Mistakes in First Aid

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samyjay

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Has anyone noticed some of the mistakes in first aid. Ill just start by listing one. On the pathology pictures, one of them is "Sacroidosis" The mentioned that is was a "caseating" granuloma, when in fact all the text, and everything we have learned mentions it is NON-caseating. please list more if guys have found any, it be nice to fix them now
 
samyjay said:
Has anyone noticed some of the mistakes in first aid. Ill just start by listing one. On the pathology pictures, one of them is "Sacroidosis" The mentioned that is was a "caseating" granuloma, when in fact all the text, and everything we have learned mentions it is NON-caseating. please list more if guys have found any, it be nice to fix them now

which edition?
 
samyjay said:
it is the 2005 edition

Something I noticed, perhaps not a mistake, was in the physiology section. When they have the diagram of the glomerulus with afferent and efferent arteriole, they show that prostaglandins act on the afferent arteriole and angiotensin II acts on the efferent. However, their actions are concentration dependent. In low concentrations, angiotensin II only constricts the efferent arteriole, but in high concentrations it constricts both. Check in Costanzo to double check with prostaglandins, she also goes into more depth with the NSAIDs.
 
2005 edition: pathology.

IBD Correction:
Crypt abscesses are found in both Crohn's and UC. Both diseases are thought to be immune-mediated diseases triggered by infectious organisms. 'Cobblestone' necrosis is not specific for Crohn's, for example this pattern may be found in ischemic changes. Less than 50% of Crohns actually have granulomas, although this is specific if you find it.

Bottomline: UC is continous, mucosal, and restricted to the colon. Crohn's is discontinous, has transmural inflammation, and may be in the colon, small intestine (or rarely even the stomach).

Note of interest: Smoking is a risk factor for Crohn's, yet it is protective for UC.
 
ForceField said:
Something I noticed, perhaps not a mistake, was in the physiology section. When they have the diagram of the glomerulus with afferent and efferent arteriole, they show that prostaglandins act on the afferent arteriole and angiotensin II acts on the efferent. However, their actions are concentration dependent. In low concentrations, angiotensin II only constricts the efferent arteriole, but in high concentrations it constricts both. Check in Costanzo to double check with prostaglandins, she also goes into more depth with the NSAIDs.

ok I was listening to goljan audio today. He said that PGE act on the afferent arteriole, and Angiotensin II constricts the efferent arteriole. SO FA is right here. In diabetics, 1) the efferent arteriole is hyalinized so this puts alot of pressure on the GFR. 2) Gycosylation of the amino acids mess up the negative charge of proteins so Heparan Sulfate on the basement membrane cant repel the protein so these 2 things lead to protein in the urine for diabetics. It's called microalbumuria.

EDIT:give diabetics ACE inhibitor to ease the pressure on the glomerulus. But this will do nothing for the glycosylation, so diabetics really need to watch their sugar to avoid chronic renal disease.
 
omarsaleh66 said:
ok I was listening to goljan audio today. He said that PGE act on the afferent arteriole, and Angiotensin II constricts the efferent arteriole. SO FA is right here. In diabetics, 1) the efferent arteriole is hyalinized so this puts alot of pressure on the GFR. 2) Gycosylation of the amino acids mess up the negative charge of proteins so Heparan Sulfate on the basement membrane cant repel the protein so these 2 things lead to protein in the urine for diabetics. It's called microalbumuria.

EDIT:give diabetics ACE inhibitor to ease the pressure on the glomerulus. But this will do nothing for the glycosylation, so diabetics really need to watch their sugar to avoid chronic renal disease.

Who gave you this audio?
 
carrigallen said:
2005 edition: pathology.

IBD Correction:
Crypt abscesses are found in both Crohn's and UC. Both diseases are thought to be immune-mediated diseases triggered by infectious organisms. 'Cobblestone' necrosis is not specific for Crohn's, for example this pattern may be found in ischemic changes. Less than 50% of Crohns actually have granulomas, although this is specific if you find it.

Bottomline: UC is continous, mucosal, and restricted to the colon. Crohn's is discontinous, has transmural inflammation, and may be in the colon, small intestine (or rarely even the stomach).

Note of interest: Smoking is a risk factor for Crohn's, yet it is protective for UC.

For the purposes of Step 1, aren't we looking for "trends" in the way these diseases present? To me, it looks like there are no blatant errors in the material that FA presents except for that Crohn disease is infectious (it is of unknown etiology but may have been triggered as you said). Also, to further clarify your point, Crohn disease can affect all parts of the GI tract (even the mouth!). However, the generalities that I hope we are going to be tested on seem to be fairly good in what is listed in First Aid. I wouldn't call the descriptions that they give absolutely pathomnemonic, but they seem sufficient for our purposes.

For instance, if they give a history involving only the rectum, a crypt abscess, and developing a couple of years later to adenocarcinoma of the colon, it would seem quite ridiculous to choose Crohn's disease and then argue that those are broad generalities to the diseases.
 
Pox in a box said:
For the purposes of Step 1, aren't we looking for "trends" in the way these diseases present? To me, it looks like there are no blatant errors in the material that FA presents except for that Crohn disease is infectious (it is of unknown etiology but may have been triggered as you said). Also, to further clarify your point, Crohn disease can affect all parts of the GI tract (even the mouth!). However, the generalities that I hope we are going to be tested on seem to be fairly good in what is listed in First Aid. I wouldn't call the descriptions that they give absolutely pathomnemonic, but they seem sufficient for our purposes.

For instance, if they give a history involving only the rectum, a crypt abscess, and developing a couple of years later to adenocarcinoma of the colon, it would seem quite ridiculous to choose Crohn's disease and then argue that those are broad generalities to the diseases.

Looks like someone is waving the white flag.
:laugh: :laugh: :laugh: :laugh: :laugh:
 
Edward_J_Goljan said:
Was this audio recorded from the kaplan lectures without permission?

The audio is all over the Internet, just do a quick search.

Dr. Goljan's lectures are available on Ebay.
 
This may or may not be right, but I just noticed this while studying (2004 edition), please correct me if I am wrong.

In the gallstones section it says risk factors for cholesterol stones include Crohn's and cystic fibrosis, but in Robbins it says those two are risk factors for pigment stones.
 
PluckyDuk8 said:
This may or may not be right, but I just noticed this while studying (2004 edition), please correct me if I am wrong.

In the gallstones section it says risk factors for cholesterol stones include Crohn's and cystic fibrosis, but in Robbins it says those two are risk factors for pigment stones.

You're right. Robbins (7th ed.) says for pigmented stones:

"Certain risk factors are well established for the development of pigment stones. Disorders that are associated with elevated levels of unconjugated bilirubin in bile include hemolytic syndromes, severe ileal dysfunction (or bypass), and bacterial contamination of the biliary tree.

Pigment Stones
Demography: Asian more than Western, rural more than urban
Chronic hemolytic syndromes
Biliary infection
Gastrointestinal disorders: ileal disease (e.g., Crohn disease), ileal resection or bypass, cystic fibrosis with pancreatic insufficiency"

For cholesterol stones:

"Cholesterol Stones
Demography: Northern Europe, North and South America, Native Americans, Mexican Americans
Advancing age
Female sex hormones
Female gender
Oral contraceptives
Pregnancy
Obesity
Rapid weight reduction
Gallbladder stasis
Inborn disorders of bile acid metabolism
Hyperlipidemia syndromes"​

Good call.
 
If you are going to pretend to be Dr. Goljan at least get the middle initial correct.

Edward_J_Goljan said:
Was this audio recorded from the kaplan lectures without permission?
 
2005: page 263-Evolution of an MI
"No visible change by light microscopy in 2-4 hrs"

Then the caption in image 80 says
"contraction band necrosis is the first visible change, occuring in one to two hours"

Hrm
 
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