This is an abdominal aortic aneurysm which ruptured, evidenced by: hypotension, pulsatile abdominal mass, the guarding and rigidity in the periumbilical region. (Pathoma page 70, FA 2018 page 298) Additional findings would include decreased femoral pulses.
A- Patient is hypotensive/hypovolemic, you probably won't see normal ankle, and brachial indices.
B - Aortic regurgitation is seen in thoracic aortic aneurysms secondary to syphilis, or cystic medial degeneration in marfans/ehler's danlos. Could also be due to aortic root dilatation from aortic dissection.
C/D - both are seen classically in aortic dissection.
Always be kind! Spending a few extra minutes will make him feel better, solidify your relationship, and not really waste too much of your time. She passed away on this same day, he must be very sad and having someone to talk to can change everything.
AR disease. She's got all the symptoms, she must have both defective genes. Genetic testing for the 36 most common mutations shows a detectable mutation (G551D) in one allele of the CFTR gene. What about the 2nd gene... we KNOW she has the disease. It wasn't detected.
Patient had Cushing disease. Basically had to work out what high cortisol does. All 5 options had 1 thing that was wrong, and 1 that right.
(A) Hyperkalemia and numerous bruises
(B) Hypertension and muscle weakness
(C) Hypocalcemia and hyperglycemia
(D) Hypoglycemia and fat pads between the scapulae
(E) Jaundice and thinning of the skin
D was wrong because it causes hyperglycaemia. E was wrong becasue there's no jaundice associated with high cortisol. Opted to not go for A or B, as I wasn't sure about the electrolyte issues related with cortisol.
Patient had ALS. Combination of UMNL + LMNL --> only answer option that had anything to do with these was atrophy (LMNL). Also, remember that their MCC of death is due to respiratory/ diphragmatic failure!
Alpha (I Error) -- Confidence Interval
Beta (II Error) -- Power
Values have an inverse relationship with each other
"pink, soft, granular, edematous wound" describes granulation tissue, which appears around day 3 and last several weeks. At this time, there is also an abundance of fibroblasts, endothelial cells (which contribute to angiogenesis with up regulation of VEGF) and macrophages as well as keratinocytes.
The infraorbital nerve is a major branch and is the termination of V2. Fractures at the infraorbital region can damage the inferior rectus and the V2 branch, which supplies sensation beneath the eye and till the upper lip.
Next time your attending asks you your top differential for a 2nd trimester pregnant female coming in with severe acute bleeding, say "cervical cancer" and when they question you, flash this question at them as the source. Ah, NBME really prepares us for the real world.
History and image are a type 4 HSR. This is T cell induced. Cd40L --> Cd40 is T cell --> B cell CD28 (on T cell) --> binds to APC's (including Langerhans cells); CD80/ 86/ B7
Options with ICAM, I immediately crossed out because they're associated with margination and rolling, etc. CD45 isn't mentioned in regards to T cells (or anywhere I might add). Leaving us with the 2 options I mentioned above ^
FA 2020 pg 399
misoprostol clinical use - prevention of NSAID induced peptic ulcers
MOA: PGE1 analog in effect causes decrease acid production and increase secretion of gastric mucous barrier.
FA 2020 ,pg 195 Metronidazole MECHANISM Forms toxic free radical metabolites in the bacterial cell that damage DNA. Bactericidal, antiprotozoal.
pg 251 Disulfiram-like reaction 1st-generation Sulfonylureas, Procarbazine,certain Cephalosporins, Griseofulvin, Metronidazole
acetaldehyde accumulates in disulfiram as acetaldehyde dehydrogenase is blocked
PG 353 Biguanides Metformin ADVERSE effect GI upset, lactic acidosis (use with caution in renal insufficiency) clue "sx began after drinking champagne -an alcohol"
pg 610 lisinopril adverse effects: Cough, Angioedema (both due to bradykinin; contraindicated in C1 esterase inhibitor deficiency), Teratogen (fetal renal malformations), increase Creatinine (dec. GFR), Hyperkalemia, and Hypotension. good thing HCTZ is not on the option pg 609 hydrochlorothiazide adverse effects: Hypokalemic metabolic alkalosis- can have nausea and vomiting, hyponatremia, hyperGlycemia, hyperLipidemia, hyperUricemia, hyperCalcemia. Sulfa allergy
FA 2020 PG 258
Absolute risk reduction BY DEFINITION : The difference in risk (not the proportion) attributable to the intervention as compared to a control.
ARR = (c/c + d ) - ( a/ a + b )
I assumed c+d as 50 for azithromycin and a+b as 50 for erythromycin
= 15/50- 5/50 = .3 -.1 = .2
in FA the example is If 8% of people who receive a placebo vaccine develop the flu vs 2% of people who receive a flu vaccine, then ARR = 8%–2% = 6% = 0.06.
why is the MCV elevated in this question when it's supposed to be normocytic non hemolytic aplastic anemia?
this is a great example of why I struggle with this silly nbme and steps. Are we testing knowledge here or semantics?
Overthinking screwed me. The question stem asks for a chance for a sister to get the same alleles, not that she is homozygous with them. So I picked 75% instead of 25%. At the top of it, they put 2D6*4(I thought that means that pt. has 4 copies of alleles(two from each parent like HLA). They have to make questions impossible to understand.
FA 2020 PG 212 Common in normal aging increase risk of atrial fibrillation where there's possible Isolated atrial amyloidosis where ANP is fibril protein --)
pg 511 FA 2020
DORSAL Midbrain lesion consequence: Parinaud syndrome—vertical gaze palsy, pupillary light-near dissociation, lid retraction, convergence-retraction nystagmus
seen in Stroke, hydrocephalus, pinealoma --- present in patient
The patient has UTI secondary to E. coli. The organism is resistant to ampicillin and sensitive to cephalosporins. I think alot of people are confused over why penicillin binding protein alteration wasn't the correct answer so here is my take:
Ampicillin - Penicillin antibiotic, with a beta lactam ring.
Mechanisms of resistance - Penicillinase (Beta lactamase which cleaves the beta lactam ring of penicillin drugs making them ineffective) OR PBP alteration (penicillin binding protein alteration).
Ceftriaxone - third generation Cephalosporin. Mechanisms of resistance - CEPHALOSPORINASE (Another type of beta lactamase), OR PBP alteration.
The question asks, which mechanism of resistance does the organism produce that causes ampicillin to be inactivated BUT ceftriaxone to be resistant.
It's the TYPE of beta lactamase produced by the two drugs that are different. so Beta lactamase production against Ampicillin (Penicillinase) would inactivate Ampicillin but NOT Ceftriaxone (cephalospoirinase).
If the mechanism of resistance were penicillin binding protein alteration, BOTH drugs would be resistant, because that mechanism of resistance is SHARED by both drugs.
It's a shitty question, which is nitpicky and goes after a pretty dumb detail.