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Why would the urine Potassium be so high if it is type 1 ? Shouldnt it be type 2?
@krewfoo99 I think it's RTA2 (Fanconi syndrome), he is losing all kinds of Na, K, Cl which should be reabsorbed in PCT.
I would say because this happened between two bacteria, but in transduction what causes the acquisition of bacterial resistance is coming from a bacteriophage, which is a virus that infects bacteria, but that is never hinted at the question!
Quick Overview of the involved topics and answer choices that are relevant in this question:
Transduction: Involves phage, cleaves DNA and takes a part with it as it is packaged. Generalized is when is happens by accident. Specialized is an excision event.
Transformation: bacteria takes up naked DNA around it and incorporates it therefore becoming "transformed" e.g. (SHiN) S. Pneuma, H. Influenza type B, and Neisseria.
Transposition: Jumping from one location to another within same bacterial organism (e.g. from chromosome to plasmid)
Conjugation: Above mentioned plasmid gets transferred from conjugal bridge from one bacteria to another.
Easy here...first both are G-ves which likely have a sex pilus and if cultured together as in this case transfer their plasmid. Transduction need phage. Transposition is exchange of genetic material inside the bacteria b/n the dna and the plasmid or vv (FA2019)
I'm confused about the phosphate level in questions like these. Decreased calcitriol would decrease phosphate absorption while PTH decrease lowers phosphate excretion. I'm assuming that the PTH decrease has the greater effect with serum phosphate levels?
PTH = "Phosphate trashing hormone" if PTH is high Phosphate must be low - they are always opposite (unless d/t renal failure then Phosphate will be high - kidneys will be unable to get rid of phosphate)
So low Ca d/t low PTH does not effect 25 H. Vit D ... only 1,25 H Vit D (active Calcitriol)?
Clarification because I was confused: PTH stimulates kidney to produce 1,25-(OH)2 D3 (calcitriol) via 1α-hydroxylase in proximal convoluted tubule. Therefore, without parathyroid glands, low PTH, 25,D is not converted and therefore not down (normal or up). phosphate "trashed" by PTH as eloquently stated above.
Here the primary defect is high up from the parathyroid gland, there is decresed or no PTH which normally trashes phosphate but not in this case so serum PHOSPHATE INCREASES and the serum calcium is low because PTH should have prevented the urine calcium so there is calciuria and no resorption from bone-LOW CALCIUM, Vitamin-D is independent of PTH so stays NORMAL
So this patient has a leaking berry aneurysm which undergone to surgery and repaired but in two days she developed widening of the SA space which could be explained by increased CSF production but a decreased in absorption, which is due to blockage of the arachinoid granulations by the leaked red and white cells therefore there is a decreased movement of the CSF via the arachinoid villi