FIRST AID 2012 Renal Flashcards
1
Q
What is the course of the ureters?
A
They pass under the uterine artery and under the ductus deferens.
Mneumonic: “Water under the bridge”
2
Q
What is the 60-40-20 rule?
A
60% total body water
40% ICF
20% ECF
3
Q
Of our total body weight, how much is water and how much is nonwater?
A
60% total body water
40% nonwater mass
4
Q
Of the 60% total body water, how much is extracellular fluid and how much is intracellular fluid?
A
1/3 extracellular fluid
2/3 intracellular fluid
5
Q
Of the extracellular fluid, how much is plasma and how much is interstitial volume?
A
1/4 plasma volume
3/4 interstitial volume
9
Q
The glomerular filtration barrier is responsible for filtration of plasma according to what two factors?
A
- size
2. net charge
10
Q
What are the 3 things that make up the glomerular filtration barrier?
A
- fenestrated capillary endothelium (size barrier)
- fused basement membrane with heparin sulfate (negative charge barrier)
- epithelial layer consisting of podocyte foot processes
12
Q
How do you calculate renal clearance?
A
C = (U x V)/ P
U = urine concentration V = urine flow rate P = plasma concentration
13
Q
- C = GFR
A
- Clearance < GFR = net tubular reabsorption of substance
- Clearance >GFR = net tubular secretion of X
- Clearance = GFR = no net secretion or reabsorption
14
Q
What is used to calculate GFR? Why? What is normal GFR?
A
Inulin is used to calculate GFR b/c it is freely filtered and is not reabsorbed or secreted.
Normal GFR is 100 mL/min.
15
Q
What is another way to write out this equation?
A
GFR = Kf [(Pgc - Pbs) - (TTgc - TTbs)]
GC = glomerular capillary
BS - bowman’s space
TTbs normally equals zero
16
Q
How do you measure plasma volume?
A
Radiolabeled albumin
17
Q
How do you measure extracellular volume?
A
Inulin
18
Q
What is normal osmolarity?
A
290 mOsm
20
Q
How do you calculate a filtration fraction (FF)? What is considered to be normal FF?
A
FF = GFR / RPF
Normal FF = 20%
24
Q
What effect will prostaglandins have on the afferent arteriole, RPF, GFR, and FF?
A
Dilate afferent arteriole
Increase RPF
Increase GFR
Constant FF
25
Q
What effect will ATN II have on the efferent arteriole, RPF, GFR, and FF?
A
Constriction efferent arteriole
Decrease RPF
Increase GFR
Increase FF
26
Q
Under what situations is the charge barrier of the glomerular filtration barrier lost?
A
In nephrotic syndrome which results in albuminuria, hypoproteinemia, generalized edema, and hyperlididemia
28
Q
What will happen to RPF, GFR, and FF (GFR/RPF) upon afferent arteriole constriction?
A
Decreased RPF
Decreased GFR
No Change in FF
29
Q
What will happen to RPF, GFR, and FF upon efferent arteriole constriction?
A
Decreased RPF
Increased GFR
Increased FF
30
Q
What will happen to RPF, GFR, and FF upon increased plasma protein concentrations?
A
No change in RPF
Decreased GFR
Decreased FF
31
Q
What will happen to RPF, GFR, and FF upon decreased plasma protein concentrations?
A
No change in RPF
Increased GFR
Increased FF
32
Q
What will happen to RPF, GFR, and FF upon constriction of the ureter?
A
No change in RPF
Decreased GFR
Decreased FF
33
Q
What is reabsorbed in the early proximal tubule of the nephron?
A
All of the glucose and amino acids.
Most of the bicarbonate, sodium, chloride, and water.
38
What is the concentrating segment of the nephron?
Thin descending loop of Henle (it passively reabsorbs H2O via medullary hypertonicity b/c it is impermeable to sodium).
Urine becomes hypertonic.
39
What happens at the thick ascending loop of Henle?
Actively reabsorb Na+/K+/Cl- and indirectly induce paracellular reabsorption of Mg2+ and Ca2+.
Unlike the thin descending limb, the thick ascending limb is impermeable to H2O.
42
What happens at the early distal convolute tubule?
Active reabsorption of Na+ and Cl-.
Known as the diluting segment. Makes urine hypotonic.
46
Can creatinine clearance be used to measure GFR?
Yes, but it slightly overestimates GFR b/c creatinine is secreted by renal tubules (inulin isn't).
47
Collecting Tubules
CAI --> Proximal Tubule
Thiazides --> TAL
Loops --> Distal Convoluted Tubule
K+ sparing diuretics --> Collecting Tubules
48
What 3 things stimulate the kidneys to secrete Renin?
1. Decreased BP (JG cells)
2. Decreased Na+ delivery to Macula Densa cells
3. Increased sympathetic tone (beta-1 receptors)
49
What can be used to estimate effective renal plasma flow (ERPF)?
PAH
50
Why is PAH clearance used to estimate ERPF?
It is both filtered and actively secreted in the proximal tubule. Therefore, this means that all PAH that enters the kidney is excreted.
52
What are the 6 actions of ATN II?
1. Acts at AT II receptors on VSM --> vasoconstriction --> increase BP
2. Constrict efferent arterioles --> Increase FF to preserve GFR in low-volume states (ie decreased RBF)
3. Stimulates the adrenal gland to secrete aldosterone
4. Stimulates the posterior pituitary to secrete ADH
5. Increase proximal tubule Na+/H+ activity --> H2O reabsorption
6. Stimulates hypothalamus --> thirst
53
How is this equation different from the equation: RBF = RPF (1-Hct)?
ERPF underestimates true RPF by ~10%
56
What are the 4 roles that the kidney plays in endocrine functions?
1. Erythropoietin - released in response to hypoxia from endothelial cells of peritubular capillaries
2. 1,25-(OH)2 vitamin D - the proximal tubule converts 25-OH vit D to active form 1,25-(OH)2 vit D --> increased intestinal absorption of Ca2+ and phosphate.
3. Renin - secreted by JG cells in response to decreased renal arterial pressure and increased renal sympathetic discharge (beta1).
4. Prostaglandins (ie PGE2) - paracrine secretion vasodilates teh afferent arterioles to increase GFR
57
How does PTH directly and indirectly affect the kidneys on Ca2+ and Phosphate regulation?
Directly - acts directly on kidneys to increase renal Ca2+ reabsorption and decrease renal phosphate reabsorption.
Indirectly - stimulates proximal tubule cells to make 1,25 - (OH)2 vit D by stimulating 1alpha-hydroxylase --> increases intestinal absorption of Ca2+ and phosphate.
58
What is used to estimate GFR?
creatinine
59
What effect does ANP have on the kidney?
Secreted in response to increased atrial pressure, it acts on the proximal convoluted tubule by dilating the afferent and constricting the efferent arterioles --> increases GFR and increases Na+ filtration with no compensatory Na+ reabsorption in distal nephron.
Net result: Na+ loss and volume loss
60
What causes release of PTH?
2. increased plasma phosphate
| 3. decreased plasma 1,25 (OH)2 vit D
61
What effect does PTH have on the kidney?
1. At the DCT --> increases Ca2+ reabsorption
2. At the PCT --> decreases phosphate reabsorption
3. increases 1,25 (OH)2 vit D production
62
What can cause hyperkalemia?
1. insulin deficiency (decreased Na/K ATPase)
2. beta blockers (decreased Na/K ATPase)
3. acidosis, severe exercise (increased K/H exchanger)
4. hyperosmolarity
5. digitalis (blocks Na/K ATPase)
6. cell lysis
63
What can cause hypokalemia?
1. insulin (increased Na/K ATPase)
2. beta agonists (increased Na/K ATPase)
3. alkalosis (increased K/H exchanger)
4. hypoosmolarity
64
What is used to estimate RPF?
PAH
65
How do you calculate the filtered load?
Filtered load = GFR x Plasma concentration
72
What drug will inhibit the effect of prostaglandins on the afferent arteriole?
NSAIDS
73
What drug will inhibit the effects of ATN II on the efferent arteriole?
ACEI
76
What's the compensatory response?
metabolic acidosis
hyperventilation (immediate)
77
What's the compensatory response?
metabolic alkalosis
hypoventilation (immediate)
78
What's the compensatory response?
respiratory acidosis
increased renal [HCO3-] reabsorption (delayed)
79
What's the compensatory response?
respiratory alkalosis
decreased renal [HCO3-] reabsorption (delayed)
80
What are some causes of respiratory acidosis?
Hypoventilation
- 1. airway obstruction
- 2. acute lung disease
- 3. chronic lung disease
- 4. opioids, narcotics, sedatives
- 5. weakening of respiratory muscles
81
What are some causes of AG metabolic acidosis?
```
Ketoacidosis
Uremia
Salicylate poisoning
Methanol poisoning
Acetaminophen poisoning
Lactic acidosis
Ethylene glycol poisoning
```
Paraldehyde or Phenformin
Iron tablets or INH
82
What are some causes of normal non-anion gap metabolic acidosis?
1. diarrhea
2. glue sniffing
3. renal tubular acidosis
4. hyperchloremia
83
What are some causes of respiratory alkalosis?
1. Hyperventilation (early high-altitude exposure)
| 2. Aspirin ingestion (early)
84
What are some causes of metabolic alkalosis with compensation (hypoventilation)?
1. diuretic use
2. vomiting
3. antacid use
4. hyperaldosteronism
85
What is RTA Type 1?
Defect in collecting tubule's ability to excrete H+.
Associated with hypokalemia and risk for calcium-containing kidney stones.
86
What is RTA Type 2?
Defect in proximal tubule HCO3- reabsorption.
Associated with hypokalemia and hypophosphatemic rickets.
87
What is RTA Type 4?
Hypoaldosteronism or lack of collecting tubule response to aldosterone.
Associated with HYPERKALEMIA and inhibition of ammonium excretion in proximal tubule.
Leads to decreased urine pH due to decreased buffering capacity.
88
RBC casts signify...
1. glomerulonephritis
2. ischemia
3. malignant HTN
89
WBC casts signify...
1. tubulointerstitial inflammation
2. acute pyelonephritis
3. transplant rejection
91
What does PTH do on the early proximal tubule?
Inhibit Na+/Phosphate cotransport --> phosphate excretion.
92
What does ATN II do on the early proximal tubule?
Stimulate Na+/H+ exchange --> increase Na+ and H2O reabsorption.
93
Why is the presence of casts so important in hematuria/pyuria?
Casts signify that the hematuria/pyuria is of renal origin.
Bladder cancer, kidney stones produce hematuria with NO CASTS.
94
What diseases can cause hematuria but will not create casts in the urine?
1. bladder cancer
| 2. kidney stones
95
Inhibit Na+/Phosphate cotransport --> phosphate excretion.
PTH
96
What diseases are classified under nephritic syndrome?
1. Acute poststreptococcal glomerulonephritis
2. Rapidly progressive glomerulonephritis
3. Berger IgA glomerulonephropathy
4. Alport syndrome
5. Diffuse proliferative glomerulonephritis
6. Membrano-proliferative glomerulonephritis
97
What diseases are classified under nephrotic syndrome?
1. Focal segmental glomerulonephritis
2. Membranous glomerulonephritis
3. Minimal change disease
4. Amyloidosis
5. Diabetic glomerulonephropathy
6. Diffuse proliferative glomerulonephritis
7. Membrano-proliferative glomerulonephritis
98
What diseases are classified under both nephritic and nephrotic syndrome?
1. Diffuse proliferative glomerulonephritis
| 2. Membrano-proliferative glomerulonephritis
99
Stimulate Na+/H+ exchange --> increase Na+ and H2O reabsorption.
ATN II
108
Impermeable to Na+
Thin descending loop of Henle
111
Impermeable to H2O
Thick ascending loop of Henle
115
What does PTH do on the early distal convoluted tubule?
Increases Ca2+/Na+ exchange --> Ca2+ reabsorption.
116
What happens at the collecting tubules of the nephron?
Reabsorb Na+ in exchange for secreting K+ and H+ (regulated by aldosterone).
117
What does aldosterone do on the collecting tubules?
Inserts Na+ channels on luminal side of the principal cell.
118
What does ADH do on the collecting tubules?
It binds to V2 receptors to insert aquaporin H2O channels on the luminal side of the principal cell.
136
What cleaves angiotensinogen from the liver into angiotensin I?
Renin
137
What cleaves angiotensin I into angiotensin II?
ACE
138
Where does ACE come from?
Lungs and kidneys
145
What role does ANP play in RAAS?
ANP acts as a "check" on RAAS. It relaxes VSM via cGMP --> increase GFR and therefore decrease renin.
148
osmolarity or low blood volume?
Low blood volume > osmolarity
149
What is in the juxtaglomerular apparatus?
JG cells and macula densa.
159
How can NSAIDs cause acute renal failure?
They inhibit the renal production of prostaglandins which are needed to maintain GFR by vasodilating the afferent arterioles.
174
What clinical s/s are seen with low serum [Na+]
disorientation, stupor, coma
175
What clinical s/s are seen with high serum [Na+]
neurologic: irritability, delirium, coma
176
What clinical s/s are seen with low serum [Cl-]
secondary to metabolic alkalosis, hypokalemia, hypovolemia, increased aldosterone
177
What clinical s/s are seen with high serum [Cl-]
secondary to non-anion gap acidosis
178
What clinical s/s are seen with low serum [K+]
U waves on ECG, flattened T waves, arrhythmias, paralysis
179
What clinical s/s are seen with high serum [K+]
Peaked T waves, wide QRS, arrhythmias
180
What clinical s/s are seen with low serum [Ca2]
tetany, neuromuscular irritability
181
What clinical s/s are seen with high serum [Ca2+]
delirium, renal stones, abdominal pain, not necessarily calciuria
182
What clinical s/s are seen with low serum [Mg2+]
neuromuscular irritability, arrhythmias
183
What clinical s/s are seen with high serum [Mg2+]
delirium, decreased deep tendon reflexes, cardiopulmonary arrest
184
What clinical s/s are seen with low serum [phosphate]
low-mineral ion product causes bone loss, osteomalacia
185
What clinical s/s are seen with high serum [phosphate]
high-mineral ion product causes renal stones, metastatic calcifications
268
Granular ("muddy brown") casts signify...
1. acute tubular necrosis
269
Waxy casts signify...
1. advanced renal disease/CRF
270
Hyaline casts are...
nonspecific.
276
What disease can cause pyuria but no casts in the urine?
1. acute cystitis
293
neutrophil-related injury to glomeruli
Nephritic syndrome
296
cytokine injury to podocytes; loss of negative charge on GBM
Nephrotic syndrome
299
HTN
both
302
Pitting Edema
both
305
RBC casts and hematuria
Nephritic syndrome
308
Massive proteinuria (>3.5 g/day, frothy urine)
Nephrotic syndrome
