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–Primary condition in which glomerular abnormality is the only disease present or secondary condition such as; DM has a chronic effect/ microvascular complication(loose kidney, eye, leg) or SLE/lupus causes renal problems
–Triggers include immunologic, nonimmunologic (hypertension, drugs/ibroprofen, chemicals, DM) and hereditary. –TEST QUESTION When it comes to renal disease & glomerular dysfunction injury results from antibody reaction & antigen-antigen complexes trapped in glomerular membrance. “Glob” –Immune mechanisms implicated: –Injury resulting from antibody reaction –Injury resulting from circulating antigen-antibody complexes trapped in glomerular membrane. Source of antigen may be unknown. |
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T/F? When it comes to renal disease & glomerular dysfunction injury results from antibody reaction & antigen-antigen complexes trapped in glomerular membrance. “Glob” |
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=i inflammation. Produces proinflammation |
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=other one. Nephrotic syndrome-constellation of clinical findings that results from increases glomerular permeability to plasma proteins. Big and fat and tend to glob things up |
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clinical correlate acute proliferative inflammation.
Onset of oliguria as GFR decreased followed by hematuria(blood in urine) with red cell casts(globs/clogged things up, becomes very concentrated looks brownish), proteinuria(protein in urine). |
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Decreased GFR leads to hypertension and edema WHY? |
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If glomerular filtration rate is down, not filter enough blood thru kidney can reabsorb/or excrete things like suppose to. If you can’t absorb enough blood and no water either. How do you get edema? Things are backed up, too slow for absorption or excretion, and then you have fluid retention and decreased urine output, the first sign you are getting into trouble. BP goes up, too much volume on board and you have edema. Fluid leaks into tissue. |
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What is relationship between strep oropharynx infection and kidney disease? |
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–Caused by renal limited disorder such as post strep infection (7-12 days post pharyngitis or impetigo) or secondary complicating disorder such as SLE/lupus. rarely goes on to kidney disease but depends on early recognition and effective treatment, like to hydrate them.
–Elevated antistreptoccal antibody (ASO) titer –Excellent prognosis with rare CKD |
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1st sign your patient is getting into trouble, decreased urine output. |
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Why would we see protein in the urine? |
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Why would we see protein in the urine? Because amount of protein has exceeded renal threshold & can’t be absorbed. Membrane all globbed up with other stuff, you reach your renal threshold, protein get excreted in urine. Not suppose to happen. You are not suppose to have protein in urine. |
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Rapidly Progressive Glomerulonephritis |
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Definition
Severe glomerular injury and we don’t know what caused it. •Focal and segmental proliferation of glomerular cells with recruitment of ***monocytes and macrophages start to clogg up the works and doesn’t allow kidney to do it’s job.
•Associated causes; SLE/lupus, small vessel vasculitides, and Goodpasture syndrome |
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-not a specific disease - constellation of clinical findings that results from increases glomerular permeability to plasma proteins –Primary disorder or secondary to changes of systemic diseases such as ***DM or SLE- can cause inflammantion(systemic lupus erythematosus) –Massive proteinuria, lipiduria, ***hypoalbuminemia*** generalized edema, and hyperlipidemia –Disruption of ***coagulation*** system-risk for thrombotic complications. Overactive platelets, DVT, blood clots |
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T/F? Can force a fluid shift by giving them abumin IV and force water from tissues & deposit into vascular space and can be filtered and excreted in the urine. |
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Diabetic Glomerulosclerosis |
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–Occurs in both Type 1 and 2 DM –Widespread thickening of the glomerular capillary basement membrane occurs in almost all with DM and can occur ***without evidence of proteinuria*** |
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Hypertensive Glomerular Disease |
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–Mild to moderate hypertension causes sclerotic changes in ***renal arterioles*** in 15% –Most prevalent and aggressive ***among AA*** |
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Tubulointerstitial Disorders
Pyelonephritis |
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–inflammation of parenchyma and pelvis =damage to kidney tissue that could lead to loss of the kidney if not treated. |
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Tubulointerstitial Disorders
Acute Pyelonephritis onset? |
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Definition
***bacterial infection*** of upper urinary tract: source lower urinary tract (vesicoureteral reflux) and bloodstream; |
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Tubulointerstitial Disorders
Signs of Acute Pyelonephritis |
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Definition
-shaking -chills, -fever, -headache, - ill, - pain over costovertebral angle (CVA tenderness)
-starts in the bladder, unrecognized, untreated and the bug crawls up the ureters into the kidney. |
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Tubulointerstitial Disorders
What decreases renal blood flow in Pyelonephritis? |
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Definition
-NSAID, -diuretics, contrast, immunosuppressive(transplant) drugs) , obstructing urine flow (Vit C and sulfonamides); direct damage to kidney, or hypersensitivity/allergic reactions |
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•Renal cysts are fluid filled sacs or segments of dilated nephron interspersed with normally functioning nephrons; -may arise as a developmental abnormality but most are hereditary |
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Autosomal Dominant Polycystic Kidney disease |
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Definition
•Cysts may also me found in liver, pancreas •Mitral valve prolapse; 10-30% cerebral aneurysm •May also have chronic colonic diverticula •***Sympthoms: Pain, hematuria, infection, hypertension*** •Progress is slow, ESRF uncommon < 40 •Treatment supportive, if pt. takes good care of self, but may proceed to dialysis and transplantation •Avoid any antiflammatory drug. Never get Motrin, Aleve. |
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Kidney stones –Etiology may include increases in blood an urinary levels of stone components, interactions among components, anatomic changes ,metabolic and endocrine influences, |
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How does diet & disease impact development in Renal calculi? |
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Stop drinking milk if in 20’s but not at 50 yrs old. -Diet restrictions of foods high in oxalate. -High conc of calcium in blood and urine. -***dietary/intestinal absorption factors and UTI*** |
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Prevention measures for Renal calculi? |
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Definition
fluid intake plus correcting cause with diet/meds |
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Urinary tract infections etiology? |
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Definition
in development of UTI host defenses are matched against the virulence of the pathogen. |
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In Urinary tract infections Catheters provide? |
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Definition
provide a means for enrty of bacterial into urinary tract. |
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Urinary tract infections are the Second most common type of bacterial infection from what pathogen virulence? |
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–Escherichia coli(E.Coli) •Distal urethra has pathogens, urine sterile |
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Urinary tract infections Diagnosis by? |
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Definition
-presence of 10,000 to the 5 or more bacterial per ml of urine. -Based on symptoms & examination of urine. |
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Urinary tract infections have an Increased risk from what two things? |
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Definition
_urinary obstruction(urine remains in bladder and microbial growth and bug climbs the urether to infect kidneys. -Reflux(urine from urether move into the bladder), neurogenic bladder, sexually active women, diseases of prostate, elderly, instrumentation |
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What are the symptoms of a Urinary tract infection? |
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Frequency, dysuria, abdominal/back discomfort |
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What are the Manifestations of UTI? |
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-Upper UTI(pyelonephritis) -Elderly may not have symptoms-at risk, mental confusion only symptom |
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Renal neoplasms Wilms Tumor symptoms |
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Definition
–Large asymptomatic abdominal mass -hypertension -microscopic -gross hematuria |
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Renal neoplasms Wilms Tumor population at risk |
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Renal neoplasms Wilms Tumor survival rate |
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–Silent disorder and symptoms denote advanced disease; hematuria and renal mass on ultrasound –Cause unclear: smoking, obesity, occupational, asbestos –Incidence peaks 55-84 years of age –Prognosis depends on stage; 30% if metastasis |
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