Factors that contribute to the progression of disease is glomerular hypertension, hyperfiltration, fibrosis, tubulointerstitial inflammation. Patho theory of CKD=loss of nephron mass with progressive kidney damage causes the surviving nephrons to sustain normal kidney function.