running quiz series

[drmajumdar]

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hi guys, I'm a med student from India, interested in interacting with med-students from all over the world to get a global perspective. thanx a lot again.

by the way, i have this idea which i have been thinking about for sometime. it would be quite interesting to run a quiz series right here on SDN. it goes like this, someone posts a question which he/she has found really interesting and the challenge for all other guys is to answer the question. the first person to answer the question will post another question...and so on. it might also be a question which the med-student hasn't found the answer to.

participation and criticism are both welcome.

 

[drmajumdar]

since nobody seems to take up the gauntlet, i'll start the series.....so here goes.

We all know Sickle Cell disease protects against malaria. so the question is

1. which type of malaria is it protective against?
and 2. more interestingly which type of malaria does it predispose to?

 

[francisdoss]

since nobody seems to take up the gauntlet, i'll start the series.....so here goes.

We all know Sickle Cell disease protects against malaria. so the question is

1. which type of malaria is it protective against?
and 2. more interestingly which type of malaria does it predispose to?

Hw many types of malaria is there out there? I alwys though there is only 1 type of malaria.

 

[mjl1717]

Hw many types of malaria is there out there? I alwys though there is only 1 type of malaria.

3 types:

P. falciparum
P. ovale
P. malarie

as I remember sickle cell is protective against P. falciparum.

 

[DocVirk]

1. which type of malaria is it protective against?
and 2. more interestingly which type of malaria does it predispose to?

I like the idea of a quiz series, but I am stumped on the first question...

1. SA or SS protects against P falciparum, but this may only be shown in papers because P falciparum is the most deadly and problematic of the malaria parasites.
2. I have no idea...

Now I'm going to drop out of medical school, because obviously I have learned nothing in all of my time...🙁

 

[crazy_cavalier]

I think that first question was obscenely useless.


Here's a new one for you. A patient presents with complaints about fatigue. Physical examination reveals depapillation of the tongue. An inquiry into the patient's eating pattern shows very low leafy vegetables and a probable folate deficiency. What would you expect to see in a sample blood smear taken from this patient?

a.) Increased hematocrit
b.) Microcytic RBC
c.) Hypersegmented neutrophils
d.) All of the above
e.) None of the above

 

[bjackrian]

I think that first question was obscenely useless.


Here's a new one for you. A patient presents with complaints about fatigue. Physical examination reveals depapillation of the tongue. An inquiry into the patient's eating pattern shows very low leafy vegetables and a probable folate deficiency. What would you expect to see in a sample blood smear taken from this patient?

a.) Increased hematocrit
b.) Microcytic RBC
c.) Hypersegmented neutrophils
d.) All of the above
e.) None of the above

c? Low folate=decreased thymidilate synthesis-->decreased cell division. You get a macrocytic anemia because pre-M checkpoint can't get passed. Hematocrit should be decreased due to macrocytic anemia. Not sure about the hypersegmented neutorphils, but that soudns familiar.

Or I could be pulling this out of my derriere...I hated biochem 👎

 

[thesauce]

I think that first question was obscenely useless.


Here's a new one for you. A patient presents with complaints about fatigue. Physical examination reveals depapillation of the tongue. An inquiry into the patient's eating pattern shows very low leafy vegetables and a probable folate deficiency. What would you expect to see in a sample blood smear taken from this patient?

a.) Increased hematocrit
b.) Microcytic RBC
c.) Hypersegmented neutrophils
d.) All of the above
e.) None of the above

I think it's C. How about this one:

During her internal medicine rotation, a 3rd year medical student is asked to evaluate a patient with a known pyruvate kinase deficiency. While interviewing the patient, the medical student remembers learning about another disease with similar characteristics. Which disease is most clinically similar:

A. alpha thalassemia
B. beta thalassemia
C. Glucose-6-phosphate dehydrogenase deficiency
D. Hereditary spherocytosis
E. Iron deficiency anemia

 

[crazy_cavalier]

I think it's C. How about this one:

During her internal medicine rotation, a 3rd year medical student is asked to evaluate a patient with a known pyruvate kinase deficiency. While interviewing the patient, the medical student remembers learning about another disease with similar characteristics. Which disease is most clinically similar:

A. alpha thalassemia
B. beta thalassemia
C. Glucose-6-phosphate dehydrogenase deficiency
D. Hereditary spherocytosis
E. Iron deficiency anemia

C was right for the folate question.

Is the one above E?

 

[neurodoc]

How about this one?

Skin pigmentation seems to follow a latitudinal gradient; that is, people who live at the Equator show more melanin than people living at higher latitudes.

This is not exactly consistent, however. The Innuit, who live above the Arctic Circle, have darker skin than Swedes, for example.

One can assume that skin pigmentation is the result of evolution by natural selection. What selects for skin color? It has been suggested that increased skin pigmentation protects equatorial populations from UV injury and skin cancer. Another hypothesis is that it protects them from hypervitaminosis D, and, conversely, that pale skin for higher latitude dwellers protects them from rickets, by allowing for greater vitamin D synthesis...

This is really a quite interesting question, and worth discussing.😍

 

[neurodoc]

Or how about this one? Afro-Americans have a high incidence of hypertension. Why is this? One explanation is that African-Americans came to the US on slave ships. The trans-Atlantic crossing was streeful and many died, especially of dehydration and starvation. Furthermore, those who survived the crossing were put to work on plantations in the American southeast, and many of those did not survive the rigors of the plantation. Those who survived the crossing and the rigors of the plantation did so becauise they were able to retain sodium. This was a good thing for their survival. It was a bad thing, in that it led to fluid retention and hypertension. As we now know, Afro-Americans have a greater than average rate of hypertension and suffer from high rates of stroke, renal failure, and cardiovascular disease as a consequence of that.

I mention this because it seems that this burden of disease on Afro-Americans is a direct result of the slave trade and natural selection.

Nick

 

[DocVirk]

I think the pyruvate kinase question is C- G6PD deficiency. They are both red cell enzymopathies that cause hemolytic anemia. Correct me if I'm wrong...

Here's another question

A trauma alert comes into the ED with a 3 cm wide stab wound to the cervical spine area. Upon examination, the patient has lost the sensation of pain in much of his right side, and has lost motor control of much of his left side. Describe the lesion and name the syndrome he is experiencing...😕

 

[thesauce]

I think it's C. How about this one:

During her internal medicine rotation, a 3rd year medical student is asked to evaluate a patient with a known pyruvate kinase deficiency. While interviewing the patient, the medical student remembers learning about another disease with similar characteristics. Which disease is most clinically similar:

A. alpha thalassemia
B. beta thalassemia
C. Glucose-6-phosphate dehydrogenase deficiency
D. Hereditary spherocytosis
E. Iron deficiency anemia

Yes, the answer is C and for that reason. Well done!

 

[thesauce]

I think the pyruvate kinase question is C- G6PD deficiency. They are both red cell enzymopathies that cause hemolytic anemia. Correct me if I'm wrong...

Here's another question

A trauma alert comes into the ED with a 3 cm wide stab wound to the cervical spine area. Upon examination, the patient has lost the sensation of pain in much of his right side, and has lost motor control of much of his left side. Describe the lesion and name the syndrome he is experiencing...😕

He's got Brown-Sequard. The LEFT half of the cervical spinal cord was severed, correct?

 

[thesauce]

Okay, new one:

Each statement below concerning osteoclasts is true except that they:

A. are found in Howship's lacuna
B. resorb bone
C. are stimulated by calcitonin
D. are mutlinucleated
E. help remodel bone

 

[epalantequevoy]

3 types:

P. falciparum
P. ovale
P. malarie

as I remember sickle cell is protective against P. falciparum.

There are actually 4 types:

Falciparum
Ovale
Malariae
Vivax

 

[neurodoc]

I think the pyruvate kinase question is C- G6PD deficiency. They are both red cell enzymopathies that cause hemolytic anemia. Correct me if I'm wrong...

Here's another question

A trauma alert comes into the ED with a 3 cm wide stab wound to the cervical spine area. Upon examination, the patient has lost the sensation of pain in much of his right side, and has lost motor control of much of his left side. Describe the lesion and name the syndrome he is experiencing...😕

Hemitransection of the spinal cord. This is the Brown-Sequard Syndrome. You didn't discuss the dissociated sensory loss, where pain and temperature sense is lost on the opposite side from loss of vibratory and light touch sensation. Brown-Sequard is a classic syndrome that illustrates the functional neuroanatomy of the spinal cord.😎

 

[xlithiumx]

Okay, new one:

Each statement below concerning osteoclasts is true except that they:

A. are found in Howship's lacuna
B. resorb bone
C. are stimulated by calcitonin
D. are mutlinucleated
E. help remodel bone

C is the correct answer for this one. Calcitonin inhibits the function of osteoclasts.

Next some cardiovascular physiology...

What will be the net effect on heartrate, mean arterial pressure, and central venous pressure following an intravenous injection of acetylcholine??

A. all increase
B. HR up, arterial pressure down, central venous pressure up
C. HR down, arterial pressure down, central venous pressure up
D. HR up, arterial pressure up, central venous pressure down
E. all decrease

 

[nintendo]

Yes, the answer is C and for that reason. Well done!

Hey i thought C..but i was just thinking krebs cycle..does that make it a lucky guess?

 

[nintendo]

C is the correct answer for this one. Calcitonin inhibits the function of osteoclasts.

Next some cardiovascular physiology...

What will be the net effect on heartrate, mean arterial pressure, and central venous pressure following an intravenous injection of acetylcholine??

A. all increase
B. HR up, arterial pressure down, central venous pressure up
C. HR down, arterial pressure down, central venous pressure up
D. HR up, arterial pressure up, central venous pressure down
E. all decrease

C..Parasympathetic response? Or is it E? Or am I already a bad doctor? Maybe I should just go to sleep.

 

[xlithiumx]

C..Parasympathetic response? Or is it E? Or am I already a bad doctor? Maybe I should just go to sleep.

try again

 

[drmajumdar]

since nobody seems to take up the gauntlet, i'll start the series.....so here goes.

We all know Sickle Cell disease protects against malaria. so the question is

1. which type of malaria is it protective against?
and 2. more interestingly which type of malaria does it predispose to?

the correct answer is alsthough HbS is protective against P.falciparum malaria, esp. in children, it has been shown to increase risk of getting P.vivax malaria, esp in adults.

 

[drmajumdar]

I think that first question was obscenely useless.


Here's a new one for you. A patient presents with complaints about fatigue. Physical examination reveals depapillation of the tongue. An inquiry into the patient's eating pattern shows very low leafy vegetables and a probable folate deficiency. What would you expect to see in a sample blood smear taken from this patient?

a.) Increased hematocrit
b.) Microcytic RBC
c.) Hypersegmented neutrophils
d.) All of the above
e.) None of the above

although it might be irrelevant to the American students, given that malaria isn't really a problem in the US, it is VERY much relevant to the global health scenario where malaria is responsible for millions of deatjs.

the answer to your question is "hypersegmented neutrophils"

 

[drmajumdar]

Next some cardiovascular physiology...

What will be the net effect on heartrate, mean arterial pressure, and central venous pressure following an intravenous injection of acetylcholine??

A. all increase
B. HR up, arterial pressure down, central venous pressure up
C. HR down, arterial pressure down, central venous pressure up
D. HR up, arterial pressure up, central venous pressure down
E. all decrease[/QUOTE]

Is it C. HR down, arterial pressure down, CVP up

 

[xlithiumx]

Next some cardiovascular physiology...

What will be the net effect on heartrate, mean arterial pressure, and central venous pressure following an intravenous injection of acetylcholine??

A. all increase
B. HR up, arterial pressure down, central venous pressure up
C. HR down, arterial pressure down, central venous pressure up
D. HR up, arterial pressure up, central venous pressure down
E. all decrease

Is it C. HR down, arterial pressure down, CVP up

Turns out the answer is B, HR up, arterial pressure down, central venous pressure up.

This is true because the circulating ACh you injected stimulates muscarinic receptors on arterioles causing vasodilation. This lowers the mean arterial pressure. The aortic and carotid sinus baroreceptors then respond by sending less stimulation to the cardiovascular medullary center which in turn sends sympathetic stimulation to the heart and vessels. This accelerates the heartrate and increases peripheral venous tone, but does not increase arteriolar tone because the ACh is still providing vasodilation. Thus, you get increased HR, increased central venous pressure, and decreased mean arterial pressure.

 

[drmajumdar]

Turns out the answer is B, HR up, arterial pressure down, central venous pressure up.

This is true because the circulating ACh you injected stimulates muscarinic receptors on arterioles causing vasodilation. This lowers the mean arterial pressure. The aortic and carotid sinus baroreceptors then respond by sending less stimulation to the cardiovascular medullary center which in turn sends sympathetic stimulation to the heart and vessels. This accelerates the heartrate and increases peripheral venous tone, but does not increase arteriolar tone because the ACh is still providing vasodilation. Thus, you get increased HR, increased central venous pressure, and decreased mean arterial pressure.[/QUOTE]



COOL.......was thinking of the same lines.......should've taken into account the barorecptor reflex.....good question

 

[drmajumdar]

what is lhermitte's sign?

 

[neurodoc]

what is lhermitte's sign?

That is lancinating pain that runs up and down the spine in response to flexion of the neck. It indicates a lesion of the posterior columns. This may be due to a mechanical lesion (e.g.cervical spondylosis) or a neural leasion ( e.g.MS or B12 deficiency)

Nick

 

[drmajumdar]

That is lancinating pain that runs up and down the spine in response to flexion of the neck. It indicates a lesion of the posterior columns. This may be due to a mechanical lesion (e.g.cervical spondylosis) or a neural leasion ( e.g.MS or B12 deficiency)

Nick

bang on!! now for the real question, this pain can also bee found as a longterm complication of the chemotherapy given to treat a particular disease. what disease? when the pain occurs as the a complication as mentioned before, it is called Lhermitte's syndrome.

 

[neurodoc]

bang on!! now for the real question, this pain can also bee found as a longterm complication of the chemotherapy given to treat a particular disease. what disease? when the pain occurs as the a complication as mentioned before, it is called Lhermitte's syndrome.

Antineoplastic drugs, especially cisplatin and carboplatin, can cause a severe sensory polyneuropathy that especially affects the dorsal columns. So can vincristine and Taxol.

Nick

 

[drmajumdar]

C'mon guys, would love to have more of your questions!!!!

And Nick, it'll be amazing if you followed up your correct answers with new questions!

 

[neurodoc]

C'mon guys, would love to have more of your questions!!!!

And Nick, it'll be amazing if you followed up your correct answers with new questions!

I'm lazy. 🙂 It's fun to try to answer questions, but a lot more work to think up interesting questions...😳

Nick

 

[drmajumdar]

ATTENTION PLEASE. THANK YOU.



THIS IS AGAIN AN URGENT AND DESPERATE PLEA TO ALL MEMBERS TO CONTINUE WITH THE SERIES BY CONTRIBUTING QUESTIONS.

PLEEEEEEEEEEEEEASE.

THANX.



is this how the cookie crumbles

 

[felipe5]

what does a positive Throckmorton sign indicate?

 

[trudub]

what does a positive Throckmorton sign indicate?

On an Xray, 50% of the time the penis points towards the side of the pathology. That is a positive Throckmorton sign. This is one to tuck away in your mind because if you hear it and people are laughing and you don't remember what it is, you will definitely be out of the loop.

So, here is my question: How do you differentiate Crohn's disease from Ulcerative colitis? What are the associated dermatological findings with each?

 

[beefballs]

How about this one?

Skin pigmentation seems to follow a latitudinal gradient; that is, people who live at the Equator show more melanin than people living at higher latitudes.

This is not exactly consistent, however. The Innuit, who live above the Arctic Circle, have darker skin than Swedes, for example.

One can assume that skin pigmentation is the result of evolution by natural selection. What selects for skin color? It has been suggested that increased skin pigmentation protects equatorial populations from UV injury and skin cancer. Another hypothesis is that it protects them from hypervitaminosis D, and, conversely, that pale skin for higher latitude dwellers protects them from rickets, by allowing for greater vitamin D synthesis...

This is really a quite interesting question, and worth discussing.😍

no because it will just end up as an AA debate

 

[Requiem]

On an Xray, 50% of the time the penis points towards the side of the pathology. That is a positive Throckmorton sign. This is one to tuck away in your mind because if you hear it and people are laughing and you don't remember what it is, you will definitely be out of the loop.

So, here is my question: How do you differentiate Crohn's disease from Ulcerative colitis? What are the associated dermatological findings with each?

This just turned inter-disciplinary! Pharmacy student 😉


From memory (hazy): Chron's is regional enteritis, marked by fistulas, inflammation of the entire bowel wall (luminal narrowing), circumscribed ulcers and right colon predominance.

Ulcerative colitis is marked by pseudopolyps, crypt abscesses and small superficial ulcers.

I'll throw out a pharmacology question: Physician writes a script for an adult with diabetes who has hypertension; Lopresor.

Why is giving a beta-adrenoreceptor antagonist contraindicated in diabetics?

 

[xlithiumx]

This just turned inter-disciplinary! Pharmacy student 😉


From memory (hazy): Chron's is regional enteritis, marked by fistulas, inflammation of the entire bowel wall (luminal narrowing), circumscribed ulcers and right colon predominance.

Ulcerative colitis is marked by pseudopolyps, crypt abscesses and small superficial ulcers.

I'll throw out a pharmacology question: Physician writes a script for an adult with diabetes who has hypertension; Lopresor.

Why is giving a beta-adrenoreceptor antagonist contraindicated in diabetics?

Beta blockers can raise blood sugar and additionally the beta blockade can mask the tachycardia associated with hypoglycemia. I think that's it.

Next question:

What are the four pathological conditions of the Tetralogy of Fallot?

 

[trudub]

Beta blockers can raise blood sugar and additionally the beta blockade can mask the tachycardia associated with hypoglycemia. I think that's it.

Next question:

What are the four pathological conditions of the Tetralogy of Fallot?

Right Ventricular Hypertrophy, Pulmonary Stenosis, Overriding Aorta, and Ventricular Septal Defect.

Next question: What is the genetic defect associated with Down's Syndrome? What congenital defect is associated with Downs? What neurological disease are Down's patients at risk for? What cancer happens with increased incidence in Down's patients?

 

[felipe5]

Right Ventricular Hypertrophy, Pulmonary Stenosis, Overriding Aorta, and Ventricular Septal Defect.

Next question: What is the genetic defect associated with Down's Syndrome? What congenital defect is associated with Downs? What neurological disease are Down's patients at risk for? What cancer happens with increased incidence in Down's patients?

trisomy 21, endocardial cushion defects/duodenal atresia, alzheimers, ALL

now for all you ob/gyn'ers: what is usually the earliest sign of magnesium sulfate toxicity?

 

[neurodoc]

So, here is my question: How do you differentiate Crohn's disease from Ulcerative colitis? What are the associated dermatological findings with each?

Erythema nodosum (EN) and pyoderma gangrenosum (PG) are both seen in infammatory bowel disease. I believe EN is more common in Crohn's and PG is more common in UC. In both, fixed drug eruptions (to PCN) are more common than in the general population.

Nick

 

[neurodoc]

no because it will just end up as an AA debate

I suppose anything that deals with skin pigmentation could "end up as an AA debate." It's still a fascinating question, as was the other question I raised the high incidence of hypertension in African Americans, and how this might have resulted from the survival benefit of salt retention during the trans-Atlantic slave ship journey.

This is really basic evolutionary biology, and it's every bit as interesting as the association of Sickle Cell anemia with falciparum malaria, an association that is widely discussed in biology textbooks. Heck, I learned about Sickle Cell disease and malaria in my nineth grade Bio class...and that was 38 years ago...😉

Nick

 

[neurodoc]

trisomy 21, endocardial cushion defects/duodenal atresia, alzheimers, ALL

now for all you ob/gyn'ers: what is usually the earliest sign of magnesium sulfate toxicity?

The most significant signs of Mg++ toxicity are CNS depression, hypotension, flushing, and weakness. The earliest sign of toxicity is loss of the deep tendon reflexes (at the knees). In order to use this sign effectively, you should assess the knee jerks before starting MgSO4...to be sure that the patient has knee jerks to begin with. Some patients are hyporeflexic to begin with.🙂

Nick

 

[neurodoc]

Here's a case from my 3rd Year IM rotation. 51 yo Chinese male (US imigrant) is admitted from the ER for abdominal pain, N/V, jaundice, ascites, and cachexia. The IM intern orders a stool sample for O&P. As the scut-monkey I get to collect the sample from the patient's bed pan and walk it to the lab. I can't resist looking at it an notice that it looks really strange. The stool is a really shiny silver color. It's so unusual that I transfer a bit of it into another container to present at morning rounds. It's a quiet night, so I hit the books in the library, and present the case, with the show-and-tell stool sample. The intern is happy to let me present this case. Based on my reading, I'm confident enough to forgo the usual broad med student differential diagnosis for abdominal pain, jaundice, N/V etc and I boldly declare that there is only one lesion that can account for this patient's presentation. The lesion must be located at "X," and in all likelihood the etiology is "Y."

What is "X" and what is "Y?"😀

Nick

 

[Requiem]

Beta blockers can raise blood sugar and additionally the beta blockade can mask the tachycardia associated with hypoglycemia. I think that's it.

Close 🙂, B2 adrenoreceptors on the liver stimulate gluconeogenesis and glycogenolysis (hence sympathetic stimulation -> breakdown of sugar) so blocking these receptors will decrease blood sugar; dangerous combo when combined with masking the sympathetic "warning signs" diabetics become accustomed to, i.e the tachycardia you mentioned.

Even selective B1-antagonists (ie acebutolol, atenolol) should be avoided.

 

[riverie]

Here's a case from my 3rd Year IM rotation. 51 yo Chinese male (US imigrant) is admitted from the ER for abdominal pain, N/V, jaundice, ascites, and cachexia. The IM intern orders a stool sample for O&P. As the scut-monkey I get to collect the sample from the patient's bed pan and walk it to the lab. I can't resist looking at it an notice that it looks really strange. The stool is a really shiny silver color. It's so unusual that I transfer a bit of it into another container to present at morning rounds. It's a quiet night, so I hit the books in the library, and present the case, with the show-and-tell stool sample. The intern is happy to let me present this case. Based on my reading, I'm confident enough to forgo the usual broad med student differential diagnosis for abdominal pain, jaundice, N/V etc and I boldly declare that there is only one lesion that can account for this patient's presentation. The lesion must be located at "X," and in all likelihood the etiology is "Y."

What is "X" and what is "Y?"😀

Nick

ok, just a second year med student here and had to google for the answer..
is X the ampulla of Vater and Y cancer?

Here's one: A 68 yo otherwise healthy diabetic patient presents with acute shortness of breath. O2 sat on evaluation in the ER is 83%. SOB is exacerbated by exertion, but patient is in no apparent distress while on oxygen and sitting quietly in the ER. Previous 20 pack year h/o smoking, quit 15 years ago. Patient is fit and exercises 6 times a week. No recent history of surgery, trauma, bed rest or travel. No history of chronic progressive shortness of breath. On exam, patient is tachycardic and tachypneic. Some fine end-expiratory crackles are heard in the right-mid and lower-left lung fields. Breath sounds vesicular and slightly decreased throughout. CXR appears normal. What is on the top of your differential?

 

[epalantequevoy]

Here's a case from my 3rd Year IM rotation. 51 yo Chinese male (US imigrant) is admitted from the ER for abdominal pain, N/V, jaundice, ascites, and cachexia. The IM intern orders a stool sample for O&P. As the scut-monkey I get to collect the sample from the patient's bed pan and walk it to the lab. I can't resist looking at it an notice that it looks really strange. The stool is a really shiny silver color. It's so unusual that I transfer a bit of it into another container to present at morning rounds. It's a quiet night, so I hit the books in the library, and present the case, with the show-and-tell stool sample. The intern is happy to let me present this case. Based on my reading, I'm confident enough to forgo the usual broad med student differential diagnosis for abdominal pain, jaundice, N/V etc and I boldly declare that there is only one lesion that can account for this patient's presentation. The lesion must be located at "X," and in all likelihood the etiology is "Y."

What is "X" and what is "Y?"😀

Nick

Could it be cholangiocarcinoma due to opisthorchis sinensis?

 

[neurodoc]

ok, just a second year med student here and had to google for the answer..
is X the ampulla of Vater and Y cancer?

Correct: carcinoma of the ampulla of Vater. The silver stool results from blood in combination with bile obstruction. This is a localizing sign (as in the "neurologic method"). It shows that the neurologic method of clinical diagnosis is in fact useful in "general" medical diagnosis.

Move to the head of the class, riverie!

Nick

 

[neurodoc]

Here's one: A 68 yo otherwise healthy diabetic patient presents with acute shortness of breath. O2 sat on evaluation in the ER is 83%. SOB is exacerbated by exertion, but patient is in no apparent distress while on oxygen and sitting quietly in the ER. Previous 20 pack year h/o smoking, quit 15 years ago. Patient is fit and exercises 6 times a week. No recent history of surgery, trauma, bed rest or travel. No history of chronic progressive shortness of breath. On exam, patient is tachycardic and tachypneic. Some fine end-expiratory crackles are heard in the right-mid and lower-left lung fields. Breath sounds vesicular and slightly decreased throughout. CXR appears normal. What is on the top of your differential?

First of all an 83% O2 Sat is VERY low. O2 Sat is easily measured with modern equipment, but I'm amazed at often people fail to appreciate that O2 Sat levels less than 92% on room air represent a serious problem with blood oxygenation.

There are only two mechanisms that can result in such low O2 Sat: 1) decreased O2 ventilation to the alveoli; and 2) decreased blood perfusion to the alveoli. Pneumonia and bronchospasm could cause #1, and PE could cause #2. Bronchospasm should be evident on ausculation as wheezes. Pneumonia should be evident on CXR. PE should be on the top of your DDx. Time to get a V:Q scan and maybe pulmonary angiography. Look for a right axis deviation on EKG and check for D-dimers.

Nick

 

[riverie]

First of all an 83% O2 Sat is VERY low. O2 Sat is easily measured with modern equipment, but I'm amazed at often people fail to appreciate that O2 Sat levels less than 92% on room air represent a serious problem with blood oxygenation.

There are only two mechanisms that can result in such low O2 Sat: 1) decreased O2 ventilation to the alveoli; and 2) decreased blood perfusion to the alveoli. Pneumonia and bronchospasm could cause #1, and PE could cause #2. Bronchospasm should be evident on ausculation as wheezes. Pneumonia should be evident on CXR. PE should be on the top of your DDx. Time to get a V:Q scan and maybe pulmonary angiography. Look for a right axis deviation on EKG and check for D-dimers.

Nick

Correct! You're already at the head of the class, Nick. 🙂