Renal: Anatomy And Physiology

Front 1

What are the parts of the kidney from the outside to the inside?

Back 1

capsule - cortex - medulla - minor calyx - major calyx - pelvis - ureter

Front 2

What is the flow of urine beginning at the glomerulus?

Back 2

glomerulus - proximal convoluted tubues - descending loop of henle - ascending loop of henle - distal convoluted tubules - collecting duct

Front 3

What is the flow of blood into the kidney?

Back 3

renal artery - interlobar artery - interlobular artery - afferent arteriole (carries unfiltered blood in to the glomeruli) has JG cells) - in the glom blood reaches a highly unfavorable pressure gradient and a large surface area for exchange - plasma portion of the blood is forced into bowman's capsule - blood levels the via efferent arteriole - vasa recta - interlobular vein - interlobar vein - renal vein (which drains into the IVC

Front 4

What kidney is taken during transplantation? why?

Back 4

The left kidney - because it has a longer renal vein

Front 5

What is the course of the ureters?

Back 5

"water under the bridge"
they travel under the uterine artery in women and under the vas deferens in men

Front 6

What is the most common place of injury during a pelvic surgery?

Back 6

the ureters

Front 7

What is the most common place of cervical cancer mets?

Back 7

the ureters - lined by urothelium: transitional cell epithelium

Front 8

Where does water go in the body and in what precentages?

Back 8

Total body water - 60% of total body weight
2/3 of water: intracellular (40% of total body weight)
1/3 of water: extracellular (20% of total body weight)
3/4 of extracellular water: interstitial volume
1/4 of extracellular water: plasma volume

Front 9

What measures plasma volume?

Back 9

radiolabeled albumin

Front 10

What measures extracellular volume?

Back 10

inulin

Front 11

In what compartment is K high?

Back 11

HIKIN
K is high intracellularly, NaCl is low intracellularly

Front 12

What are the concentrations of K and NaCl extracellularly?

Back 12

high NaCl extracellularly, low K extracellularly

Front 13

What are the parts of the glomerular filtration barrier?

Back 13

1) fenestrated endothelium (size barrier)
2) fused basement membrane with heparan sulfate (charge barrier)
3) podocyte foot processes - filtration slits (second line of defense)

Front 14

What is lost in nephrotic syndrome? What are the symptoms of it?

Back 14

The charge barrier - results in albuminuria, hypoproteinemia, generalized edema and hyperlipidemia (because of low proteins - so liver is activated to make more and more lipoprotein is made too - also decreased lipoprotein lipase - so less degradation of lipids)

Front 15

What is the equation for renal clearance?

Back 15

Cx = UxV/Px
Cx - clearance of substance x (mL/min)
Ux = urine concentration of substance x (mg/ML)
V = urine flow (volume/time)
Px = plasma concentration of substance x (mg/ML)

Front 16

If GFR>Cx then what is happening?

Back 16

net tubular resorption of substance x

Front 17

If GFR<Cx then what is happening?

Back 17

net tubular secretion of substance x

Front 18

If GFR = Cx then what is happening?

Back 18

no net secretion of resorption

Front 19

What is used to estimate the GFR?

Back 19

inulin - because it is freely filtered and not secreted or absorbed (a little is secreted by renal tubules so it is a little overestimate of the GFR)

Front 20

What is a normal value for GFR?

Back 20

100

Front 21

What are the 2 equations for GFR?

Back 21

GFR = Uinulin x V/Pinulin
GFR = Kf(Pgc-Pbs) - (pigc - pibs)
Kf = filtration coefficient
Pgc = hydrostatic pressure of glomerular capillary
Pbs = hyrdostatic pressure of bowmans space
pigc = oncotic pressure of glomerular capillary
pibs = oncotic pressure of bowmans space (should be 0)
*If Fick's equation is positive then filtration is favored

Front 22

When using inulin to estimate GFR is it an exact measurement of the value?

Back 22

NO! It slightly overestimates the GFR - because the renal tubules secrete a tiny amount of inulin

Front 23

What is the driving force for GFR?

Back 23

net ultrafiltration pressure across the glomerular capillaries

Front 24

What can ERPF (effective renal plasma flow) be estimated by?

Back 24

PAH (para-aminohippuric acid) clearance because it is both filtered and actively secreted in the proximal tubule - all PAH entering the kidney is excreted

Front 25

What is the equation for ERPF (effective renal plasma flow)? How does it compare to true RPF (renal plasma flow)?

Back 25

ERPF = Upah x V/Ppah
ERPF underestimates true RPF by 10%

Front 26

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

Back 26

RBF = RPF/1-hematocrit
RBF = 25% x CO (25% of the cardiac output goes to the kidneys)
1-hematocrit = fraction of blood occupied by plasma

Front 27

What is the equation for filtration fraction (FF)?

Back 27

FF = GFR/RPF
FF is the fraction of RPF that is filtered across the glomerular capillaries
normal = 0.2 = 20% of RPF is filtered across glomerular capillaries

Front 28

What do prostaglandins do in the kidney vessels?

Back 28

dilate the afferent arterioles - increasing RPF, increasing GFR so FF stays constant

Front 29

What inhibits prostaglandins from dilating the afferent arterioles?

Back 29

NSAIDs - so they cause constriction of the afferent arterioles and thus decrease RPF and decrease GFR

Front 30

What are NSAID's affect in the kidneys?

Back 30

they inhibit the vasodilataion of the afferent arterioles by prostaglandins - so they decrease RPF thus decreasing GFR

Front 31

What can GFR be estimated with?

Back 31

Creatinine clearance- but it slightly overestimates GFR because a little is secreted in the proximal tubules

Front 32

What does angiotensin II do in the kidney vessels?

Back 32

vasoconstricts the efferent arterioles decreasing RPF and increasing GFR - so filtration fraction increases (FF = GFR/RPF)

Front 33

What does an ACE inhibitor do in the kidney vessels?

Back 33

inhibits the action of angiotensin II - so does not allow for the efferent arterioles to vasoconstrict so no increase in GFR

Front 34

What does constriction of the afferent arterioles do to GFR, FF, RPF?

Back 34

decrease in Pgc - so decreased RPF, decreased GFR - no change in FF

Front 35

What does constriction of the efferent arterioles do to GFR, FF, RPF?

Back 35

increase Pgc - so decrease is RPF, increase in GFR - increase in FF

Front 36

What is GFR dependent on?

Back 36

Pressure!

Front 37

What does increase plasma protein concentration do to GFR, FF and RPF?

Back 37

increased oncotic pressure in glomerular capillaries (fluid wants to go into capillaries) (pigc) - so no change in RPF, decrease in GFR - so decrease in FF

Front 38

What does a decrease in plasma protein concentration do to GFR, FF and RPF?

Back 38

decreased oncotic pressure (fluid wants to leave capillaries) no change in RPF, increase in GFR - increase in FF

Front 39

What does a constriction in the ureters do to GFR, FF and RPF?

Back 39

causes increase pressure in bowmans space (Pbs) - no change in RPF, decreased GFR - so decreased FF

Front 40

What is the equation for the filtered load?

Back 40

GFR x Px

Front 41

What is the equation for the excretion rate?

Back 41

V x Ux

Front 42

What is the equation for the reabsorption?

Back 42

Filtered - Excreted

Front 43

What is the equation for secretion?

Back 43

Excreted - Filtered

Front 44

If filtered>excreted

Back 44

reabsorption occurred

Front 45

If excreted>filtered

Back 45

secretion occurred

Front 46

What is free water clearance?

Back 46

The ability to dilute/concentrate the urine - given urine flow rate, urine osmolarity, and plasma osmolarity.

Front 47

What is the equation for free water (C H2O)?

Back 47

C H2O (free water) = total urine (V) - water occupied with solute (Cosm)

Front 48

What is the equation for C osm?

Back 48

C osm = Uosm x V/P osm

Where V = urine flow rate
use C osm for calculating free water

Front 49

What creates an isotonic urine?

Back 49

loop diuretics
CH2O = 0

Front 50

When is CH20>0 seen?

Back 50

without ADH

Front 51

When is CH20 < 0 seen?

Back 51

With ADH (retention of free water)

Front 52

Where is glucose reabsorbed?

Back 52

All of it in the proximal tubules by the Na+/glucose cotransporter

Front 53

At what serum glucose levels does glucosuria begin?

Back 53

At a blood glucose of 160-200 mg/dL (threshold)

Front 54

At what blood glucose are all transporters saturated (Tm) ?

Back 54

At a blood glucose of 350 mg/dL

Front 55

What is an important clue of diabetes mellitus?

Back 55

glucosuria

Front 56

How are amino acids resorbed?

Back 56

sodium-dependent transporters in the proximal tubules resorb amino acids by at least 3 distinct carrier systems, competitive inhibition within each group

Front 57

What happens in Hartnup's disease?

Back 57

Become deficient in neutral amino acid (tryptophan) transporter - results in pellagra (death, dementia, dermatitis, and diarrhea) - because tryptophan makes niacin!

Front 58

What are the transporters on the lumen (urine) side of the proximal tubule?

Back 58

Na+/glucose cotransporter - transports both into the cell
Na+/H+ antiporter - transports Na+ into the cell and H+ into the lumen (urine)
Cl-/Base- antiporter - transports Cl- into the cell and Base - into the lumen (urine)
*water and CO2 passively diffuse into the cells

Front 59

What are the transporters on the interstital (blood) side of the proximal tubule?

Back 59

Na+/K+ pump (K+ goes into cells, Na+ goes into the blood)
HCO3- transporter - transports HCO3- into the blood

Front 60

What does the thin descending loop of henle do?

Back 60

passively reabsorbs water via medullary hypertonicity (impermeable to sodium). Concentrating segment. Makes urine hypertonic

Front 61

What part of the nephron is the concentrating segment? What does it make the urine?

Back 61

the thin descending loop of henle - makes the urine hypertonic

Front 62

What are the transporters on the lumen side of the thick ascending loop of henle?

Back 62

Na+/K+/2Cl- transporter - brings all of them into the cell
K+ channel - K+ goes into the lumen (positive potential)
Mg2+, Ca2+ - enters cells paracellularly

Front 63

What are the transporters on the interstitum side of the thick ascending loop of henle?

Back 63

Na+/K+ ATPase - Na+ goes into the blood and K+ goes into the cell
K+ channel - K+ goes into the blood
Cl- channel - Cl- goes into the blood

Front 64

What part of the nephron is impermeable to water? and makes urine less concentrated?

Back 64

thick ascending loop of henle

Front 65

What are the transporters on the lumen (urine) side of the distal convoluted tubules?

Back 65

Na+/Cl- cotransporter - brings both into the cells
Ca2+ channel - Ca2+ goes into cells

Front 66

What are the transporters on the interstitium (blood) side of the distal convoluted tubule?

Back 66

Na+/K+ ATPase - K+ into cells, Na+ into blood
Na+/Ca2+ antiporter - Na+ into cells, Ca2+ into blood
PTH receptor - increases the Ca2+/Na+ exchange - so more Ca2+ is reabsorbed
Cl- channel - Cl- goes into the blood

Front 67

What are the 2 types of cells in the collecting duct?

Back 67

Principal cells and intercalated cell

Front 68

What 2 molecules work in the collecting ducts?

Back 68

1) aldosterone - increase Na+ resorption from the lumen (urine) - by inserting a Na+ channel on the lumen side and increase K+ secretion into the lumen (urine)
2) ADH works at V2 receptors- insert H20 channel into the lumen side - H20 goes into the cells (out of the urine)

Front 69

What receptors does ADH work at? What area of the nephron?

Back 69

works on V2 receptors in the collecting duct (inserts a H20 channel into the lumen side) so water is reabsorbed into the blood

Front 70

What are the transporters in principal cells on the lumen (urine) side in the collecting ducts?

Back 70

Na+ channel - Na goes into the cell
K+ channel - K+ goes into the lumen (urine)
aquaporin (H20 channel) - inserted by ADH

Front 71

What are the transporters in principal cells on the interstitial (blood) side?

Back 71

Na+/K+ ATPase - K+ goes into cell, Na+ goes into the interstitium (blood)

Front 72

What receptors does principal cells have?

Back 72

Aldosterone receptor (aldosterone causes Na+ resorption and H+ and K+ secretion (K+ in prinicpal cells) (H+ in intercalated cells)??
ADH receptor (works on V2 receptors)

Front 73

What are the transporters on the lumen side of intercalated cells?

Back 73

K+/H+ antiporter - K+ goes into cell, H+ goes into lumen (urine)
H+ ATP channel - H+ goes into urine

Front 74

What are the transporters on the interstitial side of the intercalated cells?

Back 74

HCO3-/Cl- antiporter - HCO3- goes into interstitium (blood) and Cl- goes into cells

Front 75

What shifts K+ out of a cell? What do they all cause?

Back 75

Hyperkalemia
1) Insulin deficiency (inhibits Na+/K+ ATPase)
2) B-adrenergic antagnoist (decreases Na+/K+ ATPase)
3) Acidosis, severe exercise (K+/H+ exchanger)
4) hyperosmolarity (water goes into blood and K+ follows)
5) Digitalis (blocks Na+/K+ ATPase)
6) Cell lysis - increased release of K+ from inside cells

Front 76

What shifts K+ into a cell? What do they all cause?

Back 76

hypokalemia
1) insulin (stimulates Na+/K+ pump on interstitial (blood) side)
2) B agonists - stimulates Na+/K+ pump
3) alkalosis (H+/K+ exchanger)
4) hypoosmolarity - water will go into cells and K+ will follow

Front 77

What matches Na+ reabsorption?

Back 77

H20 reabsorption - water follows Na+

Front 78

Where does PTH act?

Back 78

the receptor is in the distal convoluted tubule - causes increase in Na+/Ca+ antiporter - Na+ goes into cell and Ca2+gets reabsorbed (on the interstitial side)

Front 79

When tubular fluid concentration (TF)/plasma concentration (P) > 1

Back 79

then water is reabsorbed quicker than solutes - there is a net secretion of solutes

Front 80

When tubular fluid concentration (TF)/plasma concentration (P) < 1

Back 80

then solutes are reabsorbed quicker than water

Front 81

When tubular fluid concentration (TF)/plasma concentration = 1

Back 81

solute and water are reabsorbed at the same rate

Front 82

What happens to tubular creatinine and inulin in the proximal tubule?

Back 82

they increase in concentration (not in amount) along the proximal tubule due to water resorption

Front 83

How does Cl- and Na+ reabsorption relate to one another in the proximal tubule?

Back 83

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

Front 84

What are the JG cells? what do they do?

Back 84

JG cell are modified smooth muscle of afferent arterioles - they secrete renin (leading to increase in AT II and aldosterone levels) in response to decrease renal blood pressure, decrease delivery of Na+ to the distal convoluted tubules, or activation of sympathetic (B1) tone

Front 85

What is the macula densa?

Back 85

specalized cells located in the distal convoluted tubules - sense Na+ concentration - if it low prostaglandins are released that vasodilate afferent arterioles and stimulate JG cells to secrete renin

Front 86

What does JGA defend?

Back 86

GFR - via the renin-angiotensin-aldosterone system

Front 87

Describe the RAAS

Back 87

Renin-angiotensin-aldosterone system
renin is released from the JG apparatus - converts angiotensinogen (from the liver) into angiotensin I (inactive) - then Angiotensin converting enzyme (ACE) from the liver converts angiotensin I into angiotensin II (active) this occurs in the lungs - then angiotensin II has many functions to increase BP!

Front 88

What does angiotensin II do?

Back 88

1) acts at AT II receptors in vascular smooth muscle to vasoconstrict to increase blood pressure
2) constricts efferent arterioles in the glomerulus (increases GFR, decreases RPF, increasing FF)
3) stimulates aldosterone secretion from adrenal gland (increases Na+ channel, Na+/K+ pump insertion in principal cells; enhances K+ and H+ excretion (upregulates principal cell K+ and intercalated cell H+ channels) get net reabsorption of Na+ and water
and loss of K+ and H+
4) stimulates ADH release from the posterior pituitary - to increase water reabsorption
5) increases proximal tubule Na+/H+ activity - so get water reabsorption - can cause contraction alkalosis
6) stimulates the hypothalamus to stimulate thirst

Front 89

What does aldosterone do?

Back 89

secreted from the adrenal gland - increases Na+ channels, Na+/K+ pump in principal cells, increases K+ channels in prinicpal cells and H+ channels in intercalated cells) get net Na+ and water reabsorption and loss of H+ and K+

Front 90

What affects baroceptor function; limits reflex bradycardia, which would normally accompany its pressor effects?

Back 90

angiotensin II (prevents the reflex bradycardia)

Front 91

What is ANP?

Back 91

released from atria in response to increased volume; may act as a check on the RAAS; relaxes vascular smooth muscle via cGMP, causing increased GFR and decreased renin
causes increased Na+ and H20 secretion and decreases TPR

Front 92

What does ADH primarily regulate

Back 92

regulates osmolarity but also responds to low blood volume (which takes precedence over osmolarity)
it inserts H20 channels in collecting ducts

Front 93

What does aldosterone primarily regulate?

Back 93

blood volume (in low volume states both ADH and aldo act to protect blood volume)

Front 94

What are the endocrine functions of the kidneys?

Back 94

1) Erythropoietin
2) 1,25 (OH)2 vitamin D
3) Renin
4) Prostaglandins

Front 95

What releases EPO and what does it do?

Back 95

released from the kidney - it stimulates RBC production - released in response to hypoxia from endothelial cells of peritubular capillaries

Front 96

What releases 1,25 (OH)2 vitamin D? What does it do?

Back 96

proximal tubule cells convert 25(OH)2 vitamin D into 1,25(OH)2 vitamin D, which increase intestinal reabsorption of both calcium and phosphate. PTH acts directly on the kidney and increases renal calcium but decrease renal phosphate reabsorption. PTH also directly stimulates 1 alpha hydroxylase in the proximal tubules to make 1,25(OH)2 vitamin D which increases intestinal reabsorption of calcium and phosphate

Front 97

What do NSAIDs do on the kidney?

Back 97

can cause acute renal failure - because they prevent the formation of prostaglandin which vasodilate the afferent arterioles to maintain GFR (remember GFR is all dependent on pressure) - if prostaglandins can't wok the afferent arterioles will be vasoconstricted and GFR will be decreased

Front 98

When is renin released?

Back 98

1) When there is decreased Na+ delivery to the macula densa in the distal convoluted tubules they release prostaglandins to the JG complex and it releases renin
2) When there is decreased renal blood pressure - the JG cells secrete it
3) increased sympathetic (B1) discharge

Front 99

What do prostaglandins do?

Back 99

paracrine secretion they vasodilate the afferent arterioles to increase GFR

Front 100

What converts 25(OH)2 Vitamin D to its active form? Where does it happen?

Back 100

1a hydroxylase converts inactive vitamin D to its active form (1,25(OH)2 Vitamin D) - happens in the kidney

Front 101

What does ANP do?

Back 101

secreted from the atria in response to increased stretch on receptors (increased atrial pressure) - causes increased GFR and increased Na+ filtration with no compensatory Na+ reabsorption in the distal nephron to lower volume. Net effect: Na+ loss and volume loss

Front 102

When is PTH released? What does it do?

Back 102

released when there is decreased serum Ca2+, increased serum phosphate, or decreased serum vitamin D. It causes increased resorption of calcium (from the DCT), increased phosphate secretion (PCT), and increased 1,25(OH)2 vitamin D production - which causes increased calcium and phosphate resorption from the gut

Front 103

When is AT II released? What does AT II cause?

Back 103

released in response to decrease BP. causes efferent arteriole vasoconstriction - which causes increased GFR, decreased RPF - increased FF but with compensatory Na+ reabsorption in the proximal and distal nephron. Net effect: preservation of renal function in low-volume state (increased FF) with simultaneous Na+ reabsorption (proximal and distal) to decrease additional volume loss

Front 104

When is ADH released? What does it do?

Back 104

released in response to increased plasma osmorlarity (primarily) but also decreased blood volume. Binds to receptors on the principal cells causing an increase in water channels and water reabsorption

Front 105

When is aldosterone released? What does it do?

Back 105

Released when there is a low blood volume (via AT II) or increased plasma K+ and it causes creation of more Na+/K+ pumps (principal cells), K+ channels (principal cells), and H+ channels (intercalated cells) - causes net resorption of Na+ and net secretion of H+ and K+!

Front 106

What is the pH, pCO2, HCO3- that you see for a metabolic acidosis? What does the body do to compensate?

Back 106

pH low (below 7.4), HCO3- low (MAIN disturbance), pCO2 low
*body hyperventilates

Front 107

What is the pH, pCO2, HCO3- that you see for metabolic alkalosis? What does the body do to compensate?

Back 107

pH high (above 7.4), HCO3- high (MAIN disturbance), pCO2 - high
* body hypoventilates

Front 108

What is the pH, pCO2, HCO3- that you see for respiratory acidosis? What does the body do to compensate?

Back 108

pH low (below 7.4), pCO2 high (MAIN disturbance), HCO3- high
To compensate the body increases renal HCO3- absorption

Front 109

What is the pH, pCO2, HCO3- that you see for respiratory alkalosis? What does the body do to compensate?

Back 109

pH high (above 7.4), pCO2 low (MAIN disturbance), HCO3- low
To compensate the body decreases renal resorption of HCO3-

Front 110

What is the Henderson-Hasselbach equation?

Back 110

to find pH
pH = pKa + log HCO3-/(0.03 x Pco2)

Front 111

How do you figure out respiratory compensation for metabolic acidosis?

Back 111

Pco2 = 1.5(HCO3-) +8 plus or minus 2
* For every 1 increase in HCO3 the PCO2 should increase by 0.7 is it is fully compensated

Front 112

What is the formulation for the anion gap? When do you use it?

Back 112

use it if someone has a metabolic acidosis -
anion gap = Na+ - (Cl- + HCO3-)
if the gap is larger than 12 - MUDPILES
if the gap is normal (8-12) think something else

Front 113

what are the potential causes of a respiratory acidosis?

Back 113

airway obstruction, acute lung disease, chronic lung disease, opioids, narcotics, sedatives, weakening of the respiratory muscles
would have: decreased pH, increased PCO2 (main disturbance), increased HCO3-

Front 114

What are the potential causes of a metabolic acidosis?

Back 114

first check anion gap = Na+ - (Cl- + HCO3-)
if it is normal (between 8 and 12) could be caused by: diarrhea (GI loss of HCO3-), glue sniffing, renal tubular acidosis, and hyperchloremia
if increased anion gap: (greater than 12) could be caused by:
Methanol
Uremia
Diabetic ketoacidosis
Paraldehyde or Phenformin
Iron tablets or INH
Lactic acidosis
Ethylene glycol
Salicylates

*would see low pH, low HCO3- (main disturbance) and low PCO2

Front 115

What are the potential causes of a respiratory alkalosis?

Back 115

hyperventilation (early high altitude exposure), aspirin injestion early (directly stimulates the medullary respiratory center)

Front 116

What can cause a metabolic alkalosis?

Back 116

diuretic use (volume contraction alkalosis), vomiting (loss of gastric H+), antacid use (increased HCO3-), hyperaldostronism (increased H+ secretion - so increased HCO3- reabsorption)
*would see high pH, high HCO3-, high pCO2

Front 117

What is renal tubular acidosis?

Back 117

accumulation of acid in the body due to failure of kidneys to appropriately acidify the urine

Front 118

What is the cause of RTA type 1?

Back 118

Type 1 (distal): defect in collecting ducts ability to excrete H+ (problem with transporters in intercalated cells). Associated with hypokalemia and risk for calcium-containing kidney stones

Front 119

What is the cause of RTA type 2?

Back 119

proximal: defect in the proximal tubules ability to reabsorb HCO3- - associated with hypokalemia and hyperphosphatemic ricketts

Front 120

What is the cause of RTA type 4?

Back 120

"hyperkalemic"
hypoaldosternoism or lack of collecting tubule response to aldosterone - hyperkalemia - inhibition of ammonia excretion in proximal tubules. Leads to a decrease in urine pH due to decreased buffering capacity