pt 4 Flashcards

1
Q

The greater susceptibility may of nervous system to toxicity is attributed to
Partly to:
-the fact that neurons have a (1)—- metabolic rate, with little capacity for (2)——–

-Furthermore, being electrically excitable, neurons tend to lose cell membrane integrity more readily.

-The great length of the axons is another reason why the nervous system is especially susceptible to toxic effects, because the cell body must supply its axon structurally and metabolically

A

(1) high
(2) anaerobic metabolism

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2
Q

what drugs produce brain anoxia

A

BARB

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3
Q

Contamination of food products with tricresyl phosphate was shown to produce a delayed neuropathy related to inhibition of “neuropathy target esterase” whereby there is damage to spinal nerves, the spinal cord, brain, and other tissues
This type of neuropathy also occurs following exposure to organophosphorous
insecticides

A

tricresyl phosphate

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4
Q

The cell body of neurons may be affected directly by toxicants such as ——

A

methyl mercury

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5
Q

The paraquat-induced neuronal effects resemble the manifestations in ——–disease.

A

Parkinson’s

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6
Q

—– affects neurons by intercalating with DNA, leading to a breakdown of the helical structures inhibits the synthesis of RNA and neuronal protein

Since this drug does not cross the BBB, it can affect the neurons in the dorsal
root ganglia and autonomic ganglia, but not those in the CNS.

A

Doxorubicin

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7
Q

Some axons are very long (up to 1 m), and the elements in the axons, such as ——-, are synthesized not locally but in the cell body, and are transported along the axon.

A

neurofibrils

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8
Q

β, β-Iminodiproprionitrile (IDPN) produces —–

A

Proximal Axonopathy: typical lesions through impairment of slow axonal transport of neurofilaments (phosphorylation)

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9
Q

what agents lead to CNS mitochontrial swelling

A

thallium

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10
Q

distal axonopathy is caused by ——

A

-organophosphates (TOCP (tri-o-cresyl phosphate), EPN, and leptophos) lead to DELAYED NEUROPATHY

-n-hexane and methyl n-butyl ketone

and organic solvents

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11
Q

Tetrodotoxin, the toxic principle of puffer fish, has been shown to block the action potential by blocking the ——–

A

Na+ channels

-Interference with Impulse Conduction

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12
Q

MOA of Clostridium botulinum: producing paralysis of muscles by impairing the release of (1) ——- from motor nerve endings

A

Interference with synaptic transmission

(1) acetylcholine

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13
Q

how does Black widow spider venom interfere with synaptic transmission

A

produces an excessive release of acetylcholine and results in cramps and paralysis

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14
Q

——- produces neurotoxicity by interfering with kinesin-related motor proteins in neurofilaments that are involved in fast antegrade transport of nerve signals between axons

A

Acrylamide

-This is manifested as hindlimb splay, ataxia, and skeletal muscle weakness

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15
Q

lead affects Schwann cells possibly by interfering with their —- transport

A

Ca2+

The PNS is affected before the CNS due to lead. In addition, lead affects motor nerves before the sensory, resulting in “wrist-drop” and “foot-drop.”

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16
Q

——- disrupt myelin sheath because of the high (70%) lipid content of myelin.

A

Hypocholesterolemic agents such as triparanol,

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17
Q

The pesticide ——- produces degeneration of the GANGLION CELL LAYER resulting in a neurodegerative disorder associated with destruction of the MITOCHONDRIA.
-This phenomenon is found in Leber’s optic neuropathy and Parkinson’s disease.

A

rotenone

18
Q

Acetyl ethyl tetramethyl tetralin (AETT) causes ——– through a complex mechanism

A

myelinopathy

19
Q

Clostridium botulinum, Black widow spider venom, acrylamide. lead to

A

Interference with synaptic transmission

20
Q

TRIparanol, Diphtheria toxin, rotenone, Acetyl ethyl tetramethyl tetralin (AETT).

they cause

A

Glial cells and myelin

21
Q

lead, mercury, arsenicals, tellurium (in the endonerium), are associated with ——- toxicity

A

EXTRAcellular edema

22
Q

Various parts of neurons may become edematous (CELLULAR EDEMA) following exposure to toxicants

A

-6-aminonicotinamide affects the perikaryon

-cyanide and carbon monoxide affect the axon

-ouabain and methylsulfoxime affect the presynaptic nerve endings.

23
Q

——— produce, after acute exposure, narcosis, but they induce axonopathy after repeated exposures

A

n-hexane and TOCP

24
Q

ammonia, chlorine, arsnicals lead to

A

lung local irritation

25
Q

what are toxicants that lead to cellular damage of lungs and edema, and what is their MOA?

A

Toxic gases, such as ozone and oxides of nitrogen, produce cellular damage, perhaps through generation of reactive oxygen species followed by peroxidation of cellular membranes.

26
Q

the lung serves as a conduit for chemicals into the circulation followed by activation in other tissues and development of diseases in different organs. such as ——— that enters via the lung, forms reactive intermediates in the liver, and these intermediates react with bone macromolecules subsequently resulting in leukemia

A

benzene

27
Q

On heating, such as in volcanic eruption and mining, quartz may become tridymite or cristobalite. Both of these forms are more fibrogenic than quartz.
The toxic effect stems from the ——- in a macrophage. The released lysosomal enzymes digest the macrophage, and this process, in turn, releases the silica from the lysed macrophage.

A

rupture of the lysosomal membrane

28
Q

Another major cause of pulmonary —— is asbestos.
Asbestos refers to a large number of fibrous hydrated silicates of magnesium, calcium, and others.

A

fibrosis

29
Q

——– is also a debilitating disease. It may be induced by cigarette smoking or exposure to aluminum, cadmium oxide, or oxides of nitrogen, ozone, and others.

A

Emphysema

30
Q

It was suggested that the elastic fibers surrounding and supporting the alveoli and bronchi may be damaged by the ———– under certain conditions

A

elastase released from polymorphonuclear (PMN) granulocytes

31
Q

Large airborne particles in the inhaled air are mainly deposited in the nasal passages and cause

A

They may produce hyperemia, squamous- or transitional-cell metaplasia, hyperplasia, ulceration, and, in certain cases, carcinoma.

32
Q

closely related herbicide to paraquat, ——-, although also toxic to cultured lung cells, is not toxic to the lungs either after inhalation or after ingestion.

A

diquat

33
Q

food colors, pesticides (e.g., DBCP), plastics (phthalates), metals (e.g., arsenic, tin, lead, and cadmium), and organic solvents.
A variety of other chemicals affect the ——, such as steroid hormones, alkylating agents, cyclohexylamine, and hexachlorophene.

A

testis

34
Q

both
methylmethane sulfonate (MMS) and
busulfan
produce lethal mutations

A

but MMS affects spermatids and spermatozoa whereas busulfan affects the prespermiogenic cells. These alkylating agents apparently attack the DNA of these cells with different repair mechanisms

35
Q

Tumors may develop in the testis. For example, the herbicide – may induce Leydig cell tumors.

A

linuron

36
Q

—— has been reported to induce prostate cancer in men

A

Cadmium

37
Q

Oocytes may be damaged by chemotherapeutic agents such as

A

nitrogen mustard and vinblastine, and polycyclic aromatic hydrocarbons (PAH) such as 3-methylcholanthrene and benzo[a]pyrene.

38
Q
  • ——– prevents implantation
  • ——– may interfere with ovulation and implantation of the fertilized ovum; it may also retard the development of the sex organs of the offspring
A

-Haloperidol

-Spironolactone

39
Q

——– suppresses ovarian steroid hormone secretion, interrupts regular cyclicity and inhibits embryo implantation

A

Gossypol is also toxic in the female.

40
Q

vitamins and nutrient deficiencies and cobalt, and poisons lead to —— tox

A

hemato system

41
Q

Dichloromethane exposure can also cause asphyxia hypoxia as metabolite is ——-

A

carbon monoxide!

42
Q

—– will cause oxidation of the haemoglobin to cause methaemoglobin which is unable to carry oxygen

A

Aniline