Reading...
Play button
Play button
Use LEFT and RIGHT arrow keys to navigate between flashcards;
Use UP and DOWN arrow keys to flip the card;
H to show hint;
A reads text to speech;
22 Cards in this Set
- Front
- Back
|
[Apr08][Oct08][Oct09][Aug10][?Aug12]
Central anticholinergic syndrome, which is NOT true: A. Will improve with neostigmine B. Peripheral anticholinergic symptoms C. Caused by Anti-Parkinson drugs D. CNS depression E. Associated with agitation, delirium, and ??? |
A. Will improve with neostigmine
- Neostigmine (quarternary ammonium structure) does not cross the BBB and will not have a central effect. Physostigmine (tertiary ammonium structure) DOES cross the BBB and is the treatment of choice. ACUTE ANTICHOLINERGIC SYNDROME DEFINITION Clinical syndrome resulting from antagonization of acetylcholine at the muscarinic receptor. TOXIC CAUSES Antihistamines (especially Promethazine, Trimeprazine, Dimenhydrinate) Antiparkinsonian drugs (e.g., Benztropine, Biperiden, Orphenadrine, Procyclidine) Antispasmodic agents (e.g., Clidinium, Glycopyrrolate, Propantheline) Belladonna alkaloids (e.g., Belladonna extract, Atropine, Hyoscine, L-Hyoscyamine sulphate, Scopolamine hydrobromide) Cyclic Antidepressants Ophthalmic cycloplegics (e.g., Cyclopentolate, Homatropine, Tropicamide) Phenothiazines Plants containing anticholinergic alkaloids (e.g., Atropa belladonna, Brugmansia spp, Cestrum spp, Datura spp, Hyoscyamus niger, Solanum spp). The tropane derivatives (alkaloids of solanaceous plants and related drugs) are of greatest practical importance. CLINICAL FEATURES The clinical diagnosis is based on the appearance of the anticholinergic toxidrome. This toxidrome has central and peripheral components: The central anticholinergic signs and symptoms include altered mental status, disorientation, incoherent speech, delirium, hallucinations, agitation, violent behaviour, somnolence, coma, central respiratory failure, and, rarely, seizures. The peripheral anticholinergic syndrome includes hyperthermia, mydriasis, dry mucosa membranes, dry, hot and red skin, peripheral vasodilatation, tachycardia, diminished bowel motility (even paralytic ileus), and urinary retention. Rhabdomyolysis, cardiogenic shock or cardiorespiratory arrest may occur exceptionally. Patients with closed-angle glaucoma may suffer an acute precipitation of the condition. Patients with benign prostatic hyperplasia are particularly prone to develop urinary retention. DIFFERENTIAL DIAGNOSIS Alcohol withdrawal Organic delirium (usually secondary to sepsis) Psychiatric illness Psychedelic drugs Sympathomimetic drugs RELEVANT INVESTIGATIONS Measurement of blood and urine levels of the anticholinergic agents are of little or no practical value. Other laboratory examinations may be needed as dictated by the general condition of the patient. TREATMENT Treatment is primarily supportive. The patient must be protected from self-inflicted injury. This may require physical and/or pharmacological restraint. Respiratory failure may require intubation and controlled respiration. In cases of ingestion, decontamination may be considered. Diazepam: Administer 5 to 10 mg intravenously over 1 to 3 minutes. Repeat this dose as necessary to a maximal total dose of 30 mg. The paediatric dose of diazepam is 0.25 to 0.4 mg/kg up to maximal total dose of 5 mg in children up to 5-years-old and 10mg in children over 5-years-old. Physostigmine is a specific antidote for anticholinergic poisoning and may be used under the following conditions : 1. Severe agitation or psychotic behaviour unresponsive to other treatments. 2. Clinical evidence of both peripheral and central anticholinergic syndrome. 3. No history of seizures. 4. Normal ECG, especially QRS width. 5. No history of ingestion or co-ingestion of tricylic antidepressants or other drugs that delay intraventricular conduction. 6. Cardio-respiratory monitoring in place and resuscitation facilities available. The dose of physostigmine is 1 to 2 mg (0.5 mg in children) by intravenous injection over 2 to 5 minutes. If necessary, this dose can be repeated after 40 minutes. CLINICAL COURSE AND MONITORING Complete recovery is expected over a period of hours to days. In more severe cases of anticholinergic syndrome, cardiac rhythm should be monitored and blood pressure frequently measured. Urine output should be monitored so as not to overlook urinary retention. ----------- |
|
|
[Mar10] Acetylcholine receptors are down regulated in
A. Guillain-Barre syndrome B. Organophosphate poisoning C. Spinal cord injury D. Stroke E. Prolonged NMBD use |
B. Organophosphate poisoning
thought to be the cause of the intermediate syndrome at 1-4 days post ingestion - Wiki: A - False. Effectively a denervation injury which causes UP-regulation. B - TRUE. Organophosphate poisoning causes increases in miniature-end-plate potential (MEPP), and thus can cause DOWN-regulation of ACh receptors. Apparently continuous exposure to organophosphates can cause degeneration of pre-junctional and post-junctional structures. C - False. Denervation causes UP-regulation. D - False. As for spinal cord injury. E - Prolonged NMBD use can cause UP-regulation of ACh receptors. ----------- |
|
|
[May09] Stimulation of flexor pollicis brevis compared to abductor pollicis brevis is likely to show
A. Slower recovery from NDMR B. Same recovery C. Faster recovery |
B. Same recovery
- See wiki May09. Some have queried if it should be flexor hallucis brevis. ----------- |
|
|
EM66 [Apr09][Oct09][Mar2010][Aug2010][?Aug12]
What's the most appropriate mode for neuromuscular monitoring during aneurysm clipping? A. TOF count B. TOF ratio C. Post tetanic count D. DBS E. ? |
C. Post tetanic count (PTC)
- Used to assess profound block ----------- |
|
|
IC77 [Apr07][Jul07][Mar10]
The signs of exposure to a nerve agent such as Sarin or VX include A. bronchodilation B. dry skin C. muscle fasciculation D. pupillary dilatation E. tetany |
C. muscle fasciculation
cholinergic syndrome DUMBELSS Diarrhoea Urination Meiosis Bradycardia Emesis Lacrimation Salivation Sweating ----------- |
|
|
PR01
Following the IV injection of 1 mg/kg of suxamethonium the serum K+ increase is: A. Typically 0.8-1.5 mmol/l in normal adults B. Largely prevented by pretreatment with 0.04 mg/kg d-tubocurarine C. Not exaggerated by renal failure D. Higher in patients with atypical cholinesterase E. None of the above (Related Q PR34) |
C. Not exaggerated by renal failure
- A False - 0.2-0.4mmol/L ↑ B ?False - may attenuate the hyperkalaemic response but it's not largely prevented C True Word for word in Stoelting Anesthesia and Coexisting disease : "Potassium release following administration of succinylcholine is not exaggerated in patients with chronic renal failure, although there is a theoretical concern that those with extensive uremic neuropathies might be at increased risk. Likewise, caution is indicated when the preoperative serum potassium concentration is in the high-normal range, as this finding combined with maximum drug-induced potassium release (0.5–1.0 mEq/L) could result in dangerous hyperkalemia. It is important to recognize that small doses of nondepolarizing muscle relaxants administered before the injection of succinylcholine do not reliably attenuate the succinylcholine-induced release of potassium." But renal patients have a higher starting point so more likely to get higher levels (ie the ↑ is the still the same) D False E False comment - 6 mg dtc may attenuate/prevent response ----------- |
|
|
PR02
Suxamethonium-induced hyperkalaemia: A. Is blocked by prior administration of cyclohexylamine B. May be modified by the prior administration of non-depolarizing muscle relaxants C. Is commoner in children D. Does not occur in the absence of muscle trauma E. Has a poor prognosis |
B. May be modified by the prior administration of non-depolarizing muscle relaxants
----------- |
|
|
PR04 ANZCA version [2002-Aug] Q11, [2003-Apr] Q39, [2005-Sep] Q46, [Mar06][Sep11][Mar12]
The percentage of the population which is heterozygous as regards pseudocholinesterase, thus having a dibucaine number between 30 and 80 (Sep11, Mar12 said 30-70), is A. 0.04% B. 0.4% C. 4.0% D. 14.0% E. 40.0% |
C. 4% - true: "In most Caucasian populations the frequency of occurence of heterozygotes for the normal and atypical genes is about 1 in 25, and the frequency of homozygotes for the atypical gene is about 1 in 2500. The atypical gene is rare in orientals and African blacks." Pantuck EJ: Plasma cholinesterase: Gene and variations. Anesth Analg 77:380-386, 1993
96% are Homozygous for Eu:Eu (Dibucaine number = 80) A if homozygous ----------- |
|
|
PR05
The proportion of the community which shows marked atypical pseudocholinesterase activity (dibucaine no. = 20-30) is: A. 0.4% B. 4% C. 25% D. 60% |
0.03% … so no option is correct
----------- |
|
|
PR43 [Mar93] [Apr07]
Plasma clearance of non-depolarising muscle relaxants in pregnant patients (when compared with matched non-pregnant controls) is: A. Delayed because distribution half-life is prolonged due to increased circulating blood volume in late pregnancy B. Delayed because elimination half-life is prolonged due to delayed hepatic & renal clearance due to hormonal changes in pregnancy C. Accelerated because the distribution half-life is shortened due to changes in cardiac output in pregnancy D. Accelerated because the elimination half-life is shortened due to increased hepatic and renal clearance due to hormonal changes in pregnancy E. Accelerated because the distribution half-life is shortened due to the placental transfer of the relaxant to fetal & placental tissue. |
D. Accelerated because the elimination half-life is shortened due to increased hepatic and renal clearance due to hormonal changes in pregnancy
- "The clearance of vecuronium may be accelerated during late pregnancy, possibly relecting stimulation of hepatic microsomal enzymes by progesterone as well as by cardiovascular changes and fluid shifts that occur during pregnancy" (Stoelting Pharm and phys p.238 4th ed) ----------- |
|
|
PR48 [Apr98] [Jul98] [Apr99] [Jul07][Apr08]
With regard to non-depolarising muscle relaxants: A. NDMR actions are increased with hyperkalemia B. Vecuronium exclusively (or primarily) undergoes renal elimination C. Mivacurium half-life 10 minutes D. Cisatracurium is metabolised to laudanosine by the liver E. May require larger doses if treated with phenytoin and theophylline |
E. May require larger doses if treated with phenytoin and theophylline
➭ NMDR actions increased with hypokalaemia ➭ Vecuronium metabolism: renal 30%, biliary 40%, rest hepatic ➭ Mivacurium lasts 12-20 minutes, half life approximately 2 minutes ➭ Cisatracurium is metabolised by plasma esterases and Hofmann degradation at physiological pH and temperature, eliminated by the liver ----------- |
|
|
PR54 ANZCA version [2003-Apr]
In the management of exposure to toxic nerve agents (highly potent anticholinesterases) A. early treatment with glycoprrolate is more effective than atropine B. ketamine is contra-indicated for endotracheal intubation C. oximes (eg.pralidoxime) in normal doses have no endogenous anticholinergic effects D. oximes reactivate AChE by cleavage of phosphorylated active sites E. pre-treatment with pyridostigmine prevents the effects of these agents |
D. oximes reactivate AChE by cleavage of phosphorylated active sites
- A: False. "Atropine and oximes are effective antidotes if administered early after exposure. Atropine antagonizes muscarinic side-effects and is more beneficial than glycopyrrolate, which has a shorter half-life and does not cross the blood-brain barrier." B: False. "Ketamine may be beneficial for intubation." C: False. "They (oximes) in normal doses have an endogenous anticholinergic effect." D: True. "Administered early, oximes reactivate AChE by cleavage of phosphorylated active sites." E: False. Does not prevent the effects. "Pyridostigmine bromide may be used as a pretreatment . . . (though it is not a true pretreatment, which would protect against nerve agents, but an "antidote enhancer") . . . The rationale of pyridostigmine pretreatment is that pyridostigmine carbamylation of AChE binding sites produces a reservoir of temporarily inactivated AChE. After exposure, nerve agents are unable to bind to the carbamylated enzyme. Later dissociation of pyridostigmine reactivates AChE, which, by hydrolysing acetylcholine, reduces the incidence of cholinergic crisis (in conjunction with atropine and pralidoxime). ----------- |
|
|
PR55
In patients with advanced liver disease who receive muscle relaxants A. decreased plasma clearance of vecuronium and rocuronium leading to prolonged blockade is a consistent feature B. duration of action of mivacurium is NOT affected C. initial doses should be reduced as volume of distribution is decreased D. plasma clearance of atracurium and cisatracurium is increased E. when the desired level of block is achieved with the initial dose, subsequent recovery is comparable to patients without liver disease |
A. decreased plasma clearance of vecuronium and rocuronium leading to prolonged blockade is a consistent feature
- A. decreased plasma clearance of vecuronium and rocuronium leading to prolonged blockade is a consistent feature - best answer: " Vecuronium and rocuronium, both steroid-based NMBs, have a prolonged elimination phase in severe liver disease." (doi:10.1093/bjaceaccp/mkp040 Continuing Education in Anaesthesia, Critical Care & Pain | Volume 10 Number 1 2010) B. duration of action of mivacurium is NOT affected - false: "The metabolism of succinylcholine may be slowed because of reduced pseudocholinesterase concentrations, but in practice this gives few problems." "the duration of action of mivacurium is prolonged in those patients in whom liver disease was associated with decreased plasma cholinesterase activity" (Stoelting p.217 3rd Ed) C. initial doses should be reduced as volume of distribution is decreased - false: "There is an apparent resistance to non- depolarizing neuromuscular blockers (NMBs) in patients with liver disease, which may be due to an increased volume of distribution or to altered protein binding." D. plasma clearance of atracurium and cisatracurium is increased - false: Why should clearance be increased? If anything will be decreased, but Hoffman elimination buffers this. "Atracurium and cisatracurium are suitable NMBs as they do not rely on hepatic excretion. After prolonged administration, concentrations of laudanosine (a metabolite of both atracurium and cisatracurium with potential to cause seizures) are lower with cisatracurium than atracurium due to the higher potency of cisatracurium, although this is unlikely to be of clinical significance." E. when the desired level of block is achieved with the initial dose, subsequent recovery is comparable to patients without liver disease ----------- |
|
|
PR56
The duration of action of suxamethonium may be increased by A. betamethasone B. bleomycin C. carvedilol D. neostigmine E. all of the above |
D. neostigmine
----------- |
|
|
PR58
Regarding anticholinesterases A. Pyridostigmine has slow onset B. Physostigmine does not rely on renal metabolism C. Neostigmine cannot reverse centrally acting cholinergics D. Edrophonium is less reliable in reversal |
C. Neostigmine cannot reverse centrally acting cholinergics
----------- |
|
|
PZ105 [Jul06][Apr08][Oct08]
When dealing with morbidly obese patients, there are two weight measures used to calculate drug doses, the Ideal Body Weight (IBW) and the Total Body Weight (TBW). Which ONE of the following is true? A. The dose of atracurium should be based on IBW B. The dose of propofol should be based on ?IBW C. The dose of thiopentone should be based on ?TBW D. The dose of suxamethonium should be based on TBW E. The dose of vecuronium should be based on TBW |
D. The dose of suxamethonium should be based on TBW
OR B. The dose of proposal shoold be based on IBW - CEACCP article 2004 Pharmacokinetics in obese patients Propofol - induction: IBW, Maintenance: TBW or IBW + (0.4x excess wt) TBW Suxamethonium - TBW; >140kg. Maximum 120 - 140mg. ----------- |
|
|
TMP-114 [Mar10]
Paralysed with atracurium. TOF is 1(25%). You give a dose of 0.1 mg/kg mivacurium to close the abdomen. When will you be back to TOF 1(25%)? A. 5 min B. 10 min C. 30 min D. 60 min E. 90 min |
C. 30 min
mivacurium times is extended 100% if preceeded by atracurium - See wiki. Abstract from BJA article (94!) We have studied the interaction between atracurium and mivacurium. The dose—response relationships of atracurium, mivacurium and their combination were studied in 96 ASA I or II patients during thiopentone—fentanyl—nitrous oxide—isoflurane (1.2% end-tidal) anaesthesia. Neuromuscular block was recorded as the evoked thenar mechanomyographic response to train-of-four stimulation of the ulnar nerve (2 Hz at 12-s intervals). The dose—response curves were determined by probit analysis. Isobolographic and algebraic (fractional) analyses were used to assess quantitatively the combined effect of equipotent doses of atracurium and mivacurium and to define the type of interaction between these drugs. Isobolograms were constructed by plotting single drug ED50 points on the dose co-ordinates and a combined ED50 point in the dose field. The calculated doses producing 50% depression (ED50) of the first twitch height were 50.5 (95% confidence intervals 48.9–52.1) and 20.8 (20.3–21 .3) μg kg−1 for the atracurium and mivacurium groups, respectively. Isobolographic and fractional analyses of the atracurium-mivacurium combination demonstrated zero interaction (additivism). An additional 26 patients anaesthetized with thiopentone-fentanyl-nitrous oxide—isoflurane were allocated randomly to receive either atracurium 0.5 mg kg−1 (n = 13) or mivacurium 0.15 mg kg−1 (n = 13). Additional maintenance doses of mivacurium 0.1 mg kg−1 were administered to patients in both groups, whenever the first twitch recovered to 10% of control. The duration of the first maintenance dose of mivacurium to 10% recovery of the first twitch was greater (P < 0.0005) after atracurium (25 (21.8–28.5) min) than after mivacurium (14.2 (11.9–16.6) min). However, the duration of the second maintenance dose of mivacurium after atracurium (18.3 (12.6–24) min) was similar to that of mivacurium after mivacurium (14.6 (10.6–18.6) min). We conclude that the combination of atracurium and mivacurium is additive and that the use of mivacurium after atracurium-induced neuromuscular block results in increased duration of the first (but not the subsequent) maintenance dose of mivacurium. ----------- |
|
|
TMP-Mar10-067
Regarding anticholinesterases: A. pyridostigmine has slow onset of effect B. physostigmine does not rely on renal metabolism/excretion C. neostigmine cannot reverse centrally acting cholinergics D. edrophonium is less reliable in reversal? |
C. neostigmine cannot reverse centrally acting cholinergics
does not cross BBB - By interfering with the breakdown of acetylcholine, neostigmine indirectly stimulates both nicotinic and muscarinic receptors. Unlike physostigmine, neostigmine has a quaternary nitrogen; hence, it is more polar and does not enter the CNS. Its effect on skeletal muscle is greater than that of physostigmine, and it can stimulate contractility before it paralyzes. Neostigmine has moderate duration of action, usually two to four hours.[3] Neostigmine binds to the anionic site of cholinesterase. The drug blocks the active site of acetylcholinesterase so the enzyme can no longer break down the acetylcholine molecules before they reach the postsynaptic membrane receptors. This allows for the threshold to be reached so a new impulse can be triggered in the next neuron. In myasthenia gravis there are too few acetylcholine receptors so with the acetylcholinesterase blocked, acetylcholine can bind to the few receptors and trigger a muscular contraction. ----------- |
|
|
TMP-Mar11-022
NEW. Anaesthetising an obese patient. Accelerometer on TOF 0.9. Could dose suxamethonium on ideal body weight or total body weight. With respect to 1mg/kg IBW vs. TBW you will see: A: shorter onset and faster twitch recovery B: shorter onset and similar twitch recovery C: shorter onset and slower twitch recovery D: similar speed of onset with similar speed of twitch recovery E: similar onset and longer recovery |
Similar onset and longer recovery if dosed for TBW
- See Anesth Analg 2006; 102:438-42 "The dose of succinylcholine in morbid obesity" Essentially no difference in onset time of maximum neuromuscular blockade among groups (IBW vs LBW vs TBW); however recovery interval was significantly shorter in IBW and LBW groups. In one third of patients in IBW group, intubating conditions were rated as poor. No patient in TBW group had poor intubating conditions. ----------- |
|
|
TMP-Mar11-038
Your registrar gives a Duchenne patient 1mg/kg of suxamethonium. What are you most worried about? A: hyperkalaemia B: rhabomyolysis C: MH |
A: hyperkalaemia
- From OrphanAnaesthesia 'Anaesthesia recommendations for patients suffering from DMD: 'Succinylcholine and volatile anaesthetics are best avoided because there is a risk of hyperkalemic cardiac arrest or severe rhabdomyolysis. There is no risk of malignant hyperthermia: some authors therefore agree that in special circumstances (e.g. difficult venous access) a short lasting use of inhalation anaesthesia is possible as long as the anaesthesiologist is prepared to treat acute rhabdomyolysis). ----------- |
|
|
TMP-Mar12-015
[Aug12] A 60kg female is given 50 mg of rocuronium, she is unable to be intubated, what dose of sugamadex is required to reverse the rocuronium a. 240 b. 800 c. 960 |
c. 960
-- Dosing for sugammadex 2mg/kg for moderate block 4mg/kg for profound block 16mg/kg for immediate reversal. from BJA 2010 systematic review: Moderate block - return of T2 or T1 20% or 25% Profound block - PTC 1-2 ----------- |
|
|
TMP-Sep11-131
[Mar12][Aug12] New When stimulating the ulnar nerve with a nerve stimulator, which muscle do you see twitch? A. opponens abducens B. abductor pollicis brevis C. adductor pollicis brevis D. extensor pollicis E. flexor pollicis brevis |
C. adductor pollicis brevis
----------- |
