GUT Anatomy and Physiology PDF

GUT Anatomy and Physiology Aldosterone NEPHRON NOTE: Functional unit of the kidneys are the glomerulus, vasa recta and kidney tubules...

GUT Anatomy and Physiology Aldosterone NEPHRON 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 Kidney Function Dysuria Excretory and Tubular Reabsorption Frequency – Water Urgency – Electrolytes Nocturia – Wastes Secretory OBSTRUCTION – Active Vitamin D Weak Stream – Renin Hesitancy – Erythropoietin Terminal Dribbling Incomplete emptying ANP Atrial Natriuretic Peptide Nocturia PAIN Blood Studies Flank or lumbar Blood Studies Inguinal or iliac Blood Urea Nitrogen or serum Initiation of BUN voiding Specific for kidney disease End of voiding normal value = 20-30 mg/dl Painless hematuria Blood Studies Serum Creatinine Incontinence is more specific for renal function test Stress is not affected by dietary intake or Urge hydration status Overflow can not be reabsorbed by the kidney Total tubules Mixed normal value 0.5-1.5 mg/dl Enuresis Serum Electrolytes Evaluation All electrolytes are elevated in CRF except calcium and HCO3 Diuretics may alter serum electrolytes Blood Studies Serum Creatinine is more specific for renal function test is not affected by dietary intake or hydration status can not be reabsorbed by the kidney tubules normal value 0.5-1.5 mg/dl Serum Electrolytes Lab and Diagnostic Evaluation All electrolytes are elevated in CRF except There is no single test for renal function calcium and HCO3 Best results are obtained by combining Diuretics may alter serum a number of clinical tests electrolytes Renal function is variable from time to time CBC Renal function may be within Erythropoietin activity normallimits until >50% of renal RBC – significantly low in CRF function is lost WBC  Platelets Loop Diuretics Radiology and Imaging Inhibits Na, Cl and K reabsorption at the Radiology and Imaging UTZ proximal portion of ascending Loop of Intravenous Pyelography IVP or Henle Excretory Urography Hypokalemia Retrograde Urography Use: HPN, PE, CHF, Cirrhosis MRI (with injection of contrast Furosemide (Lasix) media) Renal Angiography Potassium Sparer Blocks Aldosterone receptors in the kidneys IVP H20 and Na loss, K retention (hyperkalemia) Use: Hyperaldosteronism, HPN, edema Taken with food, 2-3 days to take effect Avoid high K diet Spironolactone (Aldactone) Carbonic Anhydrase Inhibitors Decreases the rate of Carbonic Acid and H ion production in the kidneys Increases the excretion of solute and H20 Used in treating Open-angle CYSTOSCOPY Glaucoma Acetazolamide (Diamox) Osmotic Diuretics Acts by increasing the osmotic pressure of GFR, reducing the rate of tubular reabsorption while 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) DIURETICS Thiazide Disorders blocks Na reabsorption in the distal CT UTI Na and K are excreted (HPN, edema, CHF) Lithiasis Hyponatremia and Hypokalemia ARF taken early AM CRF report sore throat – Dialysis Chlorthiazide (Diuril) – Kidney Transplant Chlorthalidone (Hygroton)  Inflammatory manifestations fever and chills Cx: Ascending infection Obstruction (stones/calculi) Management E. coli (most common C.A.) Increase fluids Warm sitz bath EMPTY the bladder Good hygiene Observe safe sexual practice Front to back stroke Acidify urine (cranberry juice, prune, plums) C/S test before giving antibiotics For urosepsis give aminoglycosides Observe complications FACTORS THAT CONTRIBUTE TO UTI FEMALE (PROXIMITY TO THE ANUS, SHORTER URETHRA) POOR HYGIENE UNSAFE SEXUAL PRACTICES BACK TO FRONT STROKE HIGH pH URINARY STASIS KIDNEY STONES OBSTRUCTION OF URINE OUTFLOW S/Sx: PAIN assessment Pain during and after urination = cystitis Pain after urination = urethritis Inguinal pain = ureteritis Flank pain = pyelonephritis LITHIASIS scratch the membrane irritating the Nephrolithiasis = kidney stone membrane leading to inflammation, Ureterolithiasis = ureter stone bleeding may occur also Cystolithiasis = bladder stone Adhesions may follow after healing Urethrolithiasis = stone at the urethra The stone is usually calcium phosphate/oxalate and uric acid – Struvite – Staghorn = large stone CALCULI (Stones) FACTORS THAT CONTRIBUTE TO STONE FORMATION HYPERURICEMIA (GA) MANAGEMENT HYPERCALCEMIA (PARATHYROIDISM) Increase fluid intake 3-4L/day DEHYDRATION Determine the CAUSE and type of stone PROLONGED IMMOBILITY (calcium or uric acid) HEREDITARY Encourage ambulation If its calcium give cranberry (acid ash diet) s/sx or ascorbic acid Pain assessment will be If its uric acid give dairy products (alkali ash dependent on the site of diet) or Allopurinol stone Flank pain = kidney or MANAGEMENT ureter Groin pain = ureter Antibiotics prophylactically Watchout for obstruction I & O, strain urine (stone must be submitted (bladder distention) to lab to identify the type of stone) Descending stone may  RENAL FAILURE Drugs: Pre→ – Sodium cellulose phosphate (GI abs. is Intra→ decreased) Post→ – Thiazide (inc. tub. Reabs., decreasing calculi formation in the kidney tubules) – Cholestyramine (binds oxalates in the feces) – Allopurinol (decreased uric acid formation) – Antibiotics (chronic UTI is a precursor to calculi formation) – Narcotics and NSAID for pain management – Antispasmodic (Probanthine) – Rowatinex to dissolve stone pre renal MANAGEMENT decreased renal tissue perfusion from: Medical and Surgical Intervention – DM (most common) Nephrolithotomy – Hypovolemia Ureterolithotomy – Shock Cystolithotomy – Hemorrhage – Burns – Impaired cardiac output – Diuretic therapy intra-renal AGN acute glomerulonephritis Infection of kidney due to immune response Previous infection from group A beta hemolytic streptococcus S/Sx – proteinuria, hematuria, oliguria, edema and HPN CGN chronic glomerulonephritis Management slowly developing disease S/Sx – same with AGN ESWL extra corporeal shock wave lithotripsy Nephrotic Syndrome Client is immersed to water, Severely damaged glomerular activity that slow waves disintegrate leads to increased capillary permeability stones (non invasive) S/Sx – proteinuria, hypoalbuminemia, – Post nsg care = increase edema and hyperlipidemia fluids, encourage Caused by CGN, DM and SLE ambulation, strain urine and watchout for obstruction and bleeding post-renal Comparatively due to obstruction or disruption to urine flow anywhere along the urinary tract: – Cystitis – Urethritis – Pyelonephritis – Urolithiasis – Injuries to the bladder and urethra – Cancer of the bladder – Prostatitis – BPH CLINICAL COURSE Acute Renal Failure Sudden decline in renal function, usually associated with increased in BUN, creatinine & elec. Causes: intra, pre and post RENAL Reversible Clinical Course: SIMILARITIES in ARF and CRF Oliguric-anuric phase may last 7-14 days ↓ waste product excretion Non-oliguric or high output chaotic acid and base regulation elevation of yet nitrogenous waste products are still electrolytes high in the blood. water retention Diuresis Phase ↓ production of erythropoietin return to normal urine output ↓active vitamin D secretions Recovery Period ↑ renin activation may take 6 months to 1 year from the initial onset s/sx Na and water retention – inc BV- edema – Chronic Renal Failure HPN – CHF - ascites Progressive deterioration of renal function ↓ BP – renin activation – angiotensin and which end fatally in uremia aldosterone production – inc BV – inc BP Dialysis or kidney transplant is necessary ↓ H ion excretion – metabolic acidosis Irreversible ↓ nitrogenous excretion – azotemia – toxic to CNS – CHANGES IN LOC Clinical Course: ↓ formation of active vit D – hypocalcemia Decreased Renal Reserve 40-70 GFR ↓ secretion of erythropoietin – anemia Renal Insufficiency 20-40 GFR ↓ electrolyte excretion – elevation of electrolytes Renal Failure 10-20 GFR in the blood End-Stage Renal Disease - decrease 10 GFR Both kidneys are severely affected and renal function is absent Let’s Diagnose! CRF Management Serum crea – elevated (normal 0.5-1.5 mg/dl) Restrict water and sodium intake Serum BUN – elevated (normal 20-30 mg/dl) ABG monitoring and NaHCO3 Serum electrolytes – all electrolytes are elevated administration except for HCO3 and Calcium Neurologic assessment CBC – anemia (due to reduced erythropoietin Dialysis production) Diet (CHON restriction, inc CHO) Renal Ultrasonography – to estimate renal size and Give vit D and calcium supplement obstruction Give synthetic erythropoietin (Epogen) Other tests that may help in detecting the cause Manage electrolyte imbalance Nursing Diagnosis Dialysis FVE related to decreased GFR and Hemodialysis sodium retention Peritoneal Dialysis Risk for infection related to reduced host defenses Altered Nutrition related to catabolic state, anorexia Risk for internal bleeding related to stress ulcer Altered thought processes related to effects of uremic toxins to CNS Nursing Diagnosis 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 ⚫ Kidney Transplant ⚫ Rejection and Infection ⚫ Donor and Recipient Preparation HLA test, ABO, Rh test ⚫ Donor Living = anemia, prone to infection, bleeding Cadaveric ⚫ Recipient Stages of Rejection (HA, AA, A, C) Drugs (Immunosuppressive and Antibiotics, prophylactically Isolation (Reverse) KIDNEY SURGERY