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shubz123

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hey guys, bit off topic q- but if in a q stem they say dysphagia with solids only does that mean esophageal Cancer? That is what goljans book and online sources say but my FA 2012 says Esophageal CA is dysphagia with solids AND liquids. For solids and liquids goljan says that is a peristalsis issues like achlasia MG etc.
Does anyone know how Cancer will present in terms of dysphagia? Thanks you
 
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sadaca said:
hey guys, bit off topic q- but if in a q stem they say dysphagia with solids only does that mean esophageal Cancer? That is what goljans book and online sources say but my FA 2012 says Esophageal CA is dysphagia with solids AND liquids. For solids and liquids goljan says that is a peristalsis issues like achlasia MG etc.
Does anyone know how Cancer will present in terms of dysphagia? Thanks you
Click to expand...
havent looked at the material in 1.5weeks but if I recall; eso cancer= slow onset of dysphagia. i.e. they will complain about solids first then to both liquids and solids but the key is that its a slow onset
 
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39. pregnant 16 year old came because of a tonic clonic seizure. unable to urina. her bp, respirations, and pulse are elevated. elevated uric acid, ldh, creatinine, ast, alt. what is the diagnosis?

drug od
eclampsia
epilepsy
renal disease
sepsis

i'm slightly leaning towards either epilepsy or drug od
 
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shok said:
39. pregnant 16 year old came because of a tonic clonic seizure. unable to urina. her bp, respirations, and pulse are elevated. elevated uric acid, ldh, creatinine, ast, alt. what is the diagnosis?

drug od
eclampsia
epilepsy
renal disease
sepsis

i'm slightly leaning towards either epilepsy or drug od
Click to expand...

eclampsia; she has all the s/sx of preeclampsia + seizures.
 
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What was the answer to the testicular biopsy photo of the infertile male? What was that a picture of - I know this is probably a super obvious question, but what am I not seeing?
 
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shok said:
is myasthenia gravis caused by binding of ach by an antibody or by binding of antibody to the ach receptor?
Click to expand...

Antibody to post-synaptic ACh receptor. I can't recall the if there's any condition with anti-ACh. Don't confuse myasthenia with lambert-eaton. There's a table in the MSK section in FA (p 429) with the differences.
 
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jayareus said:
What was the answer to the testicular biopsy photo of the infertile male? What was that a picture of - I know this is probably a super obvious question, but what am I not seeing?
Click to expand...

That was a picture of the "glomeruloid" appearance of an endodermal sinus Yolk sac tumor. I am not sure if it has an increased risk with Kleinfelters or not, but it is the most common type of testicular tumor in boys <3.
 
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Anyone know the answer to the question about a 64 yr old alcoholic man with 1 day of confusion. Disoriented, disheveled. Dehydrated, jaundiced. and has spider angiomata over face and chest. Has flapping up and down of the hands when his arms are outstretched. Abdominal distention and bulging flanks. He is administered oral neomycin. Question asks which of the following primary mechanisms of action is most likely to occur in this patient as a result of the drug treatment?

a. Binding of ammonia and other hepatically cleared toxins in the gut
b. blockade of protein synthesis in liver
c. blockade of folic acid synthesis
d. increased endotoxin production when bacterial overgrowth appears
e. killing of bacteria in the gut that generate ammonia

Please give explanation as well. Thanks!
 
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medstudent987 said:
Anyone know the answer to the question about a 64 yr old alcoholic man with 1 day of confusion. Disoriented, disheveled. Dehydrated, jaundiced. and has spider angiomata over face and chest. Has flapping up and down of the hands when his arms are outstretched. Abdominal distention and bulging flanks. He is administered oral neomycin. Question asks which of the following primary mechanisms of action is most likely to occur in this patient as a result of the drug treatment?

a. Binding of ammonia and other hepatically cleared toxins in the gut
b. blockade of protein synthesis in liver
c. blockade of folic acid synthesis
d. increased endotoxin production when bacterial overgrowth appears
e. killing of bacteria in the gut that generate ammonia

Please give explanation as well. Thanks!
Click to expand...

E. Neomycin is a nuclear bomb to bacteria.
 
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26. for short term seasonal allergy treatment, would you give an alpha adrenergic agonist or a nicotinic cholinergic antagonist?
 
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i don't think nicotinic cholinergic antagonists are used anymore except for the curoniums, which cause muscle paralysis.
 
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shok said:
26. for short term seasonal allergy treatment, would you give an alpha adrenergic agonist or a nicotinic cholinergic antagonist?
Click to expand...

I would say alpha agonist. Think about the popular allergy OTCs that have the "D" at the end of the trade name: pseudoephedrine 120 mg or 240 mg (12hr or 24hr).
 
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30. 38 y/o woman seems to have a gastrinoma (serum gastrin concentration is 2000 (normal <100). She also has multiple lipomas and two large non bleeding ulcers. she is started on a proton pump inhibitor. what measurement should you follow?

serum ca
serum cortisol
serum tissue transglutaminase
stool alpha 1 antitrypsin
urine 5hiaa

i probably wouldn't choose 5 hiaa or cortisol. leaning towards calcium
 
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32. which one of these doesn't have microtubules?
corticol thymocytes
enterocytes in duodenal crypts
erythroblasts in the bone marrow
keratinocytes in stratum basale
ventricular cardiac muscle fibers
 
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shok said:
30. 38 y/o woman seems to have a gastrinoma (serum gastrin concentration is 2000 (normal <100). She also has multiple lipomas and two large non bleeding ulcers. she is started on a proton pump inhibitor. what measurement should you follow?

serum ca
serum cortisol
serum tissue transglutaminase
stool alpha 1 antitrypsin
urine 5hiaa

i probably wouldn't choose 5 hiaa or cortisol. leaning towards calcium
Click to expand...

I wouldn't choose 5-HIAA either because it doesn't sound like carcinoid. Serum Ca makes sense due to hip fracture risk with long-term use, but she's 38, so...?
 
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38. centrilobular pallor and swelling of the heaptocytes

is this because of ribosomal disaggregation or activation of caspases?
 
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does anyone have any insight into the question which the girl with anal itching, pain with pooping, bright red blood who uses the mineral oil enema. the picture shows something brown sticking out of her butthole.
a) candida
b) lymphatic obstruction (wrong)
c) tinea cruris
d) vzv
e) venous HTN

My first thought was hemorrhoids, so I was going to go with e. But, I was under the impression what internal hemorrhoids are painless which would rule out venous HTN. I put lymphatic obstruction because I thought it would cause a fecal impaction, but I was obviously wrong. Does anyone know the right answer?

thanks
 
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Omar Little said:
does anyone have any insight into the question which the girl with anal itching, pain with pooping, bright red blood who uses the mineral oil enema. the picture shows something brown sticking out of her butthole.
a) candida
b) lymphatic obstruction (wrong)
c) tinea cruris
d) vzv
e) venous HTN

My first thought was hemorrhoids, so I was going to go with e. But, I was under the impression what internal hemorrhoids are painless which would rule out venous HTN. I put lymphatic obstruction because I thought it would cause a fecal impaction, but I was obviously wrong. Does anyone know the right answer?

thanks
Click to expand...
Venous HTN could also cause external hemorrhoids, which are painful.
 
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thanks -- one more:

5 year old boy brought to the ER. with vomiting and sleepiness, he had a flu like illness 5 days ago that she treated with aspirin. Serum studies show increased ammonia, lactate, and transaminase levels. what's the most likely cause of the patient's coma?
a) cerebral edema
b) metabolic alkalosis (wrong)
c) subarachnoid hemorrhage
d) venous sinus thrombosis
e) viral encephalitis

kid probably has Reye's syndrome, so I started with A. but I remembered a UWorld explanation saying Reye's does not cause hepatic encephalopathy (fyi - 536216). I switched it to b, because I thought the vomiting would cause the metabolic alkalosis. does anyone know the right answer?
 
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and another. I've tried searching around for these -- I guess I'm missing ones no one has questions about.
"60 year old man with no history of bleeding problems. Has PT of 11.5 PTT of 160. Which of the following inflammatory reactions is abnormal in this patient.
a) C5a generation
b) histamine release
c) Kallikrein formation
d) phagocytosis
e) platelet aggregation (wrong)

I thought it was von Willebrand's disease which causes an isolated increase in PTT and is often mild. Is it C -- no Hageman factor soyou aren't making kallkrein? thanks againl
 
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Omar Little said:
thanks -- one more:

5 year old boy brought to the ER. with vomiting and sleepiness, he had a flu like illness 5 days ago that she treated with aspirin. Serum studies show increased ammonia, lactate, and transaminase levels. what's the most likely cause of the patient's coma?
a) cerebral edema
b) metabolic alkalosis (wrong)
c) subarachnoid hemorrhage
d) venous sinus thrombosis
e) viral encephalitis

kid probably has Reye's syndrome, so I started with A. but I remembered a UWorld explanation saying Reye's does not cause hepatic encephalopathy (fyi - 536216). I switched it to b, because I thought the vomiting would cause the metabolic alkalosis. does anyone know the right answer?
Click to expand...

I would probably go with viral encephalitis tbh. In FA2012, it says that Reye's is associated with viral infection (VZV and influenza B).
 
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yeah, but I thought that was just because you have parents giving kids Tylenol for chickenpox and the flu. I was under the impression that Reye's pathogenesis is more due to mitochondrial changes.
 
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which one of these doesn't have microtubules?
corticol thymocytes
enterocytes in duodenal crypts
erythroblasts in the bone marrow
keratinocytes in stratum basale
ventricular cardiac muscle fibers

a newborn female is diagnosed with hypothyroidism 2 days after birth. ultrasonography of the neck shows no gland tissue. p/e and reflexes are normal. maternal to fetal transfer of which of the following explains the normal development in the newborn?
iodine
thyroglobulin
tsh
thyrotropin releasing hormone
t4

chloroquine spares which two plasmodium species?
really confused by this question

centrilobular pallor and swelling of the heaptocytes
is this because of ribosomal disaggregation or activation of caspases?

68 y/o woman has 1 year history of severe ab pain after meals. also has an unintentional 20lb weight los. pain is relieved when she decreases the amount of food she eats. p/e shows soft, nontender abdomen and abdominal bruit. pedal pulses diminished. which artery is stenosed?
greater pancreatic
hepatic
right gastric
superior mesenteric
supraduodenal
 
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shok said:
which one of these doesn't have microtubules?
corticol thymocytes
enterocytes in duodenal crypts
erythroblasts in the bone marrow
keratinocytes in stratum basale
ventricular cardiac muscle fibers
The question is trying to get at which cell isn't dividing which means it would be resistant to chemotherapy. Ventricular caridac muscle fibers. Pathoma Ch 1

a newborn female is diagnosed with hypothyroidism 2 days after birth. ultrasonography of the neck shows no gland tissue. p/e and reflexes are normal. maternal to fetal transfer of which of the following explains the normal development in the newborn?
iodine
thyroglobulin
tsh
thyrotropin releasing hormone
t4
I put T4 and was correct. The baby is normal, but doesn't have a thyroid, the only way it could be would be if mom gave the baby the final effector -- T4. All other require a functional thyroid gland

chloroquine spares which two plasmodium species?
vivax/ovale. This is in FA i think
really confused by this question

centrilobular pallor and swelling of the heaptocytes
is this because of ribosomal disaggregation or activation of caspases?

68 y/o woman has 1 year history of severe ab pain after meals. also has an unintentional 20lb weight los. pain is relieved when she decreases the amount of food she eats. p/e shows soft, nontender abdomen and abdominal bruit. pedal pulses diminished. which artery is stenosed?
greater pancreatic
hepatic
right gastric
superior mesenteric
supraduodenal
SMA - I think. I think you're not quoting a really important part of the question, but I think I put SMA this morning and got it right
Click to expand...
 
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newborn develops resp distress. p/e shows cyanosis, decreased breath sounds. chest xray while pt is supine shows multiple cystic appearing areas on the left and decreased aeration on the right. what is the diagnosis?
bact pneumonia
bullae related pneuothorax
congenital cystic adenomatoid malformation
congenital diaphragmatic hernia
laryngeal atresia
lobar sequestration
tracheal stenosis
 
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which would increase the flow of pulmonary lymph

endothelin 1 into pulm artery
phenylephrine in pulm artery
decreasing inspired oxygen concentration from 21% to 10%
increasing inspired co2 concentration from .3% to 3%
iv infusion of .9% saline for 5 min
iv infusion of 20% albumin solution for 5 min
 
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Omar Little said:
and another. I've tried searching around for these -- I guess I'm missing ones no one has questions about.
"60 year old man with no history of bleeding problems. Has PT of 11.5 PTT of 160. Which of the following inflammatory reactions is abnormal in this patient.
a) C5a generation
b) histamine release
c) Kallikrein formation
d) phagocytosis
e) platelet aggregation (wrong)

I thought it was von Willebrand's disease which causes an isolated increase in PTT and is often mild. Is it C -- no Hageman factor soyou aren't making kallkrein? thanks againl
Click to expand...

its probably C. XIIa converts prekalli->kallikrein. the classic vignettes for von willibrands disease usually involve signs of platelet dysfxn (epistaxis, easy bruising) which the pt doesnt have.
 
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another question. last one (I think)
a 1 year old boy is brought in. has white, pale hair that hasn't changed color since birth. His eyes are blue. During opthalmic examination, the patient turns away from the flashlight and starts crying. Which of the following is the most likely cause of the pale skin color?
a) aberrant migration of neural crest (wrong)
b) decreased number of epidermal melanocytes
c) immune destruction of melanocytes
d) inability to make melanin
e) melanin dropout to the dermis

-Thought this question was asking about albinism. The patient had blue eyes, so I thought he still had tyrinase function, and that the skin/hair hypopigmentation was a failure of neural crest to descend which can cause albinism. Is it D?
 
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Omar Little said:
another question. last one (I think)
a 1 year old boy is brought in. has white, pale hair that hasn't changed color since birth. His eyes are blue. During opthalmic examination, the patient turns away from the flashlight and starts crying. Which of the following is the most likely cause of the pale skin color?
a) aberrant migration of neural crest (wrong)
b) decreased number of epidermal melanocytes
c) immune destruction of melanocytes
d) inability to make melanin
e) melanin dropout to the dermis

-Thought this question was asking about albinism. The patient had blue eyes, so I thought he still had tyrinase function, and that the skin/hair hypopigmentation was a failure of neural crest to descend which can cause albinism. Is it D?
Click to expand...
It is D. A would be Hirschprung's Disease.
 
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Omar Little said:
thanks -- one more:

5 year old boy brought to the ER. with vomiting and sleepiness, he had a flu like illness 5 days ago that she treated with aspirin. Serum studies show increased ammonia, lactate, and transaminase levels. what's the most likely cause of the patient's coma?
a) cerebral edema
b) metabolic alkalosis (wrong)
c) subarachnoid hemorrhage
d) venous sinus thrombosis
e) viral encephalitis

kid probably has Reye's syndrome, so I started with A. but I remembered a UWorld explanation saying Reye's does not cause hepatic encephalopathy (fyi - 536216). I switched it to b, because I thought the vomiting would cause the metabolic alkalosis. does anyone know the right answer?
Click to expand...

Omar Little said:
yeah, but I thought that was just because you have parents giving kids Tylenol for chickenpox and the flu. I was under the impression that Reye's pathogenesis is more due to mitochondrial changes.
Click to expand...

The answer is A. It would be Reye syndrome which leads to hepatic encaphalopathy. The mitochondrial damage is in the liver. Here i'm a little bit hazy but hopefully google should find something that can confirm or elucidate but: Liver damage --> hyperammonemia --> hepatic encephalopathy --> astrocyte swelling. I tried looking for that uworld id but it doesn't exist for me. But FA2014 pg 361 has it leading to hepatoencephalpathy

shok said:
newborn develops resp distress. p/e shows cyanosis, decreased breath sounds. chest xray while pt is supine shows multiple cystic appearing areas on the left and decreased aeration on the right. what is the diagnosis?
bact pneumonia
bullae related pneuothorax
congenital cystic adenomatoid malformation
congenital diaphragmatic hernia
laryngeal atresia
lobar sequestration
tracheal stenosis
Click to expand...

Congenital Diaphragmatic Hernia is the answer. The big thing for me was the occasional bowel sound over the left hemithorax but hopefully someone can give a better reason.
 
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EazyE1907 said:
2) An animal study is conducted to assess the effects of smoking on pulmonary defense and maintenance mechanisms. For 1 week, normal
male rats are exposed to levels of cigarette smoke comparable to those encountered by humans who smoke cigarettes. Results of
pulmonary testing are compared with baseline levels obtained the week before the smoke exposure. Which of the following sets of changes
is most likely to be observed? Is everything low? smoking impairs mucocilliary clearance I know that much..

Mucus Production and Secretion up/down

Alveolar Macrophage Function up/down

Activity of Airway Cilia up/down


numero 2. should definitely be

Mucus Production and Secretion up

in response to cigarette smoke, combustible fumes and etc mucus production always increases. Just think of the reid index in chronic bronchitis, the submucosal mucous glands increase in size in response to cigarette smoke because they are secreting more mucous in order to clear all those nasty inhaled carcinogens

Alveolar Macrophage Function up

the inhaled carcinogens from cigarette smoke damage the lining of the alveoli. in response to this alveolar macrophages aggregate to clear up the mess

Activity of Airway Cilia down

this one should be easy. carcinogens in cigarette smoke destroy cilia cells lining the airway.

Listen to Dr. Sattar's lecture starting with obstructive pulmonary diseases. he explains all this really well. hope this helped
Click to expand...

I completely agree and that's what I was looking for in the choices, but unfortunately that was NOT one of the answer choices, so that can't be right. Anybody else have any ideas?Maybe macrophage activity goes down somehow... I don't know :-/
 
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shok said:
30. 38 y/o woman seems to have a gastrinoma (serum gastrin concentration is 2000 (normal <100). She also has multiple lipomas and two large non bleeding ulcers. she is started on a proton pump inhibitor. what measurement should you follow?

serum ca
serum cortisol
serum tissue transglutaminase
stool alpha 1 antitrypsin
urine 5hiaa

i probably wouldn't choose 5 hiaa or cortisol. leaning towards calcium
Click to expand...


Calcium should be right -- there's a UWorld question that is similar -- You should work up every pt with a gastrinoma for MEN1, which will include serum calcium (parathyroid tumors?), PTH, and pituitary hormones.
 
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What's the answer to the genetics question >> 2 year old boy with ophthalmoplegia and hypotonia, increased lactic acid
 
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rlanders85 said:
What's the answer to the genetics question >> 2 year old boy with ophthalmoplegia and hypotonia, increased lactic acid
Click to expand...

Answer is heteroplasmy. The only choices that were possible were AD and Mitochondrial. I couldn't think of any AD that would present with that constellation of sx (and that variability among family members). I'm pretty sure mitochondrial can have variable phenotypes and one of the things that can happen is leber optic neuritis.
 
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Hi everyone, all the comments have been super helpful so far! I have a few Q of my own.

1) Young man with left flank pain radiating to groin; tenderness in left flank and LLQ abdomen; mildly hypoactive bowel sounds and negative occult blood in stool.

I know the answer was speculated briefly above, but I was wondering if anyone knows the answer for sure. I narrowed it down to ureteral calculus and renal infarction (other choices being colon cancer, diverticulitis, epididymitis, torsion of testis - which none of this sounded like).

2) Old man who came in with difficulty sleeping since his wife's death 8 months ago. Wakes up early, cries thinking about her, etc; but still enjoys life with grandkids, remains active in community, etc. No suicidal ideation. Initial action?

Regular appt's to monitor patient
Neuropsych test
Sleep study
Antidepressant

Is it the first one? This patient doesn't quite sound like he has major depressive disorder...

3) Question about a man who has bullous pemphigoid: production of autoantibodies against which structure is causing sx?

Bullous pemphigoid antigen
Collagen type 7
Cystokeratin
Desmoplakin
Plakoglobin

Is the answer really obvious as "bullous pemphigoid antigen"? I thought collagen VII, desmoplakin, and plakoglobin were also components of desmosomes.

4) Middle aged man with 2 months of diarrhea and abd pain that's relieved temporarily with eating and antacids. Serum gastrin is 500 (normal 100) and gastric acid secretion is 80 (6-40). Most definitive treatment to decrease risk of complications?

Low protein diet
Antibiotics
Antihistamine
Section the vagus n to stomach
Surgically remove suspected tumor

I thought it was gastric ulcer caused by H pylori, but antibiotics wasn't correct 🙁
 
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luckyducky87 said:
Hi everyone, all the comments have been super helpful so far! I have a few Q of my own.

1) Young man with left flank pain radiating to groin; tenderness in left flank and LLQ abdomen; mildly hypoactive bowel sounds and negative occult blood in stool.

I know the answer was speculated briefly above, but I was wondering if anyone knows the answer for sure. I narrowed it down to ureteral calculus and renal infarction (other choices being colon cancer, diverticulitis, epididymitis, torsion of testis - which none of this sounded like).

2) Old man who came in with difficulty sleeping since his wife's death 8 months ago. Wakes up early, cries thinking about her, etc; but still enjoys life with grandkids, remains active in community, etc. No suicidal ideation. Initial action?

Regular appt's to monitor patient
Neuropsych test
Sleep study
Antidepressant

Is it the first one? This patient doesn't quite sound like he has major depressive disorder...

3) Question about a man who has bullous pemphigoid: production of autoantibodies against which structure is causing sx?

Bullous pemphigoid antigen
Collagen type 7
Cystokeratin
Desmoplakin
Plakoglobin

Is the answer really obvious as "bullous pemphigoid antigen"? I thought collagen VII, desmoplakin, and plakoglobin were also components of desmosomes.

4) Middle aged man with 2 months of diarrhea and abd pain that's relieved temporarily with eating and antacids. Serum gastrin is 500 (normal 100) and gastric acid secretion is 80 (6-40). Most definitive treatment to decrease risk of complications?

Low protein diet
Antibiotics
Antihistamine
Section the vagus n to stomach
Surgically remove suspected tumor

I thought it was gastric ulcer caused by H pylori, but antibiotics wasn't correct 🙁
Click to expand...

1) I put ureteral calculus and got it right.
2) Regularly monitor patient is right. He's perfectly normal, but we want to make sure he stays that way.
3) Sure is Bullous Pemphigoid Antigen. Not sure what makes up a HEMIdesmosome, but maybe that's the distinction they're making.
4) Remove the gastrinoma.
 
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Gonna show my own ignorance here (leaving off the answer choices for right now, but will post if someone needs a refresher)

1. Surgical repair of AAA in man with horseshoe kidney--what complicates this surgery?
2. Neuroendocrine brain tumor--SCLC metastasis?
3. Problem trafficking vesicles to Golgi-->increased/decreased RER, SER, lysosomes
4. Pubertal 8-year old--what do we do?
5. 12-year old boy, lower extremity atrophy and hammer toes, high-stepping gait--What's his deal?
6. Which intervention increase flow of pulmonary lymph? (see post #134)
7. Consensus on the vocal folds while swallowing, immediately after laryngeal irritation and while coughing?
8. Central cath with 4-micrometer elliptical, purple, budding organisms and the blood agar plate next to it
 
Last edited:
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bassvp said:
Gonna show my own ignorance here (leaving off the answer choices for right now, but will post if someone needs a refresher)

Section 1, Q5: Surgical repair of AAA in man with horseshoe kidney--what complicates this surgery?
Section 1, Q13: Neuroendocrine brain tumor--SCLC metastasis?
Section 1, Q34: Problem trafficking vesicles to Golgi-->increased/decreased RER, SER, lysosomes
Section 1, Q37: Pubertal 8-year old--what do we do?
Section 3, Q21: 12-year old boy, lower extremity atrophy and hammer toes, high-stepping gait--What's his deal?
Section 3, Q36: Which intervention increase flow of pulmonary lymph? (see post #134)
Section4, Q2: Consensus on the vocal folds while swallowing, immediately after laryngeal irritation and while coughing?
Section4, Q5: Central cath with 4-micrometer elliptical, purple, budding organisms and the blood agar plate next to it
Click to expand...

1-5: the answer choice with multiple arteries
1-13: (I don't remember this question)
1-34: increased RER because products back up
1-37: normal puberty
3-21: charcot-marie-tooth disease - abnormal myelin sheath
3-36: IV infusion of saline - increases hydrostatic pressure

4-5: I put Staph aureus and that was wrong; it couldn't be E. coli because that's gram negative. Then I noticed the word "budding" in the Q stem which suggests fungus anyway. Sporothrix schenckii seems wrong since there are no skin lesions; maybe it's candida albicans? :-/ Size seems right and google suggests that biofilm formation of candida on catheter surfaces is a known problem. I got tricked because I assumed it was bacterium based on gram staining and blood agar!
 
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I forgot, one more Q:

54y F admitted with acute MI, at which point there were no murmurs or signs of heart failure; but 2 days later, she has acute SOB and sweating; HR 100, RR 24, BP 160/98. Crackles bilaterally, +murmur. Which murmur is most likely?

(then they basically gave a descriptor for each murmur type "grade x/6, diastolic decrescendo murmur heard best at Y")

I have no idea what this is... is she having heart failure 2 days after her MI...?
 
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luckyducky87 said:
I forgot, one more Q:

54y F admitted with acute MI, at which point there were no murmurs or signs of heart failure; but 2 days later, she has acute SOB and sweating; HR 100, RR 24, BP 160/98. Crackles bilaterally, +murmur. Which murmur is most likely?

(then they basically gave a descriptor for each murmur type "grade x/6, diastolic decrescendo murmur heard best at Y")

I have no idea what this is... is she having heart failure 2 days after her MI...?
Click to expand...

Sounds like it could be papillary muscle rupture post-MI leading to mitral regurgitation leading to holosystolic murmur.
 
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Kid with sickle cell anemia, prophylaxis with penicillin. This decreases infection for which of the following:

E coli
H. flu
N. meningiditis
Salmonella
S. pneumoniae

Looks like the answer is Strep pneumo. How can you eliminate N. meningitidis since penicillin can be used for that as well?
 
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