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14 Cards in this Set

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DESCRIBE RENAL DISEAS ASSOC WITH 1) Diabetes mellitus:
1) Diabetes mellitus: glucose transporters get saturated resulting in glucose in urine. Have down-regulation of their Na-glucose co-transporters. Can’t reabsorb 100% glucose w/o enough transporters.IN the proximal tublule, that is the place that you essentially reabsorb all of your glucose). There should never be glucose in your urine. If you eat 40 jellys, you will not have urine that has glucose in it. If you don’t need it, it will be converted to fat. Your body is designed to store something that you need to produce energy. There is the whole sodium glucose transporter thing, the secondary active transport set up by sodium potassium pump. This co transport system has deficiencies in it or lack of transporters, the ones they do have get saturated.
DESCRIBE RENAL DISEASE ASSOC WITH URINATION
 Micturition- =WIZZING (Diseases/difficulties of should be under voluntary control, stretch receptors are involved.) bladder has tight tight junctions and stretch receptors. When bladder fills, it activates stretch receptors which sends a signal to your brain that tells your bladder that it is time to empty the bladder. You can ignore the signal-it stretches some more….will get to a place where it is no longer a voluntary issue and your body will eliminate it.
o1)Incontinence-loss of voluntary control.
Diseases that can lead to incontinence:
•CNS damage can lead to loss of voluntary control
•Aging (still a nervous sstem issue)
•Muscular control issue
oRetention - inability to empty bladder.
Usually CNS problem, or
Stretch receptor problem
Muscular control issue
75% of all stuff is reabsorbed in the proximal tubule (glucose aa , water, ….)
NAME AND DESCRIBE ALL
Tests for Renal Disease
• Inulin tests GFR
• Para-amino hippuric acid (PAH) tests renal plasma flow (then you calculate renal blood flow)
• Urinalysis-
o Cloudy: proteins (all proteins reabsorbed in the proximal tubule usually)—any plasma protein that does cross will be reabsorbed in your proximal tubule b/c they are large and charged (membrane is supposed to prohibit cross of these guys; re-upped by endocytosis which req atp), pus within the renal tubule, bacteria
o Dark: hematuria (blood), excess bilirubin , or dark yellow about hydration status
o Odor: infection=foul
• Blood Teststo look at the function of the kidney (kidney does get rid of nitrogenous wastes)
o Increased serum urea & creatinine (failure to excrete nitrogenous wastes) why=if you do not have adequate blood flow to the kidney, you cannot get rid of it. About half of the concentration of your medullary interstitium is urea.
KNOW OSMOLALITY FROM DIAGRAM FROM LAST WEEK -600.
 The urea is supposed to get into the kidney, then be reabsorbed in your medullary interstitium. If high in the blood, it didn’t get reabsorbed in your interstitium—triggers you that there is something wrong.
 You usually excrete all of your creatinine: nitrogenous waste (=osmotically active particles).
 If you lose loop of henle, you can’t lose nitrogenous wastes/osmotically active particleaffect water movement as is osmotically active. If you lose Loop of Henle, you lose your ability to affect water movement.
• Biopsy=
• culture urine specimens (if cloudy)
• measure GFR (creatinine or inulin) you have to put a substance in to measure. Normal GFR is 125 ml/min, so you filter 180L/day. You must know this. You do reabsorb 99.9% of the water. You get rid of whatever you drink. The substance you give to check this cannot be absorbed or secreted. It should be given (injected) and go through the membrane and calculated as what comes out in the urine per unit time. Blood flow to the kidney is 1L/min or 20% of cardiac output. Renal blood flow is not a measure of Renal disease.
• radiologic tests via ultrasound, MRI, or CT (look at the renal structure itself; check for tumor presence)
HGB wt is 68,000 (not just a red cell), when there is blood in the urine, it is red cells, plasma
NAME Abnormal urine constituents
• Blood (RBCs): Can get RBCs into your urine via 2 mechanisms:
o hemorrhagic condition within the kidney (secondary to tumor)
o increased glomerular permeability (generally secondary to infection (bacterial) at the glomerular-bowman’s capsule membrane. Bacteria usually infect from the nephron side (not usually from the blood side.)
 could have decreased GFR where stuff won’t cross
 Or could have an increased GFR and stuff will cross.
• Protein (proteinuria): inflammation & increased glomerular permeability (Endocytosis keeps protein from going into urine; you reabsorb 100% protein at your proximal tubule via endocytosis, unless you don’t have ATP =death.) you get inflammatory disorders at the bowmans capsule membrane so increased permeability. ?? carbonic anhydrase is 30,000-huge, crossing the membrane. Reduced plasma protein = high hydrostatic favoring and low osmotic pressure (opposing)= hosing across interstitium ie. Fluid in lung.
• Bacteria and pus (bacteriuria & pyuria)=
• Alteration of urine specific gravity: decreased specific gravity indicates potential renal failure. The particles in the urine are altering the specific gravity.
DESCRIBE DIUERETIC DRUGS
• Yield increased water & sodium loss from body. It could be about just sodium or just water
• Are prescribed for:
o HTN-
o Edema (systemic)
o CHF
o Furosemide (potent diuretic)-
 blocks NaK2CL co transporter. There is one of those in your nephron in the loop of henle so it is essentially blocking the nak2cl co transporter. You will lose the ions and water will not follow them later. All 4 molecules must be present to block the co-transporter. Is driven by the sodium uptake. Could lead to increased water loss.
 Not concentrating medullary interstitium as you did before could lose more than usual sodium & water.
 could lead to excess K loss because it is being transported on the co-transporter (so is being lost; not reabsorbed)
o Potassium sparing diuretic: (spirinolactone/thiazides)
 Can stop some of the K loss by the kidneys, but may cause hyperkalemia
LIST TYPES OF Dialysis
• Designed to do a couple of things here but can run into complications there is the potential for HIV and hepatitis infection…….
o Problems: infection, clots (increased potential for HIV & hepatitis infections)
o Dialysis tubing is semi-permeable—some things cross and some things do not.REMEBER, OUR MEMBRANES ARE DIFFERENTIALLY PERMEABLE, NOT SEMI!
o Dialysis membrane is not charged.
o Goal: rid fluid and wastes. Dialysate has less solutes in itthese wastes cross the dialysate membrane to get out of the blood.
• Peritoneal dialysis—increased time provides more continuous exchange putting into a body cavity-so the overall time you have for peritoneal dialysis. The prob with increased time is infection.
o Problem: potential infection/bacterial peritonitis.
 Antibiotics are prescribed.
o Fluid intake and diet (proteins) must be watched.
o Works because lots of blood vessels in peritoneal space to exchange w/ dialysate, during long dwell times.
In CRF, you will ultimately lose nephrons. Must watch diet! Can’t produce []’d urine and the more nephrons you lose, the more you can’t lose fluid period. As fluid not going through nephrons, nephrons die. No rid water, nitrogenous wastes, salts, etc.
DESCRIBE RENAL DISORDER CAUSING uti
Urinary Tract Infections
-women more susceptible (short urethra, proximity of vagina & anus, baths, use of tampons)
-Causes of UTI: see figure
-1)blood borne organisms (bacterial infection; most common: e. coli from intestine)pyelonephritis (kidney level)
-2)immobility =stasis of urine =(urine backflow=urine stasis due to urine can’t flow from bladder to kidney)pyelonephritis this is a kidney problem
-3) vesicoureteral reflux-valve deficiency (reflux up ureter towards kidney)cystitis
-4) obstruction (ex: prostatic hypertrophyresidual urinereflux)cystitis (bladder level)
any infection carried in the blood goes right to the kidney and affectst the glomerular bowmans capsule membrane. This is due to the amount of blood flow per unit time to the kidney. 1L/min or 360 ml/min per 100g of tissue.
DESCRIBE PYELONEPHRITIS
• Pyelonephritis: kidney level infection from urethra to renal pelvis and medullary interstitium tissue; affects all of the plumbing
o possible cause of ARF when exudates (likely bacterial) blocks urine flow—have formation of urinary casts (leukocytes and renal cells—distal/proximal tubule cells or other nephron cells—YIKES!) present in urine.
o Could lose nephrons due to build up of pressure: both backflow & continued flow thru nephron

• Pyelonephritis treatment:
o antibiotics,
o increase fluid intake (flush it out)
o treat promptly
 Without prompt treatment, leads to chronic pyelonephritis,
 scar tissue obstruction
DESCRIBE CYSTITIS
• Cystitis: bladder issue inflammation, swelling of bladder wall. (Supposed to have tight-tight junctions w/o much swelling of these cells.)
S&S: Dysuria: painful urination,
 frequency & urgency are common,
 fever, nausea, malaise, bacteriuria
NAME FOUR TYPES OF UTI'S ACCORDING TO BOOK
1) Cysititis=inflammation of teh bladder, most common site of uti.severe can cause necrosis or gangrenous cystitis, pus or suppurative cystitis, or ulcerative cystitis
PATHO=e coli, klebsiella, pseudomonaus, staph
NAME FOUR TYPES OF UTI'S ACCORDING TO BOOK
2) "non bacterial cystitis"
=neg urine cx common in women 20 -30 called urethral syndrome.
char=dysfuncton of external sphincter, vaginites, urethritis infl of glands near vagina and urethra, freq, urgency, sm urine vol, bladder fulnes
NAME FOUR TYPES OF UTI'S ACCORDING TO BOOK
3) Acute Pyelonephritis
=an infection of teh renal pelvis and interstitium.
risk factors=urinary obstruction reflux of urine (vesicoureteral reflux.
organism=ecoli, proteus, psudomonas
=spread by way of ureters ofr bloodstream.
what are predisposing factors of acute pyelonephritis
kidney stones
vesicoureteral reflux
prego
neruogenic blader
instrumentation
femal sex trauma
NAME FOUR TYPES OF UTI'S ACCORDING TO BOOK
4) chronic pyelonephritis
=persistent or recurrent autoimmunen infection of kidney with infl and scarring assoc