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Flashcards

Conditions causing impaired renal function

Whitney Willbanks Nursing Inglês 78 flashcards

Flashcards do conjunto (78)

  1. 1injury to the nephron (glomerulus, tubules, arteriole) result in alteration in____, while disorders or injury in other areas of the kidney (calyx, pelvis) result in ____--urine formation
    --problems of urine elimination
  2. 2genetic disorder (most commonly autosomal dominant) resulting in numerous fluid-filled cysts in both kidneys that enlarge the kidneys, compressing & eventually replacing functional kidney tissuepolycystic kidney disease (PKD)
  3. 3autosomal dominant PKD occurs in ____, whereas autosomal recessive is often diagnosed in ____--both children & adults (most often in adults) with symptoms usually arising in middle age
    --prenatally or during infancy
    **extremely serious, progresses rapidly, usually leads to renal failure & death in infancy or early childhood
  4. 4PKD manifestations in neonates include:--Potter facies (pronounced epicanthal folds, pointed nose, small chin, floppy/low-set ears)
    --large symmetrical masses on bilateral flanks
    --respiratory distress (fluid build up due to renal impairment)
    --hyponatremia (from fluid build up)
  5. 5clinical manifestations of PKD in adults include--lumbar/flank pain
    --swollen, tender abdomen
    --grossly enlarged, palpable kidneys
  6. 6PKD clinical manifestations in children & adults--hypertension (RAAS activation, fluid build-up)
    --hematuria (impaired filtration)
    --nocturia (unable to concentrate urine)
    --uremia (waste build-up)
  7. 7Other disorders that may occur with PKD include--brain aneurysm
    --cysts in other organs (especially liver)
    --colon diverticula
  8. 8complications of PKD--CRITICAL: renal insufficiency/CKD, cyst rupture, retroperitoneal bleeding
    --NON-CRITICAL: anemia, HTN, renal calculi
  9. 9what confirms the diagnosis of PKD?genetic testing
  10. 10What pharmacological agents are used to control symptoms and prevent complications in PKD?--antibiotics (if infection present)
    --analgesics
    --antihypertensives/diuretics
    --statins
  11. 11What is used for treatment of PKD in addition to medications?--adequate hydration
    --low salt, low protein diet
    --surgically draining cystic abscesses or retroperitoneal bleeding
    --dialysis
    --kidney transplant
    **measures to protect kidneys & delay destruction
  12. 12What are the layers of the glomerulus?--endothelial layer (fenestrated)
    --middle layer (basement membrane) that serves as barrier to large molecules
    --outer parietal epithelial layer, podocytes
  13. 13how does the endothelial layer of the glomerulus function?endothelial layer surrounds the capillaries within Bowman's capsule & fenestrations allow for rapid filtration of blood
  14. 14specialized epithelial cells of the glomerulus; form extensions (foot processes) that surround glomerular capillaries & restrict passage of large molecules into urinePodocytes
  15. 15Diffuse glomerular damage involves ___ of the glomeruli. Focal injury involves ____.--all or most of the glomeruli (>50%)
    --some of the glomeruli (<50%)
  16. 16Global glomerular damage refers todamage to the whole glomerulus
  17. 17Segmental glomerular damage indicatesonly a section of the glomerulus is damaged
  18. 18What does proliferative glomerular damage indicate?increase in glomerular cells (mesangial, endothelial, etc.)
  19. 19What causes crescents in the glomerulus?increased glomerular permeability from various glomerular insults leads to influx of inflammatory cells & proliferation of parietal layer of Bowman's capsule.
    **crescent = two or more layers of cells partially or completely filling the Bowman's space
  20. 20What does sclerosing damage to glomeruli indicate?scarring/fibrosis
    **interstitial fibrosis = scarring between glomerulus & tubules
  21. 21What are the two broad categories of glomerular disease?glomeruloNEPHRITIS
    glomeruloSCLEROSIS
  22. 22Glomerulonephritis most often occurs due to activation ofthe immune system
    **trigger often unknown
  23. 23What is a key mechanism of injury in glomerular disorders (up to 90% of cases)?HUMORAL (B-cell mediated) immune response
    **most glomerular disorders involve development of immune complexes that become deposited in the glomerulus & activate complement system
  24. 24Immune complexes deposited in the glomerulus cause--injury to capillary walls & increased permeability
    --loss of negative charge of basement membrane
    --large proteins (albumin, RBCs) pass through into filtrate & manifest as hematuria & proteinuria
  25. 25Even in absence of antigen-antibody complexes in the glomerulus, glomerular disease may occur due toplatelets & T cells
  26. 26How do platelets lead to glomerular damage?platelets aggregate, leading to thrombosis & release of vasoactive substances that increase vascular permeability
  27. 27How do T cells contribute to glomerular damage?stimulates influx of macrophages & lymphocytes that promote cellular proliferation in extracapillary space & CRESCENT formation
    **causes obstruction of blood flow, reduces GFR, leads to sclerosis & fibrosis, & ultimately renal failure
  28. 28This type of glomerulonephritis results from IgG (occasionally IgA or IgD) targeting type IV collagen in the basement membrane:anti-glomerular basement membrane (anti-GBM) glomerulonephritis
    (also known as Goodpasture disease)
    **Type 2 hypersensitivity reaction
    **often results in rapid renal failure
  29. 29anti-GBM antibodies in Goodpasture disease not only attack the glomerular basement membrane but also the _____. How is this manifested?--alveolar basement membrane
    --pulmonary hemorrhage (may present with hemoptysis)
  30. 30Cause of Goodpasture (anti-GBM) disease is not known but may be due to infection, or toxin/drug exposure. What is the treatment for this disease?--plasmapheresis to remove antibodies
    --inhibiting antibody production via corticosteroids
  31. 31What two syndromes is glomerulonephritis associated with?--nephritic syndrome
    --nephrotic syndrome
  32. 32What is the main difference between nephritic & nephrotic syndromes?--nephritic syndrome is an INFLAMMATORY immune response
    --nephrotic syndrome is NON-inflammatory
  33. 33Glomerular inflammation, cellular proliferation, & capillary damage, allowing leakage of red & white blood cells into the urine, as well as SMALL amounts of protein =nephritic syndrome (INFLAMMATORY)
  34. 34Nephritic syndrome can occur following:infection (acute post-infectious glomerulonephritis)
    **can also occur with disorders such as lupus
    **may present as rapidly progressive glomerulonephritis
  35. 35The most common cause of acute glomerulonephritis in children =post-infectious glomerulonephritis
    **risk is highest between age 5 & 12
  36. 36the most common causative organism in acute postinfectious glomerulonephritis is:group A beta-hemolytic strep
  37. 37Which characteristics/behaviors increase risk of acute postinfectious glomerulonephritis in adults?--diabetes
    --alcoholism
    --cancer
    --IV drug use
  38. 38what is the mechanism of damage in acute postinfectious glomerulonephritis?antigen-antibody complexes with IgG & complement
    **complexes form in glomerulus or circulate in the blood, activate immune system, cause proliferation of endothelial & mesangial cells, increase capillary permeability
  39. 39when do symptoms of acute postinfectious glomerulonephritis commonly present?--1-2 weeks after strep throat
    --up to 6 weeks after impetigo
  40. 40sudden hematuria with tea/cola-colored urine, dysmorphic cells in urine, proteinuria (but less than in nephrotic syndrome), & pyuria:severe complete acute nephritic syndrome
  41. 41What are the 4 main characteristics of nephritic syndrome?--hypertension
    --edema
    --hematuria
    --reduced UOP
  42. 42What causes the signs/symptoms of nephritic syndrome?--decreased GFR causes sodium & water retention & OLIGURIA; retention causes generalized edema & HTN; HTN may cause CNS symptoms: N/V, HA, seizures; fluid overload may cause pulmonary edema & renal failure
  43. 43Renal biopsy usually isn't necessary to diagnose ____ infection, but is usually indicated in ____ infection.--strep
    --staph
  44. 44In postinfectious glomerulonephritis, what may be necessary to manage fluid overload, hyperkalemia, & uremia (elevated BUN) that are not responding to therapy?dialysis
  45. 45In ~ 20% of cases of IgA vasculitis, the ____ is affected.glomerulus
  46. 46a systemic immune vasculitis that mainly affects small vessels throughout the body, most often in the skin (causing palpable purpura), occasionally in the kidneyIgA vasculitis
    **also known as Henoch-Schonlein purpura
  47. 47Most cases of IgA vasculitis occur in what age group?children between ages 3 & 15
    **more prevalent in boys
  48. 48renal involvement in IgA vasculitis is more likely in___older children & adults
  49. 49What causes nephritic syndrome in IgA vasculitis?deposition of immune complexes (most often with IgA)
  50. 50Treatment may not be necessary for mild cases of IgA vasculitis; complete remission may occur___within 1 month
  51. 51Rapidly progressing nephritic syndrome usually seen in adults > age 50, characterized by extensive crescent formation, & with serious consequences if not diagnosed early:rapidly progressing glomerulonephritis (RPGN)
  52. 52The three mechanisms of injury in rapidly progressing glomerulonephritis are:1) Goodpasture syndrome = IgG antibodies attack alveolar & glomerular basement membranes
    2) immune complexes deposited in glomeruli (postinfectious glomerulonephritis, Lupus, IgA nephritis)
    3) necrotizing = Pauci-immune glomerulonephritis
  53. 53In type 3 rapidly progressive glomerulonephritis, anti-neutrophil cytoplasmic antibodies (ANCA) in serum attack small blood vessels. This type of glomerulonephritis occurs with:systemic diseases such as granulomatous disease or microscopic polyangiitis
  54. 54In rapidly progressing glomerulonephritis, the number of crescents that form determine:severity of disease, disease prognosis
  55. 55What is treatment for rapidly progressing glomerulonephritis?--immunosuppressive therapy (corticosteroids, cyclophosphamide)
    --plasmapheresis possibly
  56. 56Glomerular disorders are usually characterized by passage of ___ molecules into the urine, while tubular disorders are usually associated with passage of ____ molecules.--large (such as albumin)
    --smaller (such as immunoglobulins)
  57. 57Nephrotic syndrome (non-inflammatory) occurs mainly due to immune injury to the ____podocytes
    **serve an important role in forming barrier against passage of proteins into urine
  58. 58Damage to podocytes in NEPHROTIC syndrome results in massive ____leakage of proteins (mainly albumin) into urine
  59. 59Proteinuria in nephrotic syndrome is > or equal to ____/day in adults or ___ mg/kg body weight in children.--3.5 g/day
    --50 mg/kg body weight
  60. 60Hematuria is usually absent or minor in nephrotic syndrome because:glomerular inflammation is usually minimal
  61. 61Massive leakage of proteins into urine in nephrotic syndrome results in ____, which reduces colloid oncotic pressure & thus causes generalized edema **sodium & water retention worsen this edemahypoalbuminemia
    **immunoglobulins are also lost in urine, increasing risk of infection
  62. 62Hypoalbuminemia in nephrotic syndrome stimulates the ___ to produce more albumin; decreased oncotic pressure also stimulates this organ to produce more lipids, leading to ____ & _____.--liver
    --hypercholesterolemia
    --hypertriglyceridemia
  63. 63Primary kidney diseases associated with nephrotic syndrome include--minimal change disease (also known as LIPOID nephrosis; most often occurs in children)
    --membranous nephropathy (membranous glomerulonephritis; most often seen in adults)
  64. 64Adults usually develop nephrotic syndrome as a result of:systemic disorders
    --diabetes
    --Lupus
    --amyloidosis
  65. 65Minimal change disease, a primary nephrotic syndrome often seen in children, is so named because:histologically there is podocyte loss but minimal change on renal biopsy & no immunoglobulin deposition
    **hematuria & HTN are usually absent, complement levels are normal, & renal function may remain normal
  66. 66In minimal change disease, impaired renal function may occur due to:intravascular volume depletion, which may lead to hemoconcentration & increased platelets, which leads to hypercoagulation & risk for thrombosis
  67. 67minimal change disease is usually treated withsteroids
  68. 68membranous nephropathy is a common cause of PRIMARY nephrotic syndrome in adults but may also be associated with:--systemic disorders (hep B)
    --autoimmune disorders
    --certain drugs (NSAIDs)
  69. 69In membranous nephropathy, histologic changes occur in the ____ (it becomes thicker), but there is no ____ as is seen in other glomerular disorders-basement membrane
    --cell proliferation (crescents)
  70. 70What causes membrane thickening in membranous nephropathy?deposition of antigen-antibody complexes
  71. 71What are the classic signs of nephrotic syndrome?--marked proteinuria
    --hypoalbuminemia
  72. 72How is membranous nephropathy treated?--immunosuppressive therapy (steroids)
    --alkylating agents (cyclophosphamide)
    --calcineurin inhibitors (cyclosporine)
    --antihypertensives for kidney protection (ACE inhibitor or ARB)
  73. 73What does focal segmental glomerulosclerosis indicate?--focal = sclerotic lesions in some glomeruli throughout the kidney
    --segmental = sclerotic lesions only in some parts of a single glomerulus
    **sclerosis is often present in NEPHROTIC syndrome
  74. 74A common cause of primary glomerulonephritis in adolescents and young adults (ages 15-30); IgA complexes deposited in mesangium, causing cell proliferation & inflammation, crescent formation, interstitial fibrosis, & segmental sclerosis:IgA nephropathy
  75. 75IgA nephropathy is the most common form of:glomerulonephritis
    **Nephrotic syndrome occurs in 5-10% of igA nephropathy cases
  76. 76What is clinical presentation of IgA nephropathy?--may be asymptomatic
    --mild proteinuria, microscopic hematuria
    --may have gross hematuria with upper respiratory infection
    --flank pain due to stretching of renal capsule
    --gradual progression over several years
  77. 77What is treatment for IgA nephropathy?--aimed at preventing CKD via management of HTN & kidney protection: ACE inhibitors/ARBs
    --low fat diet
  78. 78What conditions are associated with development of chronic glomerulonephritis?--HLD
    --HTN
    --SLE
    --DM

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Nursing FlashCards sobre Conditions causing impaired renal function, criado por Whitney Willbanks em 02-03-2024.
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