Kidney, liver, and endocrine complete Flashcards

Question

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

Answer 1

Each percentage represents how much sodium is reabsorbed at each point in the nephron

Answer 2

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

Answer 3

proximal tubule: * bulk reabsorption of solutes *bulk reabsorption of water Loop of Henle (Descending): * countercurrent mechanism (tubular fluid concentrate) * High permeability to H2O Loop of Henle (Ascending): * countercurrent mechanism (tubular fluid diluted) * No permeability to H2O Distal Tubule: * Fine tunes solute concentration (aldosterone and ADH) Collecting duct: *regulates final concentration of urine (aldosterone and ADH)

Answer 4

Carbonic anhydrase inhibitors: * Acetazolamide * Dorzolamide MOA: * Noncompetitive inhibition of carbonic anhydrase in the proximal tubule -> net loss of HCO3- and Na+ with a net gain of H+ and CL- Clinical uses: *open- angle glaucoma * altitude sickness * central sleep apnea syndrome Key side effects: * Metabolic acidosis * Hypokalemia

Answer 5

Osmotic diuretics: * Mannitol * Glycerin * Isosorbide MOA: * Osmotic diuretics are sugars that undergo filtration but not reabsorption. They inhibit water reabsorption in the proximal tubule (primary site) as well as the loop of henle. Water is excreted in excess of electrolytes. Clinical uses: * free radical scavenging * Prevention of acute kidney injury (little evidence to support this) * Intracranial HTN Key side effects: * Pulmonary overload in CHF patients * Pulmonary edema * If the blood-brain barrier is disrupted, mannitol will enter the brain and cause cerebral edema

Answer 6

Loop diuretics: * furosemide * Bumetanide * Ethacrynic acid MOA: * Loop diuretics poison the Na-K-2CL transporter in the medullary region of the thick portion of the ascending loop of Henle (primary site). The amount of sodium that remains in the tubule overwhelms the distal tubule's reabsorption capability. Thus, a large volume of dilute urine is excreted. potassium, calcium, magnesium, and chloride are lost to the urine as well. Clinical uses: * HTN * CHF/Pulmonary edema * Hypercalcemia Key side effects: * Hypokalemia, hypochloremic metabolic alkalosis * Hypocalcemia * Hypomagnesemia * Hypovolemia * Ototoxicity (ethacrynic acid > furosemide) * Reduced lithium toxicity

Answer 7

Thiazide diuretics: * Hydrochlorothiazide * Metolazone *Indapamide MOA: *Thiazide inhibit the Na-Cl transporter in the distal tubule Clinical uses: *HTN *CHF *osteoporosis (reduces Ca excretion) * Nephrogenic diabetes insipidus Key side effects: * Hyperglycemia- caution with DM * Hypercalcemia * Hyperuricemia - caution with gouty arthritis * Hypokalemic, hypochloremic metabolic alkalosis * hypovolemia

Answer 8

Potassium-sparing diuretics: * Spironolactone * Amiloride * Triamterene MOA: * Amiloride and triamterene inhibit potassium secretion and sodium reabsorption in the collecting ducts. Their function is independent of aldosterone. * Spironolactone exists in a subclass of potassium-sparing diuretics called aldosterone antagonists. By blocking aldosterone at mineralocorticoid receptors, spironolactone inhibits potassium secretion and sodium reabsorption in the collecting ducts Clinical uses: * To reduces potassium loss in a pt receiving a loop or thiazide diuretic * Secondary hyperaldosteronism Key side effects: * Hyperkalemia (risk increased with concurrent use of NSAIDs, beta-blockers, and ACE inhibitors) * Metabolic acidosis * Gynecomastia * Libido changes (spironolactone) * Nephrolithiasis (triamterene)

Answer 9

Glomerular function is measured by GFR. Clinical tests include: * Blood urea nitrogen (10-20 mg/dL) * Serum creatinine (0.7-1.5 mg/dL) * Creatinine clearance (110-150 mL/min)

Answer 10

Tubular function is measured by urine concentrating ability. Clinical tests include: * Fractional excretion of Na+ (1-3%) * Urine osmolality (65-1400 mOsm/kg). Note: if expressed as osmolarity, units of measurement are mOsm/L. * urine sodium concentration (130-260 mEq/day) * Urine specific gravity (1.003-1.030)

Answer 11

Urea is the primary metabolite of protein metabolism in the liver (amino acids -> ammonia -> urea) Because urea undergoes filtration AND reabsorption, it is a better indicator of uremic symptoms than as a measurement of GFR. <8 mg/dL- overhydration, decreased urea production: Malnutrition, severe liver disease 20-40mg/dL Dehydration Increased protein input: high protein diet, GI bleed, hematoma breakdown catabolism: trauma, sepsis Decreased GFR >50mg/dL: decreased GFR

Answer 12

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 oh hydration. * The normal ratio is 10:1 * A BUN:Cr ratio of >20:1 suggests prerenal azotemia * The aforementioned non-renal causes of elevated BUN can also affect this ratio

Answer 13

Creatinine clearance is the most useful indicator of GFR GFR = [(140-age) x body weight (kg)]/ [72 x serum Cr (mg/dL)] (x0.85 if female)

Answer 14

Fe(Na+) relates sodium clearance to creatinine clearance * if Fe(Na+) < 1% then more sodium is conserved relative to the amount of creatinine cleared. This suggests prerenal azotemia * If Fe(Na+) >3% then more sodium is excreted relative to the amount of creatinine cleared. This suggests impaired tubular function.

Answer 15

The most common cause of perioperative kidney injury is ischemia-reperfusion injury. The following patients are at risk for acute kidney injury during the perioperative period: * Pre-existing kidney disease * Prolonged renal hypoperfusion *Congestive heart failure *Advanced age *sepsis *jaundice *high-risk surgery (use of aortic cross-clamp and liver transplant)

Answer 16

Theses are 3 modern methods used to classify the severity of renal injury: * RIFLE criteria: Risk, Injury, Failure, Loss, End-Stage Kidney Disease Risk: * SCr: increase in SCr to >1.5x baseline * UOP< 0.5 mL/kg/hr for >6hrs Injury: * SCr: increase in SCr to >2x baseline *UOP < 0.5 mL/kg/hr for >12 hrs Failure: *Increase in SCr to >2x baseline *UOP <0.3 mL/kg/hr for >12hr or...Anuria for >12hr Loss * need for renal replacement therapy >4 weeks End-stage * need for renal replacement therapy >3 months Acute Kidney Injury Network (AKIN) Risk * Increase in SCr > 1.5-2x baseline or...>0.3mg/dL * UOP< 0.5 mL/kg/hr for >6hrs Injury * Increase in SCr >0.5mL/kg/hr for >12hrs * UOP <0.5 mL/kg/hr for >12 hrs Failure * Increase in SCr >3x baseline or... >0.5mg/dL to absolute value >4mg/dL or....Need for renal replacement therapy * UOP < 0.3mg/kg/hr >12 hr or... anuria for >12hr last one is Kidney Disease Improving Global Outcomes (KDIGO) These systems grade renal function on serum creatinine and urinary output. Serum creatinine (not urine output) is a more sensitive indicator of renal dysfunction. Their methods highlight that kidney injury occurs along a continuum.

Answer 17

Prerenal injury: Hypoperfuison * Perfusion impaired as a result of hypovolemia, decreased cardiac output, systemic vasodilation, renal vasoconstriction, or increased intra-abdominal pressure. There is no intrinsic damage...yet Treatment: * the risk of prerenal azotemia is reduced by maintaining MAP >65mmHg and providing appropriate hydration * The restoration of renal blood flow with IVF, hemodynamic support, and/or PRBCs (if insufficient DO2) * renal prostaglandins mediate vasodilation in the kidney. NSAIDs reduce prostaglandin synthesis, so avoid them if prerenal injury is a concern. * An improvement in UOP following an intravenous fluid bolus confirms the diagnosis of prerenal azotemia (Azotemia- elevated levels of urea and other nitrogen compounds in the blood)

Answer 18

Intrinsic injury: Parenchymal dysfunction * While intrinsic injury can be caused by injury to the tubule, glomerulus, or the interstitial space, we will focus our discussion on acute tubular necrosis * ATN is usually caused by ischemia (medulla at highest risk) or nephrotoxic drugs (IV contrast dye, abx, NSAIDs) Treatment: * Restore renal perfusion * Supportive

Answer 19

Postrenal injury: Obstruction * Postrenal AKI is the result of an obstructive phenomena * The source of the obstruction can arise anywhere between the collecting system and the urethra treatment: * Relieve the obstruction

Answer 20

The most common cause of CKD is diabetes mellitus The second most common cause of hypertension

Answer 21

Chronic kidney disease is a progressive and irreversible disorder that reflects the ongoing inability of the kidneys to sustain their normal functions We can use GFR to stage chronic kidney disease Stage: 1: normal : GFR >90 2: Mildly decreased: GFR 60-89 3: Moderately decreased: GFR 30-59 4: Severely decreased: 15-29 5: Kidney Failure (requires dialysis): <15

Answer 22

Uremic pts are at increased risk of bleeding. * bleeding time is a measure of platelet function. It is elevated by uremia and is the most accurate predictor of bleeding risk * if PT, PTT, and platelet counts are normal * The first-line treatment is desmopressin (von Willebrand factor VIII) * Cryoprecipitate may be used to provide VIII-vWF, however, its use is associated with an increased risk of viral transmission * Dialysis improves bleeding time, so it should be performed within 24hrs of surgery

Answer 23

Causes of anemia with CKD: * Decreased erythropoietin production leads to normochromic normocytic anemia * Excess parathyroid hormone replaces bone marrow with fibrotic tissue Treatment: * Exogenous EPO or darbepoetin + iron supplementation * Blood transfusion is not a first-line treatment because it increases the risk of HLA (human leukocyte antigens) sensitization and future rejection of a transplanted kidney.

Answer 24

Decreased excretion of non-volatile acid contributes to a gap metabolic acidosis * Gap acidosis is the result of an accumulation of nonvolatile acids * The pt will develop a compensatory respiratory alkalosis (HTN) * Acidosis shifts the oxyhemoglobin association to the right. This partially compensates for anemia (release)

Answer 25

Hyperkalemia is the result of impaired excretion. Dialysis is indicated when serum potassium exceeds 6 mEq/L Other treatments that reduce serum potassium include: * Glucose (25-50g) + Insulin (10-20 units) * Hyperventilation ( for every 10 mmHg decrease in PaCO2, the serum potassium level is reduced by 0.5 mEq/L) *calcium chloride (1g) does not change serum potassium concentration. Instead, it raises threshold potential in the myocardium and reduces the risk of lethal dysrhythmias

Answer 26

renal osteodystrophy is caused by: * decreased vit D production *secondary hyperparathyroidism Pathophysiology: * An inadequate supply of Vit D impairs calcium absorption in the GI tract * The body responds to hypocalcemia by increasing parathyroid hormone release. This action demineralizes bone to restore the serum calcium concentration * The net result is a decreased bone density and increased risk of bone fractures

Answer 27

Dialysis is the concentration of AKI tx. There are 5 indications for its use: * Volume overload * Hyperkalemia * Severe metabolic acidosis * Symptomatic uremia * Overdose with a drug that is cleared by dialysis

Answer 28

hypotension is the most common event during dialysis. This is due to intravascular volume depletion and osmotic shifts

Answer 29

Compound A is produced when sevoflurane is degraded by soda lime. In theory, this can be toxic to the kidneys (there is no good human data) The FDA recommends that sevo be administered at a rate of 1L/min for no more than 2 MAC hours. After 2 MAC hours have elapsed, the fresh gas flow should be increased to 2L/min

Answer 30

Factors associated with increased compound A production include: * High concentrations over a long period of time * Low fresh gas flow * High temperature of CO2 absorbent * Increased CO2 production * Desiccated soda lime

Answer 31

Opening of the nAChR at the neuromuscular junction can increase serum potassium by 0.5-1 mEq/L for up to 10-15 min * Succ's is safe in pts with renal failure with a normal potassium level * in the pt with hyperkalemia (K+ >5.5mEq/L), the normal response to succ's may increase serum potassium to a dangerous level

Answer 32

Due to their organ independent elimination, cisatracurium and atracurium are more predictable agents in this population

Answer 33

Roc primarily undergoes hepatobiliary elimination. >70% hepatic and 10-25% renal. However, it is associated with an unpredictably increased duration of action. Possible causes include a reduced clearance. altered protein binding, and/or an increased potency. Vecuronium is metabolized by 3-OH vecuronium. Its duration is prolonged as a function of decreased clearance and an increased elimination half-life. 40-50% metabolized by the liver and 50-60% by the kidney. Pancuronium is primarily eliminated by the kidneys >85% and 15% liver. and has no use in this population

Answer 34

Both anitcholinesterases and anticholinergics used to reverse neuromuscular blockers undergo renal elimination, and thus share a similar increase in duration. They do not require dosage adjustments

Answer 35

Morphine is metabolized to morphine-6-glucuonide. 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 of normeperidine can cause convulsions. Fentanyl, sufentanil, afentanil, and remifentanil do not produce active metabolites and are better choices with renal failure. Hydromorphone may or may not produce an active metabolite (depends on the reference) Hydromorphone is metabolized to an active metabolite, hydromorphone-3-glucuronide. This can cause prolonged respiratory depression and myoclonus. The literature is inconsistent on this one. Whether or not hydromorphone produces an active metabolite, renal impairment does necessitate a dose reduction

Answer 36

Prevention of contrast-induced nephropathy (CIN): * Use nonionic iso- or low-osmolar contrast instead of hyperosmolar contrast * Use the lowest volume of contrast as the procedure will allow * withholding other drugs with known nephrotoxic effects *IV hydration with 0.9% NaCl prior to administration of contrast dye *Sodium bicarbonate injection or infusion * N-acetylcysteine is a free radical scavenger. It has fallen out of favor for lack of efficacy.

Answer 37

Rhabdomyolysis 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 (pH <5.6), myoglobin precipitates in the proximal tubule * This results in tubular obstruction and acute tubular necrosis * In addition, myoglobin scavenges nitric oxide, leading to renal vasoconstriction and ischemia

Answer 38

Preventative strategies include: * Maintenance of renal blood flow and tubular flow with IV hydration * Osmotic diuresis with mannitol * UOP should be kept >100-150 mL/hr * Sodium bicarbonate and/or acetazolamide to alkalize the urine As an aside, hemolysis from a hemolytic reaction is treated in the same way

Answer 39

Some antibiotics increase the risk of AKI. This risk is reduced with IV fluids, correction of correctable risk factors, and close monitoring of serum trough levels Nephrotoxic antibiotics: * Aminoglycosides (gentamycin, tobramycin, amikacin) * Amphotericin B (antifungal) * vancomycin- (glycopeptide antibiotic) * Sulfonamide (Trimethoprim, sulfadiazine, Bactrim) * tetracyclines (Lymecycline, methacycline, doxycycline) * Cephalosporins (Cephalexin, ceftriaxone, cefotaxime)

Answer 40

Calcineurin inhibitors (cyclosporine and tacrolimus) are immunosuppressant agents used to prevent rejection of transplanted organs. Side effects include HTN and renal vasoconstriction. Sirolimus is a non-calcineurin inhibitor that carries a much lower risk of nephrotoxicity

Answer 41

distilled water has an osmolality of zero. This creates a dilutional effect that increases the risk of hyponatremia, hypo-osmolality, hemolysis, and hemoglobinuria (renal failure)

Answer 42

Glycine metabolism can increase ammonia production, and 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- 48 hours

Answer 43

yes and no. 0.9% NaCl or LR would be great choices, however they're highly ionized, so they're good conductors of electricity. Therefore, these fluids are contraindicated when unipolar electrocautery is used. The introduction of bipolar cautery in newer resectoscope permits use of ionic solutions

Answer 44

Cardiopulmonary: * Circulatory overload: * HTN * Reflex bradycardia * CHF * Pulmonary edema * Dysrhythmias * Myocardial infarction CNS: * Restlessness * N/V * Cerebral edema * Seizures * Coma Metabolic: * Hyponatremia Misc.: * Hemolysis * Hypo-osmolality

Answer 45

* Support oxygenation and cardiovascular support * Tell the surgeon to abort the procedure * Lab data: Electrolytes, hematocrit, creatinine, glucose, and 12- lead EKG * If Na > 120mEq/L, then restrict fluids and give furosemide (loop diuretic) * If Na <120mEq/L, then give 3% NaCl at <100 mL/hr (discontinue when Na+ >120 mEq/L) * Correcting serum Na too quickly increases the risk of central pontine myelinolysis * Midazolam may be used for seizures * Proceed with tracheal intubation and mechanical ventilation if the pt has difficulty with oxygenation and/or pulmonary edema (chest auscultation and CXR will be helpful)

Answer 46

Bladder perforation can occur if the resectoscope punctures the bladder wall * Inadvertent stimulation of the obturator nerve through the bladder wall can cause lower extremity movement, which may cause the resectoscope to puncture the bladder wall. * This complication is more easily recognized in a conscious patient, especially if sensory anesthesia does not extend much beyond T10 * Presentation includes abdominal and/or shoulder pain * A reduction of irrigation fluid return is an early sign of bladder rupture * Treatment is supportive (IVF, pressors, etc) with serial assessment of H&H and transfusion as indicated * The pt will require emergent suprapubic cystostomy or possibly exploratory laparotomy

Answer 47

ESWL delivers shock waves in rapid succession that are directed at the stone. * Because the acoustic impedance of water and human tissue is roughly similar, the shock wave moves through the body until it reaches the body-stone interface. * at this point, the energy is released, breaking up the stone, producing smaller small stone fragments that are eliminated via the urine * It's important that there's nothing between the energy source and the stone.

Answer 48

absolute: * Pregnancy * Risk of bleeding (bleeding disorder or anticoagulation) Relative contraindications: * Pacemaker / ICD * Calcified aneurysm of the aorta or renal artery * UTI (untreated) * Obstruction beyond the renal stone * Morbid obesity

Answer 49

The shock wave can produce dysrhythmias (probably due to mechanical influence), and the pulse wave is timed to the R wave on the EKG to minimize the risk of "R-on-T" phenomenon.

Answer 50

The livers functional unit is the lobule (otherwise known as the acinus) Arterioles: terminal branches of: hepatic artery and portal vein Capillaries: sinusnoids Venules: central vein

Answer 51

since portal vein blood drains the intestine, the liver receives a significant bacterial load. Kupffer cells (part of the reticuloendothelial (fixed phagocytic cells) system) remove the bacteria before the blood drains into the vena cava

Answer 52

The flow of bile: * Bile is produced by the hepatocytes * The canaliculi drain bile into the bile duct * The bile ducts converge to form the common hepatic duct * The cystic duct (from the gallbladder) and the pancreatic duct join the common hepatic duct before it empties into the duodenum * The sphincter of Oddi controls the flow of bile released from the common hepatic duct * Contraction of the sphincter of Oddi (narcotics) increase biliary pressure

Answer 53

The liver receives around 30% of CO (1500mL)

Answer 54

The liver is supplied by 2 vessels: portal vein & hepatic artery * Aorta -> Splanchnic organs -> portal vein -> liver * Aorta -> Hepatic artery -> liver Portal vein supplies (alpha 1): * 75% of liver blood flow * 50% of oxygen content (lower O2 saturation) Hepatic artery supplies (alpha 1 and beta 2): * 25% of liver blood flow * 50% of oxygen content (higher O2 saturation)

Answer 55

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

Answer 56

Portal vein: Normal pressure- 7-10 mmHg Diagnostic for portal HTN: >20-30mmHg Sinusoids: Normal: 0 mmHg Diagnostic for portal HTN: >5mmHg

Answer 57

Hepatic artery perfusion pressure = MAP- Hepatic Vein pressure Hepatic arterial buffer response: This is a fancy way of saying that a reduction in portal vein flow is compensated by an increased hepatic artery flow * this response is mediated by adenosine (direct vasodilator effect only on hepatic artery, not portal vein) * Severe liver dx impairs this response

Answer 58

General anesthesia as we all neuraxial anesthesia reduce liver blood flow as a function of decreased MAP

Answer 59

Since the hepatocytes produce so many proteins, its easier to learn what they do NOT produce: * Von Willebrand factor: Vascular endothelial cells * Factor III (tissue factor): Vascular endothelial cells * Factor IV (calcium): Diet * Factor VIII (antihemophilic factor): Liver sinusoidal cells (not hepatocytes) and endothelial cells

Answer 60

Vitamin K is required to synthesize factors II, VII, IX, and X, and absorption of vitamin K is dependent on the presence of bile in the gut (1972) Anticoagulants that are dependent on Vitamin K: Proteins S,C,Z

Answer 61

The liver produces all of the plasma proteins except for immunoglobulins (gamma globulins). * Albumin: Provides oncotic pressure and is a reservoir for acidic drugs * Alpha-1 acid glycoprotein: is a reservoir for basic drugs * Pseudocholinesterase metabolizes succinylcholine and ester-type local anesthetics

Answer 62

Stimulus: Hyperglycemia -> Release of insulin (pancreatic beta cells)- Metabolic process is glycogenesis-> glucose turned into glycogen (storage) Stimulus: Hypoglycemia-> Release of: Glucagon (pancreatic alpha cells) and Epi (adrenal medulla)-> metabolic process ( Glycogenolysis and gluconeogenesis) -> glucose is normalized by glycogen (storage)-> glucose and Non-carbohydrates turned to glucose such as amino acids, pyruvate, lactate, and glycerol (triglycerides) the liver is an important regulator of serum glucose. It also clears insulin from the circulation. Therefore, pts with liver failure are at risk of hypoglycemia.

Answer 63

Amino acid deamination allows the body to convert proteins to carbohydrates and fats. Some of these are utilized in Kreb's cycle to produce ATP * the deamination process produces a large quantity of ammonia. The liver converts ammonia to urea, which is eliminated by the kidney. * Failure to clear ammonia (hepatic failure or portosystemic shunting) leads to hepatic encephalopathy

Answer 64

Bilirubin: * The erythrocyte's life cycle is 120 days. Aged RBCs are processed by the reticuloendothelial cells in the spleen * In the spleen: Hemoglobin -> heme -> unconjugated bilirubin (this component is neurotoxic) * Unconjugated bilirubin is lipophilic. It's transported to the liver bound to albumin * the liver conjugates bilirubin with glucuronic acid. This increases its water solubility * Conjugated bilirubin Is excreted into the bile, metabolized by intestinal bacteria, and eliminated in the stool

Answer 65

PT: * Normal value = 12-14 sec * Very sensitive for acute injury ( Factor 5 and 7 t1/2 is 4-6hrs) Albumin: * Normal value= 3.5- 5.0 g/dL * Not sensitive for acute injury (t1/2= 21 days)

Answer 66

AST (10-40 units/L) and ALT (10-50 units/L) * Marked elevation of both suggest hepatitis * AST/ALT ratio > 2 suggest cirrhosis or alcoholic liver dx

Answer 67

5'-nucleotidase (0-11 units/L) is the MOST specific indicator of biliary duct obstruction Y Glutamyl transpeptidase (0-30 units/L) Alkaline phosphatase (45-115 units/L) is not very specific (it's also in bone, placenta, and tumors)

Answer 68

Type A = 50% Type B= 35% Type C= 15% Type D= Co-infection with type B

Answer 69

Type A= oral-fecal Type B= Percutaneous or sexual content Type C= Percutaneous Type D= Percutaneous

Answer 70

Type A: * Pooled Gamma Globulin * Hep A vaccine Type B: * Hep B immunoglobulin * Hep B vaccine Type C: * Interferon + Ribavirin

Answer 71

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 called N-acetyl-p-benzoquinoneimine ( NAPQI) * With normal acetaminophen dosing, NAPQI is conjugated with glutathione. The conjugated metabolite is not toxic. * Acetaminophen overdose consumes the liver's supply of glutathione * Since the conjugation substrate isn't available, the concentration of NAPQI rises, and this leads to hepatocellular injury Treatment consists of oral N-acetylcysteine within 8 hours of acetaminophen overdose

Answer 72

The liver metabolizes desflurane, isoflurane, and halothane to inorganic fluoride ions and trifluoroacetic acid (TFA) Halothane hepatitis is believed to be the result of an immune-mediated reaction caused by TFA. Up to 20% of halothane is metabolized, so it makes sense that halothane metabolism produces significant quantity of TFA. By comparison 0.02% Des and and 0.2% Isoflurane are metabolized. These drugs produce minuscule quantities of TFA, however, there is a theoretical risk that they can cause hepatitis, particularly in sensitized patients. Sevoflurane does not produce TFA.

Answer 73

Unless you provide anesthesia in a third world country, you'll probably never touch halothane. You should still know this stuff, however. Risk factors: * Age >40 * Female gender * Greater than 2 exposures * Genetics * Obesity * CYP2E1 induction (alcohol, isoniazid, phenobarbital)

Answer 74

Most common= alcoholism- alcohol is the most common cause of drug-induced hepatitis Second most common- Hepatitis C

Answer 75

* If acute hepatitis: Non-emegergent surgery should be postponed until symptoms have resolved and liver function tests return to normal * If chronic hepatitis- The pt may proceed to surgery so long as the condition is stable Your primary objectives are to preserve hepatic blood flow and avoid drugs that can potentiate hepatocellular injury. Some pts may be sensitive to the CNS effects of anesthetic drugs, while alcoholics experience a higher tolerance

Answer 76

* Use isoflurane (preserve hepatic blood flow the best) * Avoid halothane (Don't use if in OR) * Avoid PEEP (increases resistance to hepatic drainage) * Ensure normocapnia * Liberal use of IV fluids * Regional anesthesia is ok as long as there are no coagulation defects

Answer 77

Avoid hepatotoxic drugs or those that inhibit CYP450: * Acetaminophen * Halothane * Amiodarone * Antibiotics: PCN, tetracycline, and sulfonamides

Answer 78

Anesthetic requirement: * MAC is decreased in the acutely intoxicated pt * MAC is increased in the chronic alcohol abuser that is not intoxicated * Alcohol potentiates GABA. There is an increased effect of benzodiazepines * Alcohol inhibits NMDA receptors

Answer 79

Alcohol abuse creates a state of dependency. Signs and symptoms of withdrawal begin 6-8 hrs after the blood alcohol concentration returns to normal and peak at 24-36 hrs * Early s/sx: Tremors and disorder perception (hallucinations, nightmares) * Late s/sx: Increased SNS activity (tachycardia HTN, Dysrhythmias), N/V, insomnia, confusion, agitation * Treatment: Alcohol, beta-blockers, alpha-2 agonists

Answer 80

Delirium tremens occurs after 2-4 days without alcohol * S/sx- grand mal seizures, tachycardia, hyper- or hypotension, and combativeness * Treatment: Diazepam (or other benzo) and beta-blockers

Answer 81

Alcoholics are often deficient in vit B12 (thiamine) Wernicke-korsakoff syndrome is characterized by a loss of neurons in the cerebellum, and this is brought on by thiamine deficiency

Answer 82

* Non-alcoholic fatty liver dx (most common cause of liver dx) - Fatty infiltration (d/t obesity, metabolic dx) * Alcohol abuse: fatty infiltration * Alpha-1- antitrypsin deficiency: Genetic (this diseases also causes emphysema) * Biliary obstruction: Inflammation and tissue destruction * Chronic hepatitis: Inflammation and tissue destruction * Right-sided heart failure: Increased hepatic vascular resistance * Hemochromatosis: Iron overload * Wilson disease: Genetic (copper accumulates in the tissues)

Answer 83

Cirrhosis is 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.

Answer 84

As the number of hepatocytes dwindles, so does the liver's ability to perform all of its essential functions. * The number of blood vessels passing through the liver is reduced, which increases hepatic vascular resistance (Portal HTN) * To partially offset the increased resistance, the body creates collateral vessels that bypass the liver; these are called portosystemic shunts * Since this blood bypasses the liver, drugs and toxins (ammonia) remain in the systemic circulation for a longer period of time

Answer 85

The MELD score uses a logarithmic calculation that examines 3 factors of hepatic function: Bilirubin, INR, and serum creatinine * low risk= <10 * Intermediate risk= 10-15 * High risk = >15

Answer 86

The modified Child-Pugh score examines 5 factors of hepatic function: albumin, PT, bilirubin, ascites, and encephalopathy * Class A (5-6 points)= 10% risk of perioperative mortality * Class B (7-9 points)= 30% risk of perioperative mortality * Class C (10-15 points)= 80% Risk of perioperative mortality If a pt with a class A or B disease that is otherwise optimized, it is reasonable to proceed with surgery. A pt with call C disease should be managed medically until hepatic function improves.

Answer 87

Hyperdynamic circulation * Decreased SVR and 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 (low platelets) Ascites: * Decreased Oncotic pressure * Decreased Protein binding * Increased volume of distribution * Drainage -> hypotension

Answer 88

Restrictive defect: Ascites and/or pulmonary effusion reduce pulmonary compliance Respiratory alkalosis: Hypoxemia -> compensatory hyperventilation Hepatopulmonary syndrome: Pulmonary vasodilation -> intrapulmonary shunt -> hypoxemia Portopulmonary HTN: PAP > 25 mmHg in the setting or portal HTN

Answer 89

Decreased hepatic clearance -> increased ammonia -> cerebral edema -> increased ICP * Increased Ammonia is treated with lactulose, abx, and reduced protein intake

Answer 90

Renal Hypoperfusion: Decreased GFR-> increased RAAS -> NA and H2O retention (dilutional hyponatremia may occur) Hepatorenal syndrome: Decreased GFR -> renal failure (liver transplant is the definitive treatment)

Answer 91

The TIPS procedure (transjugular intrahepatic portosystemic shunt) bypasses a portion of the hepatic circulation by shunting blood from the portal vein (hepatic inflow vessel) to the hepatic vein (hepatic outflow vessel) This reduces portal pressure and minimizes back pressure on the splanchnic organs. In turn, it reduces the likelihood of bleeding from esophageal varices and reduces the amount of ascites. It is also a temporary treatment for hepatorenal syndrome. Hemorrhage is a significant risk during the TIPS procedure as well as pneumothorax, also portal vein puncture and heart dysrhythmias

Answer 92

Cholecystokinin (CCK) stimulates gallbladder contraction, and this increases the flow of bile into the duodenum * Production and release = duodenum * Release due to food ingestion (fat and amino acids) and also increased vagal stimulation (PNS= rest and digest)

Answer 93

Cholecystitis: inflammation of the gall bladder: Cholecystectomy Cholelithiasis: Gallstones: Cholecystectomy Choledocholithiasis: Stones in the common bile duct -> May be the result of inflammation of the pancreatic head which obstructs the common bile duct: endoscopic retrograde cholangiopancreatography (ERCP)

Answer 94

The incidence of gallstones increases with obesity, aging, rapid weight loss, pregnancy, and women >men * remember the 3 F's: Fat, female, and 40

Answer 95

Signs and symptoms: * Leukocytosis * Fever * RUQ pain- Pain is worse with inspiration (murphy's sign)

Answer 96

You can relax the sphincter of Oddi with: glucagon, naloxone, or nitroglycerin. Glycopyrrolate and atropine may help as well. * Using naloxone in a surgical pt is a poor choice * glucagon increased the risk of PONV Opioids can precipitate spasm of the sphincter of Oddi. This is a problem if it causes a false-positive during a cholangiogram. This is one are where the texts conflict with real-work practice. We've never withheld narcotics for this reason

Answer 97

the hypothalamus communicates with the posterior pituitary gland through a series of neural connections, and it communicates with the anterior pituitary gland with a group of releasing and inhibiting hormones

Answer 98

The pituitary gland resides in the sella turcica, and it is connected to the hypothalamus by the pituitary stalk * Anterior pituitary: Adenohypophysis * Posterior pituitary gland= neurohypophisis

Answer 99

FLAT PIG: Follicle-stimulating hormone Luteinizing hormone Adrenocorticotropic hormone Thyroid stimulating hormone Prolactin Growth hormone

Answer 100

*Follicle-stimulating hormone -> germ cell maturation and ovarian follicle growth (females) * Luteinizing hormone-> testosterone production (males) and ovulation (females) * Adrenocorticotropic hormone -> adrenal hormone release * Thyroid stimulating hormone-> thyroid hormone release * Prolactin -> lactation * Growth hormone-> cell growth

Answer 101

Antidiuretic hormone ->water retention Oxytocin-> uterine contraction and breast feeding

Answer 102

Excess growth hormone * Distorted facial features (difficult to mask) * Large tongue, teeth, and epiglottis (difficult larygnoscopy) * Subglottic narrowing and vocal cord enlargement (difficult ett placement -use a smaller tube) * Turbinate enlargement (Risk of epistaxis- avoid nasal intubation if possible) * OSA is common * Increased risk of HTN, CAD, and rhythm disturbances * Glucose intolerance * skeletal muscle weakness * Entrapment neuropathies are common

Answer 103

Source: T3: Directly released from the thyroid T4: Mostly extrathyroid conversion of T4 to T3, a small amount is released from the thyroid Where concentration is highest T3: In the blood (think of T4 as a delivery vehicle) T4: In the target cell- T4 is converted to T3 (think of T3 as the active form) Protein binding T3: more T4: less Potency T3: less T4: More Half-life: T3- 7 days T4- 1 day

Answer 104

TSH stimulates the iodide pump. Iodine is a substrate that the thyroid requires to synthesize triiodothyronine (T3) and thyroxine (T4). When iodine is not available (dietary deficiency), the thyroid is unable to produce a sufficient quantity of T3 and T4

Answer 105

Thyroid hormone increases myocardial performance independent of the ANS: * Increased chronotropy * Increased inotropy * Increased lusitropy * decreased SVR Thyroid effects the ANS that impact cardiac function: * Increased number and sensitivity of cardiac beta receptors * Decreased number of cardiac muscarinic receptors

Answer 106

Increased BMR-> Increased O2 consumption -> increased CO2 production -> increased minute ventilation (increased Vt and RR)

Answer 107

thyroid hormone does not affect the brain, and by extension, hyper- and hypothyroidism do NOT affect MAC. They do, however, affect the speed of anesthetic induction when a volatile agent is used. * Hyperthyroidism= slower induction (d/t higher CO) * Hypothyroidism = faster induction (d/t lower CO)

Answer 108

* Most common: Grave's disease (autoimmune) * Myasthenia gravis * Multinodular goiter * carcinoma * pregnancy * Pituitary adenoma * amiodarone (less common)

Answer 109

* Most common: Hashimoto's thyroiditis (autoimmune) * Iodine deficiency * Hypothalamic-pituitary dysfunction * neck radiation * thyroidectomy * amiodarone (more common)

Answer 110

Hyperthyroidism: Low TSH + High T3 and T4 Hypothyroidism : High TSH + low T3 and T4

Answer 111

Myxedema coma occurs with end-stage hypothyroidism. Coma is a consequence (not a cause) of severely impaired thyroid function. Cretinism is caused by neonatal hypothyroidism that leads to physical and mental retardation

Answer 112

Thionamides= propythiouracil (PTU), methimazole, carbimazole These agents inhibit thyroid synthesis by blocking iodine addition to the tyrosine residues on thyroglobulin. PTU also inhibits the peripheral conversion of T4 and T3 * These agents require 6-7 weeks to achieve a euthyroid state * They are only available PO but can be crushed and given via OGT/NGT

Answer 113

Beta blockers reduce SNS stimulation and inhibit peripheral conversion of T4 to T3

Answer 114

Pregnancy breast feeding mothers

Answer 115

Hyperthyroidism: * Do NOT proceed to elective surgery until the pt is euthyroid. Successful medical management may require upwards of 6-8 weeks * Emergency surgery warrants administration of beta-blocker, potassium iodide, glucocorticoid, and PTU Hypothyroidism: * Okay to proceed to surgery if mild to moderate disease

Answer 116

A goiter can cause tracheal deviation and/or tracheomalacia On boards, goiter = awake intubation. The next best response is a technique that maintains spontaneous ventilation

Answer 117

Avoid sympathomimetics, anticholinergics, ketamine, and pancuronium

Answer 118

Thyroid storm is a medical emergency that can occur in hyperthyroid AND euthyroid pt It is generally brought on by stressful events: infection, surgery, etc. It most commonly occurs 6-18 hours after surgery Common s/sx include: * Fever > 38.5 decrees C * Tachycardia/tachyarrhythmias (afib) * HTN * CHF * Shock * Confusion and agitation * N/V * under anesthesia, thyroid storm can mimic MH, pheochromocytoma, neuroleptic malignant syndrome, and light anesthesia

Answer 119

Remember the four B's when treating the pt with thyroid storm * Block synthesis (methimazole, carbimazole, PTU, Potassium iodide) * Block release (radioactive iodine, potassium iodide) * Block T4 to T3 conversion (PTU, propranolol, glucocorticoids) * Block beta receptors (propranolol, esmolol) Other treatments include: * cardiopulmonary support * active cooling measures (cold IVF, ice packs) * PTU or methimazole can be given via OGT/NGT if during surgery * Beta-blockers * treat fever with acetaminophen * avoid aspirin- it can dislodge T4 from plasma proteins -> increase unbound fraction * management is the same in pregnant and non-pregnant pts

Answer 120

The RLN innervates all of the intrinsic laryngeal muscles except for the cricothyroid muscle (innervated by the SLN). Injury to the RLN can cause airway obstruction * unilateral injury-> ipsilateral vocal cord is positioned midline on inspiration = hoarsness * bilateral injury -> both cords are positioned midline on inspiration -> airway obstruction * Have pt say the letter "E" or "moon" to assess nerve injury * A NIM ETT provides the ability to assess RLN integrity intraoperatively. When the electrode on the tube are positioned between the vocal cords, a current can be applied to assess RLN function * At the end of the procedure, Direct Laryngoscopy can be used to assess vocal cord function as well as identify glottic edema

Answer 121

Resection of parathyroid glands (without reimplantation) -> hypocalcemia at least 6-12 hours after surgery. Most s/sx of hypocalcemia are the result of increased nerve and muscle irritability. * Muscle spasm-> tetany * Laryngospasm * Mental status changes * Hypotension * Prolonged QT interval * Paresthesia's * Chvostek's sign: tapping on the angle of the jaw (facial nerve/masseter muscle)-> facial contraction on ipsilateral side * Trousseau's sign: muscle spasm in hand or forearm in response to BP cuff inflation for 3 minutes

Answer 122

Hypothyroidism is associated with delayed gastric emptying-> increased risk of aspiration

Answer 123

The adrenal cortex has 3 zones that synthesize and release: * Mineralocorticoids (aldosterone) * glucocorticoids (cortisol) * androgens (dehydroepiandrosterone) Notice that the cortical layers (outside to inside) spell GFR. Remember what each one releases with: "salt, sugar, sex"

Answer 124

Cortisol production is 15-30 mg/day, with a normal level of 12mg/dL. Stress can increase cortisol production upwards to 100mg/day, with a serum level up to 30-50mg/dL during and after major surgery

Answer 125

Cortisol improves myocardial performance by increasing the number and sensitivity of beta receptors on the myocardium Cortisol is also required for the vasculature to respond to the vasoconstrictive effects of catecholamines

Answer 126

pay attention to the following: * no glucocorticoid effects = aldosterone * No mineralocorticoid effects = dexamethasone, betamethasone, triamcinolone

Answer 127

Triamcinolone is commonly administered in the epidural space to treat lumbar disc disease. This drug is unique because it is associated with a higher incidence of skeletal muscle weakness. It's also more likely to cause sedation (not euphoria) and anorexia (not increased appetite)

Answer 128

Conn's syndrome= too much aldosterone * primary- increased aldosterone release from the adrenal gland * Secondary- usually due to increased renin release or aldosterone secreting tumor remember that aldosterone is a mineralocorticoid, so Conn's syndrome will present with s/sx of mineralocorticoid excess: * HTN (Na+ and water retention) * Hypokalemia (K+ wasting) * Metabolic alkalosis (H+ wasting)

Answer 129

Long term licorice ingestion (glycyrrhizic acid) causes a syndrome that highly resembles hyperaldosteronism (Conn's syndrome)

Answer 130

Treatment: * Aldosterone antagonists- spironolactone or eplerenone * Potassium supplementation * Na+ restriction * Removal of aldosterone secreting tumor

Answer 131

Although they present similarly, the etiologies are a little different: * Cushing's syndrome= too much cortisol * Cushing's disease = too much ACTH (Increases cortisol and androgen production) Causes of Cushing's Syndrome * Exogenous causes (steroid medications) * Endrogenous causes (overproduction of cortisol)- Pituitary tumor (cushings dx), Aderenal tumor, other cause

Answer 132

Glucocorticoids effects: * Hyperglycemia * Weight gain (central obesity, buffalo hump, moon face) * Increased risk of infection * osteoporosis * Muscle weakness * Mood disorder

Answer 133

* HTN (NA+ and water retention) * Hypokalemia (K wasting) * Metabolic alkalosis (H+ wasting)

Answer 134

* women become masculinized (hirsutism, hair thinning, acne, amenorrhea) * Men become feminized (gynecomastia, impotence)

Answer 135

Remember that cortisol has glucocorticoid, mineralocorticoid, and androgenic effects, so Cushing's will present as an excess of these three things. Glucocorticoid effects: Hyperglycemia weight gain (central obesity, buffalo hump, moon face) Increased infection osteoporosis muscle weakness Mineralocorticoid effects * HTN (NA+ and water retention) * Hypokalemia (K wasting) * Metabolic alkalosis (H+ wasting) Androgenic effects: * women become masculinized (hirsutism, hair thinning, acne, amenorrhea) * Men become feminized (gynecomastia, impotence)

Answer 136

Diabetes insipidus ( too little ADH). this complication is usually transient.

Answer 137

Adrenal insufficiency= too little mineralocorticoid, glucocorticoid, and androgen * Primary (Addison's): adrenal glands don't secrete enough steroid hormone (most common is autoimmune) * Secondary: decreased CRH or ACTH release (most common is exogenous steroid use) Presentation: * Muscle weakness/ fatigue * Hypotension * hypoglycemia * Hyponatremia * Hyperkalemia * metabolic acidosis (usually mild) * Anorexia * N/V * Hyperpigmentation of knees, elbows, knuckles, lips, and buccal mucossa

Answer 138

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

Answer 139

Adrenal insufficiency is a chronic state, but it can deteriorate into an acute adrenal crisis if the pt is faced with additional stress (infection, illness, sepsis, or surgery). This is a medical emergency * Hemodynamic instability / collapse * fever * hypoglycemia * impaired mental status

Answer 140

* Steroid replacement therapy ( hydrocortisone 100mg + 100-200 mg q24hr) * ECF volume expansion (D5NS is best) * Hemodynamic support

Answer 141

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

Answer 142

The answer depends on how much exogenous steroid the pt is receiving and for how long.

Answer 143

Glucose is the primary stimulator of insulin release from the pancreatic beta cells. Therefore, anything that increases serum glucose will also increase insulin release. Things that stimulate insulin release * Anything that raises blood glucose with stimulate insulin release * PNS stimulation (occurs after eating a meal) * SNS stimulation ( increase blood glucose -> insulin release) Hormones: * Glucagon (it raises BG -> increase insulin release) * Catecholamines * Cortisol * Growth hormone Drugs * Beta agonists (albuterol)

Answer 144

Anything that decreases serum glucose will also decrease insulin release Hormones: * Insulin (decrease glucose-> decrease insulin release) Drugs: * Volatile anesthetics * Beta antagonists

Answer 145

the insulin receptor is made up of 2 alpha and 2 beta subunits that are joined together by disulfide bonds. When insulin binds to the receptor, the beta subunits activate tyrosine kinase, which then activates insulin-receptor substrates (IRS). The insulin cascade turns on the GLUT4 transporter, which increases glucose uptake by skeletal muscle and fat.

Answer 146

Glucagon is secreted by pancreatic alpha cells. It's a catabolic hormone that promotes energy release from adipose and the liver. Said another way. Its a physiologic antagonist to insulin. Things that stimulate glucagon release: * Anything that reduces blood glucose will stimulate glucagon release * hypoglycemia * stress * trauma * Sepsis * beta agonists

Answer 147

* Anything that increases blood glucose will inhibit glucagon release * insulin * somatostatin

Answer 148

Glucagon (1-5mg IV) increases myocardial contractility, heart rate, and AV conduction by increasing the intracellular concentration of cAMP. It does this independently of the autonomic nervous system, which is useful in the following situations: * Beta-blocker overdose * CHF * Low cardiac output after MI or cardiopulmonary bypass * improving MAP during anaphylaxis glucagon is also administered during ERCP to relax the biliary sphincter (side effect =N/V)

Answer 149

also known as growth hormone- inhibiting hormone, regulates endocrine hormone output from the islet cells. It's release by delta cells. * it inhibits insulin AND glucagon * It also inhibits splanchnic blood flow, gastric motility, and gall bladder contraction

Answer 150

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

Answer 151

* Fasting plasma glucose >126 mg/dL * Random glucose level >200mg/dL + classic symptoms * Two hour plasma glucose > 200mg/dL during oral glucose tolerance test * HGB A1C >6.5%

Answer 152

Hyperglycemia >180 mg/dL -> glycosuria ->osmotic diuresis -> hypovolemia -> classic symptom triad: Polyuria, dehydration, polydipsia (excess thirst)

Answer 153

Diabetes is classified as either type I or type II * T1DM is characterized by a lack of insulin production * T2DM is characterized by a relative lack of insulin and insulin resistance

Answer 154

TRDM= Autoimmune response (early in life) T2DM= obesity ( later in life, but prevalence is increasing in obese children)

Answer 155

* More common with Type 1 diabetes mellitus * usually caused by infection * not enough insulin-> ketoacidosis, hyperosmolarity (from increased glucose), and dehydration * Patient is hyperglycemic (> or equal to 250 mg/dL), but cells are starved for fuel * Acetone causes fruity-smelling breath * Treatment = volume resuscitation, insulin, K+ after acidosis subsides

Answer 156

* More common with Type 2 DM * Usually caused by insulin resistance or inadequate production * Enough insulin is produced to prevent ketosis but not hyperglycemia * Hyperglycemia (>600mg/dL) significantly increases serum osmolarity (>330 mOsm/L) * Compared to DKA, HSS is associated with a greater elevation in glucose and osmolarity * Glycosuria (sugar in urine) leads to dehydration and hypovolemia * Mild metabolic acidosis may occur (usually >7.3 and no anion gap) * Treatment= volume resuscitation, insulin, correct electrolytes

Answer 157

Microvascular: Neuropathy (sensory, motor, autonomic), Retinopathy, nephropathy Macrovascular: Coronary artery disease, Peripheral vascular disease, Cerebrovascular disease Other: Stiff joint syndrome, poor wound healing-> infection, cataracts, glaucoma

Answer 158

ANS dysfunction: * painless myocardial ischemia (referred pain pathways are dysfunctional) * Reduced vagal tone -> tachycardia * Risk of dysrhythmias * Orthostatic HoTN * Impaired respiratory compensation to hypoxia and hypercarbia -> increased sensitivity to anesthetic drugs * Delayed gastric emptying -> increased risk of aspiration * Impaired thermoregulation -> increased risk of hypothermia * regional anesthesia may worsen neurologic defects in the pt with diabetic polyneuropathy * Diarrhea and constipation

Answer 159

DM can cause glycosylation of the joints -> stiff joint syndrome with reduced ROM or AO joint the prayer sign suggests glycosylation and an increased risk of difficult intubation

Answer 160

MOA: Inhibit gluconeogenesis and glycogenolysis in the liver and decrease peripheral insulin resistance. Examples: metformin Key facts: * Does not cause hypoglycemia * Risk metabolic acidosis * Often used for polycystic ovarian dx

Answer 161

MOA: stimulate insulin secretion from pancreatic beta cells Examples: glyburide, glipizide, glimepiride key facts: * risk of hypoglycemia * avoid if there is a sulfa allergy

Answer 162

MOA: stimulate insulin secretion from pancreatic beta cells Examples: Repaglinide, Nateglinide Key facts: * Risk of hypoglycemia

Answer 163

MOA: decrease peripheral insulin resistance and increase hepatic glucose utilization Examples: Rosiglitazone, pioglitazone Key facts: * Does NOT cause hypoglycemia * Black box warning d/t risk of CHF

Answer 164

MOA: slows digestion and absorption of carbohydrates from the GI tract Examples: Acarbose, Miglitol Key facts: * Does NOT cause hypoglycemia

Answer 165

MOA: increases insulin release from beta cells, decreases glucagon release from alpha cells, and prolongs gastric emptying Examples: Exenatide, liraglutide Key facts: * Risk of hypoglycemia

Answer 166

MOA: increase insulin release from pancreatic beta cells and decrease glucagon release from alpha cells. Examples: Suffix- liptin Key facts: * risk of hypoglycemia

Answer 167

MOA: decrease glucagon release from pancreatic alpha cells and reduce gastric emptying Ex: pramlintide Key facts: * Risk of hypoglycemia if co-administered with insulin * Does not alter insulin levels * Does cause N/V

Answer 168

* highest risk if insulin is given during fasting * S/sx: SNS stimulation (tachycardia, HTN, Diaphoresis) * Difficult to diagnose under GA (even harder if pt is on beta-blocker) * Possible cause of delayed emergence * Rebound hyperglycemia (Somogyi effect) may cloud diagnosis * Tx: D50 (50-100mL) or glucagon (0.5-1mg IV or SQ)

Answer 169

Insulin allergy was more common when animal-derived insulin products were used. Chronic NPH use (or fish allergy) may sensitize the pt to protamine. This may not manifest until a large dose of protamine is administered (cardiac surgery)

Answer 170

* Epinephrine * Glucagon * Cortisol

Answer 171

* Monoamine oxidase inhibitors (Phenelzine, isocarboxide, selegine) * Salicylates (aspirin) * Tetracycline

Answer 172

Carcinoid syndrome is associated with the secretion of vasoactive substances from enterochromaffin cells. It is usually associated with tumors of the GI tract, but it can also arise from locations outside the GI tract as well (lungs) These tumors tend to release histamine, serotonin, kinins, and kallikrein

Answer 173

Histamine: Bronchoconstriction, Vasodilation, HoTN, flushing (head and neck) Kinins and Kallikrein: Bronchoconstriction, vasodilation, HoTN, flushing (head and neck), increases histamine release from mast cells Serotonin: Bronchoconstriction, vasoconstriction, HTN, supraventricular tachydysrhythmias, increased GI motility (diarrhea, abd pain) * the most common signs are flushing and diarrhea

Answer 174

Carcinoid crisis is life-threatening and can occur in pts with carcinoid syndrome. S/sx include: * Tachycardia * Hyper- or Hypotension * intense flushing * abd pain * diarrhea

Answer 175

* Somatostatin (octreotide or lanreotide) inhibits the release of vasoactive substances from carcinoid tumors * Antihistamines (H1 and H2: Diphenhydramine + ranitidine or cimetidine) * 5-HT3 antagonists * Steroids * Phenylephrine or vasopressin for HoTN

Answer 176

* Histamine releasing drugs: morphine, meperidine, atracurium, thiopental, and succinylcholine (if possible) * Succ's induced fasciculations can cause hormone release from the tumor * Exogenous catecholamines can potentiate hormone release * Sympathomimetic agents: ephedrine and ketamine

Answer 177

* Glomerulus * bowman's capsule * Proximal tubules * Distal tubules

Answer 178

loop of henle collecting duct

Answer 179

1. Maintenance of extracellular volume and composition 2. Blood pressure regulation 3. Excretion of toxins and metabolites 4. Maintenance of acid-base balance 5. Hormone production 6. blood glucose homeostasis

Answer 180

Antidiuretic hormone (ADH)

Answer 181

Aldosterone

Answer 182

1. lungs 2. Kidneys

Answer 183

1. Erythropoietin 2. Prostaglandins 3. Calcitriol (active vit D3)

Answer 184

it decreases 10% per decade

Answer 185

Afferent and efferent arterioles

Answer 186

1. myogenic 2. juxtaglomerular apparatus + tubuloglomerular feedback 3. Renin-angiotensin-aldosterone system 4. prostaglandins 5. Atrial natriuretic peptide 6. Sympathetic nervous system

Answer 187

1. decreased renal perfusion pressure 2. SNS activation 5. Tubuloglomerular feedback

Answer 188

Sodium * Plasma osmolarity = 2[Na+] + glucose/18 + BUN/2.8

Answer 189

280-290 mOsm/L

Answer 190

Mostly in the supraoptic nuclei of the hypothalamus, although the paraventricular nuclei produce a little bit

Answer 191

Peripheral vasoconstriction

Answer 192

Expansion of plasma volume via increased water reabsorption in the kidneys

Answer 193

Natriuretic peptides stimulate sodium and water excretion in the collecting ducts. They also inhibit renin release.

Answer 194

1. Prostaglandins 2. Natriuretic peptide 3. Dopamine

Answer 195

1. arterial blood pressure 2. afferent arteriole resistance 3. efferent arteriole resistance

Answer 196

substance is transferred from the tubule to the peritubular capillaries

Answer 197

substance is transferred from the peritubular capillaries to the tubule

Answer 198

substance is removed from the body in the urine

Answer 199

distal tubules

Answer 200

Ascending loop of henle

Answer 201

Spironolactone

Answer 202

1. to reduce potassium loss in a pt receiving a loop or thiazide diuretic 2. Secondary hyperaldosteronism amiloride is a potassium sparing diuretic

Answer 203

1. Hyperkalemia 2. Metabolic acidosis 3. gynecomastia 4. libido changes (spironolactone) 5. Nephrolithiasis (triamterene)

Answer 204

1. NSAIDs 2. Beta-blockers 3. ACE inhibitors

Answer 205

1. pre-existing kidney dx 2. Prolonged renal hypoperfusion 3. CHF 4. Advanced age 5. Sepsis 6. Jaundice 7. High risk surgery (use of aortic cross= clamp and liver transplant)

Answer 206

1. RIFLE 2. AKIN 3. KDIGO

Answer 207

Bleeding time

Answer 208

1. anemia 2. fatigue 3. N/V 4. Anorexia 5. Coagulopathy

Answer 209

decreased production of erythropoietin leads to normochromic normocytic anemia

Answer 210

Decreased excretion of non-volatile acids

Answer 211

1. high concentrations over a long period of time 2. low fresh gas glow 3. high temperature of CO2 absorbent 4. Increased CO2 production

Answer 212

Benzylisoquinolines: atracurium, cisatracurium, mivacurium

Answer 213

Fentanyl, sufentanil, afentanil, and remifenatnil. They dont produce active metabolites like morphine, meperidine, and hydromorphone (maybe)

Answer 214

1. Direct muscle trauma 2. muscle ischemia 3. prolonged immobilization 4. MH 5. Succ's in a pt with Duchenne muscular dystrophy

Answer 215

<110 mEq/L

Answer 216

2-5 mL/min of resection time

Answer 217

abdominal and shoulder pain

Answer 218

1. liver 2. spleen 3. stomach

Answer 219

1. pancreas 2. small intestine 3. colon

Answer 220

1. SNS stimulation 2. Pain 3. Hypoxia 4. propranolol

Answer 221

all transgastric views

Answer 222

RSI. Pts are at risk of gastric regurgitation and pulmonary aspiration. Also, not all pts will be NPO

Answer 223

1. Hyperventilation 2. D50+ insulin 3. Bicarbonate 4. Albuterol 5. Furosemide 6. CVVHD

Answer 224

1. nervous system 2. endocrine system

Answer 225

HoTN and prolonged QT interval

Answer 226

1. Parathyroid gland releases PTH 2. Osteoclasts in bone release Ca+2 3. Ca+2 is reabsorbed in the kidneys 4. Ca+2 absorption in the gut increases in the presence of vit D

Answer 227

cortisol, cortisone, aldosterone

Answer 228

aldosterone, it's 3,000 times more potent than cortisol

Answer 229

Prednisone. Of all the synthetic steroids, it most closely resembles cortisol

Answer 230

1. aldosteronoma 2. pheochromocytoma 3. primary hyperthyroidism

Answer 231

Renovascular HTN

Answer 232

* HTN * Hypokalemia * Metabolic alkalosis

Answer 233

1. attention to aseptic technique 2. Carefully position to reduce skin and bone injury 3. Consider post-op steroid supplementation 4. Diabetes insipidus following resection 5. Considerations for hyperaldosteronism

Answer 234

1. Transsphenoidal resection of the pituitary gland 2. Pituitary radiation 3. Adrenalectomy (if adrenal tumor)

Answer 235

1. Polyuria 2. Dehydration 3. Polydipsia

Answer 236

Increases formation of active vitamin D Stimulates bone resorption Inhibits renal calcium excretion

Answer 237

bile duct obstruction and erythrocyte destruction

Answer 238

A triad of features defines hepatopulmonary syndrome: an A-a gradient >15mmHg on room air or PaO2 <80mmHg, evidence of pulmonary vascular dilation (typically with demonstrable right-to-left shunt), and portal HTN (HVPG >5mmHg). A diagnosis or cirrhosis is not required for the diagnosis of HPS. High mean PAP and PVR with portal HTN are features of portopulmonary HTN. Again, cirrhosis is not required for the diagnosis of PPHTN.

Answer 239

Acute tubular necrosis (ATN), an intrinsic renal event, is the primary cause of perioperative acute kidney injury. ATN occurs following ischemia-reperfusion injury and/or as a result of the nephrotoxic effects of periopertative drug administration. volume depletion and/or HoTN are considered pre-renal events, while ureteral, bladder, or urethral obstruction are post-renal events

Answer 240

Nephrotoxic syndrome is characterized by excessive protein loss into the urine; this syndrome is often associated with chronic kidney disease. Chronic glomerulonephritis usually occurs as a result of antigen-antibody complexes accumulating in the glomerular membrane. This reduces the glomerular capillary filtration coefficient due to both thickened glomerular membranes and decreased numbers of glomerular capillaries. Pyelonephritis affects the function of the renal medulla impairing the countercurrent multiplication mechanism for concentrating urine; it is commonly associated with marked impairment of the ability to concentrate urine.

Kidney, liver, and endocrine complete Flashcards

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