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I am the Object of My Pimp's Affection


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If the ddx is simply CP, 10 isn't hard..... but 10 menstrual-related causes of CP?

Ectopic endometrium, blood-loss anemia, psychogenic secondary to PMS (hate going there, though)... that's all that comes to mind.

Others (adding to doboy's list):

6. pericarditis

7. pleurisy

8. pneumonia

9. PE

10. CVD-related vasculitis, such as SLE

11. MVP

12. costochondritis

13. muscle strain (diaphragm, intercostals, chest wall)

14. traumatic

15. esophageal spasm

16. esophageal rupture (Boerhaave) vs. Mallory-Weiss

17. esophagitis (fungal like Candida, viral like HSV)

18. Hiatal hernia

19. zoster

20. pulmonary HTN

21. cardiomyopathy

CP ddx is HUGE :D

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  • 2 weeks later...

From another thread...

I am working with a very very very smart doctor, we were discussing asthma exacerbation associated with URI, specifically viral influenced asthma attacks. She asked me what we can do to prophylax (protect) the patient from having an asthma attack from this viral upper respiratory infection (common head cold) and I discussed various medicines which stabilize the inflammatory response that causes an asthma attack. She shot down every one of my

ideas, and then told me Viruses don't cause the same asthma response as allergens, they effect a different route to cause bronchospasm.....so the medications would be ineffective.

 

It's a great thread and I don't want to hijack it by going off on this tangent... but as is consistent with (one of) my weakness(es), I've gotta know. Unfortunately I have knees, shoulders, imms schedules and lots more to be reading about before getting back to clinicals tomorrow. So does anyone know HOW a respiratory virus provokes bronchospasm?

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From another thread...

 

 

It's a great thread and I don't want to hijack it by going off on this tangent... but as is consistent with (one of) my weakness(es), I've gotta know. Unfortunately I have knees, shoulders, imms schedules and lots more to be reading about before getting back to clinicals tomorrow. So does anyone know HOW a respiratory virus provokes bronchospasm?

 

LA, the question you are asking has many, many, many answers. There is t-cell mediated immunopathology, recruitment of neutrophils and macrophages to the virus-infected cells leading to cellular damage, release of IL-11, IL-8, and other chemo/cytokines that contribute to localized inflammation, and other scenarios that contribute to localized (and on a macroscopic level) inflammation. Further, there is evidence of viruses interfering with acetylcholine regulation leading to bronchoconstriction.

 

But as a guiding principle, viruses usually cause asthma by the infammatory response (non-IgE mediated) aimed at them in the lung (some recent literature suggests a significant role for NK cells which are not responsive to corticosteroids), not by the common underlying pathology (IgE mediated) commonly known as "asthma."

 

G

 

PS - now you got me reading asthma articles... :)

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  • 2 weeks later...
Guest leavinthelab

I'll stop lurking and take a stab...

Neuroleptic malignant syndrome is characterized by fever, rigidity and cognitive changes. It is reported to occur in people taking central dopaminergic drugs and occurs within the first few days to weeks of starting the meds.

 

Is it differentiated from malignant hyperthermia by onset and drug exposure? (Since malignant hyperthermia occurs within an hour or so following administration of anesthetic meds)

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I'll stop lurking and take a stab...

Neuroleptic malignant syndrome is characterized by fever, rigidity and cognitive changes. It is reported to occur in people taking central dopaminergic drugs and occurs within the first few days to weeks of starting the meds.

 

Is it differentiated from malignant hyperthermia by onset and drug exposure? (Since malignant hyperthermia occurs within an hour or so following administration of anesthetic meds)

 

Nice, leavin. The main difference I was thinking of is the setting in which it occurs- as you mentioned, after inhalational agents-OR, ICU, etc...

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Some things that I needed to know for ER rotation...

 

How do you treat a patient with SVT (supraventricular tachy) that is hemodynamically stable?

 

What if they are hemodynamically unstable with SVT?

 

Name as many causes of PEA (pulseless electrical activity) as you can...

 

First thing(s) to administer to a patient with PEA?

 

With what ratio of lidocaoine/bicarb do you buffer lidocaine?

 

In what parts of the body do you not use lidocaine with epinephrine?

 

X-ray sign that is seen with a kid that has epiglottitis?

 

X-ray sign that is seen with viral croup?

 

X-ray sign that is seen in a patient that has a fracture to the proximal end of the radius (not talking about anterior fat pad)?

 

Invasive and non-invasive immediate (temporary) treatments for a patient that has PEA due to cardiac tamponade?

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Not sure if you have received any responses, but here is what I found on a quick search.

 

White Clot Syndrome: It has been reported that patients on heparin sodium may develop new thrombus formation in association with thrombocytopenia, resulting from irreversible aggregation of platelets induced by heparin the so-called ''white clot syndrome.'' The process may lead to severe thromboembolic complications like skin necrosis, gangrene of the extremities that may lead to amputation, myocardial infarction, pulmonary embolism, stroke and possibly death. There, heparin sodium administration should promptly be discontinued if a patient develops new thrombosis in association with thrombocytopenia.

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I did a quick search and this is what I found, hope it helps.:D

 

White Clot Syndrome: It has been reported that patients on heparin sodium may develop new thrombus formation in association with thrombocytopenia, resulting from irreversible aggregation of platelets induced by heparin the so-called ''white clot syndrome.'' The process may lead to severe thromboembolic complications like skin necrosis, gangrene of the extremities that may lead to amputation, myocardial infarction, pulmonary embolism, stroke and possibly death. There, heparin sodium administration should promptly be discontinued if a patient develops new thrombosis in association with thrombocytopenia.

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I did a quick search and this is what I found, hope it helps.:D

 

White Clot Syndrome: It has been reported that patients on heparin sodium may develop new thrombus formation in association with thrombocytopenia, resulting from irreversible aggregation of platelets induced by heparin the so-called ''white clot syndrome.'' The process may lead to severe thromboembolic complications like skin necrosis, gangrene of the extremities that may lead to amputation, myocardial infarction, pulmonary embolism, stroke and possibly death. There, heparin sodium administration should promptly be discontinued if a patient develops new thrombosis in association with thrombocytopenia.

 

:rolleyes: This is a "pimping" session thread, so it's more for posing a question to test the knowledge of students out there on the forum- not for my own knowledge.... (ie I wouldn't ask the question unless I knew the answer!)

 

thanks though :rolleyes: :rolleyes:

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