Renal - Embryology + Anatomy + Physiology

Front 1

Pronephros

Back 1

Develops by week 4, then degenerates

Front 2

Mesonephric duct

Back 2

From mesonephros to cloaca; gives off ureteric bud near metanephros (stimulate nephrons)
Degenerates in females, becomes ductus deferens in males

Front 3

Mesonephros

Back 3

Temporary kidney for 1st trimester

Front 4

Metanephros

Back 4

Becomes permanent kidney, appears in week 5, continues developing until birth

Front 5

Ureteric bud derivatives

Back 5

Ureter, pelvis, calyx, collecting duct
Fully canalized by week 10

Front 6

Metanephros derivatives

Back 6

Glomerulus through to DCT

Front 7

Most common site of obstruction in fetus

Back 7

Ureteropelvic junction

Front 8

Patent urachus

Back 8

Patent allantois with bladder; fistula forms with bladder once umbilical cord is cute --> urine leaking from umbilicus

Front 9

Potter's syndrome

Back 9

Oligohydramnios --> limb, facial deformities, pulmonary hypoplasia

Front 10

Potter's syndrome cause of death

Back 10

Pulmonary hypoplasia
(Oligohydramnios)

Front 11

Potter's syndrome causes

Back 11

ARPKD, posterior urethral valves, bilateral renal agenesis
(Oligohydramnios)

Front 12

Horseshoe kidneys are trapped under which structure?

Back 12

IMA

Front 13

Horseshoe kidney commonly associated with which condition?

Back 13

Turner's syndrome

Front 14

Multicystic dysplastic kidney

Back 14

Ureteric bud + metanephros abnormal interaction --> nonfunctioning kidney with cysts

Front 15

Compensation in asymptomatic multicystic dysplastic kidney

Back 15

Hypertrophy of contralateral kidney

Front 16

Renal arterial supply

Back 16

Renal --> segmental --> interlobar --> arcuate --> interlobular

Front 17

Ureters pass under which structures?

Back 17

Under uterine artery (in female) and ductus deferens (in male)

Front 18

60-40-20 Rule

Back 18

60% body weight = total body water (TBW)
40% of TBW = ICF
20% of TBW = ECF

Front 19

Glomerular filtration barrier

Back 19

1) Fenestrated capillary endothelium
2) Fused, - charge BM (heparan sulfate)
3) Podocyte foot process epithelial layer

Front 20

Renal clearance formula

Back 20

Clearance [x] = UxV/Px = mL/min
(Vol of plasma completely cleared of x per unit time)

Front 21

Normal GFR value

Back 21

~ 100 mL/min

Front 22

How does using creatinine affect GFR?

Back 22

Slight overestimation of GFR (creatinine is also secreted)

Front 23

How to measure Effective Renal Plasma Flow (ERPF)

Back 23

Use PAH - filtered + actively secreted = all PAH entering kidney is excreted

Front 24

Renal Blood Flow formula

Back 24

RBF = RPF / (1 - Hct)

Front 25

How does using PAH affect RPF values?

Back 25

Underestimates true RPF by 10%

Front 26

Filtration fraction formula + normal value

Back 26

FF = GFR / RPF = 20% normally

Front 27

Which substance dilates afferent arterioles?

Back 27

Prostaglandins

Front 28

Which substance constricts efferent arterioles?

Back 28

Ang-II

Front 29

Afferent arteriole constriction - change in RPF, GFR, FF

Back 29

RPF: decrease
GFR: decrease
FF: no change

Front 30

Efferent arteriole constriction - change in RPF, GFR, FF

Back 30

RPF: decrease
GFR: increase
FF: increase

Front 31

Increase plasma protein conc. - change in RPF, GFR, FF

Back 31

RPF: no change
GFR: decrease
FF: decrease

Front 32

Decreased plasma protein conc. - change in RPF, GFR, FF

Back 32

RPF: no change
GFR: increase
FF: increase

Front 33

Ureter constriction - change in RPF, GFR, FF

Back 33

RPF: no change
GFR: decrease
FF: decrease

Front 34

How to calculate Filtered Load + Excretion Rate

Back 34

Filtered load = GFR x [Plasma concentration]
Excretion rate = V x [Urine concentration]

Front 35

How to calculate reabsorption and secretion

Back 35

Reabsorption = filtered load - excreted load
Secretion = excreted load - filtered load

Front 36

Threshold plasma glucose conc. for nephric reabsorption + Tm for glucose

Back 36

Threshold = 160 mg/dL
Tm (saturation) = 350 mg/dL

Front 37

Hartnup's disease + which protein level affected

Back 37

Neutral AA transporter deficiency in PCT: results in tryptophan deficiency (pellagra)

Front 38

Cx < GFR indicates

Back 38

Net tubular absorption of x

Front 39

Cx > GFR indicates

Back 39

Net tubular secretion of x

Front 40

Cx = GFR indicates

Back 40

No net tubular secretion or reabsorption of x

Front 41

Cell responsible for renin secretion

Back 41

Granular cells of juxtaglomerular cells (afferent arteriole)

Front 42

Changes stimulating renin secretion

Back 42

1) Decreased blood volume (JG cells)
2) Decreased Na+ delivery (MD cels)
3) B-receptor stimulation (increase sympathetic tone)

Front 43

Ang-II effects 6)

Back 43

1) AT1 receptors - peripheral vasoconstriction
2) Eff. arteriole constriction --> raise GFT
3) Aldosterone --> Na+, water reabsorption
4) ADH --> water reabsorption
5) Increase Na+/H+ exchanger in PCT --> Na+, HCO3-, water reabsorption
6) Hypothalamus --> thirst

Front 44

ADH vs. aldosterone regulation

Back 44

ADH: regulates osmolarity
Aldosterone: regulates blood volume;
In low-vol states, both work to increase blood volume

Front 45

JGC components + main purpose

Back 45

JG cells (afferent arteriole) + MD cells (DCT)
Maintains GFR via RAAS

Front 46

EPO produced by which cells?

Back 46

Interstitial cells of peritubular capillary bed in response to hypoxia

Front 47

Where is 25-OH vit D converted to active form? Which enzyme responsible?

Back 47

PCT cells
1a-hydroxylase

Front 48

How do NSAIDs cause renal failure?

Back 48

Decrease PG production --> cause afferent arteriole constriction --> decrease GFR/FF

Front 49

ANP effect

Back 49

Increased GFR and Na+ secretion *without compensatory Na+ reabsorption in DCT* (vs. Ang-II)

Front 50

Factors stimulating PTH secretion

Back 50

Decreased serum Ca2+
Increased serum phosphate
Decreased serum calcitriol

Front 51

PTH effects

Back 51

Increase Ca2+ reabsorption in DCT
Decrease phosphate reabsorption in PCT
Increase calcitriol production

Front 52

Aldosterone main effects

Back 52

Increase Na+ reabsorption
Increase K+ secretion
Increase H+ secretion

Front 53

Hyperkalemia causes ("DO Insulin LAB work")

Back 53

Digitalis
hypoOsmolarity
Insulin deficiency
Lysis of cells
Acidosis
B-receptor antagonist

Front 54

Hypokalemia causes

Back 54

hyperOsmolarity
Insulin
Alkalosis
B-receptor agonist

Front 55

Hyper/hyponatremia symptoms

Back 55

Irritability, stupor, coma

Front 56

Hypokalemia & hyperkalemia presentation on ECG

Back 56

Hypo: U waves, flattened T waves
Hyper: wide QRS, peaked T waves

Front 57

Hypocalcemia & hypercalcemia symptoms

Back 57

Hypo: tetany, seizures
Hyper: renal stones, bone pain, abdo groans, psychiatric moans

Front 58

Hypomagnesemia & hypermagnesemia symptoms

Back 58

Hypo: tetany, seizures
Hyper: decreased DTR, bradycardia, lethargy, hypotension, cardiac arrest, hypocalcemia

Front 59

Hypophosphatemia & hyperphosphatemia symptoms

Back 59

Hypo: bone loss, osteomalacia
Hyper: renal stones, metastatic calcifications, hypocalcemia

Front 60

Respiratory acidosis cause & compensation

Back 60

Cause: hypoventilation (PCO2 rise)
Compensation: increase renal reabsorption of HCO3- (delayed)

Front 61

Respiratory alkalosis cause & compensation

Back 61

Cause: hyperventilation (PCO3 fall)
Compensation: decrease renal absorption of HCO3- (delayed)

Front 62

Metabolic acidosis cause & compensation

Back 62

Cause: increased H+ or increased HCO3- loss
Compensation: hyperventilation (immediate)

Front 63

Metabolic alkalosis cause & compensation

Back 63

Cause: decreased H+ or increased HCO3- absorption
Compensation: hypoventilation (immediate)

Front 64

Henderson-Hasselbalch equation

Back 64

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

Front 65

Winter's equation + use

Back 65

PCO2 = 1.5(HCO3-) + 8 +/- 2
Predicts respiratory compensation for metabolic acidosis
(If expected is different than observed --> mixed acid-base)

Front 66

Anion gap equation + normal value

Back 66

[Na+] - [Cl-] - [HCO3-] = 8 - 12 mEq/L

Front 67

Causes of respiratory acidosis

Back 67

Hypoventilation:
Airway obstruction, lung disease, opioids, sedative, resp muscle weakening

Front 68

Causes of metabolic acidosis with increased anion gap
(MUDPILES)

Back 68

Methanol
Uremia
Diabetic ketoacidosis
Propylene glycol
Iron tables, INH
Lactic acidosis
Ethylene glycol
Salicylates (late)

Front 69

Causes of metabolic acidosis with normal anion gap
(HARD-ASS)

Back 69

Hyperalimentation
Addison's disease
Renal tubular acidosis
Diarrhea
Acetazolamide
Spironolactone
Saline infusion

Front 70

Respiratory alkalosis causes

Back 70

Hyperventilation (eg. high altitude exposure)
Salicylates (early)

Front 71

Metabolic alkalosis causes

Back 71

Loop diuretics
Vomiting
Antacid use
Hyperaldosteronism

Front 72

Renal tubular acidosis type 1 (distal)

Back 72

Defect in H+ secretion in CT
Urine pH > 5.5, hypokalemia
Risk for calcium stones

Front 73

Renal tubular acidosis type 2 (proximal)

Back 73

Defect in HCO3- reabsorption in PCT
Urine pH < 5.5, hypokalemia
Risk for hypophosphatemic rickets, seen in Fanconi's syndrome

Front 74

Renal tubular acidosis type 4 (hyperkalemic)

Back 74

Low aldosterone or defect in aldosterone response in CT
Hyperkalemia --> decreased urine pH, decreased buffering capacid