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Renal > Clinical Correlations of Renal Physiology and Disease > Flashcards

Clinical Correlations of Renal Physiology and Disease Flashcards

1
Q

Exaplain the relationship between normal water input and output

A

input it 1-1.5 L

output is 1-1.5 in urine and 0.5 in insensible loss like stool, sweat, and pulmonary

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2
Q

WHat is osmolarity? What is the bigegst component?

A

Osmolarity is total solute/ECF volume

biggest component is Na (140mEq/L and is regulated by amount of ECW)

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3
Q

how does the body respond to hypertonicity?

A

It wants to get back to isotonicity!

  • stimulate hypothalamic receptors
  • increase thirst which increases water intake
  • also increase ADH release which causes renal water retention
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4
Q

How does the body respond to hypotonicity?

A

it wants to get back to isotonicity!

  • inhibit hypothalamic receptors
  • decrease ADH release which leads to renal water excretion
  • also decrease thirst which leads to decreased water intake
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5
Q

What 2 things stimulate ADH release?

A
  1. osmoreceptor control
  2. baroreceptor control
    1. hypovolemia (low Na) is the main driver
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6
Q

How does osolarity chaneg throughout the tubular fluid?

A
  • iso-osmotic in the proximal tubule
  • in the descednign loop of henle is increases in osmolarity
  • in the ascending loop of henle is decreases in osmolarity
  • it slowly increases throughout the distal tubule and collecting tubule and duct
  • drastically increases in the medullary collecting duct until it is a concentrated urine! ADH is responsible for the big incerase in osmolarity!
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7
Q

A man drinks a gallon of wate then runs, he is hypovolemic. what lead him to osmotic failure?

A

He had hypovvolemia due to sweating and losing Na. so he did like decrease ADH leading to renal water excretion like he should have!

He also ignore his decreased thirst and drank water anyway!

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8
Q

What are the clinical manifestations of hyponatremia?

A

prominent when change in Na occurs rapidly

signs and symptoms:

  • nausea
  • vomiting
  • weakness
  • headache
  • lethargy
  • seizures
  • respiratory depression
  • death
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9
Q

What factors alter water balance?

A
  • appropritely elevated ADH
    • volume depletion
  • excessive water intake
    • hypotonic fluids
  • altered renal water handling
    • chronic kidney disease
  • inappropriate secretion of ADH
    • Cancer (eg small cell lung)
    • CNS disease
    • pulmonary disease
    • drugs
      • narcotic
      • antiemetics
      • SSRIs
      • antipsychotics
      • antiseizure
    • HIV
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10
Q

what is the primary determinant of ECF osmolarity? ECF osmolarity is tightly regulated by what?

A

primary determinant of ECF osmolarity is Serum Na

ECH osmolarity is tightly regulated by changes in thirst and ADH secretion

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11
Q

What is required to prevent hypoosmolarity due to increased water intake?

__________can precipitate hyponatremia and hypoosmolarity since urinary dilution is impaired (osm>300mOsm/kg0

A

excretion of dilute urine (osm<100mOsm/kg) is required to prevent hypoosmolarity due to increased water intake

inappropriately elevated ADH can precipitate hyponatremia and hypoosmolarity since urinary dilution is impaired (osm>300mOsm/kg)

(what happen to the hyovolemic man)

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12
Q

What is glomerular filtration rate? what is it usually estimated on?

A

GFR: amount of plasma filtered through glomeruli per unit time

usually estimated based on serum creatine

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13
Q

what is serum creatine? what is it used for? what are its limitations?

A
  • breakdown product of skeletal muscle
  • production remains constant over time
  • filtered at the glomerulus (like inulin) and creatine clearance can be used to estimate GFR
  • the fold increase in serum Cr estimates the fold decrease in GFR (ie if Cr double GFR 1/2s)
  • limitations: ulike inulin, creatine is also secreted in the nephron and creatine clearance overestimates GFR
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14
Q

What is the equation for Creatine Clearance?

A
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15
Q

What is the Cockcroft-Gault equation? and what do you multilpy by if female?

A

If female multiply by 0.85

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16
Q

GFR under what value is often underestimated with the MDRD equation, so labs using MDRD should only report those as ______`

other than MDRD what other equation is often used to represent GFR?

A

GFR>60 often underestimated with MDRD, so labs using MDRD should onyl report those as >60

CKD-EPI also used

17
Q

Serum creatine can be used to estimate GFR is what 3 things are true? When are creatine based measures of GFR inaccurate?

A
  1. CrCl can be calculated by U*V/P
  2. GFR can be estimated by Cockcroft-Gault
  3. the fold change in serum Cr can estimate the fold chaneg in GFR

serum creatine based GFR estmates can be inaccurate due to extremes of age, obesity or muscle mass

18
Q

what 3 inputs influence control of tubular Na reabsorption?

A

renal sympathetic tone

hormonal

blood pressure

these inputs ultimately effect tubular Na channels and transporters

19
Q

What 2 things directly effect the tubule? and what is their effect?

A
  • renal sympathetic nerves:
    • multiple tubular receptrs stimulate Na reabsorption
  • Angiotensin II
    • tubular receptors
    • increases activity of proximal tubule Na/H counter transporter
    • aldosterone excretion
20
Q

How does aldosterone influence tubular Na reabsorption?

A
  • stimulates Na reabsorption in cortical collecting duct principal cells
  • about 2% of filtered load of Na has its excretion dependent on aldosterone action
  • increases number of luminal Na channels and basolateral Na/K/ATPases
21
Q

_____ activation leads to ADh release

A

baroreceptor activation leads to ADH release to control water reabsorption

22
Q

mechanistically how does ADH stimulate increased water reabsorption on the late distal tubules, colecting tubules and colelctingducts?

A

ADh binds to the receptor which is a Gs (GPCR) which activates AC which increases concentration of cAMP which activates PKA whic leads to placement of aquaporin channels to increase water reabsoprtion

23
Q

what is the osmolarity of urine?

A

1200

24
Q

the systemic respone to decreased ECF volume involves what 3 things? What do these factors lead to? How is this clinically reflected?

A
  • baroreceptor and sympathetic nerve activation
  • activation of renin-angII-aldo system
  • increased ADH

these 3 factors (inresponse to decreased ECF volume) lead to enhanced renal tubular Na and water reabsorption

this is clinically reflected by low urine Na, low FENa, and elevated urine osmolarity

25
Q

serum ca levels are regulated by what? what do these 2 things lead to?

A
  • serum Ca level is regulated by PTH and 1, 25, OH vitamin D levels which act to increase serum Ca
    • PTH leads to increased resorption from boen
    • 1, 25 OH vitamin D increases intestinal absorption
26
Q

What happens to 25-OH Vit D in the kidney?

A

25-OH Vit D is converted to 1, 25-OH Vit D (active form) in the kidney

27
Q

______ is reposnible for phosphate excretion

A

kidneys is also responsible for phosphate excretion

high serum phos levels increase PTH secretion that leads to less phosphate reabsorption in the renal tubule

28
Q

So what do we see in kidney disease?

A
  • Low 1, 25 OH vitamin D levels
    • low serum Ca
  • Less phosphate excretion in urine
    • high serum phosphate levels
  • low serum Ca and high serum phosphorous leads to increase in PTH secretion
  • High PTH leads to calcium reabsoprtion from bone to increase serum Ca (unfortnately this causes even higher phosphorous)
29
Q

SO how does chronic kidney disease impact active vitamin D production? what does this lead to?

A

chronic kidney disease decreases active vitamin D production leading to decreased calcium absorption, hypocalcemia, and secondary hyperparathyroidism

leads to phosphorous retention leading to secondary hyperparathyroidism

secondary hyperparathyroidism leads to increase bone turnover and extraosseous calcification

Renal (7 decks)

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