What would a rupture of the fallopian tube look like then? Compared to normal spillage..
Can anyone justify why they did not describe an increased MCHC? FA 2019 says spherocytosis has high MCHC, and they did not even have it on the upper end of normal.
We know that the defecation process is modulated by the parasympathetic and voluntary nervous systems, with tonic stimulation of the sympathetic nervous system (thank god, so we aren't just pooping and peeing with erections all the time).
S2,S3,S4 roots all provide input to the anal canal, urethral sphincters, and to the erectile apparatus.
We know that the pelvic splanchnic nerves, arise from these nerve roots (S2, S3, S4). Pelvic splanchnic nerves cause detrusor muscle contraction (urination), peristalsis in the hindgut (defecation), and mediate erection.
The other nerve that arises from S2,S3,S4 is the pudendal nerve, which mediates basically the same stuff, it mediates urination (ext. urethral sphincter relaxation), defecation (ext anal sphincter relaxation), and emission.
This question says that a patient with a 10 year history of DM Type 1 has fecal incontinence (presumably diabetic neuropathy) which of the following additional symptoms will this dude have? we know from our anatomy run down, that this is caused by damage to the pudendal nerve, who regulates the ext. anal sphincter, leading to fecal incontinence. The pudendal nerve is from S2,S3,S4 nerve roots so the diabetic neuropathy is occurring here. The only other answer choice with innervation from S2,S3,S4 is the pelvic splanchnic nerves which leads to erection, damage to the S2,S3,S4 nerve roots cause lack of erection or inability to maintain erection (impotence).
Just for completeness sake, I want to elaborate on HbH. THIS CAN LITERALLY ONLY HAPPEN if a Thalassemia minima, mated with a cis deletion-thalassemia minor patient. AKA Thalassemia MINIMA: a patient with only one alpha gene missing (from the normal 4 alpha genes present), mated with Thalassemia MINOR: two alpha genes with two absent alpha genes (CIS deletion ONLY).
This combo can produce HbH disease. Which presents with severe hypochromic microcytic anemia.
This was literally the most vague shit I've ever read.
But basically my reasoning was that:
Endometriosis of the ovary would cause chocolate filled cysts, and there would be cyclical menstrual pain. This patient is asymptomatic, so this is ruled out.
Ectopic pregnancy would present with a growing fetus or fetal tissue in the ampulla, fallopian tube, ovarian surface. This is an acute emergency, not a cyst, and would present like acute appendicitis, severe lower abdominal pain on either the right or left side. Again, nope.
I couldn't rule out malignancy by any rational thought process, but in this patient demographic with absolutely 0 symptoms, and one single fluid filled cyst I was thinking of a follicular cyst (FA 2018 pg 628). It kinda helped that I was instinctively leaning towards PCOS as a diagnosis the moment I heard cysts in a young woman, and I knew that the cysts in PCOS are due to anovulation.
Couple of Uworld questions on this, but basically Type 1 diabetics have a CD4+ T cell response to their pancreatic islets, which target beta cells in the pancreas. This leads to almost absent insulin secretion in these patients. OVERTIME, the autoimmune reaction to the beta cells causes damage to alpha cells in the pancreas, leading to a decreased ability to increase serum glucose levels appropriately as a counter balance to insulin.
The reason it wasn't related to catecholamine based increase in glycogen phosphorylase is because GLUCAGON is the primary hormone responsible for increasing glucose levels, not catecholamines.
I don't think this question was going after pregnancy related increase in prolactin. That could lead you to the correct answer, but imo, they mentioned she had an MRI for head trauma, which could mean there was damage to the pituitary stalk, in which case the ONLY hormone which will increase when there is damage to the stalk is prolactin, because it is under constant inhibition by dopamine. Prolactin obviously stimulates lactotropes.
This was just how I got to the answer. You could very well have gotten to the correct answer by simply using the pregnancy logic, its probably easier.
RA is a type 3 hypersensitivity reaction which has two components.
CD 4+ T cells will infiltrate tissue and react to autoantigens present in the synovial joint, this causes TNF-alpha and IL-1 to be released. These inflammatory cytokines will cause the initial inflammatory reaction. These cytokines ALSO activate B cells.
B cells produce rheumatoid factor as well as anti cyclic citrullinated peptide antibody. They bind the autoantigens and form IMMUNE complexes that deposit on the synovium. They cause complement to be activated. Hence the classic Type 3 hypersensitivity reaction, it is composed of 3 things: 1. antigen 2. antibody 3. complement
Next, you need to know that serum sickness (FA) is ALSO a type 3 hypersensitivity reaction, this time it is due to penicillin or a monoclonal antibody, basically some antigenic drug, which causes antibody to bind and then deposit complement.
Just wanted to add in addition to others comments, there are TWO types of breast cancer, SPORADIC (amplification, overexpression of estrogen/progesterone receptors) and then there is HEREDITARY breast cancer. IF the question stem mentioned a family history of breast cancer in say the mother or some family relative, then loss of heterozygosity would be the correct answer. What is imperative to understand is that her2/neu is a receptor tyrosine kinase, and when its over expressed on cells in the breast THAT is what leads to breast cancer. In BRCA1/2 mutations, these are tumor suppressor genes, hence they require Knudson's two hit hypothesis in order for cancer to develop. Since this question specifically mentioned HER2/neu it is safe to say that this is overexpression and has nothing to do with BRCA1/2 mutations.
Process of elimination using the stem, this kid has no vitamin deficiencies that correspond to his clinical symptoms. Plus his diet was weird to me, so I selected dietary change.
30 years construction worker, insulation, shipbuilding, plumbing? Asbestosis fine inspiratory crackles = restrictive lung disease bilateral parenchymal opacities, RETICULAR pattern = pulmonary fibrosis pattern on CXR PLEURAL PLAQUES = Cherry on top, extra info, Asbestosis.
All of this points to a restrictive lung disease with an INTERSTITIAL pattern. Even if you didn't get asbestosis, but understood that this pathologic process is restrictive in nature, you can get the right set of changes on PFT. This is a pathologic interstitial disease, not myasthenia gravis or polio, so DLCO will decrease. IF this was myasthenia gravis, and it asked for the same set of findings your DLCO WOULD BE NORMAL, your Alveolar arterial gradient would be normal!!
Live Attenuated Vaccines:
Attention! Please Vaccinate Small Beautiful Young Infants with MMR Regularly!
Adenovirus Polio virus (Sabin) Varicella Small Pox BCG Yellow Fever Influenza (Intra nasal) MEASLES, MUMPS, Rubella Rotavirus
If you were like me and were thinking that this is acute tubular necrosis because the UW tables/FA passage mention HF as a cause of ATN, then read below.
You have to understand that acute kidney injury exists on a spectrum when it comes to renal blood flow decreases. If you have a patient who is oliguric and who has had renal blood flow loss (due to excessive diuretic overuse, HF, hemorrhage, ischemia of basically any cause) the first thing to happen is PRERENAL AZOTEMIA. Afterwards, you progress to acute tubular necrosis, where you will get the classic decreases urine osmolality, urine Na+ decreases, FeNa+ increase, and serum BUN/Cr decreases.
Remember this is a spectrum for renal blood flow decreases, the more severe the more chances it will progress to ATN. In this case, its prerenal azotemia, so only choice D makes sense.
The thing that threw me of was the 74% neutrophil count. Does anyone have an explanation for this?
This is a tricky question. The another big point of confusion here is that sweat actually causes a hyperosmotic volume contraction. This occurs because the content of sweat is composed primarily of water more so than salt. With that said, its unlikely that this patient will be hyponatremic. If anything she will be hypernatremic.
Abnormal phagolysosome fusion in pulmonary alveolar macrophages of rats exposed chronically to cigarette smoke.
Differences between Naked and Enveloped viruses:
IS THE VIRUS: Inactivated by heat, detergents, acid and organic solvents like ether and alcohols?
YES = ENVELOPED, the lipid envelope basically holds the proteins needed to attach to the human cells, by dissolving the envelope, the virus loses its ability to infect and therefore survive.
NO = NAKED
Got this from Kaplan
o Greater Splanchnic (T5-T10)= Symp innervation foregut o Lesser Splanchnic (T9-T12)= Symp to hindgut o Vagus nerve= Parasymp of proximal GI system until splenic flexure o Pelvic Splanchnic (S2-S4)= Parasymp to bowel and bladder
Heres a summary of the Autonmomics of that area!
Firstly, I chose ADH. When I thought twice in review, I picked crossed ADH and picked ANP. My logic to cross ADH: 1. The main inducer of ADH are Osm and BP/vlomue. THis pt, Osm obviously not high, Bp obviously not low. So, nonsense in increased ADH. 2.You may see AngII also induces ADH. But it seems to be a minor inducer. Meanwhile, if it is exactly high AngII→ high ADH. Then, Aldo must be high as well, and High Aldo →Salt preserving→ HOW CAN serum Sodium be LOW? "Low Cardiac output→ High RASS (AngII Aldo ADH)" pathway is WATER-SODIUM retention. NOT pure WATER retention Please correct me
Meningiomas most often occur near the surfaces of the brain, especially the parasaggital regions. They are often asymptomatic, and grossly it appears as a round mass attached to dura. It will compress the cortex (explaining the headaches), but it will not invade. They are also the most common primary benign CNS tumor. Women are more commonly affected, which is supported by the vignette.
A: Astrocytomas are usually found in the posterior fossa, and are the most common primary CNS tumor in children
B: Glioblastoma multiforme is usually seen within the cerebral hemispheres, and shows signs of necrosis and hemorrhage.
C: Melanoma can metastasize to the brain, but this would likely form in multiple spots, and they would not be outside of the parenchyma
E: Squamous epithelial would similarly be metastasis and therefore also be multiple lesions inside the parenchyma
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
"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.