Anatomy Flashcards
Kidney taken during donor transplantation
Left kidney
Reason left kidney taken during donor transplantation
Longer renal vein
Vessels used to attached new kidney in transplantation
Iliac artery and vein
Structure that may be damaged during ligation of uterine or ovarian vessels
Ureters
Consequence of damage to ureters during ligation of uterine or ovarian vessels
Obstruction or leakage
Components of glomerular filtration barrier
Basement membrane, podocytes, endothelial cells
Cells that detect sodium and stimulate JG cells to secrete renin
Macula densa cells
Cells stimulated by macula densa cells to secrete renin
JG cells
Location of macula densa cells
Inside distal convoluted tubule
Location of JG cells
Between distal convoluted tubule and afferent arteriol
Cells that function to clean debris from the glomerulus
Mesangial cells
Renal vein drains into what major vessel
Inferior vena cava
Major vessel renal arteries branch from
Abdominal aorta
Structures ureters pass under
Uterine artery or vas deferens
Urine path
Pyramids - calyces - renal pelvis - ureter - bladder
Renal blood flow
Renal artery - segmental artery - interlobar artery - arcuate artery - interlobular artery - afferent arteriole - glomerulus - efferent arteriole - vasa recta/peritubular capillaries - venous outflow
Total body water percentage
60%
Compartment made up of interstitial fluid and plasma
Extracellular compartment
Percentage of ECF that makes up interstitial fluid
75%
Fraction of total body water that makes up ECF
2/3
Percentage of total mass of person that makes up ECF
40%
Percentage of total mass of person that makes up ICF
20%
Normal hematocrit percentage
45%
Formula for calculating HCT %
HCT % = 3 x [Hb] in g/dL
Method for measuring plasma volume
Radiolabeling albumin
Method for measuring extracellular volume
Inulin or mannitol
Formula for measuring ECF volume
ECF = grams infused/equilibrium concentration
Can be inulin or mannitol
Fraction of total body water that makes up ICF
20%
Responsible for filtration of plasma according to size and charge selectivity
Glomerular filtration barrier
Type of collagen found in glomerular filtration barrier
Type IV collagen
Layer of glomerular filtration barrier podocytes are found in
Epithelial layer
Components of basement membrane
Type IV collagen chains and heparan sulfate
Type of endothelium found in glomerular filtration capillaries
Fenestrated capillary endothelium
Glomerular filtration charge barrier properties
Negative charged glycoproteins prevent positive charge molecule entry
Glomerular filtration barrier structure preventing entry of > 100nm molecules and/or blood cells
Fenestrated capillaries
Glomerular filtration barrier structure preventing entry of > 50-60 nm molecules
Slit diaphragm
Structures that make up slit diaphragm in glomerular filtration barrier
Podocyte foot processes interposed with basement membrane
Volume of plasma from which a substance is completely cleared per unit time
Renal clearance (Cx)
If clearance of substance is less than GFR
Net tubular reabsorption
If clearance of substance is more than GFR
Net tubular secretion
If clearance of substance is equal to GFR
No net tubular secretion or reabsorption
Formula for renal clearance
Cx = UxV/Px Ux = urine concentration of substance X Px = plasma concentration of substance X V = urine flow rate (ml/min)
Substance used to calculate GFR because it is freely filtered and is neither reabsorbed or secreted
Inulin
What is normal GFR
100 ml/min
Substance that is an approximate of GFR
Creatinine
Incremental reductions in GFR define what disease
Chronic kidney disease
Formula for GFR
GFR = U(inulin) x V/P(inulin) = Clearance(inulin)
Substance used to measure effective renal plasma flow
para-aminohippuric acid (PAH) clearance
Effective renal plasma flow formula
eRPF = U(PAH) x V/P(PAH) = Clearance(PAH)
Formula for renal blood flow
RBF = RPF/(1 - Hct)
Formula for calculating plasma from Hct
Plasma = 1 - Hct
Measurement that underestimates true renal plasma flow slightly
Effective renal plasma flow
Measurement that overestimates GFR
Creatinine clearance
Formula for calculating filtration fraction
GFR/RPF
What is the normal filtration fraction (%)
20%
Formula for calculating filtered load (mg/min)
GR x plasma concentration
GFR can be best estimated with what measurement
Creatinine clearance
RPF can be best estimated with what measurement
PAH clearance
Lipid compounds that dilate afferent arteriole
Prostaglandins
Drugs that prevent constriction of efferent arteriole
ACE inhibitors
Peptide hormone that preferentially constricts efferent arteriole
Angiotensin II
Effect of ACE inhibitor
Blocks angiotensin II, increases renin, dilates efferent arteriole
Effects of afferent arteriole constriction
Decreased GFR, RPF
No change in FF
Effects of efferent arteriole constriction
Increased GFR, FF
Decreased RPF
Effect of increased plasma protein concentration
Decreased GFR, FF
No change in RPF
Effect of decreased plasma protein concentration
Increased GFR, FF
No change in RPF
Effect of constricting ureter on glomerular dynamics
Decreased GFR, FF
No change in RPF
Effect of dehydration on glomerular dynamics
Decreased GFR and severe decrease in RPF
Increased FF
Drugs that inhibit prostaglandin synthesis
NSAIDs
Glomerular arteriole that is affected by NSAIDs
Afferent arteriole
Effect of NSAIDs on glomerular arteriole
Vasodilates afferent arteriole
Formula for calculating excretion rate
V x [U] of substance
Formula for reabsorption rate
Reabsorption rate = filtered - excreted
Formula for secretion rate
Secretion rate = excreted - filtered
Formula for calculating fraction of excreted sodium
Fe(Na) = P(cr)/U(cr) x U(Na)/P(Na)
Section of renal tubule that reabsorbs glucose
Proximal convoluted tubule
Percentage of glucose reabsorption in healthy individual
100%
Plasma glucose concentration glucosuria begins
200 mg/dL
Rate at which all glucose transporters are saturated
375 mg/min
Mechanism of gestational diabetes
Decreased ability of PCT to reabsorb glucose
Glucose transporter located in proximal convoluted tubule
SGLT2
Drugs that inhibit SGLT2 and permit glucosuria at glucose plasma concentrations < 200 mg/dL
Flozin drugs
The region of substance clearance between threshold and glucose transporter saturation
Splay
Section of renal tubule that contains brush border
Early PCT
Section of renal tubule that generates and secretes NH3
Early PCT
Hormone that inhibits sodium-phosphate contransport leading to phosphate excretion
PTH
Peptide hormone that stimulates sodium-H+ transporter leading to increased sodium, water and bicarb reabsorption
Angiotensin II
Consequence of stimulating sodium-H+ transporter leading to increased sodium, water and bicarb reabsorption
Contraction alkalosis
Section of renal tubule where 60-80% of sodium is reabsorbed
Early PCT
Section of renal tubule that is impermeable to sodium
Thin descending loop of Henle
Function of thin descending loop of Henle
Passively reabsorb water, concentrate urine
Section of renal tubule that makes urine hypertonic
Thin descending loop of Henle
Section of renal tubule that is impermeable to water
Thick ascending loop of Henle
Thick ascending loop of Henle has paracellular transport of what ions
Calcium and magnesium
Mechanism of paracellular transport of calcium and magnesium in thick ascending loop of Henle
Positive lumen potential generated by potassium back leak
Section of renal tubule that makes urine less concentrated
Thick ascending loop of Henle
Drug that inhibits carbonic anhydrase
Acetazolamide
Side effect of acetazolamide
Renal tubular acidosis type II
Condition that affects sodium-potassium pump at PCT
Hyperkalemia
How do potassium and chloride move from tubule to interstitium
Diffusion down electrochemical gradient
Drugs that act on thick ascending loop of Henle
Loop diuretics (furosemide)
Amount of sodium reabsorbed at thick ascending loop of Henle
10-20%
Section of renal tubule that makes urine fully dilute
Early DCT
Ions absorbed at DCT
Sodium and chloride
Hormone that increases calcium-sodium exchange leading to calcium reabsorption
PTH
Amount of sodium reabsorbed in DCT
5-10%
Drugs that act on DCT
Thiazide diuretics
Section of renal tubule that is regulated by aldosterone
Collecting tubule
Effect of ADH binding to V2 receptor
Insertion of aquaporins on apical side of principal cell
Site of action of potassium sparing diuretics
ENaC channel on principal cell
Renal tubular defect associated with increased excretion of nearly all amino acids, glucose, bicarb, and phosphate causing renal tubular acidosis
Fanconi syndrome
Site of action of Fanconi syndrome
Proximal renal tubule
Type of acidosis caused by Fanconi syndrome
Renal tubular acidosis type II
Autosomal recessive disorder presenting similar to chronic loop diuretic use
Bartter syndrome
Site of action of Bartter syndrome
Na/K/2Cl cotransporter in thick ascending loop of Henle
Findings in Bartter syndrome
Causes hypokalemia, metabolic alkalosis with hypercalciuria, hypochloremia, increased renin
Components of the juxtaglomerular apparatus
Macula densa cells, mesangial cells and JG cells
Autosomal recessive disorder presenting similar to being on life-long thiazide diuretics
Gitelman syndrome
Site of action of Gitelman syndrome
Na/Cl cotransporter in DCT
Findings in Gitelman syndrome
Hypokalemia, hypomagnesemia, metabolic alkalosis, hypocalciuria, hypochloremia
Autosomal dominant disorder causing a gain of function mutation presenting like hyperaldosteronism
Liddle syndrome
Site of action of Liddle syndrome
Increased activity of Na channel in collecting duct
Findings in Liddle syndrome
Hypertension, hypokalemia, metabolic alkalosis
Treatment for Liddle syndrome
Amiloride
Hereditary deficiency of 11-B-hydroxysteroid dehydrogenase leading to excess cortisol levels
Syndrome of Apparent Mineralocorticoid Excess (SAME)
Findings in Syndrome of Apparent Mineralocorticoid Excess
Low aldosterone, hypertension, hypokalemia, metabolic alkalosis
Acquired form of Syndrome of Apparent Mineralocorticoid Excess is caused from what
Eating licorice - has glycyrrhetinic acid which inhibits 11-B-hydroxysteroid dehydrogenase
Treatment for Syndrome of Apparent Mineralocorticoid Excess
Corticosteroids
Mechanism of exogenous corticosteroids in Syndrome of Apparent Mineralocorticoid Excess
Decrease endogenous cortisol production leading to decrease mineralocorticoid receptor activity
Function of 11-B-hydroxysteroid dehydrogenase
Convert cortisol to cortisone
Function of renin
Convert angiotensinogen to angiotensin I
Function of ACE
Convert angiotensin I to angiotensin II and breakdown bradykinin
Mechanism of renin release
JG cells secrete due to low BP, sympathetic discharge from B1 effect, macula densa cells from low sodium
Angiotensin II effects on afferent arteriole
Vasoconstrict to raise FF to preserve kidney function in low volume states
Angiotensin II effects on posterior pituitary
Secrete ADH for aquaporin insertion in principal cells for water reabsorption
Angiotensin II effects on vascular smooth muscle
Binds ATII receptor causing vasoconstriction and raising BP
Angiotensin II effects on hypothalamus
Stimulates thirst
Angiotensin II effects on PCT
Increase Na/H+ activity to increase Na, HCO3, water reabsorption
Cells that release atrial natriuretic peptide (ANP)
Atrial myocytes in response to increased volume
Function of ANP
Relaxes smooth muscle via cGMP to increase GFR and decrease renin secretion
Also…
Dilates afferent arteriole, constricts efferent arteriole and promotes natriuresis
Function of ADH
Regulates osmolarity.
Also responds to low blood volume states
Function of aldosterone
Regulate ECF volume and Na content.
Also responds to low blood volume states
Increases K excretion during hyperkalemia
Mechanism of B-blockers on juxtaglomerular apparatus (JGA)
Bind B1-receptors of JGA, decreasing renin which lowers BP
Glycoprotein released by interstitial cells in peritubular capillary bed in response to hypoxia
Erythropoietin
Function of erythropoietin
Stimulate RBC proliferation in bone marrow
Consequence of low erythropoietin
Anemia
Active form of vitamin D
1,25-(OH)2 Vitamin D3
Site of conversion to active form of vitamin D
Cells of PCT
Enzyme that converts 25-OH vitamin D3 to 1,25-(OH)2 Vitamin D3
1a-hydroxylase
Hormone that acts with 1a-hydroxylase to convert 25-OH vitamin D3 to 1,25-(OH)2 Vitamin D3
PTH
NSAID side effect in low renal blood flow states
Acute renal failure
Effect of prostaglandin on renal vasculature
Vasodilates afferent arteriole to increase RBF
Direct sympathomimetic secreted by PCT cells which dilates interlobular arteries, afferent and efferent arterioles at low doses and acts as vasoconstrictor at higher doses
Dopamine
Effect of vasodilatory effects of dopamine on renal vasculature
Increase renal blood flow, little to change in GFR
Hormone secreted in response to low Ca, 1,25-(OH)2 Vitamin D3 and increased plasma phosphate
PTH
Effect of PTH
Increases Ca reabsorption, phosphate secretion and 1,25-(OH)2 Vitamin D3 production
Net effect of atrial natriuretic peptide
Water and Na loss
Digitalis MOA
Blocks Na/K/ATPase shifting K out of cells and H+ into cells
Effect of hypo-osmolarity on potassium
Hypokalemia
Effect of alkalosis on potassium
Hypokalemia
Effect of B-blockers on potassium
Hyperkalemia
Effect of insulin on potassium
Hypokalemia
Effect of hyperosmolarity on potassium
Hyperkalemia
Insulin MOA in hypokalemia
Increases Na/K/ATPase activity shifting K into cells
Effect of high blood sugar on potassium
Hyperkalemia
High blood sugar MOA in hyperkalemia
Solvent drag pulls K out of cells
Effect of succinylcholine on potassium
Hyperkalemia
Succinylcholine MOA
Increase risk in burns and muscle trauma lysis cells leaking K out of cells
Effect of cell lysis on potassium
Hyperkalemia - K leaks out of cells
Primary disturbance in Bartter syndrome
Increased urinary calcium
Primary disturbance in Gitelman syndrome
Decreased urinary calcium
Primary disturbance in Liddle syndrome
Decreased aldosterone
Primary disturbance in Primary hyperaldosteronism
Increased aldosterone
Primary disturbance in renin-secreting tumor
Increased renin
Renal disorder with a primary disturbance of increased urinary Ca and secondary high renin and aldosterone with normal BP
Bartter syndrome
Renal disorder with a primary disturbance of decreased urinary Ca and secondary high renin and aldosterone, low Mg with normal BP
Gitelman syndrome
Renal disorder with a primary disturbance of decreased aldosterone and secondary high BP, low renin and aldosterone
Liddle syndrome
Renal disorder with a normal to high BP, low renin and aldosterone
SIADH
Renal disorder with a primary disturbance of increased aldosterone and secondary high BP and low renin
Primary hyperaldosteronism
Renal disorder with a primary disturbance of increased renin and secondary high BP and aldosterone
Renin-secreting tumor
Metabolic acidosis immediate compensatory response
Hyperventilation
Plasma changes in metabolic acidosis
Primary disturbance - low bicarb
Compensatory - low pH, low PCO2
Metabolic alkalosis immediate compensatory response
Hypoventilation
Plasma changes in metabolic alkalosis
Primary disturbance - high bicarb
Compensatory - high pH, high PCO2
Respiratory acidosis delayed compensatory response
Increased renal bicarb reabsorption
Plasma changes in respiratory acidosis
Primary disturbance - high PCO2
Compensatory - low pH, high bicarb
Plasma changes in respiratory alkalosis
Primary disturbance - low PCO2
Compensatory - high pH, low bicarb
Henderson-Hasselbalch equation
pH = 6.1 + log [HCO3-]/0.03 PCO2
How do you determine metabolic acidosis
Look at pH, bicarb and PCO2 if all low more likely metabolic acidosis
Causes of increased anion gap acidosis
MUDPILES: Methanol Uremia Diabetic ketoacidosis Propylene glycol Iron tablets or INH Lactic acidosis Ethylene glycol (oxalic acid) Salicylates (late)
Causes of normal anion gap acidosis
HARDASS: Hyperalimentation Addison disease Renal tubular acidosis Diarrhea Acetazolamide Spironolactone Saline infusion
Causes of Respiratory acidosis in hypoventilation
Airway obstruction Acute lung disease Chronic lung disease Opioids, sedatives Weakening of respiratory muscles
Formula to calculate anion gap
AG = Na - (Cl + HCO3)
Causes of respiratory alkalosis in hyperventilation
Hysteria Hypoxemia (high altitude) Salicylates (early) Tumor Pulmonary embolism
Causes of metabolic alkalosis in H+ loss/HCO3- excess
Loop diuretics
Vomiting
Antacid use
Hyperaldosteronism
Winters formula
PCO2 = 1.5 [HCO3] + 8 (+/-) 2
A disorder of the renal tubules that leads to normal anion gap metabolic acidosis
Renal tubular acidosis
Mechanism of hypokalemia in RTA type 1
Since H+ not excreted, K+ excreted to luminal charge
Findings in RTA type 1
Urine pH > 5.5, hypokalemia
Causes of RTA type 1
Amphotericin B, analgesics, congenital anomalies of urinary tract
Mechanism of RTA type 1
Inability of a-intercalated cells in collecting duct to excrete H+ and regenerate bicarb
Treatment for RTA type 1
Oral bicarb
Findings in RTA type 2
Urine pH < 5.5, hypokalemia
Mechanism of hypokalemia in RTA type 2
Increased bicarb in lumen leads to negative lumen which pull K+ into lumen increasing excretion
Causes of RTA type 2
Fanconi syndrome, carbonic anhydrase inhibitors
Mechanism of RTA type 2
Inability of PCT to reabsorb bicarb
What causes acidification of urine in RTA type 2
a-intercalated cells in collecting duct acidify urine
Other name for RTA type 1
Distal renal tubular acidosis
Other name for RTA type 2
Proximal renal tubular acidosis
Mechanism of hyperkalemia in RTA type 4
Hypoaldosteronism
Mechanism of RTA type 4
Hypoaldosteronism causes hyperkalemia decreasing ammonia synthesis in PCT decreasing ammonium excretion
Findings in RTA type 4
Urine pH < 5.5
Hyperkalemia, hyperchloremia
Hyponatremia