A good way to think about this is that angiotensin II is present at the ANGII receptors. If you give an angiotensin receptor blocker such as losartan. this will displace the angiotensin II present in the receptors. thus increasing the levels of angiotensin II in serum.

incidence = number of new cases/ new cases+ population at risk. new cases= 250. People at risk that year 5050 (including new cases. In one point they were a population at risk) 250/ 5050= 4.9%

I think the key to understanding this question is that the boy has above average height. Leptin stimulates the release of GH (https://www.ncbi.nlm.nih.gov/pubmed/12122085) Children with Cushing syndrome have short stature https://www.ncbi.nlm.nih.gov/pubmed/16675933) insulin inhibits GH secretion https://www.ncbi.nlm.nih.gov/pmc/articles/PMC425166/) I think that both a high caloric diet in fats and glucose can make you fat so you can eliminate those answer choices.

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.

When conjugated bilirubin (CB) is less dan, 30% of total bilirubin----> increased the production of unconjugated bilirubin or decreased uptake. Hemolysis is the possible answer choice.

CB is 30%-50% mix-hyperbilirubinemia (Ex. Hepatitis or Alcholol) CB is more than 50% --> Obstruction (intra or extrahepatic)

PDA flows from aorta to pulmonary artery decreasing afterload. Therefore cardiac output increases

High glucose leads to more insulin production in the fetus (recall that the hormone insulin is anabolic) ---> large fetus (9lb,1oz)---> problems in labor.

chronic kidney disease --> decreased EPO --> decreased hematocrit chronic kidney disease --> decreased PO4- excretion --> increased PTH chronic kidney disease --> decreased 1,25 dihydrovitD (calcitriol) --> increased PTH

This has been a tough concept for me to get, but I think I'm finally there:

The stem is describing primary adrenal insufficiency, or Addison's.

• ACTH is being over-produced to stimulate the adrenals to produce cortisol, but they can't respond, either due to atrophy or destruction (TB, autoimmune: DR4, etc.)
• The first 13 amino acids of ACTH can be cleaved to form α-MSH, which stimulates melanocytes, causing hyperpigmentation

I think it has something to do with glycine (due to its small size it can fit in many places where other amino acids can not and hence it provides “structural compactness” to the collagen, i.e. put a kink in the alpha helix). If glycine is misplaced by something else, I don’t think pro-collagen can form its correct secondary structure.

I think it has something to do with glycine (due to its small size it can fit in many places where other amino acids can not and hence it provides “structural compactness” to the collagen, i.e. put a kink in the alpha helix). If glycine is misplaced by something else, I don’t think pro-collagen can form its correct secondary structure.