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.

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.

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

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.

Nowhere have I been able to find why the hell this is a thing.

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)

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

https://www.jacionline.org/article/S0091-6749(18)31602-6/pdf

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.

Bronchophony= pneumonia Expiratory stridor= tracheobronchial obstruction (mass/foreign body) Inspiratory stridor = laryngeal obstruction Succussion splash= test for pyloric stenosis

When there is a fractured rib it will cause a trauma pnemothorax which can cause air to escape and become trapped under the skin leading to crepitus.

Use the Hardy-Weinberg equation

1. Take the square root of 1/1600, and that will give you the frequency of the recessive allele = 1/40.
2. Calculate the frequency of the dominant allele with p+q=1, which is p= 0.975.
3. They are telling you to calculate the frequency of the disease carriers, which is with the equation 2pq.
4. They want only the disease carriers in which deletion is present. To calculate this, use the q value (1/40) and multiply by 80% in this should give you 0.02.
5. Finally, calculate for 2Pq 2 (0.975)(0.02)= 0.04 = 1/25.

This is a conditional called craniocleidodysplasia. The kid on Stranger Things with the lisp has the disorder. No collar bones, too many teeth, frontal bossing => craniocleidodysplasia. CBFA1 is a gene highly implicated in osteoblast function.

As a rule of thumb, if you give someone an ACE inhibitor and they get a problem, they had renal artery stenosis (usually bilaterally, or so we were taught at our med school). Probably has to do with decreased GFR thanks to decreased Angiotensin II–selective vasoconstriction of the efferent arteriole => decreased sodium delivery to macula densa => increased renin release.