Kidney & Diuretics & Liver Flashcards
What is contained in the renal cortex?
Most parts of the nephron
Glomerulus, Bowman’s capsule, proximal and distal tubule
What is contained in the renal medulla?
The inner part of the kidney. (more @ risk for hypoxia)
Loop of Henle & Collecting Ducts
-The medulla is divided into pyramids. The APEX of each pyramid is called the papilla. This part has a lot of collecting ducts.
Discuss the drainage of the papilla
Papilla drains urine > minor calyxes > major calyces > renal pevlics > ureter
What are the 2 key hormones that govern how the kidney regulates ECF volume and composition?
-Aldosterone controls na+ and h2O reabsorption (together)
-ADH controls plasma osmolarity
What is calcitrol?
Calciferol is synthesized from Vit. D ingestion or following UV light exposure. In the liver its converted to inactive vit d.
In the kidney under control of parathyroid hormone vid d is converted to the active form.
Calicitriol = 3 functions = absorb calcium in intestines, bone to store calcium, and kidney to reabsorb calcium and phosphate
how much blood flow do kidneys receive
20 - 25%
Discuss blood flow of kidneys
renal artery > renal segmental artery > interlobar artery > arcuate artery > interlobular artery > afferent arteriole > glomerular capillary bed > efferent arteriole > peritubular capillary bed > venules
Discuss TG feedback
JG apparatus is located in distal tubule
Specifically the region that passes btw afferent and efferent arterioles. JG cells recognize changes in sodium/water concentration. & Release renin
Discuss the surgical stress response on kidneys
Transient state of vasoconstriction and sodium retention. This persists for several days resulting in oliguria and edema.
What contributes to vasodilation
Kinins
Prostaglandins
ANP
What casues the release of renin by the JG cells
- decreased perfusion
- sns activation (B1)
- TG feedback
What converts angiotensinogen to AT1
RENIN
and ACE converts AT 1 to AT 2
List the effects of AT 2
Vasoconstriction of peripheral vessels and efferent arteriole
Aldosterone and ADH release
Na+ reabsorption in the PCT
Thirst
Where is aldosterone produced?
Zone GLOMERULOSA of the adrenal gland.
It stimulates the Na/K ATPASE pumps in the distal tubules and collecting duct.
Results in = sodium/water reabsorption, k and h excretion
Where is ADH produced?
Suproptic and paraventricular nuclei of the hypothalamus. Released from posterior pituitary gland.
Increased blood volume from V2 stimulation in collecting ducts (incr’d cAMP)
Increased SVR from V1 stimulation in the vasculature (IP3, DAG, CA)
DA1 vs DA2 receptors
DA 1 @ renal vasculature, renal tubules
= increased cAMP = vasodilation, diuresis
DA2 @ presynaptic SNS nerve terminal
= decreased cAMP and decr’d NE release
Fenoldopam
= selective DA1 receptor agonist that increases RBF.
0.1 - 0.2 mcg/kg/m
may offer renal protection during aortic surgery and during CPB
How much of the RBF is filtered at glomerulus?
RBF = 1000 - 1250 mL/m
GFR = 125 ml/m ~ 20% of RBF
The remaining 80% is delivered into the peritubular capillaries
What are the 3 determinants of glomerular hydrostatic pressure?
MAP, afferent arteriole resistance, efferent arteriole resistance
glomerular hydrostatic pressure is the most important determinant of GFR!!
Describe the fate of sodium at each location in the nephron
PCT = 65%
LOH = 20%
DCT = 5%
CD = 5%
What are the key functions of each part of the nephron
PCT = bulk reabsorption of solutes, water
LOH Descending= countercurrent mechanism (tubular fluid concentrated) and high permeability to H2O
LOH (Ascending) = countercurrent mechanism (tubular fluid diluted) and no permeability to water
Distale Tubule = fine tunes solute concentrations (ADH and aldosterone)
Collecting Duct = regulates final concentration of urine (aldosterone and ADH)
List 3 tests of GFR and give normal values
BUN (10 - 20)
Cr (0.7 - 1.5)
Cr Cl (110 - 150 mL/m)
List 4 tests of tubular function
Fractional excretion of Na+ % = 1 - 3%
Urine osmolaliity = 65 - 1400 msOsm/kg
Urine sodium concentration = 130 - 260 mEq/day
Urine specific gravity = 1.003 - 1.030
BUN
Urea is the primary metabolite of protein metabolism in the liver.
Amino acids - ammonia - urea
B/c urea undergoes filtration AND reabsorption, it is a better indicator of uremic symptoms than as a measurement of GFR>
What is included in the differential diagnosis of a low BUN?
< 8
overhydration
d/t decreased urea production - malnutrition or severe liver dx
High BUN?
20 - 40
dehydration
increased protein input, catabolism, or decr’d GFR
What is the BUN:Creatinine ratio?
Helps us evaluate the status of hydration. Nml = 10:1
> 20:1 = prerenal azotemia
or non-renal causes of elevated BUN can cause this
What is the best indicator of GFR?
CREATINE CLEARANCE
(140 - age) x kg/ 72x cr
if female multiply by 0.85
How do you interpret the fraction excretion of sodium?
Fe(Na+) < 1% = prerenal azotemia b/c more sodium is conserved relative to the amount of creatine cleared
> 3% = impaired tubular function
Carbonic anhydrase inhibitors
Acetazolamide, Dorzolamide
Noncompetitive inhibition of carbonic anhydrase in the PCT - net gain of H+, Cl- and loss of HCO3 and Na
ADR: metabolic acidosis and hypokalemia!
Osmotic diuretics
-Mannitol, glycerin, isosorbide
Sugars that undergo filtration but not reabssorption. PCT and LOH are the primary sites.
Loop diuretics
furosemide, bumetanide, ethacrynic acid
poison the Na/K/2CL transporter in the medullary region of the LOH. The amount of sodium remaining in the tubule overwhelms the distal tubule reabsorption capability. Thus, a large volume of dilute urine is excreted. Potassium, calcium, magnesium, and chloride are also lost to the urine.
ADR: hypokalemia, hypochloremic metabolic alkalosis, ototoxicity (ethacrynic acid > furosemide), reduced lithium clearance
Thiazide diuretics
HCTZ, metolazone, indapamide
Inhibit the NaCl transported in the distal tubule
treats osteoporosis by reducing calcium excretion.
ADR: hyperglycemia, hypercalcemia, hyperuricemia, metabolic alkalosis (hypochloremic hypokalemia)
Potassium sparing diuretics
Spironolactone, amiloride, triamterene
Inhibit k secretion and sodium reabsorption in the collecting ducts. (A&T) Thus, function is independent of aldosterone.
Spironolactone exists in a subclass called aldosterone antagonissts.
Treats secondary hyperaldosteronism.
ADR: metabolic acidosis, gynecomastia, decreased libido (spir), nephrolithiasis (triamterene)
CKD and acid/base balance
Decreased excretion of non-volatile acid contributes to a gap in metabolic acidosis.
Gap acidosis = accumulation of nonvolatile acids
Discuss pathophys of renal osteodystrophy
-D/t = decreased vitamin D production and secondary hyperparathyroidism
-inadequate supply of vit d impairs calcium absorption in GI.
-body increases PTH which gets ca+ from bones.
What are the arterioles of the liver? Aka what is its blood supply?
Hepatic artery and portal vein
The central vein is the hepatic “vein” that actually drains blood.
The sinusoid is the capillary equivalent
Describe the flow of bile from its site of production to release into the duodenum
-Hepatocytes make the bile
-Canaliculi drain bile into the bile duct
-The bile ducts converge to form the common hepatic duct
-The cystic duct (from the gallbladder) and the pancreatic duct join the common hepatic duct before it empties into the duodenum
-Sphincter of Oddi controls flow of bile released
How much blood flow does the liver receive?
30% = 1500 mL
Celiac artery provides blood flow to
Liver, Spleen, Stomach
Comes from aorta. Has a1 and b2 receptors
Superior mesenteric artery provides blood flow to
Pancrease, SI, Colon
Inferior mesenteric artery provides blood flow to
Colon
Portal vein has what receptors on it
alpha 1 only
What is normal portal vein pressure
7 - 10 mmHg
PORTAL HTN > 20 - 30 mmHg
What is the hepatic arterial buffer response
Hepatic Artery Perfusion Pressure = MAP - Hepatic Vein Pressure
A reduction in portal vein flow is compensated by an increased hepatic artery flow. This is mediated by adenosine. Severe liver disease impairs this response.
What coagulation factors are NOT produced by hepatocytes
Factor 3, 8, & vwF & factor 4
What plasma proteins are produced by the liver
All except for immunoglobulins
Albumin & acidic drugs
Alpha 1 acid glycoprotein & basic drugs
Pseudocholinesterase metabolizes sux & esters
Glycogenesis
Hyperglycemia - insulin releaased from beta cells - glucose stored as glycogen
Glycogenolysis & Gluconeogenesis
Hypoglycemia - glucagon released from pancreatic alpha cells - glycogen broken into glucose
Epi released from adrenal medulla - non-carbs made into glucose
LIVER PLAYS IMPORTANT ROLE IN GLUCOSE METABOLISM
Discuss bilirubin
Aged RBCS (> 120 d) are processed by reticuloendothelial cells in the spleen
-Hgb -> Heme -> Unconjugated bilirubin which binds with albumin
-Transported to the liver. Conjugated with glucuronic acid.
-Now it’s water-soluble, and it can be excreted into bile.
AST/ALT
AST = 10 - 40
ALT = 10 - 50
AST/ALT > 2 = cirrhosis or alcoholic liver dx
Name 3 tests of biliary duct obstruction. What. is the most specific?
5 Nucleotidase = 0 - 10 = MOST SPECIFIC
Y Glutamyl transpeptidase = 0 - 30
Alk phos = 45 - 115 (not v. specific b/c its in bone, placenta, tumors)
Prehepatic lab dx
Unconjugated bilirubin will be high
caused by hemolysis, hematoma reabsorption
Hepatocellular injury
Conjugated bilirbuin, AST/ALT/ PT all high
caused by cirrhosis, alcohol abuse, drugs, viral infection, sepsis, hypoxemia
Cholestatic
Conjugated bilirubin, alk phos, y glutamyl all high
PT, AST/ALT albumin don’t change until late
Due to biliary tract obstruction and sepsis
Which type of viral hepatitis has the highest incidence
Type A = 50%
Type B = 35%
Type C = 15%
Type D = coinfection w/B
Anesthetic technique to maintain blood flow
Isoflurane
Liberal use of fluids
Normocapnia
Avoid: amio, PCN, tetracycline, sulfa
MELD score
Low risk < 10
Intermediate risk = 10 - 15
High risk > 15
