Neoplasia is new tissue growth that is unregulated, irreversible, and monoclonal.
Clonality can be determined by glucose-6-phosphate dehydrogenase (G6PD) enzyme isoforms. G6PD is X-linked.
*For more information check out Ch. 3 Neoplasia in Pathoma
Fever -> rule out left ventricular failure TMP-SMX prophylaxis -> rule out Pneumocystis jiroveci Kidney transplant but no WBC/RBC in urine -> rule out transplant rejection
Leaving CMV and atypical mycobacterium as the remaining two options. CMV is more likely in a transplant patient.
LV stopped working, pressure backed up into pulm circuit. Pulm circuit roughly is made of 3 "parts" - the capillaries, interstitial space, and the alveoli.
In cardiogenic shock, the extra blood increases capillary hydrostatic pressure, driving fluid into the interstitial space. Compared to the alveoli, the interstitial space now has more fluid (thus more interstitial hydrostatic pressure and less oncotic pressure due to ratio of fluid to protein), and as a result of this unbalancing of forces, fluid moves into the alveoli --> pulmonary edema.
A big thing here too is noticing that the ALP is decreased. Osteoblast activity is measured by bone ALP. I think that was the main focus here and not that you necessarily need to know the CBFA1 gene mutation.
Page 2 has a great picture
While the lifetime risk in the general population is just below 1%, it is 6.5% in first-degree relatives of patients and it rises to more than 40% in monozygotic twins of affected people. Analyzing classic studies of the genetics of schizophrenia done as early as in 1930s, Fischer concludes that a concordance rate for psychosis of about 50% in monozygotic twins seems to be a realistic estimate, which is significantly higher than that in dizygotic twins of about 10–19% (ncbi.nlm.nih.gov/pmc/articles/PMC4623659/#ref3)
Itraconazole requires the acidic environment of the stomach to be absorbed. Omeprazole inhibits the H+/K+ pump of the stomach, thereby decreasing the acidity of the stomach. So when the patient takes Omeprazole and Itraconazole together, Itraconazole won't be absorbed into the body. That's why it has no effect.
It's recommended to take medications at least 2 hours prior to taking an antacid.
You can cross out the top three answer choices, A,B,C. You wont be reabsorbing anything in the PCT in fanconi's syndrome. Looking at hypokalemia, hyponatremia, and hypophosphatemia now. Hypokalemia can't be correct because even though potassium is lost it will be reabsorbed at the later thick ascending loop and if that doesnt make sense, the body will adjust for low serum potassium but activating the H+/K+ pump on cells. It isn't hyponatremia because at the collecting duct principal cells, reabsorption will occur. This leaves hypophosphatemia as the correct and only answer choice.
Nowhere have I been able to find why the hell this is a thing.
Missense mutations involve a nucleotide substitution resulting in changed amino acids. Sometimes the effects of missense mutations may be only apparent under certain environmental conditions; such missense mutations are called conditional mutations. Many missense mutations result in proteins that are still functional, at least to some degree.
Also, all the other answers would probably leave you with either a greatly altered or non-functional protein.
Bifid carotid pulses are seen in Aortic stenosis or regurgitation
Carotid Bruit is heard with atherosclerosis of common carotid artery
Slow rising decreased volume carotid pulse is characteristic of aortic stenosis.
Cannon waves are seen in complete AV block, as right ventricle and atria contract independently.
Patient's symptoms began 30 min after mowing lawn (i.e. after doing physical activity). He has severe chest pain and is cool, clammy, diaphoretic. He has increased pulmonary artery pressure and increased left atrial pressure. Taken altogether, this is cardiogenic shock.
Cardiogenic shock is a heart pump problem -- the LV isn't working.
When the LV, isn't working, it causes a back up in the direction opposite to how blood normally flows. Therefore, blood will back up in the lungs.
This causes increased capillary hydrostatic pressure --> this drives more fluid into the interstitium --> this causes increased interstitial hydrostatic pressure --> there is now more fluid than normal in the interstitium --> this affects the protein ratio within the interstitum --> this causes decreased interstitial oncotic pressure.
Goljan had a lecture that mentioned that "If a patient has galactorrhea, review every drug they're taking since many drugs cause galactorrhea."
The only thing of possible relevance in this Q-stem is that she takes a medication, therefore the answer of "drug effect" is the most likely reason for her galactorrhea.