First Aid Step 1 - Renal - Anatomy, Embryology, Physiology

Front 1

What are the 3 embryologic precursers of the renal system and when do they occur?

Back 1

Pronephros (week 4, then degenerates).

Mesonephros (functions as interm kidney for 1st trimester; later contributes to male genital system).

Metanephros (permanent; first appears in 5th week of gestation; nephrogenesis continues through 32-36 weeks of gestation)

Front 2

What is the uteric bud derived from and what does it make?

Back 2

Derived from caudal end of mesonephros and gives rise to ureter, pelvises, calyces, and collecting ducts.

Front 3

When does th ureteric bud canalize fully?

Back 3

By the 10th week

Front 4

What does the ureteric bud interact with and what does this interaction induce?

Back 4

Ureteric bud interacts with the metanephric mesenchyme. This interaction indues differentiation and formation of glomulerulus through to the distal convoluted tubule

Front 5

What does aberrant interaction between the metanephric mesenchyme and the ureteric bud cause?

Back 5

May result in several congenital malformations of the kidney

Front 6

What struture is the last to canalize in the renal system?

Back 6

The ureteropelvic junction

Front 7

What is Potter's syndrome? What is the cause of death?

Back 7

Oligohydramnios -> compression of fetus -> limb deformities, facial deformities, and pulmonary hypoplasia (which is the cause of death).

Front 8

What are causes of Potter's syndrome?

Back 8

Autosomal Recessive Polycystic Kidney Disease (ARPKD), posterior urehtral valves, bilateral renal agenesis

Front 9

What is a horseshoe kidney and how do they arise? What is the prognosis?

Back 9

Inferior poles of both kidneys fuse. As they ascend form the pelvis during fetal development, horseshoe kidneys get trapped under inferior mesenteric artery and remain low in the abdomen. The kidneys function normally

Front 10

What condition are horsehoe kidneys associated with?

Back 10

Turner syndrome

Front 11

What is a multicystic dysplastic kidney and what causes it?

Back 11

Abnormal interaction between ureteric bud and metanephric mesenchyme. This leads to a nonfunctional kidney consisting of cysts and connective tissue.

Front 12

What are the symptoms of multicystic dysplastic kidney?

Back 12

If unilateral (most common, generally asymptomatic with compensatory hypertrophy of the contralateral kidney. Often diagnosed prenatally via ultrasound

Front 13

What is the anatomical course of the ureters?

Back 13

Ureters pass UNDER the uterine artery and UNDER the ductus deferens (retroperitoneal).

"water (ureters UNDER the bridge (uterine artery, vas deferens"

Front 14

What percentage of total body weight is nonwater and water mass?

Back 14

40% non-water, 60% water mass

Front 15

What percentage of total body water is extracellular vs intracellular fluid?

Back 15

1/3 extracellular, 2/3 intracellular (60-40-20 rule: 60% of body is water - 40% ICF, 20% ECF)

Front 16

What percentage of extracellular fluid is plasma vs interstitial volume?

Back 16

1/4 plasma, 3/4 interstitial

Front 17

How is plasma volume measured?

Back 17

Radiolabeled albumin

Front 18

How is extraceullar volume measured?

Back 18

Inulin

Front 19

What is normal osmolarity of body fluid?

Back 19

290 mOsm/L

Front 20

What is the function of the glomerular filtration barrier?

Back 20

Responsible for filtration of plasma according to size and net charge.

Front 21

What are the 3 main components of the glomerular filtration barrier?

Back 21

1. Fenestrated capillary endothelium (size barrier)

2. Fused basement membrane with heparan sulfate (negative charge barrier)

3. Epithelial layer consisting of podocyte foot processes

Front 22

In what condition is the charge barrier of the glomerular filtration barrier lost and what does it result in?

Back 22

Nephrotic syndrome. Results in albuminuria, hypoproteinemia, generalized edema, and hyperlipidemia

Front 23

What can be used to calculate GFR and why?

Back 23

Inulin clearance bc it is freely filtered and is neither reabsorbed nor secreted

Front 24

What is the formula for calculating GFR?

Back 24

GFR = Uinulin x V/Pinulin = Cinulin = Kf((P(GC) - P(BS)) - (pi(GC) - pi(BS))) where GC = glomerular capillary and BS = Bowman's space (pi(BS) normally zero)

Front 25

What is the normal GFR?

Back 25

100 mL/min

Front 26

How accurately does creatinine clearance estimate GFR?

Back 26

Slightly overestimates bc creatinine is moderately secreted by renal tubules. Is is an approximate measure

Front 27

What changes in GFR define the stages of chronic kidney disease?

Back 27

Incremental reductions in GFR

Front 28

How can estimate ERPF (effective renal plasma flow) and why?

Back 28

PAH clearance because it is both filtered and actively secreted in the proximal tubule. All PAH entering the kidney is excreted.

Front 29

What is the formula for ERPF?

Back 29

ERPF = U(PAH) x V/P(PAH) = C(PAH)

Front 30

What is the formula for RBF (renal blood flow)?

Back 30

RBF = RPF/(1-Hct)

Front 31

How accurate is ERPF in estimating RPF?

Back 31

It underestimates true RPF by ~10%

Front 32

What is the formula for filtration fraction?

Back 32

FF = GFR/RPF

Front 33

What is a normal FF?

Back 33

20%

Front 34

What is the formula for filtered load?

Back 34

Filtered load = GFR x plasma concentration

Front 35

How do NSAIDs affect renal blood flow, RPF, GFR, and FF?

Back 35

They inhibit the afferent arteriole (prostaglandins dilate afferent arteriole). Increases RPF, increases GFR, FF remains constant

Front 36

How do ACE inhibitors affect renal blood flow, RPF, GFR, and FF?

Back 36

Inhibits efferent arteriole. Angiotension II preferentially constricts efferent arteriole. Decreases RPF, increases GFR, FF increases

Front 37

What is the effect of afferent arteriole constriction on RPF, GFR, and FF?

Back 37

Decreases RPF, decreases GFR, no change in FF

Front 38

What is the effect of efferent arteriole constriction on RPF, GFR, and FF?

Back 38

Decreases RPF, increases GFR, increases FF

Front 39

What is the effect of increased plasma protein concentration RPF, GFR, and FF?

Back 39

No change in RPF, decreases GFR, decreases FF

Front 40

What is the effect of decreased plasma protein concentration on RPF, GFR, and FF?

Back 40

No change in RPF, increased GFR, increased FF

Front 41

What is the effect of constriction of the ureter on RPF, GFR, and FF?

Back 41

No change in RPF, decreased GFR, decreased FF

Front 42

How do you calculate reabsorption and secretion rate?

Back 42

Filtered load = GFR x plasma concentration.

Excretion rate = V x Ux.

Reabsorption = filtered - excreted.

Secretion = excreted - filtered

Front 43

Where is glucose reabsorbed in renal system, by what transporter, and how much?

Back 43

Glucose at a normal plasma level is completely reasorbed in the proximal tubule by the Na/glucose co-transport.

Front 44

At what point does glcuosuria occur and at what point are all glcuose transporters fully saturated (Tm)?

Back 44

At plasma glucose of ~160mg/dL, glucosuria begins (threshold). At 350 mg/dL, all transporters are fulled saturated (Tm)

Front 45

How does pregnancy affect reabsorption of glucose and amino acids?

Back 45

Normal pregnancy reduces reabsorption of glucose and amino acids in the proximal tubule, leading to glucosuria and aminoaciduria

Front 46

How are amino acids reabsorbed in the kidneys?

Back 46

Na-dependent transporters in proximal tubule

Front 47

What is Hartnup's disease?

Back 47

Deficiency of neutral amino acids (tryptophan) transporter. Results in pellagra

Front 48

What is the function of the early proximal tubule?

Back 48

Contains brush border. Reabsorbs all of the glucose and amino acids and most of the bicarb, Na, Cl, Phosphate, and water. Generates and secretes ammonia, which acts as a buffer for secreted H+

Front 49

What type of absorption occurs in the early proximal tubule?

Back 49

Isotonic

Front 50

How does PTH affect early proximal tubule?

Back 50

Inhibits Na/phosphate cotransport -> phosphate excretion

Front 51

How does angiotensin II affect early proximal tubule?

Back 51

Stimulates Na/H exchange -> inc Ha, H20, bicarb reabsorption (permitting contraction alkalosis)

Front 52

How much of Na is reabsorbed in early proximal tubule?

Back 52

65-80%

Front 53

What is the function of the thick ascending loop of Henle?

Back 53

Actively reabsorbs Na, K, and Cl. Indirectly induces the paracellular reabsorption of Mg and Ca through (+) lumen pontential generated by K backleak. It is impermeable to H2). It makes urine less concentrated as it ascends

Front 54

How much Na is reabsorbed in the thick ascending loop of Henle?

Back 54

10-20%

Front 55

What is the function of the early distal convoluted tubule?

Back 55

Actively reabsorbs Na, Cl. Makes urine hypotonic.

Front 56

How does PTH affect the early distal convoluted tubule?

Back 56

Increases Ca/Na exchange -> Ca reabsorption.

Front 57

How much Na is reabsorbed in the early distal convoluted tubule?

Back 57

5-10%

Front 58

What is the function of the collecting tubules?

Back 58

Reabsorbs Na in exchange for secreting K and H (regulated by aldosterone)

Front 59

How does aldosterone affect the collecting tubules?

Back 59

Acts on mineralocorticoid receptor -> insertion of Na channel on the luminal side

Front 60

How does ADH affect the collecting tubules?

Back 60

Acts as V2 receptor -> insertion of aquaporin H2O channels on the luminal side.

Front 61

How much Na is reabsorbed in the collecting tubules?

Back 61

3-5%

Front 62

How does tubular inulin concentration change along the proximal tubule?

Back 62

Tubular inulin increases in concentration (but not amount) along the proximal tubule as a result of water reabsorption

Front 63

How do Cl and Na reabsorption compare in the kidneys?

Back 63

Cl reabsorption occurs at a slower rate than Na in the proximal 1/3 of the proximal tubule and then matches the rate of Na reabsorption more distally. Thus, its relative concentration increases before it plateaus

Front 64

What stimulates renin release from the kidneys?

Back 64

Increase in blood pressure (JG cells), decrease in Na delivery (macula densa cells), and increased sympathetic tone (B1 receptors)

Front 65

What stimulates conversion of angiotensinogen to ATI?

Back 65

Renin

Front 66

Where is angiotensinogen made?

Back 66

Liver

Front 67

Where is ACE made?

Back 67

Lung and kidney

Front 68

What stimulates the conversion of AT I -> AT II?

Back 68

ACE

Front 69

Besides ATI, what othe rmolecule does ACE affect?

Back 69

Decreases bradykinin production

Front 70

How does ATII affect vascular smooth muscle?

Back 70

Acts at AT1 receptors on vascular smooth muscle -> vasoconstriction -> inc BP

Front 71

How does ATII affect glomerular blood flow?

Back 71

Constricts efferent arteriole of glomerulus -> increases FF to preserve GFR in low-volume states (ie when RBF decreases)

Front 72

How does ATII affect aldosterone and therefore the kidneys?

Back 72

ATII -> aldosterone in adrenal glands -> increase Na channel and Na/K pump insertion in principal cells; enhances K and H excretion (upregulates principal cell K channels and intercalates cell H channels) -> creates favorable Na gradient for Na and H2O reabsorption

Front 73

How does ATII affect ADH?

Back 73

ATII -> ADH (posterior pituitary) -> inc H2O channel insertion in principal cells -> H2O reabsorption

Front 74

How does ATII affect proximal tubule Na/H activity?

Back 74

Increases proximal tubule Na/H activity -> Na, bicarb, and H2O reabsorption (can permit contraction alkalosis)

Front 75

How does ATII affect hypothalamus?

Back 75

Stimulates hypothalamus -> increase thirst

Front 76

How does ATII affect baroreceptor function?

Back 76

It limits reflex bradycardia, which would normally accompany its pressor effects. It helps to maintain blood volume and blood pressure

Front 77

What is ANP and what is its function?

Back 77

Released from atria in response to increased volume; may act as a "check" on renin-angiotensin-aldosterone system; relaxes vascular smooth muscle via cGMP, causing increased GFR and decreased renin

Front 78

What does ADH regulate?

Back 78

Primarily regulates osmolarity but also responds to low blood volume, which takes precendence over osmolarity

Front 79

What does aldosterone regulate?

Back 79

Primarily regulates blood volume; in low-volume states, both ADH adn aldosterone act to protect blood volume

Front 80

What are the components of the juxtaglomerular apparatus?

Back 80

Consists of JG cells (modified smooth muscle of afferent arteriole) and the macula densa (NaCl sensor, part of teh distal convoluted tubule).

Front 81

What is the function of JG cells?

Back 81

Secrete renin in response to decreased renal blood pressure, decreased NaCl delivery to distal tubule, and increased sympathetic tone (B1 cells)

Front 82

How does JGA defent GFR?

Back 82

Via the renin-angiotensin-aldosterone system

Front 83

How can beta blockers decrease BP?

Back 83

Inhibits B1-receptors of the JGA, causing decreased renin release.

Front 84

When is by where is erythropoietin secreted?

Back 84

Released by interstitial cells in the peritubular capillary bed in response to hypoxia

Front 85

What is vitamin D converted to in the kidneys and by what?

Back 85

Proximal tubule: 1-alpha-hydroxylase converts 25-OH vitamin D into 1,25 (OH) vitamin D (active form)

Front 86

What does PTH do to vitamin D in kidney?

Back 86

Stimulates 1-alpha hydroxylase, increasing 1,25-vit D (active form)

Front 87

When is renin released by the kidneys?

Back 87

Secreted by JG cells in response to dec renal arterial pressure and increased renal sympathetic discharge (B1 effect)

Front 88

How does paracrine secretion of prostaglandins affect GFR?

Back 88

Vasodilates the afferent arteriole to increase GFR

Front 89

What affect do NSAIDs have on renal function?

Back 89

They can cause acute renal failure by inhibiting the renal produciton of prostaglandins, which keep the afferent arterioels vasodilated to maintain GFR

Front 90

What is the effect of ANP (atrial natriuretic peptide) on the kidney?

Back 90

Secreted in response to increased atrial pressure. Causes increased GFR and increased Na filtration with NO compensatory Na resabsorption in the distal nephron.

Net effect: Na loss and volume loss

Front 91

What is the effect of PTH on the kidney?

Back 91

Secreted in response to dec plasma Ca, increased plasma phosphate, or dec plasma 1,25-Vit D. Causes increased Ca reabsorption (PCT), increased 1,25-vit D production.

Additional effect: Increased Ca and phosphate absorption from the gut

Front 92

What is the effect of ATII on the kidneys?

Back 92

Synthesized in response to dec BP. Causes efferent arteriole constrction -> inc GFR and inc FF but with compensatory Na reabsorption in proximal and distal nephron.

Net effect: preservation of reanl function in low-volume state (inc FF) with simultaenous Na reabsorption (both proximal and distal) to dec additional volume loss

Front 93

What is the effect of aldosterone on the kidneys?

Back 93

Secreted in response to dec blood volume (via ATII) and inc plasma K. Causes inc Na reabsorption, inc K secretion, and inc H+ secretion.

Front 94

What is the effect of ADH (vasopressin) on the kidneys?

Back 94

Secreted in response to inc plasma osmolarity and dec blood volume. Binds to receptors on principal cells, causing inc number of water channels and inc H2O reabsorption

Front 95

What drugs/conditions shift K out of the cell (causing hyperkalemia)?

Back 95

Digitalis, hyperosmolarity, insulin deficiency, lysis of cells, acidosis, beta-adrenergic antagonist

Front 96

What drugs/conditions shift K into the cells (causing hypokalemia)?

Back 96

Hypo-osmolarity, insulin (inc Na/K ATPase), alkalosis, beta-adrenergic agonists (inc Na/K ATPase). (INsulin shifts K INto cells)

Front 97

What are the signs/symptoms of low serum Na?

Back 97

Nausea and malaise, stupor, coma

Front 98

What are the signs/symptoms of high serum Na?

Back 98

Irritability, stupor, coma

Front 99

What are the signs/symptoms of low serum K?

Back 99

U waves on EKG, flattened T waves, arrhythmias, muscle weakness

Front 100

What are the signs/symptoms of high serum K?

Back 100

Wide QRS and peaked T waves on EKG, arrhythmias, muscle weakness

Front 101

What are the signs/symptoms of low serum Ca?

Back 101

Tetany, seizures

Front 102

What are the signs/symptoms of high serum Ca?

Back 102

Stones (renal), bones (pain), groans (abdominal pain), psychiatric overtones (anxiety, altered mental status), but not necessarily calciuria

Front 103

What are the signs/symptoms of low serum Mg?

Back 103

Tetany, arrhythmias

Front 104

What are the signs/symptoms of high serum Mg?

Back 104

Decreased deep tendon reflexes, lethargy, bradycardia, hypotension, cardiac arrest, hypocalcemia

Front 105

What are the signs/symptoms of low serum phosphate?

Back 105

Bone loss, osteomalacia

Front 106

What are the signs/symptoms of high serum phosphate?

Back 106

Renal stones, metastatic calcifications, hypocalcemia

Front 107

What are the changes in pH, PCO2, and HCO3- in metabolic acidosis?

Back 107

Dec pH, dec PCO2 (compensatory), dec bicarb (1st)

Front 108

What are the changes in pH, PCO2, and HCO3- in metabolic alkalosis?

Back 108

Inc pH, inc PCO2 (compensatory), inc bicarb (1st)

Front 109

What are the changes in pH, PCO2, and HCO3- in respiratory acidosis?

Back 109

Dec pH, inc PCO2 (1st), inc bicarb (compensatory)

Front 110

What are the changes in pH, PCO2, and HCO3- in respiratory alkalosis?

Back 110

Inc pH, dec PCO2 (1st), dec bicarb (compensatory)

Front 111

What is the compensatory response to metabolic acidosis and what is the time frame?

Back 111

Hyperventilation (immediate)

Front 112

What is the compensatory response to metabolic alkalosis and what is the time frame?

Back 112

Hypoventilation (immediate)

Front 113

What is the compensatory response to respiratory acidosis and what is the time frame?

Back 113

Inc renal bicarb reabsorption (delayed)

Front 114

What is the compensatory response to respiratory alkalosis and what is the time frame?

Back 114

Dec renal bicarb reabsorption (delayed)

Front 115

What is the Henderson-Hasselbalch equation?

Back 115

pH = 6.1 + log (bicarb)/(0.03*PCO2)

Front 116

How can you calculate the predicted respiratory compensation for simple metabolic acidosis? What does it mean if there is a significant difference between measured and predicted PCO2?

Back 116

Using Winter's formula (PCO2 = 1.5(bicarb) + 8 +/- 2. If the measured pCO2 is much different from predicted pCO2, then a mixed acid-base disorder is likely present

Front 117

What are causes of respiratory acidosis?

Back 117

Hypoventilation (airway obstruction, acute lung disease, chornic lung disease, opioids, sedatives, weakening of respiratory muscles)

Front 118

What are the 2 types of causes of metabolic acidosis?

Back 118

Increased anion gap and normal anion gap

Front 119

How do you calculate anion gap and what is normal?

Back 119

AG = Na - (Cl + bicarb). Normal is 8-12

Front 120

What are the causes of increased anion gap metabolic acidosis?

Back 120

MUDPILES:
Methanol (formic acid)
Uremia
Diabetic ketoacidosis
Propylene glycol
Iron or INH
Lactic acidosis
Ethylene glycol (oxalic acid)
Salicylates (late)

Front 121

What are the causes of normal anion gap metabolic acidosis?

Back 121

HARD-ASS:
Hyperalimentation
Addison's disease
Renal tubular acidosis
Diarrhea
Acetazolamide
Spironolactone
Saline infusion

Front 122

What are the causes of respiratory alkalosis?

Back 122

Hyperventilation (ex: early high-altitude exposure), salicylates (early)

Front 123

What are the causes of metabolic alkalosis?

Back 123

Loop diuretics, vomiting, antacid use, hyperaldosteronism

Front 124

What is the defect in type 1 ("distal") renal tubular acidosis and what are the signs/symptoms? What is the urine pH?

Back 124

Defect in collecting tubule's ability to excrete H+. Untreated pts have urine pH >5.5. Associated with hypoK. Increased risk for calcium phosphate kidney stones as a result of inc urine pH and bone resorption

Front 125

What is the defect in type 2 ("proximal") renal tubular acidosis and what are the signs/symptoms? What is the urine pH? What condition can it be associated with?

Back 125

Defect in proximal tubule bicarb reabsorption. May be seen with Fanconi's syndrome. Untreated pts have urine pH <5.5. Associated wtih hypokalemia. Inc risk for hypophosphatemic rickets.

Front 126

What is the defect in type 4 ("hyperkalemic") renal tubular acidosis and what are the signs/symptoms? What is the urine pH?

Back 126

Hypoaldosteronism or lack of collecting tubule response to aldosterone. The resulting hyperK impairs ammoniagenesis in the proximal tubule, leading to dec buffering capacity and inc urine pH