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Pathophysiology
Renal Exam 3
| Question | Answer |
|---|---|
| What is the concern of protein loss through the kidneys? | The concern is that the glomerulus is damaged and proteinuria is an indicator of nephritic syndrome |
| How does protein loss through the kidneys happen? | It occurs when the basement membrane of the glomerulus is damaged and when the split pores are genetically mutated |
| What in the kidneys is damaged to allow protein loss? | The basement membrane of the glomerulus is damaged ….. also if the split pores are genetically mutated |
| When protein is high as in nephritic syndrome what s/s will you see? | Proteinuria, edema, hypoalbuminemia, hyperlipidiemia & lipiduria, hypercoaulability, antithrombin III is excreated in excess in the urine, changes in protein C & S…. |
| Hyperfibrinogemia, impaired fibrinolysis, decreased immunity, trace mineral & Vit D deficiency, Hyperparathyrodisim, neural osteodystrophy & decreased Ca+ are also s/s of ____? | nephritic syndrome |
| ____ is the principal selectivity barrier of the glomerulus? | basement membrane is the principal selectivity barrier of the glomerulus |
| What does the basement membrane of the glomerulus prevent from passing through? (hint there are 3 things) | The basement membrane of the glomerulus prevents plasma proteins, erythrocytes, & leukocytes from passing through. |
| ____ are negatively charged & repelled by the basement membrane? | plasma proteins are negatively charged & repelled by the basement membrane |
| ____ have a thin diaphragm of protein that restricts the filtration of some ____ that make it through the basement membrane? | SLIT PORES have a thin diaphragm of protein that restricts the filtration of some PLASMA PROTEIN that make it through the basement membrane |
| ____ is an important protein in the slit pores? | Nephrin is an important protein in the slit pores |
| A pt with genetically mutated slit pores will have what kind of urine? | massive proteinuria (protein in urine) |
| ___ & ___ are not usually present in urine? | proteins & blood cells |
| If the ___ is injured, blood cells & proteins may filth through and be found in the urine? | glomerulus |
| ___ is an IMPORTANT sign of basement membrane dysfunction? | proteinuria |
| ___, ____, & ____ are normally reabsorbed completely in the early proximal tubule? | Nutrients, Vitamins, & Small proteins are normally reabsorbed completely in the early proximal tubule |
| Why does the glomerular capillary oncotic (colloid osmotic) pressure exit? | it exists b/c proteins are present in the blood |
| What are negatively charged & attract positive ions, which subsequently attract water? | plasma proteins |
| What keeps plasma proteins from being pushed against the capillary wall? | The glomerular capillary colloidal osmotic pressure opposes filtration by holding H2O & ions in the capillaries which are attracted to the plasma proteins |
| ___ & ___ are attracted to the plasma proteins? | Ions & water are attracted to the plasma proteins |
| Pressure is decreased at ___ & progressively increases along the length of the ___? | pressure is decreased at the afferent end & progressively increases along the length of the capillary |
| Normally plasma proteins do not filter into the ___? | Bowman capsule |
| If plasma proteins filter into the bowman capsule they would create ____? | Bowman capsule oncotic pressure |
| ___ would enhance glomerular filtration b/c proteins attract cations & water? | Bowman capsule oncotic pressure that is created with plasma proteins filter into the bowman capsule |
| In a healthy kidney the bowman capsule oncotic pressure is ___? | negligible |
| As blood passes through the capillaries, continued filtration leaves a greater concentration of proteins in the capillaries which ___ the oncotic pressure? | raises |
| T/F Normal urine contains proteins? | False normal urine DOES NOT contain proteins |
| T/F A small amount of protein in the urine is insignificant? | True |
| When should you investigate urine for glomerular capillary disease? | when a pt excretion of protein is more than 150mg/24 hrs |
| Proteinuria can cause the urine to be ___? | foamy |
| ___ is a collection of symptoms caused by glomerular disease? | Nephritic Syndrome |
| Nephritic Syndrome is characterized by an ___ in glomerular capillary wall permeability to ___? | Nephritic Syndrome is characterized by an increase in glomerular capillary wall permeability to serum proteins |
| The predominant abnormality in nephritic syndrome is the loss of …? | The predominant abnormality in nephritic syndrome is the loss of LARGE amounts of protein in the urine (↑ 3.5g/day) |
| Hypoalbuminemia, hyperlipidemia, edema, hypercoagulability, altered immunity & lipiduria are present secondarily to proteinuria in ____? | nephritic syndrome |
| What is the most common cause of nephritic syndrome in adults? | Diabetic neuropathy |
| What is the most common cause of nephritic syndrome in children? | minimal change disease |
| ___ is when hydrostatic & colloid oncotic pressures are not balanced in independent areas & periurbital areas? | edema |
| In nephritic syndrome hypercoagulability is due to altered clotting factors such as ….? | (antithrombin III is excreted in excess in the urine; changes in protein C & S, hyperfibrinogenas is a result of ↑ hepatic production impaired fibrinolysis, & ↑ ability of plts to aggregate are probable contributors to an incident of thromboembolic event |
| What trace minerals are deficient in nephritic syndrome? | Zinc, Fe- & copper |
| If a pt’s urine dipstick results revel protein in the urine what are the possible disorders? (Hint there are 6) | renal HTN, glomerulepathies, nephritic syndrome, renal artery or vein thrombosis, & pyllonephritis |
| Bowman capsule drains the glomerular filtrate directly into the ____ segment, where 2/3 of ___ & ___ are rapidly reabsorbed? | Bowman capsule drains the glomerular filtrate directly into the Proximal Tubule segment (Proximal Convoluted Tubule), where 2/3 ofH2O & electrolytes are rapidly reabsorbed |
| What three things are normally reabsorbed completely in the early proximal tubule? | Nutrients, Vitamins, & small proteins |
| The ___ is the site of most HCO3 ion reabsorption, whereas Cl- ion is reabsorbed in where? | The early proximal tubule is the site of most HCO3 ion reabsorption, whereas Cl- ion is reabsorbed in the late proximal tubule |
| The proximal tubule is made up of ___ ___ & convoluted to provide a greater surface area for reabsorption? | cuboidal epithelium |
| In the proximal Tubule (cuboidal epithelium) the epithelial cells in this segment have ___ that form a brush border next to the filtrate & substantially increase the apical surface area? | microvilli |
| Proximal tubule cells have high aderiosine triphosphate (ATP) requirements b/c most reabsorption utilizes active transport mechanisms that are dependent on ____ pumps in the basoleteral membrane? | Na+-K+ ion pumps |
| H2Ois reabsorbed passiveley through water channels made of ___ called what? | H2O is reabsorbed passively through water channels made of proteins called agnaporin 1 |
| Reabsorption of solutes creates the osmotic force for what? | Passive H2O reabsorption |
| What is the average rate of the Glomerular Filtration Rate (GFR) & how is it determined? | 125ml/min & it is determined by the filtration pressure in the glomerali & by the permeable surface area of the glomerular membrane |
| GFR is the product of what? | GFR is the product of filtration pressure & permeability constant determined by the physical principles of filtration across a capillary membrane |
| The main driving force for filtration in the GFR is ___ by exerting a force against ___? | hydrostatic pressure in the glomerular capillaries by exerting a force against glomerular capillary walls |
| As blood circulates through capillaries the ___ ___ pushes blood against the walls & fluid is filtered out? | hydrostatic pressure |
| One of the most important physiologic regulations of GFR is ____? | blood volume |
| More blood -> more pressure, more pressure-> ____ GFR, and the opposite is true. | increased |
| Auto-regulation in the GFR adjusts for large swings in __? | BP |
| Decreased renal blood flow causes decreased GFR which leads to what? | leads to decreased excretory & reabsorbtive capabilities of tubules causing decreased drug excretion & metabolites, decreased secretion of H+, decreased urine concentration, increased renal threshold of glucose |
| In the kidney’s tubule system, where is most glomerular filtrate reabsorbed? | Proximal Tubule segment (Proximal Convoluted Tubule) |
| What is GFR? | Glomerular Filtration Rate average of 125ml/min |
| What does the GFR tell you about kidney function? | it tells you the overall function of the kidneys if the GFR leads to decreased excretory & reabsorbtive capabilities of tubules causing decreased drug excretion & metabolites, decreased secretion of H+, decreased urine concentration, increased renal thre |
| The most common causative agents of renal system infection are ____ such as what? | gram negative bacteria such as Escherichia Coli (enterobacter & proteus). E. Coli 80% of the time |
| ____ is an infection of the renal pelvis & interstitium? | Pyelonephritis |
| Acute Pyelonephritis - bacterial colonization commonly occurs in the renal papilla as a result of what? Which intereferes with what? Allowing what? | Acute Pyelonephritis - bacterial colonization commonly occurs in the renal papilla as a result of the increased osmolarity which interferes with WBC & complement function, thus allowing bacteria to multiply |
| In Acute Pyelonephritis Bacteria ascending from the ___ urinary tract seed in the renal calices & papillae first, whereas infection from ____ source starts in the ___ of the kidney? | Bacteria ascending from the lower urinary tract seed in the renal calices & papillae first, wereas infection from ahematogenons source starts in the medulla of the kidney. |
| Regardless of the cause of acute pyelonephritis w/in ___ the infection spreads to the parenchyma & creates what? That results in what? | Regardles of the cause, w/in 2-3days the infection spreads to the parenchyma & creates a widespread inflamtory response that results in arterial construction & edema in the infected portions of the kidneys. |
| In Acute Pyelonephritis renal scarring resulting in compressed kidney function is __ in otherwise healthy adults if the infection is promptly managed? | Rare |
| In Acute Pyelonephritis in what pts is renal scarring more common? | Infants, Children, Pregnat women, & adults with other comobiditis that inhibit either diagnosis, mgnt, or response to antibiotic therapy. |
| In acute Pyelonephritis prevention of renal scaring is dependent on what? | It is dependent on prompt & effective Tx of the infection in all age groups |
| T/F S/S of acute pyelonephritis does not vary amoung age groups? | False it does vary amoung the age groups |
| What is the s/s of acute pyelonephritis in adults? | classic- fever & chills of sudden onset, flank pain, UTI symptoms such as dysuria & urinary frequency or urgency. The hallmark symptom is tenderness or pain at the costovertebral angle on palpation |
| What is the hallmark s/s of acute pyelonephritis? | The hallmark symptom is tenderness or pain at the costovertebral angle on palpation |
| FYI - algia = ___ ex:nephralgia = kidney ___ | pain, pain |
| Neither renal or uretal pain is altered by changes in ___ ___? | body position |
| (Acute Pyelonephritis) UTI's including pyelonephritis should be suspected in infants, children & elderly pts with generalized symptoms such as? | such as irritability, fever & malaise & decreased oral intake, occasional manifestation with abdominal pain, N/V |
| What is chronic pyelonephritis characterized by...and is a consequence of ___? | Chronic pyelonephritis is characterized by unilateral or bilateral pathologic changes in the kidney as a consequence of infection |
| What are the classic manifestations of chronic pyelonephritis? | Small atrophic kidneys with diffuse scarring & bunting of the calices are classic manifestations of chronic pyelonephritis |
| In chronic pyelonephritis individuals at risk have bacteriuria associated with? Give examples | In chronic pyelonephritis individuals at risk have bacteriuria associated with obstructive uropathy such as renal calculi, neurologic deficits, vesicouretal reflux, or intrinsic renal disorder. |
| In chronic pyelonephritis; as a result of ___ infections, chronic intersitial inflamation develops with __ & ___ infiltration of the renal tissue? | As a result of recurerent infections, chronic interstitial inflamation develops with lymphocyte & plasma cell infiltration of the renal tissue. |
| (Chronic Pyelonephritis): The interstitium has degrees of ___ or ____ with casts. fibrosis of the interstitium, including the renal tubules, decreased # of functional nephrons. | dilated or atrophic renal tubules |
| T/F Chronic pyelonephritis has the same s/s of acute pyelonephritis? | True |
| What is cystitis? | Cystitis is the inflammation of the bladder urothelium |
| Cystitis may result from what? | may result from bacterial, fungal or paracitic infections, chemical irritants, foreign bodies (stones), or trauma |
| Cystitis most commonly results from ___? | bacterial infection |
| What bacteria is the most common cause of cystitis? | E. Coli is responsible for 80% of cases of bactreial cystitis |
| Why is bacterial cystitis more common in females? | It is more common in females than males b/c of shorter urethra as well as a colonization ronte from the rectum & vagina to the urethra. |
| Research shows that women who have recurent bacterial cystitis have ___,___, & ___that enhance binding properties of ___? | Research demonstrated that women who have recurrent bacterial cystitis have uroepithelial, vaginal, & buccal epithelial cells that enhance binding properties of E. Coli |
| Name 4 things that increase the incidence of cystitis. | decreased vaginal pH, decreased estrogen levels, & lewis bloog group LE (a-b-) & LE (a+b-) pheontypes are associated with increased incidence of cystitis |
| What are some OTHER risk factors of cystitis? | sexual activity, use of spermicides, catheterization, DM, poor hygiene, & type A bladder dysfunction/urin stasis |
| What are the s/s of cystitis? | 10% asymptomatic; frequency; urgency; dysuria (painful urination); flank pain & pain in the suprapubic area, low back, or both |
| In cystitis flank pain is ___ & can indicate what? | Flank pain is usually more serious & can indicate an infection protimal to the bladder |
| How may the urine appear visually in cystitis? | Visually, heamturia or cloudy urine may be evident |
| What will the urinalysis of a pt with cystitis show? | urinalysis shows colonization of known bacterial pathogen, WBCs, RBCs & nitrites |
| What is the difference between UTI and pyelonephritis? | Pyelonephritis is an infection of the renal pelvis whereas a UTI can be an infection in the bladder, urethra, ureters or kidneys. UTIs may be asymptomatic |
| What are the s/s of a UTI? | Some are asymptomatic. Urgent need to urinate (often w/ only a few drops of urine to pass); burning sensation when urinating; cloudy or blood-tinged urine; strong odor to the urine. |
| What are the s/s of a UTI that has spread? | pain in the lower back as well as fever, chills, N & V |
| What are the differences in s/s of UTIs and pyelonephritis? | In pyelonephritis fever & chills have a sudden onset, flank pain, UTI symptoms such as dysuria & urinary frequency or urgency. chills and fever only happen in UTIs that have spread |
| Between pyelonephritis and UTIs which is more serious? | pyelonephritis |
| What is the most common causitive bacteria for UTI? | E. Coli |
| What is a Nephroblastoma or Wilm's tummor & who does it occur in? | A malignant neoplasm of the kidney occurring in young children before the fifth year in 75% of the cases. |
| What is the most common abdominal tumor in children? | Nephroblastoma or Wilm's Tumor |
| T/F Nephroblastoma or Wilm's tummor cannot be found in adults? | False it can be found in adults but it is rare in pts >15 yrs |
| In nephroblastoma or Wilm's Tummor what is the most common age group? males & females are ___ affected. | most cases onset is b/t 3-5 yrs. males & females equally affected |
| What is the primary etiological basis of wilm's tumors? What does this defect result in? | a defect on chromosome 11p13 is the primary etiologic basis of Wilm's defect. This defect results in abnormal growth A metanephric blastema w/o NL differentiation N2 tubules & glomeruli |
| 15% of children with Wilm;s tumors have other abnormalities, including what? | including Wilm's aniridia-genital anomaly - retardation syndrome, bech with- wiedemann syndrome, hemihypertropy, musculoskeletal anormalities & other genitonurinary abnormalities |
| What is the s/s of Wilm's Tumor? | A tumor mass of the flank or abdomen is palpable in 80% of cases. abdominal pain, HTN, & microscopic hematuria |
| ___ is initially identified by a parent or physician on routine physical exam. | Nephroblastoma or Wilm's Tumor |
| What are the s/s that indicate a subscapular hemorrhage of the wilm's tumor? | Sudden onset of pain & fever & findings of an abdominal mass, anemia, & HTN indicate subscapsular hemorrhage of the Wilm's Tumor. |
| What are the most frequent early signs of a Wilms Tumor? | The most frequent early signs are hypertesopm, a palpable mass, pain and hematuria. |
| Where would you see a Wilms tumor? | Abdonmen or flank |
| ___ is a syndrome of disorders characterized by an abrupt onset of hematuria & proteinuria in conjunction with azotemia & renal Na+ & H2O | acute glomerulonephritis |
| What are the s/s of acute glomerulonephritis? | abrupt onset of hematuria & proteinuria in conjunction with azotemia & renal Na+ & H2O |
| ___ is an infection process that indirectly causes or tirggers acute glomerulsnephritis by activating ____? | Post-streptococcal glomerulonephritis is an infection process that indirectly causes or triggers acute glomerulsnephritis by activating inflammatory cells. |
| What does the circulating inflmmatory cells infiltrate in Post-streptococcal glomerulonephritis? | Circulating inflammatory cells infiltrate the glomerular caillary walls & establis antibody-antigen compleses w/in the glomeruli. |
| In Post-streptococcal glomerulonephritis what is dispersed once the antibody-antigen complex that has been establised in the glomerullar capillary wall? what is relased as a result & what does this do to the glomerular wall? | cerndement is deposited & attracts neutrophils & monocytes. Lysosomal enzymes are then released & damage glomerular walls. |
| What results in Post-streptococcal glomerulonephritis once the glomerular wall has been damaged? | The change in the structure of the glomerular wall results in a more permeable membrane. In essence, larger gaps in the glomerular wall decreases SA for filtering & allows previously restricted molecules to enter the glomerular space. |
| In Post-streptococcal glomerulonephritis after the glomerular wall has been damaged 2 other processes are thought to take place. What are they? | 1. Local vasoactive componets such as angiotenain & leukotrines contract messangical cells & reduce perfusion to glomerular capillares & 2 the bowman space may also be damamged as a result of fibrin deposition & criescent formation (accumulation of prolif |
| In Post-streptococcal glomerulonephritis what is fluid retention due to? | Fluid retention is due to a decrease in GFR & distal tubule H20 & Na+ reabsorption. |
| In Post-streptococcal glomerulonephritis what does the H20 & Na+ reabsorption due? | H20 + Na+ reabsorption increases the vascular & extracelluar fluid volume of the pt |
| In Post-streptococcal glomerulonephritis hematuria & evidence of RBC casts result why? | Hematuria & evidence of RBC casts result b/c erythrocytes are now able to cross the more permable glomerular or peritubular walls N2 proximal tubule fluid (which is eventually urine) |
| What is the most common s/s or finding of Post-streptococcal glomerulonephritis? | Gross hematuria manifested as smokey or coffee-colored urine is the most common finding |
| What are the classic indicators of glomerulonephritis & what does it represent? | Red cells casts are classic indicators of glomerulonephritis & reperesent erythrocytes that have crossed from the glomerular capillary N2 the tubule & then asumed the shape of the tubule. |
| In glemerulonephritis what type of cell cast will be present? | Red cell cast are classic indicators.White cell casts may also be present, particullary with inflammation in the glomerulus & interstitium. |
| In glomerulonephritis ____ is generally present in the urine? | proteinuria |
| In glomerulonephritis what are the systemically manifestations? | Systemically, disruptions r/t fluid volume changes are major manifestations - periorbital edema most common & dependent areas cause lower extremity edema, apcites & plueral effusion |
| If the glomerulonephritis is thought to be psot streptococcal whatantibodies are evaluated and what will BUN & Creaton levels tell you? | If the glomerulonephritis is thought to be post streptococcal antibodies such as antistneptolysin O & antistneptokinase are evaluated. BUN & Creaton levels evalate/estimate the extent of renal damage |
| Glomerulonephritis can lead to ____ which requires dialysis? What does dialysis due for the pt or what can happen to the pts kidneys? | Glomerulonephritis can lead to rapidly progressive glomerulonephritis which requires dialysis which may allow pt to return to NL normal fx or the pt may progress to renal failure. |
| ___ is a sudden, severe decrease in renal function that is ptoentially reversiable? | Acute renal failure |
| What type of renal failure is potentially reversiable? | Acute renal failure |
| What type of kidney failure is associated with decrease in GFR, decreae in I/O over several hrs-days? | Acute renal failure |
| What are the s/s of acute renal failure? | Oliguria or anuria (rare) & usually azotemia (retention of nitrogenous wastes) |
| ___ is a broad term used to organize a wide variety of etologic factons. | ARF Acute Renal Failure |
| In ___ failure - 60% or more of community-????????????? ARF. What is the underlying factor? | Prerenal failure - 60% or more of community-acquired ARF. The underlying factor is diminished perfusion of the kidney. |
| In ____ the functional componets of the kidney are intact, but decreased blood flow to the kidney ultimately results in____? | Prerenal failure, the functional components of the kidney are intact, but decreased blood flow to the kidney ultimately results in decreased GFR |
| In Prerenal failure normally, the kidney can maintain a stable ___ in the face of ___, ___, or ___ through autoregulation, primarily by alteration in the ___ & ___? | Normally, the kidney can maintain a stable GFR in the face of HoTN, reduced blood volume, or reduced CO through autoregulation, primarily by alteration in the afferent & efferent arterioles |
| In Prerenal failure when mean systemic areterial pressure drops below ___, GFR is sharply reduced. | 70mHg |
| What are some causes of prerenal failure? | Hypovolemia-hemorrhage, shock, third spacing, buma, dehydration, decreased CO-caridiogenic shock, dysrhythmia, tamponade, CHF, MI, thromboembodic obstruction of renal vascular share the commorbility of reduced renal perfusion & often are referred to as is |
| T/F Usually, prerenal oliguria is easily reveresed if cause is identified? | True |
| In prerenal failure decreased GFR affects ___ & thus decreases urine volume eliminated because why? | Decreased GFR affects production of filtrate & thus decreases urine volume eliminated, b/c of the slow mvt through the renal tubules, more Na+ & H2O are reabsorbed N2 the bloodstream. |
| In prerenal failure glomerular hypoperfuma increases ___,___, & ___ which results in __ & __ retntion? I/O decreases to ____ | Glomerular hypoperfusion increases renin, angiotension II, & aldosterone production which results in Na+ & H20 retention. I/O decreases to <500ml/24hrs. |
| In prerenal failure when I/O decreases to <500ml/day ___ develops, indicating retention of ___ products reflected by ____? | When I/O decreases to <500ml/day azotemia develops, indicating retention of nitrogenous waste products reflected by increased BUN |
| The hemodynamic alterations that occur in ARF if allowed to progress will lead to what? | The hemodynamic alterations that occur in ARF if allowed to progress will lead to renal enclothelial ischemia. |
| What does renal enclothelial ischemia lead to in ARF? | It leads to increased in endothelin-1 & a disruption in the release of the vasodilator nitric oxide, further decreasing renal blood flow. |
| What is endothelin-1? | a potent vasoconstrictor |
| In ARF accumulation of inflmmatory __, __, & ___ leads to obstruction in the renal ____? | Accumulation of inflammatory cytokines, leukocytes, & fibrin leads to obstruction in the renal micorcirculation |
| Name some meds that contribute to prerenal failure. | NSAIDS & ACE Inhibitors |
| In what type of renal failure is the common etiologic factor is obstruction of urine flow @ some point distal to kidney itself? | Postrenal failure |
| In postrenal failure obstruction must be ___ to produce failure? | bilateral |
| What are the causes of postrenal failure? | BPH, calculi (stones), UTI, tumors, strictures, altered bladder contraction |
| How does postrenal failure manifest? | manifest as oliguria or anuria |
| In postrenal failure the obstruction of urine flow initially produces an increase in ___ pressure w/in the kidney & subsiquently increases the pressure in the ____? | The obstruction of urine flow initially produces increase in netrograde pressure w/in the kidney & subsiquently increases the pressure in the Bowman capsule of theglomerulus |
| In postrenal failure the elevated pressure in the bowman capsule causes the elevated tubular pressure. The elevated tubular pressure opposes ____ and production of urine is impaired b/c ____? | The elevated tubular pressure opposes glomerular capillary filtration pressure and production of urine is impaired b/c of decreased GFR |
| In Postrenal failure why does azotemia develop? | Azotemia develops b/c the kidneys ability to carry out nitrogenous waste meterials is impaired |
| What type of renal failure produces the most derangement in renal function? | Intrarenal failure |
| In intrarenal failure what part of the kidney is damaged? | The functional unit of the kidney, the nephron itself is damaged. |
| In intrarenal failure what might be the site of injury and what can the injury lead to? | the glomerulus may be the site of injury or most commonly, the renal tubules may be injured with the injury leading to acute tubular necrosis (ATN). |
| In intrarenal failure how long can recovery take? | B/C the nephron itself has been affected; recovery can take weeks to months |
| If the nephron is severly damaged & no recovery is possible what may it lead to? | CRF |
| What is the most common cause of intrarenal acute renal failure? | (ATN) Acute Tubular Necrosis |
| What are the causes of (ATN) Acute Tubular Necrosis? | prolonged prerenal ARF, trnasfusion reaction, Rhabdomyolyois), nephrotoxic acute tubular necrosis(prolonged postrenial ARF, antibiotics, contrast, heavy metals) & inflamation |
| What are the heavy metals that can cause ATN? | lead, murcury, carbon tetrachloride, insecticides, fungicides, cytotoxic drugs |
| What are some cytotoxic drugs that can cause ATN? | chemotherapy, hemolytic-uremic syndrome |
| What are two inflammations that can cause ATN? | acute glomerulonephritis & acute pyelonephritis |
| ___ is a result of either ischemic or nephrotoxic injury to the tubules? | ATN |
| ATN: injured tubular epithelial cells release intracellular debris N2 the ___, which in combination with proteins is the ___ result in formation of ____. | AtN: injured tubular epithelial cells release intracellular debris N2 tubular lumen, which in combination with proteins is the tubules result in formation of epithelial casts. |
| The epithelial casts in the tubules along with slughed ischemic & necrotic cells cause what in ATN? | cause hernial obstruction which increases pressure in tubules & eventually backs up & increases pressure in the bowman capsule, slowing GFR & furter damaging the glomeruli & tubules. |
| What is an important part of ATN pathology? | The back leak of filtrate that is caused by the epithelial casts along with sloughed ischemic & necrotic cells causing the herrinal obstruction is an important part of ATN pathology |
| A pt with ATN that has lead to a herrinal obstruction,what can happen to the kidney? | a herrinal obstruction causes decreased renal vascular perfusion, which leads to the kidney becoming hypoxic |
| In Intrarenal failure ___ releasead by the kidney result in congestion of the vascular bed by WBCs & pHs | Cytokines |
| In Intrarenal failure ischemic endothelial cells also release a variety of mediators such as ____ that constrict the intrarenal blood vessels, further contributing to the ____ & ____? | Ischemic endothelial cells also release a variety of mediators such as endothelin that constrict the intrarenal blood vessels, further contributing to the vascular congestion & impaired perfusion |
| Both Prerenal & Postrenal failure have I/O symptoms of ___ &___? | oliguria & anuria |
| Intrarenal failure has an I/O symptoms of ___ &___? | oliguria or nonoliguria |
| What happens to the specific gravity in prerenal failure? | It is increased in prerenal failure |
| What happens to the specific gravity in intrarenal failure? | It is decreased in intrarenal failure |
| What happens to the especific gravity in postrenal failure? | It is variable in postrenal failure sometimes increased other times decreased |
| What happens to the Na+ level in urine in prerenal failure? | Urine Na+ is decreased in prerenal failure |
| What happens to the Na+ level in urine in intrarenal failure? | Urine Na+ is increased in prerenal failure |
| What happens to the Na+ level in urine in postrenal failure? | Urine Na+ is variable |
| What happens microscoply in prerenal failure? | Prerenal failure microscopically Normal |
| What happens microscoply in intarenal failure? | Intarenal failure microsopically Casts |
| What happens microscoply in postreanl failure? | postrenal failure microsopically Increased WBC, bacteria possibly |
| What is the BUN/Creat ratio of prerenal failure? | >20:1 in prerenal failure |
| What is the BUN/Creat ratio of intrarenal & Postrenal failure? | 10:1 in both intrarenal & postrenal failure |
| What are some pre renal causes of acute renal failure? | Hypovolemia, hepatorenal syndrome, vascular problems such as atheroembolic disease & reanl vein thrombosis (complication of nephrotic syndrome)& infection usually sepsis |
| hypovolemia a cause of prerenal filaure is usually from ___ or ___ and fluid loss or excessive use of ___? | usually from shock or dehydration & fluid loss or excessive use of diuretics. |
| Hepatorenal syndrome in which renal ___ is compromised in ____ can cause pre renal failure | Hepatorenal syndrome in which renal perfusion is compromised in liver failure can cause pre renal failure |
| What are some causes of Renal Failure? | toxins, medications; rhabdomyolysis; hemolyisis; multiple myeloma; sickle-cell disease; lupus erythematosus; glomerulonephritis; Goodpasture's syndrome; Wegener's granulomatosis or acute lupus nephritis with systemic lupus erythromatosus |
| Name some toxins or medications that can cause pre renal failure? | (e.g. some NSAIDs, aminoglycoside antibiotics, iodinated contrast, lithium, phosphate nephropathy due to bowel preparation for colonoscopy with sodium phosphates) |
| What is rhabdomyolysis? The resultant release of ___ in the blood affects the kidney; it can be caused by ___ (especially in ____ and extensive blunt trauma), statins, stimulants and some other drugs | rhabdomyolysis (breakdown of muscle tissue) - the resultant release of myoglobin in the blood affects the kidney; it can be caused by injury (especially crush injury and extensive blunt trauma), statins, stimulants and some other drugs |
| What are some causes of post renal failure? | Medication interfering with normal bladder empthying (eg anticholinergics); benign prostatic hypertrophy or prostate cancer; kidney stones; due to abdominal malignancy (eg ovarian ca, colorectal ca); & obstructed urinary catheter |
| What are s/s of prerenal ARF? | Dizziness; dry mouth; low blood pressure (hypotension); rapid heart rate; slack skin; thirst; weight loss; Urine output is usually low. The pt may also have symptoms of heart or liver disease |
| What are s/s of intrinsic ARF? aka intrarenal failure | Fever, rash, arthralgia (joint pain; flank pain; headache, dizziness, confusion, seizure, oliguria, edema, HTN, papilledema, & heart failure |
| What are s/s of postrenal ARF? | Pain, difficult urination, distended bladder, edema, HTN, pain in lower back, lower abdomen, groin, genitalia, SEVERE Hematuria |
| What classifies a pt of having oliguria? | <500ml/day |
| What classifies a pt of having anuria? | <50ml/day |
| What are the s/s of renal failure? | Nl perfusion is diminished with decreased I/O, when oliguric-anuria phase last 1-2 weeks, some pts have little or no oliguric phase & begin to make lg quantities of dilute urine signifying restoration of tubular patency phase last 2days-2wks. Increase pho |
| How long can the oliguric to anuric phase last | 1-2 weeks |
| Some pts have no oliguric phase & begin to make large quantities of dilute urine signify8ing restoration of tubular patency. How long does this phase last? | 2days -2 weeks |
| In ARF pts can have an ___ in phosporone with ___ createn clearance of ____ ml/min (NL= 125ml/min), crystals form from _____in __, ___, ___, ___, & ___- classified as osteodystrophies & metastatic calcifications. | increases in phophorone with decreased creat clearance <25ml/min (NL = 125 ml/min), crystals form from excess calcium phosphate in soft tissue, lungs, joints, brain, & heart- classified as osteodystrophies & metastatic calcifications |
| In ARF small decrease in plasma ioniced calcium levels leads to ____ stimulation, ___ stimulation, bone reasorption, & enhanced renal secreation of _____, impaired Vit ___, hydroxylation contributed to ___ & ___levels. | Small decreases in plasma ionized calcium levels leads to parathryoid hormone (PTH) stimulation, osteoclasts stimulation, bone reasorption, & enhanced renal secretion of phosphate (phosphate excretion is impired in renal failure), impired Vit D & hydroxyl |
| In ARF hyperkalemia is a s/s that may lead to what? | hyperkalemia may lead to dysrhythmias or cardiac arrest, metabolic acidosis, decreased erythropoietin(a hormone growth factor essential for erythropoiesis in BM) leading to decreased Hct & Hbg & hyperparathyroidism |
| ___ is also d/t the continued release of renin by the kidney; which activates the ____? Ultimately this process results in the release of ___ from teh ___, which increases the retention of __ & ___ thus exacerbating the fluid overload problem | HTN is also d/t the continued release of renin by the kidney; which activates the renin-angiotensisn mechanism. Ultimately this process results in the release of aldosterone from the adrenal cortex, which increases the rentention of Na+ & H2O thus exacerb |
| Why does fluid volume overload devleop in renal failure that leads to HTN? | Fluid volume overload develosp because the kidney can no longer excreate H2O & Na. JVD plumonary pulses raies in lungs, peripheral edema. HTN are s/s of fluid volume overload |
| What is a s/s of fluid volume overload? | HTN |
| How would renal damage or failure lead to HTN in a person? | The kidney can no longer excreate H20 & Na, which leads to fluid volume overload which leads to HTN. |
| Fluid volume overload may lead to ___ intolerance producing an ___ in blood sugar level | Fluid volume overload may lead to CHO intolerance producing an increase in blood sugar level |
| Why are ACEI drugs helpful, especially in patients with Diabetes? | ACEIs & ARBs reduce proteinuria & enhance glomerular hernodyamics. The use of ACEIs appears to slow the progression of CRF by proteting the kidney from hemodynamically mediated glomerular damage. Also in pts with Diabetes The risk of developing macroalbum |
| ACEIs block all production & interfere with constriction of the ___ arteriole. This can be particuallry detremental to renal fx in pts who require high filtration pressure, such as those with ___ or ____? | ACEI's block all production & interfere with constriction of the efferent arteriole. This can be particullarly detremental to renal fx in pts who require high filtration pressures, such as those with polycystic kidney disase or collecting system obstructi |
| Blood flows to the kidneys from the ___ through the ___ that divide N2 several interlobar arteries. | Blood flows to the kidneys from the abdominal aorta through the renal arteries that divide into several interlobar arteries. |
| When the interlobar arteries reach the border of the __ 7 ___, they branch into the arcuate arteries that then travel along the ____ & branch further to form small interlobular arteries (going into the ___) & branch extensively to from the ____? | When they reach the border of the medulla & cortex, they branch into the arculate arteries that then travel along the cortical medullary border & branch further to form small interlobular arteries (going into the cortex) & branch extensively to form the a |
| The afferent arterioles divide to form ___ capillaries, which coalesce to form the ____? | The afferent arterioles divide to form flomerular capillairies, which coalesce to form th eefferent arterioles. |
| Each nephrone has its own ___, capillary, & ___? | Each nephrone has its own afferent arteriole, capillary , & efferent arteriole |
| As the unit of kidney function, a nephone must accomplish what 3 functions? | 1. filtration of water soluble substances from the blood 2. reabsorption of filtred nutrients 3. secretion of wastes or excess substances into the filtrate |
| Chemical mediators are thought to be released in response to maculadensa signals, including vasoactive _____. Drugs that inhibit cycloxygenase, such as ___ & ___, interfere with ___ production & may precipitate excessive revovascular constriction in some | Chemical mediators are thought to be released in response to maculadensa signals, including vasoactive PROSTOGLANDINS. Drugs that inhibit cycloxygenase, such as ASA & NSAIDs, interfere with prostoglandin production & may precipitate excessive revovascular |
| Prostoglandins have ___ properties. | Prostoglandins have vasodilating properties |
| ___ is composed of the glomerulus, the maculer densa, & specialized ___ cells, which are located arround the glomerular arterioles. | The juxtaglomerular apparatus is composed of the flomerulus, the mcculer densa & specialized juxtaglomerular cells, which are located arround the glomerular arterioles |
| ___ produces & releases renein | Juxtaglomerular cells |
| ___ is an enzyme that converts angiotensinogen to angiotensin I. | renin |
| Angiotensin I is then converted to Angiotension II by ___ cells in the ___ capillary, which possesses angiotensin-converting enzyme activity. | Angiotension I is then converted to Angiotension II by endothelial cells in the glomerular capillary, which possess angiotension converting enzyme activity |
| __ is a potent vasoconstrictor that constricts the ___ thus increasing GFR? | Angiotension II is a potent vasoconstrictor that constricts the efferent arterole, thus increasing GFR |
| How do prostaglandins help the kidneys? | The kidney increases prostaglandin synthesis to modulate renal vascular resistance. |
| Why is renin released? | A decrease in arterial blood pressure; a decrease in NaCL levels in the ultra-filtrate nephone or sympathetic nervous system activity (that also controls blood pressure acting through the beta 1 adrenergic receptors |
| Renin is secreted from ______ (of the afferent arterioles), which are activated via signaling (the release of _____) from the macula densa, which respond to the rate of fluid flow through the distal tubule, by decreases in renal perfusion pressure (throug | Renin is secreted from juxtaglomerular cells (of the afferent arterioles), which are activated via signaling (the release of prostaglandins) from the macula densa, which respond to the rate of fluid flow through the distal tubule, by decreases in renal pe |
| ___ activates the renin-angiotensin system by cleaving angiotensinogen, produced by the liver, to yield angiotensin I, which is further converted into angiotensin II by ACE, the angiotensin-converting enzyme primarily within the capillaries of the lungs. | Renin activates the renin-angiotensin system by cleaving angiotensinogen, produced by the liver, to yield angiotensin I, which is further converted into angiotensin II by ACE, the angiotensin-converting enzyme primarily within the capillaries of the lungs |
| What is Renin's primary function? | Renin's primary function is therefore to eventually cause an increase in blood pressure, leading to restoration of perfusion pressure in the kidneys. |
| Kidney stones form when there is a decrease in ____ volume or an excess of stone-forming substances in the ____. The most common type of kidney stone contains ____ in combination with either oxalate or phosphate. Other chemical compounds that can form sto | Kidney stones form when there is a decrease in urine volume or an excess of stone-forming substances in the urine. The most common type of kidney stone contains calcium in combination with either oxalate or phosphate. Other chemical compounds that can for |
| ____ through reduced fluid intake or strenuous exercise without adequate fluid replacement increases the risk of kidney stones. | Dehydration through reduced fluid intake or strenuous exercise without adequate fluid replacement increases the risk of kidney stones. |
| ___ to the flow of urine can also lead to stone formation. Kidney stones can also result from ___; these are known as ___ or infection stones. | Obstruction to the flow of urine can also lead to stone formation. Kidney stones can also result from infection in the urinary tract; these are known as struvite or infection stones. |
| Name some conditions that can lead to kidney stones. | gout; hyperclciuria; hyperparathyroidism, kidney disease such as renal tubular acidosis and some inherited metabolic conditions including cystinuria & hyperoxaluira. Chronic diseases such as diabetes and HTN; Inflammatory bowel disease; pts who have had a |
| What are some medications that put a pt at risk for kidney stones? | protease inhibitors Crixivan (indinavir), a drug used to treat HIV infection; diuretics, calcium-containing antiacids |
| While some kidney stones may not produce symptoms (known as "silent" stones), people who have kidney stones often report the sudden onset of _____ in their low back and/or side, groin, or abdomen. Changes in body position do not relieve this ____. The ___ | While some kidney stones may not produce symptoms (known as "silent" stones), people who have kidney stones often report the sudden onset of excruciating, cramping pain in their low back and/or side, groin, or abdomen. Changes in body position do not reli |
| Renal calculi consist of combined organic material taht initially form the __ or ___ of the kidney? | calicles or pelvis of the kidney |
| The calculi may then migrate down the urinary tract & cause what? | pain, obstruction, & infection |
| The presence of a stone or calculus anywhere in the urinary tract is termed ___? | nephrolithiasis |
| Factors influencing calculus formation are what? | supersteration (increased concentration of the offending solute), an abnormal pH, or low urine volume. |
| A complex interrelationships between conditions conducive to crystallization, cellular response to crystals, & the presence of matrix materials to ehhance mineralization & substained activity of the usual process that inhibit Ca formation is involved in t | etiologic progression of calculi |
| What are some inhibitors to stone formation? | Inhibitors to stone formation include pyrophosphate, citrate, megnesium, & certain macromolecules such as glycoproteins,. Forms when Citrates & Magnesium is difcient in urine, hypercalciema |
| When the calculus is in the ___ no symptoms appear unless an infection or obstruction of the kidney is present? | pelvis |
| What is the hallmark s/s of reanl stones? | PAIN |
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jmilbur4
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