CPR Exam 2 - RENAL

183 flashcards · Other · by Jared Blackwell

1. What is the thin descending limb permeable to?

   Water via AQP1.

2. What is the thick descending limb permeable to?

   Salt.

3. Diabetes Insipidus

   Produce large volume of dilute urine resulting in hypernatremia. Either Neurogenic- failure to secrete ADH Nephrogenic- kidney unresponsive to ADH.

4. Syndrome of Inappropriate ADH (SIADH)

   Excessive ADH secretion. Retaining water when you shouldn't. -Hypotonic Hyponatremia (decreased Posm and decrease Na+). Carbamazepine, cyclophosphamide. Small lung cancer.CNS disorders. Pulmonary disease.

5. How does diabetes mellitus and congestive heart failure affect ADH?

   They both increase synthesis of ADH.

6. Do we change intracellular volume?

   No, because it's regulated by K+. Intracellular fluid is predominately potassium K+.

7. How does SNS affect the kidneys?

   Constricts arterioles with more effect on afferent arteriole than efferent arteriole. Diameter of afferent arteriole is larger than efferent under normal conditions.

8. What does Angiotensin II do?

   Vasoconstricts afferent & efferent (more) arterioles causing decrease in RBF and maintain GFR. At proximal tubule ANG II increases NaCl/H20 reabsorption via NHE3. Works on adrenal glands to secrete Aldosterone. Goes to post. pituitary to secrete ADH onto the collecting duct.

9. Where does ANG II work on in the kidney?

   ANG II goes to the proximal tubule and tells the NHE3 (Sodium Hydrogen Exchanger) to work harder. More sodium is reabsorbed. Water follows Na+.

10. How does aldosterone affect the kidney?

    Permeates the collecting duct to bind mineralocorticoid receptor. Increases synthesis of Na/K ATPase and ENaC (Epithelial Sodium Na channel). Aldo also increases the number of open ENaC.

11. What does spironolactone do?

    Binds mineralocorticoid receptor (MR) and blocks aldosterone actions. K+ sparring. (may cause hyperkalemia). Used for Heart failure, cirrohsis, primary hyperaldosteroism.

12. Aldosterone affects on tubular epithelium?

13. Catecholamines' affects on tubular epithelium?

14. What does ANP do?

    Decreases Na+ reabsorption in collecting duct via inhibition of ENaC. If volume depleted no activation of ANP b/c you want to absorb Na+.

15. Substances that affect afferent/efferent arterioles.

16. Dilation and constriction of afferent/efferent arterioles.

17. Where is potassium reabsorbed?

    Mostly, 90% in proximal tubule and thick ascending limb. 70% proximal tubule. 10-25% in thick ascending limb via NKCC2 & Na/K ATPase.

18. Where is potassium secreted?

    Distal tubule and thick ascending limb.

19. What structures does the ureteric bud form?

    The collecting duct and ureter, pelvis, calyxes.

20. What structures does the metanephric mesenchyme form?

    The glomerulus to distal tubule. All nephron except collecting duct.

21. What do loop diuretics do?

    Inhibit NKCC2 cotransporter at thick ascending limb. Prevents sodium, potassium, & chloride to be reabsorbed. Furosemide. K+ wasting. Hypokalemia.

22. What does a decrease in medullary blood flow (vasa recta) do?

    Increases ability to produce concentrated urine.

23. What is the diluting segment of nephron?

    The thick ascending limb. NKCC2 cotransporter reabsorbs sodium, potassium, chloride to generate osmotic gradient.

24. Hypertonic Hyponatremia

    >290 mOsmo. Presence of effective osmole moves water from ICF to ECF. Ex. Mannitol, glycine, marked hyperglycemia.

25. Effects of lithium on nephron?

    Lithium disrupts V2 receptor on collecting duct and ADH cannot work. Nephrogenic diabetes insipidus. Hypernatremia.

26. What is the first step in evaluating patient with hyponatremia?

    Evaluate plasma osmolality. If HIGH --> glucose, mannitol, glycine. [Hypertonic Hyponatremia]. Normal--> Lipids, protein Low--> Further workup. [Hypotonic Hyponatremia].

27. Causes of Hypovolemic Hypotonic Hyponatremia

    GI loss, blood loss, sweating: Urine Na+ LOW. Urine Osm High. Diuretics: Urine Na+ high. Urine Osm high. Primary adrenal insufficiency: Cortisol normally suppresses ADH--> increase ADH. Decreased aldosterone loses salt/water further increases ADH. High ADH, High urine Osm.

28. Causes of Euvolemic Hypotonic Hyponatremia?

    SIADH Urine Na+ high >40. Urine Osm high. Psychogenic Polydispisia Urine Osm LOW Hypothyroidism.

29. Causes of Hypervolemic Hypotonic Hyponatremia?

    ADH increased too much. Low urine Na+. High urine Osm. Heart failure, cirrhosis, kidney failure

30. Describe how excess water and restricted water affects osmolality, water, and urinary osmolality.

    Excess water-> Decrease osmolality-> Decrease ADH -> Increase water excretion -> Decrease urinary osm.

31. How should a healthy patient respond to hyponatremia?

    Urine should be diluted. Low urine Osm. Low urinary sodium (<30mEq/L). If urine is diluted then kidneys are responding appropriately. ADH level is low and problem is outside of kidneys.

32. Can thiazides cause hyponatremia.

    YES. Sodium reabsorption is blocked in distal tubule. Osm in CD rises and more sodium excreted in urine. However, it leaves medullary Osm intact and water leaves collecting duct causing hyponatremia.

33. What do loop diuretics do to osmolality in medulla?

    Block NKCC2 which diminishes Osm in medulla. Less water is draw out of collecting duct. More sodium goes to collecting duct and osmolality in collecting duct is higher so less water is drawn out. It diminishes the osmolality in the medulla because the pump NKCC2 that is inhibited is responsible for maintaining high osm in medulla. Thus blocking it causes less drawing force to remove water from CD.

34. What is the urinary osmolality and urine sodium levels in SIADH?

    Too much ADH leas to hyponatremia. HIGH urinary Osm. HIGH urinary Na+.

35. Are patients with SIADH fluid overloaded (hypervolumic)? i.e. crackles, lower extremity edema.

    No. Euvolumic. Fluid retention due to ADH BUT body lowers RAAS. Lower aldosterone increases Na+ in urine and worsens hyponatremia. Lower aldosterone also decreases water reabsorption by kidneys so still keeps normal volume.

36. How do you treat patient with SIADH?

    Fluid restriction. Increase solute intake.

37. What is the urinary osmolality in Psychogenic Polydipsia?

    LOW urine osmolality. Kidneys working but they're drinking too much water. Fluid restriction.

38. What are the causes of hypervolumic, euvolemic, & hypovolemic hyponatremia?

    Hypervolumic= CHF, renal failure, Cirrohis Euvolemic= SIADH, hypothryoidism, polydispsia, diet. Hypovolemic= Dehydration, Diuretics, primary adrenal disease.

39. How do you treat diabetes insipidus?

    Water. Vasopressin or desmopressin. D5 dextrose.

40. What do principal cells do?

    In collecting duct, respond to aldosterone and reabsorb NaCl ENaC. Main regulator of K+ excretion. Respond to ADH to become water permeable.

41. What do intercalated cells do?

    In collecting duct they secrete H+. Beta secrete HCO3-.

42. Where is HCO3- reabsorption take place?

    80% of HCO3- is reabsorbed in the proximal tubule.

43. Where does ammoniagenesis take place?

    Proximal tubule: metabolism of glutamine produces NH4+ and HCO3-.

44. Symptoms of Hypovolemic Hypotonic Hyponatremia?

    Hypotension Tachycardia Flat neck veins Orthostatic hypotension

45. Who most often experiences hypernatremia?

    Elderly who don't experience thirst normally. People unable to communicate.

46. What happens when you dilate afferent arteriole?

    Increases RBF and GFR.

47. What happens when you constrict efferent arteriole?

    Decrease RBF and Increase GFR.

48. What happens to RBF and GFR if there is increased protein levels in the blood?

    Lower GFR and no change in RBF.

49. How does kidney autoregulate GFR/RBF with changes in blood pressure?

    Myogenic Feedback "Bayliss Effect" Responds to changes in BP. Tubuloglomerular Feedback Responds to changes in NaCl conc. Macula Densa at end of thick ascending limb detects Na+ and signals afferent arteriole.

50. What is the myogenic mechanism for high BP?

    Afferent arteriole constricts less blood flow comes in bringing pressure down. Efferent arteriole dilates from decreased renin and dilation lets more blood leave capillary.

51. What are the effects of NSAIDs on the nephron?

    Prostaglandins dilate afferent arteriole. NSAIDs will constrict afferent arteriole: Decrease RBF Decrease GFR Acute renal failure and acute heart failure.

52. What does angiotensin II do to GFR & RBF/

    Constricts efferent arteriole preferentially which decreases RBF and maintains/increases GFR.

53. What do ACE inhibitor do to GFR & RBF?

    Block angiontensin II and increases RBF and decreases GFR & FF. *May develop acute renal failure b/c decreased GFR.

54. What does hyperkalemia do to an EKG?

    Peaked T-waves and QRS widening.

55. Acidosis, Insulin defeciency, Beta blockers, Digoxin, Lysis of cells, and Hyperosmolarity can all cause what?

    Hyperkalemia. Acidosis: High level of acid around drives H+ inside cell in exchange for potassium causing high levels of K+ principal cell. Insulin increases Na+/K+ pump. Insulin deficient makes K+ to stay outside cell causing hyperkalemia. Digoxin inhibits Na/K pump leaving K+ outside of cell. Catecholamines drive pump to work harder. Beta blockers will block catecholamine effect raising K+ in plasma.

56. What does hypomagnesia do to potassium levels?

    Promotes urinary K+ loss causing hypokalemia. Cannot fix K+ until magnesium is corrected.

57. What drug targets the collecting duct?

    Amioloride: Blocks ENaC, spares K+. Usually first choice diuretic.

58. Where is the regulatory site for K+ excretion?

    Principal cell on collecting duct. ENaC creates an electrochemical gradient because chloride comes after sodium leaving a negative charge. Allows K+ to leave to lumen.

59. How does thick ascending limb handle K+?

    Reabsorbs 10-25% of K+. As Na+ increases, Na+ is transported with K & Cl via NKCC2. Na+ is then reabsorbed by blood via Na/K ATPase which reduces ATP stimulating efflux of luminal K+ channel, recycling it. Increases NKCC2.

60. How does aldosterone affect potassium?

    Increases K+ secretion from principal cells. Increases number of Na+ and K+ channels on luminal side Enhances Na/K ATPase

61. What does increased potassium concentration do to principal cells?

    Same as aldosterone--> increase K+ secretion. Increases Na+ and K+ channels on luminal side. Enhances Na/K ATPase.

62. How does distal flow rate affect potassium?

    Increased flow rate and urine will increase K+ secretion. Favorable K+ gradient for secretion to tubular fluid. Reduced flow rate and urine will decrease potassium secretion.

63. Increased flow rate and urine will do what to potassium?

    Increased flow rate and urine will increase K+ secretion. Favorable K+ gradient for secretion to tubular fluid. Reduced flow rate and urine will decrease potassium secretion.

64. Distal Na+ delivery will do what to potassium secretion?

    Na+ enters with ENaC leaving negative charge (b/c chloride slower). Na/K ATPase will pump more K+ into cell and K+ will go to negative lumen side.

65. What do alpha-intercalated cells do to potassium?

    They reabsorb K+ via H/K ATPase. Secrete H+ in exchange for K+ reabsorption.

66. What does insulin and B2 agonists do to potassium?

    Insulin & B2 agonist enhance Na/K ATPase, increase secretion.

67. What does alkalosis do to potassium?

    H+ will leave cell to decrease pH and K+ will enter cell in order to maintain electronegativety.

68. What is hyperkalemic periodic paralysis?

    Acute attacks caused by sudden movement of K+ into cell. Stress, high carb, rest after exercise. Familial autosomal dominant mutation in dihydropyridine calcium channel in skeletal muscle. Thyrotoxicosis is acquired.

69. How does sustained vomiting affect potassium?

    Sustained vomiting causes metabolic alkalosis due to loss of HCL. Alkalosis increases bicarbonate past reabsorbtion threshold. HCO3- must be paired with Na+ which increases distal delivery of Na+ increasing K+ loss. Volume depletion stimulates RAAS which increases Aldosterone to stimulate principal cell to open luminal Na+ and K+ channels and enhance Na/K ATPase.

70. Hypokalemia with metabolic alkalosis and normo-hypotension caused by?

    Loop & thiazide diuretics Bartter's syndrome Gitelman's syndrome

71. What type of receptors does base (trigone) of bladder have?

    The base of bladder has alpha-adrenergic receptors.

72. What type of receptors does the body of the bladder have?

    The body of bladder has beta-adrenergic receptors.

73. How does bladder empty?

    ACh binds muscarinic receptor to contract detrusor.

74. How does bladder store urine?

    NE binds beta receptors on bladder body to relax detrusor. NE also binds alpha receptors on base to constrict bladder neck/proximal urethra.

75. Osteodystrophy Earliest signs will present in phalanx.

76. Calcium Oxalate Stones Hyperoxaluria occurs with high oxalate or LOW Ca2+ diet. Fat malabsorption (Crohn's): Fat binds calcium leaving oxalate free to be absorbed in gut. Hypercalcemia

77. Hallmarks of Glomerular Hematuria?

    Blood in urine is coca-cola color. Red cell casts. Dysmorphic RBCs. Proteinuria. LOW urine Na+; <20 mEq/L.

78. How does nephrotic syndrome cause Fatty casts/Oval fat bodies?

    1) Decreased protein 2) Decreases albumin 3) Increases liver activity 4) Hyperlipidemia 5) Fatty casts/Oval fat bodies.

79. Classical presentation of Nephrotic Syndrome?

    Frothy urine. Peripheral & periorbital edema. May mistake for allergic rxn. High cholesterol. Proteinuria.

80. Post-streptococcal Glomerulonephritis

    Follows group A B-hemolytic strep infection. Immune complex deposit in kidney. Will see hypocomplementemia (also lupus, MPGN). Mostly children 5-12 years old 2-3 weeks after strep infection. Granular IgG w/ immunofluorescence. Electron microscopy: Subepithelial "humps."

81. IgA Nephropathy (Berger's Disease)

    Most common form of glomerulonephritis. Repeated episodes of hematuria. Overactive immune system increases IgA due to respiratory infection and GI infection. IgA complex --> mesangium. No hypocomplementemia. Granular immunofluorescence stained for IgA. Recurrent episodes of hematuria since childhood. Episodes follow UTI. Days after infection while post-strep GN is weeks after. Henoch-Schonlein Purpura IgA nephropathy w/ extra-renal involvement. Most common childhood vasculitis. Palpable purupur…

82. Diffuse Proliferative Glomerulonephritis (DPGN)

    SLE patients. Presents with Lupus features: Fever Rash Arthritis Immune complex deposition. Lupus Nephritis Type I & II are mild Type III & IV are same but type III is focal and IV is diffuse. Type V leads to nephrotic syndrome- membranous nephropathy. Subendothelial deposits drive immune response. Anti-dsDNA. Hypocomplementemia (also post-strep, MPGN). "Wire looping" Capillary loops thickened. Granular immunofluorescence "Full house" picks up IgG, IgA, IgM, C3, C1q. **DPGN may present as nephr…

83. Rapidly Progressive Glomerulonephritis (RPGN)

    Presence of "crescent" within glomeruli. Formed by inflammation. Severe with rapid onset often presenting with acute renal failure. Fatigue, anorexia. Elevate BUN & Cr. RBC casts. Type I: Linear IF anti-GBM antibodies. Type 2 hypersensitivity because Abs against tissue antigens. Goodpasture's Syndrome: Antibody against type IV collagen found in GBM and alveoli. Hemoptysis and nephritic syndrome. Young adult male with hemoptysis and hematuria. Type II: Granular IF Immune complex deposition (type…

84. Alport Syndrome (Hereditary Nephritis)

    X-linked defect in type IV collagen. Triad: Hematuria Hearing loss Ocular disturbances Male child with triad and family history.

85. Classical presentation of Nephritic Syndrome?

    Dark urine (RBCs) Swelling/Edema Fatigue Proteinuria (< 3.5 g/day).

86. Minimal Change Disease

    Podocytes become flattened and protein spills into urine. Loss of anion charge barrier GBM causes loss of albumin. Normal light micrscopy and immunofluorescence. Only finding is effacement foot processes by EM. Sometimes due to immune trigger (days before). Viral infection (URI). Allergic Rxn (bee sting). Immunization. "Selective" proteinuria ONLY albumin in urine (not immunoglobulin). Most common cause of nephrotic syndrome in children. Child with recent URI. Responds well with steroids.

87. Focal Segmental Glomerulosclerosis (FSGS)

    Caused by podocyte injury. More serious version of minimal change disease and often progresses to chronic renal failure. Does NOT respond to steroids. Pink/dense deposition of collagen in glomerulus. Only portion and some glomeruli involved. Immunofluorescence C3 IgM Sclerotic segments have collapse of basement membrane and hyaline deposition. Effacement of podocytes seen on EM. Most common cause of nephrotic syndrome in blacks. Often idiopathic but may be secondary to HIV, Sickle cell, heroin…

88. Membranous Nephropathy

    Thick glomerular basement membrane. Immune complex deposition in basement membrane. IF shows granular deposits of IgG and C3 staining. Immune complex deposits in subepithelium and podocytes lay down extra basement membrane on top of complex "spike and dome" pattern. Electron microscopy shows "electron dense deposits." Often idopathic. Autoantibodies against phospholipase A2 receptor (PLA2R) antigen expressed on podocytes. Secondary causes: SLE (most lupus renal disease cause nephritic syndrome…

89. Diabetic Nephropathy

    Non-enzymatic glycosylation of basement membranes causing leaking of proteins. Long term effects: sclerosis of glomeruls. Proteinuria. Can develop into nephrotic syndrome.

90. Amyloidosis

    May cause nephrotic syndrome. Apple-green birefringence with Congo red stain. Kidney most commonly involved organ with amyloidosis.

92. Etiology of Minimal Change Disease?

    Cytokines damage podocytes, often Idiopathic.

93. What disease is associated with minimal change disease?

    Hodgkin Lymphoma Massive production of cytokines by Reed-Sternberg cells.

94. Light microscopy and immunofluorescence findings in minimal change disease?

    Normal. Only finding is effacement of podocytes on EM.

95. Epidemiology of minimal change disease?

    Most common cause of nephrotic syndrome in children. Child with recent URI - days before.

96. Epidemiology of Focal Segmental Glomerulosclerosis (FSGS)

    Most common cause of nephrotic syndrome in African-Americans.

97. What is the generalized treatment for Nephrotic Syndrome?

    ACE inhibitors and ARBs Reduce intraglomeruluar pressure Reduce proteinuria. Loop diuretics with low sodium diet. Statin to treat hyperlipidemia. Strict control of BP.

98. Etiology of Focal Segmental Glomerulosclerosis (FSGS)

    Idiopathic Podocyte damage due to genes encoding slit diaphragms.

99. Secondary causes of Focal Segmental Glomerulosclerosis (FSGS)

    HIV Sickle cell Heroin users Obesity

100. Minimal Change Disease Generalized edema: