to snoo-finity ... and beyond!
to snoo-finity ... and beyond!
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.
Which of the following reasons is why this question is bull?
1) Using the word "cyclic" instead of tricyclic for clarity
2) Knowing all of epidemiology of all drugs
3) having to reason out that anticholinergic effects are probably the worst over alpha1 or H1 effects to no certainty.
4) The crippling depression of studying for days-to-weeks on end to probably do average on the test.
Perfect image which can explain everything in this question!
if one still doesn't understand to add on .. 1000 cm^3 = 1000 ml 1000ml = 1 Litre
There's an episode in scrubs the person is orange i looked up "too much carrot" they look orange NBME language strikes again
Explanations for this are too complicated. Think of it like this:
You've got a piece of mutated DNA that is able to be digested by a restriction endonuclease, that means the DNA was transcriptionally available to begin with. AKA it was not methylated, because as we know, methylation = heterochromatin which is transcriptionally inactive. that means methylase was mutated
Only other plausible answer was DNase, and if it was mutated it would be inactive, not overactive.
I overthought this one big time. Since the question said the mass was pressing on the outside of the trachea, I figured that during inspiration, b/c the chest expands, so more space, so the mass would have less effect on the trachea as the chest expands (and conversely, it'd have more of an effect during expiration as the chest wall retracts). Apparently, it was just straight up blockage and I thought waaay to hard. Oops.
When ZES is suspected, the initial test recommended is a fasting serum gastrin (FSG) determination in the absence of antisecretory therapy (Sensitivity- 98–100% in ZES patients various series. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5757869/
Hereditary angioedema (HAE) caused by C1-esterase inhibitor deficiency is an autosomal-dominant disease resulting from a mutation in the C1-inhibitor gene. HAE is characterized by recurrent attacks of intense, massive, localized subcutaneous edema involving the extremities, genitalia, face, or trunk, or submucosal edema of upper airway or bowels. Routine long-term prophylaxis with either attenuated androgens or C1-esterase inhibitor has been shown to reduce the frequency and severity of HAE attacks.
Hypoxic pulmonary vasoconstriction (HPV), also known as the Euler-Liljestrand mechanism, is a physiological phenomenon in which small pulmonary arteries constrict in the presence of alveolar hypoxia (low oxygen levels). By redirecting blood flow from poorly-ventilated lung regions to well-ventilated lung regions, HPV is thought to be the primary mechanism underlying ventilation/perfusion matching.[1][2] The process might initially seem counterintuitive, as low oxygen levels might theoretically stimulate increased blood flow to the lungs to increase gas exchange. However, the purpose of HPV is to distribute bloodflow regionally to increase the overall efficiency of gas exchange between air and blood. While the maintenance of ventilation/perfusion ratio during regional obstruction of airflow is beneficial, HPV can be detrimental during global alveolar hypoxia which occurs with exposure to high altitude, where HPV causes a significant increase in total pulmonary vascular resistance, and pulmonary arterial pressure, potentially leading to pulmonary hypertension and pulmonary edema. Several factors inhibit HPV including increased cardiac output, hypocapnia, hypothermia, acidosis/alkalosis, increased pulmonary vascular resistance, inhaled anesthetics, calcium channel blockers, positive end-expiratory pressure (PEEP), high-frequency ventilation (HFV), isoproterenol, nitric oxide, and vasodilators.
either bladder cancer (unilateral in this case) or transitional cell carcinoma (also uni) are precipitated by smoking inhalant toxic injury. BUT what matters more than the cause is that the reader recognize that this is without a doubt
obstructive hydronephrosis with dilated pelvicalyceal system and cortex of kidney showing atrophy and thinning.
Assuming that the pt lost blood from the MVA - this would further enhance the renal ischemia (PCT and ascending LOH are both very sensitive to ischemic conditions 30 minutes of blood loss is enough to exacerbate the already ischemic conditions.
Prosthetic valves are one of the causes of extravascular hemolysis so suspect this in a patient that has symptoms of anemia such as fatigue, pallor, jaundice. Further supporting evidence in this patient is the increased indirect bilirubin. Also, look for elevated LDH, decreased haptoglobin.