Toxic pulmonary diseases

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19 Terms

1
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club cell

___________: Non-ciliated cell that produces surfactant and serves as the progenitor cell in the airways for Epithelial repair.

2
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surfactant, progenitor, epithelial

Club cells produce _______ and serve as ______ calls in the airways to aid in ________ repair

3
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smooth endoplasmic reticulum, club cell secretory protein (CC10), phospholipase A2

Club cells contain a lot of _________, and secrete ________ in response to adrenergic stimuli, which inhibits __________

4
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fog fever

Acute bovine pulmonary edema and emphysema is commonly referred to as ________

5
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cattle no dry pasture over winter being switched to lush pasture RICH IN L-TRYPTOPHAN

What is the common inciting factor of Acute bovine pulmonary edema and emphysema?

6
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l-tryptophan, rumen, 3-methyl indole

After being switched to lush pasture, _____________ is metabolized in the _______ to ___________

7
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it's eructated and inhaled or absorbed through rumen wall

What happens to 3-methyl indole after its made in the rumen from L-tryptophan?

8
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club cells, cytochrome p450, metabolites are incredibly toxic

After being absorbed into the lungs, 3-methyl indole is metabolized by _______ using _________.

Why is this bad?

9
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type 1 pneumocytes, interstitial pneumonia

After 3-methyl indole is converted to toxic metabolites, these cause damage to __________ causing a _______________

10
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increased permeability, pulmonary edema, interstitial emphysema, respiratory distress

The damaged lung tissue becomes leaky, leading to _________, ___________, _________ and _________, which can be fatal.

11
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cool

She said to make sure you knew these 9 steps of "acute bovine pulmonary edema and emphysema".

It's basically the last couple terms I just went through, but the specific shortened steps are on slide 4 of lecture 11 if you want to check them.

Cool?

<p>She said to make sure you knew these 9 steps of "acute bovine pulmonary edema and emphysema".</p><p>It's basically the last couple terms I just went through, but the specific shortened steps are on slide 4 of lecture 11 if you want to check them.</p><p>Cool?</p>
12
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beef cattle in spring, 2-10 days,

Who is the prime suspect for getting fog fever?

This usually occurs ___________ days after switching to a lush pasture.

13
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sudden death, frothing at the mouth, dyspnea, 50%

what are the clinical signs of Fog fever?

morbidity is about ________%

14
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pale, soft and rubbery, dorsocaudal, interstitial edema, emphysema

Affected lungs (fog fever) are often ________, ______ and _______ especially in the ________ lung lobes.

There is significant _________ and ________. This correlates with the clinical signs of dyspnea and frothing at the mouth.

15
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moldy sweet pototes, perilla mint, brassica spp

What plants are included in a differential diagnosis for toxic pneumonia in ruminants

16
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4-ipomeanol, type I pneumocytes, S-methyl cystine sulfoxide.

Moldy sweet potatoes contain _________.

Perilla mint (perilla ketones) can also damage _______________.

Plants in the Brassica family (decorative cabbages) contain _______________________>

17
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laryngeal and respiratory tract edema

Smoke inhalation causes thermal injury like __________________ and _______________ from inhalation of heated air and damage to epithelium

18
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type I pneumocytes

Chemical injury from smoke inhalation includes damage to _______________________

19
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true, duh

true/false: There are many causes for pulmonary toxicity, including chemicals, plants, etc, so obtaining a good history is necessary for diagnostics