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APEXANESTHESIA > UNIT 10 Kidney, Liver, Endocrine > Flashcards

UNIT 10 Kidney, Liver, Endocrine Flashcards

1
Q

Discuss the anatomy of the renal cortex and medulla

A

renal cortex = outer part of the kidney
- contains most parts of the nephron (glomerulus, Bowman’s capsule, proximal tubules, distal tubules)

renal medulla = inner part of the kidney

  • contains the parts of the nephron not in the renal cortex (loops of Henle & collecting ducts)
  • divided into pyramids
  • apex of each pyramid is called the papilla; contains lots of collecting ducts
  • papilla drain into minor calyxes
  • multiple minor calyxes converge to form major calyxes
  • multiple major calyxes converge to form the renal pelvis, which empties urine into the ureter

the calyces, pelvis, and ureters have the capability to contract and push urine toward the bladder

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2
Q

Describe the anatomy of the nephron.

A

the nephron is the functional unit in the kidney. Pay particular attention to the nephron as well as its blood supply

afferent arteriole –> glomerulus –> efferent arterial

Bowman’s capsule –> PCT –> LOH –> distal tubule –> collecting duct

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3
Q

how does the kidney contribute to the volume and composition of the ECF?

A

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

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4
Q

how do they kidneys help to regulate blood pressure? what other systems also contribute to blood pressure regulation?

A

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
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5
Q

how does the kidney eliminate toxins and metabolites?

A

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.

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6
Q

how does the kidney contribute to acid-base balance? Which other organ is essential to this process?

A

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.

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7
Q

what stimulates the kidney to release EPO? what does EPO do after it’s released?

A

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

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8
Q

what is calcitriol, and what does it do?

A

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
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9
Q

How much blood flow do the kidneys receive (% of CO and total flow)?

A

20-25% of CO

1000-1250mL/min

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10
Q

discuss the path blood flows after it enters the renal artery.

A 
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
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11
Q

discuss the significance of renal autoregulation

A

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

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12
Q

describe the myogenic mechanism of renal autoregulation.

A

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

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13
Q

how does tubuloglomerular feedback affect renal autoregulation?

A

the juxtaglomerular apparatus is located in the distal tubule, specifically the region that passes b/n the afferent and efferent arterioles

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

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14
Q

how does the surgical stress response affect renal blood flow?

A

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.

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15
Q

list the steps involved in the RAAS pathway.

A

RAAS plays an integral role in the regulation of systemic vascular resistance and the composition of the extracellular volume. By extension, it greatly influences CO and arterial BP.

  1. decreased renal perfusion
  2. SNS activation (beta1)
  3. tubuloglomerular feedback
    - -> renin release

angiotensinogen –> angiotensin 1 (via renin) –> angiotensin 2 (via ACE) –) vasoconstriction, aldosterone and ADH release, Na+ reabsorption, and thirst

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16
Q

list the three conditions that increase renin release, and give examples of each.

A
  1. decreased renal perfusion pressure
    - hemorrhage
    - PEEP
    - CHF
    - liver failure w/ ascites
    - sepsis
    - diuresis
  2. SNS activation (beta1)
    - circulating catechols
    - exogenous catechols
  3. 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.
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17
Q

where is aldosterone produced, and what is its function

A

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.

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18
Q

where is antidiuretic hormone produced, and what is its function?

A

ADH is produced in the supraoptic and paraventricular nuclei of the hypothalamus. 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
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19
Q

what clinical situations increase ADH release?

A

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
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20
Q

list 3 mechanisms that promote renal vasodilation

A

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)
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21
Q

compare and contrast the location and function of the dopamine 1 and 2 recepotrs

A

there are two types of dopamine receptors: DA1 and DA2

  • 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
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22
Q

what is the mechanism of action of fenoldapam? why is it used?

A

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
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23
Q

how much of the RBF is filtered through the glomerulus? Where does the rest go?

A 
RBF = 1000-1250mL/min
GFR = 125mL/min or 20% of RBF

filtration fraction is 20%
the remaining 80% is delivered to the peritubular capillaries

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24
Q

what are the 3 determinants of glomerular hydrostatic pressure?

A

glomerular hydrostatic pressure is the most important determinant of GFR.

three determinants:

  • arterial blood pressure
  • afferent arteriole resistance
  • efferent arteriole resistance
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25
Q

how do changes in afferent arteriole diameter, efferent arteriole diameter, and plasma protein concentration affect net filtration pressure?

A

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
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26
Q

define reabsorption, secretion, and excretion.

A

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

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27
Q

describe the fate of sodium at each location in the nephron

A 
PCT 65%
LOH 20%
DCT 5%
CD 5%
urine 5%
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28
Q

what are the key functions of each part of the nephron?

A

PCT:
- bulk reabsorption of solutes and water

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)

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29
Q

describe the mechanism of action, clinical use, and key side effects of carbonic anhydrase inhibitors.

A

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
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30
Q

describe the mechanism of action, clinical use, and key side effects of osmotic diuretics.

A

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

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31
Q

describe the mechanism of action, clinical use, and key side effects of loop diuretics.

A

MOA: poison the Na-K-2Cl transporter in the medullary region of the thick aLOH. THe amount of Na+ that remains in the tubule overwhelms the DCT reabsorption capability. Thus, a large volume of dilute urine is excreted. K+, Ca++, Mg++, and Cl- are lost to the urine as well.

clinical uses:

  • HTN
  • CHF/acute pulmonary edema
  • hypercalcemia

key side effects:

  • low K+, Ca++, Mg++
  • hypochloremic met acidosis
  • hypovolemia
  • ototoxicity
  • reduced lithium clearance

ex:
- furosemide
- bumetanide
- ethacrynic acid

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32
Q

describe the mechanism of action, clinical use, and key side effects of thiazide diuretics.

A

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

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33
Q

describe the mechanism of action, clinical use, and key side effects of potassium sparing diuretics.

A

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

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34
Q

list 3 tests of GFR and give the normal values for each.

A

BUN (10-20mg/dL)
creatinine (0.7-1.5mg/dL)
creatinine clearance (110-150mL/min)

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35
Q

list 4 tests of tubular function and give the normal values for each.

A

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)
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36
Q

what is included in the differential diagnosis of a low BUN? how about a high BUN?

A

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

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37
Q

what is the BUN: creatinine ratio? What do the numbers mean?

A

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

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38
Q

what is the best indicator of GRF? How is this value calculated?

A

creatinine clearance

GFR = [(140-age)kg)]/[72cr]

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39
Q

how do you interpret the fraction excretion of sodium?

A

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

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40
Q

how can you use renal function tests to differentiate between prerenal oliguria and acute tubular necrosis?

A

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
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41
Q

what is the most common cause of perioperative acute kidney injury? who is at the highest risk?

A

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.
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42
Q

what are the two modern methods used to classify the severity of acute renal injury?

A

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.

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43
Q

what is the most common cause of prerenal injury? What is the treatment?

A

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.

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44
Q

what is intrinsic renal injury? What is the treatment?

A

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

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45
Q

what is postrenal injury? What is the treatment?

A

obstruction
- source of obstruction can arise anywhere b/n the collecting system and the urethra

tx: relieve the obstruction

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46
Q

what are the first and second most common causes of CKD?

A
  1. DM

2. HTN

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47
Q

define the 5 stages of CKD.

A
  1. normal, GFR >90
  2. mild decrease, GFR 60-89
  3. mod decrease, GFR 30-59
  4. severe decrease, GFR 15-29
  5. kidney failure, requires dialysis, GFR <15
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48
Q

how does uremia affect coagulation? how can bleeding be minimized in these patients?

A

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
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49
Q

why are patients w/ CKD often anemic? What is the treatment for this?

A

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.

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50
Q

how does CKD affect acid base balance?

A

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.
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51
Q

How does CKD affect serum K+ concentration. How is hyperkalemia treated in this patient population?

A

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
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52
Q

discuss the patho of renal osteodystrophy.

A

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

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53
Q

list 5 indications for dialysis

A
  1. volume overload
  2. hyperkalemia
  3. severe metabolic acidosis
  4. symptomatic uremia
  5. OD w/ a drug that is cleared by dialysis
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54
Q

what is the most common complication of dialysis?

A

hypotension

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55
Q

what re the FGF recommendations for sevo? Why is this?

A

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

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56
Q

what factors increase compound A production w/ sevo?

A
  • high concentration over long period of time
  • low FGF
  • high temp of CO2 absorbent
  • increased CO2 production
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57
Q

discuss the use of succinylcholine in the patient w/ renal failure

A

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.
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58
Q

which class of NMB provides the most predictable duration of action in patients w/ CKD?

A

d/t their organ independent elimination, cisatra and atra are more predictable agents in this population

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59
Q

discuss the use of the aminosteroid NMB in patients w/ CKD.

A

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

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60
Q

How do you dose the reversal agent for the patient w/ CKD?

A

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

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61
Q

discuss the use of opioids in the patient w/ CKD.

A

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

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62
Q

what steps can be taken to prevent nephrotoxicity from radiologic contrast media?

A
  • 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)
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63
Q

how does rhabdomyolysis affect renal function?

A

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.
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64
Q

how can you prevent or minimize renal injury in the patient w/ rhabdomyolysis?

A
  • 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.

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65
Q

which antibiotics are nephrotoxic?

A

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
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66
Q

what are calcineuron inhbitors and how do they affect renal function?

A

(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
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67
Q

what is the risk of distilled water when used for irrigation during TURP?

A

distilled water osm = 0
this creates a dilutional effect that increases the risk of hyponatremia, hypoosmolality, hemolysis, and hemoglobinuria (renal failure)

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68
Q

what is the risk of glycine when used for irrigation during TURP?

A

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

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69
Q

Can NS or LR be used as an irrigation solution for TURP? Why or why not?

A

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

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70
Q

describe the presentation of TURP syndrome.

A

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

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71
Q

what is the treatment for TURP syndrome?

A
  • 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.
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72
Q

discuss bladder perforation that can occur w/ TURP.

A

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
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73
Q

describe how extracorporeal shock wave lithotripsy breaks up kidney stones

A

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
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74
Q

list the absolute and relative contraindications to ESWL.

A

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

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75
Q

how does ESWL affect cardiac conduction? What is done to minimize this risk?

A

can produce dysrhythmias. the pulse wave is timed to the T wave on the EKG to minimize “R on T” phenomenon.

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76
Q

what is the functional unit of the liver? Describe its anatomy.

A

lobule, otherwise known as the acinus.

arterioles = terminal branches of hepatic artery and portal vein

capillaries = sinusoids

venules = central vein

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77
Q

what is the function of Kupffer cells?

A

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.

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78
Q

describe the flow of bile from its site of production to release in the duodenum.

A

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.
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79
Q

how much blood flow does the liver receive (% of CO and total)?

A

30% of CO (1500mL)

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80
Q

which vessels supply blood to the liver? which provides comparatively more blood flow? which provides more oxygen?

A

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

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81
Q

what determines how much blood is delivered to the portal vein?

A

the portal vein receives venous blood that has passed through the splanchnic circulation

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82
Q

what is the normal portal vein pressure? what value is diagnostic of portal hypertension?

A

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
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83
Q

what is the hepatic arterial buffer response?

A

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
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84
Q

how do general and neuraxial anesthesia affect hepatic blood flow?

A

reduce HBF as a function of decreased MAP

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85
Q

What coagulation factors are NOT produced by hepatocytes?

A

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)

86
Q

what coagulation factors are vitamin K dependent? what anticoagulants are dependent on vitamin K?

A

II, VII, IX, and X
absorption of vitK is dependent on the presence of bile in the gut

anticoagulants that are dependent on vitK: proteins C, S, Z

87
Q

what plasma proteins are produced by the liver?

A

all of the plasma proteins except for immunoglobulins (gamma globulins)

albumin: provides oncotic pressure and is a reservoir for acidic drugs

alpha1 acid glycoprotein is a reservoir for basic drugs

pseudocholinesterase: metabolizes succinylcholine and ester type LA

88
Q

discuss glycogenesis, glycogenolysis, and gluconeogenesis. what is the stimulus for each? how does each affect serum glucose?

A

stimulus: hyperglycemia –> release of insulin (beta cells)
- -> glycogenesis (glucose into glycogen for storage)

stimulus: hypoglycemia –> release of glucagon (alpha cells) and epi (adrenal medulla)
- -> glycogenolysis (glycogen into glucose) AND
- -> gluconeogenesis (noncarbs into glucose)

89
Q

discuss the role of the liver and amino acid deamination. what happens when the liver is unable to perform this function?

A

amino acid deamination allows the body to convert proteins to carbohydrates and fats. some of these are utilized in the Krebs cycle to produce ATP.

  • produces large quantity of ammonia (converted to urea)
  • failure to clear ammonia leads to hepatic encephalopathy
90
Q

where does bilirubin come from? how is it cleared from the body?

A

RBC life cycle: 120 days; aged RBCs are processed by reticuloendothelial cells in the spleen

in the spleen: Hgb –> heme –> unconjugated bili (neurotoxic)

  • unconjugated bili is transported to the liver bound to albumin
  • liver conjugates w/ glucuronic acid to increase H2O solubility
  • conjugated bili is excreted in the bile, metabolized by intestinal bacteria, and eliminated in the stool
91
Q

what are the best tests of hepatic synthetic function? which is best for acute injury? why?

A

PT: normal 10.9-12.5sec
- very sensitive for acute injury (factor V, VII t1/2= 3-6hrs

albumin: normal 3.5-5g/dL
- not sensitive for acute injury (t1/2 = 21 days)

92
Q

name two tests of hepatocellular injury.

A

AST (10-40) and ALT (10-55)

  • marked elevation of both suggests hepatitis
  • AST/ALT ratio >2 suggests cirrhosis or alcoholic liver disease
93
Q

name 3 tests of biliary duct obstruction. which is the most specific?

A

5’nucleotidase (0-11) is the most specific indicator of biliary duct obstruction

Y glutamyl transpepidase (0-30)

alkaline phosphatase (45-115) is not very speicifc (its also in bone, placenta, and tumors)

94
Q

how can you use these hepatic function tests to aid your differential diagnosis of hepatic dysfunction?

A

prehepatic: increased unconjugated bilirubin
- causes: hemolysis, hematoma reabsorption

hepatocellular injury: increased conjugated bilirubin, increased AST, ALT, increased PT
- causes: cirrhosis, EtOH abuse, drugs, viral infection, sepsis, hypoxemia

cholestatic: increased conjugated bilirubin, increased ALP, GTP, 5’NT
- late disease: labs similar to hepatocellular injury
- causes: biliary tract obstruction, sepsis

95
Q

which type of viral hepatitis has the highest incidence?

A

A 50%
B 35%
C 15%
D co-infection w/ B

96
Q

how is each type of viral hepatitis transmitted?

A

A oral fecal
B percutaneous or sex
C percutaneous
D percutaneous

97
Q

what is the prescribed prophylaxis regimen after exposure to hepatitis A, B, or C?

A

A: pooled gamma globulin, hep A vaccine

B: hep B immunoglobin, hep B vaccine

C: interferon + ribaviron

98
Q

how can acetaminophen cause hepatic injury? What is the treatment?

A

glutathione is a substrate for many phase 2 conjugation reactions. It increases a substance’s water solubility, so that the substance can be excreted in the bile or by the kidney

  • acetaminophen produces a toxic metabolite N-acetyl-p-benzoquinoneimine (NAPQ)
  • NAPQI is normally conjugated w/ glutathione to a nontoxic substance
  • acetaminophen OD consumes the liver’s supply of glutathione.
  • since conjugation substrate isn’t available, NAQPI concentration rises –> hepatocellular injury

tx: N-acetylcysteine w/in 8hrs of OD

99
Q

how can halogenated anesthetics cause hepatic injury? which agent presents the greatest risk?

A

des, iso, and halo –> inorganic fluoride ions and trifluoroacetic acid (TFA)

halothane hepatitis is believed to be the result of an immune mediated rxn to TFA.

  • up to 40% of halothane is metabolized (vs. 0.02% des, 0.2% iso)
  • thus halo = greatest risk, others have minimal risk.

sevo doesn’t produce TFA

100
Q

what are the risk factors for halothane hepatitis?

A 
age >40
female
2+ exposures
genetics
obesity 
CYP2E1 induction (alcohol, isoniazid, phenobarbital)
101
Q

what are the first and second most common causes of chronic hepatitis?

A 
#1 alcoholism
#2 hepatitis C
102
Q

is the patient w/ acute hepatitis a candidate for surgery? how about chronic hepatitis?

A

primary objectives: preserve HBF and avoid drugs that can potentiate hepatocellular injury

if acute: nonemergent surgery should be postponed until symptoms resolve + LFTs are normal

if chronic: surgery ok if condition is stable.

103
Q

which anesthetic techniques can be used to maintain HBF?

A
  • iso (preserves HBF best)
  • avoid halothane)
  • avoid PEEP (increases resistance to hepatic drainage)
  • ensure normocapnia
  • liberal IVF use
  • RA is ok as long as no coagulation defects
104
Q

which drugs should be avoided in the patient w/ hepatitis?

A

hepatotoxic drugs or those that inhibit CYP450:

  • tylenol
  • halothane
  • amiodarone
  • abx: PCN, tetracycline, sulfonamides
105
Q

how is the anesthetic requirement altered in the alcoholic patient? Why?

A

MAC is decreased in the acutely intoxicated patient

MAC is increased in the chronic alcoholic that isn’t intoxicated

alcohol potentiates GABA; there is an increased effect of benzos.
alcohol inhibits NMDA receptors.

106
Q

what are the signs, symptoms, and treatment for alcohol withdrawal syndrome?

A

s/s begin 6-8hrs after the blood alcohol concentration returns to near normal
- peaks at 24-36hrs

early: tremors, disordered perception (hallucinations, nightmares)
late: increased SNS activity, N/V, insomnia, confusion, agitation

tx: alcohol, BB, a2 agonists

107
Q

what are the s/s and tx for delirium tremens?

A

occurs after 2-4days w/out alcohol

s/s: grand mal seizures, tachycardia, hyper or hypotension, and combativeness

tx: benzo + BB

108
Q

why are alcoholics susceptible to Wernicke-Korsakoff syndrome?

A

deficient in vitamin B1 (thiamine)

Wernicke-Korsakoff syndrome is characterized by a loss of neurons in the cerebellum, and this is brought on by thiamine deficiency

109
Q

list the etiologies of cirrhosis and the cause of each.

A

alcohol abuse d/t fatty infiltration

alpha1 antitrypsin deficiency d/t genetic (also causes emphysema)

biliary obstruction d/t inflammation and tissue destruction

chronic hepatitis d/t inflammation and tissue destruction

hemochromatosis d/t iron overload

RV failure d/t increased hepatic vascular resistance

Wilson disease d/t genetic (copper accumulates in the tissues)

110
Q

what is cirrhosis?

A

characterized by cell death, where healthy hepatic tissue is replaced by nodules and fibrotic tissue. This reduces the number of functional hepatocytes as well as the number of sinusoids

111
Q

how does cirrhosis affect liver blood flow? What is the consequence of this?

A

number of blood vessels passing through the liver is reduced–> increased hepatic vascular resistance (portal HTN)

to partially offset the increased resistance, the body creates collateral vessels that bypass the liver (portosystemic shunts)

since this blood bypasses the liver, drugs and toxins (ammonia) remain in the systemic circulation longer.

112
Q

what is the MELD score, and what do these numbers mean?

A

log calculation w/ 3 factors: bilirubin, INR, and serum creatinine

low risk <10
intermediate risk 10-15
high risk >15

113
Q

what is the Child-Pugh score?

A

examines 5 factors of hepatic function: albumin, PT, bilirubin, ascites, and encephalopathy

Class A (5-6pts) = 10% risk of periop mortality
Class B (7-9pts) = 30% risk of periop mortality
Class C (10-15pts) = 80% risk of periop mortality

ok for surgery w/ A and B as long as they are otherwise optimized.
C should be managed medically

114
Q

describe the cardiovascular changes that accompany cirrhosis.

A

hyperdynamic circulation:

  • decreased SVR, BP; increased CO
  • increased RAAS = increased blood volume
  • increased peripheral blood flow (shunting) = increased SvO2
  • decreased response to vasopressors
  • diastolic dysfunction

portal HTN

  • increased hepatic vascular resistance = increased backpressure to proximal organs
  • esophageal varices = bleeding
  • splenomegaly = thrombocytopenia

ascites

  • decreased oncotic pressure
  • decreased protein binding
  • increased Vd
  • drainage –> hypotension
115
Q

describe the pulmonary changes that accompany cirrhosis

A

restrictive defect d/t ascites and/or pulmonary effusion reduces compliance

resp alkalosis: hypoxemia results in compensatory hyperventilation

hepatopulmonary syndrome: pulmonary vasodilation –> shunt –> hypoxemia

portopulmonary HTN: PAP >25 in the setting of portal HTN

116
Q

what is the etiology of hepatic encephalopathy? What is the treatment?

A

decreased hepatic clearance = increased ammonia = increased ICP

tx: reduce ammonia: lactulose, abx, reduced protein intake

117
Q

describe the renal changes that accompany cirrhosis.

A

renal hypoperfusion: decreased GFR = increased RAAS = Na+ and H2O retention

hepatorenal syndrome: decreased GFR = renal failure (liver transplant is definitive treatment)

118
Q

what is the TIPS procedure?

A

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

119
Q

which hormone stimulates bile release? what is the stimulus for release?

A

cholecystokinin (CCK) sitmulates gallbladder contraction, and this increases the flow of bile into the duodenum.

production and release: duodenum
release d/t food ingestion (fat and amino acids) and also d/t increased vagal stimulation (PSNS = rest and digest)

120
Q

describe the pathophysiology and treatment of cholecystitis, cholelithiasis, and choledocholithiasis.

A

cholecystitis (inflammation of the gallbladder) tx: cholecystectomy

cholelithiaiss (gallstones) tx: cholecystectomy

choledocholithiasis (stones in the common bile duct: may be d/t inflammation of the pancreatic head that obstructs common bile duct) tx: ERCP

121
Q

who is at highest risk for developing gallstones?

A 
obesity 
aging
rapid weight loss
pregnancy
women > men

“fat female forty”

122
Q

what are the s/s of gallstones?

A

leukocytosis
fever
RUQ pain: worse w/ inspiration (Murphy’s sign)

123
Q

what drugs can be used to relax the sphincter of Oddi?

A 
glucagon 
- increases risk of PONV
naloxone
- bad choice in surgical pt
nitroglycerine
glyco/atropine may also help
124
Q

compare and contrast the architecture of the nervous system and endocrine system.

A

nervous system = wired

  • electrochemical
  • neurotransmitters
  • synapse
  • specific cell target
  • fast speed
  • short duration

endocrine system = wireless

  • travels in blood
  • hormones
  • endocrine, paracrine, autocrine
  • more widespread target
  • slow speed
  • long duration
125
Q

compare and contrast positive and negative feedback loops in the endocrine system.

A

negative feedback: hormone reduces it’s own release via short or long loops

positive feedback: hormone increases it’s own release

pathway: 
hypothalamus
anterior pituitary
endocrine gland
hormone
target tissue
126
Q

compare and contrast how the hypothalamus communicates w/ anterior and posterior pituitary glands.

A

posterior pituitary via neural connections

  • ADH produced by supraoptic nuclei
  • oxytocin produced in paraventricular nuclei
  • carried by axonal transport along the pituitary stalk

anterior pituitary via releasing and inhibiting hormones

  • released into the hypophyseal portal vessels
  • transported along the pituitary stalk to influence hormone secretion by anterior pituitary gland
127
Q

name the 7 hypothalamic hormones, and identify their effects on the anterior pituitary gland

A

luteinizing hormone releasing hormone

  • increased FSH
  • icnreased LH

corticotropin releasing hormone
- increased ACTH

thyrotropin releasing hormone
- increased TSH

prolactin releasing factor and prolactin inhibiting factor
- prolactin

growth hormone releasing hormone and inhibiting hormone
- GH

128
Q

where is the pituitary gland located? what is another name for the anterior and posterior pituitary glands?

A

in the sella turcica, and it is connected to the hypothalamus by the pituitary stalk.

anterior = adenohypophysis
posterior = neurohypophysis
129
Q

what hormones are released from the anterior pituitary gland?

A 
"FLAT PIG"
FSH
LH
ACTH
TSH
Prolactin
GH
130
Q

what is the function of each anterior pituitary hormone?

A

FSH: germ cell maturation and ovarian follicle growth (females)

LH: testosterone production (males) and ovulation (females)

ACTH: adrenal hormone release

TSH: thyroid hormone release

prolactin: lactation

GH: cell growth

131
Q

what hormones are released from the posterior pituitary gland? What are their functions?

A

ADH: water retention
oxytocin: uterine contraction and breast feeding

132
Q

compare and contrast the presentation and treatment of SIADH and DI.

A

SIADH: too much ADH

  • d/t TBI, CA, lung dz, carbamazepine
  • presents as hyponatremia w/ hypotonic osm
  • can be euvolemic or hypervolemic
  • low UOP w/ high urine osm, Na+
  • tx: fluid restriction +/- hypertonic saline, demeclocycline

DI: too little ADH

  • d/t pit surgery, TBI, SAH
  • presents as polyuria w/ low urine osm, Na+
  • can be hypovolemic or euvolemic, w/ high serum osm and Na+
  • tx: DDAVP, supportive
133
Q

what are the anesthetic implications of acromegaly?

A
  • distorted facial features = difficult mask
  • large tongue, teeth, epiglottis = difficult DL
  • subglottic narrowing + VC enlargement = use a smaller tube
  • turbinate enlargement = epistaxis risk, avoid nasal ETT
  • OSA is common
  • increased risk of HTN, CAD, dysrhythmias
  • glucose intolerance
  • skeletal m weakness
  • entrapment neuropathies are common
134
Q

compare and contrast T4 and T3

A

T4

  • directly released from thyroid
  • highest concentration in the blood (think of it as a delivery vehicle)
  • high PB, low potency
  • t1/2 7 days

T3

  • some released from thyroid, but most is extrathyroid T4 conversion
  • highest concentration at the target cell (think of it as active form)
  • less PB, high potency
  • t1/2 1 day
135
Q

how does iodine deficiency affect T3 and T4

A

TSH stimulates the iodide pump. Iodine is a substrate that the thyroid requires to synthesize T3 and T4. When iodine isn’t readily available, the thyroid is unable to produce a sufficient quantity

136
Q

how does thyroid hormone affect cardiac function?

A

increases myocardial performance independent of the ANS:

  • increased chronotropy
  • increased inotropy
  • increased lusitropy
  • decreased SVR

effects on the ANS that impact cardiac function

  • increase # and sensitivity of cardiac B receptors
  • decrease # of cardiac muscarinic receptors
137
Q

how does thyroid hormone affect the respiratory system?

A

increased BMR –> increased O2 consumption –> increased CO2 production –> increased MV (Vt and RR)

138
Q

how does thyroid hormone affect MAC?

A

it doesn’t affect the brain, and by extension, hyper/hypothyroidism don’t affect MAC.

They do however, affect the speed of anesthetic induction when IA is used:

  • hyper = slower induction d/t higher CO
  • hypo = faster induction d/t lower CO
139
Q

what is the most common etiology of hyperthyroidism? What are the other causes?

A

most common: graves (autoimmune)

others:
- myasthenia gravis
- multinodular goiter
- carcinoma
- pregnancy
- pituitary adenoma
- amiodarone

140
Q

what is the most common etiology of hypothyroidism? What are the other causes?

A

most common: Hashimoto’s (autoimmune)

others:
- iodine deficiency
- hypothalamic-pituitary dysfunction
- neck radiation
- thyroidectomy

141
Q

how are TSH, T3, and T4 levels affected by hyper and hypothyroidism?

A

hyperthyroidism: low TSH + high T3 and T4
hypothyroidism: high TSH + low T3 and T4

142
Q

what is the difference b/n myxedema coma and cretisim?

A

myxedema coma occurs w/ end stage hypothyroidism. coma is a consequence (not a cause) of severely impared thyroid function

cretinism is caused by neonatal hypothyroidism that leads to physical and mental retardation

143
Q

list 3 thionamides that can be used to treat hyperthyroidism. What is their mechanism of action?

A

thionamides: propylthiouracil (PTU), methimazole, carbimazole

inhibit thyroid synthesis by blocking iodine addition to the tyrosine residues on thyroglobulin. PTU also inhibits the peripheral conversion of T4 to T3

  • require 6-7 weeks to achieve a euthyroid state
  • only available PO, but can be crushed and given via OGT
144
Q

why are beta blockers used to treat hyperthyroidism?

A

reduce SNS stimulation and inhibit peripheral conversion of T4 to T3

145
Q

what are contraindications to radioactive iodine?

A

pregnancy

breast feeding

146
Q

when is it ok for a patient w/ hyperthyroidism to undergo surgery? how about the hypothyroid patient?

A

hyper:
- do not proceed to elective surgery until pt is euthyroid.
- emergency surgery warrants administration of BB, potassium iodide, glucocorticoid, and PTU

hypo: ok to proceed if mild to moderate disease

147
Q

what is the best way to secure the airway in a patient w/ a large goiter?

A

on boards, goiter = awake intubation

the next best response is a technique that maintains spontaneous ventilation

148
Q

which anesthetic agents should be avoided in the hyperthyroid patient?

A

sympathomimetics
anticholinergics
ketamine
pancuronium

149
Q

describe the presentation of thyroid storm

A

medical emergency that can occur in hyperthyroid and euthyroid patients

  • generally brought on by stressful events (infection, surgery, etc.)
  • most commonly occurs 6-18hrs after surgery

s/s

  • fever >38.5C
  • tachycardia/arrhythmias
  • HTN
  • CHF
  • shock
  • confusion and agitation
  • N/V

under anesthesia, thyroid storm can mimic:

  • MH
  • pheo
  • neuroleptic malignant syndrome
  • light anesthesia
150
Q

how do you manage the patient w/ thyroid storm?

A
  • cardiopulmonary support
  • active cooling measures
  • PTU, methimazole
  • BB
  • tx fever w/ tylenol
  • avoid aspirin (it can dislodge T4 from plasma proteins and increase unbound fraction)
  • management is the same in pregnant and nonpregnant pts
151
Q

discuss recurrent laryngeal nerve injury in the context of thyroidectomy.

A

RLN innervates all the intrinsic muscles except cricothyroid. Injury can cause upper airway obstruction

  • unilateral = hoarseness
  • bilateral = a/w obstruction
  • phonate “E” or “moon” to assess for nerve injury
  • NIMS tube provides ability to assess for nerve injury intraoperatively
  • at end of procedure DL can be used to assess VC function as well as glottic edema.
152
Q

why is hypocalcemia a potential complication of thyroidectomy? How and when does it present?

A

resection of parathyroid glands w/out reimplantation –> hypocalcemia at least 6-12hrs post-op.

s/s (d/t increased nerve and muscle irritability):

  • m spasm –> tetany
  • laryngospasm
  • MS changes
  • hypotension
  • prolonged QT
  • paresthesias
  • Chvosteks (jaw) and Trousseau’s (forearm)
153
Q

how does hypothyroidism affect gastric emptying?

A

delays it

–> increased risk of aspiration

154
Q

what are the 3 zones of the adrenal cortex? What substance does each synthesize?

A

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)

155
Q

describe the steps involved in the RAAS.

A
  1. decreased renal perfusion, SNS activation (B1), and/or tubuloglomerular feedback
  2. increased renin released from juxtaglomerular cells

renin: angiotensinogen –> angI
ACE: ang1 –> ang2
- vasoconstriction

ang2 = increased aldosterone

  • increased Na+, H2O reabsorption
  • increased K+, H+ excretion
156
Q

how much cortisol is produced per day? what is the normal cortisol level?

A

15-30mg/day
normal serum level 12mcg/dL

stress can increase cortisol production upwards of 100mg/day, w/ serum level 30-50mcg/dL during and after major surgery

157
Q

how does cortisol affect cardiovascular function?

A

improves myocardial performance by increasing the number and sensitivity of B receptors on the myocardium

cortisol is also required for the vasculature to respond to the vasoconstrictive effects of catechols.

158
Q

compare and contrast the glucocorticoid and mineralocorticoid potencies of the endogenous and synthetic steroids.

A
  • *no glucocorticoid effects = aldosterone
  • *no mineralocorticoid effects = dexamethasone, betamethasone, triamcinolone

glucocorticoid effect (anti-inflammatory)

  • cortisol > cortisone > aldosterone
  • dexamethasone = betamethasone > fludrocortisone
  • minimal: prednisone, prednisolone, methylprednisolone, triamcinolone

mineralocorticoid effect (sodium retaining potency)

  • aldosterone&raquo_space;» cortisol > cortisone
  • fludrocortisone by far the most
  • prednisone, prednisolone, and methylprednisolone = minimal
  • dexamethasone, betamethasone, triamcinolone = none

** study equivalent dosing + duration of action (all in the 8-54hr range)

159
Q

what are the unique side effects of epidural triamcinolone?

A

(treats lumbar disc disease)

unique b/c it’s associated w/ higher incidence of skeletal m weakness. It’s also more likely to cause sedation (not euphoria) and anorexia (not increased appetite)

160
Q

what is Conn’s syndrome? how does it present?

A

too much aldosterone

  • primary: increased release from adrenal gland
  • secondary: d/t increased renin release or aldosterone secreting tumor

presents w/ s/s of mineralocorticoid excess:

  • HTN (Na+, H2O retention)
  • hypokalemia (K+ wasting)
  • met alkalosis (H+ wasting)
161
Q

chronic consumption of what food can produce a syndrome that resemble hyperaldosteronism?

A

long term licorice ingestion (glycyrrhizic acid)

162
Q

what is the treatment for Conn’s syndrome?

A

aldosterone antagonists: spironolactone or eplerenoee

K+ supplementation
Na+ restriction
removal of aldosterone secreting tumor

163
Q

what is the difference b/n Cushing’s syndrome and Cushing’s disease?

A

although they present similarly, etiologies are a litle different.

Cushings syndrome = too much cortisol
Cushings disease = too much ACTH

164
Q

What are glucocorticoid effects?

A
  • hyperglycemia
  • weight gain (central obesity, buffalo hump, moon face)
  • increased risk of infx
  • osteoporosis
  • muscle weakness
  • mood disorder
165
Q

what are mineralocorticoid effects?

A
  • HTN
  • hypokalemia
  • met alkalosis
166
Q

What are androgenic effects?

A

women become masculinized (hirsutism, hair thinning, acne, amenorrhea)

men become feminized (gynecomastia, impotence)

167
Q

how does Cushing’s syndrome present? Why?

A

cortisol has glucocorticoid, mineralocorticoid, and androgenic effects, so it will present w/ excess of these 3 things:

glucocorticoid:
- hyperglycemia
- weight gain + abnormal fat pattern
- increased infx risk
- osteoporosis
- muscle weakness
- mood disorder

mineralocorticoid

  • HTN
  • hypokalemia
  • met alkalosis

androgenic: feminzation/masculanization

168
Q

what endocrine disorder can occur after transsphenoidal resection of the pituitary gland?

A

DI, usually transient

169
Q

describe the presentation of adrenal insufficiency

A

too little mineralocorticoid, glucocorticoid, and androgen

  • primary (Addisons): adrenal glands dont secrete enough hormone (usually autoimmune)
  • secondary: decreased CRH or ACTH (usually exogenous steroid use)

presentation:
- muscle weakness/fatigue
- hypotension
- hypoglycemia
- hyponatremia
- hyperkalemia
- met acidosis
- anorexia
- N/V
- hyperpigmentation of knees, elbows, knuckles, lips, and buccal mucosa

170
Q

what is the treatment for adrenal insufficiency?

A

steroid replacement therapy (15-30mg cortisol equivalent/day)

171
Q

what is acute adrenal crisis? How does it present?

A

adrenal insufficiency is a chronic state, but it can deteriorate into an acute crisis if the pt is faced w/ additional stress (infection, illness, sepsis, surgery). This is a medical emergency:

  • hemodynamic instability/collapse
  • fever
  • hypoglycemia
  • impaired MS
172
Q

what is the treatment for acute adrenal crisis?

A

steroid replacement therapy (hydrocortisone 100mg + 100-200mg Q24hrs)

ECF volume expansion (D5NS is best)

hemodynamic support

173
Q

describe the surgical stress response in patients on chronic steroid therapy

A

exogenous steroid supplementation suppresses ACTH release from the anterior pituitary gland. Some patients on chronic steroid therapy won’t be able to increase cortisol release in response to perioperative stress.

174
Q

How do you determine who should receive perioperative steroid supplementation?

A

yes if prednisone >5mg/day x3 weeks (or equivalent dosing)

higher risk for HPA suppression if dose >20mg/day

175
Q

what are the 4 endocrine hormones produced by the pancreas? which cell types produce each one?

A 
alpha = glucagon
beta = insulin
delta = somatostatin
PP = pancreatic polypeptide
176
Q

what conditions increase insulin release?

A

glucose is the primary stimulator; thus anything that increases serum glucose will stimulate insulin release

  • PNS stim after meal
  • SNS stim
  • hormones: glucagon, catechols, cortisol, GH
  • beta agonists
177
Q

what conditions decrease insulin release?

A

anything that decreases serum glucose will also decrease insulin release

  • hormones: insulin, somatostatin
  • IA
  • B blockers
178
Q

describe the physiology of the insulin receptor.

A

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

179
Q

what factors stimulate glucagon release?

A

secreted by alpha cells. It’s a catabolic hormone that promotes energy release from adipose and the liver (physiologic antagonist to insulin)

decreased glucose stimulates glucagon release (which increases glucose)

  • stress
  • trauma
  • sepsis
  • B agonists
180
Q

what factors inhibit glucagon release

A

increased glucose inhibits glucagon release (which decreases glucose)

  • insulin
  • somatostatin
181
Q

what are the other uses for glucagon?

A

1-5mg IV increases myocardial contractility, HR, AV conduction by raising the intracellular concentrations of cAMP.
since it’s independent of the ANS, it’s useful in:
- BB OD
- CHF
- low CO after MI or CPB
- improving MAP during anaphylaxis

also helpful during ERCP to relex SOO (side effect = N/V)

182
Q

what is somatostatin?

A

aka growth hormone-inhibiting hormone

regulates endocrine hormone output from the islet cells

  • it’s released by delta cells
  • inhibits insulin AND glucagon
  • also inhibits splanchnic blood flow, gastric motility, and gall bladder contraction
183
Q

what is pancreatic polypeptide?

A

inhibits pancreatic exocrine hormone secretion, gallbladder contraction, gastric acid secretion, and gastric motility

184
Q

what are the diagnostic criteria for diabetes mellitus?

A

fasting glucose >126

random glucose >200 + classic symptoms

2hr glucose >200 during oral glucose tolerance test

HgbA1C >6.5%

185
Q

what is the classic triad of DM? Why does it occur?

A

polyuria
dehydration
polydipsia

  • hyperglycemia –> glycosuria (acts as osmotic diuretic) –> hypovolemia
186
Q

what’s the difference b/n type I and type II diabetes mellitus?

A 
T1DM = lack of insulin production
T2DM = relative lack of insulin + insulin resistance
187
Q

what are the most common causes of T1DM and T2DM?

A 
T1DM = autoimmune (early in life)
T2DM = obesity (later in life, but prevalence is increasing in obese children)
188
Q

discuss diabetic ketoacidosis

A
  • more common w/ T1DM
  • usually d/t infection
  • not enough insulin –> ketoacidosis, hyperosmolarity (from increased glucose) + dehydration
  • BS >250, but cells are starved for fuel
  • met acidosis = Kussmaul respirations
  • acetone = fruity breath
  • tx: volume resus, insulin, K+ after acidosis subsides
189
Q

discuss hyperglycemic hyperosmolar state.

A
  • more common w/ T2DM
  • usually d/t insulin resistance or inadequate production
  • enough insulin is produced to prevent ketosis but not hyperglycemia
  • BS >600 = sign increase in osm
  • glycosuria –> dehydration and hypovolemia
  • mild met acidosis may occur (no anion gap)
  • tx: volume resus, insulin, correct e-lytes

c/w DKA, HHS = higher BS and osm

190
Q

describe the long term complications associated w/ DM.

A

microvascular:
- neuropathy
- retinopathy
- nephropathy

macrovascular:
- CAD
- PVD
- CVD

other:
- stiff joint syndrome
- poor wound healing –> infection
- cataracts
- glaucoma

191
Q

how does DM affect the ANS?

A
  • painless myocardial ischemia (referred pain pathways are dysfunctional)
  • reduced vagal tone = ST
  • risk of dysrhythmias
  • orthostatic hypotension
  • impaired resp comp to hypoxia and hypercarbia
  • delayed gastric emptying
  • impaired thermoregulation
  • RA may worsen neuro defects
  • diarrhea and constipation
192
Q

what is the prayer sign?

A

DM can cause glycosylation of the joints –> stiff joint syndrome w/ reduced ROM of AO joint

prayer sign suggests joint glycosylation and an increased risk of difficult intubaiton

193
Q

what is the mechanism of action of the biguanides? list an example from this drug class.

A

MOA: inhibit gluconeogenesis and glycogenolysis in the liver and decrease peripheral insulin resistance

ex: metformin

key facts:

  • does NOT cause hypoglycemia
  • risk: met acidosis
  • often used for polycystic ovarian disease
194
Q

what is the mechanism of action of the sulfonylureas? List examples from this drug class.

A

MOA: stimulate insulin secretion from pancreatic beta cells

ex: glyburide, glipizide, glimepiride

key facts:

  • risk of hypoglycemia
  • avoid if sulfa allergy
195
Q

what is the mechanism of action of the meglitinides? List examples of this drug class.

A

MOA: stimulate insulin secretion from the pancreatic beta cells

ex: repaglinide, nateglinide

key facts:
- risk of hypoglycemia

196
Q

what is the mechanism of action of the thiazolidinediones? List examples from this drug class.

A

MOA: decrease peripheral insulin resistance and increase hepatic glucose utilization

ex: rosiglitazone, pioglitazone

key facts:

  • does NOT cause hypoglycemia
  • black box warning d/t risk of CHF
197
Q

what is the mechanism of action of the alpha-glucosidase inhibitors? List examples from this drug class.

A

MOA: slows digestion and absorption of carbs from GI tract.

ex: acarbose, miglitol

key facts: does NOT cause hypoglycemia

198
Q

what is the mechanism of action of the glucagon-like peptide1 receptor agonists? List examples from this drug class.

A

MOA: increases insulin release from beta cells, decrease glucagon release from alpha cells, and prolongs gastric emptying

ex: exenatide, liraglutide

key facts: risk of hypoglycemia

199
Q

what is the mechanism of action of the dipeptidyl-peptidase-4 inhibitors? List examples from this drug class.

A

MOA: increase insulin release from pancreatic beta cells and decrease glucagon release from alpha cells

ex: suffix -liptin

key facts: risk of hypoglycemia

200
Q

what is the mechanism of action of the amylin agonists? List examples from this drug class.

A

MOA: decrease glucagon release from pancreatic alpha cells and reduce gastric emptying

ex: pramlintide

key factors: risk of hypoglycemia if co-administered w/ insulin

201
Q

compare and contrast the onset, peak, and duration of exogenous insulin preparations.

A

very rapid acting (lispro, aspart, glulisine)

  • onset 5-15min
  • peak 45-75min
  • DOA 2-4hrs

rapid acting (regular)

  • onset 30min
  • peak 2-4hrs
  • DOA 6-8hrs

intermediate acting (NPH)

  • onset 2hrs
  • peak 4-12hrs
  • DOA 18-28hrs

long acting (detemir, glargine)

  • onset 1.5-2hrs
  • peak: detemir 3-9hrs, glargine has no peak
  • DOA up to 24hrs

ultra long acting (degludec)

  • onset 2hrs
  • no peak
  • DOA 40+hrs
202
Q

discuss the presentation, risks, and treatment of hypoglycemia in the perioperative period.

A
  • highest risk = insulin admin during fasting
  • s/s: SNS stim (tachy, HTN, diaphoresis)
  • difficult to diagnose under GA (esp w/ BB)
  • possible cause of delayed emergence
  • rebound hyperglycemia (Somogyi) effect may cloud diagnosis
  • tx: D50 (50-100mL) or glucagon (0.5-1mg IV or SQ)
203
Q

discuss the association b/n insulin and allergic reactions.

A

insulin allergy was more common when animal derived insulin was used

chronic NPH use (or fish allergy) may sensitize the pt to protamine (may not manifest until a large dose is administered - cardiac surgery)

204
Q

what drugs counter the hypoglycemic effect of insulin?

A

epi
glucagon
cortisol

205
Q

what drugs extend or enhance the hypoglycemic effect of insulin?

A

MAOI
salicylates
tetracycline

206
Q

discuss the patho of carcinoid syndrome.

A

associated w/ secretion of vasoactive substances from enterochromaffin cells.
usually associated w/ tumors of the GI tract, but can also arise from locations outside of the GI tract as well (lungs)

release histamine, serotonin, kinins, kallikrein

207
Q

what are the systemic effects of the hormones released by a carcinoid tumor?

A

most common: flushing, diarrhea

histamine:
- bronchoconstriction
- vasodilation, hypotension, flushing (head and neck)

kinins, kallikrein

  • bronchoconstriction
  • vasodilation, hypotension, flushing
  • increases histamine release from mast cells

serotonin

  • bronchoconstriction
  • vasoconstriction, HTN, SVTs
  • increased GI motility (diarrhea, abdominal pain)
208
Q

what are the s/s of carcinoid crisis?

A

life threatening

tachycardia
HTN or hypotension
intense flushing
abdominal pain, diarrhea

209
Q

what drugs are used in the treatment of carcinoid crisis?

A

somatostatin (octreotide or lanreotide): inhibits release of vasoactive substances from carcinoid tumors

antihistamines (H1 and H2: benadryl + ranitidine or cimetidine)

5-HT3 antagonists

steroids

phenylephrine/vasopressin for hypotension (no ephedrine)

210
Q

what drugs should be avoided in the patient w/ carcinoid syndrome?

A

histamine releasing drugs (morphine, meperidine, atra, thiopental, sux)

sux-induced fasciculations can cause hormone release from the tumor

exogenous catechols can potentiate hormone release

sympathomimetic agents: ephedrine and ketamine

APEXANESTHESIA (12 decks)

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