Medication Flashcards
22.2 The diabetic medication that, as part of its therapeutic effect, significantly prolongs gastric emptying is
a) dulaglutide
b) sitagliptin
c) metformin
d) gliclazide
e) acarbose
a) dulaglutide
The primary mechanism of action of dulaglutide, as an incretin mimetic hormone or an analogue of human glucagon-like peptide-1, is to increase insulin secretion when glucose levels are elevated, decrease glucagon secretion, and delay gastric emptying in an effort to lower postprandial glucose level.
Acarbose:
Acarbose is a complex oligosaccharide that acts as a competitive, reversible inhibitor of pancreatic alpha-amylase and membrane-bound intestinal alpha-glucoside hydrolase.
Pancreatic alpha-amylase hydrolyzes complex carbohydrates to oligosaccharides in the small intestine
By delaying the digestion of carbohydrates, acarbose slows glucose absorption, resulting in a reduction of postprandial glucose blood concentrations.
-> causes delayed gastric emptying but is not necessarily a part of its therapeutic effect
20.1 Prolonged block post mivacurium
A)Sugammadex 4mg/kg
B)Neostigmine 100microg/kg
C)FFP 20ml/kg
D)Pralidoxime
E)Wait for it to wear off
E)Wait for it to wear off
> Neostigmine inhibits plasma cholinesterases (that could slow mivacurium metabolism), but effects are less than the inhibition of acetylcholinesterases, resulting in a “net” reversal of nondepolarizing block. Dose in stem inappropriate though.
> Administration of whole blood or FFP is not recommended unless there is another primary indication for the transfusion.
> In patients with homozygous pseudocholinesterase deficiency, will result in prolonged NMB; monitor and await.
22.1 A 74-year-old man presents for a femoral popliteal artery bypass procedure for peripheral limb ischaemia. Regarding its role in modifying his perioperative cardiovascular risk, clonidine
a. Increased stroke
b. No change in complications
c. Increased death
d. Increased non fatal MI
e. Increased risk of non fatal cardiac arrest
e. Increased risk of non fatal cardiac arrest
POISE II
* clonidine 200mcg per day - did not reduce the rate of composite outcome of death or nonfatal MI - but it increased the risk of clinically important hypotension and nonfatal cardiac arrest
* aspirin initiation or continuation – no significant effect on rate of composite of death or non fatal MI but increased risk of major bleeding
22.2 The medication most strongly associated with an acute primary hypotensive reaction following transfusion of blood products is
a. aspirin
b. celecoxib
c. hydralazine
d. metoprolol
e. labetalol
f. perindopril
f. perindopril
Hypotensive transfusion reactions, which account for almost 3% of all transfusion reactions, are associated with patients treated with angiotensin-converting enzyme inhibitors. The current hypothesis suggests that they are caused by bradykinin-induced vasodilation in the absence of allergic, hemolytic, or septic mechanisms. The hypotension observed frequently is unresponsive to conventional therapy with catecholamines. The suggested intraoperative management includes cessation of transfusion and washing red blood cells before blood replacement.
Hypotensive reactions to transfusion may not always be recognized. To prevent these reactions, clinicians have several options: they may discontinue the ACE inhibitor (elective transfusion), not use a leukoreduction filter (if the patient has no absolute requirement for leukoreduced blood components), use washed cellular components, or use components that have undergone leukoreduction at the collection facility or the hospital blood bank before transfusion (since bradykinin is degraded during storage).
22.2 A 45-year-old male received a heart transplant one month ago. He develops a new supraventricular tachyarrhythmia without hypotension during a gastroscopy. The most appropriate therapy is
a) Adenosine
b) Amiodarone
c) Digoxin
d) Esmolol
e) Verapamil
d) Esmolol
Management of Arrhythmias After Heart Transplant
https://www.ahajournals.org/doi/10.1161/CIRCEP.120.007954
In asymptomatic patients, additional cardiac monitoring such as 24-Holter or an event monitor can be useful to assess the SVT burden, and a trial of atrioventricular nodal blockers (β-blockers preferably) can be attempted with caution in view of potential risk of bradycardia. Calcium channel blockers such as diltiazem and verapamil are contraindicated in patients taking immunosuppression such as tacrolimus and cyclosporine as it can impair the metabolism CYP3A, which increases the levels of these drugs potentially causing renal toxicity.
The use of adenosine in the management of SVT has remained a subject of controversy for over a quarter century. In the past, adenosine was contraindicated in patients post-OHT due to its supersensitivity and presumed risk of prolonged atrioventricular block.
Thus, based on the aforementioned data, in patients with OHT, adenosine is feasible and safe at reduced doses (starting at 1.5 mg for patients ≥60 kg) as long as patients are closely monitored, with dose escalation as needed. Furthermore, the 2010 American Heart Association guidelines on advanced cardiovascular life support also recommended lowering the initial dose of adenosine to 3 mg for the acute management of SVT in patients with OHT.
23.1 The glucagon-like peptide-1 receptor (GLP-1) agonist semaglutide is associated with
A. delayed gastric emptying
B. hypoglycaemia
C. hyperlactataemia
a) delayed gastric emptying
22.1 A drug which does NOT increase the defibrillation threshold in a patient with an implanted cardioverter defibrillator is
a. Amiodarone
b. Atropine
c. B-blocker
d. Flecainide
e. Sotalol
e. Sotalol
Drugs that INCREASE defibrillation threshold:
+ Amiodarone (Chronic)
+ Atropine
+ lignocaine
+ Diltiazem
+ Flecainide
+ Verapamil
+ Venlafaxine
+ Anaesthetic agents.
Drugs that DECREASE defibrillation threshold:
- Sotalol
- Amiodarone (acute)
- Nifekalant
Drugs with No Change in DFT
= B- blocker
= Disopyramide
= Procainamide
= Propafenone
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6304797/
22.1 The mechanism of action of tranexamic acid is to inhibit the formation of
a. Plasminogen
b. Plasmin
c. Fibrin
d. fibrinogen
b. Plasmin
Plasminogen activation results in increased conversion of plasminogen to plasmin, the latter an enzyme that breakdowns the fibrinogen in blood clots.
Tranexamic acid is a synthetic derivative of lysine that exerts antifibrinolytic effects by blocking lysine binding sites on plasminogen molecules, inhibiting the interaction of plasminogen with formed plasmin and fibrin.
As a result, inhibition of plasminogen activation results in stabilization of the preformed fibrin meshwork produced by secondary hemostasis.
23.1 In subarachnoid block for caesarean section, hyperbaric local anaesthetic compared to regular local anaesthetic has been shown to reduce the
a. Risk of total spinal
b. Analgesic properties
c. Onset of anaesthetic
d. Offset of anaesthetic
e. Chance of inadequate anaesthetic
reduce onset time
c) faster onset of anaesthetic
https://pubmed.ncbi.nlm.nih.gov/28708665/ agrees with faster onset but for non obstetric surgery
UTD
hyperbaric bupivacaine because of its rapid onset and the option to modify the spinal level by changing the position of the operating table. Plain bupivacaine (ie, slightly hypobaric, prepared in saline) may also be used for spinal anesthesia for CD. The literature comparing safety and efficacy of hyperbaric with isobaric bupivacaine for CD is inconclusive
20.1 IgE-related penicillin anaphylaxis crossover rate with cephazolin
a. 0.1%
b. 1%
c. 5%
d. 10%
1%
BJA ED
20.2 Idarucizumab reverses the anticoagulant effect of
a) Clopidogrel
b) Rivaroxaban
c) Dabigatran
d) Apixaban
e) Rivaroxaban
c) Dabigatran
Idarucizumab (Praxbind) is a monoclonal antibody to dabigatran
Dabigatran bleeding may be treated with:
- idarucizumab
- haemodialysis
- TXA will decrease fibrinolysis and has some effect
- FFP also has some effect
Humanized monoclonal antibody fragment (Fab) indicated in patients treated with dabigatran (Pradaxa) when reversal of the anticoagulant effects are needed for emergency surgery or urgent procedures, or in the event of life-threatening or uncontrolled bleeding
- 5 g IV, provided as 2 separate vials each containing 2.5 g/50 mL (see Administration)
- Limited data support administration of an additional 5 g
Dosage Modifications
Renal impairment: Renal impairment did not impact the reversal effect of idarucizumab; no dosage adjustment required
Hepatic impairment: Not studied
Dosing Considerations
This indication is approved under accelerated approval based on a reduction in unbound dabigatran and normalization of coagulation parameters in healthy volunteers; continued approval for this indication may be contingent upon the results of an ongoing cohort case series study
22.2 When used for prolonged analgesia in a healthy adult, the recommended maximum dose of ropivacaine via continuous infusion or bolus dosing in a 24-hour period is
a) 450mg
b) 600mg
c) 770mg
d) 1200mg
c) 770mg
Product info: Fresenius-Kabi
When prolonged epidural blocks are used, either by continuous infusion or repeated bolus administration, the risks of reaching a toxic plasma concentration or inducing local neural injury must be considered. Cumulative doses of up to 800 mg ropivacaine for surgery and postoperative analgesiaadministered over 24 hours were well tolerated in adults, as were postoperative continuous epidural infusions at rates up to 28 mg/hour for 72 hours.
product info: pfizer
When prolonged blocks are used, either through continuous infusion or through repeated bolus administration, the risks of reaching a toxic plasma concentration or inducing local neural injury must be considered. Experience to date indicates that a cumulative dose of up to 770 mg ropivacaine hydrochloride administered over 24 hours is well tolerated in adults when used for postoperative pain management: i.e., 2016 mg. Caution should be exercised when administering ropivacaine for prolonged periods of time, e.g., > 70 hours in debilitated patients
21.2 Of the following drugs, the least likely to cause pulmonary vasodilation when used at low
doses in patients with chronic pulmonary hypertension is
a) Dopamine
b) Dobutamine
c) Vasopressin
d) Milrinone
dopamine
- least likely to cause pulmonary vasodilation (all the others do to my knowledge)
- From UP TO DATE:
> At low doses of 1 to 3 mcg/kg per min, dopamine acts primarily on dopamine-1 receptors to dilate the renal and mesenteric artery beds
> At 3 to 10 mcg/kg per min (and perhaps also at lower doses), dopamine also stimulates beta-1 adrenergic receptors and increases cardiac output, predominantly by increasing stroke volume with variable effects on heart rate.
> At medium-to-high doses, dopamine also stimulates alpha-adrenergic receptors, although a small study suggested that renal arterial vasodilation and improvement in cardiac output may persist as the dopamine dose is titrated up to 10 mcg/kg per min
*clinically, the haemodynamic effects of dopamine demonstrate individual variability
Dobutamine (inodilator):
- selective β1-agonist that increases cardiac contractility and reduces pulmonary vascular and systemic vascular resistances
Vasopressin:
- vasopressin may have pulmonary vasodilatory effects in addition to a systemic vasoconstrictive effect
Milrinone (inodilator):
- the phosphodiesterase-3 inhibitors, milrinone and enxoimone, have positive inotropic effects combined with the capacity to reduce RV afterload (‘inodilators’) without significant chronotropic effect, but they can be associated with significant systemic hypotension
22.1 A 30-year-old parturient presents in labour. She has a history of Addison’s disease from autoimmune adrenalitis and has been taking prednisolone 6 mg daily for ten years. On presentation the patient is given hydrocortisone 100 mg intravenously. The most appropriate steroid replacement regimen the patient should receive during labour is
a. 25mg TDS hydrocortisone
b. 8mg/hr hydrocortisone
c. 6mg PO prednisone
8mg/hr
Guidelines for mx of glucocorticoids during the perioperative period for patients with adrenal insufficiency
https://associationofanaesthetists-publications.onlinelibrary.wiley.com/doi/10.1111/anae.14963
23.1 The next patient on your endoscopy list is a 50-year-old woman who has been scheduled for gastroscopy and colonoscopy under sedation, after unsatisfactory
proceduralist-supervised midazolam and fentanyl sedation in the past. She states that she has egg anaphylaxis and carries an adrenaline (epinephrine) auto-injector.
The most appropriate agent to use for her sedation is
A. Propofol
B. Ketamine
C. Remifentanil
D. Sevofluarane
A
The situation in adults is straightforward: there is convincing evidence that propofol is safe in patients who are allergic to peanut and/or soy and/or egg.
BJA Ed
https://academic.oup.com/bja/article/116/1/11/2566111
21.2 The oral morphine equivalent of tapentadol 50 mg (immediate release) is
a) 5mg
b) 10mg
c) 15mg
d) 20mg
e) 25mg
c) 15mg
Oral Tapentadol 25mg = 8mg Oral Morphine
Oral Oxycodone 5mg = 8mg Oral Morphine
Oral Tramadol 25mg = Oral Morphine 5mg
Oral Hydromorphone 4mg = Oral Morphine 20mg
S/L Buprenorphine 200mcg = 8mg Oral Morphine
IV Oxycodone 5mg = Oral Morphine 15mg
IV Morphine 5mg = Oral Morphine 15mg
IV Hydromorphone 1mg = Oral Morphine 15mg
20.1 The substance that should be avoided in a patient with history of anaphylaxis to MMR vaccine is
a) Protamine
b) Penicillin
c) Sulphonamides
d) Gelofusine
gelofusin
Anaphylaxis after vaccination is probably due to anaphylactic sensitivity to gelatin or neomycin, not an egg allergy
22.2 A patient presents for endoscopic retrograde cholangiopancreatography (ERCP) with a history of previous post-ERCP pancreatitis. The management most likely to reduce the likelihood of pancreatitis is
a) Gentamicin
b) PR indomethacin
c) Creon post op
d) Preop smoking cessation
b) PR indomethacin
APMSE 5th edition 8.6.1.3: Only rectal NSAIDs are effective for reducing post ERCP pancreatitis, particularly indomethacin. Epidural > PCA for severe acute pancreatitis
A Randomized Trial of Rectal Indomethacin to Prevent Post-ERCP Pancreatitis
https://www.nejm.org/doi/full/10.1056/NEJMoa1111103
Nonsteroidal antiinflammatory drugs (NSAIDs) are potent inhibitors of phospholipase A2, cyclooxygenase, and neutrophil–endothelial interactions, all believed to play an important role in the pathogenesis of acute pancreatitis. NSAIDs are inexpensive and easily administered and have a favorable risk profile when given as a single dose, making them an attractive option in the prevention of post-ERCP pancreatitis. Preliminary studies evaluating the protective effects of single-dose rectal indomethacin or diclofenac in post-ERCP pancreatitis have been conducted, and a meta-analysis suggests benefit.
Results
A total of 602 patients were enrolled and completed follow-up. The majority of patients (82%) had a clinical suspicion of sphincter of Oddi dysfunction. Post-ERCP pancreatitis developed in 27 of 295 patients (9.2%) in the indomethacin group and in 52 of 307 patients (16.9%) in the placebo group (P=0.005). Moderate-to-severe pancreatitis developed in 13 patients (4.4%) in the indomethacin group and in 27 patients (8.8%) in the placebo group (P=0.03).
Conclusions
Among patients at high risk for post-ERCP pancreatitis, rectal indomethacin significantly reduced the incidence of the condition.
The amount of intravenous potassium chloride required to raise the plasma potassium level from 2.8 mmol/L to 3.8 mmol/L in a normal adult is approximately
a. 10mmol
b. 20mmol
c. 30mmol
d. 100mmol
e. 200mmol
e. 200mmol
K+ < 3.0 mmol/L: 200-400 mmol of potassium are required to raise it by 1 mmol/L
K+ > 3.0 mmol/L: 100-200 mmol of potassium are required to raise it by 1 mmol/L
Hypokalaemia P. GLOVER
https://www.cicm.org.au/CICM_Media/CICMSite/CICM-Website/Resources/Publications/CCR Journal/Previous Editions/September 1999/05-Sept_1999_Hypokalaemia.pdf
If the serum potassium level is greater than 3 mmol/L, 100-200 mmol of potassium are required to raise it by 1 mmol/L; 200 - 400 mmol are required to raise the serum potassium level by 1 mmol/L when the potassium concentration is less than 3mmol/L, assuming a normal distribution between cells and the intracellular space, and a linear relationship between plasma potassium and body deficit (which has been described, i.e. 0.27 mmol/L/100 mmol deficit/70 kg), exists. The rate of administration of potassium will be influenced by the presence and seriousness of the pathophysiological changes caused by hypokalaemia. The underlying disorder should also be treated simultaneously.
22.2 A 48-year-old man is day two post-laparoscopic high anterior resection. He has used 42 mg of intravenous morphine in the past 24 hours. You wish to start him on oral tapentadol immediate release. The most appropriate equianalgesic dosage would be
a) 50mg six times a day
b) 100mg six times a day
c) 200mg six times a day
d) 300 mg six times a day
a) 50mg six times a day
42mg IV Morphine = 126mg Oral Morphine
126/8= 15.75
15.75 x 25 = 393.75 (*400mg/day Tapentadol)
Option 50mg 6 times a day = 300mg
As direct OME to tapentadol conversion is 400mg, a 300mg dose represents a 25% dose reduction, which is line with a 25-50% dose reduction due to incomplete cross-tolerance during opioid rotation.
Oral Tapentadol 25mg = 8mg Oral Morphine
Oral Oxycodone 5mg = 8mg Oral Morphine
Oral Tramadol 25mg = Oral Morphine 5mg
Oral Hydromorphone 4mg = Oral Morphine 20mg
S/L Buprenorphine 200mcg = 8mg Oral Morphine
IV Oxycodone 5mg = Oral Morphine 15mg
IV Morphine 5mg = Oral Morphine 15mg
IV Hydromorphone 1mg = Oral Morphine 15mg
23.1 The bioavailability of an oral dose of ketamine is approximately
A. 10%
B. 20%
C. 40%
D. 70%
E. 80%
B. 20%
25% (a few studies have higher ranges but typically around 20-25%)
https://doi.org/10.1192/bjp.bp.115.165498
20.1 The anti-emetic action of aprepitant is via receptors for
A. Serotonin
B. Neurokinin-A
C. Dopamine
D. Substance P
E. Glycine
D. Substance P
Development of aprepitant, the first neurokinin-1 receptor antagonist for the prevention of chemotherapy-induced nausea and vomiting (2011)
https://www.ncbi.nlm.nih.gov/pubmed/21434941
Aprepitant acts centrally at NK-1 receptors in vomiting centres within the central nervous system to block their activation by substance P released as an unwanted consequence of chemotherapy.
23.1 Of the following drugs, the LEAST suitable for managing atrial arrhythmias in a patient with a left ventricular assist device is
A. Metoprolol
B. Amiodarone
C. Digoxin
D. Diltiazem
d) diltiazem
Nondihydropyridine calcium channel blockers should be used cautiously in patients with HFrEF because of their negative inotropic effects, and the role of these agents in LVAD recipients remains unclear
https://www.ahajournals.org/doi/10.1161/CIR.0000000000000673
Should also avoid sotolol