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CR&R > Quiz 3 > Flashcards

Quiz 3 Flashcards

1
Q

Where is the GBM found relative to the glomerulus and Bowman’s space?

A
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2
Q

Through what structure in the glomerular capillary does plasma flow before crossing the GBM? After crossing, it passes between podocytes through what structure in order to enter Bowman’s space?

A

Fenestrations

Filtration slits

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3
Q

What is the GFR?

A

The sum of the individual filtration rates of all glomeruli in both kidneys

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4
Q

What is the optimal GFR of normal kidney function? What range is still considered normal?

A
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5
Q

What range of GFR values is considered kidney disease?

A
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6
Q

What range of GFR values is considered kidney failure?

A
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7
Q

What substances should not pass through the GBM?

A
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8
Q

What is the equation that represents how to theoretically determine GFR with Starling forces?

A
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9
Q

How much ATP is required per minute for glomerular filtration to occur?

A
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10
Q

What happens to Glomerular capillary oncotic pressure as plasma moves from the AGA to the EGA?

A

It increases as plasma volume is filtered into BC, so that pressure is equalized at the EGA and no further filtration occurs

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11
Q

What substance is used to measure GFR in experiments? What clinical substance is used to approximate GFR for patients?

A
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12
Q

How is creatinine clearance calculated?

A
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13
Q

What is RPF?

A
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14
Q

Why is Para-AminoHippuric acid (PAH) used in order to estimate renal plasma flow (RPF)?

A
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15
Q

What is the equation used to calculate RPF (using PAH)?

A
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16
Q

What equation can be used to calculate RPF involving HCT?

A
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17
Q

What is the filtration fraction of the kidneys?

A

*Also know it is the ratio of the GFR to the RPF

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18
Q

What is the relationship between FF, GFR, and RPF?

A
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19
Q

What effect does dilation of the AGA have on RPF? On GFR? on FF? What is an example of a substance that causes this effect?

A
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20
Q

What effect does constriction of the AGA have on RPF? On GFR? on FF? What is an example of a substance that causes this effect?

A
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21
Q

What effect does constriction of the EGA have on RPF? on GFR? on FF? What is an example of a substance that causes this effect?

A
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22
Q

What effect does increased albumin in the plasma have on RPF? On GFR? On FF?

A
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23
Q

What can cause an increase in hydrostatic pressure in Bowman’s space?

A
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24
Q

How does increasing the hydrostatic pressure in Bowman’s space affect GFR? RPF? FF? What can cause this to occur?

A
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25
Q

In absence of autoregulation of GFR what would occur in situations of high BP? Of low BP?

A
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26
Q

What two autoregulation mechanisms are used by the kidneys to regulate GFR and RPF over a wide range of MAP?

A
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27
Q

How does the myogenic mechanism work in autoregulation of GFR?

A
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28
Q

How does the tubuloglomerular feedback mechanism work in autoregulation of the GFR?

A
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29
Q

What are some limits on auto-regulation of GFR? What drugs can interfere with autoregulation?

A
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30
Q

What is filtrate called once it moves from BS into the nephron tubules?

A

Tubular fluid

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31
Q

What is the direction and exchange rate of Na+ and K+ in the tubular cell Na+/K+ ATPase?

A
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32
Q

What are two hormones that stimulate the Na+/K+ ATPases in renal tubular cells?

A

Insulin
Epinephrine

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33
Q

Which tubule of the nephron experiences the highest volume of substance traffick?

A

The proximal tubule

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34
Q

Which renal tubule is responsible for absorption of all glucose and AA’s, as well as most of the HCO3?

A
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35
Q

What is the proximal tubule responsible for absorbing and secreting?

A
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36
Q

What PCT transporter is principally responsible for reabsorption of glucose? What substance is co-transported?

A
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37
Q

Most symporters in the PCT use what substance for cotransport?

A

Na+

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38
Q

What two mechanisms allow for water reabsorption in the PCT?

A

Aquaportins (AQP1)
Tight junctions

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39
Q

How is bicarbonate reabsorbed in the PCT? Which carbonic anhydrase is found in the apical surface of the cell, and which on the interior?

A
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40
Q

As water diffuses through the tight junctions in the PCT what molecules are able to follow it as a result of solvent drag?

A
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41
Q

T/F: The DTL of the loop of Henle is permeable to salt but NOT water

A

False, the exact opposite

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42
Q

As tubular fluid travels through the DTL of the loop of Henle, what is the change in osmolality?

A

300 mOsm to about 1200 mOsm

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43
Q

What types of channels allow Na+ reabsorption in the TAL of the loop of Henle but not water?

A
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44
Q

Where is magnesium predominantly reabsorbed in the renal tubules?

A
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45
Q

What molecules are reabsorbed from the tubular fluid by the NKCC2 transporters?

A

Na+
K+
2 Cl-

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46
Q

What is the counter-current multiplier? What two processes is it essential for?

A
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47
Q

What transporter is the target of loop diuretics? What effect does this have on the tonicity of the renal medulla? What is the net effect on urine production?

A
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48
Q

Why can loop diuretics cause a decrease in plasma potassium levels?

A
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49
Q

Which transporter allows K+ to leak back into the filtrate in the TAL?

A
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50
Q

What transporter in the DCT is responsible for reabsorbing Na+ and Cl- ions from filtrate in to DCT cells? What type of diuretics target this transporter?

A

NCC symporter

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51
Q

The CD of the kidneys are impermeable to water under what condition? Under what condition are they impermeable to salts?

A
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52
Q

How does ADH lead to water reabsorption in the DCT/CD?

A
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53
Q

How does aldosterone lead to sodium reabsorption in the DCT/CD?

A
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54
Q

How much of total Na+ reabsorption occurs in the DCT/CD? Is it more or less impactful on Na+ homeostasis than PT malabsorption?

A
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55
Q

What structures are included in the renal corpuscle?

A

Glomerulus
Bowman’s capsule

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56
Q

What equation can be used to represent excretion from the kidneys?

A

Excretion = Filtration - Reabsorption + Secretion

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57
Q

What percentage of nephrons are classified as cortical? Where are they located? What is the relative length of the loops of Henle?

A
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58
Q

What capillaries receive blood from the EGA in cortical nephrons?

A
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59
Q

What percentage of nephrons are classified as juxtamedullary? Where are they located? What is the relative length of the loops of Henle?

A
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60
Q

What capillaries receive blood from the EGA in juxtamedullary nephrons?

A
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61
Q

What are the three parts of the glomerular filtration apparatus (GFA)?

A

1) Fenestrated glomerular capillary
2) GBM
3) Podocytes with filtration slits

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62
Q

What is the purpose of the counter-current exchanger in the renal medulla?

A
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63
Q

Where are macula densa cells found?

A

DCT

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64
Q

Does maximally dilute urine require the presence of Aldosterone, ADH, both or neither?

A
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65
Q

Does maximally concentrated urine require the presence of Aldosterone, ADH, both or neither?

A

*With ADH, no aldosterone

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66
Q

Does urine with the same osmolality of body fluids require the presence of Aldosterone, ADH, both or neither?

A
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67
Q

What are the 3 unique cell types that compose the juxtaglomerular apparatus?

A

1) JG cells (granular cells)
2) Macula densa
3) Mesangial cells

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68
Q

What is the function of juxtaglomerular cells? What are the 3 situations that activate them?

A
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69
Q

What is the role of macula densa cells in the JG apparatus? What occurs when a drop in tubular fluid Na+ concentration is sensed?

A
70
Q

Small tumors (less than 1.5cm diameter) found in the renal cortex, comprising branching, papillomatous structures with complex fronds would most likely represent what type of neoplasm?

A

Renal papillary adenoma

71
Q

What type of renal neoplasm is present in 25-50% of patients with tuberous sclerosis?

A

Angiomyolipoma

72
Q

An epithelial neoplasm comprised of large eosinophilic cells with small nuclei and large nucleoli; also presenting as a tan/brown tumor would most likely be classified as what type of neoplasm?

A

Oncocytoma

73
Q

Tuberous sclerosis is caused by a loss-of-function mutation in which genes?

A

TSC1 or TSC2

74
Q

What manifestations characterize tuberous sclerosis?

A

Lesions of the cerebral cortex that produce epilepsy and intellectual disability

75
Q

What percentage of renal cancers are renal cell carcinomas?

A

85%

76
Q

The VHL gene mutation is associated with what type of renal cell carcinoma?

A

Renal clear cell carcinoma

77
Q

The MET gene mutation is associated with what type of renal cell carcinoma?

A

Renal papillary carcinoma

78
Q

What cellular abnormalities can be found in renal chromophobe carcinoma ? What can it be difficult to distinguish from?

A

Prominant cell membranes and pale eosinophilic cytoplasm
*A halo around the nucleus is often seen

It can be difficult histologically to distinguish from oncocytoma

79
Q

What percentage of renal clear cell carcinoma cases are familial? What percentage are sporadic?

A

Familial: 5%
Sporadic: 95%

80
Q

At what systolic and diastolic values is a blood pressure classified as Stage 1 HTN? Is one measurement sufficient?

A
81
Q

Each increment of ____ mmHg in SBP or ____ mmHg in DBP doubles the risk of death from stroke, heart or vascular disease.

A
82
Q

What are the 6 broad causes of HTN?

A
83
Q

What two criteria could classify hypertension as stage 1?

A
84
Q

What two criteria could classify hypertension as stage 2?

A
85
Q

What is essential hypertension?

A

Hypertension of no single, definable cause

AKA primary hypertension

86
Q

What is secondary hypertension?

A

Hypertension with a known etiology (potentially reversible)

87
Q

What is resistant hypertension?

A
88
Q

What is malignant hypertension?

A
89
Q

What is the main difference between hypertensive urgency and hypertensive emergency?

A
90
Q

What is a better phrase than “hypertensive urgency”?

A

Severe uncontrolled hypertension

91
Q

What immediate treatment steps are indicated for a hypertensive urgency (severe uncontrolled HTN)?

A
92
Q

What immediate treatment steps are indicated for a hypertensive emergency?

A
93
Q

What are the 5 most common causes of secondary hypertension?

A
94
Q

What type of cells surround the glomerulus just outside of Bowman’s space?

A

Parietal cells

95
Q

What are the four main compartments of the kidney to be considered in pathologies?

A

Glomeruli
Tubules
Interstitium
Vessels

96
Q

What is a common mechanism of glomerular injury?

A
97
Q

What are common mechanisms of vessel injury in the kidneys?

A
98
Q

What are common mechanisms of tubular or interstitial injury in the kidneys?

A
99
Q

What disease state is visible here?

A

End Stage Renal Disease
-sclerotic glomeruli
-poor tubule visualization
-lots of inflammatory cells

100
Q

What are the different cells (labeled 1-4) in this electron microscope picture?

A
101
Q

What are the different cells/structures/spaces (labeled 1-6) in this electron microscope picture?

A
102
Q

What is the difference between primary and secondary glomerular disease? What are the two major manifestations of glomerular disease?

A
103
Q

What is a simple definition of nephrotic syndrome? What are three notable clinical features?

A

Massive proteinuria
Edema
Foamy urine (due to protein)

104
Q

What are two notable pathologies that patients with nephrotic syndrome have increased susceptibility to?

A
105
Q

What is a simple definition of nephritic syndrome? What are 5 notable clinical features?

A

Hematuria (w/ casts)
Proteinuria
Dysmorphic RBCs
Azotemia (increased BUN)
Coke-colored urine

106
Q

How do immune complexes activate the classical complement pathway?

A
107
Q

What is the difference in location between sub-epithelial, sub-endothelial and mesangial immune complex deposition?

A
108
Q

What type of immune complex deposition is occuring in this picture?

A

Subendothelial IC deposition

109
Q

What type of immune complex deposition is occuring in this picture?

A

Subepithelial IC deposition

110
Q

What are possible etiologies for granular-pattern inflammation (left) vs linear-pattern inflammation (right)?

A
111
Q

What type of renal tumor is visible here?

A

Renal papillary adenoma

112
Q

What type of renal tumor is visible here? How is it described?

A

Renal papillary adenoma

Well-circumscribed, greyish-white to yellow nodules

113
Q

What renal tumor is visible here? What disease is associated with it in 25-50% of patients? What renal crisis are these patients suceptible to?

A

Angiomyolipoma

Tuberous sclerosis

Spontaneous retriperitoneal hemorrhage

114
Q

What renal tumor is visible here? How is it described?

A

Well-circumscribed, mahogany brown-yellow

115
Q

What is one difference that can be used to differentiate oncocytoma nad chromophobe RCC histologically?

A

Chromophobe RCC presents with “halos” around the nuclei of affected cells

116
Q

What is Benign Nephrosclerosis?

A

Luminal narrowsing of arterioles/small arteries caused by hyalinization of walls (hyaline arteriosclerosis)

*grossly may appear leathery and granular

117
Q

What kidney tumor is visible here? How is the appearance described?

A

Malignant nephrosclerosis

*The rupture of capillaries gives rise to petechiae that give the kidney a “flea-bitten” appearance

118
Q

What are two notable microscopic findings for malignant nephrosclerosis?

A
119
Q

What is the most common cause of renal artery stenosis?

A
120
Q

What is the 2nd most common cause of renal artery stenosis? What are two important RF?

A
121
Q

What is the main clinical impact of renal artery stenosis?

A
122
Q

What are the expected clinical findings in benign nephrosclerosis? What are the expected clinical findings in maligant nephrosclerosis?

A
123
Q

What subtype of renal cancer represents 70-80% of cancer findings?

A

Renal clear cell carcinoma

124
Q

What type of renal pathology is visible here?

A

Renal clear cell carcinoma

125
Q

Renal clear cell carcinoma has a tendency to invade into what vascular structure?

A

The renal vein

126
Q

What percentage of renal cell carcinomas are sporadic?

A

95%

127
Q

What gene inactivation is associated with the cases of renal cell caricinoma that are genetic?

A

Inactivation of the Von-Hippel-Lindau gene (VHL)

128
Q

What notable pathology visible here is unique to the type of cancer occuring? What type of cancer is it?

A

“peri-nuclear halos”

Chromophobe carcinoma

129
Q

Of renal clear cell carcinomas, renal papillary carcinoma and chromophobe carcinomas, which have the best prognosis?

A

Chromophobe carcinomas

130
Q

What type of renal cancer can be seen here?

A

XP11 translocation renal cell carcinoma

131
Q

What elements of the triphasic appearance (Wilm’s tumor) are located by the red and greens arrows, respectively, as well as the yellow circle?

A

RA: Stromal component
GA: Epithelial component
YC: Blastemic component

132
Q

What is a unique feature of this particular sample of a Wilm’s tumor? What is the influence on the prognosis?

A

Anaplastic presentation

Worse prognosis for anaplastic presentation

133
Q

What three notable syndromes carry an associated risk of Wilm’s tumor?

A
134
Q

What effect can heavy menstruation have on urine protein readings?

A

Elevated urine protein readings due to difficulty in obtaining a clean-catch sample

135
Q

What are 3 situations in which a false positive result for blood on urinalysis can be obtained?

A

1) Hemoglobin in urine (i.e. intravascular hemolysis)
2) Myoglobin in urine (rhabdomyolysis)
3) Semen in urine

136
Q

Presence of what vitamin on some disticks can lead to false negative for hematuria?

A

Vitamin C (ascorbic acid)

137
Q

In what two kidney diseases are white cell casts seen?

A
138
Q

In what type of kidney diseases can fatty casts be seen?

A
139
Q

With what kidney disease can waxy casts be seen?

A
140
Q

In what kidney pathology can “muddy brown” casts be seen?

A
141
Q

In what type of kidney pathology can hyaline casts be seen?

A
142
Q

What are the five types of kidney stones pictured here?

A
143
Q

What isthe Kidney Disease: Improving Global Outcomes (KDIGO) definition of acute renal failure?

A
144
Q

What is oliguria?

A

Less than 500mL/day of urine output

145
Q

What is anuria?

A

Urine output of less than 50mL/day

146
Q

What is indicated by a FeNa of less than 1%? What is the formula for FeNa?

A
147
Q

What acronym is used to indicate emergent need of dialysis?

A
148
Q

pH persistantly below what level despite management is indicative for dialysis? Hyperkalemia above what level is indicative for dialysis?

A
149
Q

What is the primary absorption site of magnesium in the nephron?

A

The TAL

150
Q

How does hypomagnesemia affect potassium?

A

Magnesium blocks the ROMK channel, so hypomagnesemia can lead to worse potassium losses through ROMK

151
Q

What is the difference in primary indication for loop diuretics vs thiazide diuretics?

A

Loop- diuresis for hypervolemia
Thiazide- HTN, nephrolithiasis

152
Q

What is a potential treatment for a patient with normal kidney function with stage 2 hypertension?

A

Losartan + hydrochlorothiazide

153
Q

What effect does aldosterone have on urinary excretion of potassium?

A

Aldosterone increaeses renal excretion of potassium

154
Q

What should generally be given in orde to treat hypokalemia? What should be given if the patient is acidemic?

A

Potassium chloride is generally the best

If the patient is acidemic, give potassium citrate

155
Q

What is the preferred treatment for hyperkalemia? What are next steps?

A

First step, IV calcium gluconate (stabilize myocardium)

Then insulin and glucose (also bicarbonate) given to push K+ into the cells

156
Q

What are the two main actions of PTH?

A
157
Q

What are the two main effects of calcitriol? How are these effects undone?

A
158
Q

What is the overall effect of FGF23? What releases it?

A

FGF23 is released by osteoclasts and osteoblasts in response to calcitriol and high phosphate

It has a phosphaturic effect

159
Q

What are the two main functions of calcitonin?

A

To reduce plasma calcium and phosphorous

160
Q

Which diuretic increases urinary calcium?

A

Loop diuretics (also maybe CAIs)

161
Q

Which diuretics increase plasma calcium?

A

Thiazide diuretics
Potassium sparing

162
Q

Which diuretics increase urinary magnesium?

A

Thiazide diuretics

163
Q

Does a patient with a an eGFR of 60 without other markers of kidney of kidne damage have CKD?

A

No!

164
Q

What are typical differences in prior creatinine in AKI CKD?

A
165
Q

What are main differences in kidney size in AKI vs CKD?

A
166
Q

What are the main differences in exam findings and labs between AKI and CKD?

A
167
Q

In proteinuric CKD, what medications may be used even though they can have a reductive effect on the GFR?

A

ACEi or ARBs

168
Q

What transporter creates most of the gradiant driving bicarbonate reabsorption in the PCT?

A

the Na/K ATPase

169
Q

Does ammonia or titratable acids have a greater capacity to bind acid in the renal tubules?

A

Ammonia; titratable acids can only accomodate a “fixed” amount, about 30mmol of acid excretion per day

170
Q

Where is ammonia generated in the kidney?

A

the PCT

171
Q

What effect does hypokalemia/hyperkalemia have on ammonia production?

A

Hypokalemia: Stimulates ammonia production

Hyperkalemia: Reduces ammonia production

172
Q
A

CR&R (8 decks)

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