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STEP 1 (3) > Renal-Embryo/Anatomy/Phsyiology > Flashcards

Renal-Embryo/Anatomy/Phsyiology Flashcards

1
Q

What are the three stages of embryo development?

A

Pronephros- week 4, then degenerates

Mesonephros- functions as intermediate kidney for 1st trimester and later contributes to male genital system

Metanephros- permanent; first appears in 5th week of gestation and continues to development through weeks 32-36 of gestation

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2
Q

What is the uretic bud?

A

derived from the caudal end of the mesonephric duct; gives rise to the ureter, pelvises, calyces, and collecting ducts; fully canalized by week 10 gestation

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3
Q

What is the last part of the embryonic kidney system to canalize?

A

the ureteropelvic junction (most common site of obstruction (hydronephrosis) in fetus

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4
Q

What is Potter sequence (syndrome)?

A
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5
Q

What are the major causes of Potter sequence (syndrome)?

A

ARPKD, obstructive uropathy (e.g. posterior urethral valves), and bilateral renal agenesis

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6
Q

What is this?

A

Horseshoe kidney, where the inferior poles of both kidneys fuse and get trappd under the inferior mesenteric artery as they ascend. Kidneys will function normally.

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7
Q

What are some causes of horseshoe kidney?

A

ureteropelvic junction obstruction, hydronephrosis, renal stones, infection, chromosomal aneuploidy (E.g. Edwards, Down, Patau, Turner), and rarely renal cancer

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8
Q

What is multicystic dysplastic kidney?

A

Due to abnormal connection between the uretic bus and metanephric mesenchyme leading to a nonfunctional kidney consisting of cysts and CT.

If unilateralm generally asymptomatic with compensatory hypertrophy of the contralateral kidney (often diagnosed prenatally via ultrasound)

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9
Q

What is a duplex collecting system?

A

bifurcation of the uretic bud before it enters the metanephci blastema creating a Y-shaped bifid ureter

can also occur when two uretic buds reach and interact with the metanephric blastema

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10
Q

Duplex collecting system is strongly associated with what?

A

vesicoureteral reflex and/or ureteral obstruction (increases risk of UTIs)

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11
Q

left kidnye is taken during donor transplant becuase it has a longer renal vein

A
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12
Q
A
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13
Q

Where do the ureters run?

A

under the uterine artery and under the vas deferens to enter the bladder

procedures involving ligation of the uterine vessels in the cardinal ligament may damage the ureter

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14
Q

Describe fluid distribution in the body

A

TBW= 60% of body mass (Intracellular (2/3, 40%), EXC= 1/3, 20%)

EXC= 75% interstitial, 25% plasma (measured by radiolabeled albumin)

RBC volume= 2.8L (normal HCT= 45%= 3*Hb in g/dL)

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15
Q

How is extracellular volume measured?

A

inulin

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16
Q

What is normal serum osmolarity?

A

285-295 mOsm/kg H2O

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17
Q

What is the glomerular filtration system composed of?

A

fenestrated capillary endothelium (size barrier)

Fused BM with heperan sulfate (negative charge barrier)

epithelial layer consisting of podocyte foot processes

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18
Q

The glomerular charge barrier is lost in what disease?

A

nephrotic syndrome (causing albuminuira, hypoproteinemia, generalized edema, and hyperlipidemia)

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19
Q

How is renal clearance measured?

A

Cx= UxV/Px= volume of plasma from which the substance is completely cleared per unit time, where:

Cx= clearance of X (mL/min), Ux= urine conc of X (mg/mL), Px= plasma conc of X (mg/mL), V= urine flow rate (mL/min)

Cx < GFR, then net tubular reabsorption of X

Cx > GFR, then net tubular secretion of X

Cx = GFR, no net secretion or absorption

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20
Q

______ clearance can be used to calculate GFR because it is freely

A

Inulin

GFR= Uinulin x V/Pinulin = Cinulin

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21
Q

GFR= Kf*[(PGC-PBS)- (piGC- piBS)

GC= glomerular capillary

BS= Bowman space

piBS= normally equals 0

A

Normal GFR= 100 ml/min

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22
Q

Creatinine clearance is an approximation of GFr but slightly overestimates GFR because it is moderately secreted by renal tubules

A
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23
Q

Effective renal plasma flow (eRPF) can estimated using ____________

A

para-aminohippuric acid (PAH) clearance because it is both filtered and secreted in the PCT resulting in near 100% excretion of all PAH entering the kidney

eRPF= UPAH x V/PPAH= GPAH (eRPF underestimates true renal plasma flow (RPF) by 10%)

RBF= RPF/(1-Hct)

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24
Q

What is the equation for filtration fraction (FF)?

A

FF= GFR/RPF (normal= 20%)

Filtered load (mg/min)= GFR (ml/min) * plasma conc (mg/mL)

again, GFR is estimated with creatinine and RPF is estimated with PAH clearance

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25
Q

How do NSAIDs affect the kidneys?

A

prostaglandings preferentially dilate the afferent arterioles (blocked)

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26
Q

How does angio II affect glomerular filtration?

A

angio II constricts the efferent arteriole (to decrease RPF and increase GFR (so FF increases)

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27
Q

How does afferent arteriole constriction affect GFR, RPF, and FF?

A

decrease GFR and RPF (FF same)

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28
Q

How does efferent arteriole constriction affect GFR, RPF, and FF?

A

increase GFR and FF

decrease RPF

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29
Q

How does increased plasma protein conc affect GFR, RPF, and FF?

A

decrease GFR and FF

no change in RPF

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30
Q

How does decreased plasma protein conc affect GFR, RPF, and FF?

A

increased GFR and RR

no change in RPF

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31
Q

How does constriction of the ureter affect GFR, RPF, and FF?

A

decrease GFR and FF

no change in RPF

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32
Q

Eqn for filtered load= GFR*Px

Excretion rate= V*Ux

Reabsorption= filtered - excreted; Secretion= excreted- filtered

A
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33
Q

Glucose at a normal plasma level is completely reabsorbed where?

A

in the PCT via Na/glucose cotransport

NOTE: At a level of 200mg/dL, glucosuria begins (threshold). At 375mg/dL, all transporters are fully saturated (may be less in pregnancy)

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34
Q

Amino acid clearance

A

Na+ depenent transporters in the PCT reabsorb amino acids

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35
Q

What is Hartnup disease?

A

AR disease of deficiency of neutral AA (e.g. tryptophan) transporters in the proximal renal tubular cells and on enterocytes leading to neutral aminoaciduria and decreased gut absorption leading to pellagra-like symptoms (tryptophan is needed for conversion to niacin)

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36
Q

How is Hartnup disease tx?

A

high protein diet and nicotinic acid

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37
Q

What are the main functions of the PCT?

A

reabsorb all glucose and amino acids and most HCO3-, Na+ (65-80%), Cl-, PO43-, K+, and H20 (isotonic reabsorption)

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38
Q

How does PTH affect PCT reabsorption?

A

inhibits PO43-/Na+ cotransport, causing PO43- excretion

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39
Q

How does angiotension II affect the PCT?

A

it stimulates the Na+/H+ exchange (NHE) resulting in more Na+, H20, and HCO3- reabsorption

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40
Q

How does Acetazolamide act as a diuretic?

A

The mechanism of diuresis involves the proximal tubule of the kidney. The enzyme carbonic anhydrase is found here, allowing the reabsorption of bicarbonate, sodium, and chloride. By inhibiting this enzyme, these ions are excreted, along with excess water, lowering blood pressure, intracranial pressure, and intraocular pressure.

By excreting bicarbonate, the blood becomes acidic, causing compensatory hyperventilation with deep respiration (Kussmaul respiration), increasing levels of oxygen and decreasing levels of carbon dioxide in the blood

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41
Q

What happens in the thin descending loop of Henle?

A

passive reabsorption of H2O via increasing medually hypertonicity as it descends

Makes urine hypertonic (concentrates)

42
Q

What happens in the thin ascending loop of Henle?

A

passive transport/reabsorption of Na+ and Cl-

43
Q

What happens in the thick ascending limb of henle?

A

active reabsorption of NaK/2Cl (blocked by loop diuretics), indirect paracellular reabsorption of Mg2+ and Ca2+ through positive lumen electrical potential generated by leak of K+

Impermeable to H20 (makes urine less concentrated as it ascends)

Absorbs 10-20% of Na+

44
Q

What happens in the DCT?

A

active reabsorption of Na and Cl (cotransporter) and Na+ via ENaC channels (5-10% of Na+ reabsorbed)

makes urine more dilute (hypotonic)

45
Q

How does PTH affect the DCT?

A

it increases Ca2+/Na+ exchange, increasing Ca2+ reabsorption

46
Q

The Na/Cl cotransporter in the DCT is the site of action of what drug class?

A

thiazide diuretics

47
Q

What are the main cells of collecting tubules?

A

principle cells

alpha and beta intercalated cells

48
Q

What happens in principle cells?

A

reabsorption of Na+ in exchange for secreting K+ and H+ (regulated by aldosterone) (3-5% Na+ reabsorbed)

49
Q

How does aldosterone affect CT principle cells?

A

it acts on mineralcorticoid receptors to increase protein synthesis that results in increased apical K+ conductance, increase NaKATPase activity, and increased ENac channels

50
Q

How does ADH affect principle CT cells?

A

it binds to apical AQP-2 channels to increase H20 reabsorption when serum osmolarity is too high (V2 receptors)

51
Q

a-intercalated (left)

b-intercalated (right)

A
52
Q

ENaC channels are the target of what drug?

A

amiloride, triamterene

53
Q

What are the major renal tubular defects?

A

Fanconi syndrome (PCT)

Bartter syndrome (thick ascending limb)

Gitelman syndrome (DCT)

Liddle syndrome (CT)

Syndrome of apparent mineralcorticoid excess (CT)

54
Q

What is Fanconi syndrome?

A

a generalized reabsorptive defect in the PCT marked by excess secretion of nearly all amino acids, glucose, HCO3-, and PO43- and resulting in metabolic acidosis

55
Q

What are some causes of Fanconi syndrome?

A

hereditary defects (e.g. Wilson diseasae, tyrosinemia, glycogen storage disease), ischemia, multiple myeloma, nephrotoxins/drugs (ex. expired tetracyclines, tenofovir), lead poisoning

56
Q

What is Bartter Syndrome?

A

AR reabsorptive defect in the thick ascending loop of Henle affecting the NaK2Cl cotransporter resulting in hypokalemia and metabolic alkalosis with hypercalcemia

57
Q

What is Gitelman Syndrome?

A

AR resorptive deficiency of NaCl in the DCT (less severe than Bartter syndrome) resulting in hypokalemia, hypomagnesia, metabolic alkalosis, and HYPOcalcemia

58
Q

What is Liddle Syndrome?

A

AD gain of function mutation resulting in ENaC channels in the CT resulting in HTN, hypokalemia, metabolic alkalosis, and hypoaldosterone

59
Q

How is Liddle Syndrome tx?

A

Amiloride

60
Q

What is syndrome of apparent mineralcorticoid excess?

A

hereditary deficiency of 11B-hydroxysteroid dehydrogenase, which normally converts cortisol into cortisone in mineralcorticoid receptor-containing cells before cortisol can act, resulting in excess cortisol, which can act on mineralcorticoid receptors resulting in HTN, hypokalemia, and metabolic alkalosis

61
Q

Only PAH and creatinine have net secretion

A
62
Q

How is angio II made?

A

renin is made in the kidneys and converts angiotensinogen to angio I in the liver.

Angio I is converted to angio II in the lungs via ACE

63
Q

What causes renin release from the kidneys?

A

decreased BP (JG cells)

decreased Na+ delivery (macula densa cells)

increased sympathetic tone (b1-receptors)

64
Q

What is a breakdown product of ACE converting angio I to II?

A

bradykinin

65
Q

What are the effects of Angio II?

A
  • vasoconstriction of vascular smooth muscle (BP up)
  • constricts efferent arteriole on glomerulus (increase FF to preserve renal function when RBF is low)
  • promotes aldosterone release from the adrenal gland
  • promotes ADH release from the posterior pituitary
  • increases the PCT NHE exchanger
  • stimulates the hypothalamus to cause thirst
66
Q

What are the effects of aldosterone?

A

increases Na+ channel and NaKATPase pump insertion in principle cells

enhances K+ and H+ excretion

increases Na+ and H20 reabsorption

67
Q

What are ANP and BNP?

A

released from the atria (ANP) and venticles (BNP) in response to increased stretch (preload) to relax vascular smooth muscle/promote diuresis via cGMP mediated increase in GFR and decrease renin release

68
Q

Describe the juxtaglomerular apparatus

A

consists of mesangial cells, JG cells (modified smooth muscle of the afferent arteriole), and the macula densa (NaCl sensor, part of DCT)

JG cells secrete renin in response to decreased renal blood pressure and increased sympathetic tone (B1). Macula densa cells sense decreased NaCl delivery to the DCT and cause adenosine release to promote vasoconstriction

Note that B1-blockers can decrease BP by inhibiting B1-receptors of the JGA to inhibit renin release

69
Q

When is EPO made?

A

releases by interstitial cells in peritubular capillary beds in response to hypoxia

70
Q

How do prostaglandins affect renal function?

A

they dilate the afferent arterioles to increase RBF (NSAIDs can precipiate renal failure)

71
Q

What is another major function of the PCT?

A

conversion of 25-OH vitD from the liver to the active form, 1,25-(OH)2-vit D via PTH mediated 1a-hydroxylase

72
Q

Overview of Angio II in the kidneys

A

synthesized in reponse to low BP and causes efferent arteriole constriction to increase GFR and FF but with compensatory Na+ reabsorption in the proximal and distal nephron

Net effect: perservation of renal function in low-vulme states with simultaneous Na+ reabsorption

73
Q

Overview of ANP in the kidneys

A

secreted in response to increased atrial pressure and causes icnreased GFR and Na+ filtration with no compensatory Na+ reabsorption (net effect is Na+ loss and volume loss)

74
Q

Overview of PTH in the kidneys

A

secreted in response to hypocalcemia, hyperphosphatemia, or low vitD3 levels. Caused increased calcium reabsorption (DCT), decreased phosphate reabsorption in the PT, and vitD3 conversion in the PT via 1a-hydrolase

75
Q

What things cause an extracellular K+ shift causing hyperkalemia?

A

digitalis

hyperosmolarity

lysis of cells

acidosis

b-blockers

high blood sugar (low insulin)

76
Q

What things cause an intracellular K+ shift causing hypokalemia?

A

hypo-osmolarity

alkalosis

B-adrenergic agonist

insulin (increased NaKATPase activity)

77
Q

How does hyponatremia present?

A

nausea and malaise stupor, coma, seizures

78
Q

How does hypernatremia present?

A

irritability, stupor, coma

79
Q

How does hypokalemia present?

A

U waves on ECG, flattened K waves, arryhthmias, muscle spasm

80
Q

How does hyperkalemia present?

A

wide QRS and peaked T waves on ECG, muscle weakness

81
Q

How does hypocalcemia present?

A

tetany,seizures, QT prolongation

82
Q

How does hypercalcemia present?

A

stones (renal), bones (pain), groans (abdominal pain), and psyhiatric overtones (altered mental status)

83
Q

What are the changes seen in metabolic acidosis?

A

decreased HCO3- (primary) (acidosis results) causing immediate hyperventilation resulting in decreased PO2

84
Q

What are the changes seen in metabolic alkalosis?

A

increased HCO3- (primary) (alkalosis results) causing immediate hypoventilation resulting in increased PO2

85
Q

What changes are seen in respiratory acidosis?

A

increased PCO2 resulting in delayed increased renal HCO3- rebabsorption

opposite in respiratory alkalosis

86
Q

Henderson-Hasselbach Eqn

A

pH= 6.1+ log[HCO3-]/0.03PCO2

87
Q

What is the Winter’s formula?

A

eqn for predicting respiratory compensation for a simple metabolic acidosis

PCO2= 1.5[HCO3-] +8 +/- 2

If the measured PCO2 is significantly different from the predicted PCO2, a mixed acid-base disorder is likely present

88
Q

1st step in handling acidosis/alkalosis

A

check arterial pH

pH < 7.35 = acidemia

p > 7.45 = akalemia

89
Q

What to do if pH < 7.35 = acidemia?

A

check pCO2

pCO2 > 40 mmHg (respiratory acidosis)

pCO2 < 40 mmHg (metabolic acidosis with compensation; hyperventilation)

90
Q

What are the main causes of respiratory acidosis?

A
  • airway obstruction
  • acute lung disease
  • chronic lung disease
  • opiods, sedatives
  • weakening of respiratory muscles
91
Q

What to do if What to do if pH < 7.35 = acidemia and pCO2 < 40 mmHg (metabolic acidosis with compensation; hyperventilation)?

A

check anion gap (Na - (Cl+ HCO3))

92
Q

What is a normal anion gap?

A

8-12 mEq/L

93
Q

What are some causes of normal anion gap, metabolic acidosis?

A

HARD-ASS

Hyperalimentation

Addison Disease

Renal tubular acidosis

Diarrhea

Acetazolamide

Spironolactone

Saline infusion

94
Q

What are some causes of increased anion gap, metabolic acidosis?

A

MUDPILES:

Methanol (formic acid)

Uremia

Diabetic keotacidosis

Propylene glycol

Iron tablets or Isoniazid

Lactic Acidosis

Ethylene glycol (oxalic acid)

Salicyclates

95
Q

Describe Type I (distal) RTA

A

urine pH > 5.5

defect in ability of a-intercalated cells to secrete H+ leading to no new HCO3- being generated and causing metabolic acidosis

associated with hypokalemia and increased risk for calcium phosphate kidney stones (due to icnreased urine pH and bone turnover)

96
Q

What are some causes of Type I (distal) RTA?

A

ampho B toxicity

analgesic nephropathy

congenital anomalies (obstruction) of the urinary tract

97
Q

Describe Type II (proximal) RTA

A

urine pH < 5.5

defect in PCT HCO3- reabsorption causing increased excretion of HCO3- in urine and subsequent metabolic acidosis (urine is acidified by a-intercalated cells in the CT, also causing hypokalemia)

risk of hypophosphatemic rickets

98
Q

What are some common causes of Type II RTA?

A

Fanconi syndrome and carbonic anhydrase inhibitors

99
Q

Describe Type IV (hyperkalemic) RTA

A

hypoaldosteronism causes hyperkalemia causing decreased NH3 synthesis in the PCT, resulting in decreased NH4+ excretion.

urine pH < 5.5

100
Q

What are the main causes of Type IV (hyperkalemic) RTA?

A

decreased aldosterone production (e.g. diabetic hyporeninism, ACE inhibitors, ARBs, NSAIDs, heparin, cyclosporine, adrenal insufficiency) or aldosterone resistance (e.g. K+-sparing diuretics, nephropathy due to obstruction, TMP/SMX)

STEP 1 (3) (16 decks)

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