Allergy, Endo, Rheum Flashcards
(36 cards)
Insulin and protein? Insulin’s receptor, and insulin and Na/ATPase
Insulin makes protein by building amino acids
Glut 4 receptor translocation
Increases Na/K ATPase which decreases serum potassium
Does stimulation of insulin receptor increase cAMP?? Does CAMP increase insulin? What kind of receptor is insulin, and what are it’s cellular effects?
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
IV insulin onset and duration
SQ insulin onset and duration
NPH insulin and onset
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.
One u it of insulin should decrease BG by how much?
A single unit of insulin should supposedly decrease glucose by about 25 points
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
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.
Main cause for acidity and increased lactic acid is what-like what’s missing intracellularly, and breakdown of what process is causing it?
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.
Osmotic diuresis leads to loss of which electrolytes. What happens to sodium on this situation?
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
DKA occurs in states of ______ deficiency concurrent with up regulation of what?
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
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?
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).
DKA and emergent/urgent/elective surgery:
KIM what about managing DKA intraoperatively:
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.
No SUX in DKA
True because of hyperkalemia
On the boards, goiter =
Hyperthyroidism and induction agents you should avoid:
How to assess goiter pre-operatively:
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.
Emergency surgery in a patient with goiter (hyperthyroidism)-can start a gtt or what?
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
Recurrent laryngeal nerve innervates
all but one muscle of the vocal cords (cricothyroid muscle – external branch of superior laryngeal nerve).
Unilateral vs bilateral transection of RLN
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.
What happens to Parathyroid during these surgeries? Reactive airway edema s/p thyroidectomy, and what you should do about it.
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.
You should always be thing about _____ post thyroidectomy? And then what to do about it?
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).
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
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).
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?
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.
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?
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.
How should patients with pheochromocytoma be managed prior to surgery-which meds should they be put on, what are you watching? Similarity to PET?
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.
Pancironium has which kind of activity, and shouldn’t be used with pheo-why?
Vagolytic, and shouldn’t be used with pheo due to that.
No sux in pheo-why? What drug isbokay with pheo?
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.
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
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!
