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Path Quiz 1 > chemical injury > Flashcards

chemical injury Flashcards

1
Q

what are the three types of cell injury?

A

reversible, permanent, lethal

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2
Q

what are some potential causes of cell injury?

A

point here is that there’s lots of ways

  • anoxia
  • immune and autoimmune mediated
  • inherited genetic abnormalities
  • microbiologic agents - bacteria, virus, fungi
  • nutritional deficiency
  • physical agents: trauma, radiation, heat, cold
  • toxic chemicals
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3
Q

what is a xenobiotic?

A

biologically active chemical that is not “us” - ie it’s from the environment

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4
Q

what are three examples of things that will cause cellular ATP deficiency?

A

systemic anoxia

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5
Q

what are three ways that we recognize toxic chemicals?

A

epidemiology
analysis of human tissues
experimental toxicology (FDA, pharmaceutical industry, academic research)

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6
Q

what tissues does CCl4 injure?

A

liver, kidney, lung - focusing on the liver

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7
Q

what does liver histology of CCl4 injury look like?

A

after 8 hr: coagulation necrosis, vaccules in some of the cells around the central vein, cells a bit farther from central vein swollen, lipid vaccules, when get further from central vein, cells will look normal and unaffected
under EM - dilated ER, granular cytoplasm which represents protein content in fluid, some clear vacuoles in ER that are lipid, mitochondria normal (not swollen yet)

24 hrs: more cells swollen, more with clumped chromatin, some with larger lipid vacuoles
under fat stain - (oil, red O) fat collected in cells around central vein, dark ring around the damaged cells because those cells live longer than then ones right by the central vein and so have more time to absorb fat

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8
Q

what is the process of metabolic activation of CCl4 in the liver?

A

liver detoxifies, but generates CCl3 radical in the process in ER cytochromes - this affects the sER and rER first
effect on sER results in cell swelling
effect on rER results in decreased protein synthesis

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9
Q

what are the three effects of CCl4 on hepatic lipid metabolism?

A

1: decreased lipoprotein synthesis
2: decreased transport, glycosolation, and secretion of VLDL
3: increased TG in cytoplasm

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10
Q

what are the potential hydroxy radical interactions?

A
  • lipid peroxidation - target is unsaturated lipids
  • base damage in DNA and RNA
  • proteins - enzyme inactivation
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11
Q

what are our defenses against free radical damage?

A

antioxidants including vitamin E, ascorbic acid, glutathione

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12
Q

how long does it take for the liver to resolve from CCl4 induced injury?

A

24 hours if there’s not too much damage (ie the dose is too large)
by 48 hrs, the necrotic cells are being removed as a result of necrosis and inflammation

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13
Q

what cells are CCl4 toxic to?

A

only those that have cytochrome enzymes to take it apart and form the free radical
requires metabolic activation

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14
Q

what is cis platinum used for clinically?

A

chemotherapy

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15
Q

what are the side effects of cis platinum?

A

diarrhea
renal failure
weight loss, kidneys swell

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16
Q

what is cis in cis platinum?

A

two chlorides on the same side - if trans, not really toxic

17
Q

what do the Cl on cis-DDP do within cells?

A

at physiologic pH, these Cl leave the molecule

bind to bases in DNA, can bind protein to DNA by binding guanine and the protein, can create crosslinks between strands

all damage DNA - cell will shut down DNA synthesis - stops cell division - cell will repair damage or undergo apop if it can’t repair it

18
Q

what are the effects of cis-DDP in the small intestine? what would you see histologically (over time)?

A

8 hrs: mitosis has stopped, apoptosis begins (clumped chromatin), vili begin to shorten

24 hrs: vili shorter, less reabsorptive surface => diarrhea
no mitoses, more evidence of apoptosis

3 days: vili very short, crypts dilated - looks like they don’t have cells but actually lined by flattened surviving epithelial cells, lots of dark blue spots

4 days: gut begins to recover - vili longer, crypts recovering

5 days: vili even longer - mitotic cells visible

19
Q

what are the effects of cis-DDP in the kidney? what would you see histologically?

A

get initial renal failure and then gets better
after 3-5 days, some tubules that look normal, but regions of swollen cytoplasm = injured cells
or pink cytoplasm, clumped chromatin = necrotic cells

after 7 days, wide lumens, flat epithelium in tubules

after 14, renal structure beginning to be recreated

20
Q

what does cis-DDP affect in the kidney?

A

not dividing cells so not affecting mitosis

damage likely due to combination of membrane effects and effects on enzymes

21
Q

how would you reduce the toxicity of cis-platin clinically?

A

nephrotoxicity makes it dose limiting
keep patient well-hydrated
give cisPt as prolonged infusion
treat for a day and then rest the patient
alter the chemical form of cisPt - carboplatin is les nephrotoxic than cisplatin

22
Q

what is hormesis?

A

biologic effect of a low dose (non-toxic dose) of a xenobiotic that is toxic at a higher dose

  • such effects sometimes promote cell survival by activation cellular defense mechanisms
23
Q

what happens to absorbed lead?

A

incorporated into bone and teeth - competes with Ca
high levels can cause CNS disturbances
peripheral neuropathies predominate in adults
interferes with normal remodeling of cartilage in epiphyses
inhibits enzymes involved in heme synthesis

24
Q

what are the major anatomic targets of lead?

A 
bone marrow
blood
nervous system
GI tract
kidneys
25
Q

what changes would you expect to see in blood and marrow due to lead?

A

inhibition of ferrochelatase => scattered ringed sideroblasts
microcytic, hypocrhormic anemia with mile hemolysis in peripheral blood
punctate basophilic stippling of the red cells

26
Q

what are ringed sideroblasts? when do they occur?

A

red cell precursors with iron-laden mitochondria that are detected with prussian blue stain

in blood and bone marrow that’s been poisoned with lead

27
Q

what does mercury do when absorbed?

A

easily lipid soluble
accumulates in brain => disturbs neuromotor, cognitive, and behavioral functions
binds with high affinity to thiol groups

28
Q

what can protective against mercury poisoning?

A

intracellular glutathione, acting as thiol donor

main protector in CNS and kidney

29
Q

what is the consequence of arsenic poisoning?

A

GI, cardiovascular, and CNS disturbances
often fatal
likely due to interference with mitochondrial oxidative phosphorylation - trivalent arsenic can replace phosphates in adenosine triphosphate

see sensorimotor neuropathy
increased risk of cancer development - skin tumors on palms and soles of feet

30
Q

what is the result of cadmium poisoning?

A

obstructive lung disease caused by necrosis of alveolar macrophages
kidney damage - tubular damage that may progress to end-stage renal damage
skeletal abnormalities associated with Ca loss
DNA damage

Path Quiz 1 (12 decks)

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