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M1 Block 4 > Week 3 > Flashcards

Week 3 Flashcards

1
Q

OPC: What are 1 common dysfunctions of the sacrum?

A

L on L torsion

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2
Q

OPC: For sacrum, what might you deduce if there is asymmetry at the base but not the ILA?

A

Means there is more likely a innominent dysfunction than a sacral dysfunction

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3
Q

CPR: How do you calculate filtration fraction?

A

FF = GFR/RPF

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4
Q

CPR: What is normal FF?

A

Normal FF is 20%

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5
Q

CRP: What can you use to estimate renal plasma flow? Why?

A
  • Est via PAH
  • Since PAH is 100% excreted and largely secreted by the PCT
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6
Q

CPR: What do you use to estimate GFR?

A

Est. via creatinine clearance

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7
Q

CPR: How to calculate renal clearance?

A

Cx = (Ux * V) / Px

where X is substance
U is urine concentration substance
V is urine flow rate
P is plasma concentration

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8
Q

CPR: What is Renal clearance

A

Volume of plasma cleared of a substance in a defined amount of time

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9
Q

CPR: What does Mannitol do to fluid movement in the body?

A

Mannitol infusion puts lots of solutes into the ECF which drives water out of the ICF into the ECF

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10
Q

CPR: What makes up the basement membrane of the glomerulus?

A

Type 2 Collagen

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11
Q

CPR: Explain changes to GFR, RPF, and FF change when:
Afferent arteriole constriction

A

Afferent arteriole constriction:
- GFR decreased
- RPF decrease
- Filtration fraction is unchanged

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12
Q

CPR: Explain changes to GFR, RPF, and FF change when:
Efferent arteriole constriction

A

Efferent arteriole constriction:
- GFR increased
- RPF decreased
- Filtration fraction increased

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13
Q

CPR: Explain changes to GFR, RPF, and FF change when:
Increased plasma oncotic pressure

A

Increased plasma oncotic flow:
- GFR: decreased
- RPF: unchanged
- Filtration fraction: decreased

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14
Q

CPR: Explain changes to GFR, RPF, and FF change when:
Decreased plasma oncotic pressure

A

Decreased plasma oncotic pressure
- GFR: increased
- RPF: Unchanged
- Filtration fraction: increased

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15
Q

CPR: CPR: Explain changes to GFR, RPF, and FF change when:
Increased ureteral constriction

A

Increased ureteral constriction
- GFR: Decreased
- RPF: no change
- Filtration fraction: decreased

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16
Q

CPR: CPR: Explain changes to GFR, RPF, and FF change when:
Dehydration

A

Dehydration:
GFR: Decreased
RPF: Decreased?
FF: Increased b/c RPF decreases even more than GFR

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17
Q

CPR: Explain Prostaglandin effects in the kidney
What inhibits prostaglandins?

A
  • Afferent arteriole vasodilation (counteract Ang II)
  • NSAIDS are COX inhibitors which can block prostaglandin production allowing too much vasoconstriction
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18
Q

CPR: How to calculate eGFR?

A

eGFR = U creatinine * V / P creatinine

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19
Q

CPR: How do you calculate RBF?

A

RBF = RPF/ (1-Hct)

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20
Q

CPR: Where is glucose reabsorbed?

A
  • 100% of glucose is reabsorbed in the Proximal convoluted tubule
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21
Q

CPR: When does Glucose start to saturate _____________ transporters?

A

SGLT2 transporters saturated when glucose is > 200 mg/min

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22
Q

CPR: Why might pregnant women have glucosuria?

A
  • During pregnancy blood volume increases
  • Increase in GFR resulting in increased glucose filtration which can oversaturate SGLT2 transporters so some glucose gets into the urine
  • Can occur even when plasma glucose is normal
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23
Q

CPR: What are extrinsic factors contributing to control of GFR?

A
  • Extrinsic = neurohumoral
    1. SNS
    2. Ang II
    3. Prostaglandins
    4. Endothelial-derived nitric oxide
    5. Endothelin
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24
Q

CPR: What are intrinsic factors contributing to control of GFR?

A

Intrinsic = local = autoregulation =
1. Myogenic mechanism
2. Macula densa

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25
Q

CPR: Describe the _________________ myogenic mechanism and the effect it exerts on GFR

A
  • B/t 60-160 MAP, the GFR needs to maintain constant renal blood flow
    1. Increasing stretch of the blood vessels, the body senses there is increased MAP
    2. The stretching activates stretch sensitive Ca+2 receptors on the afferent arterioles = vasoconstriction
    1a. Decreased stretch of the blood vessels, the body senses a decrease in MAP
    2a. Without stretch, the Ca+2 sensitive receptors are closed and allow the afferent arteriole to dilate
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26
Q

CPR: Describe how the ________________ tubuloglomerular feedback at the macula densa exerts its effect on the GFR when there is increased MAP

A
  • On the DCT, the macula densa senses increased MAP which means increased GFR. Increased GFR means increased NaCl filtered which tells the juxtaglomerular cells proximal to the afferent arteriole to constrict causing afferent arteriole constriction
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27
Q

CPR: Describe how the ________________ tubuloglomerular feedback at the macula densa exerts its effect on the GFR when there is decreased MAP

A
  • On the DCT, the macula densa senses decreased MAP and thus there is decreased GFR meaning there is decreased NaCl filtration. This tells the juxtaglomerular cells to allow the afferent arteriole to vasodilate
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28
Q

CPR: Other than glucose, what is reabsorbed at the PCT?

A

~ 70%: Na+, Cl-, PO 4 -3 , K+, HCO 3 -

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29
Q

CPR: Where are SGLT2 transporters? What do they do?

A
  • They are cotransporters that move Na+ and glucose from the PCT to the cell
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30
Q

CPR: Describe how HCO 3 - , _________________, moves into the peritubular capillary in the PCT

A
  • Uses bicarbonate buffer system
  • CO2 can freely diffuse from the PCT to the cell since it is a gas
  • In the cell, carbonic anhydrase converts to CA & H2O and is subsequently transformed into: HCO 3 - & H+
  • Lastly, a HCO 3 - /Na+ cotransporter moves these molecules from cell to peritubular capillary
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31
Q

CPR: How does PTH affect reabsorption at the PCT?

A
  • Parathyroid hormone decreases Na+/PO 4 -3 cotransport to peritubular capillary
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32
Q

CPR: Describe what happens at the thick ascending loop of Henle

A
  • Urine dilution due to reabsorption of Na
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33
Q

CPR: Describe how Na is reabsorbed at the Thick ascending loop of Henle

A
  1. Na/K+ ATPase active transporters at the peritubular cell side push Na+ out of the cell against its gradient
  2. On the loop side, K+ channels drive [K+] down its concentration gradient and out of the cell into the thick ascending loop
  3. This has created a gradient for the NaKCC channels to reabsorb: Na+, 2 Cl-, K+ to come into the cell
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34
Q

CPR: Describe how Mg+2 and Ca+ are reabsorbed in the Thick Ascending loop of Henle

A
  1. Both use paracellular movement from the loop to move into the peritubular capillary
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35
Q

CPR: Describe K+ and Cl- reabsorption from the cell into the Peritubular capillary at the Thick Ascending loop of Henle

A
  1. High [K+] in the cell
  2. Increased [Cl-] concentration due to co-transport with Na+ drives both K+ and Cl- to use passive transport down their concentration gradients out of the cell and into the peritubular capillary
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36
Q

CPR: Describe reabsorption at the Thin descending loop of Henle

A
  • Here only permeable to H2O
  • This portion of the nephron is very salty which creates a concentration gradient to pull water out of the loop and into the medulla
  • Urine concentration occuring here
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37
Q

CPR: What is Bartter syndrome? What happens to the urine and plasma?

A
  • Autosomal recessive disorder
  • Defect in the NaKCC channels that disallows reabsorption of Na, K+, Cl- from the renal tubule into the cell
  • Causes: metabolic alkalosis, hypercalciuria, hypokalemia
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38
Q

CPR: Describe the gradient that influences movement of Mg+2 and Ca+2 into the peritubular capillary at the thick ascending loop of Henele

A
  • On the apical side of the cell that faces the loop, there is excretion of K+ ions down the concentration gradient that makes the loop + charged overall
  • This + charge creates a Mg+2 & Ca+2 concentration gradient to make these + ions want to flow down via paracellular movement to the peritubulular capillary
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39
Q

CPR: Describe the movement of Na+ & Cl- in the Distal convoluted tubule

A
  1. Na+ & Cl- use a symporter on the apical side for reabsorption
  2. On the basal side, uses active transport- Na+/K+ ATPase to move sodium into the peritubular capillary
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40
Q

CPR: Which side is apical and basal of the cells in the nephron

A
  • APICAL SIDE FACES THE LUMEN OF THE TUBULE
  • BASAL SIDE FACES THE PERITUBULAR CAPILLARY
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41
Q

CPR: Describe the movement of Mg+2 and Ca+2 at the DCT

A
  • On the apical side, both flow down the concentration gradient using individual transporters for each
  • On the basal side, Ca+ is reabsorbed into the peritubular capillary via Ca+ efflux and Na+ influx (Na+ moving with its concentration gradient which is secondary active transport)
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42
Q

CPR: Describe the influence of Parathyroid hormone on the DCT

A
  • In the peritubular capillary, PTH binds to a receptor on the basal side of the DCT
  • This causes the Na+/Ca+ channel to increase action and thus drive more Ca+ reabsorption
  • Overall goal is to increase Ca+ levels in the body
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43
Q

CPR: What is Gitelman Syndrome? Describe how this changes plasma and urine

A
  • NaCl channel reabsorption problem at the DCT
  • Thus there decreased reabsorption of both ions
  • Causes: hypocalcuria, hypokalemia, hypomagnesium, & metabolic alkalosis
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44
Q

CPR: Where do thiazide diuretics work? What do they do?

A
  • Exert their effect at the DCT
  • Decrease activity of the Na/Cl- cotransporter and thus decrease Na+ reabsorption to decrease water retention
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45
Q

CPR: What is the reflection coefficient?

A
  • Its value is indicative of what is permeable to a membrane
  • Represented by σ
  • If σ=1, then the membrane is only permeable to water
  • IF σ=0, then membrane is permeable to another substance, i.e. Na+, Cl- etc
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46
Q

CPR: What is the osmolarity of a solution with 1 mole of Na+/Cl-? What is the osmolarity of a solution with 1 mole of glucose? Why are they different even tho each is one mole?

A

1 mole Na+/Cl- is 2 osm/L, 1 mole of glucose is 1 osm/L. B/c Na+ & Cl+ can be broken up in a solution into separate ions while glucose cannot

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47
Q

CPR Lab: What levels of the sympathetic trunk does the greater splanchnic nerve arise from?

A

Greater splanchnic nerve arises from the sympathetic trunk levels at T5-T9

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48
Q

CPR Lab: What is the most common cause of hemoptysis?

A
  • Source from bronchial artery
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49
Q

CPR: During dehydration, most water will be reabsorbed at the PCT, why?

A
  • Since 70-75% of Na is reabsorbed in the PCT
  • Anytime Na is reabsorbed water will follow
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50
Q

CPR: Where in the nephron is Na reabsorption hormonally independent?
Where in the nephron is Na reabsorption based on hormones or outside factors?

A
  • PCT: Sodium reabsorption is always 70-75% at the PCT regardless of hormones present & thus the same amount of water is reabsorbed here too
  • DCT: Sodium reabsorption in the DCT is dependent on what hormones are present, i.e. low or high ADH, dehydration, volume overload
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51
Q

CPR: What are juxtaglomerular cells?
What are granular cells?
Where are they found & what do they do?

A
  • Juxtaglomerular cells AKA granular cells are found at the afferent arteriole and are part of the juxtaglomerular feedback mechanism
  • These cells secrete renin
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52
Q

CPR: For someone with a juxtaglomerular tumor, what class of drugs would be administered and why?

A
  • ACE Inhibitors
  • The tumor will cause increased release of Renin = HTN, so the ACE inhibitors will prevent this
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53
Q

CPR: What cells are the initial start of the tubuloglomerular feedback system?

A
  • Osmoreceptors in the macula densa of the DCT sense flow of NaCl in filtrate
  • The macula densa communicates with the glomerulus
  • High flow of NaCl in the filtrate will cause GFR to be decreased
  • Low flow of NaCl in the filtrate will cause GFR to be increased
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54
Q

CPR: T/F prostaglandins dilate afferent and efferent arterioles of the kidney

A

True, prostaglandins dilate both Afferent and Efferent arterioles

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55
Q

CPR: What do intercalated cells do in the collecting tubule? Are they also found other places?

A
  • Intercalated cells include β & α cells
  • Found both at the DCT and collecting tubule
  • α cells activated in metabolic acidosis to secrete H+ & Cl- ions
  • β cells activated in metabolic alkalosis to secrete HCO3- & K+
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56
Q

CPR: α cells are more commonly activated, why?

A
  • Metabolic acidosis is more common than metabolic alkalosis
  • Since α cells secrete H+ & Cl- ions to the renal tubule and cause Bicarb Reabsorption
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57
Q

CPR: How does dopamine affect renal perfusion?

A
  • Dopamine causes vasodilation & thus can be administered as a protective measure for acute renal failure
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58
Q

CPR: Where are NKCC2 channels found?
What drugs act on them?

A
  1. NKCC2 are Na-K+-Cl- symport channels for reabsorption at the thick ascending loop of Henle
  2. Furosemides inhibit NKCC2 channels from reabsorbing and thus encourage diuresis
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59
Q

CPR: Why are NSAIDS such as Naproxen, _______________, and _____________________ not recommended for patients with renal disturbances?

A
  • Naproxen, Ibuprofen, Idomethacin are all NSAIDS
  • NSAIDS inhibit prostaglanding production & thus can place patient at risk for renal injury due to increased pressure
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60
Q

CPR: Explain how Furosemide works

A
  • Furosemide is a loop diuretic that works by inhibiting NKCC2 symporters at the ascending loop of Henle
  • Stimulate prostaglandin release & thus has a vasodilatory effect
  • Vasodilation increases renal blood flow that leads to increased GFR and enhanced drug delivery
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61
Q

CPR: What does Endothelin do?

A
  • A peptide hormone found in smooth muscles that causes contraction
    -Potent vasoconstrictor
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62
Q

CPR: T/F: Loop diuretics stimulate renin release

A

True, since loop diuretics have vasodilatory effects, the increased RPF will induce tubuloglomerular feedback and initiate renin release

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63
Q

CPR: What does Aldosterone do?
Where does it come from?

A
  • Aldosterone is secreted by the adrenal cortex
  • Aldosterone stimulates K+ secretion by the principal cells of the collecting tubules
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64
Q

CPR: What does spironolactone do? Where does it exert its effects?

A
  • Is a aldosterone antagonist
  • Thus it works at the DCT & Collecting duct
  • Is a diuretic via inhibiting the action of aldosterone and reducing the amount of Na reabsorption
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65
Q

CPR: What do Naturetic peptides do?

A
  • Naturetic peptides include atrial Naturetic peptide and BNP (from ventricle) that cause vasodilation, natriuresis and diuresis in response to volume expansion
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66
Q

CPR: Describe how sympathetic activation impacts renal hemodynamics

A
  1. SNS activation causes vasoconstriction of afferent arteriole and stimulates renin release & its cascade
  2. vasoconstriction of afferent arteriole causes decreased RPF thus decreasing glomerular capillary hydrostatic pressure thus decreasing GFR overall reducing net filtration pressure
  3. Peritubular capillary hydrostatic pressure decreases and thus peritubular capillary oncotic pressure is stronger favoring increased peritubular reabsorption and secretion of NaCl
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67
Q

CPR: What does Tm mean?

A

Tm = reabsorption

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68
Q

CPR: How to calculate Tm?

A

Tm/Reabsorption = Filtration - Excretion

Tm = (GFR X Pc) - (Uflow -Uconc)

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69
Q

GFR: In normal kidneys, which of the following is true of the osmolarity of renal tubular fluid that flows through the early distal tubule in the region of the macula densa?

A

Hypotonic compared with plasma

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70
Q

CPR: What is the major determinant of GFR regarding hydrostatic and osmotic pressures?

A

The major determinant of GFR is glomerular capillary hydrostatic pressure

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71
Q

CPR: Ang II causes constriction of both afferent and efferent arteriole, most significant constriction occurring:

A

Ang II causes constriction of efferent arteriole and increases hydrostatic capillary pressure & GFR

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72
Q

CPR: What are the repercussions of ureterblockage?

A

Increasing Bowman’s capsule pressure and opposing filtration, thus decreasing GFR

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73
Q

CPR: Why is colloid osmotic pressure in Bowman’s capsule not considered the opposing force to glomerular capillary hydrostatic pressure in healthy individuals?

A

In healthy individuals, protein should not be filtered through the glomerulus
- Thus colloid osmotic pressure in Bowman’s capsule should be 0 & therefore cannot be an opposing force
- Thus the opposing force to glomerular filtration is plasma osmotic pressure

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74
Q

CPR: What substances might be found in glomerular filtrate?

A
  • Small molecular substances
  • Ions
  • Glucose
  • Amino acids
  • Urea
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75
Q

CPR: How to calculate Net filtration pressure of the glomerulus?

A

NFP = (Out + out) - ( In + in)

NFP = (Hydrostatic P capillary + Oncotic P Bowman’s ) - (Oncotic P capillary + Hydrostatic P Bowmans )

  • note, Oncotic pressure in healthy individuals should be 0
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76
Q

CPR: Explain how GFR and filtration fraction are changed when the efferent arteriole is vasoconstricted

A
  • RPF decreases
  • But GFR increases since there is increases resistance = increased hydrostatic pressure in the glomerular capillary
  • Filtration Fraction = GFR / RPF
  • FF gets larger since the ratio is becoming larger
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77
Q

CPR: What happens to filtration fraction when the afferent arteriole is vasoconstricted and efferent arteriole unchanged?

A
  • Filtration fraction does not change b/c both GFR and RPF are decreased and thus the ratio is the same
  • FF = GFR/RPF
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78
Q

CPR: A researcher in a laboratory wants to use an agent that will cause simultaneous constriction of the afferent and efferent arterioles in the kidney and therefore decrease both the renal blood flow and glomerular filtration rate. What mechanism/substance is the best choice for induction?

A
  • Norepinephrine
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79
Q

CPR: Why is the osmolarity of renal tubule fluid that flows through the early distal tubule hypotonic?

A
  • As filtrate flows up the ascending loop of Henle the solutes are reabsorbed
  • Since this portion is impermeable to water, overall dilution of the filtrate is occurring
  • So in the early DCT, this portion is considered the diluting segment of the renal tubule
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80
Q

CPR: What is the osmolarity of filtrate when it reaches the early distal tubule?

A

100 mOsm/L

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81
Q

CPR: What tends to decrease potassium secretion by the cortical collecting duct?

A
  • A diuretic that inhibits the action of aldosterone, i.e. spironolactone
  • Blockade of the action of aldosterone with spironolactone inhibits potassium secretion
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82
Q

CPR: When GFR decreases by 50%, what substance would be found to have increased the greatest in plasma concentration and why?

A
  • Normally, creatinine is filtered at the glomerulus
  • It is not secreted or reabsorbed and nearly entirely excreted and, thus is an indicator of eGFR
  • If GFR decreases, then less is being filtered, thus less creatinine is being sent to the nephron loops and stays in the plasma
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83
Q

CPR: Why does metabolic acidosis decrease intracellular K+ concentration and K+ secretion in the collecting duct?

A
  • Increased H+ concentration inhibits potassium secretion by reducing the activity of the Na/K+ ATPase pump in the principle cells
  • Thus less K+ is less K+ is moved into the cell
  • Thus there is less K+ in the cell to passively diffuse across the luminal membrane into the collection tubule
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84
Q

CPR: Where is the majority of K+ secreted?

A
  • K+ secreted in the late DCT & collecting tubule
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85
Q

CPR: Describe the movement of PAH through the tubules

A
  • At the GFR, PAH filters freely through
  • However, the largest contribution of PAH to the filtrate comes from secretion by the proximal tubule
  • No reabsorption
  • Indicator of renal plasma flow
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86
Q

CPR: Describe how increased ADH induces aquaporin insertion at the ___________________________.

A
  • ADH is secreted from the posterior pituitary gland
  • Causes insertion of aquaporins at the apical principle cell of the collecting duct
  • V2 receptors in principle cells stimulated > G s insertion of endosomes containing aquaporin 2
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87
Q

GFR: If PAH secretion is blocked, why is the clearance considered equal to the GFR?

A
  • PAH contribution comes largely from PCT secretion
  • If PAH secretion is blocked, then the only contribution of PAH is from the filtrate and urine is from glomerular filtration & thus would match GFR
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88
Q

CPR: What does + Free Water clearance mean?

A
  • Dilute urine is being formed
  • Too much H20 is being secreted
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89
Q

CPR: What does - Free Water clearance mean?

A
  • Excess solutes are removed from the blood and water being reserved
  • Concentrated urine
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90
Q

CPR: What is Free Water clearance?

A

Comparing Urine osmolarity / Plasma osmolarity

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91
Q

CPR: What does it mean if a substance appears in the renal artery but not in the renal vein?

A
  • The substance is not filtered
  • Entirely secreted by the peritubular capillaries
  • Clearance is equal to the renal plasma flow
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92
Q

CPR: What are the normal values for human pH?

A

7.4 +/- 0.5
7.35 - 7.45

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93
Q

CPR: What is the normal value [CO2]?

A

1.3 mM

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94
Q

CPR: What is the normal value of P CO2?

A

40 mmHg in the arterial

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95
Q

CPR: What is the normal value of [HCO3]?

A

24 mM

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96
Q

CPR Lab: What does I 8 10 EGGS AAT 12 mean?

A

Diaphragm openings
- I 8: Inferior vena cava found at the level of T8
- 10 Eggs: Esophagus found at level of T10 & CN 10
- AAT 12: Azygos vein, ascending aorta, thoracic duct found at level of T12

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97
Q

CPR Lab: What is ligamentous arteriosum a remnant of?

A

Ductus arteriosus

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98
Q

CPR Lab: What does the phrenic nerve innervate?

A

Diaphragm

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99
Q

CPR Lab: What level of the the sympathetic trunk does the greater splanchnic nerve arise?

A

The greater splanchnic nerve arises from the sympathetic trunk at levels T5-T9

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100
Q

CPR Lab: What does the innermost intercostal nerve innervate?

A

Intercostal nerves

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101
Q

CPR Lab 4: Name the nerve, artery, vein found in the posterior mediastinum

A

In order from superior to inferior most
- Nerve: Intercostal nerve
- Artery: Posterior intercostal A.
- Vein: Posterior intercostal V.

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102
Q

CPR Lab: List the impressions for visceral organs on their posterior surface of the L lung?

A
  • L lung: Descending aorta impression & arch of aorta
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103
Q

CPR Lab: Name the fissures of each lung & what lobe they separate

A
  • L: Oblique fissure separates the superior and inferior lobe
  • R: Oblique fissure separates the inferior and middle lobe
  • R: Horizontal fissure separates the superior and middle lobe
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104
Q

CPR Lab: List the impressions on the posterior surface of the R lung:

A

CASE
C: Cardiac notch
A: Arch Azygos vein
S: Superior vena cava
E: Esophageal

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105
Q

CPR Lab: What is on the R lung that if ruptured is a common cause of hemoptysis?

A

Brachial Artery of the R lung common cause of hemoptysis

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106
Q

CPR Lab: list the structures on the Arch of Aorta to know:

A
  • Brachiocephalic trunk > gives rise to R common carotid and subclavian
  • Left common carotid
  • Left subclavian
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107
Q

CPR Lab: What structure is proximal to the L recurrent larygneal N?

A

The L recurrent laryngeal nerve travels under the ligamentum arteriosum to reach the vocal cords

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108
Q

CPR Lab: List the branches of the SVC need to know

A
  • R & L brachiocephalic veins come off the SVC
  • They travel under the arch of aorta
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109
Q

CPR Lab: What is the carina?

A

The point of the main bronchus divides into L & R secondary/lobar bronchi

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110
Q

CPR Lab: On the L side of the mediastinum, what two structures associated with the Azygos vein are found?

A
  • Ascending is the Accessory Hemiazygos vein
  • Descending branch is the Hemiazygos vein
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111
Q

CPR Lab: What is the Pulmonary ligament and where is it found?

A
  • Found on both lungs proximal to the hilum
  • Where the visceral and parietal pleura meet
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112
Q

CPR Lab: What is important to remember about the costodiaphragmatic recess? Where is it found?

A
  • Found more laterally
  • The costodiaphragmatic recess is a narrow space in the pleural cavity where the costal and diaphragmatic pleura meet
  • On XR needs to have sharp points, if there are rounded points here it is an indication of pleural effusion
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113
Q

CPR Lab: what are the muscles found on the posterior rib cage in the mediastinum?

A

Innermost intercostal M.

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114
Q

CPR: What type of water movement is occurring in burns, diarrhea, hemorrhage?

A
  • Iso-osmotic volume contraction
  • Loss of both solutes and water
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115
Q

CPR: What type of water shift is occurring in severe dehydration (pathological caused by: __________) , alcoholism or water deprivation

A
  • Severe dehydration can be caused by low ADH and so too much water is excreted
  • There is hyperosmotic volume contraction
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116
Q

CPR: Where does aldosterone come from?

A

Adrenal glands secrete aldosterone

117
Q

CPR: What kind of water volume shift is occurring during Adrenal insufficiency?

A
  • Adrenal insufficiency = decreased Aldosterone
  • Decreased Na+ reabsorption paired with water excretion = Hypo-osmotic volume contraction
118
Q

CPR: What type of water shift is occurring in SIADH or water intoxication?

A
  • Too much H20 being reabsorbed = Hypotonic Volume expansion
  • Water moves from ECF to ICF = cellular expansion
119
Q

CPR: What type of water movement is occurring in infusion of isotonic saline?

A

Isotonic volume expansion
- ECF and ICF osmolarity stay the same, volume increased in ECF

120
Q

CPR: What type of water movement is occurring in High NaCl intake?

A

Hyperosmotic volume expansion

121
Q

BSE: When does age contribute to generalizability of a study?

A
  • If age is a large population, i.e. 18-65 then the study is more generalizable
  • If the age is a narrower window, 45-65, this makes the study less generalizable
122
Q

CPR: Why are sacral physiologic dysfunctions most often Type I?

A
  • Think common compensatory pattern, at the Lumbar spine there is commonly a sidebent L, rotated R type I dysfunction
  • So then if common pattern is a type I dysfunction then this would be more physiologic
123
Q

CPR: List examples of Iso-osmotic volume contraction related to water shift if body fluid compartments

A
  • Burns
  • Diarrhea
  • Hemorrhage
124
Q

CPR: Give examples of hyperosmotic volume contraction related to water shift if body fluid compartments

A
  • Severe dehydration
  • Severe dehydration due to sweating
  • Severe dehydration due to low ADH
  • Severe dehydration due Diabetes insipidus nephrogenic
  • Alcoholism
125
Q

CPR: List examples of Hypo-osmotic volume contraction related to water shift if body fluid compartments

A
  • Adrenal insufficiency causing low Alodsterone
126
Q

CPR: List examples of Iso-osmotic volume expansion related to water shift if body fluid compartments

A

Infusion of isotonic saline

127
Q

CPR: List examples of Hyperosmotic volume expansion related to water shift if body fluid compartments

A
  • High NaCl intake
128
Q

CPR: List examples of hypo-osmotic volume expansion related to water shift if body fluid compartments

A
  • Syndrome of inappropriate ADH secretion
  • Water intoxication
129
Q

CPR: What is the total body water for a 70 kg man?

130
Q

CPR: What is the extracellular fluid volume for a 70 kg man?

131
Q

CPR: What is the intracellular volume of a 70 kg man?

132
Q

CPR: What is the interstitial fluid volume of a 70 kg man?

133
Q

CPR: What is the plasma volume of a 70 kg man?

134
Q

CPR: What does increasing obesity do to Total body water?

A

Decreases total body water percentage

135
Q

CPR: How to calculate osmolarity

A

Osmolarity = concentration * number of particles in solution

Osmolarity = C in (mol/L) * n

136
Q

CPR: What % of NaCl is isotonic to plasma? What % of glucose solution is isotonic to plasma?

A
  • 0.9% NaCl is isotonic to plasma volume
  • 5% glucose is isotonic to plasma
137
Q

CPR: What transporters does Aldosterone activate?

A

Activates ROMK & ENaCC for Na+ reabsorption

138
Q

CPR: Why does diarrhea lead to metabolic acidosis?

A
  • Loss of gastric juices which contains bicarbonate
  • Without bicarbonate have acidosis
139
Q

CPR: What is the normal osmolarity in the body?

A

280-300 mOsm

140
Q

CPR: What is being lost while sweating?

A
  • Sweating causes loss of more water than salt
  • Hyperosmotic volume contraction
141
Q

CPR: Generally speaking, what does Parathyroid hormone do?

A

PTH increases Ca+ reabsorption and increases Phosphate excretion

142
Q

CPR: What is the main buffering mechanism in the ECF?

A

Bicarbonate is the most important ECF buffer

143
Q

CPR: What is the difference between volatile acids and fixed acids?

A
  • Volatile acids can be exhaled out
  • Fixed acids use kidneys for excretion
144
Q

CPR: When is pH buffering considered compensated?

A

pH between 7.35-7.45 is considered buffered

145
Q

CPR: Name a volatile source of acid

146
Q

CPR: List fixed sources of acid

A
  • Sulfuric acid & Phosphoric acid from catabolism
  • Keto acids and lactic acid
  • Acids from diet and drugs
147
Q

CPR: List 3 mechanisms of acid buffering

A
  1. Body fluids using bicarbonate via ECF & Hgb via intracellular, rapid but temporary
  2. Lungs: exhalation to remove CO2
  3. Renal H+ excretion and bicarbonate generation-slow but powerful
148
Q

CPR: Acid/Base balancing - If the primary disorder is respiratory (CO2), how is compensation achieved?

A

If the primary disorder is respiratory (CO2) then compensation is by renal adjustments of HCO3 excretion

149
Q

CPR: Acid/Base balancing - If the primary disorder is metabolic (HCO3-), how is compensation achieved?

A

If the primary disorder is metabolic (HCO3) then compensation is by respiratory adjustments of CO2

150
Q

CPR: During acid-base disturbance, how can highly abnormal values of HCO3- or CO2 exist with a normal arterial pH?

A

The body is in a final state of acid base balance
- The pH of the blood is normal because the metabolic or respiratory compensation has balanced the original abnormal value

151
Q

CPR: Describe respiratory regulation of Acid-Base balance

A
  1. Low pH sensed by carotid A. receptors because of increased H+ ions
  2. Send signal to increase ventilation to remove free CO2 and will decrease P CO2
  3. Convert H+ ions to carbonic acid to CO2 for exhalation
  4. Correction by 50-75% in 3-12 minutes and have a feedback gain of 1.0-3.0
152
Q

CPR: What is the most important renal tubular buffer?

A

Phosphate
2 PO 4 3-

153
Q

CPR: What is the second most important renal tubular buffer?

A

Ammonia
NH 3

154
Q

CPR: What are protein buffers? Where are they?

A

Located intracellular b/c Hemoglobin is considered a H+ buffer
When Hgb is at capillaries, H+ binds to hemoglobin for removal

155
Q

CPR: What is the most important buffer in ECF?

A

Bicarbonate is the most important

156
Q

CPR: Where is the majority of bicarb (________________) reabsorbed?

A

HCO 3 -
~ 85% reabsorbed here
- Also reabsorbed in Loop of Henle and Collecting duct

157
Q

CPR: About 90-95% of HCO 3 - is reabsorbed in the Proximal tubule and Thick Ascending Loop of Henle & _____________ _____________. Describe the movement

A
  • Occurring in the early DCT
    1. Na+/H+ antiporter on the Apical surface of cells pushes H+ into the tubule for excretion
    2. CO2 passively diffuses on the basal cell surface into the cell from the peritubular capillary
    3. CO2 & H2O in the cell combine to form bicarb, HCO3-
    4. Na/HCO3- cotransporter on the apical surface transport both bicarb and Na+ into the peritubular capillary
  • Since Na+ & HCO3- are in the renal tubule here, the HCO3- combines with H+ that are being pushed into the tubule that are then transformed into H20 & CO2 which can passively diffuse into the cell
158
Q

CPR: What is the expected bicarbonate value in uncompensated ____________ acidosis?

A

HCO3- < 24 mEq/L is metabolic acidosis

159
Q

CPR: What is the expected CO2 value in uncompensated _________________ acidosis?

A

P CO2 greater than 40 mmHg is respiratory acidosis

160
Q

CPR: What is the expected bicarbonate value in uncompensated ________________ alkalosis?

A

HCO3- greater than 24 mEq/L is metabolic alkalosis

161
Q

CPR: What is the expected CO2 value in uncompensated ___________________ alkalosis?

A

P CO2 less than 40 mmHg is respiratory alkalosis

162
Q

CPR: What is the difference between what is lost in vomiting vs diarrhea

A
  • Vomiting: Losing HCl from stomach acid
  • Diarrhea: Loss of Bicarbonate in gastric & pancreatic juices
163
Q

CPR: Describe how Aldosterone increases BP

A
  • Aldosterone increases ENaCC channels formation & Increases channel activity (Na+ reabsorption)
  • Increases ROMK channel synthesis & channel activity (K+ secretion & excretion)
  • These channels are present in the cortical collecting duct
  • Induces phosphorylation of Aldosterone receptors that increases Pendrin channels with increase Cl- reabsorption = inc. ECF volume
164
Q

CPR: What is another name for hyperaldosteronism?
What is the resulting change in plasma in this disease?

A
  • Hyperaldosteronism = Conn disease
  • Leads to hypokalemia b/c too much K+ is excreted
  • Hypokalemia induces phosphorylation of aldosterone receptors which upregulates the activity of Pendrin (in collecting duct), a channel that secretes Cl- and reabsorbs HCO3- on the apical cell
  • Excess reabsorption of HCO3- causes metabolic alkalosis
165
Q

CPR: Describe the secretion/formation/generation of Ammonium in the PCT

A
  • PCT: Ammonium & Bicarb generated, NH4+ secreted
    1. Liver makes glutamine which is secreted from the peritubular capillary into the PCT cell where it is broken down into: 2 NH4+ & 2 HCO3-
    1a. HCO3- is reabsorbed on basal side along with Na+
    1b. 2 NH4+ use NHE counter transporter (channel that can counter transport Na+ into cell and H+ or NH4+ into the renal tubule)
166
Q

CPR: Describe the reabsorption of Ammonium in the TALH

A
  • TALH has NaKCl channel for reabsorption
    1. NaKCl: NH4+ can be reabsorbed on the apical cell instead of K+
    2. Once in the medulla, the NH4+ disassociates into NH3 & H+
    3. The NH3+ can then be used by the collecting duct for NH4+ secretion later
167
Q

CPR: What do loop diuretics bind to in order to exert their effects?

A
  • Loop diretics bind to NaKCCl channels to prevent reabsorption of solutes
  • Decreases medulla osmotic pressure
  • Since NH4+ can also use NaKCCl channels, loop diuretics can block NH4+ reabsorption
  • Can lead to metabolic alkalosis
168
Q

CPR: Describe the movement of Ammonium at the Collecting duct

A
  • Collecting duct has 2 types of intercalated cells: α & β
  • Both types of cells have H+/K+ ATPase & Na+/H+ ATPase, depending on the cell type depends if these channels are basal or apical sided
  • At the collecting duct, NH3+ is excreted and thus can combine with the H+ that is secreted by α cells to become NH4+ that is trapped in the collecting duct to be excreted
169
Q

CPR: What does aspirin poisioning do?

A
  • Increases H+ reabsorption and induces metabolic acidosis
170
Q

CPR: What does DM do to H+ protons?

A
  • Diabetes mellitus increases H+ production and leads to metabolic acidosis
171
Q

CPR: How does diarrhea contribute to metabolic acidosis?

A
  • Diarrhea is the loss of gastric & pancreatic juices which are rich in bicarbonate, HCO3-
  • Low HCO3- = metabolic acidosis
172
Q

CPR: What do carbonic anhydrase inhibiting drugs do to H+ in the body?

A
  • Carbonic anhydrase inhibiting drugs decrease H+ secretion & excretion leading to metabolic acidosis
173
Q

CPR: Chronic renal failure and ________________ disease are contributors to metabolic acidosis

A

Addison’s disease

174
Q

CPR: What is the anion gap?

A

The body has both cations and anions
- Cation contributor: Na+
- Anion contributor: Cl-, HCO3-, & unmeasurable anion (b/c such low levels)
- The unmeasurable portion is the anion gap
- Should change in proportion to Cl- changes

175
Q

CPR: What is Hyperchloremic acidosis?

A
  • Acidosis wherein HCO3- levels decrease causing Cl- levels increase causing the equilibrium to shift and anions to decrease. Proportions are changed
176
Q

CPR: List 4 possible causes of hyperchloremic acidosis

A
  1. Diarrhea
  2. Carbonic anhydrase inhibitors
  3. Addison’s disease
  4. Renal tubular acidosis
177
Q

CPR: What is normochloremic metabolic acidosis?

A
  • Decreased bicarbonate causes acidosis, Cl- levels should increase to balance cation levels, **but Cl- levels remain the same!, rather anion levels increase to equilibrate the cations
  • Anion gap is increased
178
Q

CPR: List 7 cases of normochloremic metabolic acidosis

A
  1. Diabetic ketoacidosis (β hydroxybuterate)
  2. Aspirin poisoning
  3. Methanol poisoning
  4. Starvation
  5. Lactic acidosis
  6. Chronic renal failure
  7. Salicylic acid
179
Q

CPR: List 3 causes of respiratory acidosis

A
  1. Emphysema
  2. Brain damage
  3. Pneumonia
180
Q

CPR: List 4 causes of metabolic alkalosis

A
  1. Increase base intake
  2. Vomiting gastric acid
  3. Mineralcorticoid excess
  4. Overuse of diuretics causing hypokalemia, increased H+ secretion and increased HCO3- reabsorption & generation
181
Q

CPR: Why does vomiting cause metabolic alkalosis?

A
  • Vomiting gastric acid means losing Cl- that is contained in gastric acid
  • Loss of acid = alkalosis
182
Q

CPR: Describe 2 major mechanisms of overuse of diuretics causing metabolic alkalosis

A
  1. Diuretic causing K+ secretion, excretion & hypokalemia
    1a. This increases H+ excretion and HCO3- reabsorption & generation
  2. Diuretics decrease volume, specifically ECF volume which initiates the Renin-AngII-Aldosterone system
    2a. Aldosterone increases ROMK & ENaCC channels which increases Cl- reabsorption leading to HCO3- reabosorption since they have a cotransporter, H+ secretion
183
Q

CPR: How can high altitude contribute to respiratory alkalosis

A
  • Hyperventilation due to low P O2
184
Q

CPR: Excess _____________ (Conn’s syndrome) may cause _____________.

A

Excess aldosterone (Conn’s syndrome) may cause alkalosis

185
Q

CPR: List 4 substances that are filterable through the glomerulus:
List 2 substances that are not filterable in the glomerulus:
(not all emcompassing)

A

Filterable:
1. Glucose
2. Electrolytes (K+, Na+, Mg+)
3. Inulin
4. Water
Non filterable:
1. Myoglobin
2. Albumin

186
Q

CPR: How does rhabdomyolysis cause kidney damage?

A
  • Rhabdomyosis is muscle fiber damage
  • There is a release of lots of myoglobin into the bloodstream which is filtered at the kidney
  • Causes kidney damage since it is not supposed to be filtered
187
Q

CPR: How does hypertension & diabetes allow proteins to pass through the glomerulus?

A
  • Proteins are - charged
  • Glomerulus is highly - so cations are highly filterable
  • Aside from their size, proteins do not filter b/c they are - charged and repelled by the glomerulus
  • DM & HTN removes the negative charges and thus removes one of the barriers that prevents proteins from being filtered under normal circumstances
188
Q

CPR: What is the normal GFR per minute?
What is the normal GFR per day?

A
  • 125 mL/min
  • 180 L/day
189
Q

CPR: How do you calculate filtered load? What does filtered load represent?

A

Filtered load is the amount filtered
Filtered load = GFR - P x

where P x is plasma concentration of a substance

190
Q

CPR: How to calculate glomerular filtration?

A

GF = K F * (H PC - H B - Colloid PC

191
Q

CPR: Define autoregulation of renal blood flow

A

Autoregulation are feedback mechanisms that are intrinsic to the kidney that normally keep renal blood flow and GFR relatively constant, despite marked changes in arterial blood pressure (75-160 mmHg)

192
Q

CPR: Pressure naturesis is what type of kidney regulation?
What is pressure naturesis?

A
  • Pressure natruesis: increases arterial pressure decreases renal tubule na+ reabsorption
  • Pressure naturesis is a type of autoregulation of renal blood flow and GFR
193
Q

CPR: List two examples that can increase the resistance of afferent arterioles and how this affects RPF

A
  • Shock and heart failure increase afferent arterioles resistance
  • This lowers RPF decreasing hydrostatic pressure in the capillary
194
Q

CPR: If GFR is increased and RPF is decrease what happens to filtration fraction?

A

FF increases since

FF = GFR/RPF

195
Q

CPR: What controls vasoconstriction of the afferent arterioles?

A
  • SNS stimulation
  • Significant levels of Ang II
196
Q

CPR: What controls efferent arterioles constriction?

A
  • Moderate levels of Ang II
  • Strong SNS stimulation
197
Q

CPR: When there is severe constriction of efferent arterioles there is a steep rise in __________ pressure. How does this increase reabsorption?

A
  • The increase in osmotic pressure decreases GFR
  • Downstream the increases osmotic pressure of the capillary is a strong force to encourage reabsorption from the tubule
198
Q

BSE: What is the CDC’s 3rd official cause of death? (Estimate)

A

Medical errors

199
Q

BSE: What is Evidence based medicine?

A
  • The conscientious, judicious and reasonable use of modern, best evidence in making decisions about the care of individual patients
  • Must combine study results with the physicians own clinical judgement and patient preferences
200
Q

BSE: What is the evidence based medicine triad?

A

Merging of the three following:
1. Patient values & expectations
2. Individual clinical expertise
3. Best external evidence

201
Q

BSE: The following studies are considered ____________ ( or observational)

A
  • Case reports
  • Case series
  • Cross sectional studies
202
Q

BSE: These types of studies are considered: _____________
- Randomized control studies

A
  • Randomized/control studies are considered evaluative or interventional
203
Q

BSE: What are the 3 reasons for development of evidence based medicine?

A
  1. Driven to cope with information overload
  2. Driven by cost control
  3. Driven by public impatience for the best in diagnostics and treatment
204
Q

BSE: What is the goal of Evidence based medicine

A
  • To make the best clinical decision for any patient
  • Quality improvement approach will ask whether the care is: appropriate, efficient, effective
205
Q

CPR: How to calculate filtered load?

A

Filtered load = GFR X P s

FL = GFR * Plasma concentration substance (mg/min)

206
Q

CPR: How to calculate excretion load?

A

Excretion load = U s * Volume

where U s is urine concentration of a substance

207
Q

CPR: Where does reabsorption of water start?

A

Water reabsorption of H2O starts at the PCT?

208
Q

CPR: Describe the tight junctions at the PCT

A
  • Tight junctions here are actually not very tight
  • Lends to H20 & ions, i.e. Na+, Ca+, Mg+ , to easily diffuse down their concentration gradient
209
Q

CPR: What do SGLT2 inhibitors do?

A
  • Promote osmotic diuresis
  • In PCT, since 100% glucose is reabsorbed here, they are on the apical cell surface
  • Co-transport Na+ & Glucose into the cell
  • Inhibiting this is a target for diabetics, since the drug will block reabsorption into the peritubular capillary & therefore allowing excretion of glucose via urine
210
Q

CPR: Describe the treatment of SIADH using glucose supplement

A
  • In the PCT, using SLGT inhibitors aim to promote osmotic diuresis by disrupting the gradient that water uses to diffuse into the peritubular capillary
  • Adding more glucose will further increase the water content in the renal tubule that does not get excreted thus counteracting urine retention caused by too much ADH
211
Q

CPR: List the primary active transporter that drives secretion and excretion in the tubules of the kidney

A
  • Na+/K+ ATPase which removes Na+ from cell and K+ into cell
  • Makes intracellular [Na+] low so that Na+ wants to come in
  • Makes cell negatively charged
212
Q

CPR: List 4 major transporters in the PCT that use 2ndary active transport

A
  1. SGLT2 co-transporters: on apical membrane to co transport Na+ & Glucose, reabsorb 90% glucose. SGLT1 channels reabsorb 10% glucose from PCT
  2. GLUT: on basal PCT to put glucose into the capillary
  3. Na+/H+ counter transporter: On apical PCT cell to reabsorb Na+ and secrete H+
  4. Na+/Amino acid co-transporter: Apical PCT cell to Reabsorb Amino acids & Na+ into cell
213
Q

CPR: Describe water reabsorption at the PCT

A
  • Iso-osmotic water reabsorption, b/c for every 1 Na+ reabsorbed, 1 water reabsorbed as well
  • No change in tubule osmolarity!
214
Q

CPR: Na+ reabsorption in the PCT drives reabsorption of what other molecules?

A
  • Amino acid
  • Ca+2
  • K+
  • Bicarbonate (HCO3-) (early PCT)
  • Cl- (late PCT)
215
Q

CPR: Describe how Cl- and Bicarb are reabsorbed at the PCT & which portions

A
  • Cl- is late PCT
  • Bicarb is early PCT
  • Both follow Na+ reabsorption here, where the Na+/H+ Counter transporter drives Bicarb reabsorption
216
Q

CPR: What drives H+ secretion in the Pct?

A

Na+/H+ counter transporter on apical membrane

217
Q

CPR: List what is secreted by the PCT

A
  • H+
  • PAH
  • Creatinine
  • Organic acids & bases
  • Drugs & toxins
218
Q

CPR: List what is reabsorbed in the PCT:

A
  1. Glucose
  2. Amino acids
  3. Na+
  4. K+
  5. Phosphate PO4 -3
  6. Cl-
219
Q

CPR: Where does PTH exert it’s effect in the kidney?

A
  • PTH decreases PO4 -3 and thus increases it’s secretion
  • Since PO4 -3 is reabsorbed at the PCT, this is where it exerts its effects
220
Q

CPR: What does PTH do?

A
  • Increase Ca+ reabsorption and decrease PO4PO4 -3 reabsorption/increase excretion
221
Q

CPR: How does the treatment for glaucoma effect the kidney?

A
  • Tx is a carbonic anhydrase inhibitor which decreases HCO-3 reabsorption which places pt at risk of metabolic acidosis
222
Q

CPR: Define T m

A

T m is the transport maximum
The maximum amount of a substance that can be transported per minute

223
Q

CPR: Describe the two fold way that Na+ reabsorption in the PCT drives Cl- reabsorption

A
  1. Na+ reabsorption makes the renal tubule - which drives Cl- out of the tubule towards a more + charge
  2. Na+ is followed by water, which increases [Cl-], such that osmolarity is increased and [Cl-] wants to flow down its concentration gradient
224
Q

CPR: What drug and physiologic process is used to treat brain edema?

A
  • Use mannitol
  • Use principle of osmotic diuresis: increase what is filtered from the blood but not easily reabsorbed which increase osmolarity in the renal tubule to discourage water reabsorption and increase urine output
225
Q

CPR: How does Na+ reabsorption drive urea reabsorption?

A
  • Na+ reabsorption increases H2O reabsorption
  • Decreased water in the renal tubule increases [urea concentration] and thus urea wants to flow from high to low concentration and into the cell
226
Q

CPR: Define osmotic diuresis

A

Uses substances that are filtered from the blood but not easily reabsorbed by the renal tubules (rea, mannitol, and sucrose) to increase the concentration of osmotically active molecules in the tubules and osmotic pressure
- Decrease water reabsorption and increase urine output

227
Q

CPR: Why is the use of mannitol for treatment of brain edema place the patient at risk of hyperkalemia?

A
  • Since less H20 is being reabsorbed, the plasma has increased osmolarity
  • Driving K+ out of the cell and into the blood plasma
228
Q

CPR: Compare the tonicity of filtrate vs. blood plasma at the thin and thick ascending portion of the Loop of Henle

A
  • Filtrate tonicity < Plasma tonicity
  • Since Na+/K+/ 2 Cl- (& NH4+ instead of K+) will dilute the filtrate and make the plasma have more solutes
229
Q

CPR: What is the driving force for allowing secondary active transport of the Na/K+/Cl- cotransporter in the ascending loop of Henle?

A
  • Na/K+ ATPase makes the [Na+] low in the cell to encourage reabsorption of Na+
230
Q

CPR: What does Na+/K+ ATPase primary active transport create a gradient for in the Thick ascending portion of the loop of Henle?

A
  • Low [Na] concentration in the cell
  • Encourages the Na/K+/2Cl- co transporter
  • Also encourages Na/H+ counter transporter for H+ secretion and Na+ reabsorption on the apical cell of the thick ascending loop of Henle
231
Q

CPR: What drives reabsorption of Mg+2 & Ca+2 in the thick ascending loop of Henle?

A
  • There is a +8 charge in the tubule which creates an electrogradient that encourages + charged Mg+2 & Ca+2 down their concentration gradient via paracellular transport
232
Q

CPR: Describe how Loop Diuretics exert their effects on the kidney and how they predispose patients to hypokalemia & metabolic alkalosis

A
  • Loop diuretics bind to Na/K+/2Cl- transporter at the Cl- site
  • Inhibit reabsorption of Na+/K+/2Cl- such that K+ is being excreted
  • Since NH4+ can be reabsorbed in place of K+ this also d/c reabsorption of NH+
  • NH4+ drives secretion of HCO3-
  • Increased [HCO3- plasma] = metabolic alkalosis
233
Q

CPR: What is Addison’s Disease?

A

Hyperaldosteronism = overdrive in the late DCT & cortical collecting duct at the principle cells = hyperkalemia & metabolic acidosis

234
Q

CPR: What are 3 factors that increase Aldosterone secretion?

A
  1. Ang II
  2. Excess K+
  3. Adrenocorticotropic hormone
235
Q

CPR: Contrast the excretion mechanisms of K+ vs Na+

A
  • Na+: the more that is intake the more is excreted, if there is less Na+ intake there is less excreted
  • K+: if there is excess ingested then more is excreted, if less K+ is ingested K+ is still excreted!
236
Q

CPR: _____________________ causes vasoconstriction of the efferent arteriole. Discuss how this induces changes in peritubular capillary hydrostatic pressure and increases peritubular colloid osmotic pressure

A
  • Ang II vasoconstricts efferent arterioles
  • Decreases peritubular hydrostatic pressure by decreasing renal plasma flow
  • Increases filtration fraction which increases peritubular colloid osmotic pressure b/c increased GFR which created more concentrated peritubular blood
237
Q

CPR: What does low renal clearance tell you about a substance?

A

That the substance is being reabsorbed

238
Q

CPR: How to calculate reabsorption rate?

A

Reabsorption rate = Filtered load

FL = GFR * plasma glucose

239
Q

CPR: Why is a filterable substance with low renal clearance going to have high concentration?

A
  • Since clearance represents excretion, if there is no secretion this means the substance is completely reabsorbed
  • Thus, as moving along the tubule will have lower concentration and be highest prior to the PCT where reabsoprtion starts
240
Q

CPR: Hypoxemia causes:

A
  • Respiratory acidosis
241
Q

CPR:
1. Diuretic therapy causes significant volume _______________ and activates: _______________
2. Overuse causes:

A
  1. Diuretic therapy causes significant volume loss and activates RAAS to increase aldosterone secretion
  2. Overuse causes hypokalemia inducing metabolic alkalosis leading to muscle weakness, cramping, irritability and neuromuscular excitability
242
Q

CPR: What is normal anion gap?

A

B/t 4-12 mEq/L

243
Q

CPR: What contributes normochloremic metabolic acidosis?

A
  • Diabetic ketoacidosis
  • Lactic acidosis
  • Chronic renal failure
  • Salicylic acid
  • Aspirin poisoning
244
Q

CPR: Why does normal diarrhea have a normal anion gap?

A
  • B/c in diarrhea the Bicarb is secreted but this is an instance of hyperchloremic metabolic acidosis such that the Cl- will increase to compensate for decrease in Bicarb
245
Q

CPR: What comprises extracellular fluid?

A
  • Extracellular fluid consists of plasma and interstitial fluid
246
Q

CPR: How to calculate interstitial volume?

A
  • Interstitial volume = ECF - plasma volume
247
Q

CPR: How to calculate vital capacity?

A

Vital capacity = Tidal volume - Residual volume

248
Q

CPR: What is functional residual capacity?

A

Total amount of air in lungs at baseline?

249
Q

CPR: How to calculate functional residual capacity?

A

Functional residual capacity = Expiratory reserve volume + Residual volume

250
Q

CPR: How do changes in elastin change lung compliance?

A

Decreased elastin = increased compliance

251
Q

CPR: What spinal levels do referred pain from the kidney/ureter come from?

252
Q

CPR: What is the ANS innervation of the kidneys and ureters?

A

Lesser/Least Splanchnic nerves

253
Q

CPR: What regions do the kidneys span normally? Where is the best place to palpate them?

A
  1. Kidneys span from 10th rib to 12th rib
  2. They are more palpable through T12-S2 dermatome levels through posterior muscular wall
254
Q

CPR: What structure does the superior mesenteric artery pass over making this structure a potential site for restriction if the artery forms an aneurysm?

A

Superior mesenteric artery off the descending aorta can compress the renal vein on the L side of the body
- Note it can only compress the LEFT side since the descending aorta travels more proximal to the L side of the body

255
Q

CPR: What are common site of obstruction or distention from kidney stones?

A
  1. Ureter where they cross the iliac A.
  2. Renal Pelvis
  3. Piercing wall of bladder
256
Q

CPR: What are common site of obstruction or distention from kidney stones?

A
  1. Ureter where they cross the iliac A.
  2. Renal Pelvis
  3. Piercing wall of bladder
257
Q

CPR: What is the sequence that describes passage of contents from blood inside the glomerulus capillary to the urinary space of the glomerulus?

A

Blood > Fenestrations of Endothelial Cells > Basement membrane > Urinary space

258
Q

CPR: The sequence of blood contents from inside the glomerular capillary to the urinary space of the glomerulus follows:
Blood > Fenestrations of Epithelial cells > Basement Membrane > Urinary space. What about the podocytes and mesangial cells?

A
  1. Pedicels of podocytes surround almost all the SA of glomerular capillaries. But they internalize contents that filter through fenestrations and digest contents, thus do not allow contents to pass through
  2. Same principle for mesangial cells. Also can phagocytize contents which eliminates contents from urinary glomerular space
259
Q

CPR: T/F Macula densa cells regulate water exchange across the DCT

260
Q

CPR: What do juxtaglomerular cells secrete?

A

Secrete renin

261
Q

CPR: What do sympathetic projections to the adrenal gland innervate?

A
  • Adrenal gland: blood vessel smooth muscle
  • Adrenal gland medulla: neurons
262
Q

CPR: What is the direction of movement of kidneys during embryologic development?

A

Kidneys will migrate from pelvic region to the abdomen

263
Q

CPR: What causes a horseshoe kidney?

A

Both kidneys get trapped in pelvis and fuse together to one single kidney

264
Q

CPR: Where/what are Wilm’s tumor?

A
  • Primary form of kidney tumor
  • Tends to be pediatric
  • Genetically based neoplasia
  • Genetic mutation that disrupts Tumor suppressor gene
265
Q

CPR: Describe the cell type in the PCT, DCT, and collecting duct

A
  • Here cells are simple cuboidal epithelium
266
Q

CPR: Describe cell type in the loop of Henle

A

Simple squamous epithelium

267
Q

CPR: Where does ADH come from?

A

Released from pituitary gland

268
Q

CPR: Describe the layers of ureter tissue

A
  • Mucosa: stratified transitional epithelium with umbrella cells
  • Muscularis: smooth muscle
  • Adventitia: connective tissue
269
Q

CPR: What are umbrella cells?

A
  • Specialized cells found in the luminal mucosa of ureters
  • They have special transmembrane proteins that cross-link to form plaques that are protective against urine
270
Q

CPR: T/F The ureters cross the L & R common iliac artery after their bifurcation into external and internal iliac artery

A

False, ureter cross over L & R common iliac artery before they become internal and external iliac A.

271
Q

CPR: Ureters have muscularis layer formed by what type of muscle? What type of innervation occurs here?

A

Muscularis layer is smooth muscle
Innervation by PNS

272
Q

CPR: Describe the tissue layers of the bladder

A
  1. Mucosa: stratified transitional epithelium with umbrella cells
  2. Submucosa: connective tissue with many WBC
  3. Muscularis: some presence
  4. Adventitia: connective tissue
273
Q

CPR: What is Antibody- mediated Glomerular nephritis?

A
  • Auto-immune attack against antigen in basement membrane
  • Inflammatory damage to glomerulus that impairs filtration
274
Q

CPR: What changes occur to the renal function in diabetic nephropathy?

A

Thickening of basement membrane and arteriosclerosis that causes progressive failure of renal function

275
Q

CPR: What is pyelonephritis?

A
  • Inflammation and neutrophil accumulation in collecting duct
  • Secondary to bacterial infection via urinary tract
276
Q

CPR: What is Sickle cell neuropathy?

A
  • Due to reduced oxygen in vasa recta of renal medulla, normal erythrocytes convert to sickle shape, occlude blood flow and induces ischemic damage
277
Q

CPR: What is cystitis?

A

Inflammation of bladder mucosa due to infection

278
Q

CPR: What is urethritis and what is a common cause of the condition?

A
  • Inflammation due to infection
  • Commonly caused by Chlamydia
279
Q

CPR: How do Tubular obstruction and urinary tract obstruction change GFR?

A
  • Note: these are not physiological regulators of GFR, rather pathological
  • They cause back up of fluid through the nephron to the glomerulus
  • Increasing Bowman’s capsule Hydrostatic pressure which decreases filtration and thus decreasing GFR
280
Q

CPR: How to calculate GFR using K f ?

A

GFR = K f * Net filtration pressure

281
Q

CPR: Describe the peritubular capillary starling forces and how they favor water movement across cortical segments

A
  • Peritubular capillary Hydrostatic pressure is low = little secretion out of the capillary
  • Peritubular capillary oncotic pressure is high = increased reabsorption due to protein free fluid
282
Q

CPR: Describe how high protein diet is beneficial in patients with SIADH

A
  • Increased protein in diet = increased AA filtration through glomerulus = increased tubule amino acid content and increased reabsorption at the PCT
  • This drives increased NaCl reabsorption at the PCT to increase plasma osmolarity
  • In doing so, helps counteract the excess pure water being reabsorbed
283
Q

CPR: Tubuloglomerular feedback = ___________ ______________

A

Tubuloglomerular feedback = Macula densa feedback

284
Q

CPR: How can a high protein diet influence tubuloglomerular feedback?

A
  • Overall, high protein increases NaCl reabsorption in the PCT = increased plasma osmolarity
  • Macula densa senses the increased NaCl/osmolarity at the DCT
  • Inducing decreased NaCl reabsorption at the DCT and telling the juxtaglomerular cells to increase afferent arteriole resistance and reduce GFR
285
Q

CPR: What patient population is pursed lip breathing beneficial?

A
  • In patients with obstructive diseases where alveoli are damaged
  • Ex. in emphysema there is destruction of alveoli and decreased alveolar pressure
  • Normally, alveolar pressure is greater than pleural pressure which prevents collapsing
  • If alveoli are damaged, pleural pressure can collapse airway earlier than in normal people = air trapping
  • By pursing the lips while breathing, this lengthens the airway and inducing increased resistance = increased pressure in the alveoli to help prevent collapse
286
Q

CPR: Describe how endothelial dysfunction can contribute to increased BP

A
  1. Endothelial dysfunction (HTN, atherosclerosis) can cause vascular damage to the endothelium of blood vessels
  2. If endothelium is damaged, this can decrease production of vasodilator, Endothelial-derived nitric oxide
  3. EDRF-NO protects against excessive vasoconstriction
  4. If this is blocked, can allow too much vascular resistance which will induce decreased GFR & thus decreased Na+ excretion to allow HTN
287
Q

CPR: What is the difference between EDRF-NO (________ _________ ______ _________) and Endothelin ?

A
  • Endothelial-derived nitric oxide (EDRF-NO) is a vasodilator
  • Endothelin is a vasoconstrictor
288
Q

BSE: What is this describing?

A Type I error occurs when you reject a null hypothesis that is actually true, essentially concluding a significant effect exists when there isn’t one

A

This is a Type I error AKA false positive

289
Q

BSE: What is this describing?

You fail to reject a null hypothesis that is actually false, meaning you miss a real effect

A

Type II Error aka False negative

M1 Block 4 (5 decks)

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