Urinary System Midterm Review

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Urinary System Midterm Review
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Urinary System Midterm Review 2010
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  1. What are the direct effects of aldosterone on the tubule?
    • potassium secretion (CCD)
    • hydrogen ion secretion (CCD)
    • sodium reabsorption (CCD)
  2. What is the research tool Para-aminohippurate (PAH) used to measure?
    effective renal plasma flow
  3. What is the prevelance of chronic kidney disease in the US?
    • ~13% of US pop. has CKD
    • most in stage 3/5
    • most in E coast and South
  4. What are the metabolites removed by the kidney?
    • urea
    • uric acid
    • creatinine
    • urobilinogen
    • (drugs)
    • (chemicals)
  5. What are the homestasis functions of the kidneys?
    • blood pressure
    • volume status
    • osmolality
    • ion balance (Na, K, etc.)
    • pH
    • gluconeogenesis
  6. What hormones are secreted by the kidney?
    • erythorpoietin
    • 1,25-dihydroxy Vit. D
    • renin
  7. What portion of the kidney is naturally hypoxic and vulnerable to injury?
    nephron: renal medulla

    risk: papillary necrosis; acute tubular necrosis
  8. What are the effects of renal artery stenosis?
    • ischemic renal disease
    • activation of renin-angiotensin system --> HTN
  9. How is the concentration gradient of the renal medulla maintained?
    • vasa recta and Loop of Henle --> countercurrent system
    • -hairpin shape
    • -slow blood flow
  10. What are the layers of the glomerular filtration barrier?
    • podocyte epithelium with diaphragms
    • basement membrane
    • fenestrated capillary endothelium (w/ glycocalyx)
  11. What are the 3 basic functions of the kidney?
    • 1. filtration
    • 2. reabsorption
    • 3. secretion
  12. What is fractional excretion? What is the FE of water? of Na?
    • fractional excretion = % of filtered substance in urine
    • FE of water = 1%
    • FE of Na = 0.5%
  13. (filtration, reabsorption, secretion)
    Which function causes the majority of filtrate "loss"?
    What function is affected by diuretics?
    Which function characterizes the PCT?
    • majority of filtrate "loss": reabsorption
    • diuretics --> secretion
    • PCT: reabsorption
  14. What are the FE (fractional excretion) of glucose, urea, and penicillin?
    • glucose: 0%
    • urea: ~50%
    • penicillin: 100%
  15. What substances are reabosorbed mostly in the PCT?
    • water (65%)
    • sodium (65%)
    • potassium (65%)
    • HCO3 (80-90%)
    • Calcium (80%)
    • phosphate (90%)
    • glucose (100%)
    • uric acid (90%)
  16. What substances are secreted in the PCT?
    • cations: creatinine, drugs (tremethoprim, cimetidine)
    • anions: hippurate, drugs (diuretics, penicillin, cephalosporins, salicylates)
  17. What are some special metabolic functions of the PCT?
    • ammoniagenesis (from glutamine, utilizes Na-H antiporter into tubule)
    • calcitriolgenesis (i.e. 1,25(OH)Vit. D generation)
  18. What happens when the macula densa senses low Cl- in the DCT?
    • stimulates adenosine release --> stimulates smooth muscle cells of afferent arteriole
    • vasoconstriction --> decreased capillary hydrostatic pressure
    • decreased RBF, decreased ultrafiltration
  19. What triggers the granular cells of the afferent arteriole to release renin?
    • macula densa senses low Cl- concentration --> PGE2 release
    • decreased baroreceptor stretching
    • increased sympathetic tone from hypotension
  20. What does the macula densa sense?
    • Cl- concentration in DCT
    • DCT flow
  21. What substance is reabsorbed mostly in the Loop of Henle?
    Mg
  22. What reabsorption occurs in the DCT?
    fine tuning of Ca2+ concentration
  23. What are some special features of the DCT?
    thiazide-sensitive NaCl cotransporter (regulated by PTH and calcitriol)
  24. What kinds of secretion occurs in the cortical collecting duct?
    principal cells: secrete K via ROMK hannels

    intercalated cells: secrete H+ via H-ATPase
  25. How does ADH affect the medullary collecting duct?
    • ADH inserts aquaporin 2 channels into tubule membrane
    • stimulates water reabosrption in MCD
  26. What part of the renal tubule is stimulated to reabsorb K during hypokalemia?
    Medullary collecting duct
  27. What type of filtration is glomerular filtration?
    • ultrafiltration
    • -convective transport
    • -semi-permeable filtration barrier
    • -"solvent drag"
    • -Starling forces

    NOT a series of filtration (i.e. not a strainer/colander)
  28. What types of molecules are freely filtered by the glomerulus?
    • freely filtered:
    • <7,000 MW
    • water
    • electrolytes
    • aminoacids
    • monosachharides
    • higher FE
  29. What types of molecules are NOT freely filtered by the glomerulus?
    • NOT freely filtered:
    • >7,000 MW
    • small molecules not bound to large proteins
    • large proteins (e.g. albumin)
    • cells
    • lower FE
  30. What factors affect single glomerular filtration rate?
    • Kf: filtration coefficient = permeability x surface area
    • hydrostatic pressure of capillary
    • oncotic pressure of capillary
    • hydrostatic pressure of Bowman's space
    • oncotic pressure of Bowman's space (~0)
  31. What happens to capillary hydrostatic pressure, renal blood flow and net ultrafiltration pressure when the pressure of the Efferent Arteriole increases?
    • capillary hydrostatic pressure: increases
    • renal blood flow: decreases
    • net ultrafiltration pressure: increases
  32. What happens to capillary hydrostatic pressure, renal blood flow and net ultrafiltration pressure when the pressure of the Efferent Arteriole decreases?
    • capillary hydrostatic pressure: decreases
    • renal blood flow: increases
    • net ultrafiltration pressure: decreases
  33. What happens to capillary hydrostatic pressure, renal blood flow and net ultrafiltration pressure when the pressure of the Afferent Arteriole increases?
    • capillary hydrostatic pressure: decreases
    • renal blood flow: decreases
    • net ultrafiltration pressure: decreases
  34. What happens to capillary hydrostatic pressure, renal blood flow and net ultrafiltration pressure when the pressure of the Afferent Arteriole decreases?
    • capillary hydrostatic pressure: increases
    • renal blood flow: increases
    • net ultrafiltration pressure: increase
  35. What is the perfusion pressure range of GFR autoregulation?
    perfusion pressure: 90-200mmHg
  36. What are the effects of Low-Dose angiotensin II?
    • constircts the efferent arteriole more than the afferent arteriole
    • increases capillary hydrostatic pressure
    • increases GFR
  37. What are the effects of High-Dose angiotensin II?
    • constricts the efferent arteriole as much as afferent arteriole
    • decreases capillary hydrostatic pressure
    • decreases GFR
    • maintains BP
    • systemic vasoconstrictor
    • increases aldosterone secretion
    • increases ADH secretion
    • increases thirst
  38. What is renal blood flow?
    RBF = 20% of cardiac output = volume/time
  39. What is renal plasma flow?
    RPF = RBF x plasma volume = RBF x (1-hematocrit)

    normal RPF = 600 mL/min
  40. What is the glomerular filtration rate?
    GFR = filtration fraction x RPF = ~20% x RPF

    normal GFR = 125 mL/min
  41. Why do we need to maintain GFR?
    • fluid balance
    • electrolyte balance
    • acid-base-balance
    • elimination of metabolic products

    defective GFR --> edema
  42. What is edema?
    clinical sign of volume overload

    can be caused by defective GFR
  43. What process does the GFR reflect?
    • renal function
    • i.e. how well are kidneys filtering plasma
  44. What are the 3 basic mechanisms of metabolic clearance?
    • stool
    • metabolism into an inactive form
    • renal clearance (i.e. kidney excretion)
  45. What can renal clearance be used to measure?
    • GFR
    • RPF
    • (measurements depend on substances)
  46. What are the fundamental characteristics of glomerular filtration?
    • entirely passive process --> no ATP demand
    • filtrate: ~180 L/day
    • urine: ~2 L/day
    • dependent on Starling forces
  47. How can you measure GFR?
    clearance method: meaure clearance rate of certain substance with certain qualities

    substance: freely filtered, constant/stable plasma level, not metabolized, not reabsorbed, not secreted

    creatinine clearance*: freely filtered and not reabsorbed but some secretion --> clinical GFR

    • 1. eyeball
    • 2. 24 hr rine collection --> creatinine clearance
    • 3. lothalamate clearance (research)
    • 4. Cockcroft-Gault Equation
    • 5. MDRD Equation
  48. What are normal creatinine excretion levels for males and females?
    • males: 20-25 mg/kg of body weight
    • females: 15-20 mg/kg of body weight
  49. What is the difference between using renal clearance to measure GFR vs. RPF?
    • GFR clearance: substance NOT secreted
    • RPF clearance: substance completely secreted
  50. How can you measure RPF?
    • renal clearance: substance freely filtered and not reabsorbed but completely secreted
    • amount delivered to kidney = amount excreted

    substance: PAH (para-aminohippurate)

    not useful clinically like GFR is
  51. What determines serum creatinine concentration?
    • muscle mass
    • renal function: GFR
    • (drugs/medications)
  52. How does serum creatinine concentration relate to GFR?
    if GFR >55 mL/min: large change in clearance relates to small change in serum level

    if GRF <55 mL/min: small change in clearance relates to large change in serum level

    i.e. GFR dysfunction has exponential relationship to serum creatinine concentration
  53. What are the major problems of the 24 hour urine collection method to measure GFR?
    • inadequate collection
    • overestimates of GFR at lower levels because of creatinine secretion
  54. What are the variables, pros, and cons of the Cockcroft-Gault equation?
    variables: age, sex, serum concentration, weight

    • pros:
    • used for drug dosing
    • measures creatinine clearance

    • cons:
    • may overestimate GFR in obese/edematous
    • does not measure GFR
  55. What are the variables, pros, and cons of the MDRD equation?
    variables: serum creatinine, age, sex, +/- African American

    • pros:
    • measures GFR (iothalamate clearance)
    • weight not a variable
    • measures steady state creatinine
    • works well at low levels of renal function

    • cons:
    • based on biased study (mostly whites, no diabetics, avg GFR 40 mL/min)
    • does not measure acute renal failure
    • inaccurate at high levels of renal function
    • not valid for body extremes (e.g. <18yo, >70yo, pregnant women, obsese, starved, amputees)
    • not valid for Asians
  56. What are the biomarkers for the 5 stages of Chronic Kidney Disease?
    (requires 2+ GFR measurements 3mo apart)

    • I/II: proteinuria, hematuria (GFR: >60 mL/min)
    • III: complications possible (GFR: 30-60)
    • IV: complications iminent (GFR: 15-30)
    • V: renal replacement therapy (GFR: <15)
  57. What are the subcompartments of the extracellular volume (ECV) of the body and their weight?
    ECV = plasma volume + interstitial volume

    • plasma volume = 5% of body weight
    • interstitial volume = 15% of body weight
  58. What are the fluid compartments of the body and their respective weights?
    • TBW = 60% of body weight (men)
    • ICV = 40% of body weight
    • ECV = plasma + interstitium = 20% of body weight
  59. What changes the size of the ECV and the ICV?
    ECV volume changes = increases/decreases in water and sodium concentrations

    • ICV volume changes = increased/decreased movement of water between ECV and ICV
    • i.e. based on osmolarity of ECV
  60. What does a person's plasma sodium concentration reflect?
    plasma sodium levels reflect free water status (i.e. osmolality)

    plasma sodium levels do NOT reflect total body sodium concentration
  61. How is total body sodium estimated?
    analysis of the ECV
  62. How is the size of the ECV estimated?
    history and physical exam
  63. What are the effects of increased sodium intake?
    increased sodium intake --> increased sodium in ECV --> increased ECV osmolality

    • increased ECV osmolality --> increased movement of water from ICV to ECV
    • i.e. ECV swelling and ICV shrinkage

    • - increased BP
    • - increased central venous pressure
    • - increased edema
  64. What are the effects of decreased sodium intake?
    decreased sodium intake --> decreased sodium in ECV --> decreased ECV osmolality

    • decreased ECV osmolality --> increased movement of water from ECV to ICV
    • i.e. ECV shrinkage, ICV swelling

    • - decreased BP
    • - orthostatic hypotension
    • - increased HR
  65. What determines oncotic pressure within a capillary?
    • albumin in plasma
    • sodium in plasma
  66. How does heart failure affect body fluid pressure and volume?
    • capillary hydrostatic pressure increases
    • edema (lower extremeties)
  67. How does liver failure and nephrotic syndrome affect body fluid pressure and volume?
    • capillary Oncotic pressure decreases (decrease in plasma albumin)
    • edema (face, upper exteremities)
  68. What are some signs of ECV excess?
    • increased central venous pressure (JVP)
    • edema and anasarca (i.e. extreme generalized edema)
    • fluid in lungs (i.e. pulmonary edema)
    • increased transcellular space (e.g. ascites, pleural effusion, etc.)
  69. What are the causes and effects of sodium depletion?
    • causes:
    • hemorrhage
    • vomiting
    • diarrhea

    • effects:
    • low blood volume (weakess, diziness, orthostasis, nausea)
    • insufficient blood volume (orthostatic hypotension)
  70. What parameter determines hypo/hypernatremia?
    water levels in body
  71. How do hyponatremia and hypernatremia relate to urine concentration?
    • dilute urine reflects hypernatremia
    • concentrated urine reflects hyponatremia
  72. What happens to urine when ADH is inhibited?
    • water not reabsorbed into blood vessel: dilute urine
    • increased plasma sodium levels: hypernatremia
  73. What are the common causes of hyponatremia (i.e. water excess)?
    • excessive intake
    • increased ADH influence (e.g. SIADH)
    • increased reabsorption of water from kidneys
  74. What causes release of ADH?
    • decrease in plasma volume (e.g. hemorrhage)
    • baroreceptors signal posterior pituitary
  75. What are some effects of hyponatremia?
    decreased ECV osmolarity --> ICV swelling --> cells swell

    • neuron damage
    • brain compression within cranium
    • intracranial swelling --> death
    • chronic: loss of electrolytes, osmolytes, ICV osmolarity decreases
  76. What are clinical markings of hyponatremia?
    • intracranial swelling and neuron damage:
    • headache
    • confusion
    • coma
    • convulsions
  77. How should you treat hyponatremia clinically?
    slowly: avoid neurological consequences from rapid swelling/shrinking of neurons --> demyelination

    • slowly increase osmolarity of ECV --> increase sodium intake (<12 mEq/L)
    • restrict free water intake

    • treat with IV saline to increase plasma volume without increasing osmolarity --> stops ADH release
    • (often plasma sodium will slowly increase on own)
  78. What could result from rapid correction of hyponatremia?
    • osmotic demyleination
    • central pontine myelinosis
  79. What can cause hypernatremia (i.e. free water depletion)?
    • dehydration
    • increased water loss with age (skin, lungs, kidneys)
    • decreased water reabsorption
  80. Why do hypernatremic patients not show signs of edema or changes in BP?
    hypernatremia does not reflect an increase in total body sodium

    therefore, BP and edema levels are unaffected
  81. What are some effects of hypernatremia?
    increase in plasma osmolarity --> increase in ECV osmolarity --> water moves out of ICV

    ICV shrinkage --> neurologic confusion
  82. What is the most common clinical finding of free water excess/depletion disorders?
    neurological symptoms (e.g. confusion)
  83. Can a patient be ECV depleted and have hyponatremia?
    yes

    low ECV treated with free water
  84. What factors cause/prevent hyper-/hypo-volemia status?
    • sodium intake
    • angiotensin II
    • aldosterone
    • sympathetic nervous system
    • natriuretic peptides (ANP, BNP, dopamine)
  85. How do our bodies control sodium balance and determine size of ECV?
    • 1. sodium reabsorption (renal tubule)
    • 2. sodium retention (low GFR, high angiotensin II, activation of sympathetic NS, high aldosterone)
  86. What is EABV (effective arterial blood volume)?
    based on intravascular volume, cardiac output, and vascular capacitance

    • abstract term that refers to the adequacy of the arterial blood volume to "fill" the capacity of
    • the arterial vasculature.

    Normal EABV exists when the ratio of cardiac output to peripheral resistance maintains venous return and cardiac output at normal levels
  87. What reduces EABV?
    • reduce actual arterial blood volume (e.g. hemorrhage, dehydration)
    • increase arterial vascular capacitance (e.g. cirrhosis, sepsis)
    • reduce cardiac output (e.g. congestive heart failure)
  88. How does a low EABV trigger sodium retention in the kidneys?
    • reduced renal blood flow --> triggers macula densa --> renin release -->--> sodium retention in CCD
    • stimulates ADH release
  89. What happens when there is an increase in the ECV but a decrease in the EABV?
    • stimulates sodium retention mechanisms
    • ADH released
  90. What factors increase natriuresis (i.e. sodium excretion into urine)
    • increased GFR
    • dopamine (acts on PCT)
    • natriuretic peptides (e.g. ANP, BNP) (act on CD)
  91. How do our bodies control water balance and control serum sodium concentration?
    • medullary concentration gradient:
    • sodium exits ascending LOH
    • urea exits CD
  92. How do we make more dilute urine?
    increase sodium reabsorption from renal tubule
  93. How do we make concentrated urine?
    stimulate ADH --> increase water reabsorption from the CD tubule
  94. Is hydrostatic pressure constant along capillary length?
    • no:
    • pressure higher at beginning
    • pressure very low in venules (where much of interstitial fluid is reabsorbed)
  95. What are some common causes of peripheral edema?
    • local factors (e.g. venous obstruction, lympyhatic obstruction)
    • heart failure (diastolic and systolic)
    • cirrhosis
    • kidney disease (e.g. volume overload, nephrotic syndrome)
  96. How is heart failure related to peripheral edema?
    • (forward)
    • heart failure: decreased cardiac output --> decreased EABV --> sodium retention mechanisms activated

    • (backward)
    • heart failure: increased right atrial pressure --> increased central venous pressure --> increased capillary pressure

    • i.e. "forward" heart failure --> --> sodium retention --> edema
    • i.e. "backward" heart failure --> --> increased hydrostatic pressure --> edema
  97. How is nephrotic syndrome related to edema?
    1. glomerular injury --> proteinuria --> decreased serum protein --> decreased capillary oncotic pressure --> edema

    2. glomerular injury --> increased sodium retention --> edema
  98. How do you treat edema?
    • treat underlying cause
    • salt (NaCl) restriction
    • mechanical measures (e.g. compression hose, limb elevation)
    • diuretics (i.e. block Na reabsorption)
  99. What are the (5) types of diuretics and where do affect the renal tubule?
    • 1. carbonic anhydrase inhibitors: PCT
    • 2. osmotic diuretics: PCT (and other places)
    • 3. loop diuretics: LOH
    • 4. thiazide diuretics: DCT
    • 5. K-sparing: CCD
  100. How do you identify a patient's diuretic threshold dose?
    • case by case
    • observe: watch for marked diuresis 2-4 hours post-dosage
  101. What if furosemide (i.e. loop diuretic) administration causes diuresis but no weight loss?
    suspect diet very high in sodium
  102. What factors contribute to acute diuretic adaptation/tolerance (i.e. "rebound sodium retention") and to chronic diuretic adaptation/tolerance (i.e. "braking phenomenon")
    • 1. general factors (e.g. sodium intake, compliance, NSAID interaction)
    • 2. renal impairment
    • 3. nephrotic syndrome
  103. How can renal impairment contribute to diuretic adaptation?
    • decreased GFR
    • decreased number of funtioning nephrons
    • impaired secretion
  104. How can nephrotic syndrome contribute to diuretic adaptation?
    • binding of free drung in lumen
    • increased volume distribution
    • tubular resistance
  105. How can we treat diuretic adaptation/tolerance?
    • diet: sodium restriction
    • discuss compliance
    • bedrest: increases diuretic effect with severe edema
    • adjust loop diuretic: increase dosage to threshold, decrease sodium retention rebound, switch to IV
    • additive measures: use different types of diuretics to effect more of tubule
    • IV albumin infusion
  106. Where is most of the potassium in the body?
    • 98% intracellular
    • vast majority in muscle cells (least in plasma)
  107. Why is it important to maintain intracellular and extracellular potassium levels and how is this done?
    intracellular/extracellular potassium levels determine resting membrane potential (i.e. excitability)

    Na-K-ATPase pump: 3Na out, 2K in
  108. What happens when you eat a meal with regards to potassium?
    • if K+ stays only in ECV:
    • ECV potassium concentration increases
    • increased K+ uptake by cells
    • increased urinary K+ excretion
  109. What stimulates potassium traffic INTO cell?
    • beta-agonists (e.g. epinephrine)
    • insulin
    • high plasma pH (i.e. alkalosis)
  110. What stimulates K+ traffic OUT OF cell?
    • low plasma pH (i.e. acidosis)
    • osmolality
    • beta-adrenergic blockers
  111. How do beta-agonists (e.g. epinephrine) increase K+ in ICV?
    • 1. directly stimulate Na-K-ATPase pump
    • 2. inhibits effect of (thiazide) diuretics (i.e. decreases K+ secretion effect of thiazide diuretics)
  112. How do beta-adrenergic blockers increase K+ in ECV?
    1. prevents cellular uptake of K+ (via Na-K-ATPase pump?)
  113. What promotes/causes hyperkalemia?
    • beta-adrenergic blockers
    • low plasma pH (i.e. acidosis)
    • osmolality
  114. What promotes/causes hypokalemia?
    • beta-agonists (e.g. epinephrine)
    • insulin
    • osmolality
    • high plasma pH
  115. How does plasma pH determine potassium serum concentration?
    low plasma pH (acidosis) --> K+ out of cell --> increase net positive charge

    high plasma pH (alkalosis) --> K+ into cell --> decreses net positive charge
  116. What determines the amount of urinary K+ excretion?
    K+ secretion into renal tubule (post-filtration and post-reabsorption)

    • TAL (NKCC)
    • DCT: principal cells (Na-K-ATPase pump)
    • CCD: principal cells: aldosterone (Na-K-ATPase & Na/K channels), distal flow of Na/H2O, plasma K+
  117. How does aldosterone affect K+ secretion?
    aldosterone --> increases K+ secretion in CCD

    • 1. increase # of Na/K channels in apical membrane of principal cells
    • 2. increases activity rate of basememnt membrane Na-K-ATPase pumps
  118. What stimulates aldosterone release?
    • low sodium diet
    • low BP
    • increased renin secretion
    • increased plasma angiotensin II

    • increased K+ intake
    • hyperkalemia
    • acidosis
  119. What are the effects of aldosterone stimulation?
    • increased tubular sodium reabsorption (kidney CD)
    • increased K+ secretion (principal cells CD)
  120. How does distal flow rate of Na/H2O relate to K+ secretion?
    distal flow of Na/H2O --> increased sodium flow to CCD lumen --> increased uptake by principal cells

    increased cellular sodium uptake --> increased K+ secretion
  121. How does the serum K+ level affect K+ secretion?
    • 1. increased aldosterone release
    • 2. increased K+ movement into lumen
    • 3. increased activity of Na-K-ATPase in principal cells
  122. Where does virtually all of the urine K+ regulation occur?
    cortical collecting duct of distal nephron of kidney
  123. What happens to the net charge of the renal tubule lumen with increased sodium reabsorption by principal cells?
    increased sodium reabsorption --> increased K+ secretion into lumen (Na-K-ATPase basement memb.) --> increased (-) charge in lumen
  124. How is the renal tubule affected by a change from a normal to a low K+ diet?
    • DCT: secretion of K+ --> reabsorption of K+
    • CCD: high secretion of K+ --> low secretion of K+
  125. Does a high sodium diet affect K+ secretion?
    No

    • dual effect counteracts itself:
    • 1. increased sodium flow to distal nephron --> increased K+ secretion
    • 2. high sodium --> high BP --> decreased aldosterone --> decreased K+ secretion
  126. What happens to cellular resting membrane potential during hyperkalemia? hypokalemia?
    hyperkalemia: K+ efflux --> less (-)/more (+) --> lower threshold --> more excitable

    hypokalemia: K+ influx --> more (-)/less(+) --> higher threshold --> less excitable
  127. What are clinical features of hyperkalemia?
    • muscle weakness (skeletal and cardiac)
    • changes in heart rate
    • bradyarrhythmias
    • sharp/peaked T waves
    • prolonged QRS
    • loss of P waves
    • sine waves on ECG (pre-death)
  128. What 3 fundamental mechanisms determine K+ disorders?
    • 1. intake
    • 2. shift
    • 3. excretion
  129. What are some risk factors for developing hyperkalemia?
    • serum K+ > 6mmol/L
    • rate rise
    • acidosis
    • hypoxia
    • hyperglycemia
    • cell breakdown
    • drugs (e.g beta-blockers and digoxin inhibit Na-K-ATPase)
  130. What contributes to pseudohyperkalemia?
    • cell breakdown
    • hemolysis
    • leukocytosis
  131. What are some clinical features of hypokalemia?
    • muscle weakness
    • fatigue
    • constipation
    • ventilatory failure
    • cardiac arrhythmias
    • rhabdomyolysis (breakdown of muscle fiber)
    • polyuria
  132. What factors can affect the distal delivery of Na/H2O to the CCD?
    • heart failure
    • volume depletion (intense)
    • decreased sodium intake
  133. What inhibits renin production?
    • NSAID
    • beta-blockers
  134. What inhibits renin action?
    renin inhibitors (e.g. aliskiren)
  135. What inhibits ACE action?
    ACE inhibitors (e.g. lisinopril)
  136. What inhibits the action of aldosterone?
    • heparin
    • cyclosporin
    • lacrolimus
    • spironolactone
    • eplerenone
    • aldosterone agonists
  137. What inhibits the production of aldosterone?
    angiotensin receptor (AT1R) blocker (e.g. losartan)
  138. What inhibits the intracellular aldosterone receptors?
    • amiloride triampterene
    • trimethoprim pentamidine
  139. What are the causes and treatments for primary hypo-aldosteronism?
    • causes:
    • adrenal insufficiency (e.g. Addison's disease)

    • tx:
    • hormone replacement: mineral- & gluco-corticoids
    • hydrocortisone
  140. What are the clinical features of primary hypoaldosteronism?
    • hyperkalemia
    • low BP
    • hyponatremia
    • weight loss
    • pigmentation
    • increased ACTH
  141. What are the clinical features of hypo-reninemic hypoaldosteronism?
    acidosis
  142. What are the causes and treatments for hypo-reninemic hypo-aldosteronism?
    • causes:
    • renin is suppressed because of interstitial disease and hypervolemia
    • renal impairment
    • diabetic nephropathy
    • associated metabolic acidosis (Type IV RTA)

    • tx:
    • loop diuretics (e.g. lasix)
    • fludrocortisone
  143. What may contribute to aldosterone resistance?
    • drugs (e.g. K-sparing diuretics, trimethoprim, pentamidine)
    • tubulo-interstial disease
    • (rare) genetic abnormalities
  144. What may contribute to hyperkalemia?
    • intake
    • shift (e.g. hyperglycemia, acidosis, drugs, cell breakdown)
    • decreased nephron # (e.g. renal failure)
    • decreased aldosterone action (e.g. primary hypoaldosteronism, hypo-renin hypoaldosteronism, aldosterone resistance, trimethoprim, pentamidine, K-sparing diuretics, tubulo-interstitial disease, genetic disorders)
    • decreased distal Na/H2O flow (e.g. hypovolemia, heart failure)
  145. How do you treat hyperkalemia?
    • 1. stabilize (IV Ca2+ gluconate)
    • 2. temporary shift (insulin, beta-agonist, albuterol nebulizer, sodium bicarbonate)
    • 3. remove K+ (loop diuretic +/- fludrocortisone, ion exchnage resin for GI, Kayexalate, dialysis)
  146. Can intake be the sole cause of hypokalemia?
    No
  147. What metabolic disorder is associated with hypokalemia?
    metabolic alkalosis
  148. What can cause hypokalemia?
    • beta2-agonists (e.g. albuterol, catecholamines)
    • alkalosis
    • periodic paralysis (e.g. thyrotoxicosis)
    • increased K+ excretion (e.g. diarrhea, vomiting, hyperaldosteronism)
  149. How does vomiting relate to hypokalemia?
    vomiting --> loss of H+ --> alkalosis --> more flow of NaHCO3 --> more K+ secretion

    vomiting --> volume depletion --> low BP --> increased aldosterone --> more K+ secretion
  150. What is the most common cause of hypokalemia?
    diuretics (especially loop diuretics and thiazide diuretics)
  151. How do diuretics contribute to hypokalemia?
    • increase distal flow of NaCl --> increase K+ secretion
    • volume depletion --> increased aldosterone --> increased K+ secretion

    loop diuretics: directly stimulate renin by blocking NKCC in macula densa (i.e. illusion of low flow)
  152. What can lead to metabolic acidosis?
    net effect of loss of base (i.e. loss of base or addition of acid)

    e.g. diarrhea (loss of bicarbonate)
  153. How is acid/base homeostasis maintained?
    • 1. ventilation : CO2 control
    • 2. kidneys: regeneration of HCO3 buffer by excreting acid
  154. How are metabolic disorders diagnosed?
    • 1. arterial blood gas (ABG)
    • 2. anion gap
    • 3. delta/delta (mixed acid base disorders)
    • 4. identify underlying causes
  155. What do you need to know to determine arterial blood gas (ABG)?
    • 1. what is the arterial pH?
    • 2. what is the serum HCO3?
    • 3. check arterial PCO2
    • 4. compensatory responses: baseline never achieved with compensation
    • -lungs: quick compensation (minutes)
    • -kidneys: slow compensation (days)
  156. What type of toxicity may contribute to a mixed acid/base disorder?
    salicylate toxicity (e.g. aspirin)
  157. What type of acidosis disorders feature a raised anion gap?
    • lactic acidosis
    • ketoacidosis
    • renal failure
    • poisoning (e.g. methanol, ethylene glycol, aspirin)
  158. What types of acidosis do not feature an anion gap?
    • GI HCO3 loss (e.g. diarrhea)
    • renal tubular acidosis
  159. What contributes to lactic acidosis?
    • hypotension
    • tissue ischemia
    • lactate levels (e.g. exercise)
  160. What contributes to ketoacidosis?
    • diabetes
    • hyperglycemia
    • serum/urine ketones
    • starvation
    • alcoholic ketoacidosis
  161. Which disorder's causes mimics the causes of hypokalemia?
    metabolic alkalosis
  162. What contributes to metabolic alkalosis?
    net loss of acid

    • volume depletion (e.g. vomiting, diuretics)
    • volume expansion (e.g. hypertension)
    • hyperaldosteronism --> increased H+ secretion, increased Na/H2O flow
  163. How do you treat metabolic alkalosis?
    first: treat more critical condition of hypokalemia

    • volume replacement (normal saline)
    • K+ replacement
  164. What substance increases efferent arteriole pressure?
    angiotensin II
  165. What substance increases afferent arteriole pressure?
    PgE2
  166. What inhibits PgE2?
    NSAID
  167. What controls ADH secretion?
    • physiologic stress (e.g. pain, nausea, etc.)
    • increased osmolality
    • SIADH
    • decreased EABV
    • volume depletion
    • edema (e.g. CHF, cirrhosis, nephrotic syndrome)
  168. What type of potassium disorder develops if you inhibit the renin-angiotensin system?
    hyperkalemia

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