when a follicle doesn't rupture (aka anovulation) then it will form a cyst.
After everything its jjust an epidem ques. Below 55 vs Above 55 years
Alcoholic = pancreatic insufficiency. Linoleic, oleic, and palmitic acid can be absorbed without pancreatic lipases since they're just free fatty acids. Triglycerides need to be broken down by lipases before absorption.
Bile acids are the main method for eliminating cholesterol, not pancreatic enzymes
Dont get confused with club feet. Clubfoot is a birth defect where one or both feet are rotated inward and downward.[1][4] The affected foot and leg may be smaller than the other.[1] In about half of those affected, both feet are involved.[1] Most cases are not associated with other problems.[1] Without treatment, people walk on the sides of their feet, which causes problems with walking.[2] The exact cause is usually unclear.[1] A few cases are associated with distal arthrogryposis or myelomeningocele.[2]
Borderline personality disorder- feelings of "emptiness," suicidality, self-mutilation, unstable relationships, and more common in women than in men. A common defense mechanism in this disorder is "splitting" in which people are seen as entirely good or entirely bad. Borderline personality disorder is also part of the Cluster B personality disorders, which are associated with substance abuse.
Integral membrane proteins are found within the plasma membrane and span the whole length across. The inside of the membrane is very hydrophobic due to the long carbon chains. Extensive hydrophobic interactions between the protein side chain and the lipid tails will help anchor the protein in the membrane.
Ritonavir inhibits CYP450! So you can use it to boost the concentration of the other Protease inhibitors by preventing their metabolism by CYP450!
From First Aid- schizotypal personalities exhibit eccentric appearance, odd beliefs or magical thinking, and interpersonal awkwardness. These describe the several layers of clothes, belief in psychic abilities and crystals, and poor eye contact.
A) Borderline- unstable moods with impulsivity, self-mutilation, suicidality, and a sense of emptiness, along with a greater likelihood in women B) Dependent- those with an excess need for support and low self-confidence C)Histrionic- excessively emotional, seeks attention, sexually provocative, concerned with appearance ("actor's disease") D) Narcissistic- grandiosity, entitled, lacks empathy, demands 'the best' E) Schizoid- voluntary social withdrawal, limited emotional expression, content to be on their own
I chose this b/c its the most common pathogen for skin infections
So if you didn't h8 bedbugs enough, they can apparently also serve as vectors for drug-resistant bacteria including MRSA HOW FUN IS THAT
Bed bugs themselves are not known to be carriers of illness, but they can leave itchy bites. The girl is likely to scratch these bites, abrade the skin, and thus increase the risk of a staph skin infection (since staph aureus is the most common skin infection pathogen)
Patient present to the clinic with classical symptoms of tetanus. Tetanus toxin work via inhibition of GABA/glycine release from Renshaw inhibitory cells. Without these inhibitory signals on the postsynaptic neuron, they are continuously activated causing muscle tetany.
binding to the MHC class II receptor and triggering the release of cytokines - superantigens
binding to the neuromuscular junction and prevention of ACh release - botulinum toxin
blockage of a GTP-binding protein resulting gin the accumulation of cAMP - pertussis toxin
blockage of presynaptic inhibition of spinal motor reflexes - tetanus toxin
prevention of protein synthesis by blocking elongation of the polypeptide chain - diphtheria toxin, Pseudomonas aeruginosa exotoxin A
So there’s 100 residents, and the prevalence after 2 years is =10 at the beginning, +5 in the first year, +10 second year, and -3 that healed, for a total prevalence of 22 residents or 22/100=22 percent. Thus, prevalence = above the standard. For incidence, it’s 15 new cases out of 90 residents over the 2 years (100 total residents – 10 that already had ulcers), or 15 new ulcers per 180 patient⋅years. This would be 83.3 new ulcers per 1000 patient⋅years if you extrapolated it out -- basically (1000/180) * 15 -- thus, incidence = above the standard.
The patient started receiving post-surgical subcutaneous anticoagulation therapy, so most likely either unfractionated heparin or low molecular weight (LMW) heparin. Unfractionated heparin's primary anticoagulation ability comes from working with antithrombin III to block coagulations factors II and X.
However, heparin can also bind to a platelet protein called Platelet Factor 4 (PF4), found in alpha-granules. When it binds PF4, the new heparin-PF4 molecule is immunogenic. The immune response to this generates anti-heparin-PF4 Ig. Platelets already have Ig receptors on their surfaces, so when these anti-heparin-Pf4 Ig trigger the receptors on the platelets, these platelets degranulate. The degranulation kicks off further clotting, leading to a drop (often more than 50%) in platelet count.
More simple from FA 2019: Heparin-induced thrombocytopenia is due to development of IgG antibodies against heparin-bound platelet factor 4 (PF4) Antibody-heparin-PF4 complex activates platelets => thrombosis and thrombocytopenia
The treatment of cholera is mostly supportive - you want to rehydrate the patient by giving them an isotonic saline since they're losing a lot of fluids.
Why does methylation cause loss of resistance to GATC restriction endonuclease? Does this have to do with methylation of U to T?
Methylase methylates DNA, making the DNA resistant to restriction endonucleases
*https://d2jmvrsizmvf4x.cloudfront.net/7Pf4zZ3TuGwLTRKvUGYL_methylatedrestriction.jpg
Me reading this question stem: .....do you mean which of the following ENZYMES?
The most important hints to the question are as follows, with #2 being the most specific:
1) patient reports pain with overhead motion and reports recurrent overhead motion during work. Overhead motion can damage the supraspinatus muscle due to impingement by the acromion.
2) Pain is worst with internal rotation of the shoulder - this is consistent with the findings of the empty-can test, which indicates a supraspinatus injury.
Enzyme A stands in for Phospholipase A2, turning phospholipids in the cell membrane into arachidonic acids. From there, Enzyme B stands for Cyclooxygenase (COX), while Enzyme C stands for 5-Lipoxygenase (5-LO). 5-LO produces 5-HPETE, which is turned into leukotrienes. Leukotrienes play a double role in events like asthma, because they cause bronchoconstriction (seen in this patient) and by acting as chemical attractants for inflammatory cells, whose activity will close the airway further. By blocking COX (presumably with an NSAID), we leave more of the substrate arachidonic acid for 5-LOX to ultimately convert into leukotrienes. This is the basis for aspirin-intolerant-asthma, which is frequently associated with nasal polyps. (Samter's triad).
https://www.karger.com/article/FullText/355949
D) Prostacyclin synthase . E) Thromboxane synthase
This question is disguised. What they are really asking is "what is the sole determinant of species survival"? The only answer is the ability to procreate. Because DNA Polymerase has proof-reading activity, progeny will be unaffected by RNA Polymerases lack of proof-reading activity.
https://en.wikipedia.org/wiki/Proofreading_(biology)
Here is a little bit on proofreading.Hope it helps
this patient's uterus was increased in size compared to a 12 week uterus. she had grape like structures and no fetus. this would indicate a hydatidiform mole. this patient also had no fetal parts so it would be a complete mole.
according to pathoma, a hydatidiform mole is an "abnormal conception characterized by swollen and edematous villi with proliferation of trophoblasts"
also in a complete mole, most villi are hydropic and trophoblasts will proliferate diffusely around these hydronic villi.
the sheetlike masses of syncytiotrophoblasts would indicate a choriocarcinoma.
She just completed the course of rituximab, which targets CD20 receptors. B-cell deficiency can predispose to bacterial infections.
b) BM failure is not associated with rituximab c) wrong d) wrong e) this occurs w/in 7-10 days of starting treatment, and would not occur after completing a 4-month course of rituximab.
MHC I function is integral to cancer suppression. MHC I displays endogenously synthesized proteins and presents them to CD8+ T cells. The failure to display MHC I, or MHC I display of non-self (and by extension cancerous) proteins triggers a cellular immune response, leading to destruction of the cell.
The proteasome is used for the degradation of worn out, senescent, or malformed proteins. As cancer develops, more mutations lead to increased wrong proteins. Only by expression of the proteasome, or its over-expression, can these mutant proteins be degraded fast enough to not be displayed by MHC I and lead to the cell being killed. Bortezomib blocks the proteasome, so the mutant proteins are displayed on the surface, allowing the immune system to recognize and kill pathological cells.
MOA of proteosome inhibitors for MM. TLDR: is that they basically block the proteosome from functioning so that myeloma cells can't recycle protiens (they make a ton of them) and when they can't be recycled they build up and thats toxic to the cell and it dies.
beyond that the question is basically asking if the inhibition of proteosomes isnt specific to the Myeloma cells and it inhibited other cells' proteosomes what would be effected?
MHC class I is present on all nucleated cells (all cells in the body except RBC) and function to present endogenous antigens to CD8+ t cells to be destroyed (for example Viral DNA in an infected cell). The way they do this is by taking the protien it needs to present and breaking it down into much smaller peptide chains (so it can fit on the MHCI. If this step was inhibited in other cells then the the Presentation of MHC I wouldnt be able to present their antigens to CD8+ T cells and Natural killer cells. as the question implies.
The question was super tricky because if you don't know how proteosome inhibitors work then you start looking for an answer that would explain how they would kill tumor cells as well. I got it wrong too. It required knowledge of the way MHC I presents peptides.
Trihexphenidyl and Benztropine are antimuscarinics that can treat the resting tremor and rigidity of parkinsonism.
To expand on this, what we think happens with Parkinson's disease (and parkinsonianism) is an imbalance between dopamine and acetylcholine. It makes more sense if you look at this diagram, paying particular attention to the indirect pathway. Loss of dopaminergic (DA) neurons from the substantia nigra (SNc) results in constant activation of those ACh secreting neurons, which ultimately results in inhibition of thalamus from initiating movements. Therefore, using anticholinergics help with parkinsonianism secondary to haldol.
Hemochromatosis, aka "bronze diabetes". Cannot be Addison due to the hyperglycemia and normal BP
Did anyone think that influenza was right? I understand that Herpes-Z can cause pneumonia but why is this answer better over influenza?
Critical points for this question: 5 year old boy, immunosuppressed because of chemotherapy, 2 day history of fever, cough, shortness of breath, febrile (101.8 F), respirations 46/min, with cyanosis and generalized vesicular rash. Extensive nodular infiltration.
Of the options listed only measles and VZV give a rash. A rash from measles usually starts rostrally and descends caudally, and is flat and erythematous. By contrast, VZV (chickenpox) presents with generalized rash that quickly transitions from macular to papular then to vesicular.
2/3 1/25 1/4
He has a 2/3 chance of being heterozygous (not 2/4 b/c we know he for sure doesn't have CF)
1/25 chance in the population
1/4 chance of a heterozygous couple having a child with CF
Posterior cord syndrome occurs due to infarction of the posterior half of the spinal cord, from occlusion of the posterior spinal artery. Our patient presents with decreased sensation to pinprick below the level of the knees as well as walking with a wide-based gait, likely indicating loss of proprioception. The patient is also anemic with hyper-segmented neutrophils.
Hypersegmented neutrophils are typically caused by an inability to make enough DNA, caused by a lack of necessary precursors and vitamins including B9 (folate) and B12 (cobalamin). If the patient is folate deficient, we see elevated homocysteine deficiency. If the patient is B12 deficient, we see elevated methylmalonic acid and homocysteine levels. Hyperhomocysteinemia can increase thrombosis. Thrombosis in the posterior spinal artery can cause posterior cord syndrome. In addition, lack of vitamin B12 impairs myelin formation and leads to Subacute Combined Degeneration, which affects the Spinothalamic tract (accounting for decreased pinprick sensation), Corticospinal Tract, and Dorsal Column-Medial Lemniscus Tract (accounting for the reduced proprioception.
A) Anterior cord syndrome- loss of motor command, as well as bilateral loss of heat and pain, the patient has not lost motor function, so it cannot be this. B) Central cord syndrome- presents as a combination of motor and sensory loss, usually with bladder dysfunction. This patient does not display motor loss or bladder dysfunction. C) Hemicord syndrome- Also called Brown-Sequard, this is complete injury to either the left or right side of the spinal cord. It presents with motor dysfunction and reflex dysfunction ipsilaterally at the level of the lesion; loss of upper motor command below the lesion ipsilaterally (spastic paresis); loss of dorsal column-carried sensation ipsilaterally at and below the lesion; and loss of pain and temperature sensation contralaterally 2 to 3 vertebra below the lesion. E) Segmentary syndrome- a congenital failure to develop part of the spinal cord. The new onset of symptoms at 82 years old makes this an unlikely diagnosis,.
Personally my issue with this question is that I though B12 causes demyelination in both the LCST and the DCML (SCD) but they are testing the mechanism here really with the whole methylamonic acid bit and the impaired myelin synthesis
If you're curious
But doesn't subacute combined degeneration lead to impairment in DCML, spinocerebellar and corticospinal tract? I get the ataxic gait - DCML/spinocerebellar. But the sensation to pinprick, wouldn't that be the spinothalamic tract? That is not usually affected in subacute combined degeneration.
Can anyone further explain this?! I could eliminate a few item choices and I guessed correctly, just need more information! Thanks
The patient underwent removal of a rectal tumor which had involvement with the prostate. The prostatic capsule is rich with nerves including the pelvic splanchnic nerves, a set of parasympathetic nerves responsible for PNS autonomic regulation. Erections are a parasympathetic function.
A) Gray rami from the sympathetic chain- erections are a parasympathetic function, not sympathetic. Emission of sperm is a sympathetic function, and is directed by the inferior hypogastric nerve. C) Pudendal- the pudendal nerve is a somatic nerve that receives sensation from the penis, posterior scrotum, clitoris, and labia, as well as being responsible for some movement of the pelvic floor, and ejaculation. D) Superior hypogastric nerve- a sympathetic nerve, this contributes to the hypogastric plexus and may also contribute to sympathetic control of emission. E) Ventral ramie of S2-S4- These rami contribute to the pudendal nerve.
An asymptomatic 30-year-old woman comes to the physician for ...
Anovulation