UNIT 10 Kidney, Liver, Endocrine Flashcards
Discuss the anatomy of the renal cortex and medulla
Cortex = outer part of the kidney: has GFR
- Glomerulus, Bowman’s capsule, proximal tubules, distal tubules
Medulla = inner part of the kidney: has catecholamines 80% epi, 20% norepi
- loops of Henle & collecting ducts
- divided into pyramids
- the calyces, pelvis, and ureters have the capability to contract and push urine toward the bladder
Describe the anatomy of the nephron.
the nephron is the functional unit in the kidney
afferent arteriole –> glomerulus –> efferent arterial
Bowman’s capsule –> PCT –> LOH –> distal tubule –> collecting duct
how does the kidney contribute to the volume and composition of the ECF?
there are 2 key hormones that govern how the kidney regulates ECF volume and composition:
- aldosterone: controls ECF volume (Na+ and water are reabsorbed together)
- ADH (vasopressin) controls plasma osm (water is reabsorbed, but Na+ isn’t)
the kidneys also regulate K+, Cl-, phos, mag, H+, bicarb, glucose, and urea
how do they kidneys help to regulate blood pressure? what other systems also contribute to blood pressure regulation?
the kidneys provide intermediate and long term blood pressure control:
- long term BP control is carried out by the thirst mechanism (intake) and sodium and water excretion (output)
- intermediate control of BP is carried out by the RAAS
- short term control of BP is carried out by the baroreceptor reflex
how does the kidney eliminate toxins and metabolites?
glomerular filtration and tubular secretion clear the blood of metabolic byproducts, toxins, and drugs.
like the liver, the kidney is capable of phase I and phase II biotransformation.
how does the kidney contribute to acid-base balance? Which other organ is essential to this process?
the key organs of acid-base balance include the lungs and the kidneys.
the lungs excrete volatile acids (CO2) and the kidneys excrete non-volatile acids
the kidneys maintain acid-base balance by titrating H+ in the tubular fluid, which creates acidic or basic urine.
what stimulates the kidney to release EPO? what does EPO do after it’s released?
EPO is released in response to inadequate O2 delivery to the kidney. Clinical examples include anemia, reduced intravascular volume, and hypoxia (high altitude, cardiac, and/or pulmonary failure)
EPO stimulates stem cells in the bone marrow to produce erythrocytes
severe kidney disease reduces EPO production and leads to chronic anemia
what is calcitriol, and what does it do?
calciferol is synthetized from ingested vitamin D or following exposure to UV light
- in the liver, calciferol is converted to 25[OH] vitamin D3 (inactive D3)
- in the kidney (under control of PTH), inactive D3 is converted to calcitriol (1,25 [OH]2 Vitamin D3 (active form))
calcitriol has three functions. It stimulates:
- the intestine to reabsorb Ca++ from food
- the bone to store Ca++
- the kidney to reabsorb Ca++ and phosphate
How much blood flow do the kidneys receive (% of CO and total flow)?
20-25% of CO
1000-1250mL/min
discuss the path blood flows after it enters the renal artery.
renal artery interlobar arteries arcuate arteries interlobular arteries afferent arterioles glomerular capillary bed (filtration) efferent arteriole peritubular capillary bed (reabsorption and secretion) venules interlobular veins arcuate veins interlobar veins renal vein
discuss the significance of renal autoregulation
the purpose of autoregulation is to ensure a constant amount of blood flow is delivered to the kidneys over a wide range of arterial blood pressures. glomerular filtration becomes pressure dependent when MAP is outside the range of autoregulation
when renal perfusion is too low, RBF is increased by reducing renal vascular resistance
when renal perfusion is too high, RBF is decreased by increasing renal vascular resistance
there is little agreement about the range of RBF autoregulation. We like 50-180
describe the myogenic mechanism of renal autoregulation.
if the renal artery pressure is elevated, the myogenic mechanism constricts the afferent arteriole to protect the glomerulus from excessive pressure
when the renal artery pressure is too low, the myogenic mechanism dilates the afferent arteriole to increase blood flow going to the nephron
how does tubuloglomerular feedback affect renal autoregulation?
juxtaglomerular apparatus is located in the distal tubule- renin is created here
tubuloglomerular feedback about the Na+ and Cl- composition in the distal tubule affects arteriole tone. In turn, this creates a negative feedback loop to maintain RBF
how does the surgical stress response affect renal blood flow?
the surgical stress response induces a transient state of vasoconstriction and sodium retention. This persists for several days, resulting in oliguria and edema. vasoconstriction of the renal vasculature during this time predisposes the kidneys to ischemic injury and nephrotoxicity from drugs administered during the perioperative period.
List the 3 steps involved in the RAAS pathway.
- decreased renal perfusion
- SNS activation (beta1)
- tubuloglomerular feedback
- -> renin release
angiotensinogen –> angiotensin 1 (via renin) –> angiotensin 2 (via ACE) –) vasoconstriction, aldosterone and ADH release, Na+ reabsorption, and thirst
list the three conditions that increase renin release, and give examples of each.
- decreased renal perfusion pressure
- hemorrhage
- PEEP
- CHF
- liver failure w/ ascites
- sepsis
- diuresis - SNS activation (beta1)
- circulating catechols
- exogenous catechols - tubuloglomerular feedback (the macula densa in the distal tubule contains chemoreceptors that monitor [Na+] and [Cl-] in tubular fluid
- decreased Na+, Cl- in distal tubule.
where is aldosterone produced, and what is its function
steroid hormone that is produced in the zona glomerulosa of the adrenal gland
by stimulating the Na+/K+ ATPase in the principle cells of the distal tubules and collecting ducts, aldosterone causes:
- sodium reabsorption
- water reabsorption
- potassium excretion
the net effect is that aldosterone increases blood volume but doesn’t affect osm.
where is antidiuretic hormone produced, and what is its function?
ADH is produced in the supraoptic nucleus hypothalamus and helps retain water. It is released from the posterior pituitary gland in response to
- increased osm of the ECF
- decreased blood volume
how ADH increases BP:
- increased blood volume from V2 receptor stimulation in the collecting ducts
- increased SVR from V1 receptor stimulation in the vasculature
what clinical situations increase ADH release?
while anesthetic agents do not directly affect ADH homeostasis, they do impact arterial blood pressure and venous blood volume. In turn, these changes increase ADH release. Examples include:
- PEEP
- PPV
- hypotension
- hemorrhage
list 3 mechanisms that promote renal vasodilation
there are 3 pathways that promote renal vasodilation:
- prostaglandins (inhibited by NSAIDs)
- atrial natriuretic peptide (increased RAP –> Na+ and water excretion)
- dopamine-1 receptor stimulation (increased RBF)
compare and contrast the location and function of the dopamine 1 and 2 recepotrs
- DA1 (increased cAMP) are present in the kidney and splanchnic circulation –> vasodilation, increased RBF/GFR, diuresis, Na+ excretion
- DA2 (decreased cAMP) are present on the presynaptic adrenergic nerve terminal –> decreased NE release
what is the mechanism of action of fenoldapam? why is it used?
selective DA1 receptor agonist that increases RBF.
low dose (0.1-0.2mcg/kg/min) is a renal vasodilator and increases RBF, GFR, and facilitates Na+ excretion w/out affecting arterial blood pressure - it may offer renal protection during aortic surgery and during CPB
how much of the RBF is filtered through the glomerulus? Where does the rest go?
RBF = 1000-1250mL/min GFR = 125mL/min or 20% of RBF
filtration fraction is 20%
the remaining 80% is delivered to the peritubular capillaries
what are the 3 determinants of glomerular hydrostatic pressure?
glomerular hydrostatic pressure is the most important determinant of GFR.
three determinants:
- arterial blood pressure
- afferent arteriole resistance
- efferent arteriole resistance
how do changes in afferent arteriole diameter, efferent arteriole diameter, and plasma protein concentration affect net filtration pressure?
constriction of afferent arteriole:
- decreased RBF
- decreased GFR
constriction of efferent arteriole:
- decreased RBF
- increased GFR
- increased filtration fraction
increased plasma protein
- decreased GFR
- decreased filtration fraction
decreased plasma protein
- increased GFR
- increased filtration fraction
define reabsorption, secretion, and excretion.
reabsorption: substance is transferred from the tubule to the peritubular capillaries
secretion: substance is transferred from the peritubular capillaries to the tubule
excretion: substance is removed from the body in the urine
describe the fate of sodium at each location in the nephron
**PCT 65%** LOH 20% DCT 5% CD 5% urine 5%
what are the key functions of each part of the nephron?
PCT:
- bulk reabsorption of solutes and water 65%
LOH (descending):
- countercurrent mechanism
- high permeability to H2O
LOH (ascending)
- countercurrent mechanism (concentrates urine)
- no permeability to H2O
DCT:
- fine tunes solute concentration (aldosterone and ADH)
collecting duct:
- regulates final concentration of urine (aldosterone and ADH)
describe the mechanism of action, clinical use, and key side effects of carbonic anhydrase inhibitors.
MOA: noncompetitive inhibition of carbonic anhydrase in the PCT –> net loss of bicarb and Na+ w/ a net gain of H+ and Cl-
clinical uses:
- open angle glaucoma
- altitude sickness
- central sleep apnea
key side effects:
- metabolic acidosis
- hypokalemia
carbonic anhydrase inhibitors:
- acetazolamide
- dorzolamide
describe the mechanism of action, clinical use, and key side effects of osmotic diuretics.
MOA: sugars that undergo filtration but not reabsorption. They inhibit water reabsorption in the PCT (primary) as well as the LOH. Water is excreted in excess of electrolytes
clinical uses:
- free radical scavenging
- prevention of AKI
- intracranial HTN
key side effects:
- volume overload in CHF
- pulmonary edema
- if BBB disrupted, can cause cerebral edema
ex:
- mannitol
- glycerin
- isosorbide
describe the mechanism of action, clinical use, and key side effects of loop diuretics.
clinical uses:
- HTN
- CHF/acute pulmonary edema
- hypercalcemia
key side effects:
- low K+, Ca++, Mg++
- hypochloremic met acidosis
- hypovolemia
- ototoxicity
- reduced lithium clearance
Loop diuretic drugs:
- furosemide
- bumetanide
- ethacrynic acid
describe the mechanism of action, clinical use, and key side effects of thiazide diuretics.
MOA: inhibit Na+/Cl- transporter in the distal tubule
clinical uses:
- HTN
- CHF
- osteoporosis (inhibits Ca++ excretion)
- nephrogenic DI
key side effects:
- high BS, Ca++, uremia
- low K+
- hypochloremic met alka
- hypovolemia
ex:
- HCTZ
- metolazone
- indapamide
describe the mechanism of action, clinical use, and key side effects of potassium sparing diuretics.
MOA:
- inhibit K+ secretion & Na+ reabsorption in collecting ducts (function is independent of aldosterone
- spironolactone is a subclass: aldosterone antagonists –> blocks aldosterone at mineralocorticoid receptors = inhibition of K+ secretion and Na+ reabsorption in the CD.
clinical uses:
- decrease K+ loss in pt receiving a loop or thiazide diuretic
- secondary hyperaldosteronism
key side effects:
- high K+
- met acidosis
- gynecomastia
- libido changes
- nephrolithiasis
ex:
- spironolactone
- amiloride
- triamterene
list 3 tests of GFR and give the normal values for each.
BUN (10-20mg/dL)
creatinine (0.7-1.5mg/dL)
creatinine clearance (110-150mL/min)
list 4 tests of tubular function and give the normal values for each.
tubular function is measured by urine concentrating ability. clinical tests include:
- fractional excretion of Na+ (1-3%)
- urine osm (65-1400mOsm/L)
- urine Na+ (130-160mEq/day)
- urine spec grav (1.003-1.030)
what is included in the differential diagnosis of a low BUN? how about a high BUN?
urea is the primary metabolite of protein metabolism in the liver (amino acids –> ammonia –> urea)
bc urea undergoes filtration and reabsorption, it is a better indicator of uremic symptoms than as a measurement of GFR.
BUN <8
- overhydration
- decreased urea production: malnutrition, severe liver dz
BUN 20-40
- dehydration
- increase protein input (high protein diet, GIB, hematoma breakdown)
- catabolism (trauma, sepsis)
- decreased GFR
BUN >50
- decreased GFR
what is the BUN: creatinine ratio? What do the numbers mean?
since BUN undergoes filtration AND reabsorption and creatinine undergoes filtration but NOT reabsorption, the ratio of these substances in the blood can help us evaluate the state of hydration
normal ratio is 10:1
BUN:Cr >20:1 suggests prerenal azotemia
- ratio can be affected by other non-renal causes of elevated BUN
what is the best indicator of GRF? How is this value calculated?
creatinine clearance
GFR = [(140-age)kg)]/[72cr]
how do you interpret the fraction excretion of sodium?
Fe(Na+) relates sodium clearance to creatinine clearance.
If Fe(Na+) <1% then more Na+ is conserved relative to the amount of sodium cleared; suggests prerenal azotemia
If Fe(Na+) >3% then more Na+ is excreted relative to the amount of creatinine cleared; suggests impaired tubular function
how can you use renal function tests to differentiate between prerenal oliguria and acute tubular necrosis?
prerenal oliguria:
- Fe(Na+) <1%
- urinary Na+ <20
- urine osm >500
- BUN:Cr >20:1
- normal sediment +/- casts
acute tubular necrosis
- Fe(Na+) >3%
- urinary Na+ >20
- urine osm <400
- BUN:Cr 10-20:1
- tubular epithelial cells w/ granular casts
what is the most common cause of perioperative acute kidney injury? who is at the highest risk?
most common cause = ischemia reperfusion injury
the following patients are at risk for AKI peri-op:
- pre-existing kidney disease
- prolonged renal hypoperfusion
- CHF
- advanced age
- sepsis
- jaundice
- high risk surgery (i.e. AoX and liver transplant.
what are the two modern methods used to classify the severity of acute renal injury?
RIFLE criteria:
risk, injury, failure, loss, ESRD
acute kidney injury network (AKIN)
both systems grade renal function on serum creatinine and UOP. both methods highlight that renal injury occurs along a continuum.
what is the most common cause of prerenal injury? What is the treatment?
hypoperfusion
- perfusion is impaired as a result of hypovolemia, decreased CO, systemic vasodilation, renal vasoconstriction, or increased intraabdominal pressure. There is no intrinsic damage yet.
tx:
- risk is minimized by maintaining MAP >65 and providing appropriate hydration
- restore RBF w/ IVF, hemodynamic support, and/or PRBCs
- renal PGs mediate vasodilation; avoid NSAIDs if prerenal injury is a concern
- an improvement of UOP after IVF bolus confirms the diagnosis of prerenal azotemia.
what is intrinsic renal injury? What is the treatment?
parenchymal injury
- can be caused by injury to the tubules, glomerulus, or the interstitial space, we will focus discussion on ATN
- ATN is usually caused by ischemia (medulla at higher risk) or nephrotoxic drugs (IV contrast dye, abx, NSAIDs)
tx:
- restore renal perfusion
- supportive
what is postrenal injury? What is the treatment?
obstruction
- source of obstruction can arise anywhere b/n the collecting system and the urethra
tx: relieve the obstruction
what are the first and second most common causes of CKD?
- DM
2. HTN
define the 5 stages of CKD.
- normal, GFR >90
- mild decrease, GFR 60-89
- mod decrease, GFR 30-59
- severe decrease, GFR 15-29
- kidney failure, requires dialysis, GFR <15
how does uremia affect coagulation? how can bleeding be minimized in these patients?
bleeding time is a measure of platelet function. it is elevated by uremia and is the most accurate predictor of bleeding risk
- PT, PTT, platelets are normal
- DDAVP = first line tx
- cryo may be used to provide VIII-vWF, but increased risk of viral transmission
- HD improves bleeding time, so should be performed w/in 24hrs of surgery
why are patients w/ CKD often anemic? What is the treatment for this?
causes:
- decreased EPO = normochromic normocytic anemia
- excess PTH replaces bone marrow w/ fibrotic tissue
tx:
- exogenous EPO or darbepoetin + iron supp
- blood transfusion isn’t first line tx bc it increases the risk of HLA sensitization and future rejection of a transplanted kidney.
how does CKD affect acid base balance?
decreased excretion of nonvolatile acid contributes to gap met acidosis
- pt will develop a compensatory resp alkalosis (hyperventilation)
- acidosis shifts oxyHgb dissociation curve to R (right = release); partial compensation for anemia.
How does CKD affect serum K+ concentration. How is hyperkalemia treated in this patient population?
result of impaired K+ excretion
- HD is indicated if K+ >6
other tx:
- glucose (25-50g) + insulin (10-20U)
- hyperventilation (10mmHg decrease in PaCO2, K+ decreases by 0.5)
- NaHCO3 (50-100mEq)
- CaCl 1g doesn’t change [K+], but raises threshold potential in the myocardium and reduces risk of lethal dysrhythmias
discuss the patho of renal osteodystrophy.
caused by:
- decreased vitD production
- secondary hyperparathyroidism
patho:
- inadequate vitD impairs Ca++ absorption in the GI tract
- body responds to hypocalcemia by increasing PTH release –> demineralization of bone to restore the serum calcium concentration
- net result = decreased bone density and increased risk of bone fractures
list 5 indications for dialysis
- volume overload
- hyperkalemia
- severe metabolic acidosis
- symptomatic uremia
- OD w/ a drug that is cleared by dialysis
what is the most common complication of dialysis?
hypotension
what re the FGF recommendations for sevo? Why is this?
compound A is produced when sevo is degraded by soda lime. In theory, this could be toxic to the kidneys (no good human data)
FDA recommends sevo @ 1L/min for no more than 2 MAC hours. After 2 MAC hours have elapsed, the FGF should be increased to 2L/min
what factors increase compound A production w/ sevo?
- high concentration over long period of time
- low FGF
- high temp of CO2 absorbent
- increased CO2 production
discuss the use of succinylcholine in the patient w/ renal failure
opening of the nAChR at the NMJ can increase K+ by 0.5-1 for up to 10-15mins
- sux is safe in those w/ renal failure and a normal K+ level
- if K+ is >5.5, suc may increase serum K+ to a dangerous level.
which class of NMB provides the most predictable duration of action in patients w/ CKD?
d/t their organ independent elimination, cisatra and atra are more predictable agents in this population
discuss the use of the aminosteroid NMB in patients w/ CKD.
roc primarily undergoes hepatobiliary elimination, however it is associated w/ an unpredictably increased DOA. Possible causes include a reduced clearance, altered PB, and/or increased potency.
vec is metabolized to 3-OH vec. Its DOA is prolonged as a function of decreased clearance and an increased elimination half life
pancuronium is primarily eliminated by the kidneys and has no use in this population
How do you dose the reversal agent for the patient w/ CKD?
both anticholinesterases and anticholinergics used to reverse NMB undergo renal elimination and thus share a similar increase in duration. They do not require dosage adjustments
discuss the use of opioids in the patient w/ CKD.
morphine is metabolized to morphine-6-glucuronide. this product is more potent than morphine and it relies on renal excretion; accumulation can contribute to respiratory depression
meperidine is metabolized to normeperidine. accumulation can cause convulsions
fentanyl, sufenta, alfenta, adn remi don’t produce active metabolites and are better choices w/ renal failure. hydromorphone may or may not produce an active metabolite
what steps can be taken to prevent nephrotoxicity from radiologic contrast media?
- use nonionic or low-osmolar contrast instead of hyperosmolar contrast
- use the lowest volume as the procedure will allow
- withhold other drugs w/ known nephrotoxic effects
- IV hydration w/ NS prior to contrast administration
- NaHCO3 IV or gtt
- mucomyst = known free radical scavenger (fallen out of favor d/t lack of efficacy)
how does rhabdomyolysis affect renal function?
rhabdo and myoglobinemia are sequelae of direct muscle trauma, muscle ischemia, or prolonged immobilization.
- myoglobin binds oxygen inside of the myocyte
- when it is released into the circulation, it is freely filtered at the glomerulus. In the presence of acidic urine <5.6, myoglobin precipitates in the PCT
- this results in tubular obstruction & ATN
- in addition myoglobin scavenges NO, leading to renal vasoconstriction and ischemia.
how can you prevent or minimize renal injury in the patient w/ rhabdomyolysis?
- maintain RBF and tubular flow w/ IVF
- osmotic diuresis w/ mannitol
- UOP >100-150mL/hr
- NaHCO3 or acetazolamide to alkalize the urine
as an aside, hemolysis from a hemolytic reaction is treated in the same way.
which antibiotics are nephrotoxic?
risk is reduced w/ IVF, correction of correctable risk factors, and close monitoring of serum trough levels.
- aminoglycosides (genta, tobramycin, amikacin)
- amphotericin B
- vancomycin
- sulfonamide
- tetracycline
- cephalosporins
what are calcineuron inhbitors and how do they affect renal function?
(cyclosporine and tacrolimus) are immunosuppressant agents used to prevent rejection of transplanted organs.
- side effects = HTN, renal vasoconstriction
- sirolimus = non calcineurin inhibitor that carries a much lower risk of nephrotoxicity
what is the risk of distilled water when used for irrigation during TURP?
distilled water osm = 0
this creates a dilutional effect that increases the risk of hyponatremia, hypoosmolality, hemolysis, and hemoglobinuria (renal failure)
what is the risk of glycine when used for irrigation during TURP?
glycine metabolism can increase ammonia production, and this can reduce LOC and contribute to encephalopathy.
glycine is an inhibitory neurotransmitter in the retina. It can cause blindness or blurry vision for up to 24-48hrs
Can NS or LR be used as an irrigation solution for TURP? Why or why not?
highly ionized, so they’re good conductors of electricity. Therefore, they are contraindicated where unipolar electrocautery is used.
the introduction of bipolar cautery in newer resectoscopes permits use of ionic solutions
describe the presentation of TURP syndrome.
cardiopulmonary: circulatory overload:
- HTN
- reflex bradycardia
- CHF
- pulmonary edema
- dysrhythmias, MI
CNS
- restlessness
- N/V
- cerebral edema
- seizures
- coma
metabolic: hyponatremia
misc: hemolysis and hypoosmolality
what is the treatment for TURP syndrome?
- support oxygenation and CV
- abort procedure
- labs: e-lytes, Hct, creatinine, glucose, 12 lead EKG
- if Na+>120, then restrict fluids and give lasix
- if Na+<120, then give 3%NaCl <100mL/hr
- avoid too fast of Na+ increase (central pontine myelinolysis)
- versed to treat seizures
- supportive: intubate & mechanically ventilate if needed.
discuss bladder perforation that can occur w/ TURP.
if the resectoscope punctures through the bladder wall
- inadvertant obdurator nerve stim can cause LE movement –> accidental puncture
- complication is more easily recognized in a conscious pt, esp if sensory block doesn’t extend past T10
- presentation: abdominal and/or shoulder pain
- reduction of irrigation fluid return is an early sign
- tx: supportive (IVF, pressors, etc.) w/ serial H/H assessment +/- transfusion
- pt requires emergent suprapubic cystostomy or possible ex lap
describe how extracorporeal shock wave lithotripsy breaks up kidney stones
delivers shock waves in rapid succession that are directed at the stone
- acoustic impedance of water and human tissue is roughly similar –> shock moves through body until it reaches stone
- at this point, energy is released, breaking up the stone into smaller fragments that are renally excreted
- it is important that there is nothing b/n the energy source and the stone
list the absolute and relative contraindications to ESWL.
absolute:
- pregnancy
- risk of bleeding (bldg dz or anticoagulation)
relative:
- pacemaker/ICD
- calcified aneurysm of aorta or renal artery
- UTI
- post-renal obstruction
- morbid obesity
how does ESWL affect cardiac conduction? What is done to minimize this risk?
can produce dysrhythmias. the pulse wave is timed to the T wave on the EKG to minimize “R on T” phenomenon.
what is the functional unit of the liver? Describe its anatomy.
lobule, otherwise known as the acinus.
arterioles = terminal branches of hepatic artery and portal vein
capillaries = sinusoids
venules = central vein
what is the function of Kupffer cells?
since portal vein blood drains the intestine, the liver receives a significant bacterial load.
kupffer cells (part of the reticuloendothelial system) remove the bacteria before the blood drains into the vena cava.
describe the flow of bile from its site of production to release in the duodenum.
flow of bile:
- produced by hepatocytes
- canaliculi drain bile into the bile duct
- bile ducts converge to form the common hepatic duct
- cystic duct (from gallbladder) and pancreatic duct joint the common hepatic duct before it empties into the duodenum
- SOO controls flow of bile released from the common hepatic duct
- contraction of SOO increases biliary pressure.
how much blood flow does the liver receive (% of CO and total)?
30% of CO (1500mL)
which vessels supply blood to the liver? which provides comparatively more blood flow? which provides more oxygen?
portal vein and hepatic artery
aorta –> splanchnic organs –> portal vein
aorta –> hepatic artery
portal vein supplies 75% of flow, 50% of O2 content
hepatic artery supplies 25% of flow, 50% of O2 content
what determines how much blood is delivered to the portal vein?
the portal vein receives venous blood that has passed through the splanchnic circulation
what is the normal portal vein pressure? what value is diagnostic of portal hypertension?
portal perfusion pressure = portal vein pressure - hepatic vein pressure
portal vein
- normal 7-10mmHg
- > 20-30 is diagnostic for portal HTN
sinusoidal
- normal 0mmHg
- > 5mmHg is diagnostic for portal HTN
what is the hepatic arterial buffer response?
hepatic artery perfusion pressure = MAP - hepatic vein pressure
hepatic artery buffer response: a reduction in portal vein flow is compensated by an increased hepatic artery flow
- mediated by adenosine
- severe liver dz impairs this response
how do general and neuraxial anesthesia affect hepatic blood flow?
reduce HBF as a function of decreased MAP
What coagulation factors are NOT produced by hepatocytes?
vWF (vascular endothelial cells)
factor III (tissue factor) (vascular endothelial cells)
factor IV (calcium) (diet)
factor VIII (antihemophilic factor) (liver sinusoidal cells and endothelial cells)
what is the TIPS procedure?
transjugular intrahepatic portosystemic shunt
- bypasses a portion of the hepatic circulation by shunting blood from the portal vein to the hepatic vein
- this reduces portal pressure and minimizes back pressure on the splanchnic organs + reduces likelihood of esophageal bleeding and reduces ascites
temporary treatment
hemorrhage is a significant risk
where is the pituitary gland located? what is another name for the anterior and posterior pituitary glands?
in the sella turcica, and it is connected to the hypothalamus by the pituitary stalk.
anterior = adenohypophysis posterior = neurohypophysis
what are the 3 zones of the adrenal cortex? What substance does each synthesize?
outside to inside: “GFR releases salt, sugar, sex”
outermost: zona glomerulosa releases mineralocorticoids (aldosterone)
middle: zona fasciculata releases glucocorticoids (cortisol)
innermost: zona reticularis releases androgens (DHEA)
describe the steps involved in the RAAS.
- decreased renal perfusion, SNS activation (B1), and/or tubuloglomerular feedback
- increased renin released from juxtaglomerular cells
renin: angiotensinogen –> angI
ACE: ang1 –> ang2
- vasoconstriction
ang2 = increased aldosterone
- increased Na+, H2O reabsorption
- increased K+, H+ excretion
describe the physiology of the insulin receptor.
made up of 2 alpha and 2 beta subunits that are jointed together by disulfide bonds.
when insulin binds the receptor, the beta subunits activate tyrosine kinase which then activates insulin-receptor substrates.
the insulin cascade turns on the GLUT4 transporter, which increases glucose uptake by skeletal m and fat
what is the classic triad of DM? Why does it occur?
polyuria
dehydration
polydipsia
- hyperglycemia –> glycosuria (acts as osmotic diuretic) –> hypovolemia
what are the most common causes of T1DM and T2DM?
T1DM = autoimmune (early in life) T2DM = obesity (later in life, but prevalence is increasing in obese children)
