FINAL Exam Flashcards

(166 cards)

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
How is plasma Na (therefore osmolarity) regulated?
Water balance
26
What factors promote Na reabsorption?
Sympathetics RAAS Secretion of aldosterone
27
What factors promote Na excretion?
ANP BNP Urodilatin Intrarenal PGs
28
How do PGs promote Na excretion?
They vasodilate, thus Increasing RBF, Increasing filtration and Increasing filtered load of Na+
29
What does constriction of efferent renal arteriole do to GFR and RBF?
slightly increase GFR Decrease RBF
30
Where is primary site of AGII action and what does it do? Where is the secondary site?
PCT Na reabsorption via INCreasing Na-H exchanger activity (pump out H+ and bring Na+ in) TAL, CD
31
What does AGII stimulate?
Thirst ADH secretion from posterior pituitary Aldosterone secretion from adrenal cortex
32
What are the main Renal effects of AgII?
DEC RBF DEC medullary blood flow INC tubular sodium reabsorption
33
Where does aldosterone act?
Late DCT and principal cells in CD
34
What does aldosterone primarily do? Secondarily?
K+ secretion by principal cells Na+ reabsorption via epithelium Na+ channels
35
What effect does aldosterone have on H+?
Stimulates H+ secretion via INCreased activity of ATPase in intercalated cells
36
Hyperaldosteronism leads to what?
Hypokalemia | Metabolic Alkalosis
37
What 3 factors control aldosterone secretion aka cause a release of aldosterone?
INC plasma [K+] INC plasma [ACTH] Hypovolemia
38
What are the main effects of ANP?
INcrease Na+ and water excretion
39
What does ANP do to GFR? How?
INCREASES GFR Dilates afferent arterioles, constricts efferent arterioles
40
What secretes urodilatin? In response to what?
DCT and CD INC arterial pressure and ECF volume
41
What does urodilatin suppress? What effect does it have on systemic circulation?
Na and water reabsorption by medullary CD NO EFFECT
42
What do intrarenal PGs (PGE2) do Na excretion and GFR (via what mechanisms)?
INCrease Na excretion by suppressing Na reabsorption in TAL and CD INCrease GFR by dilating renal arterioles
43
What secretes ADH?
Hypothalamus via posterior pituitary
44
What are the 2 major stimuli for ADH release?
Hyperosmolarity Volume depletion
45
What osmoreceptors are most important?
Hypothalamic > hepatic
46
What is the luminal potential in the PCT? TAL? DCT?
+/- 2 +6 to +10 -70
47
What is the major mechanism of sodium reabsorption in the PCT?
Cotransport with glucose, a.a., phosphate Countertransport with H+ (Na/H+ exchange)
48
Mechanism of sodium reabsorption in TAL?
Na, K, 2Cl cotransport
49
Mechanism of sodium reabsorption in early DCT?
Na, Cl cotransport
50
mechanism of sodium reabsorption in late DCT, CD?
Luminal Na membrane channels inserted by aldosterone
51
What is the descending limb of the loop of Henle permeable/impermeable to?
Perm - water Impermeable to Na and Cl
52
What is the ascending limb perm/impermeable to? What is this part called?
Impermeable to water diluting segment
53
What is responsible for the +6mv potential in the TAL?
K+ leak channels
54
What ions are repelled by the + luminal potential and are able to leave the lumen paracellularly?
K+, Mg2+, Ca2+
55
Where is the major site of control of salt and water balance?
Late DCT and CD
56
What does aldosterone stimulate in late DCT and CD?
Na+ reabsorption | K+ and H+ secretion
57
What does ADH stimulate in the Late DCT and CD?
Water reabsorption
58
What is responsible for the large negative potential in the DCT? What does this drive?
Cl-, it cannot get through tight junctions K+ and H+ secretion by the principal cells
59
What is the MOA for aldosterone and Na+ reabsorption in the principal cells?
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
60
How does ADH increase the water permeability of the late DCT and CD?
ADH attaches V2 receptor to basolateral membrane of the cell via cGMP which will insert aquaporin channels onto the luminal side of the membrane
61
Why does the inner medullary interstitial fluid have a high solute concentration?
Low blood flow in inner medulla allows for concentration of solutes
62
What comprises the countercurrent multiplier system (3)?
Descending and ascending loops of Henle Vasa recta CDs
63
What is responsible for half of the 1200 mOsm gradient?
Na, K, Cl cotransporter in TAL
64
What promotes urea reabsorption from the inner medullary CD?
ADH
65
If you have a high protein diet, what is your urine concentrating ability like?
INCreased
66
What is special about the vasa recta?
VERY slow blood flow
67
What is antidiuresis?
Dehydrated patient | Therefore reduction in excretion of urine
68
What is the urine like in an antidiuresing patient?
Low volume, high concentration Due to presence of ADH
69
What is happening in a patient who is diuresing?
Volume expanded Low ADH
70
What is the urine and concentration of the medullary interstitium like in a patient who is diuresing?
high volume of dilute urine excreted Lower solute concentrations in the medullary interstitium
71
How much waste is generated per day? What is the max urine concentration?
600 1200
72
Osmolar clearance equation =
(Uosm x V) / Posm
73
What happens when the kidneys excrete excess solutes?
Osmolar clearance Increases
74
Free water clearance (C) = ?
V - Cosm
75
If Uosm
Free water clearance is positive and pure water is cleared from the body (getting rid of water)
76
What does Uosm > Posm mean?
Free water clearance is negative and the body will retain pure water Ie. Cases of dehydration
77
How does ADH affect free water clearance?
Decreases it bc you are reabsorbing more water
78
Fractional excretion = ?
Amount excreted / amount filtered
79
Fractional excretion condensed formula =
(Ux X Pcr) / (Px X Ucr)
80
If FE is below 1% what does it mean?
Prerenal and AGN Sodium is avidly reabsorbed
81
If FE is greater than 2% what does it mean?
Acute Tubular Necrosis (ATN), volume expanded or Renal cause Na is excreted
82
What does the PCT reabsorb?
``` Filtered water Na K Cl Bicarbonate Ca Phosphate All the glucose and a.a. ```
83
What are the 3 causes of pseudohyponatremia which lead to errors in lab measurement of Na?
Hyperproteinemia Hyperlipidemia Hypercholesterolemia
84
What are the 2 causes of pseudohyponatremia due to dilutional hyponatremia?
``` Hyperglycemia Unmeasured osmosis (antifreeze) ```
85
Plasma solute concentration = ?
2xNa + glucose/18 + BUN/2.8
86
Osmolar gap =? What is normal?
Difference between estimated plasma osmolarity and true measured plasma osmolarity Less than 10
87
What are the causes for true hyponatremia (low sodium and low plasma osmolarity) in cases of dilute urine and low ADH?
``` Reset osmostat (pregnancy) Psychogenic polydipsia ```
88
A Uosm/Posm
Primary polydipsia Neuro(central) OR Nephro Diabetes Insipidus
89
What does a Uosm/Posm > 1 indicate with a low plasma osmolality? High plasma osmolality?
SIADH Dehydration
90
How do you differentiate between Nephro and Neuro DI?
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
will the ADH level be low or high in a patient with Neuro DI?
Low
92
What are 2 causes of hypernatremia (Na > 145)?
Extra renal water loss (excessive sweating, fever, diarrhea, vomiting) Renal water loss (ADH not working properly)
93
How does lithium act in the body? What is a result of lithium in the body?
Limits V2 receptors from making cAMP, therefore less ADH and less transcription of aquaporin channels Result is Nephro DI
94
What are 2 common causes for Nephro DI?
Hypercalcemia (assoc. with malignancies) Hyperkalemia (assoc. with acidosis)
95
What are some common causes for central DI?
Head trauma Postpartum hypophysitis (autoimmune) Hypothalamic or pituitary tumor
96
What maintains a normal BP while being volume expanded?
Initial INC in ECF volume activates atrial volume receptors that stimulate ANP secretion to return ECF volume to normal
97
What are some causes of SIADH?
``` Pulmonary tb CHF CNS issues (stroke) Intubation w/mechanical ventilation Drugs (SSRI, cyclophosphamide, Tegretol) ```
98
What are some ADH antagonists?
Conivaptin | Demeclocycline
99
What is common cause of hypervolemia? What happens?
CHF Excessive gain of salt and water --> edema
100
What does a BUN > 20 indicate?
Pre-renal cause | Hypovolemia
101
What are signs of Hypovolemia?
Orthostatic hypotension Orthostatic tachycardia Loss of skin turgor Dry mucous membranes
102
What are hyperkalemia patients at risk for?
Acidosis
103
Are diabetics at risk for hypo or hyperkalemia? Why?
Hyperkalemia bc lack of insulin to bring potassium from the plasma into the cells
104
Where is the major site of K+ regulation?
CDs
105
Who is K+ reabsorbed in the nephron?
67% PCT paracellularly 20% TAL via Na,K,2Cl cotransport
106
How does a higher flow rate affect the secretion of K+?
More dilute tubular fluid, therefore more secretion of K+ into the tubule
107
How do most diuretics affect Na, volume and K+?
Increase Na and volume to late DCT and CD, which increases K+ secretion
108
What does increased plasma [K+] stimulate?
Aldosterone secretion
109
What is Conn's disease also called? What causes it?
Primary hyperaldosteronism Aldosterone secreting tumor in adrenal cortex
110
What is a result of Conn's disease?
Hypokalemia | Metabolic alkalosis
111
What is Addison's disease also called? What causes it?
Hypoaldosteronism Destruction of adrenals and aldosterone isn't secreted
112
What is the result of Addison's disease?
Hyperkalemia | Acidosis
113
What are hypokalemic patients at risk for?
Alkalosis
114
What do diuretics do and how do they work?
Increase urine excretion by inhibiting tubular solute and water reabsorption
115
When do you use a diuretic?
When volume expanded (CHF, edema)
116
Where do osmotic diuretics work? Give example of one How does it work?
PCT Mannitol Inhibits water reabsorption and secondarily Na
117
Where do CA inhibitors work? Give example How?
PCT Acetazolamide Inhibit NaHCO3 reabsorption
118
What are some examples of loop diuretics?
furosemide Ethacrynic acid Bumetanide
119
How do loop diuretics work? What do they do to total RBF?
Inhibit Na,K,2Cl cotransporter by competing for Cl Increase RBF and dissipates high solute [ ] of medullary interstitium
120
What do loop diuretics do to the descending limb of loop of Henle?
Lessens the water reabsorption therefore decreasing the concentrating ability or our urine
121
Where do thiazide diuretics act? Example How? Result?
DCT HCTZ Inhibit Na,Cl cotransport Increased Na,Cl,K excretion and decreased Ca excretion
122
Where do potassium-sparing diuretics work? Example How?
CD Amiloride, triamterene, spironolactone Inhibit Na reabsorption and K secretion
123
What is Ca2+ required for? What can low EC Ca produce?
Neuromuscular transmission Hypocalcemic tetany
124
How does calcium affect APs?
Dampen APs by blocking Na channels
125
What kind of calcium is biologically active? What is the other kind bound to?
Free Calcium Proteins (albumin)
126
What does acidemia do to the plasma free Ca level?
Increases amount of free plasma Ca2+
127
Low levels of H+ in the plasma does what to free calcium levels?
Decreased free plasma [Ca]
128
What happens if Ca goes down?
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
Where is Calcium mostly reabsorbed? Via what mechanism?
PCT Transcellularly
130
What prevents Ca from being reabsorbed paracellularly in the DCT?
Claudin 8 (CLDN8)
131
Where does paracellular Ca reabsorption occur? Because of what?
TAL Driven by the 6mV potential
132
What effect do loop diuretics have on paracellular Ca reabsorption?
INC flow, abolish charge in the lumen, thus decreasing calcium reabsorption leading to hypocalcemia
133
What effect do thiazide diuretics have on calcium levels? Why?
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
What are the 3 effects of increasing plasma PTH?
INC bone resorption INC tubular reabsorption of calcium INC intestinal absorption of calcium
135
What transporters does Phosphate use to get into the cell and eventually into the blood?
Cell: 2Na/Pi cotransporter Blood: Pi/A- countertransporter
136
What does PTH do to PCT phosphate reabsorption? How?
Inhibits phosphate reabsorption and increases the amount of phosphate excreted Inhibits the Pi/anion countertransporter in the blood
137
What 3 forms is Mg carried in the plasma?
60% free 20% complexed w/inorganic or organic anions 20% bound to plasma proteins
138
Where is the bulk of Mg reabsorbed? How?
TAL (63%) Paracellular movement
139
What are volatile acids? Examples
Produced by metabolic processes that can be expired by your respiratory system Carbonic acid, H2CO3
140
What are fixed acids? Examples
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
What are the 3 lines of defense against pH changes in order and brief description of what they do?
1. Chemical buffers - accept H+ ions 2. Respiration - can blow off CO2 3. Kidneys - gets rid of fixed acids
142
What is the Renal response to excess acid?
All the filter bicarbonate is reabsorbed in the PCT | H+ secreted into the lumen and is excreted as ammonium in the urine
143
What is the Renal response to excess base?
Incomplete reabsorption of filtered bicarbonate Decreased H+ secretion Secretion of HCO3- in CD
144
How is most H+ excreted?
Titratable acid - conjugate base of metabolic acids (phosphate, creatinine, urate) Ammonia - MAJOR way to get rid of H+
145
Total renal H+ excretion = ?
Urinary excretion of titratable acid + ammonia - HCO3-
146
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?
PCT DCT and CD PCT
147
What do alpha-intercalated cells do? Describe the resulting blood? What stimulates them?
Actively secrete H+ via ATPase Alkalotic Aldosterone
148
What to Beta-intercalated cells do? Name the transporter
Secrete bicarbonate to eliminate excess base Bicarbonate is exchanged for Cl (counter-transporter)
149
Hyperaldosteronism leads to what?
Alkalosis | Hypokalemia
150
How many H+ ions are secreted in the reabsorption of HCO3-?
ZERO
151
What substance is bicarbonate temporarily converted to so that it may traverse membranes freely? What is this process dependent on?
CO2 Na/K ATPase
152
What is the most important buffer converted to titratable acid?
Filter HPO4(2-)
153
What does Glutamine produce? What is the ultimate result?
2 ammonium ions Acidification of the urine
154
What renal response occurs if there is a decrease in intracellular pH?
Means increased [H+], therefore will secrete more H+
155
What renal response will occur if there is increased PCO2?
Will excrete H+ ion
156
What renal consequences will occur if a CA inhibitor is administered?
Cannot reabsorbed bicarbonate, get metabolic acidosis
157
What renal response will occur if there is Increased Na reabsorption due to volume depletion?
Increase H+ secretion
158
What renal response will occur to hypokalemia?
Want to reabsorbed more K+ in exchange for secreting H+, therefore alkalosis
159
What renal response will occur if there is increased plasma aldosterone?
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
What can diuretic abuse cause? How?
Alkalemia bc there will be INC secretion of H+ as a result of the RAAS trying to retain water
161
What can cause metabolic acidosis?
Gain of fixed acids | Diarrhea
162
What can cause metabolic alkalosis?
``` Alkali ingestion (seltzers) Vomiting ```
163
What does hyper choleric acidosis mean?
Anion Gap is unchanged
164
What does a high anion gap acidosis indicated?
Normochloremic MUDPILES
165
MUDPILES mnemonic
``` Methanol, metformin Uremia DKA (diabetes, alcohol, starvation) Paraldehyde Iron, Isoniazid, Inhalants Lactic acidosis Ethylene Glycol Salicylates (aspirin), toluene ```
166
What are causes of metabolic acidosis with a normal anion gap?
Diarrhea renal tubular dysfunction CA inhibitors Addison's disease