Apex Unit 10 Kidney Liver Endocrine Flashcards
1
Q
All of the structures reside in the renal cortex EXCEPT the:
proximal tubule.
distal tubule.
collecting duct.
glomerulus
A
Collecting duct
The kidney is divided into the cortex and the medulla. The cortex is the outer region and the medulla is the inner region.
The nephron is the functional unit of the kidney. It consists of five major components: glomerulus, proximal tubule, loop of Henle, distal tubule, and collecting duct.
The renal cortex contains the glomeruli, proximal tubules, and distal tubules.
The renal medulla contains the loops of Henle and the collecting ducts.
2
Q
The kidney produces: (Select 3.)
aldosterone.
renin.
antidiuretic hormone.
angiotensinogen.
1,25 {OH]2 Vitamin D3.
erythropoietin.
A
Renin
Erythropoietin
1,25 {OH]2 Vitamin D3
Explanation:
The kidney responds to, as well as produces, a wide variety of hormones and enzymes. In this question, we asked about the compounds that are produced in the kidney.
Renin is produced by the juxtaglomerular apparatus - specifically in the fenestrated epithelium in the afferent arteriole.
Erythropoietin is synthesized in the kidney and is secreted in response to hypoxia.
Under control of parathyroid hormone, the kidneys convert inactive vitamin D3 to active vitamin D3 (1,25 [OH]2 vitamin D3).
Why are the other answers wrong?
Angiotensinogen is manufactured in the liver.
Aldosterone is synthesized in the adrenal cortex.
Antidiuretic hormone is produced by the supraoptic nuclei and paraventricular nuclei in the hypothalamus. It is released into the circulation from the posterior pituitary gland.
3
Q
Which statement BEST describes the pathway of blood through the kidney?
Glomerulus > proximal tubule > loop of Henle > distal tubule > collecting duct
Afferent arteriole > efferent arteriole > glomerular capillary bed > peritubular capillary bed
Glomerular capillary bed > afferent arteriole > peritubular capillary bed > efferent arteriole
Afferent arteriole > glomerular capillary bed > efferent arteriole > peritubular capillary bed
A
Afferent arteriole > glomerular capillary bed > efferent arteriole > peritubular capillary bed
Explanation:
At any given time, there are two types of fluid moving through the kidney: blood and tubular fluid. Knowing both pathways is essential to understanding the filtration, reabsorption, and secretion functions of the kidney.
The correct order for renal blood flow is: afferent arteriole > glomerular capillary bed > efferent arteriole > peritubular capillary bed.
4
Q
Which factor increases renin release?
Positive end expiratory pressure
Hypervolemia
Angiotensinogen
Increased chloride delivery to the macula densa
A
Positive end expiratory pressure
Explanation:
Renin release is increased by three things: reduced renal perfusion, beta-1 activation, and decreased sodium and chloride delivery to the distal tubule.
PEEP reduces venous return and may reduce cardiac output. By extension, this reduces renal perfusion and stimulates renin release.
5
Q
Antidiuretic hormone:
increases sodium reabsorption in the proximal tubule.
is produced in the posterior pituitary gland.
upregulates aquaporin-2 channels.
agonizes the V1 receptor to decrease cAMP.
A
Upregulates aquaporin-2 channels
Explanation:
ADH upregulates aquaporin-2 channels in the collecting ducts. This facilitates water reabsorption and restores blood volume and serum osmolarity.
Why are the other answers wrong?
ADH is produced in the supraoptic and paraventricular nuclei of the hypothalamus. It is released from the posterior pituitary gland.
ADH agonizes the V2 receptor (not V1) and increases (not decreases) cAMP.
It increases water reabsorption in the collecting ducts (not proximal tubule).
6
Q
All of the following enhance renal perfusion EXCEPT:
thromboxane A2.
fenoldopam.
PGE2.
atrial natriuretic peptide.
A
Thromboxane A2
Explanation:
Thromboxane A2 is a renal vasoconstrictor. Its production is increased during renal ischemia.
7
Q
Which condition increases glomerular filtration rate?
Afferent arteriolar constriction
Increased efferent arteriolar resistance
Cyclooxygenase inhibition
Increased plasma protein
A
Increased efferent arteriolar resistance
Explanation:
Glomerular filtration is dependent on renal blood flow and the hydrostatic pressure at Bowman’s capsule.
Constriction of the efferent arteriole increases hydrostatic pressure and GFR.
Constriction of the afferent arteriole reduces RBF and GFR.
Increased plasma protein raises plasma oncotic pressure and reduces GFR.
Cyclooxygenase inhibition by NSAIDs increases renal vascular resistance and reduces RBF and GFR.
8
Q
Identify the BEST tests of tubular function. (Select 2.)
BUN
Urine osmolality
Fractional excretion of sodium
Creatinine clearance
A
Fractional excretion of sodium
Urine osmolality
Explanation:
Renal function tests assess glomerular filtration or tubular function.
Tests of GFR: BUN and creatinine clearance
Tests of tubular function: fractional excretion of sodium and urine osmolality
9
Q
Anesthetic considerations for acute kidney injury include: (Select 2.)
diuretics should be used to convert oliguric to nonoliguric AKI.
hydroxyethyl starches are associated with an increased risk of renal morbidity.
renal dose dopamine prevents AKI.
prerenal azotemia can cause acute tubular necrosis.
A
Prerenal azotemia can cause acute tubular necrosis
Hydroxyethyl starches are associated with an increased risk of renal morbidity
Explanation:
Why are the other answers wrong?
Renal dose dopamine does not prevent nor treat acute kidney injury.
Attempting to convert oliguric to nonoliguric AKI with diuretics increases risk of additional renal injury as well as mortality.
10
Q
Pathophysiologic considerations for end-stage renal disease include: (Select 3.)
megaloblastic anemia.
secondary hyperparathyroidism.
gap metabolic acidosis.
obstructive ventilatory defect.
increased bleeding time.
increased prothrombin time.
A
Increased bleeding time
Gap metabolic acidosis
Secondary hyperparathyroidism
Explanation:
Uremia increases bleeding time.
A gap metabolic acidosis is the result of accumulation of non-volatile acids.
Secondary hyperparathyroidism occurs as a result of impaired active vitamin D3 production and hyperphosphatemia.
Why are the other answers wrong?
PT, PTT, and platelet count are normal.
Erythropoietin production is reduced. This contributes to a normocytic normochromic anemia. Megaloblastic anemia is associated with nitrous oxide.
Fluid overload creates a restrictive ventilatory defect (not obstructive).
11
Q
Drugs to avoid in the patient on dialysis include: (Select 2.)
meperidine.
succinylcholine.
dexmedetomidine.
vecuronium.
A
Meperidine
Vecuronium
Explanation:
This question asks about drugs that produce active metabolites that might increase morbidity in the patient with renal dysfunction.
Meperidine is metabolized to normeperidine. Accumulation of normeperidine can cause convulsions.
Vecuronium is metabolized to 3-OH vecuronium. Its duration is prolonged as a function of decreased clearance and an increased elimination half-life.
Succinylcholine and dexmedetomidine are ok to to use in the patient on dialysis, however there are some stipulations. When approaching a question like this, you’ll need to learn how to see through the shades of grey.
12
Q
All of the following reduce the incidence of contrast induced nephropathy EXCEPT:
sodium bicarbonate.
low-osmolar contrast dye.
furosemide.
fluid bolus with 0.9% NaCl.
A
Furosemide
In most cases, acute kidney injury is preventable when radiocontrast media is used.
Preventative strategies include: intravenous hydration with 0.9% NaCl, low- or iso-osmolar contrast, and sodium bicarbonate.
Furosemide can reduce intravascular volume, concentrate radiocontrast media inside the kidney, and worsen kidney injury.
13
Q
For the patient undergoing transurethral resection of the prostate, match each irrigation fluid with its unique anesthetic consideration.
A
Distilled water + Hemolysis
Glycine + Transient blindness
Sorbitol + Hyperglycemia
Normal saline + Risk of electrocution
TURP requires a continuous fluid source to facilitate visualization and irrigation of the bladder and prostate.
The ideal irrigation fluid provides good surgical visibility, is isotonic, and is absent of toxicity. Read on to review the key differences between each of the irrigation fluids (and a whole lot more).
14
Q
Which finding represents an absolute contraindication to extracorporeal shock wave lithotripsy?
Diabetes
Pregnancy
Morbid obesity
Pacemaker
A
Pregnancy
You’ll need to understand the differences between absolute and relative contraindications to ESWL. Absolute contraindications include pregnancy and bleeding disorders/anticoagulation.
Morbid obesity and the presence of a pacemaker are relative contraindications.
15
Q
Which structure is responsible for eliminating bacteria from the liver?
Sinusoid
Canaliculus
Kupffer cell
Acinus
A
Kupffer cell
The acinus (otherwise known as the liver lobule) is the functional unit of the liver.
The Kupffer cells are a type of reticuloendothelial cell that are responsible for removing bacteria and viruses that enter the liver from the intestine.
The sinusoids receive blood from the hepatic artery and portal vein. They contain large pores that permit easy passage of large molecules from the blood to the hepatocytes. The Kupffer cells are located in the sinusoids.
Bile canaliculi collect bile that’s produced by the hepatocytes.
16
Q
Which statement MOST accurately describes hepatic perfusion?
The hepatic artery provides 75 percent of liver blood flow.
The portal vein provides 50 percent of liver blood flow.
The hepatic artery provides 75 percent of the liver’s oxygen content.
The portal vein provides 50 percent of the liver’s oxygen content.
A
The portal vein provides 50 percent of the liver’s oxygen content
The liver receives a dual blood supply. It receives blood from the hepatic artery and the portal vein.
The hepatic artery provides 25 percent of liver blood flow and 50 percent of the liver’s oxygen content. It provides comparably less blood than the portal vein, but it has a higher O2 content.
The portal vein provides 75 percent of liver blood flow and 50 percent of the liver’s oxygen content. It provides comparatively more blood than the hepatic artery, but because the portal vein contains blood that has passed through the splanchnic organs, it’s O2 content is less.
17
Q
Hepatocytes produce: (Select 3)
thrombopoietin. alpha-1-acid glycoprotein. immunoglobulins. factor III. factor VII. factor VIII.
A
Thrombopoietin
Alpha-1-acid glycoprotein
Factor VII
Of all of the procoagulant proteins, factor VII has the shortest half-life. This explains why the PT is an early indicator of synthetic dysfunction.
Factor VIII is produced by the sinusoids and NOT by the hepatocytes. If the question asked about which factors are produced in the liver (not specific to the hepatocyte), then factor VIII would be a correct answer choice.
Factor III is produced by the vascular endothelium.
18
Q
Match each laboratory test with its underlying pathology.
A
Bilirubin + Hepatic clearance
Transaminases + Hepatocellular injury
Prothrombin time + Synthetic function
5’-nucleotidase + Biliary obstruction
There’s too much to cover here, but you’ll find everything you need on the next page.
19
Q
Select the statements that BEST describe hepatitis. (Select 2)
Alcohol abuse is the most common cause of chronic hepatitis.
Halothane hepatitis is an immune-mediated response.
Hepatitis A usually causes cirrhosis.
Hepatitis is usually transmitted via blood transfusion.
A
Halothane hepatitis is an autoimmune response
Alcohol abuse is the most common cause of chronic hepatitis
Hepatitis A is the most common form of viral hepatitis.
Hepatitis B and C (not A) can cause cirrhosis.
Hepatitis B and C can be transmitted in a blood transfusion, while hepatitis A and E are transmitted by the oral-fecal route. Hepatitis D is a co-infection that occurs with hepatitis B.
Halothane is metabolized to inorganic fluoride ions and trifluoroacetic acid (TFA). TFA can produce an immune mediated response leading to hepatitis.
Alcohol abuse is the most common cause of chronic hepatitis.
20
Q
All the following drugs should be avoided in the patient with acute hepatitis EXCEPT:
propranolol.
acetaminophen.
tetracycline.
amiodarone.
A
Propranolol
Propranolol is a non-selective beta-blocker that reduces portal pressure by two processes:
Decreased cardiac output (beta-1)
Splanchnic vasoconstriction (beta-2)
This makes it a useful drug in the patient with hepatitis and elevated portal pressure. Propranolol is also useful in the patient with esophageal varices.
For the patient with acute hepatitis, you should avoid drugs that are hepatotoxic or inhibit CYP450 isoenzymes.
Acetaminophen, amiodarone, and tetracycline can cause hepatotoxicity.
21
Q
Common physiologic changes in the patient with cirrhosis include all of the following EXCEPT:
decreased glomerular filtration rate.
increased cardiac output.
respiratory acidosis.
right-to-left shunt.
A
Respiratory acidosis
Patients with cirrhosis experience pulmonary vasodilation, right-to-left shunting, and hypoxemia. They hyperventilate in an effort to offset the reduction in PaO2. This creates a respiratory alkalosis (not acidosis).
A hyperdynamic circulation is common. Said another way, the SVR decreases with a reciprocal rise in CO. GFR is reduced.
22
Q
Match each phase of liver transplantation with its MOST likely complication.
A
Pre-anhepatic phase + Pulmonary aspiration of gastric contents
Anhepatic phase + Profound reduction of cardiac output
Neohepatic phase + Hyperkalemia
You must understand the time course of the three phases of liver transplantation. We’ll cover these in detail on the next page.
23
Q
All the following drugs improve biliary hypertension EXCEPT:
naloxone.
octreotide.
glucagon.
nitroglycerine.
A
Octreotide
Contraction of the sphincter of Oddi can increase biliary pressure. This may lead to two possible consequences:
Biliary colic
False-positive result of intraoperative cholangiogram
Drugs that relax the sphincter of Oddi and reduce biliary pressure include:
Glucagon Glycopyrrolate Atropine Naloxone Nitroglycerine Administering naloxone to an intraoperative patient is a poor choice, particularly when there are other alternatives available. Although there is some debate, octreotide (a somatostatin analogue) can increase biliary pressure.
24
Q
Match each term with its definition.
A
Endocrine function + Hormone enters the blood and acts at distant site
Paracrine function + Hormone acts adjacent to its site of origin
Autocrine function + Hormone acts at its site of origin
25
Which hormones are released by the anterior pituitary gland? (Select 3.)
Corticotropin-releasing hormone
Antidiuretic hormone
Prolactin
Growth hormone
Oxytocin
Luteinizing hormone
Prolactin
Luteinizing hormone
Growth hormone
Many of you will encounter a question like this one. Know which hormones are released by each region of the pituitary gland!
The posterior pituitary releases two hormones:
Antidiuretic hormone
Oxytocin
```
The anterior pituitary releases six hormones. You can remember these with the mnemonic "FLAT PiG"
Follicle stimulating hormone
Luteinizing hormone
Adrenocorticotropin
Thyroid stimulating hormone
Prolactin
ignore
Growth hormone
```
You should also be able to recognize the differences between the hypothalamic hormones and their corresponding pituitary hormones. All of these have either "releasing" or "inhibitory" in their name. We added corticotropin-releasing hormone to confuse you.
26
Anesthetic considerations for the patient with diabetes insipidus include:
three percent sodium chloride.
sodium restriction.
DDAVP.
demeclocycline.
DDAVP
Diabetes insipidus is caused by either inadequate ADH production or renal tubules that are not responsive to ADH. Either way, this causes a tremendous water loss from the body (up to 18+ L/day).
The most common cause of DI is pituitary surgery.
Treatment consists of DDAVP (a selective V2 agonist).
SC = 0.5 - 2 mcg bid.
Nasal = 5 - 40 mcg qd
The syndrome of inappropriate ADH is caused by too much ADH; the body retains too much water. Treatment includes: fluid restriction, hypertonic saline, and demeclocycline.
27
When compared to T4, which statements BEST describe T3? (Select 2.)
More protein bound
Shorter half-life
Higher concentration in the blood
Higher potency
Higher potency
Shorter half-life
You must be able to compare and contrast T4 to T3.
T4 is a prohormone
T3 has greater biologic activity
When compared to T4, the following are true of T3:
Higher potency
Shorter half-life
Less protein bound
Smaller concentration in the blood (bound + unbound fractions)
28
All of the following are consequences of excess thyroid hormone EXCEPT:
vasodilation.
hypoventilation.
tremors.
diarrhea.
Hypoventilation
Thyroid hormones increase the metabolic activity of nearly all the cells in the body. You must remember:
↑ Thyroid hormone → ↑ BMR → ↑ VO2 + ↑ CO2 Production
Vasodilation results from increased oxygen consumption. This helps improve tissue blood flow and oxygen delivery.
Increased carbon dioxide production requires that the patient increase (not decrease) minute ventilation.
Thyroid hormone excess increases the sensitivity of neuronal synapses in the spinal cord, leading to tremors.
Intestinal hypermotility results in diarrhea (risk of fluid and electrolyte imbalance).
29
A patient with untreated hyperthyroidism and atrial fibrillation presents for emergency surgery. What is the BEST intervention at this time?
Propylthiouracil
Esmolol
Amiodarone
Delay surgery until a euthyroid state is achieved
Esmolol
The hyperthyroid patient presenting for non-emergency surgery should be cancelled and managed medically until a euthyroid state is achieved. This patient requires an emergent operation, so you don't have the luxury of canceling.
Esmolol is the best option. It reduces the SNS response, and it's easily titratable. Having said this, propranolol is the only beta-blocker that inhibits the peripheral conversion of T4 to T3.
Propylthiouracil inhibits the conversion of T4 to T3, however this requires days to begin to take effect. You don't have this much time.
We said that this patient has atrial fibrillation (a common consequence of hyperthyroidism). Amiodarone would treat this, however it contains a significant amount of iodine by weight. An important side effect of this drug is that it can cause hyper- or hypothyroidism. As such, it has the potential to worsen this patient's condition.
30
All of the following are anesthetic considerations for myxedema EXCEPT:
hypernatremia.
low cardiac output.
restrictive lung disease.
impaired drug metabolism.
Hypernatremia
Hypothyroidism in its most severe form is called myxedema. This affects all the organ systems in the body.
Lack of thyroid hormone decreases heart rate, contractility, and cardiac output.
Pleural and pericardial effusions are common.
In the liver, decreased metabolism manifests as slowed biotransformation reactions.
Inappropriate secretion of ADH is common, so these patients retain free water. This contributes to a dilutional hyponatremia (not hypernatremia). Edema is a common finding.
31
Match each region of the adrenal gland with the class of hormones it produces.
Zona glomerulosa + Mineralocorticoids
Zona fasciculata + Glucocorticoids
Zona reticularis + Androgens
The adrenal gland is composed of the cortex (outer region) and medulla (inner region). You must know which hormones are produced in which regions.
Adrenal cortex:
Zona glomerulosa - mineralocorticoids (aldosterone)
Zona fasciculata - glucocorticoids (cortisol)
Zona reticularis - androgens (dehydroepiandrosterone)
Adrenal medulla:
Catecholamines (epinephrine and norepinephrine)
32
Order each drug in terms of its glucocorticoid potency.
(One is the most potent and four is the least potent)
Dexamethasone + 1
Methylprednisolone + 2
Cortisol + 3
Aldosterone + 4
33
Match each disease to its underlying pathophysiology.
Cushing's syndrome + Excess cortisol
Addison's disease + Inadequate cortisol
Conn's syndrome + Excess aldosterone
*Inadequate aldosterone almost never occurs in isolation.
34
Signs of Cushing's syndrome include: (Select 4.)
```
hypertension.
hypotension.
hyperkalemia.
hypokalemia.
metabolic alkalosis.
metabolic acidosis.
hyperglycemia.
hypoglycemia.
```
Hypertension
Hypokalemia
Metabolic alkalosis
Hyperglycemia
Cushing's syndrome results when the anterior pituitary gland releases an excessive amount of ACTH, which in turn increases cortisol release from the zona fasciculata of the adrenal cortex.
Remember that cortisol has glucocorticoid, mineralocorticoid, and androgenic effects.
35
A patient with adrenal insufficiency and sepsis requires an emergency intubation in the intensive care unit. Which drug should be avoided?
Etomidate
Propofol
Thiopental
Ketamine
Etomidate
Adrenal insufficiency is characterized by the destruction of all the cortical zones. This manifests as decreased production of mineralocorticoids, glucocorticoids, and androgens.
By inhibiting 11-beta-hydroxylase, a single induction dose of etomidate causes adrenocortical suppression for > 8 hours. This could potentially convert adrenal insufficiency to acute adrenal crisis.
Ketamine is often an attractive option in this context, but be aware that its negative inotropic properties can be unmasked in this patient population.
36
Match each pancreatic hormone with the cell type that produces it.
Glucagon + Alpha cells
Insulin + Beta cells
Somatostatin + Delta cells
Pancreatic polypeptide + PP cells
The pancreas produces two types of hormones:
Exocrine hormones are secreted into the duodenum for digestion (produced by the acini tissue).
Endocrine hormones are secreted into the systemic circulation for metabolism (produced by the islets of Langerhans).
37
Compared to type I diabetes mellitus, choose the statements that MOST accurately describe type II diabetes mellitus. (Select 2.)
It is usually caused by an autoimmune response.
Is usually associated with a thin body habitus.
It is more likely to cause hyperglycemic hyperosmolar syndrome.
Peripheral sensitivity to insulin is reduced.
Peripheral sensitivity to insulin is reduced
It is more likely to cause hyperglycemic hyperosmolar syndrome
You'll need to be able to distinguish between the key features of T1DM and T2DM.
T1DM is:
Caused by beta cell destruction.
Most commonly caused by an autoimmune response.
Typically associated with a thin and wasting body habitus.
Is more likely to be associated with diabetic ketoacidosis.
T2DM is:
Usually caused by obesity.
Associated with a relative lack of insulin production and peripheral insulin resistance.
Is more likely to be associated with hyperglycemic hyperosmolar syndrome.
38
All of the following can mask the signs of intraoperative hypoglycemia EXCEPT:
propranolol.
general anesthesia.
diabetic autonomic neuropathy.
hydrochlorothiazide.
Hydrochlorothiazide
Intraoperative hypoglycemia can be difficult to diagnose. As serum glucose falls, the SNS is activated and circulating epinephrine stimulates gluconeogenesis and glycogenolysis in the liver to restore a normal serum glucose concentration.
Anything that blunts the SNS response can potentially mask the signs of intraoperative hypoglycemia. Examples include: general anesthesia, diabetic autonomic neuropathy, and beta-blockers (propranolol).
Thiazide diuretics have a unique side effect in that they increase serum glucose. Hyperglycemia is a side effect of these drugs (hydrochlorothiazide, metolazone, and indapamide).
39
Match each oral hypoglycemic agent with its unique risk.
Metformin + Lactic acidosis
Glyburide + Cross sensitivity with sulfa allergy
Rosiglitazone + Promotes edema
Metformin disrupts mitochondrial function, ultimately reducing the intracellular concentration of ATP. Recall that pyruvate is the final product of glycolysis, and in the setting of mitochondrial dysfunction, the cell will shift to anaerobic metabolism, and produces lactate.
Glyburide is a sulfonylurea. This class of agents can cause an immunologic response in patients with a sulfa allergy.
Rosiglitazone expands the ECF, which can lead to edema.
40
Which insulin preparation can be administered intravenously?
Very rapid-acting
Rapid-acting
Intermediate-acting
Long-acting
Rapid acting
Insulin preparations can be divided into the following groups:
```
Very rapid-acting
Rapid-acting
Intermediate-acting
Long-acting
Ultra long-acting
Only regular insulin can be given IV (or IM), and regular insulin is the only short acting insulin in commercial use.
```
41
Which drugs should be avoided in the patient with carcinoid syndrome? (Select 3.)
```
Vasopressin
Octreotide
Ketamine
Rocuronium
Morphine
Norepinephrine
```
Ketamine
Norepinephrine
Morphine
Carcinoid syndrome is associated with 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 of the GI tract as well.
We tend to avoid drugs that can precipitate hormone release by the tumor, therefore avoid drugs that:
Release histamine (morphine)
Stimulate the SNS (ketamine)
Augment hormone release (norepinephrine)
Octreotide is a primary treatment for carcinoid syndrome, rocuronium doesn't release histamine, and vasopressin is an acceptable treatment for hypotension.
42
Which of the following are increased in the serum of the patient with renal osteodystrophy? (Select 2.)
Parathyroid hormone
Calcitriol
Phosphate
Calcium
Phosphate
Parathyroid hormone
There are two "P's" that are increased in the patient with renal osteodystroPhy: phosphate and parathyroid hormone. Here's why...
The active form of vitamin D (calcitriol) is produced by the kidney. When the kidney fails to produce calcitriol, the body absorbs less calcium from the GI tract and serum calcium falls.
As a result, parathyroid hormone output is increased. This causes demineralization of calcium from bone, which aims to restore the serum calcium level. The tradeoff is that the bones become weaker and more susceptible to fractures.
As GFR declines (remember this patient has kidney disease), phosphate clearance is reduced, thereby increasing the serum phosphate concentration.
43
Identify the MOST potent stimulators of antidiuretic hormone secretion. (Select 2.)
Hypernatremia
Hyponatremia
Hypervolemia
Hypovolemia
Hypernatremia
Hypovolemia
ADH is produced in the supraoptic and paraventricular nuclei of the hypothalamus. It is released by the posterior pituitary gland.
There are two mechanisms that control ADH secretion:
1. Osmolarity of the ECF (think sodium concentration):
Increased ECF osmolarity → shrinkage of osmoreceptors in the hypothalamus → ↑ ADH secretion.
2. Blood Volume:
↓ Blood volume → baroreceptor unloading in the carotid bodies, transverse aortic arch, great veins, and right atrium → ↑ ADH secretion.
44
Which substances are produced by the kidney? (Select 2.)
Antidiuretic hormone
Renin
Angiotensin II
Erythropoietin
Renin
Erythropoietin
Erythropoietin signals stem cells in the bone marrow to produce erythrocytes. Patients with renal failure make less erythropoietin, and this explains why they develop normochromic, normocytic anemia.
Renin is released by the juxtaglomerular apparatus in response to decreased renal perfusion. Renin release is the first step in the renin-angiotensin aldosterone system.
The kidneys do not produce antidiuretic hormone or angiotensin II.
45
Match each substance with its primary site of production.
Angiotensinogen + Liver
Angiotensin I + Systemic circulation
Angiotensin II + Lung
Aldosterone + Zona glomerulosa
The renin-angiotensin-aldosterone system is a hormone based system that moderates long term blood pressure control and fluid balance. There's lots of information on this page, but you MUST know all of it!
Stimulus for RAAS Activation:
The juxtaglomerular apparatus of the afferent arteriole releases renin when there is decreased renal perfusion, hypovolemia, hyponatremia, or SNS activation.
Angiotensinogen → AT I → AT II → Aldosterone:
Renin converts angiotensinogen (produced in the liver) to angiotensin I (AT I). This occurs in the systemic circulation.
Angiotensin converting enzyme (produced in the lung) converts AT I to angiotensin II (AT II).
AT II stimulates aldosterone release from the zona glomerulosa in the adrenal cortex. It is also a potent vasoconstrictor.
Function of Aldosterone:
Aldosterone acts on the principal cells in the kidney. This restores plasma volume and blood pressure by promoting Na+ and water retention.
Aldosterone also causes potassium excretion.
46
A BUN/creatinine ratio of 30 to one most likely suggests: (Select 2.)
acute tubular necrosis.
upper GI bleeding.
dehydration.
interstitial nephritis.
Dehydration
GI bleeding
Creatinine is a waste product of muscle metabolism, and urea is a waste product of protein metabolism.
The BUN/creatinine ratio is a common laboratory test that is used to distinguish between prerenal and intrinsic kidney injury. A normal BUN/creatinine is 10:1.
Both BUN and creatinine are freely filtered at the glomerulus. The difference is that BUN can undergo reabsorption in the renal tubules, while creatinine generally passes into the urine (no reabsorption or secretion).
When the kidneys conserve more water, they increase tubular reabsorption, pulling BUN back into the blood. Because BUN is returned to the blood, but creatinine is not, the BUN/creatinine ratio increases.
The differential diagnosis of an increased BUN/creatinine ratio includes dehydration, obstructive uropathy, increased protein intake, and upper GI bleeding.
Why upper GI bleeding? In the gut, heme is broken down into protein and this protein is metabolized to urea (among other things). The urea is absorbed into the systemic circulation, which ultimately increases the urea load to the kidneys. Dehydration can compound the issue.
47
The glomerular filtration rate is normally:
125 mL/min.
275 mL/min.
450 mL/min.
650 mL/min.
125 mL/min
Key numbers to know:
Renal blood flow = 650 mL/min (to each kidney) or ~ 20 percent of the cardiac output
Glomerular filtration rate = 125 mL/min
Filtration fraction = 20 percent of renal blood flow (125/650)
Fraction of ultrafiltrate excreted as urine = ~ 1 percent
48
A creatinine clearance of 70 mL/min suggests:
normal renal function.
mild renal dysfunction.
moderate renal dysfunction.
severe renal dysfunction.
Mild renal dysfunction
Creatinine clearance provides the best estimation of the glomerular filtration rate.
Values to know:
Normal = 95 - 150 mL/min
Mild dysfunction = 50 - 80 mL/min
Moderate dysfunction = 10 - 25 mL/min
Severe renal dysfunction = < 10 mL/min
49
Calculate the glomerular filtration rate for this male patient:
```
Age = 60 years
Weight = 70 kg
Serum creatinine = 2.0 mg/dL
(Enter your answer as mL/min and round to the nearest whole number)
```
39
You must know the Cockroft-Gault GFR calculation for men and women.
Creatinine clearance for a man:
(140 - age) x (weight kg) / (Serum creatinine x 72)
(140 - 60) x 70 / (2 x 72) = 39 mL/min
50
Calculate the glomerular filtration rate for this female patient:
```
Age = 40 years
Weight = 80 kg
Serum creatinine = 0.9 mg/dL
(Enter your answer as mL/min and round to the nearest whole number)
```
105 mL/min
You must know the Cockroft-Gault GFR calculation for men and women.
Creatinine clearance for a woman:
Because women generally have a smaller muscle mass, we multiple the same equation we use for a man by 0.85.
0. 85 x [(140 - age) x (weight kg) / (Serum creatinine x 72)]
0. 85 x [(140 - 40) x 80 / (0.9 x 72)] = 105 mL/min
51
Which physiologic change increases glomerular filtration?
Increased plasma osmotic pressure
Decreased renal blood flow
Increased resistance at the afferent arteriole
Constriction of the efferent arteriole
Constriction of the efferent arteriole
Glomerular hydrostatic pressure is the most important determinant of GFR.
There are three determinants of glomerular hydrostatic pressure:
1. Arterial blood pressure
2. Afferent arteriole resistance
3. Efferent arteriole resistance
Arterial Blood Pressure:
Renal blood flow (RBF) is regulated by renal vascular resistance.
By adjusting renal vascular resistance, autoregulation ensures a constant RBF when MAP = 60 - 160. This provides a constant GFR as well. (Please note that the books will cite different ranges of renal autoregulation).
Outside of the boundaries of autoregulation, RBF and GFR are directly proportional to MAP.
Afferent Arteriole Resistance:
The afferent arteriole determines how much blood is delivered to the glomerulus.
Constriction of the afferent arteriole reduces GFR
Dilation of the afferent arteriole increases GFR.
Efferent Arteriole Resistance:
Constriction of the efferent arteriole follows a biphasic pattern.
Mild constriction reduces flow towards the peritubular capillaries and increases GFR, while excessive constriction reduces renal blood flow as well as GFR.
Dilation of the efferent arteriole increases flow towards the peritubular capillaries and reduces GFR.
52
Arginine vasopressin increases the glomerular filtration rate by causing:
dilation of the afferent arteriole.
dilation of the efferent arteriole.
constriction of the afferent arteriole.
constriction of the efferent arteriole.
Constriction of the efferent arteriole
Potent vasopressors are often required to combat hypotension. Norepinephrine and vasopressin are two options.
Norepinephrine vasoconstricts the afferent arteriole, reducing glomerular filtration. This can contribute to acute renal injury.
Vasopressin constricts the efferent arteriole, increasing glomerular filtration. For this reason, it's a better option to preserve renal function when a potent vasopressor is required.
53
Identify the laboratory tests that reflect the concentrating ability of the kidney. (Select 2.)
Urine specific gravity
Creatinine clearance
Blood urea nitrogen
Fractional excretion of sodium
Urine specific gravity
Fractional excretion of sodium
Renal function tests provide assessment of either:
1. Glomerular function - measured by GFR
2. Tubular function - measured by concentrating ability
Tests of GFR:
Blood urea nitrogen (10 - 20 mg/dL)
Serum creatinine (0.7 - 1.5 mg/dL)
Creatinine clearance (110 - 150 mL/min)
Tests of tubular function (concentrating ability):
Fractional excretion of Na+ (1 - 3%)
Urine osmolality (65 - 1400 mOsm/L)
Urine sodium concentration (130 - 260 mEq/day)
Urine specific gravity (1.003 - 1.030)
54
A patient with end-stage renal disease is scheduled for a fem-fem bypass. Which of the following lab values are MOST likely to be abnormal? (Select 2.)
PT/PTT
Bleeding time
Platelet count
Hemoglobin
Hemoglobin
Bleeding time
Uremia is caused by the kidney’s inability to excrete urea and other nitrogenous waste products.
In the patient with end-stage renal disease, uremia impairs platelet function (not count). This is best measured by bleeding time.
These patients are at risk of bleeding even if the PT, PTT, and platelet counts are normal. Dialysis within 24 hours of surgery reduces uremia and improves bleeding time.
Treatment for uremic bleeding consists of replenishing von Willebrand factor VIII with desmopressin (first choice). Cryoprecipitate is an alternative, but it carries the risk of viral transmission.
Remember that erythropoietin is synthesized by the kidney, and patients with ESRD are often anemic as a result. It’s ok for them to be mildly anemic (that’s where they live), and you must always consider the risk of HLA sensitization and future rejection of a transplanted kidney.
55
Using the Acute Kidney Injury Network model for kidney injury, match each stage of acute kidney injury with the clinical finding that best defines it.
Serum creatinine 50 percent over baseline
Urine output < 0.5 ml/kg/hr x 12 hours
Serum creatinine > 4 mg/dL
Stage II
Stage 1
Stage III
stage 1 Serum creatinine 50 percent over baseline
stage 2 Urine output < 0.5 ml/kg/hr x 12 hours
stage 3 Serum creatinine > 4 mg/dL
There are two systems that we use to classify kidney injury:
RIFLE
AKIN
Both focus on serum creatinine and urine output.
They are almost identical except for the two additions on the RIFLE continuum.
While reviewing labs prior to surgery, these indices can help you stratify perioperative risk.
56
Which of the following are causes of prerenal azotemia? (Select 3.)
```
Abdominal compartment syndrome
Aortic artery clamping
Congestive heart failure
Bladder carcinoma
Aminoglycoside toxicity
Acute glomerulonephritis
```
Aortic artery clamping
Congestive heart failure
Abdominal compartment syndrome
Azotemia is an elevation in blood nitrogen levels (azot = nitrogen + -emia = blood).
```
Prerenal azotemia (or prerenal failure) is caused by inadequate renal perfusion (not enough pressure or obstruction to renal flow). Examples include:
Hypotension
Hypovolemia
Hemorrhage
Congestive heart failure
GI fluid loss
Burns
Sepsis
Trauma
Hepatic failure
Aortic or renal artery clamp placement
Abdominal compartment syndrome
Thromboembolism
Prerenal azotemia is reversed by addressing the underlying cause. If not treated, prerenal azotemia can progress to acute tubular necrosis.
```
57
Etiologies of intrarenal azotemia include: (Select 3.)
```
Vasculitis
Bladder carcinoma
Interstitial nephritis
Nephrolithiasis
Acute tubular necrosis
Ureteral clot
```
Acute tubular necrosis
Interstitial nephritis
Vasculitis
Intrarenal azotemia is another name for intrinsic kidney injury. Etiologies include:
Acute tubular necrosis (aminoglycosides, IV contrast, ischemia, myoglobin)
Acute glomerulonephritis
Vasculitis
Interstitial nephritis (allergic reactions to drugs)
```
Causes of postrenal azotemia include:
Nephrolithiasis (kidney stones)
Obstructive clots
Bladder carcinoma
Benign prostatic hyperplasia
```
58
What is the BEST way to prevent contrast-induced nephrotoxicity?
N-Acetylcysteine
Mannitol
Fenoldopam
Normal saline bolus
Sodium chloride bolus
The best way to prevent contrast-induced nephrotoxicity is adequate intravenous hydration.
Second tier methods include:
Sodium bicarbonate injection or infusion
Low volume of nonionic iso-osmolar contrast agents
Other methods have provided conflicting results. These include:
Mannitol
Fenoldopam
N-Acetylcysteine
59
What is the BEST method of renal protection following major muscle trauma?
N-acetylcysteine
Acidifying the urine
Mannitol
Norepinephrine
Mannitol
Rhabdomyolysis and myoglobinemia are sequelae of direct muscle trauma, acute muscle ischemia, and prolonged immobilization.
In the healthy myocyte, myoglobin binds oxygen. When the muscle is injured, myoglobin is released into the systemic circulation where it is highly toxic!
Myoglobin is freely filtered by the glomerulus, and in the presence of acidic urine (pH < 5.6), it is converted to ferrihematin. This substance precipitates and clogs the renal tubules. Additionally, myoglobin scavenges nitric oxide leading to renal vasoconstriction and ischemia.
The best way to prevent acute kidney injury is to maintain a urine output between 100 - 150 mL/hr. This is best accomplished by osmotic diuresis with mannitol.
The urine pH should be kept above 5.6 with sodium bicarbonate and/or acetazolamide.
60
Identify the theoretical concerns that accompany the administration sevoflurane to the patient with renal dysfunction. (Select 2.)
Trifluoroacetic acid
Carbon monoxide
Compound A
Fluoride
Fluoride
Compound A
There are two ways that sevoflurane can theoretically impair renal function. Before we go any further, however, we'd like to point out that there is no solid human data that supports these concerns.
1. Compound A (produced in the breathing circuit):
Compound A is produced when sevoflurane is exposed to soda lime.
The FDA says that a minimum FGF of 1 L/min is safe for up to 2 MAC hours.
Example: 2% x 2 hours or 1% x 4 hours.
After 2 MAC hours have elapsed, the minimum FGF is 2 L/min
.
2. Free Fluoride Ions (produced by metabolism in the liver):
~5% of sevoflurane is metabolized by the liver.
Hepatic metabolism liberates inorganic fluoride ions.
Inorganic fluoride ions are nephrotoxic; they impair the concentrating mechanism in the renal tubules.
Previous research with methoxyflurane concluded that the risk of nephrotoxicity was increased when [Fl-] exceeded 50 µM/L. This does not seem to be the case with sevoflurane.
Trifluoroacetic acid is produced by hepatic metabolism of halothane, isoflurane, and desflurane. It is responsible for causing halothane hepatitis.
61
Which factors increase the rate of compound A production with sevoflurane administration? (Select 2.)
Cold soda lime
Decreased carbon dioxide production
High inspired sevoflurane concentration
Low fresh gas flow
Low fresh gas flow
High inspired sevoflurane concentration
Compound A is produced when sevoflurane reacts with soda lime.
The rate of compound A production is increased by:
Low fresh gas flow
High inspired sevoflurane concentration
Warm soda lime
Increased CO2 production (think of conditions that increase the patient's metabolism and oxygen consumption)
62
# Choose the BEST drug to treat mild pain in the patient with a glomerular filtration rate of 25 mL/min.
Codeine
Celecoxib
Acetaminophen
Ketorolac
Acetaminophen
Renal prostaglandins are produced in the afferent arteriole, where they promote vasodilation. This helps maintain renal blood flow.
All of the NSAIDs (including COX-2 inhibitors) inhibit cyclooxygenase. This reduces renal prostaglandin synthesis, thereby increasing renal vascular resistance and reducing renal blood flow. Obviously this can be detrimental to the patient with borderline renal function.
Reduced renal prostaglandin synthesis causes the patient to retain sodium, resulting in hypertension, edema, and possibly acute renal failure. Patients who are intravascularly depleted, have a history of renal impairment, or are experiencing intraoperative oliguria are at increased risk.
Codeine is metabolized to morphine. Morphine is metabolized to morphine-6- and morphine-3-glucuronide. M6G is an active metabolite and is more potent than morphine. Since M6G is eliminated by the kidneys, the patient with renal dysfunction is at higher risk of significant respiratory depression.
63
When antagonizing rocuronium in a patient with end-stage renal disease, the dose of neostigmine should be:
increased by 25%.
increased by 50%.
decreased by 50%.
the same as the patient without end-stage renal disease.
The same as the patient without end-stage renal disease
The excretion of cholinesterase inhibitors (neostigmine, pyridostigmine, and edrophonium) is delayed in the patient with end-stage renal disease.
This offsets the prolonged duration of rocuronium in this patient population. For this reason, the dose of the cholinesterase inhibitor should be the same that you would give to a patient with normal kidney function.
64
Match the diuretic to its primary site of action.
Loop diuretics + Loop of Henle
Thiazide diuretics + Distal tubule
Carbonic anhydrase inhibitors + Proximal tubule
Aldosterone antagonists + Collecting duct
Remember the mnemonic: COLT PA. It sounds like COLT 45 - everyone's favorite malt liquor. Alcohol ... making urine ... you get the idea...
```
C = carbonic anhydrase inhibitors (proximal tubule)
O = osmotic diuretics (proximal tubule)
L = loop diuretics (thick ascending loop of Henle)
T = thiazide diuretics (distal tubule)
P = potassium sparing diuretics (collecting duct)
A = aldosterone antagonists (collecting duct)
```
65
During the preoperative evaluation of a patient with congestive heart failure, you observe the following rhythm. Which of the following drugs are the MOST likely causes for this finding? (Select 2.) (u waves)
Amiloride
Spironolactone
Bumetanide
Metolazone
Bumetanide
Metolazone
These are the types of questions that will net you big points on the NCE, because you have to connect several pieces of information together to arrive at the correct answer.
The U waves on this EKG suggest hypokalemia. Other possible EKG changes include flat or inverted T waves and ST depression. Other effects of hypokalemia include skeletal muscle weakness and enhanced effects of nondepolarizing neuromuscular blockers.
Now that we've established that K+ is low, we need to identify the diuretics that waste potassium. Only potassium sparing diuretics increase potassium reabsorption, so we can rule out spironolactone and amiloride. Therefore, bumetanide and metolazone are the most likely explanations for the patient's hypokalemia.
The likelihood of digoxin toxicity is increased in the patient with hypokalemia. This condition increases digoxin binding inside the myocyte as well as increases its pharmacologic activity.
66
A patient is scheduled for bilateral mastectomy. She presents with nausea, vomiting, polyuria, and a short QTc interval. Which of the following agents will worsen this patient's condition?
Furosemide
Mannitol
Hydrochlorothiazide
Triamterene
Hydrochlorothiazide
Hypercalcemia exists when ionized Ca+ > 1.5 mM or 10.5 mg/dL, and is a medical emergency when it exceeds 14 mg/dL. Malignancy is the most common cause of hypercalcemia, but other causes include hyperparathyroidism and thyrotoxicosis. S/sx include nausea, vomiting, polyuria, renal stones, mental status changes, and EKG changes including a prolonged PR interval, widened QRS interval, and a shortened QTc interval.
Treatment includes intravenous hydration with 0.9% NaCl and hastening calcium excretion via diuresis. Furosemide is the best diuretic to treat this condition.
Thiazide diuretics (hydrochlorothiazide) inhibit the Na-Cl exchanger in the distal tubule. This activates the Na-Ca antiporter and increases Ca+ reabsorption, ultimately increasing serum calcium.
67
Which of the following should be avoided in the diabetic patient?
Spironolactone
Hydrochlorothiazide
Triamterene
Ethacrynic acid
Hydrochlorothiazide
Thiazide diuretics are unique in this drug class in that they cause hyperglycemia. Possible mechanisms for this include reduced insulin release from the pancreas or impaired cellular glucose utilization in the body.
Loop diuretics and potassium sparing diuretics affect serum glucose concentration only minimally.
68
Which of the following are associated with ototoxicity? (Select 2.)
Furosemide
Mannitol
Ethacrynic acid
Metolazone
Furosemide
Ethacrynic acid
Ototoxicity that results in either transient or permanent deafness is a rare, yet devastating side effect of furosemide and ethacrynic acid.
The risk is increased with high plasma concentrations, when these drugs are co-administered with other ototoxic agents, and appears to be higher with ethacrynic acid.
69
In the patient with impaired renal function, mannitol is more likely to cause: (Select 2.)
hyperchloremia.
hyponatremia.
hyperkalemia.
pulmonary edema.
Hyponatremia
Pulmonary edema
As an osmotic diuretic, mannitol pulls water from ECF into the intravascular compartment. In the patient with normal renal function, this effect is short-lived and well tolerated. In the patient with impaired renal function, the increase in plasma volume has several consequences:
There is a dilutional effect. This causes hyponatremia, hypochloremia, and reduces the hematocrit. It's important to note that hyponatremia in this instance does not reflect a reduction in plasma osmolarity. Indeed, by its mechanism of action, mannitol has increased plasma osmolarity.
In the patient with myocardial dysfunction, the increased plasma volume can overshoot the Starling curve. This results in congestive heart failure and pulmonary edema.
70
A patient with central sleep apnea is prescribed acetazolamide. Which statement MOST accurately describes the mechanism of action of this drug?
Stimulation of the Na-Cl transporter in the cortical region of the loop of Henle
Inhibition of the Na-K-2Cl transporter in the ascending loop of Henle
Inhibition of bicarbonate reabsorption in the proximal tubule
Stimulation of carbonic anhydrase in the tubular fluid
Inhibition of bicarbonate reabsorption in the proximal tubule
Bicarbonate accepts H+ to form carbonic acid. In the presence of carbonic anhydrase (an enzyme), carbonic acid dissociates into CO2 and H2O. This favors a concentration gradient where HCO3- flows from the lumen of the tubule and into the cells of the proximal tubule.
H+ → HCO3- → H2CO3 → CO2 + H2O
Inhibiting carbonic anhydrase with acetazolamide disrupts this mechanism. As a result, HCO3- isn't reabsorbed. Since H+ isn't used to produce carbonic acid, it is retained by the body. Chloride is retained to maintain electroneutrality. This is the mechanism for hyperchloremic metabolic acidosis (non-gap). We can use the metabolic acidosis to our advantage by stimulating ventilation in the patient with central sleep apnea.Acetazolamide is also used to treat acute mountain sickness and periodic paralysis.
71
Propranolol reduces hepatic blood flow by causing:
portal vein dilation.
portal vein constriction.
hepatic artery dilation.
hepatic artery constriction.
Hepatic artery constriction
The liver receives a dual blood supply. It receives flow from the hepatic artery and portal vein.
The hepatic artery supplies 25 percent of liver blood flow and 50 percent of the oxygen content. It is lined with alpha-1 and beta-2 receptors. Beta-2 receptor blockade causes hepatic artery and splanchnic vasoconstriction, and this can reduce liver blood flow.
The portal vein supplies 75 percent of liver blood flow and 50 percent of the liver oxygen content. It is populated by alpha-1 receptors only; there are no beta-2 receptors here. Therefore, beta-blockers do not alter the diameter of the portal vein.
Cardioselective beta-1 antagonists would not be expected to impact hepatic blood flow by this mechanism.
72
The hepatic arterial buffer response:
removes bacteria absorbed from the gut.
maintains pH in the sinusoids.
reduces hepatic vascular resistance in patients with cirrhosis.
preserves hepatic blood flow.
Preserves hepatic blood flow
The hepatic arterial buffer response attempts to preserve hepatic perfusion when liver blood flow falls.
If portal vein flow is compromised, the hepatic artery dilates to restore hepatic perfusion.
If hepatic artery flow is compromised, the portal vein dilates to restore hepatic perfusion.
Severe liver disease impairs the hepatic arterial buffer response.
Portal vein blood contains bacteria that were absorbed from the gut. Kupffer cells kill these bacteria.
73
What is the MOST common cause of viral hepatitis?
A
B
C
D
Hepatitis A
Here are the incidences of each type of viral hepatitis in the United States:
Hepatitis A = 50%
Hepatitis B = 35%
Hepatitis C = 15%
This should make sense because hepatitis A can be transmitted by the oral-fecal route; it's much easier to acquire. Luckily, hepatitis A does not lead to chronic hepatitis, cirrhosis, or hepatocellular carcinoma.
74
Which hepatitis viruses are MOST likely to be acquired during a blood transfusion? (Select 2.)
A
B
C
E
Hepatitis B
Hepatitis C
Hepatitis B and C are most likely to be transmitted via blood transfusion.
The incidence transfusion transmitted HBV is 1: 205,000
The incidence of transfusion transmitted HCV is 1 : 935,000
HAV and HEV are usually transmitted via the oral-fecal route.
75
All of the following have been implicated in immune-mediated hepatotoxicity EXCEPT:
desflurane.
isoflurane.
sevoflurane.
halothane.
Sevoflurane
Halothane, isoflurane, and desflurane are degraded to trifluoroacetic acid, and TFA has been implicated in immune-mediated hepatotoxicity. Historically halothane is considered the biggest offender, but there is a potential for cross-sensitivity with iso and des.
Sevoflurane does not produce TFA, so it does not produce immune-mediated hepatotoxicity.
76
# Choose the MOST significant risk factors for halothane hepatitis. (Select 2.)
Obesity
Age > 40 years
Male gender
Inhibition of CYP2E1
Age > 40 years
Obesity
Just because we don't use halothane anymore, does not mean this historically significant agent won't be on the NCE.
Risk factors for halothane hepatitis include:
Female gender
Age > 40 years
Genetic predisposition
Obesity
Induction of CYP2E1 by alcohol, isoniazid, or phenobarbital
77
Identify the physiologic changes that commonly accompany liver failure. (Select 2.)
Restrictive pulmonary defect
Increased sensitivity to vasopressors
Inhibition of the renin angiotensin aldosterone system
Thrombocytopenia
Thrombocytopenia
Restrictive pulmonary disease
Thrombocytopenia is caused by:
↓ platelet production (↓ thrombopoietin and bone marrow suppression)
↑platelet consumption (splenomegaly)
Ascites and pulmonary effusions reduce pulmonary compliance, which promotes atelectasis. These changes contribute to a restrictive pulmonary defect.
The failing liver is unable to efficiently clear endogenous vasodilators (VIP, glucagon, etc), and this decreases (not increases) the response to vasopressors.
A reduction in GFR activates the RAAS.
78
Which criteria are used to calculate the modified Child-Pugh score? (Select 3.)
```
Bilirubin
Gamma-glutamyl transpeptidase
Prothrombin time
Ascites
Aspartate aminotransferase
Creatinine
```
Bilirubin
Ascites
Prothrombin time
Used as a predictor of perioperative mortality in patients with cirrhosis, the modified Child-Pugh score examines 5 factors of hepatic function:
Albumin
PT
Bilirubin
Ascites
Encephalopathy
After the score is calculated, the patient is assigned to 1 of 3 classes.
```
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 patient with class A or B disease is otherwise optimized, it is reasonable to proceed with surgery. A patient with class C disease should be managed medically until hepatic function improves.
```
79
In the patient with cirrhosis:
many collateral vessels form inside the liver.
the back pressure in the portal system is transferred to the hepatic vein.
the number of sinusoids increase.
many collateral vessels form outside the liver.
Many collateral vessels form outside the liver
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.
The number of blood vessels passing through the liver is reduced, which increases hepatic vascular resistance (portal hypertension). This causes ascites, hepatomegaly, splenomegaly, peripheral edema, and esophageal varices.
To partially offset the increased hepatic vascular resistance, the body forms collateral vessels that bypass the liver; these are called portosystemic shunts. This blood does not benefit from the liver's clearance functions.
80
Identify the statements that BEST describe the surgical procedure in the image. (Select 2.) (TIPS)
It is used to improve hepatic perfusion.
It is a definitive treatment for hepatorenal syndrome.
It is commonly known as the TIPS procedure.
It improves esophageal varices.
It improves esophageal varices
It is commonly known as the TIPS procedure
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.
Hemorrhage is a significant risk of the TIPS procedure.
81
Select the MOST efficacious treatment for hepatorenal syndrome.
Hepatic cryotherapy
Liver transplant
Transjugular intrahepatic portosystemic shunt
Dialysis
Liver transplant
Hepatorenal syndrome is caused by dehydration and a reduction in renal perfusion (↓ GFR). If not reversed, acute tubular necrosis may result. Mortality is high.
Temporary solutions: Dialysis or TIPS procedure (improves RBF)
Definitive treatment: Liver transplant
Hepatic cryotherapy utilizes subzero temperatures to treat unresectable malignant tumors.
82
Management for the patient with bleeding esophageal varices includes: (Select 2.)
TIPS procedure.
aggressive volume resuscitation.
propranolol.
reducing the hepatic venous pressure gradient to 20 mmHg.
TIPS procedure
Propranolol
Portal hypertension increases esophageal venous pressure, and this predisposes the patient to esophageal varices and hemorrhage.
Management of this patient includes:
Reducing the hepatic venous pressure gradient to less than 10 mmHg
TIPS procedure ( ↓'s HVPG)
Propranolol (↓'s HVPG) - by vasoconstriction of the splanchnic bed and hepatic artery (beta 2) as well as decreasing CO (beta 1)
Moderate, not aggressive, volume resuscitation (prevent ↑'d HVPG)
Balloon tamponade
83
Alcohol withdrawal syndrome is treated with all of the following EXCEPT:
disulfiram.
propranolol.
alcohol.
diazepam.
Disulfiram
Alcohol withdrawal syndrome presents as early as 6-8 hours after the blood alcohol level returns to near zero. Generalized tremors, cognitive changes, sympathetic discharge, agitation, nausea, vomiting, and insomnia can occur.
Alcohol withdraw syndrome can be treated with:
```
Beta blocker - tachycardia
Benzodiazepine - sedation
Alpha 2 agonist - ANS hyperactivity
Alcohol
Delirium tremens may occur 2-4 days after the last episode of alcohol consumption. It manifests as hallucinations, tachycardia, hyper or hypotension, seizures, combativeness, and hyperthermia. Treatment is similar to alcohol withdrawal with the addition of restraints, securing the airway, and correction of metabolic and electrolytes imbalances. Even with treatment, mortality approaches 10 percent.
```
Disulfiram is used as part of an alcohol abstinence program. It is not used to treat acute withdrawal.
84
Which hormones are released by the posterior pituitary gland? (Select 2.)
Prolactin
Oxytocin
Antidiuretic hormone
Growth hormone
Oxytocin
Antidiuretic hormone
While the anterior pituitary is a glandular organ, the posterior pituitary is a glial structure that contains nerve endings originating in the hypothalamus. The neurohypophysis is another name for the posterior pituitary gland.
The posterior pituitary releases two hormones: antidiuretic hormone and oxytocin.
The supraoptic nucleus produces antidiuretic hormone.
The paraventricular nucleus produces oxytocin.
These hormones are transported along the pituitary stalk (nerve fibers) towards the posterior pituitary gland, and from there, they are released into the circulation via exocytosis.
```
You can remember the hormones secreted by the anterior pituitary gland with the mnemonic "FLAT PiG"
Follicle-stimulating hormone
Luteinizing hormone
Adrenocorticotropin
Thyroid stimulating hormone
Prolactin
ignore
Growth hormone
```
85
A diagnosis of Grave's disease is consistent with:
elevated TSH.
somnolence.
decreased free T4.
protein catabolism.
Protein catabolism
Grave's disease is most common cause of hyperthyroidism. As an autoimmune disorder, TSH-receptor antibodies cause the thyroid gland to produce excess T3 and T4. This leads to s/sx of thyroid over simulation. Grave's disease is more common in women.
Lab values consistent with a diagnosis of Grave's disease include:
↑ Free T4 (not decreased)
↓ TSH (not increased)
Signs and symptoms include:
```
Insomnia
Protein catabolism and weight loss
Exophthalmos
Anxiety
Heat intolerance
```
86
Which of the following statements is true of cortisol?
It engages with receptors on the cell membrane.
It inhibits insulin release.
Its mineralocorticoid activity increases serum glucose.
An excess causes muscle wasting.
An excess causes muscle wasting.
Cortisol is a glucocorticoid. One of its primary roles is gluconeogenesis, which raises serum glucose. Hyperglycemia stimulates the pancreatic beta cells to secrete insulin.
Cortisol also possesses some mineralocorticoid properties (think aldosterone). This leads to:
Na+ retention with passive reabsorption of water
K+ secretion into the collecting ducts by principal cells
H+ secretion in the collecting ducts by intercalated cells
Cortisol acts on intracellular cytoplasmic receptors and stimulates the production of mRNA. It does not interact with membrane bound receptors. This explains why it has a delayed onset of action.
87
Which of the following stimulate growth hormone secretion? (Select 3.)
Corticosteroids
Surgery
Increased fatty acid levels
Pregnancy
Hypoglycemia
Alpha adrenergic agonists
Surgery
Hypoglycemia
Alpha adrenergic agonists
Growth hormone secretion is increased by:
```
Growth hormone releasing hormone from the hypothalamus
Stress and anxiety (including surgery)
Physiologic sleep
Hypoglycemia
Decreased free fatty acid levels
Increased blood amino acid levels
Fasting
Dopamine
Alpha-adrenergic agonists
Estrogen
GH release is not increased by corticosteroids or pregnancy.
```
88
Match each organ to the physiologic effect of its stimulation.
Adrenal cortex + Sodium reabsorption
Adrenal medulla + Systemic vasoconstriction
Atrium + Natriuresis
Posterior pituitary gland + Synthesis and insertion
Explanation:
Adrenal cortex → ↑ aldosterone → Na+ and water retention as well as K+ and H+ wasting
Adrenal medulla → ↑EPI and NE → systemic vasoconstriction
Atrial stretch → ↑ atrial natriuretic peptide release → natriuresis
Posterior pituitary → ↑ antidiuretic hormone → aquaporin synthesis and insertion in the renal collecting ducts → water reabsorption to restore osmolality
89
Which of the following is the MOST common etiology of Cushing's syndrome?
Adrenal cortex adenoma
Pituitary adenoma
Chronic glucocorticoid therapy
Cortisol secreting extra-adrenal tumor
Chronic glucocorticoid therapy
Explanation:
An over production of cortisol by the adrenal cortex is called Cushing's syndrome.
Diagnosis: Low ACTH level and a high cortisol level.
Etiologies: Chronic glucocorticoid therapy (most common cause) and adrenal cortex adenoma
Hypersecretion of corticotropin-releasing hormone by the hypothalamus is called Cushing's disease.
Diagnosis: High ACTH level and a high cortisol level.
Etiologies: Pituitary adenoma
Cortisol secreting extra-adrenal tumors can also cause hyperadrenalism.
90
Etiologies of Addison's disease include: (Select 3.)
Adrenocorticotropic hormone deficiency
Tuberculosis
Autoimmune disease
Adrenal tumor
Pituitary tumor
Corticotropin releasing hormone deficiency
Autoimmune
Adrenal tumor
Tuberculosis
Explanation:
Hypoadrenalism (adrenal insufficiency) can be primary or secondary.
Primary adrenal insufficiency is called Addison's disease. It occurs when the adrenal cortex fails to produce enough cortisol (↑ACTH level and ↓ cortisol level).
```
Causes include:
Autoimmune disease (most common cause in US)
Tuberculosis (most common cause worldwide)
Heparin induced thrombocytopenia
Diabetes type I
Hashimoto’s thyroiditis
HIV
Trauma
Adrenal tumor
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Secondary adrenal insufficiency occurs when the pituitary gland doesn't secrete enough ACTH (↓ ACTH level and ↓ cortisol level).
Causes include:
Iatrogenic (chronic glucocorticoid supplementation)
Hypothalamic or pituitary dysfunction (tumor, infection, or ablation)
As an aside, remember that a single dose of etomidate reversibly inhibits 11-beta-hydroxylase and impairs cortisol and aldosterone synthesis for 8-24 hours. Don't give it to the patient with Addison's disease.
91
Which of the following conditions is commonly associated with this EKG tracing? (u Wave)
Addison's disease
Conn’s syndrome
Acromegaly
Myxedema
Conn's syndrome
Explanation:
Primary hyperaldosteronism is called Conn's syndrome.
Remember that aldosterone:
Increases Na+ AND water retention
Wastes K+ and H+
This EKG has a U wave, and you know that this suggests hypokalemia. This patient may also present with muscle weakness.
92
All of the following hormones are released by the adenohypophysis EXCEPT?
Thyroid stimulating hormone
Luteinizing hormone
Growth hormone
Cortisol
Cortisol
Explanation:
Cortisol is released by the zona fasciculata of the adrenal cortex. Remember the mnemonic "GFR" for adrenal hormone production? You'll get to strut your stuff a little bit later in this review exam.
The adenohypophysis is another name for the anterior pituitary gland. All of the other answer choices are secreted by the anterior pituitary: growth hormone, thyroid stimulating hormone, and lutenizing hormone.
93
Somatotropin:
increases bone length following epiphyseal closure.
decreases fatty acid mobilization.
increases protein catabolism.
facilitates tissue growth.
Facilitates tissue growth
Growth hormone is also called somatotropic hormone or somatotropin. Make it a habit to learn these synonyms.
It facilitates growth of all of the tissues in the body.
It stimulates linear bone growth before epiphyseal closure.
It increases protein synthesis (anabolic effect).
It enhances fatty acid mobilization and utilization (ketogenic effect).
94
Match each steroid to its glucocorticoid potency relative to cortisol.
Aldosterone + 0x
Methylprednisolone + 5x
Fludrocortisone + 10x
Dexamethasone + 25x
95
Glucosuria is likely to occur when serum glucose exceeds:
120 mg/dL.
180 mg/dL.
240 mg/dL.
300 mg/dL.
180 mg/dL
Glucosuria is glucose in the urine. The kidney's capacity to reabsorb glucose is exceeded when serum glucose is > 180 mg/dL.
An elevated glucose load in the urine exerts an osmotic effect, so glucosuria leads to polyuria which later leads to hypovolemia. Hypovolemia activates the thirst reflex, which explains why these patients are frequently thirsty (polydipsia).
Indeed, the classic s/sx of diabetes mellitus are polydipsia, polyuria, and dehydration.
96
Which of the following are complications of Conn’s syndrome? (Select 2.)
Hypokalemia
Hypertension
Hypernatremia
Metabolic acidosis
Hypokalemia
Hypertension
Conn's syndrome occurs when there is an over production of aldosterone - usually from an adrenal tumor.
Excess aldosterone causes:
Na+ retention with passive reabsorption of water (hypervolemia + HTN)
K+ secretion into the collecting ducts by principal cells (hypokalemia)
H+ secretion in the collecting ducts by intercalated cells (metabolic alkalosis)
Remember hypokalemia moves the resting membrane away from threshold potential. This means its more difficult to generate an action potential. This explains why the patient with hypokalemia commonly experiences muscle weakness.
97
What is the cause of endemic goiter?
Decreased thyroid stimulating hormone
Increased triiodothyronine
Iodine deficiency
Decreased thyroglobulin
Decreased iodine uptake
Thyroid stimulating hormone is released from the anterior pituitary gland. It affects the thyroid gland in 2 key ways:
It tells the thyroid gland to produce T3 and T4 (this requires iodine).
It tells the follicular tissue to produce thyroglobulin colloid (this does not require iodine).
Let's go a bit deeper...
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.
Under normal conditions, there is a negative feedback loop where T3 and T4 suppress TSH release. In the patient with a hypoactive thyroid, there isn't enough thyroid hormone to suppress TSH, so TSH remains chronically elevated. This presents a problem.
Remember that we said TSH stimulates the follicles to make thyroglobulin colloid and that this does not require iodine? Well since TSH is chronically elevated, the follicles continue to produce thyroglobulin colloid, and this causes the thyroid gland to increase in size. This is the cause of endemic goiter.
98
All of the following hormones bind to to a G-protein coupled receptor EXCEPT:
epinephrine.
cortisol.
norepinephrine.
vasopressin.
Cortisol
Cellular receptors tend to be located in 1 of 3 places:
1. On the cell surface, you'll find receptors that bind catecholamine, protein, or peptide hormones (vasopressin, epi, ne)
2. In the cytoplasm is where you'll find receptors for most steroid hormones (cortisol).
3. In the nucleus is where you'll find receptors for thyroid hormones.
99
Which drug should be avoided in the patient with hyperthyroidism?
Levothyroxine
Propylthiouracil
Propranolol
Radioactive iodine
Levothyroxine
Treatment for hyperthyroidism consists of antithyroid medications, beta-blockers, and thyroidectomy.
Antithyroid medications include:
Propylthiouracil (PTU)
Carbimazole
Radioactive iodine
Radioactive iodine arrests the overproduction of thyroid hormones over a 2-4 month period. It should not be given during pregnancy or to nursing mothers, because it can ablate the offspring's thyroid gland.
Levothyroxine is synthetic T4. Obviously you wouldn't want to administer it to someone with Grave's disease.
100
Which medication should be avoided in the patient with thyroid storm?
Amiodarone
Hydrocortisone
Propylthiouracil
Propranolol
Amiodarone
A 200 mg amiodarone pill is 35% iodine by weight, and this amount of iodine is 20 times the optimal daily intake.
It can cause hypothyroidism by reducing T4 synthesis.
It can cause hyperthyroidism by inhibiting the conversion of T4 to T3.
Patients experiencing thyroid storm require steroid supplementation, because steroid metabolism is increased by the hypermetabolic state.
101
Where does propylthiouracil exert its pharmacologic effect?
Thyroid gland
Parathyroid gland
Adrenal gland
Anterior pituitary gland
Thyroid gland
Propylthiouracil (PTU) is a thionamide that blocks the reaction between iodine and tyrosine. This inhibits T3 and T4 production and also interferes with the conversion of T4 to T3.
Other thionamides include methimazole and carbimazole.
102
Match each hormone to its site of synthesis.
Zona Glomerulosa
Zona Fasciculata
Zona Reticularis
Adrenal medulla
Aldosterone
Cortisol
Epinephrine
Estrogen
Zona Glomerulosa + Aldosterone
Zona Fasciculata + Cortisol
Zona Reticularis + Estrogen
Adrenal medulla + Epinephrine
Zona Glomerulosa → Mineralocorticoids (aldosterone)
Zona Fasciculata → Glucocorticoids (cortisol)
Zona Reticularis → Androgenic hormones (estrogen & progesterone)
Adrenal medulla → Catecholamines (Epi & NE)
You can remember the order of the zones by remembering the abbreviation GFR.
103
Factors that stimulate the pancreas to increase insulin release include: (Select 2.)
beta-2 agonists.
glucagon.
alpha-2 agonists.
volatile anesthetics.
Glucagon
Beta-2 agonists
Know that anything that causes the serum glucose to increase will indirectly stimulate the release of insulin.
Glucagon
Beta-2 agonists
Hyperglycemia
104
Complications of Addison's disease include: (Select 2.)
hypokalemia.
hyperpigmentation.
hyponatremia.
hypervolemia.
Hyponatremia
Hyperpigmentation
Addison's disease decreases mineralocorticoid (aldosterone) production.
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K+ retention → hyperkalemia
Na+ and Cl- wasting → severe hypovolemia
Decreased CO results in shock-like state
Death within 3 days to 2 weeks
Addison's disease decreases glucocorticoid (cortisol) production
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Unable to store glucose as glycogen. This leads to hypoglycemia between meals.
Stress (surgery, sepsis, trauma) is poorly tolerated and may lead to demise.
Patients with Addison's disease have an elevated ACTH and this can stimulate melanocytes in the dermis and epidermis to increase melanin secretion.
105
Diagnostic criteria for diabetes mellitus includes an A1C greater than:
1. 5%.
2. 5%.
4. 5%.
6. 5%.
6.5 percent
Diagnostic criteria for diabetes mellitus includes:
Hemoglobin A1C > 6.5 percent
Fasting plasma glucose > 126 mg/dL
Two-hour plasma glucose > 200 mg/dL during an oral glucose tolerance test
Classic symptoms + random glucose of 200 mg/dL
A hemoglobin A1C correlates with an average serum plasma glucose of 126 mg/dL.
106
Rank each insulin formulation according to its duration of action.
(One is the shortest duration and four is the longest duration
Humulin N
Lantus
Humulin R
Humalog
1
2
3
4
Humalog + 1
Humulin R + 2
Humulin N + 3
Lantus + 4
Duration of each insulin formulation:
Humalog (rapid acting) = 3-5 hours
Humulin R (short acting regular) = 4-12 hours
Humulin N (intermediate acting NPH) = 10-20 hours
Lantus (long acting) = 12-24 hours
Of these formulations, only Humulin R can be given IM or IV. All of the others are administered subcutaneously.
107
Match each oral diabetic agent to its drug class.
Glipizide + Sulfonylurea
Pioglitazone + Thiazolidinedione
Metformin + Biguanide
Exenatide + GLP-1 agonist
Sulfonylureas (glipizide) increase insulin release from pancreatic beta cells.
Glucagon-like polypeptide-1 drugs (exenatide) stimulate insulin release and reduce glucagon release.
Thiazolidinediones (pioglitazone) sensitize the glucose receptor for increased uptake and also decrease hepatic glucose output.
Biguanides (metformin) reduces hepatic glucose output and increases peripheral insulin utilization.
108
When compared to diabetic ketoacidosis, a hyperglycemic hyperosmolar state is: (Select 2.)
associated with a higher serum osmolarity.
more common in patients with type 2 diabetes mellitus.
associated with a lower serum glucose.
lower blood pH.
More common in patients with type 2 diabetes mellitus
Associated with a higher serum osmolarity
Diabetic Ketoacidosis (DKA):
More common with type 1 diabetes mellitus.
Usually caused by infection.
Not enough insulin → ketoacidosis, hyperosmolarity (from increased glucose), and dehydration.
Patient is hyperglycemic (> 250 mg/dL), but cells are starved for fuel.
Treatment = volume resuscitation, insulin, K+ after acidosis subsides.
Hyperglycemic Hyperosmolar State (HHS):
More common with type 2 diabetes mellitus.
Usually caused by insulin resistance or inadequate production.
Enough insulin is produced to prevent ketosis by not hyperglycemia.
Hyperglycemia (> 600 mg/dL) significantly increases serum osmolarity (> 330 mOsm/L).
Compared to DKA, HSS is associated with a greater elevation in glucose and osmolarity.
Mild metabolic acidosis may occur (usually > 7.3 and no anion gap).
Treatment = volume resuscitation, insulin, correct electrolytes.
109
Chose the statements that BEST describe the anesthetic considerations for the patient with hyperthyroidism. (Select 3.)
Patients with mild hyperthyroidism can be cleared for elective surgery.
There is a higher incidence of corneal abrasion.
There is an increased risk for pathologic fractures during positioning.
There is increased sensitivity to muscle relaxants.
Beta blockers are contraindicated.
MAC is increased.
There is an increased sensitivity to muscle relaxants
There is increased risk of pathologic fractures during positioning
There is a higher risk of corneal abrasion
An increased cardiac output slows FA/FI, and this may be falsely interpreted as a higher anesthetic requirement. Know that MAC is unchanged!
The patient with hyperthyroidism is at risk for thyrotoxicosis, so the patient should be euthyroid for an elective procedure.
SNS stimulation can precipitate thyrotoxicosis and thyroid storm.
Avoid drugs that activate the SNS (ketamine, pancuronium, ephedrine).
Direct acting sympathomimetics are better than indirect acting drugs.
Hypercarbia and hypoxia can activate the SNS.
Beta blockers are indicated to depress the SNS.
Exophthalmos is an infiltrative process involving the eyelids and the retrobulbar fat. Lid retraction and periorbital swelling makes closing the eyes more difficult, and this increases the risk of corneal abrasion.
Position carefully. Patients are prone to osteoporosis and fractures.
Closely titrate muscle relaxants because of a higher incidence of myopathy and propensity towards myasthenia gravis.
110
All of the following are indicated in the treatment of severe hypercalcemia EXCEPT:
furosemide.
calcitonin.
0.9 percent sodium chloride.
lactated ringers.
Lactated ringers
Hypercalcemia should be treated when the serum calcium exceeds 13 mg/dL or if the patient is symptomatic. Treatment includes:
Hydration with 0.9 percent NaCl → Dilutes serum Ca+2 and increased GFR hastens diuresis
Loop diuretic → Enhances Ca+2 excretion
Calcitonin or bisphosphonates → Inhibits osteoclast bone resorption
Lactated ringers contain calcium and should be avoided.
111
A patient becomes acutely hypotensive during resection of a carcinoid tumor. What is the BEST drug to administer at this time?
Phenylephrine
Octreotide
Norepinephrine
Ketamine
Octreotide
Carcinoid syndrome is associated with secretion of vasoactive substances from enterochromaffin cells. The tumor can release vasoactive substances that increase or decrease blood pressure.
Somatostatin (octreotide or lanreotide) inhibits release of vasoactive substances from carcinoid tumors. This makes it the drug of choice if tumor secretion is the etiology of hemodynamic instability. A fluid bolus is also indicated in the context of this question.
Vasopressors can have an unpredictable effect on blood pressure. If you must give one, then phenylephrine is the best choice.
112
Which pathologic changes are expected with acromegaly? (Select 2.)
Turbinate hypertrophy
Subglottic narrowing
Microglossia
Epiglottic atrophy
Turbinate hypertrophy
Subglottic narrowing
Acromegaly results from over secretion of growth hormone after adolescence. 99 percent of the cases are associated with pituitary adenoma. A difficult mask and intubation should be anticipated. Dyspnea, stridor, or hoarseness signify airway involvement.
A larger tongue (macroglossia) and epiglottis may make laryngoscopy more difficult. Subglottic narrowing along with vocal cord enlargement should be expected with acromegaly and may necessitate a smaller endotracheal tube. Turbinate enlargement requires care with nasal intubation. Obstructive sleep apnea is common.
113
Differential diagnosis of thyroid storm should include all of the following EXCEPT:
malignant hyperthermia.
pheochromocytoma.
neuroleptic malignant syndrome.
myxedema.
Myxedema
The clinical presentation shares many characteristics with neuroleptic malignant syndrome, malignant hyperthermia, pheochromocytoma, and light anesthesia.
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Myxedema coma occurs with severe hypothyroidism. S/sx include:
Alveolar hypoventilation and hypoxia
Congestive heart failure
Pericardial effusion
Bradycardia
Hypothermia
Hyponatremia
Anesthetic considerations include:
Large tongue may increase risk of difficult intubation
Decreased anesthetic requirement
Expand intravascular volume
Treat electrolyte imbalance (risk of water intoxication)
Provide active warming
Treat with IV levothyroxine
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