to snoo-finity ... and beyond!
to snoo-finity ... and beyond!
A very similar question I have seen in Qbanks will ask why a patient with right heart failure does not develop edema and the answer is increased lymphatic drainage. I got this question wrong originally because I answered along this line of reasoning but I think in this case it all has to do with WHERE the extra pressure is coming from. In this question the pt has diastolic hypertension so you can think about the pressure as coming "forward" so constricting precapillary sphincters can prevent an increase in pressure in the capillary bed. However for right heart failure this extra fluid is coming from the OPPOSITE direction (backwards from the right heart) and constricting precapillary sphincters can do nothing (on opposite side of capillary bed) - the only way to prevent edema is to increase lymphatic drainage.
Coloboma is an eye abnormality that occurs before birth. They're missing pieces of tissue in structures that form the eye.
Colobomas affecting the iris, which result in a "keyhole" appearance of the pupil, generally do not lead to vision loss.
Colobomas involving the retina result in vision loss in specific parts of the visual field.
Large retinal colobomas or those affecting the optic nerve can cause low vision, which means vision loss that cannot be completely corrected with glasses or contact lenses.
A and J represent the gracile fasciculus, while B and I represent the cuneate fasciculus. Together they make up the dorsal column-medial lemniscal tract, responsible for pinpoint perception, proprioception, vibration, and pressure. Input is ipsilateral.
C and H make up the lateral corticospinal tract (also called the lateral cerebrospinal fasciculus), responsible for motor command of ipsilateral limbs.
D and G represent the lateral spinothalamic tract. It is responsible for pain and temperature conduction. The input arises in a limb (left lower extremity in this case), enters through the dorsal root (pictured between J and H), decussates and ascends at the anterior commissure (just behind E and F), and finally synapses on the second order neuron in the lateral spinothalamic tract. So the spinothalamic tract is responsible for contralateral pain and temperature sensation. Because our patient has lost sensation on the left, the lesion is in the right.
E and F are the anterior corticospinal tract. It is involved in motor control of proximal muscles, typically of the trunk.
Alcoholic = pancreatic insufficiency. Linoleic, oleic, and palmitic acid can be absorbed without pancreatic lipases since they're just free fatty acids. Triglycerides need to be broken down by lipases before absorption.
Bile acids are the main method for eliminating cholesterol, not pancreatic enzymes
Was it just me, or did "age at onset in years" appear RIGHT above the number of patients, rather than the mean. Which confused me for a good 3 minutes.
Maintenance dose formula is (CssCltau)/F where Css is steady-state target plasma conc. of drug, Cl is clearance, tau is dosage interval & F is bioavailability.
Neither dosage interval nor bioavailability is given, so ignoring those & plugging in the numbers (careful to convert units to mg/kg/day): (12 ug/mL * 1 mg/1000 ug) * (0.09 L/hr/kg * 1000 mL/1 L * 24 hr/1 day) = 25.92 mg/kg/day
...which isn't any of the answer choices listed. They must have rounded 0.09 L/hr/kg to 0.1 L/hr/kg, and doing so gives exactly 28.8 mg/kg/day (choice C)
So for Candida we can use
Azoles (fluconazole) (inhibit CYP450 demethylation)
Amphotercin B (pore formation in fungal cell membrane)
Caspofungin (prevent crosslinking of beta glucans in cell wall)
or Nysatin for oral or esophageal cases (pore formation)
This question is saying that she is taking an ORAL drug to treat candida vaginitis.
Amphotercin is IV
Caspofungin is also IV
so we're left with azoles
Azoles inhibit synthesis of ergosterol by inhibiting CYP 450 that converts lanosterol to ergosterol.
Critical points for this question: 5 year old boy, immunosuppressed because of chemotherapy, 2 day history of fever, cough, shortness of breath, febrile (101.8 F), respirations 46/min, with cyanosis and generalized vesicular rash. Extensive nodular infiltration.
Of the options listed only measles and VZV give a rash. A rash from measles usually starts rostrally and descends caudally, and is flat and erythematous. By contrast, VZV (chickenpox) presents with generalized rash that quickly transitions from macular to papular then to vesicular.
Attributable risk = incidence in exposed – incidence in unexposed
= 30/1,000 (smokers) - 30/3,000 (nonsmokers)
= 0.03 - 0.01
= 0.02 (so the attributable risk is about 2%)
Applying it to a population of 10,000:
= 0.02 * 10,000
= 200
What a terrible picture. They they covered up part of it with lines. WTF
He has fecal incontinence so his external sphincter is damaged, which is innervated by the pudendal n. (S2-S4). The pelvic splanchnic nerves, which mediate the erection process, are also S2-S4.
This is a type II Renal Tubular Acidosis. My Medical School Never taught this to me. Did you also go to poverty med school? I'm surprised they even gave us toilet paper.
you need to know diff bt negative pressure ventilation (which is normal ventilation) and positive presssure ventilation (which is mechanical ventilation). In negative pressrue ventilation the diaphragm contracts making a - intrapleural pressure which allows alveoli to expand. in positive ventilation (the pt diaphragm is not contracting thus not expanding chest cavitiy and not creating the - pressure) the machine is creating positive pressure inside alveoli so so alveoli expands. :)
Per UWORLD- Adenocarcinoma is associated w/ lung scarring related to granulomatous disease, old COPD (chronic) and damage due to recurrent pneumonia.
Malaria can impair hepatic gluconeogenesis and can also consume glucose for its own metabolic demands.
No diet deficiency, the patient had excess carotene due to his diet
The best I can understand, they're describing endometrial hyperplasia, a result of excess estrogen, a steroid hormone that translocates to the nucleus and binds its transcription factor.
Enzyme A stands in for Phospholipase A2, turning phospholipids in the cell membrane into arachidonic acids. From there, Enzyme B stands for Cyclooxygenase (COX), while Enzyme C stands for 5-Lipoxygenase (5-LO). 5-LO produces 5-HPETE, which is turned into leukotrienes. Leukotrienes play a double role in events like asthma, because they cause bronchoconstriction (seen in this patient) and by acting as chemical attractants for inflammatory cells, whose activity will close the airway further. By blocking COX (presumably with an NSAID), we leave more of the substrate arachidonic acid for 5-LOX to ultimately convert into leukotrienes. This is the basis for aspirin-intolerant-asthma, which is frequently associated with nasal polyps. (Samter's triad).
https://www.karger.com/article/FullText/355949
D) Prostacyclin synthase . E) Thromboxane synthase
Biggest clue was that there was no time frame given. Therefore, this seems to be a "slice in time" study, which lines up with cross sectional study.
Patient is current breast-fed, so we can eliminate fructose (fructose is found in honey and fruits and some formula, but not in breast milk). Patient has reducing substances but no glucose in the urine, so he must some non-glucose sugar. My differential for reducing non-glucose sugars in the urine is disorders fructose metabolism or galactose metabolism. We have eliminated fructose, so that leaves us with galactokinase deficiency or classic galactosemia.
Patient has polycythemia vera, as evidenced by erythrocytosis, granulocytosis, and headaches & diziness. EPO is decreased due to erythrocytosis. Decreased LAP would indicate CML, not PV.
Wasn't sure about Rickettsia, but I knew robin of ixodes was on his tricycle in the northeast and getting tortured by the vampire babes.
Because the baby's mother has Type 1 Diabetes mellitus, it is plausible that they had elevated blood glucose levels during or shortly before birth. Insulin does not cross the placenta, but glucose does, so during birth the neonate would have been hyperglycemic. This would lead to the neonatal pancreas releasing insulin, driving glucose into cells and turning down gluconeogenesis; this is why the baby is hypoglycemic right now.
B) Decreased glycogen concentration- I don't know the glycogen concentration compared to an adult patient, but a decrease in glycogen concentration would indicate glycogen/glucose release, which would not be a hypoglycemic state. C) Decreased glycogen synthase activity- decreased glycogen synthase activity indicates energy catabolism, and would lead to higher serum glucose levels. D) Decreased serum insulin concentration- decreased serum insulin would lead to higher levels of glucose in serum. E) Increased serum insulin-like growth factor- IGF does not bind nearly as well to insulin receptors as insulin does, and so would have to be in extremely high concentrations to have this effect. IGF is associated with somatic growth and muscle development.
An asymptomatic 30-year-old woman comes to the physician for ...
Anovulation