Kid had a viral URI then took aspirn -> Reye syndrome, a hepatic encephalopathy. There is increased ammonia production because of the liver damage, leading to hyperammonemia. This gets to the brain, is ocnverted to glutamine (an osmolyte). This causes the brain swelling.
It's not E) viral encephalitis because it implies the virus is directly causing the encephalitis. Instead, the viral infection -> aspirin -> liver damage -> ammonia -> crosses BBB -> converted to glutamine -> draws in water -> cerebral edema
This is metastatic renal cell carcinoma (FA2020 p605) for the following reasons:
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Niacin( Vit B3)
- inhibits lipolysis ( hormone sensitive lipase ) and hepatic VLDL synthesis /secretion .
Side effects :
Facial flushing , secondary to prostaglandin release . Pre treat with NSAIDS
- Also causes Hypergl;ycemia and Hyperuircemia , as such avoid in Gouty patients and Diabetics
ACUTE alcohol inhibits CYP → Increased bioavailability of acetominophen
CHRONIC alcohol induces CYP → Induction of cytochrome P450 enzymes that activate acetaminophen to a hepatotoxic metabolite
I got this wrong because I assumed chronic alcohol meant years and years. I guess a weekend will suffice?
Honestly, fuck this problem.
I think this is Strongyloides stercoralis (threadworm) is a roundworm whose larvae live in soil and who can cause pulmonary disease. It has the ability to penetrate skin from the soil but can also be obtained by ingesting feces contaminates soil (FA2020 p159) https://www.cdc.gov/parasites/strongyloides/gen_info/faqs.html
Most intestinal roundworms are fecal-oral route except strongyloides which can also penetrate skin, hookworm (necator americanus) which only penetrates skin, and trichinella which can come from undercooked meats (especially pork) but whose symptoms do not match that of the patient. Trichinella larvae enter the blood stream and infect muscle and can also cause trichinosis with fever, nausea, vomiting, periorbital edema, and myalgia.
This question can be answered by a process of elimination approach in my opinion: (FA2020 p638)
This leaves only 47,XXY which is Kleinfelter's syndrome and is associated with testicular atrophy and extensive fibrosis and hyalinization leading to infertility.
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
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.
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(oFmr lwolainwgS kiWi)
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FA 2019, P. 304:
2-7 days following an MI, there can be a papillary muscle rupture, leading to mitral regurgitation. Thus the murmur in the answer, specifically the description of holosystolic and cardiac apex
In eukaryotes, the 5' methylguanosine (m7G) cap is important in the initiation of translation because eukaryotic initiation factors (eIFs) identify the cap and help assemble the ribosome at that site (FA2020 p45).
The absence of a 5' m7G cap would thus require a different sequence to allow translation initiation and ribosomal entry (i.e. an internal ribosomal entry site).
The 5' and 3' untranslated regions are more important in regulation of translation and termination of translation, respectively, and their absence would not aid translation of the viral mRNA. The 3' poly-A tail is important for protection of eukaryotic mRNA from degradation and aiding in exportation from the nucleus; its absence would not aid translation. A very short open reading frame would not make a significant difference in ability to be translated (the open reading frame is the part of the mRNA able to be translated).
You want something that improves her osteoporosis, which is usually weight-bearing exercise. So avoid the swimming one, because that's just decreased gravity. The best answer is walking outside every day that could strengthen her over time.
Flow rate ( Q) = V * A
V- velocity A - cross sectional area
Our velocity is given as 20cm/sec Convert this to cm/min 20cm/sec * 60seconds = 1200cm/min
Plugging in this value into our equation for flow rate we get 1200cm/min * 2 square cm = 2400 cubic cm /min
Note : 1000 cubic cm = 1 L and therefore we can convert our answer to L/min which are the required units by dividing by 1000
= 2.4 L/min
Clomiphene is a SERM that antagonizes estrogen receptors in the hypothalamus.
If estrogen is antagonized there, there is decreased negative feedback to improve FSH and LH release to stimulate ovulation. This is very important in PCOS and other disorders with decreased fertility.
Ugh this question. The Gram stain and purple made me thing Staph aureus, but it also mentions "budding" and "elliptical" (SA is a coccus). Additionally, SA is not a common UTI infection while Candida is.
Annoying because of the Gram stain and purple descriptor.
From quora: "when decolourizer is added, the crystal violet taken up by yeast cells is retained." https://www.quora.com/Why-does-a-yeast-cell-give-Gram-positive-reaction
First order elimination: a constant FRACTION of drug is metabolized per unit time (i.e. elimination rate is proportional to the drug concentration)
This differs from zero order elimination where a constant amount of drug is metabolized per unit time (i.e. rate stays constant)
In this question:
it si cchtrao ierma ootht esaidse as ti si ihdntiere dna hwti oanarbml mleiny tsaheh, toof dpor, rmmeha toe tce.
First, notice that there's a drop in concentration after glyceraldehdye 3-phosphate to 1,3-bisphosphoglycerate. Thus, the conversion is impaired here.
Next, it's somehow remembering which freaking enzyme is involved. Which is glyceraldehyde-3-phosphate dehydrogenase in the glycolytic pathway. This is one where if you know the substrate name you know the enzyme name.
fa 2019 pg 662, Inhalation injury and sequelae. in the inhalation injury and sequelae part they say signed nasal hairs or soot in the oropharynx -> decreased activity of airway cilia as there is soot overlying them and cant function properly tobacco has silica (fa 2019 pg 663) - silica can disrupt phagolysosomes and impair macrophages -> decreased alveolar macrophage function as for the increased mucus production and secretion - idk i figured there is an irritant and your body will be trying to clear it some how, i guess think about COPD
Her calcium is only a little higher than normal (upper limit 10.2) due to the excess vitamin D supplements she took. According to FA '19 (p. 70), activated vitamin D:
-Increases intestinal absorption of calcium and phosphorus --This is what increase her calcium concentration in the serum -Increases bone mineralization (lower levels) -Increases bone resorption (higher levels)
Pink rods is describing a Gram negative bacteria, which has two membranes an outer membrane and an inner membrane (whereas Gram positives have just one thicc membrane).
Both Gram + and - bacteria have an ER, can be inhibited fluoroquinolones (though negatives > positives), both have the peptidoglycan wall (positives thicker than negatives), and either can have polysaccharide capsules.
FA 2020 p. 525.
Ash-leaf spots are pretty pathognomonic for TSC. The subependymal nodules add further support for TSC
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Just wondering if someone could explain the difference between collagen and elastin for this one? I thought either or could be used for tensile strength. Anyone have clarification, don't know why collagen is the best answer!
Did anyone else feel like the question should have been more specific as in saying "just before the consumption of a meal"? As in saying she has high ghrelin = high hunger just before she eats so point B?
Copied from NBME 22 for completeness sake:
"A good pic showing anomalous arteries in horseshoe kidney
Renal papillary necrosis is a common complication of sickle cell disease which would cause gross hematuria (FA2020 p602, p422).
Glomerulonephritis would be associated with RBC casts rather than gross hematuria (casts are present if they are released from the glomerulus or tubules). Nephrolithiasis (kidney stones) are not associated with sickle cell and would likely be associated with crystals of some sort on urinalysis. Prostatitis would likely present with more WBCs and does not commonly present with hematuria but rather urgency and dysuria. Transitional cell carcinoma is rare in the kidney and transitional cell carcinoma of the bladder is associated painless hematuria.
Peutz-Jeghers syndrome is an autosomal dominant syndrome associated with hyperpigmented macules on the mouth, lips, hands, and genetalia as well as increased risk of breast and GI cancers. [FA2020 p387]
This patient presents with the characteristic hyperpigmented macules as well as positive occult blood test which could be indicative of an underlying GI malignancy. Peutz-Jeghers is also associated with numerous hamartomas throughout the GI tract which could be associated with the patient's general GI symptoms due to their ability to cause blockage.
Sildenafil is a PDE5 inhibitor that runs the risk of causing hypotension in patients on nitrates due to the synergy of the mechanisms of action. [FA2020 p246]
Nitrates, like nitroglycerin, work by increasing NO production which in turn acts to increase cGMP in smooth muscle causing vasodilation. PDE5 inhibitors act by decreasing the breakdown of cGMP in smooth muscle, enhancing the action of NO to cause vasodilation. Thus, when combined there can be systemic vasodilation that leads to dangerous hypotension.
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Natural transformation is when bacteria take up naked bacterial chromosomal DNA in their environment (usually from cell lysis). A cell "lysate" is what remains of bacterial genes when the bacteria is dead (can be extracted from bacteria, as shown here). The SHiN bugs all can undergo transformation. You know it is transformation even without knowing which bugs can do so because it doesn't take up the DNA when DNase is added (it kills any free environmental DNA in the lysate)
This is a case of Marfan syndrome. This is a tall kid (6'3", does well on Tinder). Leads to a FBN1 gene mutation, affecting fibrillin protein.
The blood:gas partition coefficient is the ratio of concentration of anesthetic in the blood vs. in the lungs when a steady state is reached. Blood/gas partition coefficient is an expression of solubility of the drug in plasma, and less soluble agents have a faster onset/offset.
MAC (minimum alveolar concentration) is the concentration of anesthetic in the lungs where 50% of the population does not move in response to a surgical srtandard stimulus. It is analogous to ED50 in other areas of pharmacology. MAC is increased with decreasing solubility (decreaseing blood/gas partition coefficients) and decreased potency. If you think about it this would make sense because if a drug is less soluble or not as potent, you have to administer more of the drug and thus would have to have a higher minimal alveolar concentration to see an effect. [FA2020 p549]
NOTE: MAC is additive so if you mix two gases at 0.75% of their MACs, you get a total 1.5% MAC. Thus for the question, you are essentially administering the same TOTAL MAC to each group, so it is not the difference in MAC that is causing the difference observed.
The brain:gas partition coefficient, more commonly called the oil:gas partition coefficient, is used as a surrogate for the amount of anesthetic in the brain and corresponds to lipid solubility. CNS drugs must be lipid soluble or actively transported. As these are inhlaed anesthetics, the lipid solubility actually does not greatly contribute to time of onset/offset; instead the plasma solubility is the limiting factor. Oil/gas partition coefficient would be associated with the drug potency.
Neural crest cells migrate to form the aorticopulmonary septum and abnormalities associated with neural crest migration in the heart include tetrology of fallot, transposition of the great arteries, and persistent truncus arteriosus. Fusion of the aorticopulmonary septum with the muscular ventricular septum is what forms the membranous septum, so patients with a persistent truncus arteriosus will have VSD as well. (FA2020 p280)
Fatty Acid degradation
-Occurs in mitochondria or peroxisomes
First step - uptake of the fatty acids by the cell and addition of CoA to them
Second step - Uptake of the Fatty Acyl CoA molecule into the mitochondria by the Carnitine Shuttle *( which involves removal and then addition of the CoA molecule again to the fatty acid once inside the mitochondria)
Once in the mitochondria the fatty acid may undergo , Beta-oxidation ( a process in which a fatty acid is oxidized/cleaved at the Beta carbon to generate Acetyl CoA in several cycles )
An Acyl CoA dehydrogenase catalyzes the initial step
Look out for Hypoketotic Hypoglycemia in defects of fatty acid degradation
The 2 main subtypes to be aware of are -a problem with the carnitine shuttle ( systemic carnitine deficiency) - or with an Acyl CoA dehydrogenase ( eg MCAD deficiency )
Impaired reabsorption of Bicarbonate and other compounds in the Proximal convoluted Tubules ( eg amino acids , glucose phosphate )
Clinical Features : Vitamin D resistant Hypophosphatemic Rickets/osteomalacia
Fanconi syndrome presents with proximal Renal Tubular Acidosis ( normal anion gap metabolic acidosis )
IV normal saline will increase hydrostatic pressure in the vasculature. This isotonic solution is freely filtered across the capillaries, which is collected by lymphatics and can be picked up in this experiment.
Morphine stimulates mu opioid receptors to provide the desired effect of analgesia, but in doing so can also precipitate many undesired effects. This patient has multiple signs of opioid toxicity, including miosis (ie, pinpoint pupils), respiratory depression (evidenced by slow respiratory rate and respiratory acidosis), and CNS depression (eg, somnolence, coma). Morphine is primarily metabolized by the liver via glucuronidation to form 2 major metabolites. These metabolites, morphine-3-glucoronide and morphine-6-glucoronide, then undergo renal elimination via excretion in the urine. Because the metabolites are metabolically active, renal dysfunction can lead to metabolite accumulation and opioid toxicity. Morphine-6-glucoronide is particularly responsible for toxicity, acting as a more potent mu opioid receptor agonist than morphine itself.
Due to its metabolically active and renally cleared metabolites, morphine requires careful monitoring when used in patients with renal dysfunction. When opioid pain control is needed in such patients, fentanyl or hydromorphone is often preferred as these drugs are predominantly hepatically cleared.
The two sections of the nephron most susceptible to hypoxic conditions are the 1) proximal convoluted tubule and the 2) mTAL (medullary section of the thick ascending loop of Henle)
The stem is describing bullous pemphigoid, which produces IgG antibodies hemidesmosomes. (PV is IgG antibodies aginst desmoglein-1 and desmoglein-3, in the oral mucosa).
BP produces the tense blisters that have a negative Nikolsky sign (don't rupture with rubbing). This is because they're supepidermal. Surprised they didn't ask about hemidesmosomes, but I think that that the BP antigen is part of the hemidesmosomes and recruits the autoantibodies.
The answer is reassurance because this is all normal behavior. She's only snored TWICE in the past year w/ no daytime sleepiness or other problems.
It wouldn't be a sleep journal because it could imply that something is wrong, but there isn't. She's 27 and if anything she should upgrade from her husband complaining about nothing important.
IgG antibodies can cross the placenta, leading to thyroid enlargement. This can also explain the stridor and issues with respiration in the newborn. Essentially, this is causing neonatal Graves disease.
From UpToDate: "Neonatal Graves disease refers to the hyperthyroidism that is seen in a small percentage of infants born to mothers with Graves disease. Although neonatal Graves disease is usually self-limited, it can be severe, even life-threatening, and have deleterious effects on neural development"
Good explanation on reddit: https://www.reddit.com/r/step1/comments/d8aqj5/spoiler_nbme_16_hey_can_anybody_advice_how_to_get/
Essentially, A = mucinous glands (foamy cytoplasm) B = parietal cells (stain eosinophilc, P ar I etal cells stain PInk w/ a fried egg appearance. Additionally, they're above chief cells C = chief cells (stain basophilic, super dark, and below parietal cells)
Li Fraumeni syndrome is associated with a loss of function mutation in p53 (FA2020 p224, p46)
p53 is a modulator at the G1/S restriction point. p53 activation in the presence of DNA damage, misfolded protein, and hypoxia leads to activation of BAK/BAX and subsequent activation of the apoptotic pathway (p208). Thus, loss of function of p53 will lead to impaired regulation of apoptosis and uninhibited cell division in cancer cells.
Li Fraumeni syndrome is associated with multiple tumors at a young age (SBLA - sarcoma, breast, leukemia, adrenal)
This is goodpasture syndrome which has antibodies directed against alveolar and glomerular basement membranes (FA2020 p596)
The key hints are:
A continuous, machine-like murmur is characteristic of a patent ductus arteriosus (FA2020 p291, p298)
The patency of the ductus arteriosus is maintained by prostaglandins (hence why newborns who need to keep a patent ductus arteriosus due to other heart defects are put on prostaglandin drips).
In this newborn's case, the patent ductus arteriosus is not necessary (there are no signs of additional heart defect that would necessiate it) and thus we want to close it.
To close a PDA, we would want to inhibit prostaglandins somehow, and cyclooxygenase inhibitors (NSAIDs) inhibit the production of prostaglandins and thus would speed up closure of the ductus arteriosus. IV indomethacin or ibuprofen are most commonly used to close the PDA.
Though inhibition of phospholipase A2 by corticosteroids would also serve to inhibit production of prostaglandins, this is more nonspecific and could be associated with more unwanted side effects. Coritcosteroids in a newborn are more often used for neonatal respiratory distress syndrome to elicit production of surfactant.