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Final Multisystems Pharmacology > Substance Abuse 2 > Flashcards

Substance Abuse 2 Flashcards

1
Q

Examples of Hallucinogenic agents (one big one to know)

A

Big one: LSD (Lysergic acid diethylamide)

Others: ergot alkaloids, peyote/mescaline, mushrooms/psilocybin, dimethyltryptamine, bufotenine

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2
Q

Duration and potency of LSD

A

Long duration (up to 12h), very potent (.5-3ug/kg)

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3
Q

Effects of LSD on you

A

Effects: hallucinations, dizziness, mydriasis, tremor, blurred vision, altered awareness of shape & color, micropsia (things seem small),macropsia (things seem large), mood swings, detachment. You will know you’re hallucinating.

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4
Q

Mechanism of LSD

A

Mechanism: partial agonist at 5-HT2 receptors (serotonin receptors)

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5
Q

How bad is the compulsion/addictive potential of LSD?

A

No addiction/physical dependence, very little compulsive use, little cross-tolerance to other hallucinogens, but tolerance to other drugs w/ similar mechanism

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6
Q

PCP and ketamine are examples of what types of drugs?

A

Dissociative drugs

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7
Q

Alternate names for PCP (2)

A

(phencyclidine, Angel Dust)

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8
Q

Mechanism of PCP

A

Mechanism: non-competitive Glu NMDA R antagonists; act as channel blockers to dec Ca2+ conductance

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9
Q

There are both acute AND chronic effects of PCP.

What are the initial acute effects?

A

Acute effects: intoxication, blank stare, muscular rigidity, analgesia, hypersalivation, sweating, hypertensive crisis, bizarre, aggressive behavior, paranoid delusions/psychoses, convulsions

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10
Q

There are both acute AND chronic effects of PCP.

What are the chronic effects?

A

Chronic effects: difficulty in organized thinking, memory deficits, speech impairment

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11
Q

How do we treat PCP? How about the specific effects of it?

A

Tx acute sx: avoid stimuli (dark quiet room),
convulsions – diazepam,
htn – hydralazine,
psychoses – haloperidol

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12
Q

Withdrawal symptoms of PCP

A

Withdrawal: depression, anxiety, irritability, restlessness, anergia, sleep disturbances

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13
Q

What other substance in high doses causes similar effects as PCP?

A

a/w: dextromethorphan in cough syrup can produce similar effects at high doses

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14
Q

Ketamine is also known as:

A

date rape drug (Rohypnol is what is commonly referred to as the date rape drug (blocks new memory formation), but keep this link in mind in case it comes up on the faculty exam)

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15
Q

Effect of Ketamine

A

effect: hallucinations, loss of consciousness

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16
Q

Ethanol is metabolized how?

A

Metabolism: EtOH –(OH dehydrogenase)–> acetaldehyde –(aldehyde DH)–> acetic acid (taken up in Krebs cycle) *pathway requires NAD+

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17
Q

How do we excrete ethanol?

A

10% excreted unaltered in sweat, breath, urine. Rest metabolized mainly in liver. Minor pathway: CYP2E1

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18
Q

Dual mechanistic action of ethanol

A

inhibition of glutamate-activated cation currents at NMDA-R → dec neuronal excitability

potentiation of GABA-A R activated chloride currents → facilitates GABA-induced hyperpolarization, dec excitability (aka general CNS depression)

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19
Q

What does ethanol do to the liver?

A

Effects on liver: inc NADH/NAD+ ratio→ inc FA synthesis, dec FA oxidation; inc plasma FFA, dec release of TAG from liver→accumulation of TAG (labs: inc GGT, AST 2x > ALT)

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20
Q

What does ethanol due in the periphery?

A

Peripheral effects: inc gastric acid secretion, inc sympathetic tone & epi release → vasodil, heat loss, arrhythmias, inhib ADH secretion → diuresis

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21
Q

Central effects of ethanol

A

Central effects: euphoria, inc reaction time, impaired judgment, loss of emotional control, impaired gait, ataxia, loss of balance, slurred speech, analgesia, confusion, sedation

Higher order: emesis, coma, death from respiratory depression

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22
Q

What happens to chronic ethanol drinkers AND WHY?

A

Chronic effects: tolerance - metabolic(inc CYP2E1), pharmacodynamic (dec effects on NMDA, GABA R’s), physical dependence & addiction.

Fatty liver, alcoholic hepatitis, cirrhosis→ portal htn and hepatocellular carcinoma.

Other cancers: oral, larynx and esophagus.

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23
Q

What are the withdrawal symptoms of ethanol and how do we treat them?

A

Withdrawal: autonomic hyperactivity, Delerium Tremens (DT – 5-15% mortality)

Tx: benzos

24
Q

Discuss the metabolism of methanol

A

Metabolism: methanol → alcohol DH→ formaldehyde → (aldehyde DH) → formic acid.

25
Q

What two things could we use if someone overdoses on methanol?

A

Tx for overdose is ethanol, fomepizole

26
Q

Why do we worry about kids drinking ehtylene glycol? What 3 parts of it are so bad and what do they do?

A

Potent CNS depressant. Blue and tastes sweet so kids are at high risk.

  • Glycoaldehyde:renal toxicity→ renal failure and death
  • Glycolic acid: metabolic acidosis
  • Oxalic acid: oxalate crystals in urine
27
Q

What two things can we use with ethylene glycol overdose?

A

Tx: Ethanol (delay metabolism) or fomepizole (alcohol DH inhibitor)

Same as methanol!

28
Q

Babies exposed to alcohol in mom’s diet as you know can get FAS, Fetal Alcohol Syndrome.

What are the morphological features of a child with FAS?

A

Head: Mild to moderate microcephaly, microphthalmia

Lips: Short palpebral fissures, smooth philtrum, thin vermillion border of upper lip

Ear: Railroad track ear crease

Nose/Oral: Maxillary hypoplasia, micrognathia, short upturned nose, cleft lip and/or palate

Hands: Small distal phalanges, small fifth finger nails (curved: clindactylyl)

Organ: Hypotonia, fine motor dysfunction, hyperactivity, cardiac murmurs

29
Q

What is a “Death Cap” mushroom?

A

highly poisonous green toadstool that causes death when ingested

(Amanita phalloides)

30
Q

How does Death Cap Mushroom ingestion present?

A

Clinical picture: summer food poisoning (resembles other commonly ingested mushrooms)

31
Q

Discuss the two thermostable toxins we see with Death Cap mushrooms and what they do

A

Amanitins (cyclic octapeptides): direct toxin that inhibits RNA polymerase → termination of protein synthesis and cell death

Phallotoxins (cyclic heptapeptides): doesn’t cause human poisoning

32
Q

Discuss the gross features the effects of Death Cap mushrooms

A

Early or limited dz: hepatic necrosis more zonal, often (but not exclusively) centrilobular.

Eventually we get massive diffuse hepatic necrosis and hemorrhage w/ thin rim of residual viable hepatocytes surrounding the portal tracts

Complications arise from dose dependent centrilobular hepatic necrosis (greater enzymatic detoxification in central zones)

33
Q

Other drugs causing centrilobular necrosis: (2)

A

acetaminophen and carbon tetrachloride

34
Q

How do we treat someone that digests Death Cap mushrooms?

A

We don’t. Supportive only.

35
Q

Discuss the clinical presentation of tetracycline overdose

A

Clinical syndrome of tetracycline toxicity consists of hepatic disease(fatty change), azotemia and pancreatitis.

n/v and abd pain (thought to be due to the frequently concomitant pancreatitis) with modest jaundice

Complications: hemorrhagic episodes, syncope, hypotension and shock → lethargy and coma.

36
Q

Labs for tetracycline overdose?

A

Labs: Inc bilirubin, prolonged PT, inc AST, inc amylase, ALT>AST

37
Q

Gross appearence of the pancreas and liver with someone who has a Tetracycline overdose

A

Liver: mildly enlarged and yellow

Pancreas: bulky, edematous

38
Q

On histology of the pancreas, liver, and kidney, we see specific findings that are associated with high tetracycline useage. What are they?

A

Liver: microvesicular steatosis (hepatocytes stuffed with droplets of fat with some tetracycline derivative, the fat droplets may be large (macrovesicular steatosis). All hepatocytes of the acini are involved by the steatosis

Pancreas: acute inflammation

Kidney: fat accumulation in tubular epithelium with some cortical necrosis and leucine-like crystals

39
Q

How common is tylenol poisoning and just how bad is it?

A

Stats: 50% of acute liver failures and 30% mortality

40
Q

Discuss the mechanism behind tylenol toxicity (secondary to how we metabolize it)

A

Metabolism: 95% detoxified in liver by phase II enzymes → excreted in urine as glucuronate or sulfate conjugates. 5% by CYP2E to NAPQI. NAPQI usually conjugates with Glutathione, making it safe and detoxified, but when it builds up beyond the amount of GSH present, NAPQI accumulates and damages hepatocytes → centrilobular necrosis → liver failure

41
Q

How specifically does NAPQI cause toxic effects?

A

Covalent bonding to hepatic proteins → damage to cell membranes and mitochondrial dysfunction

Depletion of GSH → Hepatocytes more prone to damage by ROS

42
Q

;., mkbjhvc6+5241

“?;.l,mjnb

A

Don’s favorite numbers

43
Q

Symptoms of Acetaminophen overdose

A

Sx: N/V, Diarrhea. shock, jaundice, liver failure

44
Q

Treatment options for Acetaminophen overdose

A

Tx: Within 12 hours = N-Acetylcysteine = Restores GSH levels. Liver centriolobular necrosis = Liver Transplant

45
Q

Discuss dosages for Tylenol and what constitutes an overdose

A

Normal dose = 0.5 g vs. Overdose = 15-25 g

46
Q

Although great at protecting against pregnancy and endometrial/ovarian cancer, what bad things arise from taking Oral Contraceptives? (3)

A

Inc risk of cervical cancer in HPV (+) females

Inc risk of venous thrombosis and pulmonary thromboembolism

Inc risk of hepatic adenoma (rare benign hepatic tumor)

47
Q

Side effects of Vancomycin (random card, sorry)

A

hypersensitivity rxn, flushing (red man syndrome), nephrotoxic, neutropenia, ototoxicity, thrombophlebitis

48
Q

What are anabolic steroids made of?

A

synthetic testosterone

49
Q

What’s the problem behind taking anabolic steroids?

A

Problem: for performance enhancement the dose is 10-100x the therapeutic dose. Inc testosterone leads to inhibition of LH/FSH (via feedback inhibition) and increased estrogen (since it’s a byproduct of testosterone)

50
Q

5 cardinal signs of Anabolic steroid use in your patient and what later complications we can see

A 
Stunted growth
Acne
Gynecomastia
Testicular atrophy
Facial hair and changes in menstrual cycle in females

Later complications: psychiatric disturbances, inc risk of MI, hepatic cholestasis

51
Q

Discuss the difference between child vs. adult overdose of aspirin (typically) and what other source we can get salicylates from

A

Source: Kids = accidental overdose.

Adults = Suicide.

Also from methyl salicylate = “oil of wintergreen” = ointments

52
Q

Discuss the pathogenesis behind the effects of too much aspirin

A

Patho: → Stimulation of Respiratory System in Medulla → Alkalosis → Metabolic Acidosis → Pyruvate and lactic acid accumulation due to uncoupling of oxidative phosphorylation and Krebs Cycle inhibition. This metabolic acidosis enhances formation of non-ionized forms of salicylates which diffuse into the brain to cause neural changes

53
Q

Signs of acute aspirin overdose (not chronic)

A

Acute Sx: nausea, dizziness, tinnitus, coma

54
Q

If I take 3 grams or more of aspirin per day, what 3 organ systems will be affected most and how will they present symptom wise?

A

CNS: Headaches, dizziness, tinnitus, hearing impairment, confusion, drowsiness, seizures, coma

GI: N/V/D, erosive gastritis → bleeding and ulcers

CV: Acetylation of platelet cyclooxygenase and irreversible block of Thromboxane A2 production (needed for platelet aggregation → Excessive bleeding → Petechial hemorrhages of skin and internal viscera

55
Q

What happens if we are extra special and take aspirin with tylenol?

A

With Tylenol: Taken chronically → Tubulointerstitial nephritis with renal papillary necrosis (analgesic nephropathy)

56
Q

What can cause acute dystonic reactions and parkinsonian syndrome

A

Phenothiazine antipsychotics

57
Q

Problem with taking too many sedatives

A

Respiratory depression.

Final Multisystems Pharmacology (3 decks)

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