Capsular polysaccharide vaccines are often conjugated to proteins to improve immunogenicity. Flagellin is the only answer choice that's a protein.
I think they want you to think about how conjugate vaccine is made: polysaccharide + protein fragment (to induce T dependent immune response). Only flagellin is a protein (or at least sounds like one) in the option list.
EF2 is translational elogation factor 2, which is necessary for protein synthesis.
wikipedia (apologies): The atmosphere is composed of 78% nitrogen and 21% oxygen. Since oxygen is exchanged at the alveoli-capillary membrane, nitrogen is a major component for the alveoli's state of inflation. If a large volume of nitrogen in the lungs is replaced with oxygen, the oxygen may subsequently be absorbed into the blood, reducing the volume of the alveoli, resulting in a form of alveolar collapse known as absorption atelectasis.
I chose cardiogenic edema, but I believe this is incorrect because there is no heart failure risk at this time, so the purpose of the PEEP is certainly not to push out fluid.
FA 2017: Chronic hypoxic pulmonary vasoconstriction results in pulmonary hypertension and RVH.
Rabies attacks the nicotinic Acetylcholine receptor, and travels retrograde via dynein motors after binding AChR, according to FA.
Hi- I don't have an explanation for this but I am also curious as to why this was the answer.
It’s acute alcohol consumption so fatty change more likely. Cellular swelling indicates alcoholic hepatitis which requires chronic alcohol consumption (See FA 2019 pg 385). At least that’s the logic I used to pick fatty change.
Mixed venous oxygen saturation (SvO2) is measured in the pulmonary artery. SvO2 samples the true mixed venous blood leaving the right heart. Measurement of mixed venous oxygen saturation (SvO2) from the pulmonary artery has been advocated as an indirect index of tissue oxygenation.
In cardiogenic shock you have decreased CO --> decreased O2 delivery --> decreased SvO2.
there are two essential fatty acids: linoleic = omega 6, and alpha-linoleic = omega 3.
For this one you just had to know the glycolysis pathway. Stem told you 2,3-BPG is elevated, which is upstream of pyruvate kinase.
It said it was fatal to males in utero, and the question asked about live born offspring. Since the males aren’t being born in the first place, I said 50% females and 0% males.
this is a cervical spinal cord section. the cuneate fasciculus is intact (UE) vibration and proprioception, but the white section is the gracile fasciculus (LE) and is damaged. I think the lateral portion that is uneven is just natural/artifact.
https://ghr.nlm.nih.gov/condition/pseudocholinesterase-deficiency
"People with pseudocholinesterase deficiency may not be able to move or breathe on their own for a few hours after [fast-acting drugs, such as succinylcholine and mivacurium] are administered.
Why is does a PDA after birth result in "higher than normal left ventricular cardiac output" over increased "right ventricular PO2"? Does the pulm artery --> aorta shunt become reversed after birth, so higher oxygen aorta blood would flow back into the right ventricle? I get that more blood would be pumped to the left ventricle, resulting in RVH/LVH, but don't understand the O2 bit.
PDA flows from the Aorta ==> Pulmonary arteries, by passing the RV so there is no change in O2 in the RV.
Recurrent kidney stones should include hyperparathyroidism on your differential, couple that with gastrinoma and you’re looking at MEN 1. Lipomas are also associated with MEN 1.
I think this one is literally just asking what part of the kidney will be the most poorly perfused. That part would have the most renin. Also, the medulla doesn’t have JG cells so I guess that’s another reason why it couldn’t have the most renin.
Renal artery stenosis is going to decrease blood flow to the kidney. JG cells sense the decrease in perfusion pressure and secrete renin.
Renin is produced by the JG cells, JG cells are in the cortex (they are modified smooth muscle of the afferent arteriole).
My reasoning was that it’d be diverticulitis due to the more acute history of presentation: “fever, chills, LLQ pain for 1 day.” Crohn’s should have a longer timeline of presentation; although the skip lesions made this one really tricky. Not sure how the gross pathology photograph plays in though ...
I think it is good to note the demographics. The patient is female and old. That, along with the constipation, made me lean more towards diverticulitis. IBD usually develops in younger persons.
I picked Crohn’s too. I think the severe constipation over 5 years distracted me.
This pt has osteomalacia / rickets (since he's a kiddo). Caused by defective mineralization of osteoid (osteomalacia) or cartilaginous growth plates (rickets, only in children).
Most commonly d/t Vitamin D deficiency.
Children with rickets have pathologic bow legs (genu varum), bead-like costochondral junctions (rachitic rosary), craniotabes (soft skull).
Dec. Vitamin D (normal function is to reabsorb Ca2+ and PO4)
Dec. serum Ca2+
Dec. serum PO4
Inc. PTH
The clues for trichotillomania were the death of her grandmother suddenly, since trichotillomania is often stress-induced. I also narrowed it down by it saying the hair was in different growth stages in the patchy areas, which makes sense if she’s plucking them out at different times.
Telogen effluvium is most common in middle-aged women, so she doesn’t fit the profile (but you’re right about it being caused by stress).
My choice for Squamous Cell Carcinoma was guided by the central location of the tumor. To me, that didn’t look like the cavity you’d get with abscess but a huge tumor.
I don’t think it was cavitary; I think that was just the bronchus. I think abscesses tend to be smaller, and wouldn’t affect the surrounding parenchyma much. I wasn’t super confident in picking squamous cell carcinoma, but I did know that squamous cell carcinoma tends to be a centrally-located lung tumor.
Stretch or dilation of the cervix and vagina are strong stimuli for oxytocin secretion, mediated by neural pathways called the Ferguson reflex.
Article: https://www.sciencedirect.com/topics/neuroscience/ferguson-reflex
FA 2017: Fibrate ADRs include myopathy increased risk with statins, cholesterol gallstones
@frimmy_11 Why would protein break down after only 20 hours? Shouldn’t fat be the major contributor now? Also if protein is being used, then why isn’t valine the choice? It’s also glucogenic.
Fats are ketogenic (except odd chain FA), so they produce ketones for energy production (Acetyl-CoA) rather than glucose. If the question asked what the primary source of energy production was, it would still be glycogen (and not ketones), because this is within 24 hours. However after 24 hours the answer could be ketone bodies. Regardless, the question specifically said the pt had a serum glucose of 100, indicating that we are looking for something that provides a substrate for gluconeogenesis.
During periods of starvation, substrates for gluconeogenesis come from two sources: (1) breakdown of existing muscle, or (2) via odd-chain FA through propionyl-CoA. (*Valine also feeds into propionyl CoA, but is not involved during starvation --> see below)
(1) The alanine-pyruvate cycle provides this (glutamine in muscle + pyruvate --> alanine --> goes to liver --> transamination to alpha-ketoglutorate --> pyruvate is separated from glutamine --> glutamine goes to urea cycle, pyruvate goes on to gluconeogenesis). Lactate can also be used (this could have been a right answer if it were listed).
(2) Odd chain FAs are also glucogenic, but stearic acid (provided in the answer choice) isn’t odd chain, so it is only ketogenic and can be ruled out.
Although valine (and other branched a.a.) feed into Propionyl-CoA, they are not used in starvation because starvation strictly relies on hepatic gluconeogenesis. These a.a. are not metabolized in the liver because the liver lacks branched-chain a.a. transferase enzyme. In First Aid, Biochem section, under Fasting/Starvation, in both the “fasting state” (which is within the time frame of this question), or the “starvation state,” both utilize hepatic gluconeogenesis. My assumption is that valine is used during regular metabolism, and not during periods of starvation.
why? like does my med school suck or am I just that dumb cuz we never learned anything like this
With this question, I think they want you to recognize that the patient isn't having chest pain related to the heart. They emphasize several rib fractures and a pneumothorax but don't indicate any heart damage (lack of adventitious sounds = no pulmonary edema indicated or a lung issue related to heart problem).
The pericarditis is what's innervated by the phrenic n. Seeing as how his heart is fine, the fractured ribs are probably what are causing him pain via the intercostal nerves.
from AAFP ED of mixed organic and psychogenic origin is common. Psychogenic causes are more likely when the patient has normal erections with masturbation or when nocturnal penile tumescence is normal.
This is water intoxication. https://www.ncbi.nlm.nih.gov/pubmed/1877579
This is what I thought but not sure if it’s correct. There is a UWorld q where it describes co-administration of cortisol and epinephrine. Cortisol significantly enhances the effect of epi because cortisol has a permissive effect on maintaining the adrenergic receptors.
“The combination of a long-acting beta 2 agonist (LABA) and an inhaled corticosteroid is more efficacious in asthma and [COPD] than [...] either alone. Corticosteroids may regulate beta 2 receptor function by increasing expression of the receptor, restoring G-protein/beta 2 receptor coupling, and inhibiting beta 2 receptor downregulation.”
Secondary hyperparathyroidism (usually d/t chronic renal failure).
Lab findings include ↑ PTH (response to low calcium), ↓ serum calcium (renal failure), ↑ serum phosphate (renal failure), and ↑ alkaline phosphatase (PTH activating osteoBlasts).
Catheter placement:
https://aneskey.com/wp-content/uploads/2016/08/image00804.jpeg
Recall that the lung apex extends above the first rib.
I might be the only person on earth who got this one wrong, but regardless:
"ITT analysis includes every subject who is randomized according to randomized treatment assignment. It ignores noncompliance, protocol deviations, withdrawal, and anything that happens after randomization."[1]
FA 2017: Urinary cyanide-nitroprusside test is diagnostic. not sure how to know that it was a red color, but maybe just the fact that red seemed like a positive test result.
link to more background but not necessarily helpful for this question
Histology showed coagulative necrosis (preserved architecture of myocardial fibers) with neutrophil infiltration which hinted that the MI was within 24 hours. Most likely cause of death within first 24 hours of MI is arrhythmia. Myocardial rupture would also be visible on gross appearance of the heart, which they described in the stem.
Mottling and softening of anterior wall on autopsy suggests it was not older than 24 hrs. Death from fatal arrhythmia like V-fib most commonly occurs within one day of the MI. That said, once scar has formed in myocardial tissue it, too, can cause arrhythmia.
MI sudden death -> arrhythmia. The order of commonness is arrhythmia > cardiogenic shock > rupture.
i think this is because bilirubin is a soluble liver breakdown product of heme, but has not entered the intestine/colon for gut bacteria conversion to stercobilin or urobilin. urobilin in urine is normal.
Bullous pemphigoid antigen must be hemidesmosome. FA: bulla are "bullow" the dermis (subepidermal blister). BP also yield "tense" bulla.
Peri- or postpartum cardiomyopathy (PPCM) is a rare, life-threatening heart disease of unclear origin and is characterized by heart failure of sudden onset between the final weeks of pregnancy and 6 months after delivery. link to pubmed The clinical picture of PPCM corresponds to a dilated cardiomyopathy (DCM) with signs of severe heart failure.
2,500 students ... but you find out during your initial screen that 500 already have the disease. So, strikeout those people. That leaves 2,000 students who don’t have the disease.
Over the course of 1 year, you discover 200 students developed the infection. Thus:
200 new cases / 2,000 people who didn’t have the disease when you started your study = 10 percent
Tricky, tricky NBME ...
Don’t forget that incidence is the number of new cases which emerge in an unaffected population. Incidence is trying to get at the question -> “In a given year, how many new people develop this disease?”
In other words, you cannot count people who already have the disease. You have to exclude those people from your calculation. You want to know, among all the people out there who DO NOT have the disease, how many times this year was someone (newly) diagnosed?
Said differently still, you don’t want to “double-count” people who developed the disease before your study. As an epidemiologist, that would screw up your sense of how infective or transmissible a disease is. You want to know, “from time1 to time2 how many new cases emerged?”
Also consider this great description from the NIH’s MeSH database:
INCIDENCE: The number of new cases of a given disease during a given period in a specified population. It also is used for the rate at which new events occur in a defined population. It is differentiated fromPREVALENCE, which refers to all cases, new or old, in the population at a given time.
A 24-year-old woman with sickle cell disease comes to the ...
Serum parvovirus B19 IgM antibody test