Large embolus obstructing pulmonary blood flow = Perfusion defect There is no capillary bed around smaller bronchi/bronchioles and they form the anatomical dead space. Since embolus also obstructs blood flow, the supplied alveoli which are ventilated, turn into dead space as no exchange of gases can occur through them.
โ Shunt = Ventilation defect
Copied from NBME 22 for completeness sake:
"A good pic showing anomalous arteries in horseshoe kidney
Child has albinism. Defective melanin synthesis due to deficiency of enzyme tyrosine hydroxylase. FA 2020, page 476
Uworld QID: 1733 explains the functions of all rotator cuff muscles.
Abduction = Supraspinatous. External rotation = Infraspinatous, Teres minor. Internal rotation = Subscapularis. Adduction = Teres minor, Subscapularis.
Also, morphine-6-glucuronide is excreted renally. So, morphine would cause toxicity in patients with reduced renal functions.
Patient is suffering from Schizophrenia (1 year of symptoms). Treatment is with anti-psychotics (Risperidone: Atypical antipsychtic)
Response to EPO is typically measured by rise in plasma hemoglobin concentration over following weeks.
The process explains Interferon Gamma Release Assay (IGRA) testing. FA 2020 page 140
10^5 bacterial colonies/mL indicates lab diagnosis of UTI. Rest of the question is pretty explanatory: oxidase positive gram negative rods, producing green pigment is characteristic of Pseudomonas aeruginosa. This is a pretty common pathogen to cause nosocomial UTI with indwelling catheters.
Drug X alone has an increase in blood pressure, so it must be an agonist. When you use Angiotensin + Drug X pressure increases but not as much as would increase with Angiotensin alone. This indicates that drug x is probably a partial agonist, since a partial agonist in the presence of a full agonist works as an antagonist [No effect of Angiotensin and only raise in BP is due to effect of Drug X]
Western blotting detects proteins. Since the number of proteins detected has increased, without any change in the mRNA (detected by Northern blot) or DNA (by PCR), there has been an increase in the translation of ferritin mRNA
Amniotic fluid phospholipid analysis is used for testing fetal lung maturity via measuring surfactant production.
Fetal echocardiography would reveal any congenital heart defects if present, but would not be diagnostic of Downs syndrome
Fetal ultrasound First-trimester ultrasound commonly shows increased nuchal translucency and hypoplastic nasal bone. But I feel this is used more commonly in older women who might have chromosomal dysgenesis as the cause of downs syndrome
Fetal biopsy Pretty invasive technique, when we have a lesser invasive and more specific test available.
In addition to amazing explanation by k_tron_3000, I'd like to add that patient also has numbness and tingling in both legs. So, all sensations to the spinal cord are impaired, hinting towards damage to dorsal horns and hence sensory neuropathy.
UWorld QID: 11747 option A.
"The VVP also communicates with the azygos vein in the chest, which explains in part why breast and lung cancers frequently metastasize to the thoracic spine."
Breast โ Intercostal veins โ Azygous vein โ Vertebral venous plexus (VVP) โ Vertebrae
Is there any drug which would cause enhancement of cell membrane permeability to chloride? It seems like the MOA of ETEC & V. cholerae adenylate cyclase toxins and somewhat that of Ivacaftor used in cystic fibrosis.
Can anyone explain what does "lost her pep" means?
This is eclamsia because of the hypertension in pregnancy with symptoms of end-organ damage and failure combined with siezures (FA2020 p643).
None of the other answers are consistent with the presentation. Epilepsy alone does not cause the symptoms of end organ damage (elevated liver enzymes, lactate dehydrogenase, and inability to urinate), renal disease alone likewise would not cause the combination of symptoms. Sepsis and septic shock causes hypotension not hypertension as seen in this patient. There is no specific drug toxidrome that matches the combination of symptoms.
Vinblastine works by binding tubulin and inhibiting microtubule formation. This inhibits cell division.
Basically, this question is asking which of the following cell types is nondividing/would not need functioning microtubules.
Enterocytes in crypts (which divide to replace intestinal epithelium(, keratinocytes of the stratum basale (which divide to to replace skin), and erythroblasts (blasts are stem cells) are all dividing cells and thus could be affected by vinblastine. Cortical thymocytes are also dividing cells, as they will divide to create progeny T-cells through the process of T-cell maturation.
Thus, the only non-affected cell is ventricular cardiomyocytes.
Grade refers to the differentiation, whereas stage refers to the TNM decriptions
This is high-grade because of the "poorly demarcated... cells growing in sheets" wit a high N:C ratio. Means it's got low differentiation.
This is low-stage because there is NO METASTASIS. Even though there is invasion (and thus, a cancer), M for the TNM is most important.
The key here is this man has no history of bleeding problems yet he has an extremely prolonged PTT (associated with the intrinsic coagulation cascade pathway). This is suggestive that he is deficient in the "unnecessary" factor of the intrinsic pathway, factor XII. (FA2020 p412)
Factor XIIa (Hageman's factor) of the intrinsic pathway activates prekallikrein to kallikrein.
Histamine release, phagocytosis, and C5a generation are not associated with the intrinsic coagulation cascade. Platelet aggregation impairment could be associated with increased PTT (i.e. vWF deficiency, p428), but not that extreme of prolongation without symptoms of bleeding issues.
Fragile X syndrome is X-linked dominant inheritance associated with a trinucleotide repeat in FMR1 (FA2020 p62).
Even if you did not know this fact, fragile X syndrome (a disease affecting the X chromosome) should be X-liked of some sort.
Knowing the disease is X-linked, you can get to the answer because in the couple, the father is the only one with a family history of the disease. Whether the disease was X-linked recessive or X-linked dominant, if the father had the diseased X-chromosome he would have the disease (as males only have one X chromosome). Since the father does not have the disease, he does not have the chromosome and thus cannot pass it on. Thus, the chance of their child having the disease is 0%
Dudes and dudettes, let me tell you how high yield Pathoma Ch. 1-3 are. Dr. Sattar is the freaking man.
Anyway, this is reversible cell injury because of swelling. If the Na/K ATPase is not working, Na is not leaving. Na follows water, so water is getting stuck in the cell, leading to swelling.
Most important is recognizing that it's reversible cell injury - everything else (except PFK lol) is talking about cell death
Candida is a part of the normal flora of skin, could cause contamination of a central venous catheter. The question states that the organism is purple, budding, did not respond to broad spectrum antibiotics (aka they didn't use fluconazole or amphotericin B). Lastly, they showed it plated on blood agar and there was no hemolysis which eliminates staph (the only other possible contender here.)
Cryptococcus usually involves meningitis in immunocompromised pts. E. coli is gram negative sporothrix is usually transmitted by a thorn on a rose or someone with a history of gardening
Candida is a part of the normal flora of skin, could cause contamination of a central venous catheter. The question states that the organism is purple, budding, did not respond to broad spectrum antibiotics (aka they didn't use fluconazole or amphotericin B). Lastly, they showed it plated on blood agar and there was no hemolysis which eliminates staph (the only other possible contender here.)
Cryptococcus usually involves meningitis in immunocompromised pts. E. coli is gram negative sporothrix is usually transmitted by a thorn on a rose or someone with a history of gardening
Confidence interval increases with decreased sample size.
Why is there rhinorrhea in opioid withdrawal? And also, if stimulants like cocaine cause nasal vasoconstriction, shouldn't opioid withdrawal do the same?
If both HCTZ and loop diuretics were provided as an answer choice, further clue that hctz would be the answer choice is the presentation of the patient "feeling funny". This suggests hypercalcemia (psychiatric overtones) which is a side effect unique to HCTZ.
This one is fairly logical if you remember that bacteria LOVE our iron. So much so, that our body came up with a way around it. When an infection is detected by the body, it makes like a doomsday prepper and batons down the hatches.
"All the iron into the bones, quick (^ferritin)! Hide it from the intruders! Get those iron delivery trucks (ferritin) off the road (blood)!
with decreased ferritin comes a decrease capacity for binding iron in the blood
This seems like NADPH oxidase deficiency, as the patient has history of multiple cutaneous abscess with Staph aurues during past 9 months. Therefore, a catalase positive organism is the likely cause, besides microbiological characteristics befitting Nocardia