to snoo-finity ... and beyond!
to snoo-finity ... and beyond!
What's the echymoses supposed to be a clue about? Does this patient have DIC? Does DIC always cause hypovolemic shock?
Please help - how are you able to tell that the CT image is not at the level of duodenum?
I don't know what I'm looking for to compare and contrast a CT at the level of the duodenum vs the CT given in this Q.
Spironolactone and eplerenone are potassium-sparing diurectics that inhibit the Na/K ATPase. Na/K ATPase is on the basolateral membrane. None of the answer choices fit with this.
Amiloride and triamterene are also potassium-sparing diuretics. The mechanism is to block ENaC channels on the luminal membrane, this is choice "B."
Patient has a hemithorax + CXR shows trachea deviates towards the hemithorax --> most likely diagnosis is spontaneous pneumothorax.
Epidemiologically, spontaneous pneumothorax is most associated with thin males
please help -- If catalase-positive bacteria neutralize their own superoxide, why isn't it the case for catalase-positive bacteria to infections in everyone?
I'm not understanding the connection to NADPH oxidase deficiency.
For people asking why the data table was even included if it was not needed to answer this Q, here is a useful explanation:
The table was given because a 2x2 table is typically what you do see regarding data for case-control studies.
If the 2x2 table wasn't included, then literally everytone would pick Choice "E" as the correct answer b/c you can't calculate something without being provided numbers.
The difference in including the data-table is that:
and
Patient has red lacy rash- this fits more with HHV-6 (Roseola virus), not Parvovirus.
HHV-6 causes deformation of erythoblasts, leading to anemia.
Patient cannnot extend wrist, which is innervated by radial nerve
Patient has been on crutches, which would affect axillary nerve --> this affects deltoid muscle, which does arm abduction 15-100º (so it can normally move arm above shoulder)
The only location in the given diagram to effect all of these nerves would be location "C"
Note: normally, arm movement above the horizontal is associated with serratus anterior muscle/long thoracic nerve. However, none of the diagram locations allow for inclusion of SALT. Since the patient has been on crutches for weeks, it suggests axillary nerve involvement --> deltoid is affected
The patient is dehydrated. Need to give water to rehydrate.
Water follows solute. If sodium is added to the solution, water will follow the sodium. Now, enterocyte uptake of sodium is mediated by Sodium-Glucose transporter. Hence, the solution needs to contain sodium and glucose in order to have the enterocytes take up the sodium.
The Q is describing the genitofemoral nerve, which runs on the external surface of the spermatic cord at the superficial inguinal ring
This Q is NOT referring to ilioinguinal nerve -- the ilioinguinal nerve exits THROUGH the superficial inguinal canal whereas this Q is asking about a nerve that is EXTERNAL to the superficial inguinal canal.
See http://www.groinpainclinic.co.uk/data/images/nervesaffected.jpg
This the same as @keycompany's explanation with more explanation those that need it...
The patient is unaffected by the particular autosomal recessive disease and his brother has the autosomal recessive disease --> this means each of their parents carries the AR allele. Now, for the patient to be unaffected given that both his parents have the AR allele, it means that the patient has a 2/3 chance that he is simultaneously unaffected and a carrier.
The patient's partner is unaffected and normal Hardy-Weinberg genetics (as stated in the problem)..when this is specifically mentioned, you are to assume that the partner has a carrier frequency for the AR allele, which equal to 2pq.
The disease has a frequency in the population of 1/40000. This is q^2 --> q^2 = 1/40000. Solving for q, you get q = 1/200.
Carrier frequency is 2pq. However, for a rare disease, 2pq ≈ 2q. So, the carrier frequency for the partner = 2q = 2 * 1/200 = 1/100.
Now, the Q asks about an offspring of the patient and his partner being affected, so to have an affected child, there is a 1/4 chance of having an affected child (becasuse the patient and the partner both have a 1/2 chance of passing the allele --> you multiple these together 1/2 * 1/2).
So, multiply 2/3 * 1/100 * 1/4 = 1/600. This is P(patient being a carrier) * P(partner being a carrier) * P(having an affected offspring together).
The grammar of the actual Q was confusing.
To make better sense, it should say "Which of the following is the most likely result on the transcription of genes that inhibit cell division and that contain the consensus sequeence TATA..."
So, the Q is asking about the tp53 gene and specifically about the tp53 gene promoter region.
Promoter regions have a TATA box (obviously, meaning rich in A-T base pairs). A-T base pairing has 2 hydrogen bonds, which makes them easier to cleave --> allows for DNA transcription to occur more easily. RNA Pol does transcription of DNA into RNA.
The entire Q-stem talks about how Li-Fraumeni is due to a mutation in tp53 gene, leading to a lack of tumor suppression activity.
So, if the promoter region TATA box of the tp53 gene is mutated, then the tp53 gene will not get transcribed --> this is why there will be decreased RNA Pol binding. RNA Pol will have a reduced ability to bind tp53 --> less tumor supressor gene transcription --> less tumor suppression.
I want to re-emphasize something that @assoplasty has already stated :).
The Q-stem states serum glucose = 100, and the Q asks why the patient is able to maintain normoglycemia.
Therefore, you can immediately eliminate choices A and C because acetoacetate and beta-hydroxybutyrate are sources of energy during ketogenesis -- ketogenesis does not provide glucose energy sources.
Please help
Why is valine incorrect?
An explanation below says that valine would be converted to glucose during regular metabolism?
Regular metabolism = fed state, so why would valine even be converted to glucose?
This is the actual correct explanation:
PDA causes blood to flow from descending aorta to patent ductus arteriosus into pulmonary circulation ("right-to-left")
The "steal" from the aorta during diastole requires increased cardiac output to compensate to deliver adequate amount of blood to rest of body
Please help
Mid-systolic ejection click = pulmonic stenosis
How is pulmonic stenosis related to the patient's ASD -- does ASD cause pulmonic stenosis??
For anyone confused trying to follow @usmleuser007's comment
Slightly modified
Essential amino acids mnemonic "Ah, Three fans will try meth"the
Ah = arginine, histidine
Three = Threonine
Fans (phans)= Phenylalanine
Vill (will -- German accent pronouncing English word "will") = valine, isoleucine, leucine, lysine
Try = tryptophan
Meth = Methionine
Multiple myeloma = neoplasm of plasma cells.
Plasma cells produce secretory Ab's (aka produce Ab's) -- plasma cells do not have membrane-bound Ig (aka do not have BCR').
To recap: membrane-bound Ig = BCR while secretory Ig = Ab.
Now, anti-idiotypic antibody = antibody against antibody.
Plasma cells do not contain surface Ig -- because plasma cells only be secrete Ab's.
Therefore, anti-idiotypic antibody would not work to target myeloma cells because myeloma cells = plasma cells aka plasma cells lack surface molecules that anti-idiotypic Ab's would need to bind to/target.
See diagram: https://qph.fs.quoracdn.net/main-qimg-ae42c5c9f839fc58a3ce10feaf14c02b
The Q stem states FOXO is a transcription factor that responds to insulin signaling by altering the transcription of metabolic genes --> therefore, FOXO is a transcription factor involved in metabolism. This should make sense because insulin-receptor activation has a role in regulating metabolism.
This Q asks about reversible ways that insulin reguates FOXO transcrption factor activity.
Ubiquitin-mediated proteolysis is irreversible. Eliminate all choices except for B, D, and H.
Insulin-receptors function through PI3K signaling. PI3K signaling involves phosphorylation of serine --> serine phosphorylation is a reversible process. Eliminate H. FYI: protein/amino acid phosphorylation is always reversible.
You are left with choices B and D.
FOXO is a transcription factor --> transcription factors mediate gene activity by shuttling between the cytoplasm and nucleus. Regulating the location of FOXO transcription factor (i.e. cytoplasm vs. nucleus) will therefore reversibly modulate FOXO-mediated metabolic gene activity.
This leaves you with the correct answer: Choice B.
q^2 = 1/900 --> q = 1/30
Carrier frequency per Hardy-Weinberg formula is 2pq.
Now, for rare autosomal recessive diseases the carrier frequency of 2pq ≈ 2q.
2q = 2(1/30) = 2/30 = 1/15
Answer = 1/15
The patient has "cells arranged in infiltrating sheets" --> indicates malignant cancer cells.
The cells are neither glandular nor squamous --> the cancer is neither adenocarcinoma nor squamous cell lung cancer, respectively.
This leaves small oat cell lung cancer. SIADH is the most common paraneoplastic syndrome for small oat cell lung cancer --> leads to hyponatremia.
Knowing the LR+ value = 10 does not help to solve this Q because estimating where "10" should fall on an axis is arbitrary. Also, the data points are coordinates -- they have an X-value and a Y-value (X, Y).
The way to approach this Q is to know that a high specificity means that a positive result is very, very likely to be a true positive.
Suppose that the specificity is 0.99 -- this is 99% specificity. Then, you look at the graph. The X-axis is "1-specificity." So, suppose the best test has a specificity of 99%. Then, calculate 1-specificity = 1 - 0.99 = 0.10. You would then chose the datapoint that corresponds to having an "X-value" that is closest to the origin. In this problem, it corresponds to data point "A."
You don't even need to know a specific specificity value to solve this problem. All you need to do is understand that if the specificity is extremely high, you will need to find a datapoint that is closest to the origin -- at least for the value in the X-axis in the coordinate of the data point -- because the X-axis corresponds to a calculation of "1-specificity".
Goljan had a lecture that mentioned that "If a patient has galactorrhea, review every drug they're taking since many drugs cause galactorrhea."
The only thing of possible relevance in this Q-stem is that she takes a medication, therefore the answer of "drug effect" is the most likely reason for her galactorrhea.
Guyon Canal Syndrome is due to an Ulnar Nerve lesions and is associated with bicycle handlebar use.
Also FINGER abduction and adduction is mediated by ulnar nerve. The patient is having trouble with FINGER abduction and adduction.
The Froment sign is testing ADDUCTOR POLICIS ACTIVITY, which is mediated by the ULNAR NERVE activity. It is NOT testing thumb opposition, which would be mediated by the median nerve.
The reason "do not prescribe antibiotics until testing results are available" is incorrect is because we already have a gram stain that shows gram-negative diplococci in pairs. This is Neisseria gonorrhoeae. So, no need to wait for test results come back.
The Q-stem stating that "Testing for Neisseria and Chlamydia" is ordered" after already having done the Gram stain seems to be a distractor.
Patient's symptoms began 30 min after mowing lawn (i.e. after doing physical activity). He has severe chest pain and is cool, clammy, diaphoretic. He has increased pulmonary artery pressure and increased left atrial pressure. Taken altogether, this is cardiogenic shock.
Cardiogenic shock is a heart pump problem -- the LV isn't working.
When the LV, isn't working, it causes a back up in the direction opposite to how blood normally flows. Therefore, blood will back up in the lungs.
This causes increased capillary hydrostatic pressure --> this drives more fluid into the interstitium --> this causes increased interstitial hydrostatic pressure --> there is now more fluid than normal in the interstitium --> this affects the protein ratio within the interstitum --> this causes decreased interstitial oncotic pressure.
Patient in hypovolemic shock - the clues are low BP and COOL skin. Hypovolemic shock is caused by fluid loss.
The patient has decreased preload b/c of fluid loss, i.e. there is decreased blood volume returning to heart --> thus decreased preload.
Spleen is enlarged. Compare it to CT scan showing normal-sized spleen:
http://www.startradiology.com/uploads/scroll/18/14hiu6b3qot5.jpg
Murmurs and maneuvers: 1st thought = how does it change with preload. All murmurs except HOCM, MVP, and atrial myxoma severity is directly proportional to change in preload (i.e. increased preload=worse murmur, etc.). Because of this, DDx can be narrowed down to HOCM, MVP, and atrial myxoma right away because the murmur worsened with decreased preload (i.e. standing up) when all but exceptions with improve.
Atrial myxoma = MCC primary cardiac tumor due to proliferation of connective tissue mesenchyme; a pedunculated mass connected via stalk to atrium septum that is suspended in the atrial blood volume and moves with the volume movement.
Presentation: triad of 1) mitral valve obstruction (i.e. malaise, symptoms of cardiac failure, syncope, etc.), 2) symptoms of embolism (i.e. facial and right arm hemiparesis in patient), and 3) constitutional symptoms (i.e. fever, weight loss, symptoms resembling connective tissue disease, because tumor releases IL-6). Others include neurologic symptoms, "pseudo-mitral valve disease" auscultatory findings (i.e. diastolic murmur), and atrial enlargement (which could compress underlying structures and cause symptoms also).
Not only does standing decrease preload, which means LA volume is lower so mass isn't as "suspended" but more mobile, standing also increases the downward gravitation force, which would contribute to the tumor moving towards the base of the atrial chamber, "plopping" on the mitral valve leaflets, and potentially extending through and causing a functional type of mitral stenosis (i.e. worsening diastolic murmur). This video explains it really well: https://www.youtube.com/watch?v=slIY64nViLg&t=161s
Murmurs and maneuvers: 1st thought = how does it change with preload. All murmurs except HOCM, MVP, and atrial myxoma severity is directly proportional to change in preload (i.e. increased preload=worse murmur, etc.). Because of this, DDx can be narrowed down to HOCM, MVP, and atrial myxoma right away because the murmur worsened with decreased preload (i.e. standing up) when all but exceptions with improve.
Atrial myxoma = MCC primary cardiac tumor due to proliferation of connective tissue mesenchyme; a pedunculated mass connected via stalk to atrium septum that is suspended in the atrial blood volume and moves with the volume movement.
Presentation: triad of 1) mitral valve obstruction (i.e. malaise, symptoms of cardiac failure, syncope, etc.), 2) symptoms of embolism (i.e. facial and right arm hemiparesis in patient), and 3) constitutional symptoms (i.e. fever, weight loss, symptoms resembling connective tissue disease, because tumor releases IL-6). Others include neurologic symptoms, "pseudo-mitral valve disease" auscultatory findings (i.e. diastolic murmur), and atrial enlargement (which could compress underlying structures and cause symptoms also).
Not only does standing decrease preload, which means LA volume is lower so mass isn't as "suspended" but more mobile, standing also increases the downward gravitation force, which would contribute to the tumor moving towards the base of the atrial chamber, "plopping" on the mitral valve leaflets, and potentially extending through and causing a functional type of mitral stenosis (i.e. worsening diastolic murmur). This video explains it really well: https://www.youtube.com/watch?v=slIY64nViLg&t=161s
A very similar question I have seen in Qbanks will ask why a patient with right heart failure does not develop edema and the answer is increased lymphatic drainage. I got this question wrong originally because I answered along this line of reasoning but I think in this case it all has to do with WHERE the extra pressure is coming from. In this question the pt has diastolic hypertension so you can think about the pressure as coming "forward" so constricting precapillary sphincters can prevent an increase in pressure in the capillary bed. However for right heart failure this extra fluid is coming from the OPPOSITE direction (backwards from the right heart) and constricting precapillary sphincters can do nothing (on opposite side of capillary bed) - the only way to prevent edema is to increase lymphatic drainage.
A very similar question I have seen in Qbanks will ask why a patient with right heart failure does not develop edema and the answer is increased lymphatic drainage. I got this question wrong originally because I answered along this line of reasoning but I think in this case it all has to do with WHERE the extra pressure is coming from. In this question the pt has diastolic hypertension so you can think about the pressure as coming "forward" so constricting precapillary sphincters can prevent an increase in pressure in the capillary bed. However for right heart failure this extra fluid is coming from the OPPOSITE direction (backwards from the right heart) and constricting precapillary sphincters can do nothing (on opposite side of capillary bed) - the only way to prevent edema is to increase lymphatic drainage.
What a terrible picture. They they covered up part of it with lines. WTF
Epinephrine is the only G coupled receptor activator the list. The rest are either inter-cellular or a tyrosine kinase (insulin).
all the others a noncompetitive since they have specificity(specific ligands), NMDA is the only nonselective(hence competitive receptor), has a ligand site and ca , na and mg...hence competitive
Please help
Mid-systolic ejection click = pulmonic stenosis
How is pulmonic stenosis related to the patient's ASD -- does ASD cause pulmonic stenosis??
The hallmark of ITP is isolated thrombocytopenia.
Dec. NaCl - general volume loss Dec. K+ - Diuretic (most diuretics, except K+ sparing ones, cause hypoK+) Inc. HCO3-& pH - Volume loss -> RAAS -> aldosterone causes K+ & H+ wasting -> metabolic alkalosis; She may be vomiting as well, which is another possible cause of met. alk. Inc PaCO2 - respiratory compensation for met. alk.
Dec. NaCl - general volume loss Dec. K+ - Diuretic (most diuretics, except K+ sparing ones, cause hypoK+) Inc. HCO3-& pH - Volume loss -> RAAS -> aldosterone causes K+ & H+ wasting -> metabolic alkalosis; She may be vomiting as well, which is another possible cause of met. alk. Inc PaCO2 - respiratory compensation for met. alk.
Dec. NaCl - general volume loss Dec. K+ - Diuretic (most diuretics, except K+ sparing ones, cause hypoK+) Inc. HCO3-& pH - Volume loss -> RAAS -> aldosterone causes K+ & H+ wasting -> metabolic alkalosis; She may be vomiting as well, which is another possible cause of met. alk. Inc PaCO2 - respiratory compensation for met. alk.
This more likely to be diuretics rather than laxatives b/c
the lab study shows a renal dysfunction (BUN & Creatinine are elevated)
Most likely the patient abused loop diuretics; also knows to cause contraction alkaloids, along with renal problems such as interstitial nephritis
I got that it needed to be a potassium sparing diuretic. Is there a reason it cannot be an aldosterone antagonist? I chose blocks basolateral K+ channels as these decrease the basolateral K+/Na+/ATPase because the wording of the correct answer did not make sense to me -- assuming they were going for an ENaC blocker (and that decreased luminal permeability indicates that Na+ would be remaining in the lumen, not remaining in the principal cell as I originally thought).
If you need a different orientation for a diagram of the pathways:
Nice schematic of how horizontal gaze is coordinated through the abducens/MLF/oculomotor pathway:
https://n.neurology.org/content/neurology/70/17/e57/F1.large.jpg
In the diagram, the system is coordinating gaze toward pt’s left, which (conveniently) is the same as in the stem.
Source article: https://n.neurology.org/content/70/17/e57
Nice schematic of how horizontal gaze is coordinated through the abducens/MLF/oculomotor pathway:
https://n.neurology.org/content/neurology/70/17/e57/F1.large.jpg
In the diagram, the system is coordinating gaze toward pt’s left, which (conveniently) is the same as in the stem.
Source article: https://n.neurology.org/content/70/17/e57
Patient has a hemithorax + CXR shows trachea deviates towards the hemithorax --> most likely diagnosis is spontaneous pneumothorax.
Epidemiologically, spontaneous pneumothorax is most associated with thin males
Patient has a hemithorax + CXR shows trachea deviates towards the hemithorax --> most likely diagnosis is spontaneous pneumothorax.
Epidemiologically, spontaneous pneumothorax is most associated with thin males
please help -- If catalase-positive bacteria neutralize their own superoxide, why isn't it the case for catalase-positive bacteria to infections in everyone?
I'm not understanding the connection to NADPH oxidase deficiency.
hydrocholorothiazide is DOC for Nephrogenic Diabetes insipidus because it paradoxically causes an increase in BP by increasing sodium absorption and thus water absorption, Pathoma explains this nicely.
Desmopressin is incorrect because upon fasting (fluid restriction) ADH is increased meaning ADH is being released Centrally but is not working in the kidneys at the V2 receptors of the epithelial renal cells at Collecting duct.
On that note, Amiloride is used for Lithium induced nephrogenic DI.
Isn't it dependent on the location? I answered it coronary sinus because av node is located in Koch triangle; which composed of CSinus, Tendon of Todaro, Tricuspid annulus?
Flow Rate = Velocity x Cross-Sectional Area
2 cm^2 x 20 cm/sec x 60 sec/min x 1 L/1,000 cm^3 = 2.4 L/min
1,000 cm^3 = 1 L
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5290806/
Osler Sign is a low-sensitivity, low-specficity finding of Mockenberg Arteriolosclerosis (MA) characterized by "a palpable although pulseless, radial artery while the BP cuff is inflated above systolic pressure".
It is possible that either: a) The low-specificity of this test means it is also applicable to atherosclerosis (not just MA) b) The NBME incorrectly implies that MA is interchangable with atherosclerosis.
For people asking why the data table was even included if it was not needed to answer this Q, here is a useful explanation:
The table was given because a 2x2 table is typically what you do see regarding data for case-control studies.
If the 2x2 table wasn't included, then literally everytone would pick Choice "E" as the correct answer b/c you can't calculate something without being provided numbers.
The difference in including the data-table is that:
and
Why wasn’t the table enough to determine prevalence in the general population?
This one was a little tricky. For this one the key is the low radioiodine uptake. This patient has high T4 and low TSH which makes sense in a hyperthyroid patient, perhaps your first thought is that this patient has Grave’s disease. However, in Grave’s your thyroid is being stimulated to make more thyroid hormone from scratch and as such would have an increased radioiodine uptake because the thyroid is bringing in the required (now radiolabeled) iodine. This is why it is not Graves (“release of thyroid hormone from a thyroid stimulated by antibodies”).
So if its not Grave’s what could it be? For this you’d have to know that Hashimoto’s Thyroiditis (also known as Chronic Lymphocytic Thyroiditis and is often referred to as such on board exams to throw you off) has three phases - first they are hyperthyroid, then euthyroid, then the classic hypothyroid that you would expect with low T4 and high TSH. This was the key to this question. The reason for this is that antithyroid peroxidase antibodies in Hashimoto’s cause the thyroid to release all of its stored thyroid hormone making the patient hyperthyroid for a short period of time. After this massive release of thyroid hormone, the antibodies make them unable to make new TH and therefore they become euthyroid for a short period and then hypothyroid which you would expect! Since they can’t make new TH, the thyroid will not take up the radioiodine and therefore there will be low radioiodine uptake. Hence, “release of stored thyroid hormone from a thyroid gland infiltrated by lymphocytes.” aka “Lymphocytic (hashimotos) thyroiditis”.
I think “release of thyroid hormone from a lymphomatous thyroid gland” is referring to some kind of thyroid cancer in which case you would expect them to be describing a nodule on radioiodine uptake.
Summary video here and also a great site in general: https://onlinemeded.org/spa/endocrine/thyroid/acquire
Can someone explain how to rule out the other answer choicers?
Can someone please explain why it would not be glycogen depletion? I thought the question was talking about the Warburg phenomenon... so why not breakdown of glycogen to glucose?
I guess it would not explain the edema?
I think this picture explains it well:
http://www.groinpainclinic.co.uk/data/images/nervesaffected.jpg
Mandelian Genetics:
Man has 2/3 chance of being a carrier. (He does not have the disease). Woman carrier risk must be calculated with p^2 + 2pq + q^2. q^2 = 1/40,000 q = 1/200, p is roughly = 1 2pq = 1/100 = Carrier frequency .
Risk of having a child thus equals 2/3 x 1/100 x 1/4 = 1/600 Because: 2/3 = Man Carrier risk 1/100 = Female Carrier Risk 1/4 = Chance they each pass on the recessive gene to their offspring.
Isn't it dependent on the location? I answered it coronary sinus because av node is located in Koch triangle; which composed of CSinus, Tendon of Todaro, Tricuspid annulus?
Please help
Mid-systolic ejection click = pulmonic stenosis
How is pulmonic stenosis related to the patient's ASD -- does ASD cause pulmonic stenosis??
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.
Any idea why hyperchloremia isn't an answer? The diarrhea would cause an normal anion gap (hyperchloremic) metabolic acidosis.
Any idea why hyperchloremia isn't an answer? The diarrhea would cause an normal anion gap (hyperchloremic) metabolic acidosis.
Per google symptoms of hypochloremia and hyponatremia are very similar; however, hyponatremia includes seizures and spasms. But per my quick google search hypochloremia does not. Hypochloremia also can present with respiratory difficulties, but I didn't see that with hyponatremia.
Catheter placement:
https://aneskey.com/wp-content/uploads/2016/08/image00804.jpeg
Recall that the lung apex extends above the first rib.
Yo dawg we all about PVT TIM HaLL
Phenylalanine, Valine, TryptoDANK, Threonine, Isoleucine, Methionine, Histidine, Leucine Lysine
Wouldn't acute alcohol consumption even in moderate amount cause reversible hepatic cellular injury characterized by cellular ballooning? It should be the right answer unless the question stem means "Weekends"
please help according to winters equation the patient has a normal anion gap
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.
What's the difference between reactive granulocytosis vs lymphocytosis?
some wrong answers:
*makes sense b/c myeloblasts are precursors to granulocytes, which use MPO to fight off infections
In sarcoidosis, hypercalcemia normally suppresses the release of PTH and therefore the production of calcitriol (1,25-dihydroxycholecalciferol), but in sarcoidosis and other granulomatous diseases, activated mononuclear cells (particularly macrophages) in the lung and lymph nodes produce calcitriol (1,25-dihydroxycholecalciferol) from calcidiol (25-hydroxycholecalciferol) independent of PTH.
https://www.uptodate.com/contents/hypercalcemia-in-granulomatous-diseases
Hypo/hyperthyroidism is diagnosed with TSH w/ reflex to T4 (this just tells the lab if TSH is normal don’t check T4 but if TSH is abnormal, check T4 too). TSH wasn’t an option so T4 is the best answer.
The Stem is describing hemochromatosis, characterized by abnormal iron sensing and increased intestinal absorption. This increases Iron, increasing ferritin. In response, TIBC is decreased, which increases transferrin saturation as there is less circulating carrier molecules.
With excess iron in the blood, it will accumulate in tissues including the liver, skin, pancreas. Sequelae include dilated cardiomyopathy, hypogonadism, diabetes, arthropathy 2/2 calcium pyrophosphate deposition, nd Hepatocellular Carcinoma
why is hyperlipidemia secondary to cushing syndrome not a possibility?
As stated below, the Left crus cerebri was damaged (see what it should normally look like below). This contains the corticospinal tract. Since the corticospinal tract decusates at the medulla, below the midbrain section we're looking at, you would see Contralateral (Right) Spastic Hemiparesis
A little math here.. pH is low --> acidosis pCO2 is high --> respiratory Normal compensation should be roughly a 1 (acute) to 4(chronic) increase in bicarb per every 10 increase in pCO2.. Its lower here, so clearly not compensated and indicated additional drop in bicard --> add on metab acidosis
This is a likelihood ratio. LR+= Sens/1-Specif
Any value greater than 10 (per first aid) indicated "usefulness of diagnostic test" which is comparable to PPV (ruling in a dz). Point "A" is the closest mark to where 10 should be on the Y axis.
Is this saying there is vesicoureteral reflux? I could have sworm this same image was on form 20 or 21 and the answer was Wilms tumor
The description of bilateral lower limb loss of vibration implies DCML damage, and the absent DTRs + Romberg seem to me to be implying that he possibly has tabes dorsalis from syphilis (or something very similar in presentation).
As for the other answers, A is wrong because his motor function is intact, B is wrong because pain and temperature deficits are not mentioned, C is wrong because it implies a specific nerve is entrapped, but he has lost bilateral sensation in his entire lower extremities
D is the trickiest, and I’m not 100% sure, but I would think radiculopathy of the anterior (ventral) roots would cause motor deficits since they carry motor efferents. You might also expect that motor dysfunction to be unilateral, since it would be unlikely to have a problem with the nerve roots on both sides. also the DCML is not located near the anterior roots of the spinal cord, so if the anterior roots were affected you really wouldn’t expect to see vibratory loss.
So basically process of elimination, I do feel like sensory neuropathy is an extremely vague answer though and I wasn’t a fan of the question.
Neoplasia is new tissue growth that is unregulated, irreversible, and monoclonal.
Clonality can be determined by glucose-6-phosphate dehydrogenase (G6PD) enzyme isoforms. G6PD is X-linked.
*For more information check out Ch. 3 Neoplasia in Pathoma
This patient has small cell carcinoma. This type of cancer is associated with paraneoplastic syndromes such as: Cushing Syndrome, SIADH, or antibodies against Ca2+ channels (Lambert-Eaton) or neurons. Amplification of myc oncogenes is also common.
SIADH (Syndrome of inappropriate antidiuretic hormone secretion) is characterized by:
Body responds to water retention with aldosterone and ANP and BNP. That is what causes the increased urinary Na+ secretion which leads to normalization of extracellular fluid volume and the euvolemic hyponatremia.
Case of arteriolosclerosis.
Hyperplastic arteriolosclerosis involves thickening of vessel wall by hyperplasia of smooth muscle ('onion-skin appearance')
As stated below, the Left crus cerebri was damaged (see what it should normally look like below). This contains the corticospinal tract. Since the corticospinal tract decusates at the medulla, below the midbrain section we're looking at, you would see Contralateral (Right) Spastic Hemiparesis
Renovascular disease is the most common cause of 2° HTN in adults. Can be d/t ischemia from renal stenosis or microvascular disease. Can hear renal bruits lateral to umbilicus.
Main causes of renal artery stenosis:
Atherosclerotic plaques—proximal 1/3rd of renal artery, usually in older males, smokers.
Fibromuscular dysplasia—distal 2/3rd of renal artery or segmental branches, usually young or middle-aged females.
Lab values based off:
While I can get on board with Adjustment Disorder, I don't see how this answer is any better than Somatic Symptom Disorder. From FA:
Variety of bodily complaints lasting months to years associated with excessive, persistent thoughts and anxiety about symptoms. May co-appear with illness.
SSD belongs in a group of disorders characterized by physical symptoms causing significant distress and impairment.
Definition of adjustment disorder:
Emotional symptoms (eg, anxiety, depression) that occur within 3 months of an identifiable psychosocial stressor (eg, divorce, illness) lasting < 6 months once the stressor has ended.
If symptoms persist > 6 months after stressor ends, it is GAD.
Zollinger-Ellison syndrome: Gastrin-secreting tumor (gastrinoma) of pancreas or duodenum.
Thought this would be something regarding "bariatric surgery," but nope, just "no starchy foods, because you're pre-diabetic."
Urea cycle: Decreased citrulline and hyperammonemia can differentiate it from orotic aciduria.
The more general principle: endothelia vasodilate in the presence of high CO2; you gotta get rid of that acid somehow! Can’t let it accumulate, as lower pH within a “micro-environment” affects structure/efficiency of enzymes, proteins, etc. The more acidic a local environment, the more you expect nearby vasculature to dilate (as a means of increasing flow rate, thereby ferrying off accumulate acid).
The anesthesiologist can exploit this mechanism. By hyperventilating (blowing off CO2), the brain vasculature senses a low CO2 / “hunky-dory state,” which requires no vasodilation. In other words, the vasculature does not need to continue the ATP-consuming practice of synthesizing Nitric Oxide (NO).
Vomiting blood and cool skin indicates this is a type of hypovolemic shock. To understand shock, remember that 1) BP = TPR x CO 2) CO = SV x HR 3) SV = EDV - ESV In hypovolemic shock, you are losing fluid, so stroke volume is decreased and end diastolic volume is decreased. Decreased EDV means that the "filling volume" is decreased, which also means the preload will be decreased (https://www.cvphysiology.com/Cardiac%20Function/CF007). Also, skin is cool because you're decreasing SV --> decreased CO --> Ang II/ADH/etc is released to vasoconstrict increaseing resistance. Since there is increased resistance, there is less blood flow causing skin to be cold/clammy.
Why are "rotator cuff tear" and "rotator cuff tendnitis" wrong? is it bc both of these would show impingement sign? is there a way to DDx one from the other?