Pharmacology and toxicology Flashcards

Question

Management of propofol infusion syndrome

Answer 1

Enhanced elimination Stop the propofol infusion! "decontamination" might be impossible, but haemodalysis should be commenced to wash out propofol and its toxic metabolites Plasma exchange may be required (Da Silva et al, 2010) Specific antidote Carnitine Supportive care Pacing and atropine may be useless (the bradycardia is refractory) Vasopressors and inotropes are aso usually ineffective ECMO is the only answer if circulatory collapse with bradycardia has developed Nutrition with a satisfactory amount of carbohydrate to reduce the use of fat for metabolism. The college answer quotes a dose rate (6-8mg/kg/min) but it is unclear where the got this value from.

Answer 2

This tends to happen after about 48 hours of infusion, at over 4mg/kg/hr. The mechanism is likely the inhibition by propofol of coenzyme Q and Cytochrome C. This results in a failure of the electron transport chain, and thus the failure of ATP production. In the event of such a breakdown of oxidative phosphorylation the metabolism becomes increasingly anaerobic, with massive amounts of lactate being produced. Furthermore, fatty acid metabolism is impaired- the conversion of FFAs to acetyl-CoA is blocked, and thus no ATP is produced by lipolysis. On top of that, unused free fatty acids leak into the bloodstream, contributing to the acidosis directly.

Answer 3

Abdominal pain, nausea and vomiting is the result of the directly corrosive effect of iron. Shock is due to fluid loss into the gut Acidosis is multifactorial (see above) but is mainly lactate-driven, due to mitochondrial toxicity Hepatotoxicity is partly due to shock, and results in coma, coagulopathy and hyperbilirubinaemia Renal toxicity is partly due to shock, and partly due to direct toxicity

Answer 4

Toxicity manifests in four stages: Stage I: GI toxicity (0-6 h since ingestion): vomiting, haematemesis, abdominal pain and lethargy Stage II: "apparent stabilization" (6-12 h since ingestion) - symptoms subside Stage III: mitochondrial toxicity and hepatic necrosis (12-48 h since ingestion)- acute liver failure, coagulopathy, acute tubular necrosis, metabolic acidosis and shock. Stage IV: GI scarring (4-6 weeks since ingestion) - gastric scarring and pyloric stricture

Answer 5

Decontamination Activated charcoal has no role to play Whole bowel irrigation - until effluent turns clear - is a good strategy; much of the toxicity is related to gut ulceration, and by diluting the iron in the gut lumen you may be able to ameliorate this direct corrosive effect, even if you don't manage to prevent toxic absorption. Surgical removal of tablets - if a bezoar is clearly visible on the AXR Enhanced elimination Exhange transfusion: the removal of iron-poisoned blood is ery old-school, but it works (Movassaghi et al, 1969) Haemodialysis can be considered to help remove the iron-desferrioxamine complexes, as they are renally excreted and there may not be enough renal function to remove this product. Otherwise, apart from correcting acidosis there is no role for dialysis. Specific antidote Administer desferrioxamine, a sideramine product derived from Streptomyces pilosus. Desferrioxamine is indicated if metabolic acidosis is present or iron levels are over 90 micromol/L. Total intravenous dose should not exceed 80mg/kg/24hrs. The resulting iron-desferrioxamine complex (ferrioxamine) is water-soluble and biologically inert. Unfortunately, iron distributed into tissues in inaccessible to desferrioxamine. Also unfortunately, desferrioxiamine is far from benign, causing hypotension, ARDS, blindness and deafness (Howland, 1996). Its persistent presence in patients with no kidneys promotes the growth of such nightmarish organisms as Mucor.

Answer 6

Intubation will likely be required to protect the airway not only from the decreased level of consciousness but also from the risks of aspiration associated with whole bowel lavage. Mechanical ventilation will likely be with mandatory mode, to decrease the demands on the failing myocardium Circulatory support should consist of simultaneous fluid resuscitation, inotrope and vasopressor infusions Sedation should be rationalised, given that the patient is already in a coma before the sedation is given, and that the liver is doing little metabolically. Correction of acidosis with bicarbonate may be indicated if catecholamine responsiveness is lost. Electrolyte replacement -losses must be anticipated, the leaky gut and bowel lavage will result in potassium and phosphate depletion. Haemodialysis may be required to maintain metabolic normality, as well as to remove ammonia which may accumulate due to the acute hepatocellular necrosis Hypoglycaemia and ketosis will likely develop. The patient will need a dextrose infusion, as hepatic and skeletal muscle glycogen stores will be depleted. Nutrition will likely be parenteral for some time, depending on the extent of gastric ulceration. Coagulopathy will develop due to hepatocellular necrosis. Coagulation factor replacement will be required.

Answer 7

Tachypnoea- Metabolic acidosis Shock, circulatory collapse - Third space fluid losses Blood and fluid loss from the ulcerated gut Cardiotoxic effects, with cardiogenic shock Vasodilation due to SIRS Hypoglycaemia - Acute hepatotoxicity Coma- Hypoglycaemia, Acute cerebral oedema due to liver failure High anion gap metabolic acidosis- Lactic acidosis, Ketosis, Minor contribution from iron itself (conversion of Fe3+ to Fe2+ produces a net loss of a cation, and therefore contributes to the decrease in the SID) Hyperlactatemia - Acute hepatotoxicity and liver failure, Shock state, Direct mitochondrial toxicity Renal failure - Shock state, mitochondrial (tubular) toxicity, ATN Gastric ulceration - direct corrosive effect of the drug Haemorrhage, melaena from ulcerated gut surface

Answer 8

Glucagon, high dose insulin

Answer 9

Intralipid

Answer 10

Oxygen, potentially even hyperbaric oxygen

Answer 11

Cyproheptadine

Answer 12

Benztropine

Answer 13

Fuller's Earth, bentonite clay

Answer 14

Sodium bicarbonate

Answer 15

Sodium bicarbonate

Answer 16

Cyanocbalamin/ Sodium thiosulphate

Answer 17

Physostigmine

Answer 18

Folinic acid

Answer 19

Calcium, glucagon, high dose insulin

Answer 20

Desferrioxamine

Answer 21

Ethyl alcohol, Fomepizole

Answer 22

Pyridoxine - a co-factor in the synthesis of GABA; isoniazid interferes with this synthesis, and causes seizures in overdose. The supplementation of pyridoxine seems to prevent the worst of isoniazid toxicity

Answer 23

Ethyl alcohol, Fomepizole

Answer 24

Methylene blue, vitamin C (ascorbic acid)

Answer 25

Atropine, pralidoxime

Answer 26

Dimercaprol (also works for mercury, antimony, gold, chrome, cobalt and nickel poisoning), BAL

Answer 27

``` Blind as a bat: mydriasis, dilated pupils and the inability to accomodate Mad as a hatter: delirium Dry as a bone: inability to form sweat Red as a beet: skin flushing Hot as a hare: fever Also... ileus urinary retention tachycardia coma ```

Answer 28

SLUDGEMS: ``` Siallorhoea Lacrimation Urination Diarrhoea Gastrointestinal distress: abdominal pain due to hypermotility Emesis Miosis - constricted pupils Seizures Also... tachycardia bronchorrhoea hypothermia diaphoresis muscle fasciculations paralysis ```

Answer 29

HAH STUPOR ``` Hypertension Agitation Hyperreflexia Seizures Tachycardia Urination Piloerection Ocular- pupil dilatation, mydriasis Rhabdomyolysis ```

Answer 30

BUM HIDE: ``` Bradycardia Urinary retention Miosis Hypotension Ileus Decreased respiratory drive Emesis Also... decreased cough reflex hypothermia hyporeflexia ```

Answer 31

RASCAL ``` Rhabdomyolysis Agitation / hypervigilance Seizures Clonus Autonomic overdrive - tachycardia, hypertension Large pupils - mydriasis also... ``` hyperreflexia hyperthermia

Answer 32

FEVER LAD ``` Fever Encephalopathy Vitals unstable - hyper or hypotension, brady or tachycardia Elevated enzymes - CK Rigidity of the muscles, hypertonia Leucocytosis Acidosis Diaphoresis Also, low serum iron (acute phase response) ```

Answer 33

Serotonin syndrome has an earlier onset (~ 12hrs) Serotonin syndrome has HYPER-reflexia, whereas in NMS the reflexes are depressed Serotonin syndrome has clonus - NMS merely has rigidity Serotonin syndrome features dilated pupils - NMS does not Serotonin syndrome has hyperactive bowels, whereas NMS may have ileus

Answer 34

The indication for the use of bicarbonate in tricyclic overdose is the widening of the QRS interval Increased protein binding of TCAs in an alkaline bloodstream, thus decreasing the biologically active free fraction. Increased availability of sodium in sodium bicarbonate, as a substrate for the voltage-gated channels. Decreased binding of TCAs to the voltage gated sodium channel Correction of metabolic acidosis Volume expansion because of the dilutional effect on TCA concentration Cellular membrane hypopolarisation results from bicarbonate-induced intracellualr shift of potassium.

Answer 35

Small molecule size Highly water soluble Small volume of distribution (i.e. ideally limited to circulating volume, or the extracellular fluid) Large protein-unbound free fraction

Answer 36

``` Barbiturates Lithium Alcohols eg. ethylene glycol, methanol Paraquat Salycilates Valproate Metformin Methotrexate It is generally accepted that extracorporeal elimination is worthwhile if it increases total body clearance by 30% or more ```

Answer 37

``` Erratic electrolyte derangement - hypocalcemia - hypophosphatemia - hypoglycemia Coagulopathy - Low fibrinogen - Thrombocytopenia: on average the count decreases 20–50% from baseline - Depletion of all other coagulation factors - Complement activation leading to DIC Immune suppression - Low WCC - Depleted immunoglobulins - Depleted cytokines - Low complement Malnutrition due to adsortion of amino acids Feberile reaction to the circuit Charcoal embolization Haemolysis "Reverse adsorption" - redistribution of the toxin back into the bloodstream ```

Answer 38

Toxidromes which benefit from dialysis and haemoperfusion will also benefit from plasmapheresis. Plasmapheresis is specifically beneficial in situations where the toxin has high plasma protein binding and a low volume of distribution (i.e. limited essentially to the circulating pool of proteins) If the toxin has a large volume of distribution (i.e. it is distributed widely to the tissues) several sessions of plasmapheresis will be required. In such a situation, there will be "rebound" toxicity as sequestered toxin redistributes into the bloodstream between sessions.

Answer 39

Many drugs are either highly protein bound or highly lipophilic These qualities make them unavailable for haemodialysis or ultrafiltration clearance, which can only access the ionised water-soluble fraction Adsorption can be used to clear these substances from the bloodstream The high surface area of resins and charcoal can compete with serum proteins for drug binding. The drugs are bound reversibly by Van der Waal forces (attractive forces between molecules not due to covalent, electrostatic or hydrogen bond interaction) Large surface area of resin or charcoal filter enhances adsorption by presenting a larger contact surface for the filtered blood. Charcoal is a "broad-spectrum" adsorption agent, whereas resins typically favour lipophilic substances. Resin filters may also be impregnated with drug-specific antibodies The rate of adsorption generally depends upon the size of the granules, and the capacity of each cartridge is determined by its size (i.e. how much charcoal is inside).

Answer 40

definition - "the ideal weight associated with maximum life-expectancy for a given height". Ideal body weight (kg) = height (cm) - 100 (100 for males, and 110 for females.)

Answer 41

Gastric emptying may be increased OR decreased (and it is unpredictable). Absorption from the subcutaneous compartment will be slowed due to poor blood flow to subcutaneous fat Intramuscular injection (or intrathecal, or even intravenous for that matter) is made difficult by poor access.

Answer 42

Increased volume of distribution for lipid-soluble drugs Increased accumulation of drugs in the fat compartment Blood flow in fat is poor in people of normal weight: it is only about 5% of the total cardiac output. - In obese individuals, blood flow to fat is even poorer. Obese individuals are also likely to have a degree of heart failure which further decreases blood flow. Body fluid volume is also increased, increasing the volume of distribution of water-soluble drugs Protein binding may be altered (but this is far from clear: most papers seem to say that albumin binding is unchanged)

Answer 43

Hepatic clearance is slowed not only by decreased cardiac output but also by fatty infiltration. But, you never actually know whether metabolic activity is going to be mre or less rapid. remember that lean tissue (and potentially metabolic organ mass) may be increased. However, increased CYP450 (2E1) activity has been observed Increased Phase II conjugation activity may be present

Answer 44

Diabetes which co-exists with obesity tends to damage kidneys, slowing the renal clearance. However, glomerular filtration rate may be increased in healthy obese individuals. Biliary clearance may be slowed by bile stasis or existing bile duct disease

Answer 45

Obese people have a larger absolute lean body mass (LBM), as well as fat mass. Lean components account for 20-40% of the absolute body weight - Exactly how much muscle is hidden in any given obese individual is difficult to est accurately with the aid of standard equations. The net effect of this is that both under-dosing and over-dosing is more likely than with individuals of normal weight, and monitoring of therapeutic levels is important. Pharmacokinetic data in obesity does not exist for most drugs. In obese individuals, the ideal body weight is likely to underestimate their lead body mass, leading to under-dosing. The total body weight is likely to over-estimate the dose and lead to overdosing. Thus, in such patients, most drug dosing should be tailored to lean body weight (LBW).

Answer 46

Lean body weight is the difference between total body weight and fat mass. Lean body weight is significantly correlated to cardiac output. It is probably the best method of dose adjustment for morbidly obese patients. - easy method is to add 20% on to ideal body weight to calculate LBW

Answer 47

``` Mild overdose: Nausea and vomiting Diarrhoea Intestinal hemorrhage Haemoptysis Oliguria Minimal renal dysfunction ``` ``` Moderate overdose: Renal failure (ATN within 12-24hours) Pulmonary oedema Hepatotoxicity Pulmonary haemorrhage Shock Pulmonary fibrosis ``` Massive overdose: multi-organ system failure rapidly fatal

Answer 48

Phase I: corrosion; mucosal linings ulcerate and swell; there may be haematamesis.This is the first two days. Phase II: organ failure; between the second and fifth days following ingestion, renal failure and hepatocellular necrosis develop. Most patients with severe overdose will die during this phase. Phase III: pulmonary fibrosis; death after many days/weeks of hypoxia.

Answer 49

Decontamination Enhanced elimination Specific antidote Supportive care

Answer 50

Decontamination - Fuller's Earth: calcium montmorillonite, or bentonite - a absorbent aluminium phyllosilicate, formed from the weathering of volcanic ash. - Activated charcoal may have equal efficacy, and is more widely available Cation exchange resins (eg. resonium) may be of use The “window of opportunity” is very narrow, only a few hours at most. Absorption from the gut is very rapid. - Remove contaminated clothes - Wash skin with soap and water to prevent transdermal absorption Enhancement of elimination - Charcoal haemoperfusion works very well, but contributes little to the overall prognosis because the drug is rapidly cleared from the plasma anyway, and the pulmonary reserve is trapped there (it is not available for removal). Dialysis is probably going to be useless, as paraquat is rapidly eliminated. The alveolar and renal damage will have been done by then, so you have nothing to gain (other than a more rapid control of the acid-base disturbance). Specific antidotes None exist. Supportive management - Intubation to protect the rapidly swelling airway after corrosive ingestion - Avoidance of hyperoxia: it has been demonstrated to exacerbate the oxidative toxicity of paraquat. - Circulatory support (there will be shock from myocardial necrosis and third space losses - Analgesia and sedation which is almost palliative in its intent - many of these people will die in spite of everything you do. - Specifically, propofol seems to have some sort of unique scavenging effect.

Answer 51

Clinical features Both - Bradycardia, Hypotension, Heart block BB - HYPOglycaemia, Bronchospasm, stupor/coma/seizures CCB -Hyperglycaemia, Constipation/ileus, seizures uncommon Management: Decontamination - both Activated charcoal Enhancement of clearance - Hemoperfusion for verapimil - Hemoperfusion for metoprolol Antidote Both - Glucagon, Insulin-dextrose, Inotropes and vasopressors CCB - Ionised calcium (eg. calcium chloride)

Answer 52

``` bradycardia tachypnoea severe metabolic acidosis - predominantly due to lactate high central venous oxygen saturation (low OER) acute renal failure acute hepatic dysfunction acute heart failure and pulmonary oedema circulatory failure, shock coma and seizures ``` Diagnosis of cyanide toxicity rests on historical features which are strongly suggestive (eg. inhalation of smoke in a plastic-based fire) as well as severe lactic acidosis, and in the absence of carbon monoxide poisoning. This might be enough to merit some doses of the (reasonably safe) empirical antidote therapy. The gold standard of diagnosis is the serum cyanide level, which may take too long.

Answer 53

Lactic acidosis develops due to the uncoupling of oxidative phosphorylation: cyanide interferes with the electron transport chain by binding to the ferric Fe3+ ion of cytochrome oxidase. Neurotoxicity occurs at modest doses; initially there is CNS stimulation (dizziness, confusion, restlessness, and anxiety) which is followed by stupor, opisthotonus, convulsions, fixed dilated pupils and unresponsive coma. This is due to the cyanide-stimulated release of excitatory neurotrasmitters, such as NMDA and glutamate. Oxidative damage to lipid bilayers due to free radical generation tends to break the blood-brain barrier and causes a vasodilated SIRS-like state of cardiovascular collapse (but this tends to happen only with very large doses) The development of pulmonary oedema, pulmonary vasoconstriction and coronary artery spasm are blamed on "biogenic amines", vasoactive substances which are supposedly liberated from cyanide-affected endothelia. There is not a lot to back this up in the literature.

Answer 54

Decontamination may to be effective (however most cyanides are rapidly absorbed). Cyanide has a short half-life (~ 2 hours), but in massive overdose the decontamination of plasma by dialysis may be feasible and has contributed to the survival of at least one historical victim (Wesson et al, 1985). Hydroxycobalamin - binds cyanide and forms cyanocobalamin This is the antidote of choice Advantages include a lack of toxicity for non-poisoned victims (thus, it may be given empirically) The onset of action is rapid It may be given in the pre-hospital setting and requires no monitoring. The side efects are relatively minor; perhaps the most striking is the tendency for the body fluids to turn a vivid red-orange color. dicobalt edetate may be an alternative cobalt-based binder, but hydroxycobalamin is more widely available, and much less toxic. LITFL mentions that dicobalt edetate causes "seizures, chest pain and dyspnoea, head and neck swelling, hypotension, urticaria and vomiting" Sodium thiosulfate Sulfur donors in general act by offering a sulfur ion to the endogenous rhodanese enzyme which converts cyanide to thiocyanate Like hydroxycobalamin, this is a reasonably safe option - there are few side effects. Induction of methaemoglobinaemia Methaemoglobin binds free cyanide and forms cyanmethaemoglobin. Various drugs are available for this. Sodium nitrite and amyl nitrite are the most frequently quoted. Methylene blue is also available, but is not without its side-effects.

Answer 55

Dose-related reactions This can include adverse effects at either normal dose or overdose. These may include expected extesions of the therapeutic effect of the drug, eg. bleeding in heparin. Toxic effects eg. serotonin syndrome Side effects are included, eg. anticholinergic effects of tricyclics Non-dose-related reactions This refers to drug effects which are totally unrelated to the dose (i.e. any exposure is enough to trigger such a reaction). Allergic reactions Anaphylaxis Idiosyncratic reactions, eg. purpura or drug-induced SLE Dose and time related reactions This refers to drug effects which occur due to dose accumulation, or with prolonged use Adrenal suppression with corticosteroids is one example. Time related reactions This refers to drug effects which occur due to prolonged use in a drug which doesnt tend to accumulate. An example might be tardive dyskinesia afte decades of using typical antipsychotics Withdrawal reactions This refers to the undesired effects of ceasing the drug Classical examples might include opiate withdrawal and rebound hypertension after stopping clonidine. Unexpected failure of therapy This category has been added to describe an undesirable reduction in the drug's efficacy (or, the undesirable increase thereof) Examples may include increased clearance by dialysis and plasmapheresis, drug interactions alterinc metabolism, and the effects of critical illness on protein binding and elimination.

Answer 56

Immediate management: ABCs Identification and withdrawal of the offending agent Immediate IM adrenaline (500mcg) for anaphylaxis Hydrocortisone and antihistamines for allergic reactions Investigation need for thorough drug history search for evidence of previous drug reactions thorough history of allergies search for predisposition to adverse effects Assessment of drug interactions Investigations (such as plasma concentration measurements, biopsies, and allergy tests) Organ system function assessment (EUC, LFTs, TFTs, FBC for neutropenia, etc) Rechallenge with the drug should be considered

Answer 57

- awareness of impaired clearance mechanisms due to organ pathology - careful prescribing - attention to drug interactions - rational management of polypharmacy - monitoring of drug levels - staff education regarding safe prescribing and administration - pharmacist participation in ICU rounds

Answer 58

In any overdose, especially early, there is some proportion of the ingested drug which still has not absorbed. This unabsorbed drug could potentially be cleared from the gut This would result in a reduced total dose of the drug The reduced total dose should also result in a reduced total toxicity Ergo, the removal of undissolved drugs should reduce the toxicity of the overdose

Answer 59

Activated charcoal, single or multiple doses Induced emesis (abandoned) Gastric lavage (largely abandoned; only indicated within the first hour) Whole bowel irrigation (only indicated for iron and slow release enteric coated tablets) Surface decontamination for skin-absorbed toxins

Answer 60

The overdose is recent (within the last hour) There is reason to believe a large number of undissolved tablets is still present in the stomach or gut There is no adequate antidote to the drug, and the overdose is lifethreatening

Answer 61

hypotension hypothermia CNS depression tremor

Answer 62

``` Lactic acidosis hyperammonaemia and encephalopathy acute hepatic failure pancreatitis cerebral oedema hypernatremia Hypocalcemia Hypocarnitinemia, if you actually test for carnitine Bone marrow suppression ```

Answer 63

``` Supportive management (ventilation, vasopressors, etc) gastrointestinal decontamination with charcoal or whole bowel lavage ``` L-Carnitine supplementation: the loading dose is 100 mg/kg IV over 30 minutes (maximum 6 g) followed by 15 mg/kg IV over 10–30 minutes every 4 hours until clinical improvement occurs. (valproate metabolism depletes the stores of carnitine) Valproate is 90% protein bound and therefore poorly cleared by dialysis, but ammonia is, and therefore haemodialysis is indicated to prevent cerebral oedema

Answer 64

prevention detection/diagnosis - Hx/Exam/Ix Supportive cares - - Sedation (for comfort) - Analgesia (to combat post-opioid hyperalgesia) - Control of physiological derangements (eg. clonidine to block the sympathetic storm of opiate withdrawal) - Protection of the CNS from seizures (i.e. in benzodiazepine and alcohol withdrawal) sedation replacement

Answer 65

Airway: Airway burns, leading to airway compromise Potential acute tracheo-oesophageal fistula due to corrosive effect on oesophagus Assessment and immediate airway control is a priority Breathing: Potential aspiration of caustic gastric/oesophageal contents, thus acute lung injury Hypoxia may be present; supplemental oxygen may be required. NIV may be contraindicated in case of full-thickness oesophageal injury Circulation: Potential hypovolemic shock due to fluid loss into the corroded gut, or haemorrhage though ulcers Need for rapid fluid replacement or surgical haemostasis CVC access, as this patient is likely to require long-term TPN Neurological state: Potential for disorganised behaviour due to psychiatric condition, or obtundation due to shock Analgesia issues need to be addressed Electrolyte disturbance Absorption of corrosive agent may result in electrolyte and acid-base disturbance Fluid balance Likely, hypovolemia will exist and need correction renal impairment may be present, with implications on drug dosing Gastrointestinal problems: Extent of corrosive damage will need to be assessed by CT and/or direct endoscopy (earlier is better, before significant tissue softenting makes endoscopy risky) Perforation of hollow organs must be ruled out with CXR and/or CT Specific issues Decontamination by NG aspiration may be possible if it is safe to pass an NGT

Answer 66

``` Agents - Alcohol Barbiturates Benzodiazepines Organic solvents ``` ``` Withdrawal syndrome - CNS excitation (agitation, tremor, hallucinations, seizures) Autonomic stimulation (tachycardia, hypertension, hyperthermia, diaphoresis) ``` Management - Benzodiazepines Dexmedetomidine

Answer 67

Agents - GHB Baclofen Withdrawal syndrome - Dyskinesia, seizures, hypertension, hallucinations, psychosis, and coma. Management -Benzodiazepines

Answer 68

Agents - opiates Withdrawal syndrome - CNS excitation (agitation, tremor, hallucinations) Diarrhoea, mydriasis, nausea. Autonomic stimulation (tachycardia, hypertension, hyperthermia, diaphoresis) Management - Clonidine Dexmedetomidine

Answer 69

Agents - Caffeine Withdrawal syndrome - Head-ache (cerebral vasodilation), fatigue, and hypersomnia (motor inhibition)

Answer 70

Agents - Nicotine Withdrawal syndrome - Agitation, insomnia, poor concentration, poor gut motility, poor feed tolerance. Management - Varenicline?

Answer 71

Agents - Amphetamines Withdrawal syndrome - Agitation, dysphoria, somnolence

Answer 72

Agents - Cocaine Withdrawal syndrome - Anhedonia, irritability, exhaustion

Answer 73

Agents - cannabis Withdrawal syndrome - Agitation, insomnia, poor gut motility Management - Mirtazapine ?

Pharmacology and toxicology Flashcards

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