veryhot_post - Medical Board Vignettes - Science and Research Author Topic: Medical Board Vignettes  (Read 3094 times)

Lorenzo

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Re: Medical Board Vignettes
« Reply #60 on: March 28, 2011, 12:38:46 PM »

How do we treat this:


Metronidazole (highly preferred) or any other antibiotics + probenicid
Easy way to borrow money online. Visit www.tala.ph

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Re: Medical Board Vignettes
« Reply #61 on: March 28, 2011, 12:49:14 PM »
You are a 1st year Psychiatry Resident MD at a local hospital. You are seeing a 65 year old man who is diagnosed for clinical depression and hypermania. You look into his patient file and realize that he is recently now taking Fluoxetine , an SSRI (serotonin selective receptor inhibitor), to treat his bouts of depression. For his mania, you notice that the attending MD has prescribed him Carbomezapine. While taking the patient's history, you observe that while he talks, he has quick uncontrollable movements that involves his lips, and his tongue.

What is the cause of this ?



A: The patient clearly has the signs and symptoms of long-term anti-psychotic medication: Tarditive Dyskinesia (uncontrollable jerky movements that invovles the lips and the tongue). The cause of this was long term intake of Typical Anti-depressant --> HALOPERIDOL (HALDOL). Since the patient is recently prescribed Fluoxetine, we can surmise that the patient was taking HALDOL or any other type of Typical Anti-Psychotics, which have extrapyramidal side effects (Tarditive dyskinesia being one of them...)





Lorenzo

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Re: Medical Board Vignettes
« Reply #62 on: March 28, 2011, 12:58:25 PM »
A 28 week old fetus is delivered prematurely. As one of the OB/GYNEs on the floor , you observe that the patient has breathing difficulty. You and the neonatologist diagnose the child as having FRDS (fetal respiratory distress syndrome).

What is deficient in this child? What cell is responsible for producing this deficient material?


A: Surfactant is deficient; Alveolar Pneumocyte Type II are responsible for producing Surfactant.

PATHOPHYSIOLOGY: Surfactant is synthesized after week 35 of gestation. If there is premature delivery prior to week 35, ALWAYS expect the infant to have FRDS.

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Re: Medical Board Vignettes
« Reply #63 on: March 28, 2011, 12:59:36 PM »


As the OB/GYNE , how will you treat Fetal Respiratory Distress Syndrome?

A: Corticosteroids.

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Re: Medical Board Vignettes
« Reply #64 on: March 28, 2011, 01:03:20 PM »

What is the complication of diabetes and corticosteroid deficiency and Respiratory Distress Syndrome?


A: High insulin levels in diabetic mothers antagonize the effects of corticosteroids. Infants of diabetic mothers have a
higher incidence of respiratory distress syndrome.


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Re: Medical Board Vignettes
« Reply #65 on: September 14, 2011, 02:28:15 AM »
Pulmonary Shunt:

A pulmonary shunt is also known as a right-to-left shunt. By definition, systemic venous blood is delivered to the left side of the heart w/o exchanging  oxygen and carbon dioxide with the alveoli. A good example is blood passing through a region of atelectasis.

When a significant pulmonary shunt exists, breathing pure O2 will elevate systemic arterial PO2 a small amount , but it will never produce enough full saturation of the hemoglobin.

Failure to obtain a significant increase in arterial PO2 following administration of supplemental oxygen in hypoxemias strong evidence of the presence of a pulmonary shunt.


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Re: Medical Board Vignettes
« Reply #66 on: September 14, 2011, 02:29:30 AM »
Pulmonary Shunt:[/b]

A pulmonary shunt is also known as a right-to-left shunt. By definition, systemic venous blood is delivered to the left side of the heart w/o exchanging  oxygen and carbon dioxide with the alveoli. A good example is blood passing through a region of atelectasis.

When a significant pulmonary shunt exists, breathing pure O2 will elevate systemic arterial PO2 a small amount , but it will never produce enough full saturation of the hemoglobin.

Failure to obtain a significant increase in arterial PO2 following administration of supplemental oxygen in hypoxemias strong evidence of the presence of a pulmonary shunt.



There is increase in A-a oxygen gradient

Supplemental O2 ineffective at returning arterial PO2 to normal

End-tidal air does not reflect the arterial values



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