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FERGU > Week 1 Lectures > Flashcards

Week 1 Lectures Flashcards

1
Q

Are RBCs and plasma proteins (i.e albumin) effective osmoles between plasma and ISF?

A

Yes

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2
Q

What is oncotic pressure

A

osmotic pressure exerted by proteins

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3
Q

Are blood vessels walls permeable to salt and water? What is the significance of this?

A

Yes–thus they do not create an osmotic gradient between intravascular and interstitial space

BUT vessels are not fully permeable to proteins therefore albumin stays in the plasma

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4
Q

in the end does the hydraulic/oncotic pressure balance favor retention in the plasma or net movement of fluid out?

A

balance results in slight net movement out–lymphatics return fluid to venous circulation

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5
Q

list causes of edema

A

CHALO (Capillary-Hydraulic–Albumin–Lymphatic–Oncotic)

  1. increased capillary permeability–may occur in sepsis or certain diseases
  2. increased hydraulic pressure–increased plasma volume due to primary sodium retention; venous obstruction; decreased arteriolar resistance (and thus increased volume moving into arterioles)
  3. decreased albumin–from protein loss, particularly in glomerular disease or reduced production
  4. lymphatic obstruction–more fluid trapped in interstitium
  5. increased interstitial oncotic pressure causes more fluid drawn into interstitium
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6
Q

describe the pathophysiology of edema

A
  • -fluid moves out of the intravascular space and into the interstitial space
  • -the issue with this is that the body is extremely protective against shock; as sodium and therefore water are extravasated, the baroreceptors pick this up
  • -this results in the activation of the RAAS system and sodium is retained + vasoconstriction
  • -the trouble with this is that even though sodium is retained for the purpose of restoring inravascular pressure, this does not solve the primary issue, which is whatever let more water get into the ISF anyway
  • –in the case of hypoalbuminemia, the oncotic pressure is too low to keep fluid in the intravascular space
  • -so even though the kidney is “doing the right thing”, water just keeps moving out of the intravascular space and into the interstitium
  • -instead, the patients salt content remains high and thus their fluid load remains high as well
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7
Q

How is Na+ filtered in the golmerulus?

A

it is freely filtered

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8
Q

what is the concentration of the ultrafiltrate in the glomerulus compared to the blood?

A

they are the same (135-145 mmol/L)

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9
Q

What happens at the proximal tubule RE: Na+ and H2O reabsorption?

A

-65% of filtered Na+ and water are reabsorbed together

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10
Q

How is Na+ reabsorption accomplished in the proximal tubule once it has crossed into the cell (i.e how does it cross the basolateral membrane)?

A

Via Na+/K+ ATPase pump in the basolateral membrane

2 steps:

  1. Na+ moves across the apical (luminal) membrane from the lumen into the cell, down an electrochemical gradient established by the Na+/K+ ATPase pump
  2. Na+ moves across the basolateral membrane from the cell into the blood, against its electrochemical gradient, via the Na+/K+ ATPase pump
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11
Q

What else is reabsorbed in the PT?

A

small proteins that were filtered by the glomerulus (reabsorbed via endocytosis)

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12
Q

Describe the two mechanisms by which Na+ crosses the apical membrane (from lumen into cell) in EARLY proximal tubule

A
  1. Na+/H+ antiporter
    - -Na+ entry coupled with H+ exit from cell; H+ secretion results in NaHCO3 reabsorption into blood
  2. NA+/X- symporter–Na+ and X- both enter cell from lumen; X- crosses basolateral membrane into blood via passive transporter; X- = organic solute (glucose, aa’s, Pi, lactate); X- are almost completely removed from tubular fluid
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13
Q

What provides the driving force for reabsorption of H2O by osmosis in the early proximal tubule

A

reabsorption of NaHCO3 and NaX establishes a trans-tubular osmotic gradient that provides the driving force for passive reabsorption of H2O by osmisis

Because H2O is absorbed in excess of Cl- in the early segment of the PT, the Cl- concentration rises along the length of the segment

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14
Q

How does Na+ cross the apical membrane (from lumen into cell) in the LATE proximal tubule?

A
  1. coupled Na+/H+ and Cl-/HCO3- antiporters–Na+ entry coupled with H+ exit from cell; Cl- entry coupled with HCO3- exit from cell; H+ and HCO3- combine in the tubular fluid to form H2CO3 and reenter the cell
  2. paracellular reabsorption of Na+ and Cl- by passive diffusion– established a transcellular osmotic gradient that provides the driving force for the passive reabsorption of water by osmosis

driving force for both mechanisms is the Cl- gradient established in the EARLY proximal tubule

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15
Q

What does “paracellular reabsorption” refer to?

A

reabsorption through tight junction (rather than transcellularly through the cells lining the lumen of the PT)

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16
Q

Through which 2 pathways is water reabsorbed in the proximal tubule?

A

PT is highly permeable to water and it flows from the lumen into the blood via:

  1. transcellularly
  2. paracellularly (through tight junctions)
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17
Q

How much Na+ is reabsorbed in the loop of henle? Where?

A

25% approx (plus Cl- and K+)

Na+ mostly in the thick ascending but to lesser extent in other parts

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18
Q

How much water is reabsorbed in the loop of Henle? where?

A

about 15%

in the descending thin limb

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19
Q

Describe the 3 pathways by which Na+ is reabsorbed in the thick ascending limb of the loop of henle

A

*remember the Na+/K+ ATPase moves Na+ into the blood from the cell and thus sets up a concentration gradient along which Na+ can flow from the TAL

  1. Na+/K+/2Cl- symporter–uses the energy released by the downhill movement of Na+ and Cl- to move K+ uphill into the cell
  2. Na+/H+ antiporter–same as in early PT
  3. paracellular pathway–Na+ (and several other cations)
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20
Q

What is the significance of the TAL being impermeable to water?

A

reabsorption of NaCl and other solutes in the TAL thus reduces the osmolality of tubular fluid to less than 150mOsm/L

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21
Q

How much Na+ is reabsorbed in the distal tubule and collecting duct?

A

about 7% of filtered NaCl

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22
Q

About how much water is reabsorbed in the distal tubule and collecting duct? What does this depend on?

A

about 8-17%, depending on the concentration of ADH

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23
Q

Describe Na+ reabsorption in the early segments of the DT

A
  • Na+ and Cl- enter the cell from the lumen via the Na+/Cl- symporter
  • Na+ leaves the cell and goes into the blood via the Na+/K+ ATPase pump
  • Cl- leaves by diffusion channels in the basolateral cell membrane and paracellularly
  • impermeable to water
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24
Q

What are the 2 cells types relevant to Na+ reabsorption in the late DT and collecting duct?

A
  1. principal cells

2. intercalated cells

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25
Q

How do principal cells participate in Na+ reabsorption in the late DT/CD?

A
  • reabsorb Na+ and H2O and secrete K+
  • Na+ crosses apical membrane through diffusion through Na+ channels
  • Na+ crosses the basolateral membrane via the Na+/K+ ATPase pump
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26
Q

How do intercalated cells participate in Na+ reabsorption in the late DT/CD?

A
  • regulate acid/base balance by either (1) secreting H+ and reabsorbing HCO3- OR (2) secreting HCO3-
  • reabsorb K+ (mech not understood)
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27
Q

Angiotensin II

  1. synthesis
  2. major stimulus
  3. site of action in nephron
  4. effect
A
  1. RAAS
  2. in response to increased renin
  3. PT
  4. increase NaCl and H2O reabsorption
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28
Q

Aldosterone

  1. synthesis
  2. major stimulus
  3. site of action in nephron
  4. effect
A
  1. synthesized by glomerulosa cells in the adrenal cortex
  2. in response to increased AT II and increased plasma K+
  3. TAL; DT/CD
  4. increases NaCl reabsorption; increases NaCl and water reabsorption
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29
Q

ANP

  1. synthesis
  2. major stimulus
  3. site of action in nephron
  4. effect
A
  1. secreted by cardiac atria
  2. in response to increased ECFV
  3. CD
  4. decreases NaCl and water reabsorption
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30
Q

Urodilatin

  1. synthesis
  2. major stimulus
  3. site of action in nephron
  4. effect
A
  1. secreted by DT and CD (not present in systemic circulation)
  2. in response to increased ECFV
  3. CD
  4. decreases NaCl and H2O reabsorption
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31
Q

Adrenalin/NA

  1. synthesis
  2. major stimulus
  3. site of action in nephron
  4. effect
A
  1. sympathetic nerves (adrenaline/NA) and adrenal medulla (adrenaline)
  2. in response to decreased ECFV (i.e bleeding)
  3. PT; TAL; DT/CD
  4. increases NaCl and water reabsorption; increases NaCl reabsorption; increases NaCl and water reabsorption
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32
Q

Dopamine

  1. synthesis
  2. major stimulus
  3. site of action in nephron
  4. effect
A
  1. released by dopaminergic nerves in the kidney, also synthesized by cells of PT (opposes action of adrenalin/NA)
  2. in response to increased ECFV
  3. PT
  4. decreases NaCl and H2O reabsorption
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33
Q

ADH

  1. synthesis
  2. major stimulus
  3. site of action in nephron
  4. effect
A
  1. secreted by posterior pituitary
  2. in response to increased Posm and/or decreased ECFV
  3. DT/CD
  4. increases water reabsorption
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34
Q

Where exactly in the hypothalamus is ADH made?

A

the supraoptic and paraventricular nuclei of the hypothalamus–>then packaged into granules and passed to posterior pituitary where is is released via exocytosis

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35
Q

What triggers ADH release?

A

detection of Posm > 280 mosmol/kg by osmoreceptors in the hypothalamus

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36
Q

What are some other stimuli that can result in ADH secretion?

A
  1. decreased ECFV
  2. AT II
  3. hypoxia
  4. hypercapnia
  5. adrenaline
  6. cortisol
  7. sex steroids
  8. pain
  9. trauma
  10. psychogenic stimuli
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37
Q

How does ADH act?

A

binds to V2 receptors on CD cells and stimulates adenyl cyclase–>this raises cCAMP levels and causes intracellular vesicles containing water channels (AQP2) to fuse with the apical membrane

also binds V1 receptors on vascular smooth muscle cells, causing vasoconstriction and enhancing the effect of aldosterone on Na+ reabsorption in the DT (normal physiological concentrations of ADH are not enough to bind V1 receptors)

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38
Q

where is the JGA located in relation to the sections of the nephron?

A

in the distal tubule, approximately between the early and late distal tubule

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39
Q

What is the key to producing concentrated or dilute urine?

A

the presence of ADH

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40
Q

How does the kidney/nephron produce hypo-osmotic urine? (dilute the urine)

A

to do this, nephron must reabsorb solute from the tubular fluid and not allow water reabsorption to occur–this occurs in the ascending limb of the LoH and in the DT and CD in the ABSENCE OF ADH

  1. proximal tubule reabsorbs isoosmotic fluid with respect to plasma–this fluid enters the descending limb of the LoH
  2. the descending limb is permeable to water, less so to solute–as the fluid descends deeper into the medulla, it encounters an increasingly osmotic medullary interstitium–thus water is reabsorbed due to the osmotic gradient in this region
  3. the fluid then travels to the thin ascending limb–impermeable to water, permeable to NaCl and urea—NaCl is passively reabsorbed, urea diffuses passively into the tubule (volume of tubular fluid remains unchanged in the thin ascending limb, but NaCl decreases and urea increases. More NaCl leaves than urea enters tubular fluid and thus the fluid becomes slightly less concentrated that the surrounding interstitial fluid)
  4. moves to the thick ascending limb–this is impermeable to water and urea–only permeable to NaCl–NaCl = ACTIVELY reabsorbed from tubular fluid, which dilutes the tubular fluid
  5. fluid leaving thick ascending limb is hypo-osmotic relative to the plasma
  6. in the DT and cortical CD, NaCl is actively reabsorbed (impermeable to urea)–in ABSENCE of ADH, the DT/CD are impermeable to water and thus further dilution of tubular fluid occurs with the active reabsorption of NaCl
  7. in the medullary CD, NaCl is actively reabsorbed–slightly permeable to water and urea even in absence of ADH–overall causes FURTHER dilution
  8. urine can be diluted as much as 50 mosm/kg H2O
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41
Q

How does the kidney/nephron generate hyperosmotic urine

A

in presence of ADH

  1. steps until the DT and cortical CD are the same as when you are generating hypo-osmotic urine
  2. remember that the NaCl reabsorbed in the ascending limbs accumulates in the medullary interstitium, and is crucial for the production for hyper-osmotic urine–>this NaCl provides the driving force for water reabsorption by the medullary CD–> COUNTERCURRENT MULTIPLICATION
  3. in the DT and cortical CD, the fluid reaching these areas is hypo-osmotic w respect to surrounding interstitial fluid
  4. ADH increases water permeability of the last half of the DT and CD–> water diffuses out of the tubular lumen and thus tubule fluid osmolality increases
  5. although the fluid at this poin has the same osmolality that entered the descending thin limb, its composition has changed–less NaCl, more urea and other solutes
  6. At the medullary CD, the interstitial osmolality continues to increase as you go down into the medulla–in PRESENCE of ADH, the medullary CD is permeable to water–>tubular fluid becomes increasingly concentrated
  7. ADH also causes increased permeability to urea in the last part of the medullary CD–urea diffuses out of the tubule lumen
  8. urea can be concentrated to about 1200 mosmol/kg H2O–high concentreations of urea and other nonreabsorbed solutes
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42
Q

What are the two major classes of membrane transport proteins in the kidney?

A
  1. transporters/carriers–>bind a specific solute–>conformational change–>transfer solute
  2. channels–>interact with solute more weakly–>aqueous pores that allow specific solutes (usually inorganic ions of appropriate size and charge) to pass thru–>faster than transporters/carriers
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43
Q

What is primary active transport

A

linked to ATP hydrolysis (i.e Na+/K+ ATPase

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44
Q

What is secondary active reabsorption?

A

2 or more substances interact with a specific membrane protein, does not require ATP

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45
Q

What is secondary active secretion?

A

counter-transport

i.e Na+/H+ exchanger on apical side

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46
Q

Name a diuretic that works in the Proximal Convoluted Tubule

A

Carbonic Anhydrase Inhibitor

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47
Q

Where do Carbonic Anhydrase Inhibitors work?

A

the PCT

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48
Q

Name 5 types of diuretics

A
  1. carbonic anhydrase inhibitorys
  2. loop diuretics
  3. thiazide diuretics
  4. K+ sparing diuretics
  5. osmotic diuretics
  6. V2 antagonist
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49
Q

Name a carbonic anhydrase inhibitor

A

Acetazolamide

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50
Q

What type of drug is Acetazolamide

A

a carbonic anhydrase inhibitor (diuretic)

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51
Q

MOA of carbonic anhydrase inhibitors

A

Inhibit Na+ and HCO3- reabsorption by inhibiting carbonic anhydrase (CA)

  1. in the lumen of the tubule, CA reversibly catalyzes the conversion of H2CO3 to CO2 and H2O, a critical step in the reabsorption of HCO3-
  2. CO2 crosses the PT membrane, reacting with H2O inside the cell
  3. CA in the cytoplasm of PT cells catalyze the reformation of H2CO3
  4. H2CO3 dissociates into HCO3- and H+–HCO3- is transported into the interstitium and H+ is recycled back into the lumen of the nephron in exchange for Na+
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52
Q

Name a diuretic that works in the loop of henle

A

Loop diuretics

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53
Q

Name a loop diuretic

A

furosemide

54
Q

Where does furosemide work and what type of drug is it?

A

works in the loop of henle

it is a loop diuretic

55
Q

MOA of loop diuretics/furosemide

A

inhibits the Na+/K+/2Cl- co-transporter in the thick ascending limb o the LoH

  1. less Na+, K+ and Cl- ions are reabsorbed from the lumen of the tubule
  2. reduction in the electrochemical gradient abolished the paracellular transport of Ca2+ and Mg2+ ions
  3. Normally, the gradient is set up by the channels which allow K+ ions to move back into the lumen and Cl- ions to move into the interstitium
  4. the +/- gradient allows Ca2+ and Mg2+ ions to move downstream, towards the -ve charge in the interstitium
  5. extra Na+ in the lumen is reabsorbed downstream in exchange for intracellular H+ and K+–results in hypokalemia and metabolic alkalosis
56
Q

Name a diuretic that works in the DCT

A

Thiazide diuretics

57
Q

Name a thiazide diuretic

A

Hydrochlorothiazide

58
Q

Where does hydrochlorothiazide work, and what type of drug is it?

A

in the DCT of the nephron

it is a thiazide diuretic

59
Q

MOA of thiazide diuretics/hydrochlorothiazide

A

inhibits the Na+/Cl- co-transporter in the DCT

  1. less Na+ and Cl- are reabsorbed from the lumen of the tubule
  2. extra Na+ in the lumen is reabsorbed downstream in exchange for H+ and K+–hypokalemia and metabolic alkalosis
  3. Ca2+ in the lumen is reabsorbed by a poorly understood mechanism–hypercalcemia
60
Q

Name a diuretic that works in the collecting duct of the nephron

A

K+ sparing diuretics (aldosterone antagonists)

K+ sparing diuretics (ENaC blockers)

61
Q

Name a K+ sparing diuretic (aldosterone antagonist)

A

Spironolactone

62
Q

What type of drug is spironolactone and where does it act

A

K+ sparing diuretic (aldosterone antagonist)

in the Collecting Duct

63
Q

MOA of K+ sparing diuretics (aldosterone antagonists) /spironolactone

A

acts as an antagonist at the mineralocorticoid receptor (MR) for aldosterone

  1. normally, the MR-aldosterone complex translocates to the nucleus where it acts on DNA to increase the expression of epithelial Na+ channels (ENac) and Na+/K+ ATPase pumps on the luminal and basolateral membranes, respectively
  2. Blocking the MR thus reduces the Na+ reabsorption, producing natriuresis and diuresis
  3. reducing the basolateral concentration of Na+/K+ ATPase also causes a reduction in the excretion of K+ (therefore sparing it)
64
Q

Name a K+ sparing diuretic (ENaC blocker)

A

Triamterene, amiloride

65
Q

Where do triamterene and amiloride work? What type of drug are they?

A

Collecting Duct

K+ sparing diuretics (ENaC blockers)

66
Q

MOA of K+ sparing diuretics (ENaC blockers)/Triamterene/Amiloride

A
  1. inhibit ENaC on the luminal membrane, preventing Na+ from moving from the tubular lumen into the cell
  2. This keeps Na+ in the lumen of the tubule, therefore facilitating natriuresis and diureses
  3. Reduced entry of Na+ into the cell also reduces the amount of Na+ that can be exchanged for K+ at the ATPase pump–with the Na+/K+ ATPase pump unable to exchange Na+ for K+, the K+ stays in the bloodstream (K+ sparing)
67
Q

Where do osmotic diuretics act

A

operate throughout the renal tubule

68
Q

Name an osmotic diuretic

A

Mannitol

69
Q

What type of drug is mannitol?

A

osmotic diuretic

70
Q

MOA of osmotic diuretics/mannitol

A

freely filtered and poorly reabsorbed inert chemicals that stay in the tubule and therefor pulling water into the tubule via an increase in oncotic pressure

limited use as a diuretic
mainly used for non-diuretic indications such as an increase in intracranial pressure

avoid if patient experiences renal failure and has a low GFR

71
Q

Where do V2 antagonists work?

A

Collecting Duct

72
Q

Name a V2 antagonist

A

Tolvaptan

73
Q

MOA of V2 antagonists/Tolvaptan

A

Acts as a V2 receptor antagonist–therefore, prevents the recruitment of aquaporins at the collecting duct (blocks action of ADH)

promotes “water diuresis” with minimal impact on the electrolytes

future drug

74
Q

Benefit for using carbonic anhydrase inhibitors

A

inhibiting production of CA means that it will also inhibit production of aqueous humor, which means it can be used for GLAUCOMA

it results in loss of HCO3-, treating metabolic alkalosis

also used to treat acute mountain sickness (mechanism unknown, but it is thought that CA may contribute to CSF production)

75
Q

Adverse effects/disadvantages of Carbonic Anhydrase Inhibitors

A

works early in proximal tubule and so much Na+ is reabsorbed later making the drug less effective

side effects include metabolic acidosis, renal stones and hypokalemia

76
Q

Benefits of K+ sparing diuretics

A

prevents compensatory loss of K+ in the DT and CD and thus conserves body K+

spironolactone has a short half life (1-2 hours) but has an active metabolite that has a half life of 16 hours

can be used to treat hyperaldosteronism (spironolactone)

may prevent aldosterone aided heart failure (they reduce all cause mortality)–(spironolactone)

available in fixed dose combinations with hydrochlorothiazide

77
Q

adverse effects/disadvantages of K+ sparing diuretics

A

causes hyperkalemia, metabolic acidosis

spironolactone itself causes gynecomastia, mentural disorders, testicular atrophy, CV injury

78
Q

Benefits of loop diuretics

A

“high ceiling” diuretics

work on apical side of the lumen (must be filtered or secreted by the PT to work–NSAIDS can inhibit this secretion)

used for edema, HTN and acute hypercalcemia

more potent than thiazides

79
Q

adverse effects/disadvantages of loop diuretics

A

may reduce expected calcium and magnesium levels in the body (although some Ca2+ recovered later in nephron)

can cause alkalosis through loss of H+

is a sulfa drug–>allergies

SEs incldue electrolyte imblanaces, metabolis alkalosis, ototoxicity, hyperuricemia

they are bound to albumin, higher levels of albumin means there is less diuretic to work in the tubules

may cause much K+ loss

80
Q

Benefits to thiazide diuretics

A

acts in the DT–less compensatory mechanisms of Na+ reabsorption happening after this

promote Ca2+ reabsorption (mechanism not understood but inhibit renal stone function formation)

acts as vasodilators and decreases BP

act at luminal side (in the tubules–must be secreted through PT)

may be used for HTN, edema, or nephrogenic diabetes insipidus

has a flat dose response curve

81
Q

adverse events/diadvantages to thiazide diuretics

A

may cause alkalosis by excretion of H+ ions (secondary passive exchange)

may cause much K+ loss

looses magnesium as well

becomes ineffective ones creatinine clearance goes below 30-50mL/min (they need a FUNCTIONING KIDNEY to work)

is a sulfa drug–allergies

SE include electrolyte disturbances, metabolic alkalosis, impaired glucose tolerance, hyperlipidemia, hyperuricemia, impotency

82
Q

What types of findings can be seen on a urinary dipstick?

A
  1. glucose with or without ketones
  2. nitrites and/or WBC
  3. hematuria or proteinuria (isolated or concurrent)
83
Q

How is glucose detected on urinary dipstick?

A

with Glucose detectin: enzymatic test (glucose oxidase)

84
Q

How are ketones detected on urinary dipstick?

A

nitroprusside reaction detects ACETOACETATE and ACETONE–it does not detect beta hydroxybutarate

85
Q

In what conditions will glucose be present in the urine

A
  1. Diabetes Mellitus–glucose concentration exceeds 10mmol/L in serum
  2. Renal glycosuria–renal tubular resporption defect

also: pancreatitis, pancreatic carcinoma, pheochromocytoma, Cushings, shock, burns, pain, steroids, hyperthyroidism, renal tubular disease

86
Q

In what conditions will ketones be present in the urine?

A
  1. Diabetic ketoacidosis–diabetics without insulin cannot use glucose for fuel, so they start breaking down fats, which will produce ketones and lead to ketoacidosis–will have BOTH glucose and ketones in urine/blood
  2. fasting or starvation states

also, high fat diet, vomiting, diarrhea, hyperthyroidism, febrile state esp. in children, aspirin overdose

87
Q

How are nitrites detected on urine dipstick?

A

Humans excrete nitrates, which are turned into nitrites by bacterial nitrite reductase

88
Q

How are leukocytes detected on urine dipstick?

A

detects both lysed or intact leukocytes based on the presence of leukocyte esterase (an intracellular leukocyte enzyme)

89
Q

In what condition are nitrites present in the urine?

A

bacteriuria

false negatives: enterococci, streptococci, staphylococci

90
Q

in what conditions are leukocytes present in the urine?

A

inflammation (pyuria)

false negative results may occur in the presence of high urinary protein or ascorbic acid
–confirmatory test is microscopic analysis and culture

91
Q

How is blood detected on urine dipstick analysis

A

test detects peroxidase-like activity associated with hemoglobin

92
Q

how is proteinuria detected on urine dipstick

A

works on the principle that a change in protein concentration changes the ionic strength of the solution and leads to a color change in a pH sensitive dye in proportion to the ionic strength

normal is

93
Q

In what conditions might you find blood in urine?

A

hematuria, hemoglobinuria, myoglobinuria

94
Q

List possible causes/reasons for detection of blood (hematuria) on urine dipstick

A
  1. hematologic–coagulopathy, sickle hemoglobinopathy
  2. renal–(a) glomerular–primary glomerular disease, multisystem disease like systemic lupus and (b) nonglomerular–renal infarction, TB, pyelonephritis, tumor, trauma, polycystic kidney disease
  3. post renal–stones, tumor of ureter/bladder/urethra, cystitis, TB, prostatitis, urethritis, BPH
95
Q

List the most common reasons for nontraumatic hematuria from most common to least

A
  1. kidney stones
  2. carcinoma of kidney or bladder
  3. urethritis
  4. UTI
  5. BPH
  6. glomerulonephritis
96
Q

Why might there be protein detected on urine dipstick

A
  1. glomerular defect–lets by too much protein
  2. tubular defect–cant reabsorb proteins properly
  3. overflow proteinuria–Bence Jones protein

also: pyelonephritis, glomerulonephritis, glomerular sclerosis (diabetes), nephrotic syndrome, myelome, postural causes, preeclampsia, malignant HTN, CHF

97
Q

what does hematuria + proteinuria indicate regarding cause of pathology?

A

indicates the hematuria is from a renal source i.e like glomerulonephritis

98
Q

What are renal casts

A
  • formed cylindrical structure organized in the nephron
  • form following urine stasis (protein ppt)
  • acid pH, high salt, reduce urine flow and protein contribute to formation
  • appearance is determined by matrix (hyaline, granular, waxy) and trapped cellular constituents (rbcs, leukocytes, epithelial cells)
  • ID may be difficult but importnat (because reflects underlying renal pathology)
99
Q

what is an erythrocyte cast and what does it indicate pathologically

A

also known as RBC casts–they contain distinct RBCs

they indicate renal bleeding, glomerular injury

100
Q

what are renal tubular epithelial casts and what do they indicate pathologically

A

they contain intact or necrotic epithelial cells

renal tubular injury (acute tubular necrosis)

101
Q

what are coarse granular casts and what do they indicate pathologically

A

they are coarse refractile granules

they indicate cell degeneration and proteinuria

102
Q

What are fine granular casts and what do they indicate pathologically

A

they are semitransparent

they are non specific in etiology

103
Q

what are broad (waxy) casts and what do they indicate pathologically

A

wide width cast, formed in dilated tubules

indicate advanced renal disease

104
Q

what are leukocyte casts and what do they indicate pathologically

A

contain segmented neutrophils

indicate pyelonephritis

105
Q

what are hyaline casts and what do they indicate pathologically

A

nonspecific transparent cast

increase with exercise, dehydration and fever

106
Q

what are fatty casts and what do they indicate pathologically

A

they are refractile droplets

lipiduria, NEPHRITIC syndrome

107
Q

What are urine crystals?

A
  • common, mostly not diagnostically significant
  • usually form after voiding when urine is supersaturated with chemical constituents
  • types depend on pH of urine
108
Q

List types of acid urine crystal

A
  1. normal/common: URIC ACID, amorphous urates, sodium urate
  2. CYSTEIN (cysteinuria)
  3. cholesterol (rare, nephritic syndrome)
  4. leucine, tyrosine (rare, liver disease)
  5. bilirubin (liver disease)
  6. URIC ACID crystals
109
Q

List the types of acid, neutral, to slightly alkaline crystals

A

CALCIUM OXALATE

110
Q

list the types of alkaline urine crystals

A
  1. TRIPLE PHOSPHATE (ammonium Mg phosphate)

2. idinavir crystals (HIV patient)

111
Q

What urinary crystals might you find in an HIV patient

A

idinavir crystals

112
Q

What is a normal RBC count in urine

A
113
Q

What diseases cause an increase in RBCs in urine

A
  • variety of urinary tract diseases (prostatitis)

- dysmorphic = glomerular bleeding

114
Q

what is normal WBC levels in urine?

A
115
Q

what does an increased WBC count in urine mean

A

indicates urinary tract inflammatory and infectious disorders

116
Q

what is the normal amount of renal tubular epithelial cells in urine

A
117
Q

what do increased renal tubular cells in urine indicate

A

indicates tubular injury

118
Q

what are oval fat bodies

A

lipid laden renal cells

119
Q

what do oval fat bodies indicate pathologically when in urine

A

NEPHROTIC syndrome

120
Q

what are transitional epithelial cells

A

large and oval with central nucleus

121
Q

what do the presence of transitional epithelial cells in urine mean

A

inflammatory and malignant conditions

122
Q

where do squamous epithelial cells in urine come from

A

from distal urinary tract and female genital tract

largest cells found in urine

123
Q

are the presence of squamous epithelial cells in urine significant

A

not clinically

124
Q

what are the major pathogenic mechanisms of glomerular disease? (list)

A
  1. immune mechanism–antibody mediated and cell mediated
  2. hemodynamic–hyperperfusion/hyperfiltration and ischemic
  3. podocyte injury
  4. polyanion loss
  5. metabolic–familial, acquired
125
Q

Describe the immune mechanisms of glomerular disease

A
  1. antibody mediated–(a) immune complesex i.e post-infectious glomerular nephritis or (b) antibodies against the basement membrane i.e Goodpasture’s disease, rapidly progressive glomerular nephritis
  2. cell-mediated–possible T cell involvement in minimal change disease
126
Q

In the antibody mediated mechanism of glomerular disease, where can antibodies deposit and how does this affect symptoms?

A

either:
1. in the subendothelial/mesangial (blood vessel) side–inflammation

  1. in the subepithelial (podocyte) side–no inflammation
127
Q

Describe the hemodynamic mechanisms of glomerular disease

A
  1. hyperperfusion/hyperfiltration–increased pressure stretches podocytes causing damage
  2. ischemic–ischemia causes collagen deposition in bowman’s capsule and shrinkage of the glomerular tuft–i.e benign nephrosclerosis
128
Q

describe podocyte injury as a mechanism of glomerular disease

A

mediated by mechanical, infection, chemical or metabolic causes

i.e focal segmental glomerulosclerosis

129
Q

describe the polyanion loss mechanism of glomerular disease

A

loss of negative charge on basement membrane allowing the negatively charged albumin to move into bowman’s capsule–ie minimal change disease

130
Q

describe metabolic mechanisms of glomerular disease

A
  1. familial–ie Fabry’s disease, cystinosis
  2. acquired–i.e diabetes mellitus; overstimulation of mesangial cells leads to an increase in matrix secretion and glycosylation of matrix component prevents degredation–thickened basement membrane prevents proper filtration
131
Q

Normal urinalysis levels RE:

  1. clarity/turbidity
  2. pH
  3. specific gravity
  4. glucose
  5. ketones
  6. nitrites
  7. leukocyte esterase
  8. bilirubin
  9. RBCs
  10. WBCs
  11. protein
  12. squamous epithelial cells
  13. casts
  14. crystals
  15. bacteria
  16. yeast
A
  1. clear or cloudy
  2. 4.5-8
  3. 1.005-1.024
  4. less than 130 mg/d
  5. none
  6. negative
  7. negative
  8. negative
  9. less than 2-3 per hpf
  10. less than 2-5 per hpf
  11. less than 150 mg/d
  12. less than 15-20 per hpf
  13. 0-5 hyaline casts per hpf
  14. occasionally
  15. none
  16. none

FERGU (9 decks)

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