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PHAR 303 (toxicology) > Cardiotoxicity > Flashcards

Cardiotoxicity Flashcards

final exam

1
Q

what happens if the SA node malfunction?

A

backup pacemakers take over control of the heart:
1. AV node: slower
2. His-Purkinje system
3. At worst, ventricles can set up their own contraction (will be very slow, but you will be alive)

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2
Q

what modulates the heart rate in response to stress/exercise?

A

ANS (sympathetic –speed up– and parasympathetic –slow down–) and hormones (noradrenaline or adrenaline –speed up–)

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3
Q

how has the heart developed to keep up its high energy demand?

A
  • highly developed blood supply
  • a lot of mitochondria
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4
Q

average heart rate

A

60 bpm

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5
Q

ways toxins can interfere with mechanisms of the heart

A
  • ion channel trafficking
  • electrophysiology
  • contractility
  • with the function of mitochondria
  • generation of ROS
  • causing apoptosis or necrosis
  • causing fibrosis
  • blood-clot formation
  • ion channels (Na+, Ca2+, K+)
  • receptors for signaling molecules
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6
Q

structure of cardiac glycosides

A
  • sugar portion
  • non-sugar (aglycone) portion which is attached to R group that determines its specific type
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7
Q

types of glycosides

A
  1. Cardenolides (plants)
  2. Bufadienolides (toads and south fauna)
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8
Q

action of cardiac glycosides

A
  • inhibits Na+/K+ ATPase pump on cell membrane (which is high in concentration i heart tissue)
  • Na+ accumulates in the cell
  • higher activity of Ca2+/Na+ exchanger
  • more Ca2+ in the cardiac cells, which induces contractions
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9
Q

problems that can occur due to cardiac glycoside toxicity

A
  • atrial fibrillation
  • conduction block
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10
Q

what is atrial fibrillation? would it kill the person?

A
  • disorganized electrical signals in the atria, so contractions become independent of pacemaker activity
  • non-lethal as AV node or ventricular pacemaker activity allow for ventricular contraction, so blood gets to lungs/periphery
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11
Q

how does conduction block occur? what is seen on an EKG? would this kill the person?

A
  • occurs when electrical impulse from atria cannot pass through the AV
  • would see P-wave but no QRS complex
  • non-lethal if blocked for a short time, but can lead to ventricular fibrillation of too ling, which is lethal (blood does not get to periphery/brain)
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12
Q

why do fauna contain cardiac glycosides?

A

evolutionary protective mechanism

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13
Q

what is digoxin and where is it found?

A

cardiac glycoside found in foxglove/digitalis plant

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14
Q

toxic effects of digoxin

A
  • early symptoms can ne neurological (can affect electrically active tissue in CNS)
  • can cause v. fib, v. tach, progressive bradyarrhythmia
  • cardiac arrest from v. failure
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15
Q

pharmacokinetics of digoxin

A
  • Absorption: well absorbed orally (peak serum is 1-3 hrs)
  • Distribution: concentrates in tissue (large AVD), crosses BB (explains disorientation)
  • Metabolism: not well by CYP450s, so excreted by kidney without metabolism (so takes a couple of days)
  • Excretion: first-order, so takes a while
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16
Q

what does the oleander plant contain? what is its effect?

A
  • oleandrin (cardiac glycoside)
  • fatal to humans (even 1 leaf)
17
Q

what does lily of the valley produce?

A

convallotoxin (cardiac glycoside)

18
Q

why do Monarch butterfly lay their eggs on milkweeds?

A

since they contain cardiac glycosides so kill predator insects (they are resistant due to genetic mutation)

19
Q

who is more vulnerable to houseplant toxicity

A

children and pets

20
Q

what do Kalanchoe contain?

A

cardiac glycosides

21
Q

what toxin does Yew contain and which parts are and aren’t toxic?

A
  • cardiotoxic alkaloids
  • leaves, bark, stem flowers are toxic
  • red part of the berry is not toxic
22
Q

is there a treatment for yew poisoning? if so, what is it?

A

no, takes 30 mins to die

23
Q

effect/mechanism of Yew cardiotoxic alkaloid

A
  • inhibits cardiac conduction and causes arrythmia via blockage of Ca2+ channels (no contractions)
  • causes impairment of HR generated from SA node, AV node, and electrical system (including the electrical-mechanical coupling of the ventricular muscle)
  • see a very wide QRS complex
24
Q

effect of moldy hay (and mode of exposure)

A

fungus grows on hay and can secrete cardiac glycosides (horse can eat and humans can inhale)

25
Q

Effect of snake venom (more specifically cobra venom)

A
  • forms a pore/channel that interferes with the conduction system
  • causes necrosis of cardiac muscle (affects contractility)
26
Q

effect of anthracyclines

A
  • early (during or first year after treatment): non-specific ST-segment and T-wave abnormalities
  • late (at least one year after completion of treatment): arrythmia or congestive heart failure
  • general: mito. damage, leading to apoptosis
27
Q

what characterizes congestive heart failure?

A

low CO and other compensatory mechanisms that took place to get enough oxygen, can lead to peripheral edema, pulmonary edema, and kidney retains fluid

28
Q

effect of Herceptin

A

HER2/4 present on heart cells, so leads to loss of heart cells, so congestive heart failure

29
Q

what is Ephedra?

A

stimulant sold illegally (for weight loss and for athletes)

30
Q

effect of Ephedra

A
  • increase release of NA and A (and impair reuptake)
  • stimulate postsynaptically
  • can cause ischemic heart disease (can be severe and cause infarction by inducing vasospasms which can block blood flow)
31
Q

how can fine particles affect the heart?

A
  • alter endothelium
  • affect endothelial barrier
  • activate platelet and induce blood clot formation
  • trigger inflammation
  • atherosclerosis, which can cause clot that can block key areas
32
Q

what is a method to study the effect of fine particles on heart?

A

organoids (see which fractions of cells die)

33
Q

acute vs chronic exposure of fine particles on cardiovascular function

A
  • chronic: gradual buildup of heart disease, gradual increase in mortality risk
  • acute: bad exposure can trigger heart attack or sudden death from arrythmia
34
Q

effect of ozone (with fine particles0 on cardiovascular function

A

potentiates effects of fine particles

35
Q

major source of indoor air pollution

A

candles and incense

36
Q

mechanism of action of carbon monoxide

A
  • binds to Hb, forming carboxyhemoglobin
  • blocks binding of oxygen to Hb
  • trigger ROS production, damages the endothelium/myelin (this can occur at even low-level exposure)
37
Q

symptoms/effects of CO poisoning

A

first CNS effects (headaches, nausea, dizziness, confusion) then loss of consciousness and cardiac arrest

PHAR 303 (toxicology) (14 decks)

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