WEEK+11+Renal

4. Describe the mechanisms responsible for urine formation, including glomerular filtration, tubular reabsorption, and tubular secretion.

4. Examine the passive transport of water and ions from the proximal convoluted tubules.

5. Examine the renal regulation of the renin-angiotensin-aldosterone system.

6. Discuss the diagnostic evaluations and special procedures related to renal and urinary function and examine the abnormalities.

7. Recognize the physical characteristics of urine and identify any abnormalities that may have pathological significance.

__//**8. Examine the etiology, pathophysiology, clinical manifestations, therapeutic management and nursing management specific to the client with the following inflammatory, infectious and congenital renal disorders. (Lewis, 1165) (Heuther, 796)**//__

- Acute glomerulonephritis
Often 5-23(7-10) days after a streptococcal infection. antigen-anitbody complexes deposit on the glomerular basement membrane. This activates complement and full blown inflammatory mechanisms that damages membrane hematuria with a smokey appearance indicates bleeding in the upper tract, red blood cell casts, proteinuria, decreases GFR, oliguria, hypertension, edema around eyes or feet,
 * Patho**
 * Clinical manifestations**

Chronic glomerulonephritis
progressive leading to renal failure, encompasses several diseases to the glomerulus. (1) deposition of circulating soluble antigen-antibody complexes that lead to complement activation (2) formation of specific basement membrane antibodies (anti-GBM anitbodies) ALL of these are basically starting a full scale complement and inflammatory response, and we all know what that does!!! altered membrane permiabilty results in filtration of proteins(albumin) and RBC's. fibrin formation in the bowmans capsule leading to cresent formation which decreases renal blood flow and GFR is reduced leading to fluid retention and activation of renin exacerbating the problem
 * Patho**
 * Clinical manifestations**

__//**9. Describe the resulting changes in glomerular structure and function as a consequence of glomerulonephritis.(Lewis, 1165) (Heuther, 796)**//__ Thickening of the GBM- alters membrane permeability- allows protein and RBC's to be filtered Fibrin deposits- cresents the Bowmans capsule resulting in decreases GFR and blood flow membrane damage leads to platelet aggregation and degranulation furthering permeability issues

See #11 ~Primarily in adults ~Crescent formations in gomeruli ~fibrin and collagen lead to fibrosis of glomeruli
 * __10. Compare and contrast acute, rapidly progressive, and chronic glomerulonephritis.__** (MS p.1165-1167, ppt. p. 14-15)
 * __acute glomerulonephritis__**
 * __rapidly progressive glomerulonephritis__**

//Rapidly progressive glomerulonephritis// (RPGN) is glomerular disease associated with acute renal failure where there is rapid, progressive loss of renal function over days to weeks. Renal failure may occur within weeks to months in contrast to chronic glomerulonephritis, which develops insidiously and progresses over many years. The manifestations of RPGN are hypertension, edema, proteinuria, hematuria, and RBC casts. RPGN can occur in a variety of situations: (1) as a complication of inflammatory or infectious disease (e.g., APSGN), (2) as a complication of a multisystemic disease (e.g., systemic lupus erythematosus, Goodpasture syndrome), (3) as an idiopathic disease, or (4) in association with the use of certain drugs (e.g., penicillamine,rifampin(TB), ). Prompt diagnosis and treatment is directed toward correction of fluid overload, hypertension, uremia, and inflammatory injury to the kidney. Treatment includes corticosteroids, cytotoxic agents, and plasmapheresis. Dialysis therapy and transplantation are used as maintenance therapy for the patient with RPGN. Following renal transplantation, RPGN may recur.

~small, scarred kidneys and renal failure ~deposits of antigen-antibody complexes ~immune complexes deposited along glom. basement membrane ~fibrin deposits(crescent formations)
 * __chronic glomerulonephritis__**

//Chronic glomerulonephritis// is a syndrome that reflects the end stage of glomerular inflammatory disease. Most types of glomerulonephritis and nephrotic syndrome can eventually lead to chronic glomerulonephritis. The syndrome is characterized by proteinuria, hematuria, and the slow development of uremia as a result of decreasing renal function. Chronic glomerulonephritis progresses insidiously toward renal failure over a few to as many as 30 years. Chronic glomerulonephritis is often found coincidentally when an abnormality on a urinalysis or elevated blood pressure is detected. It is common to find that the patient has no recollection or history of acute nephritis or any renal problems. A renal biopsy may be performed to determine the exact cause and nature of the glomerulonephritis. However, ultrasound and CT scanning are generally preferred as diagnostic measures. Treatment is supportive and symptomatic. Hypertension and UTIs should be treated vigorously. Protein and phosphate restrictions may slow the rate of progression of kidney disease.

Most common in males age 5-10 in the winter or spring 5-21 days after infection by nephrotoxic strains of group A beta-hemolytic streptococci, but can occur in both sexes of all ages The clinical manifestations of APSGN appear as a variety of signs and symptoms. Generalized body edema, hypertension, oliguria, hematuria with a smoky or rusty appearance, and proteinuria may occur. Fluid retention occurs as a result of decreased glomerular filtration. The edema appears initially in low-pressure tissues, such as around the eyes (periorbital edema), but later progresses to involve the total body as ascites or peripheral edema in the legs. Smoky urine indicates bleeding in the upper urinary tract. The degree of proteinuria varies with the severity of the glomerulonephropathy. Hypertension primarily results from increased extracellular fluid volume. The patient with APSGN may have abdominal or flank pain. At times the patient has no symptoms, with the problem found on routine urinalysis. More than 95% of patients with APSGN recover completely or improve rapidly with conservative management. Accurate recognition and assessment is critical as chronic glomerulonephritis develops in 5% to 15% of the affected persons, and irreversible renal failure occurs in 1% of patients.
 * __11. Describe the risk factors, clinical manifestations, and pathophysiology of a child with poststreptococcal glomerulonephritis.__** (pilli p.1468, MS p. 1165)
 * __risk factors__**
 * __clinical manifestations__**
 * __pathophysiology__**

APSGN develops 5 to 21 days after an infection of the tonsils, pharynx, or skin (e.g., streptococcal sore throat, impetigo) by nephrotoxic strains of group A β-hemolytic streptococci. The person produces antibodies to the streptococcal antigen. Although the specific mechanism is not known, tissue injury occurs as the antigen-antibody complexes are deposited in the glomeruli and complement is activated. Complement activation causes an inflammatory reaction to the injury. The response to the injury is also a decrease in the filtration of metabolic waste products from the blood and an increase in the permeability of the glomerulus to larger protein molecules.

12. Correlate long term complications of diabetes mellitus with diabetic nephropathy. (**Lewis; 1285, 1282, & 1177, Huether 466-469, p.pt. 13)** Diabetes is the most common cause of end-stage renal disease. AGEs, activation of the polyol pathway, glucose toxicity, and protein kinase C all contribute. -Damage to the small blood vessels that supply the glomeruli of the kidney. -Tight blood glucose control is critical for prevention and delay, HTN is also accelerate the process 1) **Glycosylation;** excess glucose binds to proteins & collagen-become AGEs (advanced glycosylation endproducts) that cause tissue injury to the blood vessel walls-lead to ischemia in kidney **(p467 Huether)** 
 * 2) Polyol Pathway; **Kidneys do not require insulin for glucose transport, they use the polyol pthwy. W/ hyperglycemia, glucose is shunted to pthway & converted to sorbitol, which is very slowly converted to fructose. The resulting accumulation of sorbitrol increases osmotic pressure& attracts H2O, leading to cell injury.
 * 3) Protein Kinase C (PKC); **intracellular signaling proteins that become inappropriately activated in diff tissues by hyperglycemia. Can cause production of extracellular matrix & cytokines, vasc cell proliferation, enhances contractility, & increased permeability.
 * Microalbuminuria **; 1st manifestation of renal dysfxn; protein should not be in pee; Glomeruli basement membrane is allowing this BIG molecule to pass-not functioning properly
 * Changes in kidneys; **Alters blood vessel walls-intraglomerular HTN, diffuse hardening & thickening of the Glom. basement membrane (GBM)-obstruction or rupture of capillaries, necrosis and loss of fx, accum of sorbitrol (intracellular osmosis) and nodule glomerulosclerosis-involving nodular lesions (type I DM). Pt is prone to glomerulonephropathy, including presence of trace proteinuria
 * Treatment; **Ace inhibitors “pril” drugs; vasodilate efferent arteriole & decrease intraglomerular HTN; caution w/NSAIDS-vasoconstrict afferent arterioles, set pt up for more ischemia to kidneys

13. Examine the etiology, pathophysiology, clinical manifestations, and collaborative management the client with benign prostatic hyperplasia. The prostate gland encases the urethra (below the bladder) and with enlargement, can compress it. Growth occurs gradually until puberty, then rapidly until 30ish, when prostate reaches adult size. At 40-45 benign hyperplasia begins & continues slowly till death. Symptoms fall into 2 groups; <span style="font-size: 13.0pt; font-family: Arial; mso-fareast-font-family: Arial; mso-bidi-font-family: Arial;"> 1)  ** Obstructive; ** urinary retention; decreased output, takes a while to start peeing, stop/start stream (intermittency), dribbling after voiding, freq UTIs, overflow incontinence from retention <span style="font-size: 13.0pt; font-family: Arial; mso-fareast-font-family: Arial; mso-bidi-font-family: Arial;"> 2)   ** Irritative ** ; urgency, frequency, burning, dysuria, incontinence, bladder pain, nocturia CT, MRI, scrotal ultrasound, TRUS-transrectal ultrasound (look @ prostate) Cytourethroscopy; (internal visualization of urethra, bladder-can see strictures, ect) Prostatic Biopsy -**5 alpha reductase inhibitors**-decreases size of pros gland by blocking 5 alpha reductase & inhibiting conversion of DHT- Relief takes 3-6 mths -**a-Adrenergic Receptor Blockers-** relaxes smooth muscle around prostate and bladder neck; facilitates urine flow
 * (lewis-1414-1422, Huether 877-878, p.point p.16-17) **
 * Etiology ** ; Exact cause unknown; Prostate enlarges probably as a result of endocrine changes assoc. with the normal aging process.
 * Theories; A) ** accumulation of dihydroxytestosterone (DHT-the main intraprostatic androgen) The body still produces testosterone, even when body doesn’t need as much, then it’s converted by 5 alpha reductase to DHT. This is linked because males that don’t produce DHT don’t get BPH.
 * B) ** Another theory is that w/ age the body releases less testosterone, but still releases normal amts of estrogen, which becomes the prominent hormone and causes problems.
 * Risk factors; ** AGE #1, family hx, obesity( increased waist circ.), diet-polyunsaturated fatty acids, Etoh
 * Things that can aggravate BPH; ** Cold meds (Sudafed), pain meds, etoh, caffeine, artificial sweeteners, spicy food, acidic foods (citrus)
 * Pathophysiology; ** Enlargement of the prostate that begins in the periurethral glands (inner gland, or in middle, of prostate-Prostate cancer usually develops on outer gland). Enlargement occurs as nodules (**hyperplasia)** and glandular cells enlarge (**hypertrophy).**
 * Clinical manifestations; ** most symptoms result from urinary obstruction. Size does not predict symptoms-**location** does. Symptoms are usually **gradual.**
 * Complications; ** urinary retention; urine may eventually back up into ureters, kidneys causing hydronephritis. Pt is also predisposed to UTIs, and potential sepsis. Caliculi in bladder may develop due to residual urine. Pylonephritis-inf goes into kidney, bladder damage if untreated
 * Diagnostics; ** Hx & phys exam
 * DRE; ** dig rectal exam-palpate posterior surface for enlargement, symmetry, consistency; should feel elastic (w/ cancer-may feel hard like rock); should be done yearly after 50 yrs old.
 * PSA ( ** prostate specific antigen) **levels;** R/O prostate cancer
 * PVR; ** (post-void residual); urinary retention- Normal 0-15 mL, w/ BPH-50 mL is acceptable.
 * Noninvasive ** ;
 * Invasive; **
 * Others; **
 * UA w/ culture; ** looking for infection (bact, WBCs, hematuria)
 * Uroflometry; ** check volume of urine/sec.-shows extent of obstruction **Serum creatinine;** R/O kidney dysfxn
 * Collaborative Care ** ; goals; restore fx, relieve symptoms, prevent comp.
 * Watchful waiting-if symptoms are minimal- wait and see
 * Dietary changes; decrease Etoh, caffeine, cold meds, spicy or acidic food
 * Time void schedule-go to bathroom every 2-3 hrs, so bladder doesn’t overflow.
 * Drug Therapy;
 * Herbal Therapy; ** Saw Palmetto; may work by breaking down estrogen

14. Differentiate between acute renal injury and chronic renal injury in relation to: Etiology, Stages & Phases, Pathophysiology, Clinical Manifestations, Complications. See pages 19 - 26 of renal powerpoint.

15. Analyze the concept of acute and chronic renal injury as a multisystem disease.