Allergy, Endo, Rheum

Question 1

Insulin and protein? Insulin’s receptor, and insulin and Na/ATPase

Answer 1

Insulin makes protein by building amino acids
Glut 4 receptor translocation
Increases Na/K ATPase which decreases serum potassium

Question 2

Does stimulation of insulin receptor increase cAMP?? Does CAMP increase insulin? What kind of receptor is insulin, and what are it’s cellular effects?

Answer 2

Not to be too confusing, but cAMP DOES increase insulin secretion (but insulin secretion DOES NOT directly lead to increases in cAMP). As far as the insulin receptor goes, it is a tyrosine kinase receptor, meaning that it adds phosphate to tyrosine residues of certain proteins that go on to signal various cellular effects (as described in Endo 1). The two most commonly discussed signaling intermediaries are Protein Kinase B and PIP3, which you probably do not have to memorize (yet?) for the boards. but you definitely need to know that cAMP is not (directly) affected. cAMP is increased with beta agonism, and its destruction is decreased by phosphodiesterase inhibitors, which is a very high yield topic on the boards

Question 3

IV insulin onset and duration
SQ insulin onset and duration
NPH insulin and onset

Answer 3

IV regular insulin has an onset in minutes, and a duration of about an hour
SQ insulin has an onset of 15 minutes (great variation between sources again), peaks at about an hour or two, and lasts for about 4-6 hours.

Question 4

One u it of insulin should decrease BG by how much?

Answer 4

A single unit of insulin should supposedly decrease glucose by about 25 points

Question 5

75 year old patient found unresponsive is diagnosed with hyperosmolar, hyperglycaemic state (HHS) with serum glucose of 1450 mg/ dL and CT evidence of appendicitis. The surgeon books an exploratory laparotomy as an emergency because the patient’s BP is 65/35 and HR 125. Which of the following is the most appropriate course of action:
A. Administer an isotonic crystalloid to decrease the glucose by 50 mg per hour, proceed with surgery when the glucose is < 500
B. Administer a hypotonic crystalloid to decrease the glucose by 50 mg per hour, proceed with surgery when the glucose is < 500
C. Administer isotonic crystalloid until the MAP is 60, and proceed to surgery regardless of serum glucose
D. Administer hypotonic crystalloid until the MAP is 60, and proceed to surgery regardless of serum glucose

Answer 5

This patient has HHS, formerly called hyperosmolar, hyperglycaemic nonketotic coma (HHNC), and is due to a relative insulin deficiency, but still enough to prevent ketone body formation. If this patient had an anion gap, it would be due to lactic acidosis from hypoperfusion, not ketoacidosis. The primary problem here is osmotic diuresis from hyperglycaemia. Even though this surgery is obviously urgent, taking the patient in this extreme hypovolaemic state could be fatal. Aggressive and rapid resuscitation with isotonic crystalloid is indicated here to improve cardiac output and oxygen delivery. Hypotonic crystalloid would be more effective at treating the hyperosmolar state, but that’s not what’s going to kill him in this situation. Various concerns regarding quickly resuscitating this patient due to inducing cerebral oedema is strongly outweighed by the need for emergency surgery. Moreover, cerebral oedema in this situation is exceedingly rare, especially in the elderly.

In reality, one might not truly wait until the patient’s MAP is actually 60 mm Hg with volume only and no pressors (as the abdominal pathology may be contributing to hypotension as well). But given that patients with HHS often have a 8-10 L volume deficit on presentation, answer C remains the best of the available choice.

Question 6

Main cause for acidity and increased lactic acid is what-like what’s missing intracellularly, and breakdown of what process is causing it?

Answer 6

The primary underlying cause for this patients profound acidosis (pH 7.05 with significant respiratory compensation) is lack of intracellular glucose (for glycolysis, see ICU principles question 8) with compensatory lipolysis. Lipolysis with resultant free fatty acid release into the circulation is taken up by cells, and converted into beta-hydroxybutyrate (B-OHB) and acetoacetic acid (AA-A), which lowers the pH producing metabolic acidosis

These acids also contribute to the hyperosmolar state produced by the increased glucose, leading to further osmotic diuresis and hypovolaemic shock.

Question 7

Osmotic diuresis leads to loss of which electrolytes. What happens to sodium on this situation?

Answer 7

osmotic diuresis leads to electrolyte loss, most notably hypo-Na, K, Mg, & Phos. In the presence of extreme hyperglycaemia, sodium levels may appear lower than they actually are as additional water is pulled into the sample by the osmotic effects of glucose

Question 8

DKA occurs in states of ______ deficiency concurrent with up regulation of what?

Answer 8

DKA occurs in states when there is an insulin deficiency concurrent with an up-regulation of counter-regulatory hormones opposing insulin effects (answer C) with resultant glycogenolysis (increased glucose), gluconeogenesis (increased glucose), and lipolysis (increased ketones). Glucose levels are almost always greater than 250 mg/ dL, but rarely over 800 mg/ dL

Question 9

What is the cornerstone of DKA treatment? First which fluids do you give? What about the amount of insulin that you give? What about bicarbonate in DKA?

Answer 9

The cornerstone of treatment of DKA is fluids and insulin. Initial fluid choice should be centered around volume resuscitation to restore haemodynamic stability, preferably with an isotonic crystalloid.
After haemodynamic stability is restored, additional free water can be administered by changing the maintenance fluid to half normal saline or another hypotonic solution (therefore isotonic solution is used initially not half normal saline).
Insulin is initially bolused (0.1-0.2 units/kg), and in this patient 12 units would be a reasonable dose, not 2-5 units. An insulin gtt is started afterwards. Subcutaneous protocols have also been developed and validated as well.
Insulin is initially bolused (0.1-0.2 units/kg), and in this patient 12 units would be a reasonable dose, not 2-5 units. An insulin gtt is started afterwards. Subcutaneous protocols have also been developed and validated as well.

Treatment of the acidosis is accomplished by volume resuscitation and insulin, but bicarb is also often indicated as well. Current recommendations are 1-2 amps of bicarb (50-100 mEq) when the pH is below 7.0. Some practitioners will treat when the pH is under 7.2, but whatever the case, low bicarb levels on serum chemistries should not be what determines whether or not bicarb is used (only pH).

Question 10

DKA and emergent/urgent/elective surgery:

KIM what about managing DKA intraoperatively:

Answer 10

For urgent surgery volume resuscitation until the haemodynamics stabilize (answer “Volume replacement until the MAP is 60, then proceed to the OR”) makes sense (see question 5). For elective surgery, answer “Proceed to the OR after the anion gap closes” is the best choice as the DKA has essentially been treated.
In emergent, if no improvement after a liter of fluids, then you’ll have to go to the IR anyway, keeping in mind the following:
On top of the normal volume resuscitation needed for an ‘ex lap’ in the setting of an acute abdomen, resuscitation should include a 8-10 L possible deficit from DKA alone. Electrolytes need to be checked hourly, and replaced aggressively. Potassium, magnesium, & phosphate can usually be given empirically after a 1-2 liter bolus of crystalloid, even in the setting of moderate hyperkalaemia. Measurement of beta-hydroxybutyrate (B-OHB) is recommended, but unlikely necessary in this acute setting (focus on volume and pH). As the ketone levels decrease the anion gap will close.

Question 11

No SUX in DKA

Answer 11

True because of hyperkalemia

Question 12

On the boards, goiter =
Hyperthyroidism and induction agents you should avoid:
How to assess goiter pre-operatively:

Answer 12

cannot intubate/ ventilate/ trach situation.
Also, in the setting of hyperthyroidism, indirect sympathetic stimulants (ketamine, ephedrine) and vagolytics (pancuronium) should be avoided. Furthermore, be aware that laying the person recumbent (even in real life, just not the boards) can lead to airway collapse (in severe cases). Therefore, for patients with goiter, you should lay them down flat to look for airway obstruction in your preoperative evaluation (oral boards gem)…if they can’t lie flat awake, they’ll do worse with sedation.

Question 13

Emergency surgery in a patient with goiter (hyperthyroidism)-can start a gtt or what?

Answer 13

Control of his haemodynamics will best be accomplished with beta-blockers, which reduce the sympathomimetic effects seen with hyperthyroidism as well as (somewhat) decrease peripheral conversion of T4 to T3. Of the listed beta-blockers, esmolol has the advantage of being easily titratable, and therefore better choice in this situation.

No time to start a thyroid regimen-which could take days

Question 14

Recurrent laryngeal nerve innervates

Answer 14

all but one muscle of the vocal cords (cricothyroid muscle – external branch of superior laryngeal nerve).

Question 15

Unilateral vs bilateral transection of RLN

Answer 15

Unilateral transection usually presents with hoarseness and bilateral transection stridor and aphonia and not a normal complication of surgery. In fact, it is considered a serious complication and a source of morbidity.

Question 16

What happens to Parathyroid during these surgeries? Reactive airway edema s/p thyroidectomy, and what you should do about it.

Answer 16

Typically, the parathyroid glands are spared with total thyroidectomy, but unintentional hypoparathyroidism can present with hypocalcaemia, leading to muscle irritability (think Trousseau’s sign) and laryngospasm. This classically occurs at least 6-12 hours post-op and not in the PACU very often. Reactive airway oedema is possible following intubation, and common things being common, this presentation could very well be run-of-the-mill post-extubation stridor (answer “racaemic epi”). This should be treated with head up position and racaemic epinephrine.

Question 17

You should always be thing about _____ post thyroidectomy? And then what to do about it?

Answer 17

In any post-thyroidectomy case, the very first thing you should be on the look out for is a re-bleed. Re-bleeding in the neck causes tracheal shift, compression, and in some cases recurrent laryngeal nerve palsy. The first step of treatment is always opening the wound surgically, never attempting intubation (before dealing with the wound). Like the goiter (question 9), intubation should always be done with the principle of maintaining spontaneous ventilation (not etomidate + sux).

Question 18

Which of the following is NOT an anesthetic concern for a patient with long-standing undertreated hypothyroidism:

A. Low cardiac output
B. Hypernatraemia
C. Restrictive lung disease
D. Hypothermia
E. Decreased drug biotransformation

Answer 18

Hypothyroidism and its most severe form, myxoedema coma results in systemic implications, affecting every organ system. Contractility, stroke volume, and heart rate decrease (low cardiac output). Pleural effusions are common (as well as pericardial), leading to restrictive lung disease (restriction external to the lung), as well as hypoventilation. Patients are hypothermic and have low metabolic rates. Decreased drug biotransformation prolongs recovery from sedatives and anesthesia, but doe not affect volatile anesthetic’s MAC specifically. Patients retain free water, with resultant oedema and hyponatraemia (not hypernatraemia).

Question 19

What are causes of Cushing’s aundrome? What is Cushing’s disease? Clinical manifestations? Anesthesia considerations: ____. Do they still need steroids? What’s a treatment for volume overload and hypokalemia?

Answer 19

Cushing’s syndrome can be due to a primary tumor in the adrenal gland, increased ACTH secretion (pituitary = Cushing DISEASE; tumors = ectopic ACTH syndrome), or endogenous steroid. Classic manifestations are insulin resistance (hyperglycemia, not hypoglycaemia), hypertension secondary to hypervolaemia, osteoporosis, & hypokalaemic alkalosis. Anesthesia considerations are increased sensitivity to muscle relaxants, hypokalaemic associated arrhythmias, difficult intubation (obesity, swelling). Even though their problem is too much corticosteroids, they may require additional steroids for surgical stress. Spirinolactone is a classic treatment for volume overload and hypokalaemia.

Question 20

Pt having carpal tunnel surgery and frequently on steroids. What’s the deal with people and steroids? When to give it? Which type and why?

Answer 20

Patients receiving supplemental steroids can have an insufficient steroid production to the perioperative stress response. In severe cases, an Addisonian-like state can be seen with vasopressor resistant hypotension. Therefore, for moderately to very stressful surgeries, especially with large wounds and fluid shifts, supplemental steroids are recommended. The classic teaching is that a healthy person can produce (up to) 300 mg of cortisol in a day when maximally stressed (20 mg on a normal non-stressed day). Various regimens have been developed to deliver 200-300 mg of hydrocortisone over 24 hours for a few days to a week. Dexamethasone is a pure glucocorticoid and is not as good of a theoretical choice as hydrocortisone (perfect physiologic balance (supposedly) of mineral- and gluco-corticoid effects). For this case, the stress response is expected to be minimal and therefore no steroids are indicated unless the patient has refractory hypotension or other symptoms.

Question 21

How should patients with pheochromocytoma be managed prior to surgery-which meds should they be put on, what are you watching? Similarity to PET?

Answer 21

Patients receiving supplemental steroids can have an insufficient steroid production to the perioperative stress response. In severe cases, an Addisonian-like state can be seen with vasopressor resistant hypotension. Therefore, for moderately to very stressful surgeries, especially with large wounds and fluid shifts, supplemental steroids are recommended. The classic teaching is that a healthy person can produce (up to) 300 mg of cortisol in a day when maximally stressed (20 mg on a normal non-stressed day). Various regimens have been developed to deliver 200-300 mg of hydrocortisone over 24 hours for a few days to a week. Dexamethasone is a pure glucocorticoid and is not as good of a theoretical choice as hydrocortisone (perfect physiologic balance (supposedly) of mineral- and gluco-corticoid effects). For this case, the stress response is expected to be minimal and therefore no steroids are indicated unless the patient has refractory hypotension or other symptoms.

Question 22

Pancironium has which kind of activity, and shouldn’t be used with pheo-why?

Answer 22

Vagolytic, and shouldn’t be used with pheo due to that.

Question 23

No sux in pheo-why? What drug isbokay with pheo?

Answer 23

supposedly the fasciculations will cause catecholamine release secondary to abdominal pressure (does that mean people with pheo should be on high dose stool softeners?). Again, unfounded, as it is based on a 1960s case report that was conjecture. So far the dogma has not overtaken good ole’ propofol, so that’s our correct answer.

Question 24

During the abdominal dissection for a pheochromocytoma, the patient develops rapidly progressive hypertension and tachycardia. The next best step is:

A. Administer labetalol and hydralazine
B. Start an esmolol gtt
C. Start a nitroprusside gtt
D. Increase the depth of anesthesia with sevoflurane
E. Increase the depth of anesthesia with propofol

Answer 24

C: Start a nitroprusside gtt

Manipulation of the tumor can expel massive amounts of catecholamines and make for a wild ride intraoperatively. The goal is to administer a short acting, easily titratable agent that can be stopped and completely inactive in minutes. Of the choices, esmolol and nitroprusside both fit the bill. Nitroprusside is more effective in treating hypertension (avoiding cerebral bleeds, etc) making it the better choice (although esmolol could be used as an adjuvant to that. Nicardipine (not listed) would also be an excellent drug for this purpose. Sevoflurane and propofol at supratherapeutic levels are not as directly addressing the catecholamine problem, nor are they as quickly titratable or effective (answers “Increase the depth of anesthesia with sevoflurane” & “Increase the depth of anesthesia with propofol”). The worst thing to do is “Administer labetalol and hydralazine”. The problem here is that in minutes, the patient will be extremely hypotensive, and you’ll be pushing pressors! As an aside, I had to remove a CRNA from a room, who without calling, gave 20 mg labetalol and 20 mg hydralazine, and then called to say the patient was still too hypertensive. Needless to say we battled systolic pressures in the 50s with an epinephrine gtt for a long while soon after!

Question 25

After 20 minutes of extreme hypertension during an open removal of pheochromocytoma treated with nicardipine gtt, the patient has become suddenly hypotensive. Vitals: BP 75/55, HR 90, Sat 100%, ETCO2 32 (unchanged from induction). Which of the following has most likely happened:

A. The surgeon has entered the inferior vena cava (IVC)
B. The surgeon has ligated the adrenal vein
C. The patient has a pulmonary embolism (PE)
D. The patient has suffered a massive myocardial infarction (MI)

Answer 25

: B: The surgeon has ligated the adrenal vein

After the adrenal vein has been removed from the rest of circulation, the steady stream of supranormal catcholamines comes to an abrupt end and the patient has become profoundly hypotensive. PE and massive MI with significantly reduced cardiac output are unlikely since the ETCO2 hasn’t changed.

Question 26

Which of the following is associated with pheochromocytoma:

A. MEN-2A
B. Neurofibromatosis -1
C. Von Hippel-Lindau
D. All of the above

Answer 26

The correct answer is: D: All of the above

The whole purpose of this question is not to review these syndromes, but to realize that when one of these patients’ present on the boards, their chance of having a pheochromocytoma is very high.

Question 27

Carcinoid syndrome and what can be affected Intraoperatively. Chronic effects of carcinoid

Answer 27

Carcinoid syndrome develops when patients have carcinoid tumors that either metastasize to the liver or develop outside the gastrointestinal tract (as GI tumor secretion is metabolized by the liver). Release of vasoactive substances (serotonin, kallikrein, & histamine) can lead to profound hypotension and bronchospasm intraoperatively.
The chronic effects of carcinoid syndrome include fibrotic patches on the right heart endocardium as well as profound tricuspid regurgitation (or pulmonary stenosis). The mediators of its cardiogenic effects are generally well metabolized by the lung, thus greatly reducing these effects on the left heart.

Question 28

Mgmt of carcinoid syndrome:
Which drugs should be avoided?
Which drug should be given?

Answer 28

Management of carcinoid revolves around avoiding those things that stimulate release. Increased catecholamine surges can lead to carcinoid flares, making regional anesthesia combined with general anesthesia an attractive option (answer A). Hypotension also increases sympathetic discharge, therefore an aggressive fluid strategy to avoid hypovolaemia is reasonable
Histamine releasing drugs should be avoided (few scattered case reports about morphine induced flares). Both morphine and meperidine release histamine (answer “Perioperative morphine instead of meperidine”). Finally, preoperative octreotide (or intraoperative gtt) can decrease release of carcinoid mediators.

Question 29

The most common cause of intraoperative anaphylaxis is:

Answer 29

The most common cause of intraoperative anaphylaxis is muscle relaxants

Question 30

Differences between anaphylactic and anaphylactoid reactions: do they both release IgE? What about serum tryptase?

Answer 30

Both anaphylactoid reactions and anaphylaxis can be equally severe and life threatening. Both reactions result in mast cell release of histamine, tryptase, proteoglycans, and other inflammatory mediators, except anaphylaxis is IgE mediated. Both reactions are found at an increased rate in atopic individuals. Because serum tryptase is released from mast cells, both reactions can have elevated serum levels. There is a lot of important information in that short explanation, maybe you should read it again.

Question 31

Which of the following patient related factors is LEAST likely to be associated with a latex allergy:

A. Congenital urinary tract disorders
B. Spina bifida
C. Multiple Sclerosis
D. Health care workers
E. Allergy to banana

Answer 31

C: Multiple Sclerosis

It is everyone’s responsibility to think about latex allergy, not just the OR nurse. Essentially, people who are exposed to latex for the greatest frequency and duration are most likely to develop this allergy, such as patients with congenital urinary tract disorders, spina bifida (see neonatal question 56), spinal cord injury, and patients with multiple surgeries (especially in childhood) have increased risk (the first two listed are by far the greatest of the mentioned risk factors). Healthcare and rubber workers also have increased risk. And, believe it or not, the ABA has asked about food allergies in relation to latex allergies. The classic offenders are avocado, banana, passion fruit, pineapple, mango, kiwi, among others.

Question 32

50 year old man with a history of diabetes and coronary disease on NPH insulin, metformin, furosemide, and metoprolol has presumed anaphylaxis following rocuronium administration intraoperatively for laparoscopic cholecystectomy. Following copious crystalloid resuscitation (6 liters of lactated ringers), epinephrine gtt, diphenhydramine, famotidine, and methylprednisolone injection the patient remains significantly hypotensive. Which of the following is the next BEST step:

A. Change from LR to albumin for resuscitation
B. Add hydrocortisone
C. Transfuse PBRCs
D. Administer glucagon
E. Change from epinephrine gtt to norepinephrine gtt

Answer 32

The patient is having an inadequate response to epinephrine due to beta blockade and glucagon should be administered. Norepinepherine has been used successfully as pressor for anaphylaxis, although epinephrine gtt remains the “gold standard.” Both drugs agonize the beta receptors, therefore switching from epinephrine to norepinephrine would not be expected to be of much benefit. Some data suggests that vasopressin is an ideal second agent in refractory anaphylaxis if beta blockade is not an issue. Volume resuscitation is the cornerstone of anaphylaxis treatment, but switching from crystalloid to colloid has no significant impact (nor would PBRC transfusion for volume reasons). Hydrocortisone is a perfectly balanced steroid as far as mineral- and gluco-corticoid effects go, but methylprednisolone is a perfectly reasonable substitute. Also note that the stem question gave you the boards answer of how to treat anaphylaxis: fluids, epinephrine, H1 blockers, H2 blockers, and steroids!

Question 33

how to treat anaphylaxis:

Does switching from crystalloid to colloid help?

Answer 33

fluids, epinephrine, H1 blockers, H2 blockers, and steroids!

No.

Question 34

Cross-reactions between penicillin and cephalosporins uncommon-How uncommon?

Answer 34

and likely even less than 2%.

Question 35

45 year old woman complains of bilateral joint pain which improves throughout the day, generalized fatigue, and examination reveals painful nodules over multiple joints. Which of the following is a likely finding:

A. Obstructive pattern on spirometry
B. Dilated cardiomyopathy
C. Atlanto-axial instability
D. Recurrent laryngeal nerve palsy

What kind of lung problems? Intubating problems? Recurrent laryngeal nerve problems? Cardiac problems?

Answer 35

What is this? RA
RA has multiple end-organ effects the anesthesiologist should be aware of. First and foremost is a 25% incidence of atlanto-axial instability (answer C) secondary to both ligamentous and bony changes. Cervical spine films (extension/ flexion) are recommended, especially for patients with limited neck movement or pain with extension. Involvement of cricoarytenoid joints cause stridor and difficult intubation. Compression of the recurrent laryngeal nerves are not expected (answer “Recurrent laryngeal nerve palsy”). Restrictive lung disease is more common than obstructive in RA from both fibrosis and pleural effusions. Pericarditis, endocarditis, valvulitis, and left ventricular hypertrophy with diastolic dysfunction is more common, not dilated cardiomyopathy. Vasculitis, myocardial infarction, conduction block, and stroke are associated with RA as well.

Question 36

AS neck problems? Neuraxial and general anesthesia risks in patients with AS?

Answer 36

In AS the problem is usually cervical neck stenosis, not instability. In both AS and RA, TMJ issues can limit mouth opening. For neuraxial anesthesia, intervertebral spaces are usually reduced and ossified making placement of the block difficult. There is a suggestion that epidural haematoma is more common in AS patients perhaps due to the need for multiple attempts. Furthermore, there is a higher risk for high spinal/ epidural in AS.