This question tripped me up. I chose 'A' because the question said her living will (consistent with the husband's wishes) does not want mechanical ventilation, but it did NOT say anything about DNR...But come to think of it, what is the point of doing CPR if she cannot maintain spontaneous breathing since she seems to be in a vegetative state? That means if you do CPR and actually want to save her life, you must intubate, which goes against her will. Hence, extubate and do not resuscitate...
I think the question stem may have a mistake because according to FA (2021 p. 528), Parinaud causes light-near dissociation wherein the light pupillary reflex is impaired while accommodation is intact. The question said accommodation is impaired...Anyway, pineal gland tumor fits the best.
I got this question right from watching that House episode of the patient with phantom limb pain lol
Lymphangitis is an infection of lymph vessels, while being a complication of some bacterial infections.
-Key words in vignette is "red streak extending to elbow".
Look at this picture: https://www.jpeds.com/article/S0022-3476(13)00037-1/fulltext.
The form is made because the streak follows the shape of the lymph node. Very noticeable once you see the image.
-Superficial thromphlebitis can't be the answer because it is generally caused by clotting in woman over 40 or 6 months post partum.
Remember the question asks "most likely" but many of some of these choices can definitely be in the differential diagnosis.
SLE like other autoimmune diseases, may improve or worsen, or can present for the first time during pregnancy. Obstretic complications related to SLE: -Maternal (preeclampsia), - -Fetal (neonatal lupus, intrauterine fetal demise)--Neonatal lupus occurs due to passive placental transfer of maternal anti-SSA (Ro) and anti-SSB (La) antibodies (30% prevalent in SLE.-
-Fetal findings: -Cardiac (fetal AV block) that occurs due to maternal autoantibodies binding to fetal cardiac cells. Causes irreversible injury to AV nose. The ventricular heart rate will determine the baseline fetal heart rate and will present with fetal bradycardia (less than 110 beats per minute). - -If the heart block is prolonged, hydrops fetalis can occur.
(https://www.jpedhc.org/article/S0891-5245(13)00232-0/fulltext) Uworld Question ID (12531)
The majority of infants with CF and MI, whether simple or complex, have pancreatic insufficiency (PI). Confirmation of PI is most efficiently and effectively done by obtaining a fecal elastase. However, the fecal elastase sample should be collected from rectally delivered, formed stools and not from an enterostomy. Watery stools from either an enterostomy or rectally delivered can result in falsely low fecal elastase values. Therefore, in infants with MI and an enterostomy, PI should be assumed and fecal elastase collected at a later date after the gastrointestinal tract is back in continuity and stools are at least of a pasty consistency to confirm diagnosis. Once the infant is able to take a minimal amount of formula or breastmilk by mouth or feeding tube, PERT should be initiated at 2000–4000 lipase units per 120 mL of formula []. PERT contains lipase to digest to lipids, amylase to digest carbohydrates, and protease
you dont see a cherry rod spot on fundoscopic exam picture - indication for fluorescein angiography to CONFIRM the diagnosis. they need to ask a different question if they want us to pick doppler. nbme always wins=(
Decubitus ulcer is a pressure sore that could be anywhere on the body, and in this case is on the head because the baby can't move.
Ecthyma gangrenosum is an infection usually seen in patients who are critically ill and immunocompromised. The characteristic lesions of ecthyma gangrenosum are haemorrhagic (bloody) pustules that evolve into necrotic (black) ulcers, which doesn't really fit the description here.
Kerion is an abscess caused by a fungal infection, and likely wouldn't be ulcerative
Recluse spider bite would have more severe systemic symptoms in a child (weakness, fever, joint pain, hemolytic anemia, thrombocytopenia, organ failure, disseminated intravascular coagulation, seizures, or death) and you would see puncture wounds.
I didn't think atypical TB or scabies made sense so I didn't go into those.
Even though most small cell lung cancer shows up in late stages, and only 2% of people diagnosed are alive after 2 years, people still frequently get treatment. Usually this is both chemo and radiation, but the chemo comes first to shrink the cancer so you don't have to radiate as large an area. Chemo + radiation is also sometimes used as paliation. (https://www.ncbi.nlm.nih.gov/books/NBK482458/)
"Nerve conduction studies (NCS) and needle electromyography (EMG) are valuable for confirming the diagnosis of GBS and for providing some information regarding prognosis. In addition, electrodiagnostic studies are useful in classifying the main variants of GBS as demyelinating (eg, acute inflammatory demyelinating polyneuropathy) or axonal (eg, acute motor axonal neuropathy" UTD
Nobody has mentioned this but I think another thing that helps with this answer is that the boy was infected with all these that he was immunized for. A 12 month old should've had immunizations for H. flu, and Strep pneumo, yet he was still getting sick. This makes me think he isnt making proper antibodies --> therefore a B cell issue
The patient has SCLC (histo description: uniform, small round cells w/darkly staining nuclei). This type is unresectable (only rare cases of small tumors w/o node involvement), responds to chemo and radiation initially, given more so as palliative care.
High Calcium and low phosphorus --> probably has high PTH.
Vitamin D - leads to absorption of both calcium and phosphorus, so you would have high Ca and Ph. PTH - differentiates between Ca and Ph, it increases Calcium in the body and decreases phosphorus in the body.
BMI ≥40 --> Gastric Bypass candidate. BMI ≥35 + comorbidity --> Gastric Bypass candidate.
She has already tried weight loss without success. Plus she is a compliant patient (diet, insulin regimen, and daily glucose monitoring)
Everyone has a story and a struggle, and weight is not dependent just on our effort or workout regimen. Genetics, microbiome, and many other factors play a role. Let's not judge these patients but help them!
so you just open a bitch up without any other workup whatsoever? stupid question
I thought I heard in a Divine podcast that if the labs showed pretty clear gallstone pancreatitis you could just skip the US and go right to ERCP. Guess not.
NPPV is approved for hospice patients for palliative reasons.
This patient is struggling to breathe, which is probably causing her some degree of suffering.
NPPV is non-invasive, and could alleviate her pain while not being a curative measure.
Was anyone thinking calcium pyrophosphate? Inflammatory joint, patient with RA, no organisms seen on FNA, would be treated with steroids?
Shouldn't early salicylate OD cause resp alkalosis? I thought only late salicylate OD caused increased anion gap metabolic acidosis. I chose Methanol given her eye sxs and I thought aspirin should be ruled out due to the timing of her OD
Stabilization - Circulation
A child with exertional heat stroke may require 60 mL/kg or more of normal saline.
For children receiving treatment for heat stroke in the hospital, we suggest evaporative cooling rather than cold-water immersion. Evaporative cooling is preferred for hospital treatment of heat stroke in children because it does not interfere with efforts to maintain monitoring and ongoing resuscitation in unstable patients. Cold-water immersion is associated with significant discomfort, shivering, agitation, and combativeness; and is not clearly more efficacious for rapid cooling in the pediatric population. When evaporative cooling is not available, cold immersion is suggested.
Why echo and not angiography?
As recommended in the 2010 American College of Cardiology/American Heart Association/American Association for Thoracic Surgery thoracic aorta guidelines, echocardiography is recommended at initial diagnosis and at six months to assess the aortic root and ascending aorta in patients with MFS
Approach to diagnosis of MFS
MFS is most commonly diagnosed using the 2010 revised Ghent Criteria. These are based on the presence or absence of family history, physical examination, imaging of the aorta, and genetic testing in some cases.
The revised Ghent nosology puts greater weight on aortic root dilatation/dissection and ectopia lentis as the cardinal clinical features of MFS and on testing for mutations in FBN1. For the aortic criteria, aortic root Z score calculators are available for children and adults.
In the absence of family history of MFS
For individuals without a family history of MFS, the presence of one of any of the following criteria is diagnostic for MFS:
Aortic criterion (aortic diameter Z ≥2 or aortic root dissection) and ectopia lentis.
Aortic criterion (aortic diameter Z ≥2 or aortic root dissection) and a causal FBN1 mutation.
Aortic criterion (aortic diameter Z ≥2 or aortic root dissection) and a systemic score ≥7.
Ectopia lentis and a causal FBN1 mutation that has been identified in an individual with aortic aneurysm.
TL;DR Echo for aortic diameter
What the hell is going on here? Still no answer that makes sense. We have:
Put it all together: RIGHT tension pneumothorax
But why the hell are breath sounds decreased on the LEFT? That alone made me switch to some crazy heart crushing atelectasis answer. I honestly thing the R/L mixup may be a typo because without that the question is simple.
Still confused about this one. I guess it depends how you read that last line:
"Which of the following potential flaws is most likely to invalidate this study?"
If you read it as which flaw is most likely to be present, then I guess selection bias is most likely.
If you read it as which flaw, if present, is most likely to invalidate the study, then that type I error would be 100% likely to sink the results, guaranteed. Guess they meant the first one... Because yes p=0.01 so it's not likely they had a type 1 error.
Beef with this q.
Step Prep has the answer on this one: diaphragmatic hernia.
this question is funny, considering that post-exposure antibiotic prophylaxis is indicated "regardless of vaccination status", I guess this would be a correct option if the "study partner bad fever" were a confirmed case
"Carotid pulses are decreased. A systolic bruit is heard over the abdomen at midline. The left femoral pulse is absent and the right femoral pulse is decreased. A left femoral bruit is heard." ^What in the hell is going on here? I'm freaking out about her absent femoral pulse meanwhile they just want to ask about ACE inhibitors...
And on that subject, how do ACE inhibitors not decrease intravascular volume? "This class of agents effectively inhibits the conversion of angiotensin I to the active vasoconstrictor angiotensin II, a hormone that also promotes, via aldosterone stimulation, increased sodium and water retention. The ACE inhibitors, therefore, are capable of lowering blood pressure primarily by promoting vasodilatation and reducing intravascular fluid volume." https://pubmed.ncbi.nlm.nih.gov/2188439/
"They work by causing relaxation of blood vessels as well as a decrease in blood volume" https://en.wikipedia.org/wiki/ACE_inhibitor
Obviously angiotensin is the safest answer but I am beyond baffled about how "decreased intravascular volume" is incorrect. Anyone?
Was anyone else torn because you thought the colonic hydrogen travelled backwards up the entire gut to be exhaled via mouth fart? So that the small-bowel must have decreased pH?
Maybe just me...
Well apparently that's not how the test works. Or the human body. "The hydrogen produced by the bacteria is absorbed through the wall of the small or large intestine or both. The hydrogen-containing blood travels to the lungs where the hydrogen is released and exhaled in the breath where it can be measured." https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3155069/
What does "central hilar opacification bilaterally" on x-ray represent?
What is that black sliver on here retina?
This is hilarious, did anyone else think it could be viral pericarditis, which in another question required prompt evaluation with an echo. I initially thought EKG, then echo, then NSAIDs as the order. Apparently, we just skip the diagnosis and go straight to NSAIDs in these patients now. Unbelievable.
What a dumb question, there's literally a UWorld question about how a girl with a hx of seizures faked one and how you need to do neuro testing if they have no post-ictal confusion. I'm sorry, why are we even entertaining this if she has NO post-ictal confusion?
I'm sorry but how the hell are you supposed to know it's vulvar when it says nothing about the vulva. I was between that and polyps, but put polyps because it was on the perineum? Like how the hell is that the vulva?
Yes, this is Gilbert syndrome. Here's my beef with this question: UDP-glucuronosyltransferase is a liver enzyme. Conjugation takes place in the liver, not the serum.
Here's how you can diagnose Gilbert syndrome according to UTD: "A reduction in hepatic bilirubin-UGT activity, which is approximately 30 percent of normal" https://www.uptodate.com/contents/gilbert-syndrome-and-unconjugated-hyperbilirubinemia-due-to-bilirubin-overproduction
Here's a picture from UTD of the enzyme sitting HAPPILY WITHIN THE HEPATOCYTE: https://www.uptodate.com/contents/image?imageKey=GAST%2F52393&topicKey=GAST%2F3578&search=gilbert%20syndrome&rank=1~53&source=see_link
So how is this a "deficiency of serum glucuronosyltransferase"?
Meanwhile, according to FA2020 p394, Gilbert syndrome also causes "impaired bilirubin uptake." Aka "Impaired hepatic storage of serum bilirubin"
My rage knows no bounds.
The only reliable way to differentiate between PCP and cocaine on these exams:
Weird facts about PCP intoxication:
The only reliable way to differentiate between PCP and cocaine on these exams: + nystagmus (not present here) + catatonia/sedation
Weird facts about PCP intoxication: + May wax and wane between extreme agitation and sedation + Blank stare and flat affect + Rigidity + May not have hypertension or tachycardia
This is drug reaction with eosinophilia and systemic symptoms (DRESS)
Notably, she has been taking the drug for a year, which is not typical for DRESS.
UTD: "The reaction typically occurs two to eight weeks after drug exposure. Medications that are taken for less than two weeks or more than three months before the onset of DRESS are unlikely to be the culprit." https://www.uptodate.com/contents/drug-reaction-with-eosinophilia-and-systemic-symptoms-dress
So yes, this is not a typical timeline. However, if you ever see rash (especially on the trunk), eosinophilia, and a high-risk drug (especially TMP-SMX) you absolutely smash the medication-rash button and move on.
No other answer choice could ever explain that huge eosinophilia.
I am NOT giving a stress test to every 50 year old male smoker with hypertension and family history of MI who wants to exercise. That would be so many patients and seems like a bad use of resources.
Tell me why I'm wrong. Is it because he has so many risk factors for CHD (age, sex, smoker, hypertension, family history)?
From UTD: "CHD screening tests are generally not recommended for asymptomatic patients, and cardiac stress testing should not be part of a routine annual physical or health screening examination. However, there are other patients in whom we perform stress testing: patients who need reassurance that it is safe for them to be active, in which a stress test can help providers delineate an activity program with specific levels of exercise to achieve; and patients who have an occupation in which high levels of exertion may be routinely required (eg, farmer)." https://www.uptodate.com/contents/screening-for-coronary-heart-disease
"Rare exceptions are patients with multiple risk factors" https://www.uptodate.com/contents/selecting-the-optimal-cardiac-stress-test
Erythema infectiosum — Parvovirus B19 most classically causes erythema infectiosum (EI), a mild febrile illness with rash. It often occurs in outbreaks among school-aged children, although it can occur in adults as well . EI is also referred to as "fifth disease" since it represents one of six common childhood exanthems, each named in order of the dates they were first described.
The illness begins with nonspecific prodromal symptoms, such as fever, coryza, headache, nausea, and diarrhea (table 1). These constitutional symptoms coincide with onset of viremia. Two to five days later, the classic erythematous malar rash appears with relative circumoral pallor (the so-called slapped cheek rash). This facial rash is often followed several days later by a reticulated or lacelike rash on the trunk and extremities (picture 1A-B). https://www.uptodate.com/contents/clinical-manifestations-and-diagnosis-of-parvovirus-b19-infection
I love factitious and surreptitious pill popping patients almost as much as I love fat embolism. I pray for it on every single thyroid question, but it rarely pays off.
BIG MONEY HERE PEOPLE! Gonna buy some lotto tickets with my next pack of smokes.
How do you prevent aspiration in a patient with severe muscle weakness?
Elevation of the head of the bed
Antibiotic prophylaxis isn't an answer they usually like to see. Mainly because it can lead to antibiotic resistance.
In this paper, prophylaxis doesn't improve outcomes in patients who have already aspirated and gotten pneumonitis (inflammation without infection), so it definitely wouldn't help before this patient even aspirates. https://pubmed.ncbi.nlm.nih.gov/29438467/
NG suction addresses stomach contents, not oral secretions.
I have been waiting my entire medical career to finally get a question on fat embolism syndrome. I always pray for it every time I see a big fracture, but it never delivers.
Yes, this is CGD. But which cell? According to UTD: "These genetic defects result in the inability of phagocytes (neutrophils, monocytes, and macrophages) to destroy certain microbes." https://www.uptodate.com/contents/chronic-granulomatous-disease-pathogenesis-clinical-manifestations-and-diagnosis
FA2020: "Involves the activation of the phagocyte NADPH oxidase complex (eg, in neutrophils, monocytes)."
Seems like NADPH oxidase deficiency would involve macrophages too... So is neutrophil just the most important/well known?
Agree that this question sucks. Why not go for psychodynamic psychotherapy since the patient specifically says she would like to understand why she does these things? Not a great option but still...
This sounds most likely to be a strangulated inguinal hernia. Perhaps it is made intentionally vague on torsion vs strangulated hernia so that we just say send them to the OR. However, wouldn't valsalva help differentiate between the two and be EXTREMELY quick and easy to perform? Why would you not take 5 seconds to do valsalva and then operate? If it said "surgical consult" then okay that's reasonable, but why would you do a procedure before this simple step? What am I missing here?
"When strangulation exists, the patient may present with bowel obstruction symptoms, including nausea, vomiting, and obstipation. If bowel ischemia is present, the patient will have severe pain and may present with sepsis (hypotension, tachycardia). Before palpating the abdominal wall, it is important to inspect the skin overlying the hernia visually. Any appearance of erythematous or dusky skin is a concern for a possible strangulated hernia. An emergent surgical consult should be obtained if skin changes are noted before attempting to reduce the hernia. When evaluating a patient for a hernia, it is essential to ask the patient to increase abdominal pressure via a Valsalva maneuver." https://www.ncbi.nlm.nih.gov/books/NBK555972/
they really copied and pasted this sh!t on nbme 6-8 huh? couldn't afford another heart sound smh
they really copied and pasted this sh!t on nbme 6-8 huh? couldn't afford another heart sound smh
Cardi B voice: WHAT WAS THE REASON for the goddamn Gram - stain, like whyyyyyyyyy. That's why I put prostatitis, even though the non-tender prostate threw me off. Damn, these questions are really just read the first and last sentence huh?
I think I thought too deep into this, but isn't the cause of post-op fever on days 3-5 UTIs? I just remembered the mnemonic, but I guess I was thinking too deep..
The maneuver described is known as Finkelstein's test, which is meant to be specific for DeQuervain tenosynovitis.
Remember the tip that you can use clindamycin for anaerobes above the diaphragm, and metronidazole for below.
From UpToDate: For patients with SCLC, systemic chemotherapy is an important component of treatment, because SCLC is disseminated at presentation in almost all patients. For those with limited-stage disease, thoracic radiation therapy is used in combination with chemotherapy. Prophylactic cranial irradiation is often used to decrease the incidence of brain metastases and prolong survival. Prophylactic cranial irradiation and thoracic radiation may also be beneficial in those with a complete or partial response to initial systemic chemotherapy.
I thought with the whole <6 months or less thing he would qualify for hospice care in a skilled nursing facility? I am the only one who thinks it's a dick move to question this guy's decision making?
If the directives state mechanical ventilation be discontinued it's implied that she would rather die. Why would anyone try to resuscitate when a decision has been made to pull the plug?
Huntington Disease is a neurological disorder characterized by a classic triad of choreiform movement (in this case the bilateral writhing motions of the upper extremities), dementia/depression, and behavioural changes (aliens).
Per UW, evaluation of fetal demise includes fetal autopsy, gross and microscopic examination of placenta, membranes, cord, and karyotype and genetic analysis. Evaluation of fetal demise on moms side includes kleihauer betke test for fetomaternal hemmorhage, antiphospholipid antibodies and coag studies.
Nobody has answered this question through the lens of a learning objective quite yet so here's my 2 cents: Km is INCREASED bc this patient has an enzyme with an overall LOWER affinity (can be corrected to normal after an increase in substrate) which is characteristic of COMPETITIVE inhibition, which is why the line of the pt. is one of competitive inhibition on a LB plot
This isn't the scenario in this question, but I was wondering what would happen if you had told the parents the diagnosis and they didn't want their child to know?
Alcohol withdrawal - - > increased catecholamines - - > increased insulin (via B2) - - > cellular uptake of K+ - - > hypokalemia
This question might be tricky because the mutation of interest here is inherited from the dad side (paternal) but affects the mitochondria.
That is, the mutation is not a mutation of the mitochondrial DNA; it is of nuclear DNA which affects mitochondrial function and quality. (Mechanism unknown.)
In their explanation, the NBME says, “
Mitochondrial diseases are strictly inherited through the mother” but that is incorrect; it would be more correct for them to have said: Mitochondrial DNA mutations are strictly inherited through the mother.
That is, you can have mitochondrial problems that come from your dad. Mitochondrial DNA mutations, on the other hand, come only from mom.
So, the stem describes a “
mitochondrial disease” but it is not a mitochondrial disease dervied from a mitochondrial DNA mutation.
Yes, mitochondria are affected but the mutation is in nuclear DNA that governs the maintenance of "healthy mitochondria".
This explains why dad and dad's brother show the same “proximal muscle weakness of the lower extremities”.
Am I crazy, or does the question stem imply that this was inherited paternally?
Why couldn't this be branching enzyme impairment? They both cause cardiac symptoms (according to Amboss at least)
Both histoplasmosis and blastomycosis are associated with living in Ohio and can cause pulmonary disease. Histoplasmosis is more associated with hilar lymphadenopathy and can cause cavitations (recall from Sketchy that it can resemble Tb) - another association to note with Histo is hepatosplenomegaly. Blastomycosis is uniquely associated with extra-pulmonary involvement in the bone, prostate, and skin
I got this right because I thought of the cavernous sinus which has CN 3, CN4, CN V1 & V2. Out of all of all the options V2 is the only one that controls upper lip. For option C, pupillary reflex is controlled by CN 2 and 3, and if there is a fracture to the orbital floor the closest to the sinuses to be injured is CN5 (V2). Idk I could be wrong but if you guys agree let me know pls.
Mom and her daughter have the same sequence of FBN1. What is special is that compared to a “normal” (wild-type) FBN1, mom and daughter have one little tiny mutation in their sequence: a single nucleotide (A,T,G,C) that is different than most other folks.
(Interestingly, this nucleotide difference does not alter the amino acid encoded by this part of the gene; that makes Choice D (
change the folding of the protein) and Choice E (
truncated protein) very unlikely.)
Back to our question. Even though mom and daughter have the same mutation, mom shows no signs of Marfan syndrome; this eliminates Choice A (
disease-causing mutation in the patient and her mother).
You might think this is an example of variable expressivity (not an option but a good guess), and it might be.
In the stem they say:
The same nucleotide change is found in 15 of 200 individuals without Marfan syndrome.
Interesting! This means that in a “normal” sample of people (who have no signs of Marfan), 15 out of 200 still have this mutation.
(They don't say anything about how many Marfan people have the mutation but we don't need that information to answer the question.)
When a gene can be found in multiple “versions”, we call the gene polymorphic (literally,
So the best response is Choice B (
The graft is placed below the renal arteries and above the aortic bifurcation, which contains the IMA. IMA supplies the hindgut (distal 1/3 of transverse colon to to upper portion of the rectum).
FA 2019 pg. 357
So are we just not going to talk about how an NBME question writer just sketched this real quick and put it on a question
I always remember locus caeruleus as Marcus Aurelius (if anyone has seen the movie Gladiator) its about action and being hopped on up Nor epi would recommend
My two Leishmania questions were literally back to back lol
I don't believe this question is addressing hereditary angioedema (which is definitely a manifestation of C1-INH deficiency), but rather just overactive complement (since its inhibitor is deficient). Remember that byproducts of the complement cascade include C3a, C4a, and C5a, which are all anaphylatoxins. "Episodes of cutaneous urticaria and occasional episodes of laryngospasm" describes an allergic reaction that can be mediated by the anaphylatoxins produced in the cascade. The other answer choices would lead to decreased complement activity and therefore release of fewer anaphylatoxins.
can someone explain why it's not degranulation of eosinophils?
How would we rule out antithrombin deficiency?
So I thought about the "tombstone" picture on p.207 of Pathoma where the desmosomes are defective. The cells in the basal layer stay attached to the basement membrane, but the cells above get disconnected. So that made me think of breaking the connection between cells in the basal layer and cells above the basal layer (suprabasal).
honestly fuck them. increased direct should point you to another dx.
^ Important read, if you have the time.
Tacrolimus has the same MOA as cyclosporine
This question is describing what is literally called "Head Out Water Immersion." The pressure that the water exerts on the body is greater than the pressure that air exerts on the body. This hydrostatic pressure pushes the water in the limbs up into the central cavity (the rib cage protects from this hydrostatic pressure). Because there's more blood in the central cavity, the heart experiences an increase in volume. This is why you often need to pee more often when standing in the pool.
In summation: water pushes blood into center cavity -> increased blood volume in central cavity -> blood stretches heart -> increase in ANP
"clear-fluid-filled, tense blisters" and "subepthelial blister" with "autoantibodies" scream bullous pemphigoid, but I thought BP blisters were itchy>>painful. Contrast with pemphigus vulgaris in which pain>>itch.
This Q stem was confusing to me because I thought pain>>itch for shingles. Any thoughts?
"In addition to slightly decreased platelet count..." — why are plts slightly low in EBV infection/mono?
totally buy the answer of K+ being increased, but can somebody explain why her extreme dehydration (decreased skin turgor, excess urine output) wouldn't lead to an increase in serum [Na+]?
Pt shows classical signs of lack of platelet ADHESION. ADHESION is mediated by vWF. Platelet AGGREGATION studies test for AGGREGATION, which is mediated by fibrinogen, thus they have normal results on lab testing as they are not testing a pathway that uses vWF (very miniscule detail I know, very annoying).
Because it is a straight downward slope, you can also tell that Y and X are bound in similar ways by antibodies. What differentiates the two, then, isn't epitope binding capability, but the concentration. All else equal with binding sites, more Y with an unchanging amount of X will lead to less X bound, in a 1:1 manner.
Don't need to know this is FAP to get it right.
Father and Grandfather had it, so can assume an AD mutation in this patient. Assuming her partner is homozygous without the mutation, the risk of her AD train going to her child is 50%
Can anyone help explain what the other options would entail?
RIPE: Rifampin, Isoniazid (INH), Pyrazinamide, Ethanbutol.
RIPE treats TB.
Dirty Medicine has a great mnemonic to memorize these diseases:
Compression of the C5/C6 spinal nerves would mean the axillary nerve is compressed.
(Use the mnemonic: 5 Muskateers Assassinated 5 Rats 5 Mice, and 2 Unicorns; assassinated would be C5/C6 and axillary sounds like assassinated)
The axillary nerve innervates the deltoid muscle which abducts the upper extremity.
Bacterial vaginosis is also very common in women/people with vaginas who have sex with women/people with vaginas, and more common in that population vs gen pop.
One 2005 study of 12K vagina-owners found 45% prevalence in folx who'd had at least one partner with a vagina, vs 29% rest of study population.
(Sorry no link, just sharing from "Lesbian Health" by Dibble & Robertson.)
Hydronephrosis causes tubular atrophy from compression of the tubules by urine. Two common causes of hydronephrosis in infants and young children include pelvic-urethral obstruction and vesicourethral reflux.
Reflex erection--> somatic tactile stimuli to penis Can still happen if a spinal-cord transection occurs cranial to T10/T12.
Sympathetic--> psychogenetic erection Males with cord transections above T9 are unable to achieve psychogenic erections.
Anyone else jump to phenylephrine as a drug that would clear the sinus congestion and also happens to cause constipation? Just me... cool
Was it wrong to see blood tinged sputum, and automatically assume its cancer? since none of the others would have caused blood tinged sputum?
This probably has to do with Barr Bodies (FA 2021, pg 61). To paraphrase FA, penetrance and severity of diseases in XX individuals can be impacted. DMD is included in their list.
Due to its pink staining, I thought B was smooth muscle surrounding the corpus cavernosum. But I suppose that the cells composing the CC are contractile by themselves? And my assumption would make the penis a giant muscle — which it most certainly is not...
Pneumococcal conjugate vaccines are strongly immunogenic in infancy due to both B and T cell recruitment. They provide higher, longer-lasting antibody titers relative to pneumococcal polysaccharide vaccines. The pneumococcal polysaccharide vaccine is poorly immunogenic in infants due to their relatively immature humoral antibody response.
Why is the T normal in this patient? I would have predicted underlying infection — ie, fever — before even "early" septic shock. I selected septic shock purely for the intractable low SVR despite fluids but want to understand more about the absence of fever... Thanks!
The glomerular filtration rate (GFR) depends on the interplay of hydrostatic and oncotic pressures in the glomerular capillaries and Bowman's space. The GFR increases with higher glomerular hydrostatic pressure and decreases with increasing Bowman's capsule hydrostatic pressure or higher glomerular capillary oncotic pressure. Acute ureteral obstruction increases hydrostatic pressure proximal to the constriction. This pressure rise is transmitted back to the Bowman's space, resulting in decreased GFR.
• This patient with alcohol withdrawal most likely developed acute hypokalemia due to stress-related beta-adrenergic hyperactivity, which causes potassium to shift intracellularly. • Severe physiologic stress (eg, myocardial infarction, head injury) results in significant endogenous catecholamine (eg, norepinephrine, epinephrine) release. Epinephrine activates the beta-2 receptor, leading to increased activity of the sodium-potassium ATPase pump and the sodium-potassium-2-chloride cotransporter, both of which transport potassium intracellularly. Adrenergic activity also stimulates the release of insulin, which further promotes intracellular potassium shifting.
just as a general question, would there be low levels of 1 25-(OH)2 ?
I agree that Serum K decrease is the better answer, but wouldn't Urine K also decrease once blood sugar goes down with insulin treatment (i.e. osmotic diuresis would lessen)?