The semantics of this question made me vomit blood.
One day a patient will look me in the eyes and ask, "Where are tripetides broken down?" I will smile at them and say, "the intestinal mucosa and not the duodenum." They'll smile back and I'll walk away and think of this moment as I jump from the window.
After the cuff is tied, the cells and tissue distal to the cuff will continue consuming ATP (
ATP->ADP), but no fresh blood will be delivered to “clear” what will be an accumulating amount of ADP and other metabolites. ADP (=Adenosine) is itself a proxy of consumption and drives vasodilation of arteries! (Evolution is smart!) Increasing ADP/Adenosine in a “local environment” is a signal to the body that a lot of consumption is occurring there; thus, arteries and arterioles naturally dilate to increase blood flow rates and “sweep away” metabolic byproducts.
The poodle is hypoallergenic, and a 10/10 good boy.
at BMI 15 not only has she never had a period but she never had a meal.
Thank you NBME for the high quality pictures. It makes these exams stress free and enjoyable.
The duodenal lumen (and pancreatic proteases like CHYMOTRYPSIN) is the site where pancreatic enzymes (“endopeptidases”) cleave large polypeptides into smaller bits (=dipeptides,tripeptides). It is at the BRUSH BORDER where the smallest kinds of peptides (dipeptides,tripeptides) are broken down into their amino acids, which finally can be co-transported with Na+ into the intestinal cell.
I think about it this way:
Stent thrombosis vs re-stenosis. Stent thrombosis is an acute occlusion of a coronary artery stent, which often results in acute coronary syndrome. Can be prevented by dual antiplatelet therapy or drug-eluting stents. Re-stenosis is the gradual narrowing of the stent lumen due to neointimal proliferation, resulting in anginal symptoms.
Platelet adherence and platelet aggregation are different things and this diferrence MATTERS A LOT. Fuck you, NBME. These differences supposedly matter on some questions and not on others. Where is the consistency? Hello?
Urea Cycle Disorders > Isolated severe hyperammonemia (> 1000; i.e., no other severe metabolic disturbances
Ornithine transcarbamylase deficiency > (most common urea cycle dis.) orotic acidemia/aciduria, hyperammonemia
Organic Acidemias > Hyperammonemia, anion-gap acidosis, ketosis (from hypoglycemia)
Medium-chain acyl-CoA dehydrogenase deficiency > Hyperammonemia, hypoketotic hypoglycemia (seen in β-oxidation disorders, EXCEPT adrenoleukodystrophy)
Liver dysfunction > Hyperammonemia, LFTs messed up, older pt.
Mast cells degranulate, producing histamine which attracts eosinophils. The early stage of an allergic reaction is mast cell mediated, but the late stage (including mucus production) is mediated by eosinophils.
Patient has Spina bifida occulta which is a neural tube defect (failure of fusion of the neuropores). Sclerotomes are the part of each somite in a vertebrate embryo giving rise to bone or other skeletal tissue. Since a part of this patient's spina bifida included "abscense of spinous process" then a sclerotome was involved. Knowing that neural tube defects are an issue with fusion should be enough to get to the right answer.
If the notochord failed to develop then the entire CNS would not develop as the notochord induces formation of neural plate.
If the neural tube failed to develop then the whole CNS would not have developed.
Yolk sac is irrelevant to this patient.
When neural crest cell it has different outcomes in different tissues. Failure of neural crest to migrate in heart can cause Transposition of great vessels, Tetralogy of Fallot, or Persistent truncus arteriosus. Failure of neural crests to migrate in GI can cause Hirschsprung disease (congenital megacolon). Treacher Collins Syndrome can occur when neural crest cells fail to migrate into 1st pharyngeal arch. Neural tube defects has nothing to do with failure of neural crest migration though.
Androgen Insensitivity Syndrome - Defect in androgen receptor resulting in normal-appearing female (46,XY DSD). Functioning testes causes increased testosterone at puberty, which is converted to estrogen peripherally, giving female secondary sexual characteristics (female external genitalia). Lack of androgen receptor function leads to absent or scant axillary and pubic hair. Patients have rudimentary vagina, but uterus and fallopian tubes absent.
Androgen insensitivity syndrome is the answer but you might have considered Müllerian agenesis (Mayer-Rokitansky- Küster-Hauser syndrome).
Mullerian agenesis will have normal hormone levels and may present as 1° amenorrhea (due to a lack of uterine development) in females with fully developed 2° sexual characteristics (functional ovaries). Hair development is normal as well. Patients also have normal height.
Seems like this question did not give us much to distinguish besides height and tanner stage 1 pubic/axillary hair.
The most direct path, and most likely path, for breast cancer to metastasize to the vertebra are the intercostal veins. This was on an earlier NBME test as well. Breast cancer will cause mixed, lytic and blastic lesions once in bone.
On an unrealated note; I finally came up with a decent way to remember lytic vs. blastic cancers in bone!
kIdneY and thYroId cause lYtIc
prostate > blastate > blastic
Two breasts > two types of lesions > B reast causes B oth
Two lungs > two types of lesions (depending on type of lung cancer)
small-cell lung > "small blasts"
non-small cell > lytic
Everyone who got this question right is a cop. ༼⌐■ل͟■༽
Make a punnett square with a cross of B B+ and B B0; B+ represents 50% function while B0 represents 0% (null) function. So in this case, the husband would have a B B0 genotype while the wife has a B B+ genotype.
Cross of these two will result in the following genotypes; BB, BB0, BB+, B+B0 BB = 100% function, BB+ = 75% function, BB0 = 50% function, B+B0 = 25% function
So the answer will be 1 in 4 have a 25% function given the genotypes.
Apparently there is a completely separate spinal cord reflex where direct penile stimulation leads to an erection. This reflex only needs an intact arc in S2-S4, so as long as this region is not injured, an erection can still occur. However, with transection at C8, then the psychogenic erection reflex cannot occur, as this requires descending fibers from the cortex.
Would've been nice if they told you "2nd intercostal space" on left or right...smh
They explicitly state that the patient has been taking excess of his levothyroxine medication. Levothyroxine is the exogenous form of T4. Therefore, free T4 must be elevated. T4 is converted to T3 at most peripheral tissues, so T3 will also be elevated. Because the body has more thyroid hormone than needed, less TSH will be made, and the thyroid will be less active, taking up LESS iodine.
Per Pathoma: early inherited cases of Alzheimer's dementia are associated with mutations in presenilin-1/presenilin-2, as well as Down's syndrome. Down's would be due to an extra chromosome 21, which carries the gene for amyloid precursor protein (APP). Extra APP is converted to A-beta amyloid and this forms extracellular neuritic plaques, a prominent feature of Alzehimer's.
Important to not confuse Amyloid A protein (one of the answer choices) with Amyloid precursor protein. Deposition of AA amyloid is more associated with chronic inflammatory states, malignancy, and Familial Mediterranean Fever. Beta-2 microglobulin is another amyloid association: dialysis-associated (deposits in joints)
Flexor digitorum profundus is responsible for flexion of DIP. Medial aspect of the muscle (which flexes the 4th and 5th digit) is supplied by the ulnar nerve (C8, T1). The lateral aspect (which flexes the 2nd and 3rd digit) is innervated by the median nerve specifically the anterior interosseous branch (C8, T1). So the question is describing a laceration damaging the nerve supply to the DIP flexor of the 2nd digit (index finger). This is saying the medial nerve is being damaged (C8 and T1; lower trunk roots).
Lumbricals (1st/2nd, median; 3rd/4th, ulnar) are a group of muscles that flex at the MCP joint, and extend PIP and DIP joints.
Could remember as 'flexor digitorum profundus is profoundly long' since tendons insert on DIPs. Compared to flexor digitorum superficialis whose tendon wraps around profundus' superficially but inserts on PIPs.