Signal recognition particle (SRP) receptor, also called docking protein, is a dimer composed of 2 different subunits that are associated exclusively with the rough ER in mammalian cells. Its main function is to identify the SRP units. SRP (signal recognition particle) is a molecule that helps the ribosome-mRNA-polypeptide complexes to settle down on the membrane of the endoplasmic reticulum.
This is a case of late post-renal azotemia, as you can tell by the BUN/Cr ratio that is <15 and the 3 day history of pain. They also tell you that the hydronephrosis and lymphadenopathy are compressing the ureters so it makes sense that you would want to stent the ureters. The others are all in the wrong location: Foley catheter (penis), suprapubic tube (bladder), stent in renal arteries (self explanatory).
Pretty sure this is a case of Legionella. The fact that it didn't show up on culture but a "highly specialized" medium (in hindsight buffered charcoal yeast) yielded gram-negative rods put Legionella on my radar. The headache and dry cough also line up with it but the macrolides threw me off since I thought they were treated with fluoroquinolone. But the sketchy video for macrolides includes Legionella as a target so it worked out.
Plasmodium vivax/ovale have dormant stages where their hypnozoites can stay latent in hepatocytes and trigger malaria well after the initial infection. The only malarial drug that covers against this is primaquine. The answer choice is just worded funny - "exoerythrocytic malarial tissue stages" basically is the stage where they are in the liver/not in RBC, and chloroquine won't work for those.
"Finger-shaped" lesions is suggestive of a papilloma and the findings being on the vocal cords and epiglottis make this a laryngeal papilloma. Most common cause of laryngeal papillomas is HPV 6 and 11, per sketchy.
Remember that medullary carcinoma of the thyroid is medullary. So it's between the follicles. What's between the follicles in the thyroid? C cells that secrete calcitonin.
Something key to note is that it's called "THROMB-oxane" for a reason.
"Named after its role in thrombosis, TxA2 has prothrombotic properties, as it stimulates the activation of platelets and platelet aggregation. TxA2 is also a known vasoconstrictor and gets activated during times of tissue injury and inflammation. While the prostaglandin counterbalances its thrombotic and vasoconstrictor properties prostacyclin (PGI2), there are various physiological and pathological situations where this balanced becomes dysregulated. Increased activity of TxA2 may play a role in the pathogenesis of myocardial infarction, stroke, atherosclerosis, and bronchial asthma. Increased action of TxA2 also has implications in pulmonary hypertension, kidney injury, hepatic injury, allergies, angiogenesis, and metastasis of cancer cells."
This is a great quesiton. With the iron deficiency anemia, i was thinking of "where the blood loss could be" not so much where would the malabsorption be...
What is TARNATION is going on here!?
I also had no idea what the diagnosis was and purely went off elimination: Can't be fatty acid oxidation bc of the ketonemia, which you wouldn't be able to produce if that was the defect. Glycogen breakdown/synthesis are related to glycogen storage diseases, which the presentation didn't line up well with. Also I was thinking of a pathway that would incorporate glycerol, fructose and galactose which seemed more in line with gluconeogenesis/glycolysis. Between the last two, I went with faulty gluconeogenesis bc that would elad to his hypoglycemia. I don't know how legit or applicable that is to other questions, but thought I'd at least share in case anyone finds it helpful.
The way I think of motivational interviewing is that the goal is you want the patient to convince themself. So the goal is to get THEM to tell YOU the arguments for why they should quit.
The patient knows that smoking is bad for them. They have weighed out pros and cons in their mind and they're stuck at "I'm still going to smoke." Smoking HAS PROs: It feels great, reduces anxiety, they're used to it, and if they were to quit they'd go through awful withdrawals. But the patient also knows that there are cons. It's going to kill them.
If you start listing all the reasons why it's bad for them that they already know, they'll want to balance out the argument for why they still smoke. You're saying the cons, so they feel the need to justify the pros. BUT if you ask them what smoking is doing for them that's good, they'll feel the need to justify the cons: "Well it helps with my anxiety, but I know that's not a good enough reason to keep smoking." You can also have them argue your side by talking in the extreme in the opposite way: "So you'd NEVER see yourself quitting?" "Oh no of course I want to quit eventually!"
Here's a good list of questions to ask in each stage: https://www.aafp.org/afp/2018/1215/hi-res/afp20181215p719-t2.gif
Main groups There are two main groups of cyclins:
• G1/S cyclins – essential for the control of the cell cycle at the G1/S transition;
• Cyclin A / CDK2 – active in S phase.
• Cyclin D / CDK4, Cyclin D / CDK6, and Cyclin E / CDK2 – regulates transition from G1 to S phase.
• G2/M cyclins – essential for the control of the cell cycle at the G2/M transition (mitosis). G2/M cyclins accumulate steadily during G2 and are abruptly destroyed as cells exit from mitosis (at the end of the M-phase).
• Cyclin B / CDK1 – regulates progression from G2 to M phase.
"The flexor group of muscles is involved in pronation of the forearm and flexion of the wrist and fingers, while the extensor group of muscles is involved in the supination of the forearm and extension of the wrist and fingers."
Weakness of extension (Radial n) and pronation (Median n).
C6 damage would give you MC signs. C8 would give you ulnar signs. C7 goes to Median and Radial.
Hypocalcemia can present with muscular twitching and spams, might cause tetany, and in severe cases lead to seizures like happened in this patient.
This question can be confusing mainly because whenever u think of seizure or neurologic manifestation, you think of Sodium, but the key here is the 1 MONTH history of episodes of pins-and-needles with involuntary contraction of muscles. Also you can rule out Potassium, because although it can cause muscle cramps, spasms and weakness, it leads to cardiac abnormalities (arrhythmias).
I do not know if that was 100% correct but I agree with eliminating answers contain sensitivity or specificity because that is not a screening test and eliminating other studies as they did not mention anything about other studies, here is what I think we here have 2 numerical values 9 interval variables ) so we will use statistical test person correlation as it needs 2 interval variable and graph done by the test will give us idea about strength of the correlation. temopral relationship ( temporality )means : tests whether the outcome occurs after the effect (e.g., surgical site infection occurs after incision of the skin) dose response relationship : tests whether greater exposure usually leads to a higher occurrence of the outcome (e.g., the greater the exposure to ionizing radiation, the higher the risk of malignancy) . and both can be applicable here . source : amboss.
Can anyone explain what "diplopia" implies? I got sutck by"these clinical findings" (thinking upward gaze+ diplopia....) Or is "Diplopia" just a unspecific word in exam??
In addition to the explanation by drjungly, the question literally states that they are using national census data. They aren't sampling data from a town/city, they are taking the entire US census data from 2000. This is population level data.
Hormones/drugs use signaling pathways to exert their effect on tissues.
In particular steroid hormones, fat soluble vitamins, and thyroid hormones (T3/T4) utilize an intracellular receptor signaling pathway which translocates to the nucleus and binds to DNA, up regulating or down regulating transcription of certain genes.
PET CAT on TV is the mnemonic that is given in FA.
Vitamin D is given in FA, but Vitamin A isn't mentioned in Uworld: fat soluble (A,D,E,K) vitamins are given.
Hope this helps!
On the pedigree, it clearly shows maternal inheritance, this is what distinguishes it from literally all other options. Mitochondrial myopathies show MATERNAL inheritance (on a pedigree chart the circle aka female is affected and only the female can pass it on to her kids, an affected male can NEVER pass it on to his kids), why? Because sperm cells lose their mitochondrial DNA before fertilization, so in all of your cells, your mitochondrial DNA is from mom. Now, when mom passes down her mitochondrial DNA, she can be passing down her mutated mitochondrial DNA and a portion of normal mitochondrial DNA this mixture is called heteroplasy, it means that a person with a mitchondrial myopathy can show variability in the clinical symptoms they present with.
This means, they can be more severe in their presentation or less severe. In the vignette it states that mom has 50% mutated mitochondrial DNA versus her offspring who have 100% mutated mitochondrial DNA. Her kids presented more severely, than she did, aka variable clinical presentation in a mitchondrial myopathy = heteroplasmy.
Contrast this with variable expressivity, which occur in autosomal dominant disorders, not mitochondrial myopathies.
Specifically this process is called disuse atrophy. It is a type of atrophy, a cellular adaptation occurring in response to stress. This cellular adaptation causes protein degradation via ubiquitin proteasome pathway. This is why his calf is smaller than his other normal one.
Acetaminophen normally is degraded by hepatic glucoronidation, but in chronic acetaminophen users, this pathway becomes "saturated". So the body uses the Cyt. P-450 enzyme system to convert it to N-acetyl-benzoquinonemine (NAPQI), which causes free radical damage. The question asks, which of the following effects of alcohol most likely contributed to this patients condition?
A,B,C,D are all anti free radical generation, and would not contribute to this patients condition. This leaves E, Alcohol is an inducer (basically ramps up CYT p450) of the P450 enzyme system which causes elevated levels of NAPQI.
Capsaicin can also reverse mucosal damage caused by ulcers
very limited clues.
"The aminoglycoside antibiotics, such as gentamicin, have the potential to cause nephrotoxicity with the principal cellular injury being in the proximal tubule. Nephrotoxicity, often detected as a fall in glomerular filtration rate (GFR), is estimated to occur in 10–20% of patients who receive the drug" (Swan, 1997).
This child has minimal change disease, the most common cause of nephrotic syndrome in children. It is often primary (idiopathic) and may be triggered by a recent infection, immunization, or other immune stimulus. Histologically, there is a loss of negative glomerular charge and selectively loses albumin which is why this child also presents with proteinuria. Source: FA19 p584.1
ANP is secreted by the atrial myocytes and result in this set of physiological responses:
This patient has dermatitis herpetiformis, a blistering skin disorder characterized by pruritic papules, vesicles, and bullae (often found on elbows, knees, buttocks). Associated with celiac dz (hence mom's diet). Histo: deposits of IgA at tips of dermal papillae Tx: dapson, gluten-free diet Source: FA19 p471.2
B is labeled over the primary somatosensory cortex of the right hemisphere. This part of the brain is responsible for touch, proprioception, nociception, and temperature. Loss of touch graphesthesia and loss of two-point discrimination infer this patient suggests a lesion in the contralateral hemisphere of the affected region.
Inability to flex elbow and loss of sensation over lateral foremarm is suggestive of musculocutaneous injury.
Clues from this question include pupillary dilation and diaphoresis, agitation, confused thought process, and tachycardia. Amphetamines are reuptake inhibitors.
The clues from this question include the patient's gender and age (MS commonly affects 20-30 yr W/W), numbness and tingling in her arms and urinary incontinence (both of which are spinal cord syndromes of MS), and scattered, nonspecific white-matter plaques (periventricular plaques). Source: FA19 p511.1
this was one of the easiest questions, and its a shame i missed it.
recall : ground glass appearance which is classic. for hep B are simply antigens in the hepatocytes.
so cd8 will target those
my perspective ;
arguement lead to an adrenaline (epinephrin) rush which went straight to the old man's coronaries and squeezed the shit out of them
Why don't we see a decrease in the size of the prostate gland? Is it a difference between atrophy vs. apoptosis?
FA 2019 P.365
CCK is secreted from I cells (duodenum, jejunum) by fatty acid, amino acid.
main functions of CCK are 1. inc pancreatic secretion 2. inc gallbladder contraction 3. inc gastric emptying 4. sphincter of Oddi relaxation
Acts on neural muscarinic pathways to cause pancreatic secretion. (not endocrine stimulation) -> R/o (C)
Thymic output of T cell repertoire during the growing phases is vital, but it becomes unnecessary for repertoire maintenance during adulthood. This happens because the T cell regeneration in adulthood is almost entirely derived from homeostatic proliferation of the EXISTING T cell pool, which is sufficient to maintain a large compartment of naive CD4 T cells. Thymic T cell generation can add new naive T cells and enrich diversity, while homeostatic T cell proliferation can sustain the richness of the TCR repertoire already created. This means that the Thymic lymphocytes produced before thymectomy are long-lived naive T cells, which are maintained stable in quantity thanks to Homeostatic proliferation in adulthood.
ATTENTION DEFICIT- hyperactivity disorder.
how do we improve the attention deficit in that kid ? by increasing dopamine and norepi levels in the brain.
dopamine and norepi= biogenic amines
funstory. newyork times once reported abuse of stimulants by students so they can have an academic advantage by improving attention
blood culture + eliptical budding organisms ( likely germ tube) = candida
summary of pathogenesis
hemochromatosis = mutation on HFE gene(codes for an iron sensor)
mutation > defect in sensor > body assumes low iron.
2 organs now make attempt to increase body iron.
1, small intestine, increases expression of DMT in lumen.
2, liver decreases hepcidin, so that ferroportin can be expressed on the basolateral surface of enterocyte.
why ? so that the iron absorbed via dmt can be taken to the blood via feroportin.
lets avoid long explanations shall we .
pt. with infertility. quick test in few seconds = semen fructose
fact : seminal vesicle makes fructose.
obstruction of seminal vesicle or congenital absence = low fructose in semen = metabolic imbalance > ineffective spermatogenesis
low retic count= marrow not working .
what can explain this ? parvo virus affecting the hematopoetic stem cells , hence the low retic count,
think of the low retic count of giving a picture of a failing marrow
ignore timing and let common sense take care of it , lets go for pathogenesis.
allergic/anaphylactic= broncoconstriction and wheez vasodilat. > third spacing > shock
trasnfusion rel. acute lung injury = host neutrophil activated by donor blood product > cytokine release in pulmoanry vasc. > pulmanry edema
i would highly recommend you refrain from cramming of exact timings , as some over lap , and the wordings can be misleading,
for example, within 6 hours, can be interpreted as an event that starts in few minutes, as few minutes are part of the "within 6 hours"
here is a copy pasted link .
first, high tsh = hypothyroidism
How can hypothyroidism affect me and my baby? thyroid hormones are important to your baby's brain and nervous system development, untreated hypothyroidism—especially during the first trimester—can cause low IQ and problems with normal development.
what is collagen ? a secondary protein structure.
when you remove glycine, the most abundant amino acid , from the precursor molecule will you get a proper secondary structure ? NO
if the commoesnt cause of hyperthyroidism in pregnancy is graves dx., then why cant the THYROID ANTIBODIES.
that stuid mneuminic of MET HIS VALENTINE made me switch from alanine to valine.
A discontinue consumption of all alcoholic beverages is wrong； Is that because what She drinks is wine ? Not take it as alcohol?
If the patient is taking calcium acetate (a phosphate binder), why is his phosphorus level increased?
While solving Ethics questions, you answer them not as some doctor, but as if some saint. It's not:
Note : In another question from the same form, we have "refer" in the answer, so refering in itself isn't wrong unless you make sure that the question stem states that you DIRECTLY dealt with and understood all of your "childs" concerns.
Amboss for cyclin：
G2 checkpoint: A cell division checkpoint during the G2 phase.
Checks for DNA damage and completeness of DNA replication
Initiates mitosis by phosphorylation of various proteins (e.g., histones)
Regulated by the mitosis promoting factor (MPF), which is composed of Cdk1 and cyclin B.
Acute onset fussiness.
Something so prominent in such a prominent place (like a baby gonna need exposing his buttocks several times) and mom is like OMG NEW BABY WHAT"s THIS
i was initially picked USG (URTI > Intususception) but theres no mention of abdominal pain.
Here i am thinking who doesnt have problem in reading new words
If anyone was worried with option C like i was....the study is comparinc class A, B, C patients among those who got EPCS and those who got EST.
Not among A patient who got EPCS & C clas who got EPCS
i think the clue should have been low grade fever and dysuria. Poor guy may have a prostatitis. that dark urine threw me off.
why not prophylactic anitbiotics?
Asthma, hemoptysis, neuropathic symptoms.
Low grade fever (B symptoms).
You know its a vasculitis.
Do ANCA. IgE testing is too nonspecific to yield any value and make a dx for u. despite churg strauss having both elevated igE and eosinophilia.
Took me long time but got it right. kinda lucky.
Wedged hepatic venous pressure (WHVP) is measured by inflating a balloon at the catheter tip, thus occluding a hepatic vein branch. Measurement of the WHVP provides a close approximation of portal pressure. The HVPG is defined as the difference in pressure between the portal vein and the inferior vena cava. Thus, the HVPG is equal to the WHVP value minus the FHVP value (ie, HVPG = WHVP - FHVP). The normal HVPG is 3-6 mm Hg. 5mmHg Here-->NO cirrhosis
Yeah. Different from cardiac muscle/coronary arteries
I wrongly chose IL-2. IL-1 is a potent cytokine that can induce bone erosion in inflammatory sites such as rheumatoid joint regions via activation of osteoclasts. (via a receptor activator of NF-κB ligand (RANKL)/RANK-independent mechanism. IL-1 has a synergistic effect on RANKL-induced osteoclast formation.) https://www.jimmunol.org/content/183/3/1862
Guys here the baby is cyanotic at birth, also receiving o2 which further can close the duct. when murmur present it most likely cyanotic CHD. so infuse prostaglandin
But if no murmur present and presents early thats most like a pulmo problem like pulmo hypoplasia from con diaphargmatic hernia. there u intibate.
jesus said "Protec thy heart"
Probably HTN. COnfirm with next follow up (idk the exact time limit, but common sense is As early the better).
After that if he surely has HTN first treat with lifestyle than meds. Lifstyle in order of efficacy wt loss DASH diet Exercise Diet low in sodium ALcohol avoiding
Diveritculitis, Crohns > UC; all 3 can cause fistula. In an elderly pt diverticulitis is way more likely than new onset IBD.
I knew it had to be X-linked because it said that it was fatal to males who have it in utero, but I had a hard time deciding between dominant and recessive. Ultimately it has to be X-linked dominant because the affected mother in the second generation gave birth to unaffected sons (which can't happen in X-linked recessive). That means the mother in question is heterozygous and her daughters will have a 50% chance of inheriting the disease while her sons have to be unaffected if they live, as previous posters mentioned. I didn't figure this out until way after the test...this one was a doozy. Still not sure that it's XLD because how come nobody in the first gen has it? Guessing it was a spontaneous mutation?
I also first chose sterilization but later move it to toxin. Its very straight if u look at it that toxin is the one causing diarrhea. Sterilizing gut flora occrs everytime u take antibiotics, its predisposing to C. DIff but not actually causing diarrhea otherwise everyone would get it.
This pt has mild hypercarbia but worse FEV1. Those are her limiting factor.
EF <35 would be absolute CI. not 40.
Why cant this taken as sexual health?
Why cant this taken as sexual health?
we gonna totally forget asthma can cause total normal PFT. including FEV1
p474 / 297 fa 2019
prostaglandin e1 maintain ductal open--> if block cox = drecease PGe1 = clousere
According to Boards and Beyond ： lunate attached to radius.
falling in outstretched hand, other bones forced backwards when lunate displaced toward palm/ So in this position ,lunate dislocation is most common
So we're expecting a topical retinoic acid to clear her acute acne within 3 weeks? don't topical retinoids cause purging often?
can Gonadotrophs “hyperplasia” rather than hypertrophy?
There is absolutely no way someone is able to raise my straight leg up to 75 degrees after all these weeks sitting at the desk :).
It's TOF and all but isn't there LV enlargement in TOF(causing a boot-shaped heart) Constant R>L shunt will overload LV and cause dilation
Nothing here right now = Chemotherapy (just to be more searchable).
could it also be possible to get this by remembering the different ventricle spaces as well. i honestly didnt remember what hydrocephalus this could be. But i remembered the mnemontic LIT AFF to SAD.(Lateral ventrical, intraventricular foramina of monroe, third ventrical, cerebral aqueduct, fourth ventricle, foramina of lushka, subarachannoid, arachanoid granulations, dural venous sinus). And i recognized they were talking about a widing of subarachanoid space and thought what was the closest thing to interefere and thats how i got to B.
Also i just want to say looking at the answers i know its a communicating hydrocephalus, i just wanna know if this was also a good way to extract the answer or if i just winded up getting lucky a little LOL.
in my opinion , this was one of the most difficult questions . why ? the answer is soooooo simple that you might be mislead thinking "naaaahh cant be that easy ...nbme .. you playin witme hun?? imma choose the most complex answer and shove it in your face"
student chooses VIP, and afterwards locks him self up with his new record level low self esteem
I just wanted to add a note here. I was confused on why you would give the patient leucovorin with the MTX. The reason is that it "rescues" the normal cells from damage/death, and allows the MTX to attack only the cancer cells.
Also another connection we may need to know is that if leucovorin with 5-FU it makes it more effective/toxic at killing cancer cells!
HOW TO REMEMBER THIS
virus > mhc 1 > cd8+
SIMPLE. 3 steps.
we know this girl has cystic fibrosis .
but testing shows only 1 allele is mutated.
since she has CF, the other allele CANNOT be normal , and the only explanation to her having CF is the panel didnt detect it.
i have never herd acetylsalicylic being prescribed for gout, and i practiced for a couple of years.
so think simple, choose probenicid since its a fairly known drug in the gout world, and enjoy your 250 on step 1
Patients with irritable bowel syndrome (IBS) who have significant gastrointestinal bloating symptoms can be treated with antispasmodic medications (eg, dicycloverine) that block gastrointestinal muscarinic receptors. Those with constipation-predominant IBS are sometimes treated with lubiprostone, a chloride channel activator, to increase intestinal fluid secretion. IBS is usually marked by periods of diarrhea and/or constipation and abdominal bloating; early satiety and vomiting of undigested food would be atypical. (UW#6705)
how to rule out iron def. ? iron is absorbed in deodenum and proximal jejunum .
b12 in ileum.
this will give you the answer