FLUIDS-ELECTROLYTES-AND-GUTS.pdf

Fluids and Electrolytes Handout Arellano Lecture B. Active Transport Process - cell moves substances across a membrane through ATP FLUIDS...

Fluids and Electrolytes Handout Arellano Lecture B. Active Transport Process - cell moves substances across a membrane through ATP FLUIDS because: 1. They may be too large - help maintain body temperature and cell shape 2. Unable to dissolve in the fat core - help transport nutrients, gases and wastes 3. Move uphill against their concentration gradient 60% of an adult’s body weight, e.g., 70 kg adult male: 60% X 70= 42 Liters Infants= more water; Elderly= less water Types of Active Transport More fat= less water; more muscle= more water 1. Active Transport – requires protein carriers using Infants and elderly – prone to fluid imbalance ATP to energize it i.e. Amino acids, sodium potassium pump – 3 Na+ out, 2 K+ in TOTAL BODY WATER 60% 2. Endocytosis – moves substances into the cell 3. Exocytosis – moves substances out of the cell Intracellular Fluid 40% Extracellular Fluid 20% OSMOSIS - movement of water from low solute to high solute concentration in order to maintain balance Intravascular 5% Interstitial 15% between compartments. Osmotic pressure – amount of hydrostatic pressure needed to stop the flow of water by osmosis Arterial Fluid 2% Venous Fluid 3% Oncotic pressure – osmotic pressure Transcellular Fluid 1-2% exerted by proteins Ie. CSF, pericardial, synovial, intraocular, sweat Regulation of Body Fluids 1. The Kidney Third Space Fluid Shift/ Third “Spacing” regulates primarily fluid output by urine - loss of extracellular fluid (ECF) into a space that does not formation 1.5L contribute to equilibrium between intracellular fluid (ICF) and release Renin ECF regulates sodium and water balance - i.e. ascites, burns, peritonitis, bowel obstruction, massive 2. Endocrine regulation bleeding thirst mechanism – thirst center in hypothalamus Transport Mechanisms Antidiuretic Hormone (ADH) – increase water reabsorption on collecting duct - fluids from different compartments move from one Renin-Angiotensin-Aldosterone system – compartment to the other, to maintain fluid balance. increases sodium and water retention in the distal nephron Atrial Natriuretic Factor (ANF) – promotes Movement is dictated by the transport mechanism principle: sodium excretion and inhibits thirst mechanism A. PASSIVE TRANSPORT B. ACTIVE TRANSPORT ADH Regulation ADH – produced by the hypothalamus A. Passive Transport Process - stored and secreted by the posterior pituitary gland - substances transported across the membrane without less water in plasma, ADH secreted to energy input from the cell conserve water by reducing urine output fluid overload in plasma, ADH secretion stops - high to low concentration to excrete fluid in the kidneys by increasing urine output 2 Types of Passive Transport ADH Disorder 1. Diffusion – substances or solutes move from high Abnormally high ADH concentration – concentration to low concentration, i.e. exchange of O2 and SIADH CO2 between pulmonary capillaries and alveoli - reduced urine output (oliguria) - water retention (fluid overload) 2. Filtration – water and solutes forced through membrane by fluid or hydrostatic pressure from intravascular to interstitial area Abnormally low ADH – Diabetes Insipidus - solute containing fluid (filtrate) from higher pressure to - increased urine output (polyuria) lower pressure - water loss (fluid deficit) 3. Gastrointestinal regulation  GIT digests food and absorbs water only about 200ml of water is excreted in th I & O IMBALANCE fecal material per day 4. Heart and Blood Vessel Functions Fluid Volume Deficit (FVD) pumping action of heart circulates blood increase output, normal intake through kidneys normal output, decrease intake no intake or prolonged decreased intake 5. Lungs – insensible water loss through respiration Causes of FVD Other Mechanisms vomiting, diarrhea, GI suctioning, sweating Diabetes Insipidus 1. Baroreceptors – carotid sinus and aortic arch Adrenal insufficiency Osmotic diuresis - causes vasoconstriction and increased blood pressure Hemorrhage 3rd space fluid shift Decreased arterial pressure → Sympathetic Nervous System (SNS) → increase cardiac rate, contraction, Assessment of FVD contractility, circulating blood volume, constriction of renal arterioles and increased aldosterone ICF – cellular dehydration → Acidosis ITF – skin → poor skin turgor 2. Osmoreceptors – surface of hypothalamus senses IVF changes in Na+ concentration - artery → decreased BP, pulse (rapid thready) Increase osmotic pressure → neurons → dehydrated → - vein → decreased Central venous pressure release ADH (CVP), decreased pulmonary artery wedge pressure (PAWP) Evaluation of Fluid Status Clinical Manifestations Osmolality – concentration of fluid that affects movement of water between fluid compartments by osmosis weight loss - measures the solute concentration per kg in blood and oliguria urine concentrated urine - reported as mOsm/kg postural hypotension - normal value= 280-300 mOsm/kg flattened neck veins increased temperature Osmolarity – concentration of solutions decreased CVP - mOsm/L thirst, anorexia muscle weakness and cramps Intake and Output Laboratory Intake (I) and Output (O) must be equal BUN: Crea > 20:1 2.6L per day Increased Hematocrit (Hct) – RBC Essential= Measurable= Sensible suspended in decrease plasma volume Non-essential= estimated Measurement= Decreased K+ - GI and renal losses Insensible Increased K+ - adrenal insufficiency Decreased Na+ - increase thirst and ADH Increased Na+ - insensible losses and Sources of Fluids (Fluid Intake) diabetes insipidus 1. Exogenous sources Medical Management Fluid intake oral intake when mild oral liquids – 1,300 ml IV route, acute or severe water in food – 1,000 ml Isotonic fluids, i.e. LR for hypotensive patients water produced by metabolism – 300 ml to expand plasma volume Assess I and O, weight, CVP, level of Intravenous fluids (IVF) consciousness (LOC), breath sounds and skin Medications color Blood products Fluid challenge test – 100-200 ml X 15 min 2. Endogenous sources Nursing Management By products of metabolism Monitor and measure I and O Secretions Monitor vital signs closely Monitor skin turgor and tongue furrows Monitor urinary concentration Fluid Output Monitor mental function Sensible Loss Urine – 1,500 ml Fecal losses – 200 ml Fluid Volume Excess (FVE) Insensible Loss increased intake, normal output Skin – 600 ml normal intake, decreased output Lungs – 300 ml no output Causes of FVE Types of Fluids Heart failure, renal failure, cirrhosis of the ISOTONIC FLUIDS liver due to aldosterone stimulation or congestion - no movements of fluids Increased consumption of table salt Excessive administration of Na+ 0.9% NaCl/ Normal Saline/ NSS containing fluids in a patient with impaired regulatory mechanism Na= 154 mEq/L, Cl= 154, 308 mOsm/L SIADH not desirable as routine maintenance solution only solution administered with blood Assessment of FVE products Indications: hypovolemia, shock, DKA, ICF – cellular edema → decreased LOC metabolic alkalosis, hypercalcemia, mild - pulmonary edema → crackles Na+ deficit (bibasilar), wheezing, shortness of breath, CI: renal failure, heart failure and edema increase RR D5W – 5% Dextrose in water ITF – skin → bipedal pitting edema, periorbital edema and Anasarca 170 cal and free water, 252 mOsm/L IVF I: hypernatremia, fluid loss and – artery → increased BP, pulse (rapid dehydration bounding) CI: early post op when ADH increased due - vein → increased CVP, increased PAWP to stress, sole treatment in FVD (dilutes plasma), head injury (inc. ICP), fluid Clinical Manifestations resuscitation (hyperglycemia), caution in renal and cardiac disease (fluid overload), Distended neck veins patient with Na+ deficiency (peripheral Tachycardia circulatory collapse and anuria) Increase weight Increase urine output 10% Dextran 40 in 5% Dextrose isotonic (252 Shortness of breath and mOsm/L) wheezing/crackles Increase CVP Lactated Ringer’s Solution isotonic Na+= 130 mEq/L, K+= 4, Ca++= 3, Cl= 109, 273 mOsm/L Edema I: hypovolemia, burns, fluids lost as bile/ diarrhea, acut blood loss common manifestation of FVE CI: ph > 7.5, lactic acidosis, renal failure due to increased capillary fluid pressure, (cause hyperkalemia) decreased capillary oncotic pressure, increased interstitial oncotic pressure localized or generalized HYPOTONIC FLUID Etiology: obstruction to lymph flow, plasma albumin level < 1.5-2 g/dl, burns and - fluid will enter the cell, the cell will swell infection, Na+ retention in ECF, drugs 0.45% NaCl (half strength saline) Laboratory provides Na, Cl and free water decreased Hct, respiratory alkalosis and Na+= 77 mEq/L, Cl= 77, 154 mOsm/L hypoxemia, decreased serum Na+ and I: hypertonic dehydration, Na+ and Cl osmolality, increased BUN, Crea, depletion, gastric fluid loss decreased urine specific gravity, CI: 3rd space fluid shifts and increased ICP decreased urine Na+ level Medical Management HYPERTONIC FLUID discontinue administration of Na+ solution - fluid will go out from the cell, the cell will shrink Diuretics, i.e. Thiazide – block Na+ reabsorption in distal tubule; Loop diuretics 3% NaCl (hypertonic saline) – block Na reabsorption in ascending loop of Henle no calories Restrict fluids and salt intake Na+= 513 mEq/L, Cl= 513, 1026 mOsm/L Dialysis I: critical situations to treat hyponatremia, assist in removing ICF excess Nursing Management CI: administered slowly and cautiously (IVF overload and pulmonary edema) measure intake and output weigh daily, 2 lb wt gain = 1 L fluid 5% NaCl assess breath sounds monitor degree of edema, D10 W – 10% Dextrose in water hypertonic (505 mOsm/L) i.e. ambulatory – feet and ankles bedridden – sacral area D10 W – 20% Dextrose in water hypertonic (1011 promote rest – favors diuresis or increase mOsm/L) venous return administer appropriate medication D50 W – 50% Dextrose in water hypertonic (1700 mOsm/L) D5 NS – 5% Dextrose & 0.9 NaCl hypertonic (559 mOsm/L)  D10 NS – 10% Dextrose & 0.9 NaCl hypertonic (812 Etiology: inadequate water intake, excessive mOsm/L) salt ingestion/ hypertonic feedings without water supplements, near drowning in sea D5 LR – 5% Dextrose in Lactated Ringers water, diuretics, Diabetes mellitus/ Diabetes hypertonic (524 mOsm/L) insipidus S/Sx: polyuria, anorexia, nausea, vomiting, thirst, dry and swollen tongue, fever, dry and COLLOID SOLUTIONS flushed skin, restlessness, agitation, seizures, coma, muscle weakness, crackles, dyspnea, Dextran 40 in NS or 5% D5 W cardiac manifestations dependent on type of hypernatremia volume and plasma expander Dx: inc serum sodium and Cl level, inc serum decreas coagulation osmolality, inc urine sp.gravity, inc urine remains for 6 hours in circulatory system osmolality I: hypovolemia in early shock, improve Mgt: sodium restriction, water restriction, microcirculation (dec RBC aggregation) diuretics, isotonic non-saline soln.(D5W) or CI: hemorrhage, thrombocytopenia, renal hypotonic soln, Desmopressin Acetate for disease and severe dehydration Diabetes Insipidus Nsg: History – diet, medication, monitor VS, LOC, I & O, weight, lung sounds, monitor Na+ levels, oral care, initiate ELECTROLYTES gastric feedings slowly, Seizure precautions - elements or compounds when dissolved in water will dissociate into ions and are able to conduct an electric b. HYPONATREMIA current. Na+ < 135 mEq/L Functions: Etiology: diuretics, excessive sweating, 1. Regulate fluid balance and osmolality vomiting, diarrhea, SIADH, aldosterone 2. Transmission of nerve impulse deficiency, cardiac, renal, liver disease 3. Stimulation of muscle activity Dx: dec serum, urine sodium and osmolality, dec Cl ANIONS – negatively charged ions: S/Sx: headache, apprehension, restlessness, Bicarbonate, chloride, PO4-, CHON altered LOC, seizures( 5.0 mEq/L Etiology: IVF with K+, acidosis, hyper- alimentation, excess K+ replacement, SODIUM (Na+) decreased renal excretion, diuretics, Cancer S/Sx: nerve and muscle irritability, most abundant cation in the ECF tachycardia, colic, diarrhea, ECG changes, 135-145 mEq/L ventricular dysrythmia and cardiac arrest, Aldosterone → increase sodium skeletal muscle weakness, paralysis reabsorption Dx: inc serum K+ level, ECG: peaked T ANF → increase sodium excretion waves and wide QRS, ABGs – metabolic acidosis Functions: Mgt: K+ restrictions (coffee, cocoa, tea, dried 1. assists in nerve transmission and muscle fruits, beans, whole grain breads, milk, eggs), contraction diuretics, Polystyrene Sulfonate (Kayexalate), 2. major determinant of ECF osmolality IV insulin, Beta 2 agonist, IV Ca gluconate – 3. primary regulator of ECF volume WOF hypotension, IV NaHCO3 – alkalinize plasma, Dialysis a. HYPERNATREMIA Nsg: monitor VS, urine output, lung sounds, Crea, BUN, monitor K+ levels and Na+ > 145 mEq/L ECG, observe for muscle weakness and Associated with water loss or sodium gain dysrythmia, paresthesia and GI symptoms  inflammation of pancreas, renal failure, b. HYPOKALEMIA thyroid CA, low albumin, alkalosis, alcohol abuse, osteoporosis (total body Ca+ deficit) K+ < 3.5 mEq/L S/Sx: Tetany, (+) Chovstek’s, (+) Etiology: use of diuretic, corticosteroids and Trousseau’s, seizures, depression, impaired penicillin, vomiting and diarrhea, ileostomy, memory, confusion, delirium, hallucinations, villous adenoma, alkalosis, hyperinsulinism, hypotension, dysrythmia hyperaldosteronism Dx: dec Ca level, ECG: prolonged QT S/Sx: anorexia, nausea, vomiting, decreased interval bowel motility, fatigue, muscle weakness, leg Mgt: Calcium salts, Vit. D, diet (milk, cheese, cramps, paresthesias, shallow respiration, yogurt, green leafy vegetables) shortness of breath, dysrhythmias and Nsg: monitor cardiac status, bleeding, increased sensitivity to digitalis, hypotension, monitor IV sites for phlebitis, seizure weak pulse, dilute urine, glucose intolerance precautions, reduce smoking Dx: dec serum K+ level, ECG – flattened, depressed T waves, presence of “U” MAGNESIUM (Mg) waves, ABGs – metabolic alkalosis Mgt: diet (fruits, fruit juices, vegetables, fish, 2nd to K+ in the ICF whole grains, nuts, milk, meats), oral or IV Normal range is 1.3-2.1 mEq/L replacement Nsg: monitor cardiac function, pulses, Functions: renal function, monitor serum K+ 1. intracellular production and utilization of ATP concentration, IV K+ diluted in saline, 2. protein and DNA synthesis monitor IV sites for phlebitis 3. neuromuscular irritability 4. produce vasodilation of peripheral arteries CALCIUM (Ca++) a. HYPERMAGNESEMIA Majority of calcium – bones and teeth Mg > 2.1 mEq/L Normal serum range 8.5-10.5 mg/dl Etiology: use of Mg antacids, K+ sparing diuretics, renal failure, Mg medications, DKA, Functions: adrenocortical insufficiency 1. formation and mineralization of bones and S/Sx: hypotension, nausea, vomiting, teeth flushing, lethargy, difficulty speaking, 2. muscular contraction and relaxation drowsiness, decrease LOC, coma, muscle 3. cardiac function weakness, paralysis, depressed tendon 4. blood coagulation reflexes, oliguria, decrease RR 5. enzyme activation Mgt: discontinue Mg supplements, Loop 6. promotes absorption and utilization of diuretics, IV Ca gluconate, Hemo-dialysis Vit.B12 Nsg: monitor VS, observe DTR’s and changes in LOC, seizure precautions Regulation: b. HYPOMAGNESEMIA GIT → absorbs Ca+ in the intestine with the help of Vitamin D Mg < 1.5 mEq/L Kidney → Ca+ is filtered in the glomerulus Etiology: alcohol withdrawal, tube feedings, and reabsorbed in the tubules diarrhea, fistula, GIT suctioning, drugs, i.e. PTH → increases Ca+ by bone resorption, antacid, aminoglycosides, insulin therapy, increase intestinal and renal Ca+ reabsorption sepsis, burns, hypothermia and activation of Vitamin D S/Sx: hyper-excitability with muscle Calcitonin →reduces bone resorption, weakness, tremors, tetany, seizures, stridor, increase Ca+ and Phosphorus deposition in Chvostek and Trousseau’s signs, ECG bones and secretion in urine changes, mood changes Dx: serum Mg level, ECG – prolonged PR a. HYPERCALCEMIA and QT interval, ST depression, widened QRS, flat T waves, low albumin level Serum calcium > 10.5 mg/dL Mgt: diet (green leafy vegetables, nuts, Etiology: overuse of calcium supplements legumes, whole grains, seafood, peanut and antacids, excessive Vitamin A and D, butter, chocolate), IV Mg Sulfate via infusion malignancy, hyperparathyroidism, prolonged pump immobilization, thiazide diuretic Nsg: seizure precautions, test ability to S/Sx: anorexia, nausea, vomiting, polyuria, swallow, DTR’s, monitor I & O, VS during muscle weakness, fatigue, lethargy Mg administration Dx: inc serum Ca, ECG: shortened QT interval, ST segments, inc PTH levels, X-ray The Anions – osteoporosis Mgt: 0.9% NaCl, IV Phosphate, diuretics – CHLORIDE (Cl) Furosemide, IM Calcitonin, corticosteroids, dietary restriction (cheese, ice cream, milk, The Major Anion in the ECF yogurt, oatmeal, tofu) Normal range is 95-108 mEq/L Nsg: Assess VS, apical pulses and ECG, Increased Na+ reabsorption causes increased bowel sounds, renal function, hydration Cl reabsorption status, safety precautions in unconscious patients, increase mobility, increase fluid Functions: intake, monitor cardiac rate and rhythm 1. major component of gastric juice aside from H+ b. HYPOCALCEMIA 2. together with Na+, regulates plasma osmolality 3. participates in the chloride shift – inverse Calcium < 8.5 mg/dL relationship with Bicarbonate Etiology: removal of parathyroid gland during 4. acts as chemical buffer thyroid surgery, Vit. D and Mg deficiency, Furosemide, infusion of citrated blood, a. HYPERCHLOREMIA  Nsg: introduce TPN solution gradually, Serum Cl > 108 mEq/L prevent infection Etiology: sodium excess, loss of bicarbonate ions S/Sx: tachypnea, weakness, lethargy, deep rapid respirations, diminished cognitive ability ACID-BASE BALANCE and hypertension, dysrythmia, coma Dx: inc serum Cl, dec serum bicarbonate Mgt: Lactated Ringers soln, IV Na Bicarbonates (HCO3) bicarbonate, diuretics Nsg: monitor VS, ABGs, I & O, neurologic, present both in ICF and ECF cardiac and respiratory changes Normal range 22-26 mEq/L b. HYPOCHLOREMIA Functions: 1. regulates acid-base balance Cl < 96 mEq/L 2. component of the bicarbonate-carbonic acid Etiology: Cl deficient formula, salt restricted buffer system diets, severe vomiting and diarrhea S/Sx: hyper-excitability of muscles, tetany, hyperactive DTR’s, weakness, twitching, ACID – substance that can donate or release hydrogen ions muscle cramps, dysrythmias, seizures, coma Dx: dec serum Cl level, ABG’s – metabolic Carbonic acid, Hydrochloric aci alkalosis Mgt: normal saline/ half strength saline, diet (tomato juice, salty broth, canned vegetables, BASE – substance that can accept hydrogen ions processed meats and fruits, avoid free/ bottled water) Bicarbonate Nsg: monitor I & O, ABG’s, VS, LOC, muscle strength and movement BUFFER – substance that can accept or donate hydrogen PHOSPHATES (PO4) Hemoglobin buffer The Major Anion in the ICF Bicarbonate: carbonic acid buffer Normal range is 2.5-4.5 mg/L Phosphate buffer Reciprocal relationship with Ca Carbon dioxide is considered to be ACID because of its PTH → increase bone resorption, increase relationship with carbonic acid PO4 absorption from GIT, inhibit PO4 excretion from kidney pH measures the degree of acidity and Calcitonin → increases renal excretion of alkalinity. It is inversely related to PO4 Hydrogen. Normal ph 7.35-7.45 Functions: Decreased pH – Acidic – increased 1. component of bones hydrogen – pH below 7.35 2. needed to generate ATP Increased pH – Alkalosis – decreased 3. components of DNA and RNA hydrogen – pH above 7.45 A high CO2 → may mean acidic a. HYPERPHOSPHATEMIA A low CO2 → may mean alkalosis Serum PO4 > 4.5 mg/dL Dynamics of Acid Base Balance Etiology: excess vit. D, renal failure, tissue trauma, chemotherapy, PO4 containing Acids and bases are constantly produced medications, hypoparathyroidism in the body S/Sx: tetany, tachycardia, palpitations, They must be constantly regulated anorexia, vomiting, muscle weakness, CO2 and HCO3 are crucial in the balance hyperreflexia, tachycardia, soft tissue A ratio of 20:1 is maintained calcification (HCO3:H2CO3) Dx: inc serum phosphorus level, dec Ca level, Respiratory and renal system are active in X-ray – skeletal changes regulation Mgt: diet – limit milk, ice cream, cheese, meat, fish, carbonated beverages, nuts, dried food, sardines, dialysis ______________ Arterial Sample Venous Sample Nsg: dietary restrictions, monitor signs of impending hypocalcemia and changes in pH 7.35-7.45 7.33-7.41 urine output PaCO2 35-45mmHg 35-40mmHg b. HYPOPHOSPHATEMIA O2 Sat 93-98% 65-75% Serum PO4 < 2.5 mg/dL Etiology: administration of calories in severe HCO3 22-26 mEq/L 24-28 mEq/L CHON-Calorie malnutrition, chronic __________________________________________________ alcoholism, prolonged hyperventilation, poor dietary intake, DKA, thermal burns, respiratory alkalosis, antacids, Vit. D METABOLIC ACIDOSIS deficiency - headache, confusion, drowsiness, increased RR, S/Sx: irritability, fatigue, apprehension, nausea, vomiting weakness, hyperglycemia, numbness, paresthesias, confusion, seizures, coma Correction of the defect Dx: dec serum PO4 level Mgt: oral or IV Phosphorus correction, diet Excessive intake of chloride (milk, organ meat, nuts, fish, poultry, whole Hyperkalemia to hypokalemia grains) Low serum calcium levels treated 1st  Alkalizing agents Chemical buffers can also participate in the balance of acid-base METABOLIC ALKALOSIS 1. Carbonic acid – bicarbonate buffer 2. Phosphate buffer - decreased calcium – tingling sensation, dizziness, 3. protein buffer – ICF and hemoglobin hypertonic muscles, Atrial tachycardia Correction of the defect improve ventilation antibiotics, pharmacologic agent, suction, mechanical ventilation RESPIRATORY ALKALOSIS - lightheadedness due to decreased cerebral blood flow, numbness, tingling, tinnitus and loss of consciousness Correction of the defect breath slowly, paper bag, sedative RESPIRATORY ACIDOSIS - increased pulse and RR, mental cloudiness, feeling of fullness in the head - increased ICP, hyperkalemia Correction of the defect improve ventilation Ways to Balance Acids and Bases Excretion Acid can be excreted, and Hydrogen can be excreted in Acidotic condition Bicarbonate can be excreted in Alkalotic condition Production Bicarbonate can be produced in Acidotic condition Hydrogen can be produced in Alkalotic condition The respiratory system compensates for metabolic problems CO2 (acid) can be exhaled from the body to normalize the pH in Acidosis CO2 (acid) can be retained in the body to normalize the pH in Alkalosis The kidney can compensate for problems in the respiratory system the kidney reabsorbs and generates bicarbonate (alkaline) in Acidosis the kidney can excrete H+ excess (acidic) to normalize the pH in Acidosis the kidney can excrete bicarbonate (alkali) in conditions of Alkalosis the kidney can retain H+ (acid) in conditions of Alkalosis GUTS ALDOSTERONE ↓ H20 IN THE PLASMA ↓ ↑ ALDOSTERONE ↓ ↑ Na REABSORPTION ↑SERUM Na H20 RETENTION ↓ ↑ BLOOD VOLUME ↑ H20 IN THE PLASMA ↓ ↓ALDOSTERONE ↓ ↑ Na and H20 EXCRETION ↓ ↓ BLOOD VOLUME NOTE: Functional unit of the kidneys are the glomerulus, vasa recta and kidney tubules ( nephron ) Only the renal tubules can regenerate Acidosis — increases hydrogen secretion (kidney tubules) — increases HCO3 reabsorption Alkalosis — decreases hydrogen secretion — decreases HCO3 reabsorption ASSESSMENT IRRITATION Dysuria Frequency Urgency Nocturia OBSTRUCTION Weak Stream Hesitancy Terminal Dribbling Incomplete emptying Nocturia PAIN Flank or lumbar Inguinal or iliac Initiation of voiding End of voiding Painless hematuria Kidney Function Excretory and Tubular Reabsorption -Water -Electrolytes - Wastes Secretory -Active Vitamin D -Renin -Erythropoietin ANP Atrial Natriuretic Peptide ↓ H20 in the plasma ↓ ANP ↓ Urine Formation Oliguria ↓ ↑Blood Volume ↓ URINE CHANGES ↑H2O in the Plasma Pneumaturia ↓ Proteinuria ↑ANP Ketonuria ↓ Glucosuria ↑Urine Formation Polyuria Hematuria Pyuria ↓Blood Vloume Fecaluria  LABORATORY AND DIAGNOSTICS DIURETICS - Thiazide There is no single test for renal function blocks Na reabsorption in the distal CT Best results are obtained by combining several clinical Na and K are excreted (HPN, edema, CHF) tests Hyponatremia and Hypokalemia Renal function is variable from time to limits until time taken early AM Renal function may be within normal >50% of renal report sore throat function is lost Chlorthiazide (Diuril) Chlorthalidone (Hygroton) Blood Studies - Loop Diuretics Blood Urea Nitrogen or serum BUN Inhibits Na, Cl and K reabsorption at the proximal Specific for kidney disease portion of ascending Loop of Henle normal value = 20-30 mg/dl Hypokalemia Use: HPN, PE, CHF, Cirrhosis Serum Creatinine Furosemide (Lasix) is more specific for renal function test is not affected by dietary intake or hydration status - Potassium Sparer cannot be reabsorbed by the kidney tubules Blocks Aldosterone receptors in the kidneys normal value 0.5-1.5 mg/dl H20 and Na loss, K retention (hyperkalemia) Use: Hyperaldosteronism, HPN, edema Serum Electrolytes Evaluation Taken with food, 2-3 days to take effect All electrolytes are elevated in electrolytes in CRF Avoid high K diet except calcium and HCO3 Spironolactone (Aldactone) Diuretics may alter serum CBC - Carbonic Anhydrase Inhibitors Erythropoietin activity Decreases the rate of Carbonic Acid and H ion RBC- significantly low in CRF production in the kidneys WBC Increases the excretion of solute and H20 Platelets Used in treating Open-angle Glaucoma Radiology and Imaging Acetazolamide (Diamox) Radiology and Imaging UTZ (Ultrasound) Intravenous Pyelography IVP or Excretory Urography - Osmotic Diuretics Retrograde Urography Acts by increasing the osmotic pressure of MRI (with injection of contrast media) GFR, reducing the rate of tubular reabsorption while Renal Angiography increasing the rate of urine output Used in increased ICP tx, drug overdose IV filter must be used for infusing the solution (above 15% solution) Mannitol (Osmitrol) DISORDERS UTI Lithiasis ARF CRF -Dialysis -Kidney Transplant UTI Ureteritis= inflammation of the ureter (maybe caused by a stone in the ureter) Cystitis = inflammation of the bladder (caused by ascending bacterial infection usually E. coli) Urethritis= inflammation of the urethra (may lead to prostatitis and epididymitis) FACTORS THAT CONTRIBUTE TO UTI Medical and Surgical Intervention Female (Proximity to the Anus, Shorter Urethra) Nephrolithotomy Poor Hygiene Ureterolithotomy Unsafe sexual practice Cystolithotomy Back to Front Stroke High pH - ESWL extracorporeal shock wave lithotripsy Urinary Statis - Client is immersed to water, slow waves disintegrate Kidney Stones stones (noninvasive) Obstruction of Urine Outflow Post nsg care = increase fluids encourage ambulation, S/Sx: PAIN assessment strain urine and watchout for obstruction and bleeding Pain during and after urination = cystitis Pain after urination = urethritis RENAL Inguinal pain = ureteritis Flank pain = pyelonephritis pre renal Inflammatory manifestations fever and chills decreased renal tissue perfusion from: -DM (most common) Cx: Ascending infection –Hypovolemia Obstruction (stones/calculi) –Shock –Hemorrhage MANAGEMENT –Burns - E. coli (most common C.A.) –Impaired cardiac output - Increase fluids –Diuretic therapy - Warm sitz bath - EMPTY the bladder Intra-renal - Good hygiene - AGN acute glomerulonephritis - Observe safe sexual practice Infection of kidney due to immune response - Front to backstroke Previous infection from group A beta - Acidify urine (cranberry juice, prune, plums) hemolytic streptococcus - C/S test before giving antibiotics - S/Sx-proteinuria, hematuria, oliguria, edema and HPN - For urosepsis give aminoglycosides - Observe complications - CGN chronic glomerulonephritis slowly developing disease LITHIASIS - S/Sx: same with AGN Nephrolithiasis = kidney stone Ureterolithiasis = ureter stone - Nephrotic Syndrome Cystolithiasis = bladder stone Severely damaged glomerular activity that leads to increased capillary permeability. Urethrolithiasis= stone at the urethra S/Sx: proteinuria, hypoalbuminemia, The stone is usually calcium phosphate/oxalate and edema and hyperlipidemia uric acid Struvite Caused by CGN, DM and SLE Staghorn = large stone Post-renal FACTORS THAT CONTRIBUTE TO STONE FORMATION due to obstruction or disruption to urine Hyperuricemia (GA) flow anywhere along the urinary tract: Hypercalcemia (Parathyroidism) - Cystitis Dehydration - Urethritis Prolonged Immobility - Pyelonephritis Hereditary - Urolithiasis - Injuries to the bladder and urethra s/sx: Pain assessment will be dependent on the site of - Cancer of the bladder stone - Prostatitis Flank pain = kidney or ureter - BPH Groin pain = ureter Watch out for obstruction (bladder distention) Acute Renal Failure (50%) identify the type of stone) Progressive deterioration of renal function which end Drugs: fatally in uremia - Sodium cellulose phosphate (GI abs. is decreased) Dialysis or kidney transplant is necessary - Thiazide (inc. tub. Reabs., decreasing calculi formation Irreversible in the kidney tubules) - Cholestyramine (binds oxalates in the feces) Clinical Course: - Allopurinol (decreased uric acid formation) Decreased Renal Reserve 40-70 GFR - Antibiotics (chronic UTI is a precursor to calculi Renal Insufficiency 20-40 GFR formation) Renal Failure 10-20 GFR - Narcotics and NSAID for pain management End-Stage Renal Disease ↓10 GFR - Antispasmodic (Probanthine) Both kidneys are severely affected and - Rowatinex to dissolve stone renal function is absent. SIMILARITIES OF ARF AND CRF Give vit D and calcium supplement Give synthetic erythropoietin (Epogen) ↓ waste product excretion Manage electrolyte imbalance chaotic acid and base regulation elevation of electrolytes water retention ↓ production of erythropoietin ↓active vitamin D secretions ↑ renin activation s/sx: Na and water retention increase- increase Blood Volume-Edema-Hypertension-Congested Heart Failure-Ascites ↓BP-renin activation-angiotensin and aldosterone production-Increase Blood Volume-Increase Blood Pressure ↓H ion excretion ––metabolic acidosis ↓nitrogenous excretion –– azotemia- toxic to CNS- Change Loc ↓ formation of active vit D ––hypocalcemia ↓secretion of erythropoietin-anemia ↓ electrolyte excretion- elevation of electrolytes in the blood Let’s Diagnose! Serum creatinine -elevated normal 0.5-1.5 mg/dl) Serum BUN -elevated (normal 20-30 5 mg/dl) Serum electrolytes all electrolytes are elevated except for HCO3 and Calcium CBC -anemia (due to reduced erythropoietin production) Renal Ultrasonography - to estimate renal size and obstruction Other tests that may help in detecting the cause Nursing Diagnosis FVE related to decreased GFR and sodium retention Risk for infection defenses Altered Nutrition related to reduced host related to catabolic state, anorexia Risk for internal bleeding related to stress ulcer Altered thought processes related to effects of uremic toxins to CNS Fluids and electrolytes imbalance Impaired skin integrity related to uremic frost Constipation related to fluid restriction and phosphate binding agent administration High risk for injury (fracture) related to osteoclast activity Non compliance to therapeutic regimen related to restrictions imposed by CRF and its treatment ARF Management I&O Weighing Infection monitoring Examine gross and occult blood Diet (CHON moderate, increase CHO) Electrolyte management Neurologic assessment CRF Management Restrict water and sodium intake ABG monitoring and NaHCO3 administration Neurologic assessment Dialysis Diet (CHON restriction, inc CHO)