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COM - Renal > FINAL Exam > Flashcards

FINAL Exam Flashcards

1
Q

What is secreted in the PCT?

A

Organic anions and cations including:
Drugs and their metabolites
Creatinine
urate

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2
Q

What is the TF/P ratio of inulin?

Why?

A

3

bc water is being lost with NO change in the solute [ ]

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3
Q

TF/P ratio of glucose?

Why?

A

0

Bc all solute (glucose) is avidly reabsorbed

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4
Q

TF/P ratio of PAH

Why?

A

10

Bc water is being lost AND PAH is being secreted back into the tubular lumen

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5
Q

What provides the major driving force for reabsorption of water and other solutes?

A

PCT Na+ reabsorption

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6
Q

What happens to Cl and urea as Na and water are reabsorbed?

A

They become more concentrated in the luminal fluid

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7
Q

Is paracellular reabsorption of Cl and urea in the early PCT active or passive process?

Why?

A

Passive

Due to the modest [ ] gradient bw lumen and peritubular interstitium

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8
Q

What systems regulate plasma concentrations of glucose and amino acids?

A

Liver and endocrine

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9
Q

What is the basic mechanism of glucose and amino acid reabsorption?

A

Secondary active transport

Trans cellular only

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10
Q

How do glucose and amino acids exit the cell once inside?

A

Via facilitated diffusion through the basolateral membrane

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11
Q

What does it mean if glucose appears in the urine?

What is a disease in which this happens?

A

The sodium glucose transporters are fully saturated

Diabetes

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12
Q

Filtered load = ?

A

GFR x Pglucose

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13
Q

Why does urine output increase with diabetes?

Hint: think about glucose

A

More glucose is trapped in the tubular lumen creating a higher osmolarity. This forces water to be pulled back from the cell into the tube thus increasing the urine output

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14
Q

What are the consequences of osmotic diuretics?

A

INC water excretion

INC sodium excretion (lose salt with the water to maintain the osmotic gradient)

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15
Q

What are the organic anions?

What kind of transport in the PCT do they utilize?

A

PAH, bile salts, uric acid, creatinine

Tertiary Active Transport

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16
Q

What drugs use tertiary active transport?

A

Penicillin, Salicylates, anti-viral drugs

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17
Q

What factors promote fluid movement INTO the peritubular capillaries (2)?

A

High plasma colloid osmotic pressure (pi c)

Low hydrostatic pressure (Pc)

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18
Q

Name the 3 steps in tertiary transport of organic anions:

A
  1. Na/K ATPase creates a gradient that helps to bring sodium IN with sodium dicarboxylate anion carrier and AKG
  2. Once inside the cell, AKG is exchanged for OA- via countertransport
  3. OA- is transported from the cell to the tubular fluid via another AKG countertransport and through a OA- transporter
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19
Q

What kind of molecules are membrane permeable?

A

Non-polar, lipid soluble molecules –> aka UNCHARGED

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20
Q

What kind of pH generates neutral acids and bases?

A

Acid: low pH

Base: high pH

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21
Q

Does luminal acidification favor reabsorption or secretion of organic acids?

Why?

A

Reabsorption

Because acidic lumen neutralizes organic acid and thus it can traverse membranes

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22
Q

If a patient overdoses on aspirin, how can you promote urinary excretion of it to help leave the body?

A

Inject bicarbonate into patient to alkalinize the urine. This makes the lumen basic and the aspirin will remain charged and stuck in the lumen to be excreted

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23
Q

What is the main substance exerting osmotic pressure in cells?

Interstitial fluid?

A

K+

Na+

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24
Q

What does increased Na+ in the body do?

What may the compensating for?

A

Expands the ECF and the ECV

hypovolemia

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25
Q

How is plasma Na (therefore osmolarity) regulated?

A

Water balance

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26
Q

What factors promote Na reabsorption?

A

Sympathetics
RAAS
Secretion of aldosterone

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27
Q

What factors promote Na excretion?

A

ANP
BNP
Urodilatin
Intrarenal PGs

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28
Q

How do PGs promote Na excretion?

A

They vasodilate, thus Increasing RBF, Increasing filtration and Increasing filtered load of Na+

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29
Q

What does constriction of efferent renal arteriole do to GFR and RBF?

A

slightly increase GFR

Decrease RBF

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30
Q

Where is primary site of AGII action and what does it do?

Where is the secondary site?

A

PCT
Na reabsorption via INCreasing Na-H exchanger activity (pump out H+ and bring Na+ in)

TAL, CD

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31
Q

What does AGII stimulate?

A

Thirst
ADH secretion from posterior pituitary
Aldosterone secretion from adrenal cortex

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32
Q

What are the main Renal effects of AgII?

A

DEC RBF
DEC medullary blood flow
INC tubular sodium reabsorption

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33
Q

Where does aldosterone act?

A

Late DCT and principal cells in CD

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34
Q

What does aldosterone primarily do?

Secondarily?

A

K+ secretion by principal cells

Na+ reabsorption via epithelium Na+ channels

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35
Q

What effect does aldosterone have on H+?

A

Stimulates H+ secretion via INCreased activity of ATPase in intercalated cells

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36
Q

Hyperaldosteronism leads to what?

A

Hypokalemia

Metabolic Alkalosis

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37
Q

What 3 factors control aldosterone secretion aka cause a release of aldosterone?

A

INC plasma [K+]
INC plasma [ACTH]
Hypovolemia

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38
Q

What are the main effects of ANP?

A

INcrease Na+ and water excretion

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39
Q

What does ANP do to GFR?

How?

A

INCREASES GFR

Dilates afferent arterioles, constricts efferent arterioles

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40
Q

What secretes urodilatin?

In response to what?

A

DCT and CD

INC arterial pressure and ECF volume

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41
Q

What does urodilatin suppress?

What effect does it have on systemic circulation?

A

Na and water reabsorption by medullary CD

NO EFFECT

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42
Q

What do intrarenal PGs (PGE2) do Na excretion and GFR (via what mechanisms)?

A

INCrease Na excretion by suppressing Na reabsorption in TAL and CD

INCrease GFR by dilating renal arterioles

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43
Q

What secretes ADH?

A

Hypothalamus via posterior pituitary

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44
Q

What are the 2 major stimuli for ADH release?

A

Hyperosmolarity

Volume depletion

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45
Q

What osmoreceptors are most important?

A

Hypothalamic > hepatic

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46
Q

What is the luminal potential in the PCT?

TAL?

DCT?

A

+/- 2

+6 to +10

-70

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47
Q

What is the major mechanism of sodium reabsorption in the PCT?

A

Cotransport with glucose, a.a., phosphate

Countertransport with H+ (Na/H+ exchange)

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48
Q

Mechanism of sodium reabsorption in TAL?

A

Na, K, 2Cl cotransport

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49
Q

Mechanism of sodium reabsorption in early DCT?

A

Na, Cl cotransport

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50
Q

mechanism of sodium reabsorption in late DCT, CD?

A

Luminal Na membrane channels inserted by aldosterone

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51
Q

What is the descending limb of the loop of Henle permeable/impermeable to?

A

Perm - water

Impermeable to Na and Cl

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52
Q

What is the ascending limb perm/impermeable to?

What is this part called?

A

Impermeable to water

diluting segment

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53
Q

What is responsible for the +6mv potential in the TAL?

A

K+ leak channels

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54
Q

What ions are repelled by the + luminal potential and are able to leave the lumen paracellularly?

A

K+, Mg2+, Ca2+

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55
Q

Where is the major site of control of salt and water balance?

A

Late DCT and CD

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56
Q

What does aldosterone stimulate in late DCT and CD?

A

Na+ reabsorption

K+ and H+ secretion

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57
Q

What does ADH stimulate in the Late DCT and CD?

A

Water reabsorption

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58
Q

What is responsible for the large negative potential in the DCT?

What does this drive?

A

Cl-, it cannot get through tight junctions

K+ and H+ secretion by the principal cells

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59
Q

What is the MOA for aldosterone and Na+ reabsorption in the principal cells?

A

Aldosterone translocates to the nucleus of principal cells and helps it transcribe the proteins that are inserted into the apical membrane (ENaC) allowing Na to enter the cell

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60
Q

How does ADH increase the water permeability of the late DCT and CD?

A

ADH attaches V2 receptor to basolateral membrane of the cell via cGMP which will insert aquaporin channels onto the luminal side of the membrane

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61
Q

Why does the inner medullary interstitial fluid have a high solute concentration?

A

Low blood flow in inner medulla allows for concentration of solutes

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62
Q

What comprises the countercurrent multiplier system (3)?

A

Descending and ascending loops of Henle
Vasa recta
CDs

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63
Q

What is responsible for half of the 1200 mOsm gradient?

A

Na, K, Cl cotransporter in TAL

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64
Q

What promotes urea reabsorption from the inner medullary CD?

A

ADH

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65
Q

If you have a high protein diet, what is your urine concentrating ability like?

A

INCreased

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66
Q

What is special about the vasa recta?

A

VERY slow blood flow

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67
Q

What is antidiuresis?

A

Dehydrated patient

Therefore reduction in excretion of urine

68
Q

What is the urine like in an antidiuresing patient?

A

Low volume, high concentration

Due to presence of ADH

69
Q

What is happening in a patient who is diuresing?

A

Volume expanded

Low ADH

70
Q

What is the urine and concentration of the medullary interstitium like in a patient who is diuresing?

A

high volume of dilute urine excreted

Lower solute concentrations in the medullary interstitium

71
Q

How much waste is generated per day?

What is the max urine concentration?

A

600

1200

72
Q

Osmolar clearance equation =

A

(Uosm x V) / Posm

73
Q

What happens when the kidneys excrete excess solutes?

A

Osmolar clearance Increases

74
Q

Free water clearance (C) = ?

A

V - Cosm

75
Q

If Uosm

A

Free water clearance is positive and pure water is cleared from the body (getting rid of water)

76
Q

What does Uosm > Posm mean?

A

Free water clearance is negative and the body will retain pure water

Ie. Cases of dehydration

77
Q

How does ADH affect free water clearance?

A

Decreases it bc you are reabsorbing more water

78
Q

Fractional excretion = ?

A

Amount excreted / amount filtered

79
Q

Fractional excretion condensed formula =

A

(Ux X Pcr) / (Px X Ucr)

80
Q

If FE is below 1% what does it mean?

A

Prerenal and AGN

Sodium is avidly reabsorbed

81
Q

If FE is greater than 2% what does it mean?

A

Acute Tubular Necrosis (ATN), volume expanded or Renal cause

Na is excreted

82
Q

What does the PCT reabsorb?

A 
Filtered water
Na
K
Cl
Bicarbonate
Ca
Phosphate 
All the glucose and a.a.
83
Q

What are the 3 causes of pseudohyponatremia which lead to errors in lab measurement of Na?

A

Hyperproteinemia
Hyperlipidemia
Hypercholesterolemia

84
Q

What are the 2 causes of pseudohyponatremia due to dilutional hyponatremia?

A 
Hyperglycemia
Unmeasured osmosis (antifreeze)
85
Q

Plasma solute concentration = ?

A

2xNa + glucose/18 + BUN/2.8

86
Q

Osmolar gap =?

What is normal?

A

Difference between estimated plasma osmolarity and true measured plasma osmolarity

Less than 10

87
Q

What are the causes for true hyponatremia (low sodium and low plasma osmolarity) in cases of dilute urine and low ADH?

A 
Reset osmostat (pregnancy)
Psychogenic polydipsia
88
Q

A Uosm/Posm

A

Primary polydipsia

Neuro(central) OR Nephro Diabetes Insipidus

89
Q

What does a Uosm/Posm > 1 indicate with a low plasma osmolality?

High plasma osmolality?

A

SIADH

Dehydration

90
Q

How do you differentiate between Nephro and Neuro DI?

A

Give ADH
If the [urine] Increases and the problem is corrected, then it is Neuro
If giving ADH has no effect and does not fix the problem, then Nephro

91
Q

will the ADH level be low or high in a patient with Neuro DI?

A

Low

92
Q

What are 2 causes of hypernatremia (Na > 145)?

A

Extra renal water loss (excessive sweating, fever, diarrhea, vomiting)

Renal water loss (ADH not working properly)

93
Q

How does lithium act in the body?

What is a result of lithium in the body?

A

Limits V2 receptors from making cAMP, therefore less ADH and less transcription of aquaporin channels

Result is Nephro DI

94
Q

What are 2 common causes for Nephro DI?

A

Hypercalcemia (assoc. with malignancies)

Hyperkalemia (assoc. with acidosis)

95
Q

What are some common causes for central DI?

A

Head trauma
Postpartum hypophysitis (autoimmune)
Hypothalamic or pituitary tumor

96
Q

What maintains a normal BP while being volume expanded?

A

Initial INC in ECF volume activates atrial volume receptors that stimulate ANP secretion to return ECF volume to normal

97
Q

What are some causes of SIADH?

A 
Pulmonary tb
CHF
CNS issues (stroke)
Intubation w/mechanical ventilation
Drugs (SSRI, cyclophosphamide, Tegretol)
98
Q

What are some ADH antagonists?

A

Conivaptin

Demeclocycline

99
Q

What is common cause of hypervolemia?

What happens?

A

CHF

Excessive gain of salt and water –> edema

100
Q

What does a BUN > 20 indicate?

A

Pre-renal cause

Hypovolemia

101
Q

What are signs of Hypovolemia?

A

Orthostatic hypotension
Orthostatic tachycardia
Loss of skin turgor
Dry mucous membranes

102
Q

What are hyperkalemia patients at risk for?

A

Acidosis

103
Q

Are diabetics at risk for hypo or hyperkalemia?

Why?

A

Hyperkalemia bc lack of insulin to bring potassium from the plasma into the cells

104
Q

Where is the major site of K+ regulation?

A

CDs

105
Q

Who is K+ reabsorbed in the nephron?

A

67% PCT paracellularly

20% TAL via Na,K,2Cl cotransport

106
Q

How does a higher flow rate affect the secretion of K+?

A

More dilute tubular fluid, therefore more secretion of K+ into the tubule

107
Q

How do most diuretics affect Na, volume and K+?

A

Increase Na and volume to late DCT and CD, which increases K+ secretion

108
Q

What does increased plasma [K+] stimulate?

A

Aldosterone secretion

109
Q

What is Conn’s disease also called?

What causes it?

A

Primary hyperaldosteronism

Aldosterone secreting tumor in adrenal cortex

110
Q

What is a result of Conn’s disease?

A

Hypokalemia

Metabolic alkalosis

111
Q

What is Addison’s disease also called?

What causes it?

A

Hypoaldosteronism

Destruction of adrenals and aldosterone isn’t secreted

112
Q

What is the result of Addison’s disease?

A

Hyperkalemia

Acidosis

113
Q

What are hypokalemic patients at risk for?

A

Alkalosis

114
Q

What do diuretics do and how do they work?

A

Increase urine excretion by inhibiting tubular solute and water reabsorption

115
Q

When do you use a diuretic?

A

When volume expanded (CHF, edema)

116
Q

Where do osmotic diuretics work?

Give example of one

How does it work?

A

PCT

Mannitol

Inhibits water reabsorption and secondarily Na

117
Q

Where do CA inhibitors work?

Give example

How?

A

PCT

Acetazolamide

Inhibit NaHCO3 reabsorption

118
Q

What are some examples of loop diuretics?

A

furosemide
Ethacrynic acid
Bumetanide

119
Q

How do loop diuretics work?

What do they do to total RBF?

A

Inhibit Na,K,2Cl cotransporter by competing for Cl

Increase RBF and dissipates high solute [ ] of medullary interstitium

120
Q

What do loop diuretics do to the descending limb of loop of Henle?

A

Lessens the water reabsorption therefore decreasing the concentrating ability or our urine

121
Q

Where do thiazide diuretics act?

Example

How?

Result?

A

DCT

HCTZ

Inhibit Na,Cl cotransport

Increased Na,Cl,K excretion and decreased Ca excretion

122
Q

Where do potassium-sparing diuretics work?

Example

How?

A

CD

Amiloride, triamterene, spironolactone

Inhibit Na reabsorption and K secretion

123
Q

What is Ca2+ required for?

What can low EC Ca produce?

A

Neuromuscular transmission

Hypocalcemic tetany

124
Q

How does calcium affect APs?

A

Dampen APs by blocking Na channels

125
Q

What kind of calcium is biologically active?

What is the other kind bound to?

A

Free Calcium

Proteins (albumin)

126
Q

What does acidemia do to the plasma free Ca level?

A

Increases amount of free plasma Ca2+

127
Q

Low levels of H+ in the plasma does what to free calcium levels?

A

Decreased free plasma [Ca]

128
Q

What happens if Ca goes down?

A

PTH is released by parathyroid gland to activate Vit D and Calcitriol/Vit D3 which increases absorption of calcium from your diet

Bone resorption to increase amount of calcium that is released from your bone by osteoclastic activity

129
Q

Where is Calcium mostly reabsorbed?

Via what mechanism?

A

PCT

Transcellularly

130
Q

What prevents Ca from being reabsorbed paracellularly in the DCT?

A

Claudin 8 (CLDN8)

131
Q

Where does paracellular Ca reabsorption occur?

Because of what?

A

TAL

Driven by the 6mV potential

132
Q

What effect do loop diuretics have on paracellular Ca reabsorption?

A

INC flow, abolish charge in the lumen, thus decreasing calcium reabsorption leading to hypocalcemia

133
Q

What effect do thiazide diuretics have on calcium levels?

Why?

A

Cause hypercalcemia

Bc Na/Cl transporter is inhibited, less intracellular Na, so Na is instead exchanged via 3Na/Ca transporter that brings sodium in the cell and takes calcium into the blood

134
Q

What are the 3 effects of increasing plasma PTH?

A

INC bone resorption
INC tubular reabsorption of calcium
INC intestinal absorption of calcium

135
Q

What transporters does Phosphate use to get into the cell and eventually into the blood?

A

Cell: 2Na/Pi cotransporter

Blood: Pi/A- countertransporter

136
Q

What does PTH do to PCT phosphate reabsorption?

How?

A

Inhibits phosphate reabsorption and increases the amount of phosphate excreted

Inhibits the Pi/anion countertransporter in the blood

137
Q

What 3 forms is Mg carried in the plasma?

A

60% free
20% complexed w/inorganic or organic anions
20% bound to plasma proteins

138
Q

Where is the bulk of Mg reabsorbed?

How?

A

TAL (63%)

Paracellular movement

139
Q

What are volatile acids?

Examples

A

Produced by metabolic processes that can be expired by your respiratory system

Carbonic acid, H2CO3

140
Q

What are fixed acids?

Examples

A

Non-carbonic acids generated metabolically that are excreted in the urine and cannot be removed via ventilation

Sulfuric, phosphoric, lactic, hydrochloride acids, ketone acids, protein, nucleic acid

141
Q

What are the 3 lines of defense against pH changes in order and brief description of what they do?

A
  1. Chemical buffers - accept H+ ions
  2. Respiration - can blow off CO2
  3. Kidneys - gets rid of fixed acids
142
Q

What is the Renal response to excess acid?

A

All the filter bicarbonate is reabsorbed in the PCT

H+ secreted into the lumen and is excreted as ammonium in the urine

143
Q

What is the Renal response to excess base?

A

Incomplete reabsorption of filtered bicarbonate
Decreased H+ secretion
Secretion of HCO3- in CD

144
Q

How is most H+ excreted?

A

Titratable acid - conjugate base of metabolic acids (phosphate, creatinine, urate)
Ammonia - MAJOR way to get rid of H+

145
Q

Total renal H+ excretion = ?

A

Urinary excretion of titratable acid + ammonia - HCO3-

146
Q

Where does the the acidification of the nephron begin?

Where does a major of the acidification occur?

Where is the major site of ammonium formation?

A

PCT

DCT and CD

PCT

147
Q

What do alpha-intercalated cells do?

Describe the resulting blood?

What stimulates them?

A

Actively secrete H+ via ATPase

Alkalotic

Aldosterone

148
Q

What to Beta-intercalated cells do?

Name the transporter

A

Secrete bicarbonate to eliminate excess base

Bicarbonate is exchanged for Cl (counter-transporter)

149
Q

Hyperaldosteronism leads to what?

A

Alkalosis

Hypokalemia

150
Q

How many H+ ions are secreted in the reabsorption of HCO3-?

A

ZERO

151
Q

What substance is bicarbonate temporarily converted to so that it may traverse membranes freely?

What is this process dependent on?

A

CO2

Na/K ATPase

152
Q

What is the most important buffer converted to titratable acid?

A

Filter HPO4(2-)

153
Q

What does Glutamine produce?

What is the ultimate result?

A

2 ammonium ions

Acidification of the urine

154
Q

What renal response occurs if there is a decrease in intracellular pH?

A

Means increased [H+], therefore will secrete more H+

155
Q

What renal response will occur if there is increased PCO2?

A

Will excrete H+ ion

156
Q

What renal consequences will occur if a CA inhibitor is administered?

A

Cannot reabsorbed bicarbonate, get metabolic acidosis

157
Q

What renal response will occur if there is Increased Na reabsorption due to volume depletion?

A

Increase H+ secretion

158
Q

What renal response will occur to hypokalemia?

A

Want to reabsorbed more K+ in exchange for secreting H+, therefore alkalosis

159
Q

What renal response will occur if there is increased plasma aldosterone?

A

Increase activity of Na/K ATPase to reabsorb sodium and secrete potassium
Will also stimulate the H+ ATPase to secrete more H+ ions making the blood alkalotic

160
Q

What can diuretic abuse cause?

How?

A

Alkalemia bc there will be INC secretion of H+ as a result of the RAAS trying to retain water

161
Q

What can cause metabolic acidosis?

A

Gain of fixed acids

Diarrhea

162
Q

What can cause metabolic alkalosis?

A 
Alkali ingestion (seltzers)
Vomiting
163
Q

What does hyper choleric acidosis mean?

A

Anion Gap is unchanged

164
Q

What does a high anion gap acidosis indicated?

A

Normochloremic

MUDPILES

165
Q

MUDPILES mnemonic

A 
Methanol, metformin
Uremia
DKA (diabetes, alcohol, starvation)
Paraldehyde
Iron, Isoniazid, Inhalants
Lactic acidosis
Ethylene Glycol
Salicylates (aspirin), toluene
166
Q

What are causes of metabolic acidosis with a normal anion gap?

A

Diarrhea
renal tubular dysfunction
CA inhibitors
Addison’s disease

COM - Renal (5 decks)

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