GU Nephron Study Guide

GU Nephron: functional unit of the kidney, forms urine by filtering waste products and water from blood. Glomerular filtration: first process in urine formation GFR: Normal 90-120 when b/p is below 65-70 self-regulation processes do not maintain GFR. Decrease in renin(enzyme) and aldosterone(holds on to fluid) causes: an excretion of na, dilution of urine, a decreased thirst. Acute Kidney Injury: Rapid reduction is kidney function: resulting in failure to maintain fluid and acid based balance. Unable to maintain waste elimination, electrolyte balance, acid base balance. Occurs in a few hours and days. *reversible *Causes: Prerenal: anything before it gets to the kidney: Issue with perfusion to kidney= decrease function to kidney, decrease of amount of blood to kidney to filter and deprives kidney= leads to Intrarenal injury – issues with cardiac(blood/fluid loss, hypotension, Infection) chart 68-4 decrease in b/p 65 cause renal problem Intrarenal-damage to nephrons- within kidney, problem with nephron= decrease ability to filter blood- excessive waste build, excessive water, not able to maintain electrolyte, from nephrotoxic drugs(NSAIDS, Vanc, Contrast dye, renal drugs, Pyelonephritis) Postrenal: Lower in urinary system, blockage in tract, after the kidney, Prevents urine draining out of system, High pressure in kidney and high in waste decreases kidney function Causes: renal calculi, enlarged prostate, Stroke “bladder doesn’t empty” In any acute kidney injury- reduce urine to increase blood volume and improve kidney elimination Oliguria: urine output less than 400/day Azotemia: retention and buildup of nitrogenous wastes in blood +all healthcare providers be alert for signs of AKI, Interventions early to prevent ESKD Encourage 2-3L water daily - Evaluate I/O, fluid status, foul odor. - Report urine output less than 0.5 ml/kg/hr that persists for more than 2 hours. After 6 hours of oliguria= progression of kidney damage - Monitor increase in creatinine (0.6-1.2) over hours of days - Bun (10-20) - Potassium (3.5-5) - Urine specific (1.005-1.030) - Decreased GFR (less than 90) bad on kidneys Assessment: ask about recent surgery, trauma, transfusions, drugs history (NSAIDS) Contrast dye? HTN, NPO(can cause AKI) IV vasopressor START with oral fluids before IV Foley- check output every hour after surgery till stable Anasarca(edema) SIGNS: Tachy, thready pulse, decrease LOC, edema, increase in daily wt, reduced urine output Diagnostic: IVP( Contrast dye), U/S, CT, KUB  Onset of polyuria= recovery of AKI Phases of AKI: Onset phase: from time of event to manifestations, up to a week after event (slight increase in BUN,CREAT, normal or decrease in urine output- may not know something wrong Oliguric stage: can last 1-8 weeks, longer=worse prognosis, Urine output decreases to 400ml or less/day -400 in a shift (8 hours) Diuretic stage: gradual or abrupt return of GFR, urine output increase 1-2l day, BUN creat decrease Recovery stage: everything back to normal last 3-12 months Treatment: diuretics(increase urine output) Hemodialysis: temporary to pull off fluid and toxins, 3 days a week, 3-6 hours, creates shifts of fluid and electrolytes and may be tolerated by critically ill patients= hypotension and can worsen renal function, fluid restriction Hemodialysis can cause disequilibrium syndrome: mental status changes, seizures, coma Parenteral: AT home, 4 exchanges per day, move around, 7-10 hours at night, no PD if a lot of abdominal surgeries, don’t have to have fluid restriction CRRT: unstable patient, ICU, cant tolerate changes in blood pressure, removes 1L/hour OK with b/p being in 80’s Chronic renal failure: serum creat level is the most accurate measure of renal function Low fat, low protein, low NA diet Metabolic acidosis= increase rate, depth breathing, kussmaul respirations No NSAIDS, Tylenol, naproxen Main causes: HTN, DM- African am. More likely to develop ESKD HTN, HLD, Decrease Ca= Increase Phos IRREVERSIABLE, kidneys do not recover 11% increase d/t obesity, HTN, DM Azotemia: build up nitrogen waste in blood Uremia (build up): metallic taste, anorexia, n/v, muscle cramps, uremic frost, itching, fatigue, hiccups, edema, Uremic frost, dyspnea- coma, seizures, decrease LOC= need dialysis ASAP Stages of CKD: Stage 1: may have normal GFR greater than 90, may have abn. Urine findings, structural abn, traits: Uncontrolled HTN, DM, Congenital, Family hx, exposed nephrotoxic drugs Stage 2: GFR: 60-89, kidney nephron damage occurred, slight elevations in metabolic waste in blood, Increase output of dilute urine may occur, (BUN,Creat, uric acid, phos may be normal) Stage 3: GFR 30-59 albuminuria is present, nephron damage, azotemia, Manage B/P, DM, Ristriction of fluids, electrolyte Stage 4: 15-29 GFR, manage complications, educate on options: Stage 5: less than 15 GFR AT risk for hyponatremia Hypernatremia causes HTN, edma Priority: fluid overload: interventions- diuretics, low Na low protein diet, fluid resctrition, monitor weight, dialysis Pulmonary edema: Left sided heart failure=lungs, crackles, restlessness, anxiety, rapid heart rate, SOA, blood tinged sputum, interventions: High fowlers, give O2, Loop diuretics (lasix, bumex) monitor K+ levels, Morphine to reduce myocardial oxygen demand Increase cardiac function: Educate how to measure B/P at home, Manage HTN, give Ca channel blockers, ACEI, vasodilator (ace inhibitors, pril’s) Nutrition: reduce proteins, K+, Na, phos (high in protein, lean meats, fish, eggs, beans) good diet green leafy vegetables, rice If on dialysis need more protein, 2-4g na If not on dialysis Na restriction 1-3g Preventing infection: Preventive measures, treat incisions carefully Acute Pancreatitis: Severe and life threatening, Affects body to protect itself via its immunity Endocine: DM Exocrine: Responsible for secreating enzymes that assist in breakdown of starches, proteins, and fats, Normal enzymes are secreted in inactive form then become active in small intestine. Pancreatitis is early activation within the pancreas 4 patho in pancreatitis Lipolysis: Fats are broken down, fatty acids released and combine w/ ionized Ca= hypocalcemia (chvosteks, trousseus) Muscle spasms Proteolysis: SplitÝng of protiens by hydrolysis of peptide bonds= smaller poly peptides=causes thrombosis(blood clot) gangrene of pancreas Necrosis of blood vessels: results in bleeding ranging from minor-massive bleeding of pancreatic tissue= shock, hemorrhaging, death Inflammation: leukocytes cluster around hemorrhagic, necrotic area and form pus= pseudocyst Jaundice: from selling of head of pancreas slows bile flow through bile duct. - Treatment at hospital to control pain, may need ERCP- gallstones - Most common reason= gallstones, ETOH Assess: abd pain after drinking, eating high protein diet, Look for jaundice, Turners sign: greyblue at flanks, Cullen’s sign- grey-blue around belly button, listen to bowel sounds= paralytic ileus= peritonitis ( monitor vitals for high temp, tachy, decrease b/p) Signs: severe abd pain, mid-epigastric, sudden onset radiates to back, Finds relief in pain knees to chest, sitÝng upright and bending forward, wt loss n/v. Check Amylase, lipase, decrease Ca, Decrease Mag, high WBC Priority: Treat pain: IV pain meds, IV fluids, NPO, NG (PCA) Morphine, dilaudid, no Demerol, H2 antagonists, PPI (ranitidine, omeprazole) NG(Enternal feeding) first before TPN When start eating need: Small frequent moderate-high carb, high protein and low fat diet NO GI stimulant(coffee, cola, chocolate) Chronic pancreatitis: damage irreversible, high blood sugar(even non diabetics) ETOH primary risk factor- constant flare ups Pancreatic enzyme secretion must be reduced to produce steatorrhea(pale, bulky, frothy odor stools) clay colored stools Fat malabsorption= weight loss Treatment: pain mang, no ETOH, Pancreatic enzyme- do not mix in foods high in protein, do not chew or crush, take with all meals and snacks H2blockers, PPI, PERT Increase calories 4000-6000 Cirrhosis: Widespread fibrosis ** Falls risk** Hepatitis C- most common in US Hep B, D most common worldwide Liver largest and most vital internal organ Thrombocytopenia (low platlet) At risk for bleeding( first sign of slenomegaly) Irreversible scarring of liver, caused by ETOH, viral hepatitis (C,B,D, nonalcoholic steatohepatitis (fatty liver d/t obesity, DM and metabolic, bile duct disease, genetic Complications: Portal HTN: increase in pressure in portal vein (5mm)= obstruction of blood flow to through portal vien= causes splenomegaly d/t blood flow backs up into the spleen= veins in esophagus, stomach, intestines, and rectum become dilated= ascities= esopheal varies= hemorrhoids. Liver will not produce albumin= osmotic pressure which causes third spacing resulting in hypovolemia and edema Massive ascities cause renal vasoconstriction and triggers renin- angiotensin= results from sodium water retention Esophageal varices: veins become distended from increased portal vein pressures- will do a scope: Bleeding= life- threatening (hematemesis, or melena dark stools) Production of bile is decreased= prevents absorption of Vitamins ADEK susceptible to bleeding and easy bruising. Jaundice(pruritis) Complications: Hepatic encephalopathy Signs: sleep disturbance, mood disturbance, change LOC, speech problems- reversible with early interventions (Lactulose) If working increase in LOC Lead to encephalopathy: high protein diet, infection, Hypovolemia, hypokalemia, constipation, GI bleed, Drugs ASSESSMENT: jaundice, dry skin, rashes, petechia, ecchymosis, palmar erythema(warm, red palms) spider angiomas(nose, cheeks, chest, shoulders) ascites, edema, fetor hepaticus: fruity musty breath, Amneorrhea (no period) gynecomastia( large breast in men) Asterixis- hand flapping, anemia Measure abd. Girth: lay flat, measure largest part of abdomen over umbilicus at end of exhalation ****daily wts most reliable indicator of fluid retention*** Check ast, alt, PT/INR, albumin, ammonia usually elevated  Women that drink 2-3 ETOH daily for 10 years at risk  Men 6 drinks daily for 10 years  Binge drinking Test: CT, MRI, Biopsy, can go through jugular vein percutaneious (at risk for bleeding) EGD, ERCP Priority: fluid over load d/t third spacing Interventions: Low na diet 1-2g restriction first, give thiamine, folate, multivitamin oral or IV, Diuretic Paracentesis: at bedside, Void before procedure, monitor vitals d/t hypotension, bedrest, HOB elevated, describe to fluid, weigh patient before and after. Respiratory: listen to lungs 4-8 hours (crackles) Bun, protein, hematocrit (elevated BUN, Decreased protein, increased hematocrit= hypovolemia Managing Hemorrhage: possible GI bleed, esophageal varices : DO EARLY SCOPE TO ASSESS FOR BLEEDING Beta blocker to prevent bleeding (propranolol) Vasopressin in active bleeding (octreotide acetate) decrease portal pressure Managing Encephalopathy: High carb, high protein, moderate-fat diet No opiods, analgesics, sedatives, barbs Lactulose: promote excretion of ammonia in stool should have 2-3 stools daily, increase LOC, older adults at risk for dehydration and weakness need broad spectrum antibiotics for normal flora Education: NO over counter drugs NSAIDS, herbs, vitamins, minerals Thrombocytopenia: reduction of platelets: below 50K Wont do paracentesis if below 50K d/t risk for bleeding Use electric shaver, watch gums, soft toothbrush DIC: problem with blood clotÝng process: triggered by severe illnesses, including CA Abn. Extensive bleeding- bleeding through IV sites Sepsis causes DIC, give antibiotic and heparin d/t clotÝng then vasopressin to stop bleeding: Octreotide acetate