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Intervenous Drugs > Truelearn > Flashcards

Truelearn Flashcards

1
Q

Cholinesterase inhibitors effect on NDNMB vs DNMB?

A

Resistant to NDNMB
Sensitive to DNMB

Cholinesterase inhibitors increase the amount of acetylcholine available and therefore make nondepolarizing muscle blockade more difficult. In contrast, cholinesterase inhibitors partially inhibit pseudocholinesterase and therefore potentiate a depolarizing blockade.

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2
Q

Paradoxical muscular weakness is a risk of …..? and when is it at risk? is it preventable with administering anticholinergic medication?

A

When neostigmine is administered with larger doses or when used following the complete recovery of neuromuscular function, or a second dose is administered in patients with a small degree of residual blockade. even when an anticholinergic medication is also used.

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3
Q

Dose Upregulation of Ach receptors occurs after NMB?

A

Yes for long NMB used.

Therefore care must taken to avoid succ if planned for re-intubation

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4
Q

Endogenous catecholamine has the most effect on MAP and SVR?

A

NorEpi

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5
Q

Milirinone MoA

A

PDE III inhibitor (decreases cAMP leading to increase intercellular Ca)

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6
Q

Endogenous catecholamine primarily + alpha 1 (increasing SVR) and prolonged gtt cases finger ischemia?

A

NorEpi

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7
Q

Epi + alpha and beta at dose dependent.

Beta at dose ….
Alpha at doses …

A

1-2 mcg/min beta + causing bronchiodilatation and decrease vascular tone

2-10 mcg/min beta dominates and increase HR, contractility, and AV node conduction

If > 10 mcg/min alpha predominantly and causes generalized vasoconstriction and reflex tachycardia

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8
Q

Dopamine MoA?

A

It directly binds to alpha, beta, and dopaminergic receptors.

Also it acts indirectly by + the release of NorEpi

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9
Q

Non catecholamines sympathomimetic drugs are … and … and … (only one is used)

A

Mephentermine, metaraminol, and Ephedrine

They act in alpha and beta directly on receptors and indirectly by releasing NorEpi

Tachyphlaxis develop when NorEpi stores are depleted

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10
Q

Which NMB has an active metabolite that is nearly as potent as its parent drug?

A

Vecuronium

3-desacetyl-vecuronium is 1/3 metabolite that has 80% of the potency of vecuronium.

It causes significant prolonged action especially if used as gtt in RF ptn’s

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11
Q

Botulism toxin action?

A

It prevents the release of ACh containing vesicles into synaptic cleft

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12
Q

Contraindications to lidocaine gtt?

A

Heart block
Eplipsy
Low EF%
Patients on antiarythmic medications?

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13
Q

3 IV anesthetics decreases seizure threshold

A

Etomidate, ketamine, methohexital)

Etomidate also associated with extrapyramidal myoclonus which can mimic colonic seizure (self-limited) and getting EEG can differentiateit from seizure

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14
Q

Meperidine metabolites increases/decrease in RF patients?

A

Increase of normeperidine which causes seizure activity.

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15
Q

Which Morphine metabolites (M6G or M3G) increases/decrease in RF patients?

A

Both, M6G, has a 100-fold greater affinity for μ-receptors than morphine, promoting respiratory depression.

Where M3G, may cause myoclonus and allodynia.

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16
Q

Thiopental metabolites increases/decrease in RF patients?

A

Barbiturates, such as thiopental, have decreased protein binding in the setting of renal and/or hepatic failure. This leads to increased sensitivity due to higher concentrations of free active molecules which leads to higher concentrations of free active molecules.

17
Q

Side effects of dantrolene?

A

Hepatotoxicity with chronic po use, asymptomatic LFT elevation.

RS: plural effusion

CV: tachy

CNS: NS. Weakness, AMS, sedation

GI: N/V and cramps

Others: crystaluria, back pain and phlebitis

18
Q

Factors that influence incidence of ketamine emergence reaction?

A

Adults > Peds

Female > Male

Large doses with rapid bouls

Concurrent medications

Psychological susceptibility (certain personality, those who tend to dream at home, and who score high on Eysenck personality questionnaire).

19
Q

Selected effects of ketamine:

A
  • Dissociative sedation
  • Possible emergence delirium
  • Spinal analgesia
  • Supraspinal analgesia
  • Nystagmus, pupil dilation
  • Increased salivation
  • Increased vascular resistance from sympathetic outflow
  • Bronchodilation with preserved respiratory drive
  • Indirect myocardial stimulation (predominant)
  • Direct myocardial depression
  • Increased cerebral metabolism, CBF, and ICP
20
Q

Ketamine produces undesirable psychological reactions that are termed ‘emergence reactions’ and include …

And can be reversed by …

A

vivid dreams, illusions, misinterpretation of auditory/visual stimuli, and extracorporeal experiences (out-of-body).

These reactions typically occur in the first hour after emergence and are gone within several hours.

Physostigmine may be able to reverse the emergence reactions that are seen with ketamine. Physostigmine is a centrally acting acetylcholinesterase inhibitor that will increase the amount of acetylcholine in the brain. The theory behind this mechanism of reversal is that ketamine’s emergence reactions resemble the central anticholinergic syndrome thus, giving physostigmine may shorten the response. However, data is conflicting regarding the reliability of physostigmine for reversal of symptoms.

21
Q

Initial recovery from induction dose of thiopental due to …

A

Redistribution to peripheral tissue

Therefore, smaller induction doses needed in geriatric patients as they lose 15% in total body water with age (decreased central volume of distribution) and also, they exhibit a slower redistribution of thiopental to peripheral tissue

22
Q

The primary mechanism of thiopental termination of action by …

A

Redistribution from brain to other body tissue (not by elimination or metabolism) because it’s lipophilic and crosses BBB

23
Q

Drugs that their termination of action by redistribution are …

A

The highly lipophlic

Thiopental
Fentanyl
Method exit all
Propfol

24
Q

IV anesthetic effect on CBF and CMRO2?

A

They all decrease both with exception to ketamine.

Fentanyl has no effect on CBF or CMRO2

25
Q

The mechanism of ketamine induced analgesia is …

A

Mu opioid receptor agonist + NMDA receptor antagonism.

26
Q

A unique IV anesthetic that preserve airway reflexes and respiratory drive, analgesia, as well as increases symptomatic tone is

A

Ketamine

27
Q

Least IV anesthetic causes local tissue injury and necrosis is

A

Propofol

28
Q

Possible Contraindications To Ketamine:

A
  • Increased ICP with spontaneous ventilation
  • Intracranial mass lesion with spontaneous ventilation
  • Open eye injury or other ophthalmologic disorder (increased IOP)
  • Ischemic heart disease (as sole anesthetic agent)
  • Vascular aneurysms (as sole anesthetic agent)
  • Psychiatric disease such as schizophrenia
29
Q

When ketamine can be neuroprotactive

A

Ketamine may be neuroprotective in head-injured patients who are mechanically ventilated. Many of the negative CNS effects of ketamine can be blunted by the co-administration of other anesthetic agents.

30
Q

Etomidate can cause adrenal suppression by inhibiting the enzyme ….

A

11-β hydroxylase

Etomidate is an intravenous anesthetic drug believed to function as a GABA-agonist. It is typically used for induction of anesthesia in hemodynamically unstable patients since it has minimal effects on cardiac function or vascular tone and does not cause histamine release. Etomidate also decreases cerebral metabolic oxygen demand, cerebral blood flow, and intracranial pressure (ICP), but maintains cerebral perfusion pressure. While etomidate otherwise appears to be an ideal agent to provide long-term sedation for neurosurgical patients with elevated ICP, it is avoided due to inhibition of adrenocortical synthetic function, especially in the setting of prolonged drug exposure. However, even a single dose can cause temporary adrenal suppression. Other side effects include pain on injection, myoclonus, and postoperative nausea and vomiting.

31
Q

Nicardipine MoA and elimination?

A

Ca-channel blocker

Metabolized by liver and elimination by bile and feces.

Half life 60-100 min

Therefore in sever liver insufficiency patient’s results in prolonged half life of nicardipine

32
Q

The excitatory symptoms and tissue necrosis seen more with methohexital or thiopental? what are they?

A

Thiopental and thiamylal produce fewer excitatory symptoms with induction than methohexital, which produces cough, hiccough (hiccups), tremors, and twitching approximately five times more often. Hiccups with methohexital can be severe and cause distress for patients in the post-anesthesia recovery unit. Tissue irritation and local complications may occur more frequently with the use of thiopental and thiamylal than with methohexital.

In comparative studies, pain on injection was shown to be greater with methohexital (12%) than with thiopental (9%). Results also show phlebitis occurs more frequently with methohexital use (8%) than with thiopental use (1%). Tissue and venous irritation are more common if a 5% solution is used, rather than the standard 2% solution.

33
Q

What is the IV anesthetic DOC for ECT? why?

A

Methohexital remains the drug of choice for electroconvulsive therapy (ECT) because of longer seizure times (versus propofol), shorter awakening times (versus thiopental), and fewer side effects (versus etomidate).

For ECT, methohexital is considered to cause no change in seizure duration overall. However, compared with saline it will decrease seizure duration during ECT. Methohexital is also commonly used as an induction agent for anesthesia for electroconvulsive therapy (ECT) since, unlike many other IV anesthetics, it does not raise the seizure threshold and can increase ictal activity at low doses (e.g. 0.75 - 0.9 mg/kg).

34
Q

Well known side effect of Methohexital?

A

Seizures
Excitatory side effects (e.g., hiccups, muscle twitches) are more prominent than those seen in most other IV anesthetics.

35
Q

Mechanisms for nitroprusside toxicity?

A

Nitroprusside is metabolized to cyanide ions and toxicity can occur following lengthy infusions. The three major mechanisms for nitroprusside toxicity are

1) Cyanide ions bind to cytochrome c oxidase and inhibit cellular aerobic respiration.
2) Formation of cyanmethemoglobin which is unable to carry oxygen.
3) Thiocyanate production which causes CNS-related effects.

36
Q

he biggest risk factor for development of EPS with ondansetron is …

A

Previous history of dystonic reactions or EPS with other antiemetics

Intervenous Drugs (13 decks)

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