https://images.app.goo.gl/PKyrfPDUoeQHYvf26
This image explains it nicely
doctor refuses to give a large doses of drugs which can harm the patient and assures her to manage the pain
Why couldn't this be multiple myeloma, they look fairly similar and the patient had a long illness, leading me to multiple myeloma. I see how its osteoporosis, but how would you distinguish the two.
But doesnt TSS spare the mucous, so I picked Trimethoprim/sulfamethoxazole thinking it could be steven johnson syndrome, I overthought it way too much!! Stupid point to lose.
This is a new comment by me. I would like to be able to submit here.
His calcium is in the reference range due to bone resorption. We also see a decrease in phosphorus which hints at an increase in PTH.
Simplified version: invariant chain serves as a placeholder that sits in the antigen binding site of MHC-II before it reaches the APC endosomes,
Important because it stops MHC-II from activating against endogenous proteins prior to its arrival to the endosome.
Inside the endosome the Invariant chain is degraded by acid-activated proteases, and only then the exogenous antigens are loaded on MHC II.
MHC2 mounts peptide on endosome (breaks antigen in cytosol and combines with premade MHCII complex inside endosome and shoots it out).
MHC1 mounts peptide on ER (breaks antigen in cytosol and uptake inside the ER where forming MHC1 and antigen particle assemble together and shoots out via ER-Golgi).
Why? I though the bicep reflex would be strongest since it was not involved with the radial nerve issue.
Wait, adipose tissue scars?? What the heck is this? maybe it's that 'fibro' part...Watched all that Botched for nothin'
This difficulty score is wrong, should be like .1 lol
cGMP is broken down by phosphodiesterase so phosphodiesterase inhibitors will cause more cGMP and more vasodilation.
Epinephrine in anaphylatic shock. In this scenario she has mainly breathing problems (wheezing) so I think that for this reason B2 agonist is used.
schizophrenia in this question->hearing voices, poor hygiene and listening to internal stimuli.
Q: A previously healthy 4-year-old girl is brought to the physician because of fever [...] Ans: B, Arthrocentesis
hyperventilation = โ CO2 โ vasoconstriction of cerebral vessels โ dizziness/lightheaded.
โ pH = โ calcium levels = tetany/perioral tingling/paresthesias.
Breathing into a paper bag reverses the symptoms because recycled air has a higher concentration of carbon dioxide than normal air.
Answer: breathing into a paper bag
Kid athlete passing out suddenly + murmur changes with maneuvers.
why cant it be A? Aren't melanocytes derived from neural crest cells?
Proteoglycans are extracellular matrix molecules that have a central protein core or backbone structure with covalently attached glycosaminoglycans. Proteoglycans, cartilage, and water are the main constituents of human cartilage.
In osteoarthritis, the breakdown of articular cartilage caused by chronic repetitive use and inflammation results in the decreased synthesis of proteoglycans by the chondrocytes. The loss of this component of cartilage is reflected at the macroscopic level by cartilage degradation and bone-bone contact osteoarthritic degenerative joint disease. Decreased proteoglycan secretion is expected on arthrocentesis, synovial fluid may show few leukocytes, but otherwise will be without evidence of acute inflammation or infection.
The patient's enzyme needs more substrate to achieve the same effect as the normal enzyme.
The Km is the substrate concentration at which the enzyme achieves 50% maximal concentration.
More substrate is needed in the patient to reach the 50% maximal velocity than is needed in the normal patient so it must be that there is a mutation in the enzyme that increases Km.
The Bartholin glands, or the greater vestibular glands, are a pair of glands on either side of the posterior vaginal orifice that secretes a lubricating fluid through two small ducts into the vestibule. When one of these glands becomes blocked, a cyst may occur.
The infection is generally polymicrobial, but anaerobes such as Bacteriodes fragilis, Clostridium perfringens, Peptostreptococcus, and Fusobacterium are key pathogens.
Cryptosporidiosis presents with severe watery diarrhea in immunocompromised patients; it is diagnosed by microscopy of the stool showing red-pink oocysts on the acid-fast stain.
The patient with HIV infection and 10 days of watery diarrhea and abdominal cramps has been infected with Cryptosporidium, an intracellular parasite that causes a severe GI illness in an immunocompromised patient.
See this question in NBME 27
See this question from NBME 25.
The peripheral blood smear shows a schizont form of the parasite, although any malarial stage (gametocyte, schizont, trophozoite, or ring) can be seen on a smear and is diagnostic of infection. CHLOROQUINE effectively eradicates circulating forms if there is no resistance but has NO EFFECT ON THE HYPNOZOITE EXOERYTHROCYTIC forms of P Vivax and P ovale. Addition of PRIMAQUINE effectively treats these liver forms and prevents relapsing infection.
Pulsus paradoxus refers to the abnormal variation of systolic blood pressure between inspiration and expiration (greater than 100 mm Hg). This presents as jugular venous distension sometimes and is often seen in conditions that restrict expansion of the heart, such as cardiac tamponade.
Maternal glucose crosses the placenta while insulin does not (remember that HPL services the baby by shunting the mother's glucose to the baby by conferring insulin resistance to the mom). In response to hyperglycemia in the mom, the fetal pancreatic islet cells increase the production of insulin. If the source of glucose is quickly removed, such as after delivery, the infant has a high risk of developing hypoglycemia, which can lead to convulsions and death.
See this question in NBME 27 asking about what a 5-alpha-reductase deficiency would look like.
The SRY gene is located on the Y chromosome and is responsible for producing the testis-determining factors, which results in male gonadal differentiation. In testis development, hormones secreted by Sertoli cells (MIF Macrophage Inhibiting Factor) and Leydig cells (testosterone and DHT) promote the development of male internal and external genitalia and suppress the development of female structures. SRY gene translocation can occur during recombination in which the SRY gene on the Y chromosome becomes part of the X chromosome, leading to an XX embryo developing male characteristics.
An intensely eosinophilic globule in the liver is a Councilman body that is indicative of an underlying hepatic disease, viral Hepatitis (usually Hepatitis A), or Yellow fever. This represents a hepatocyte undergoing APOPTOSIS.
Recall that Yello Fever is caused by flavivirus/arbovirus transmitted by the Aedes mosquito causing black vomitus, jaundiced eyes, and the Councilman bodies (intensely eosinophilic apoptotic globules in the liver).
To also answer this question, one had to know that apoptosis caused by activation of the mitochondrial intrinsic pathway is triggered by cellular damage such as radiation, oxidative damage, ischemia, or toxin exposure and leads to release of cytochrome C from mitochondria. Cytochrome C in turn leads to the activation of caspase enzymes. Viral hepatitis primarily leads to apoptosis through the extrinsic rather than the intrinsic pathway.
Morbilliform skin rash is HIGH-YIELD for a drug reaction, the most severe being Drug reaction with eosinophilia and system symptoms (DRESS). It is associated with the use of allopurinol, anticonvulsants, antibiotics like TMP-SMX, and sulfa drugs. This is a potentially fatal delayed hypersensitivity reaction.
It is also related to a severe rash Stevens-Johnson syndrome or Toxic epidermal necrolysis which is also caused by anti-epileptic drugs (especially lamotrigine), allopurinol, sulfa drugs, and penicillin.
See here in FA 2020 for a list of extrahepatic manifestations in HepC and HepB. Importantly HepC can induce essential mixed cryoglobulinemia. It presents with palpable purpura in association with arthralgia and peripheral neuropathies caused by immune-complex type III hypersensitivity mediated vasculitis.
The triad is weakness, arthralgia, and palpable purpura. Keep in mind peripheral neuropathy, hematuria, and hepatosplenomegaly and most importantly, Hepatitis C.
This image is clinically extremely similar to the image for Fibromuscular dysplasia in FA 2020 on pp300.
90% of hypertension is 1ยฐ (essential) and related toยCO orยTPR. The remaining 10% is mostly 2ยฐ to renal/renovascular diseases such as fibromuscular dysplasia (characteristic โstring of beadsโ appearance of the renal artery, usually seen in women of child-bearing age) and atherosclerotic renal artery stenosis or to 1ยฐ hyperaldosteronism.
This question should be easy but if you didn't go through all the options, or if you're like me and tunnel-vision on seemingly right options, then you can miss "gimme" points on a question like this. We know that DNA plasmids in bacterial are circular and don't really have a terminal end or beginning but rather have DNA synthesis sites where DNA polymerases can attach to begin replication.
See this question in block 1 about GVHD.
See also these tables on transplant rejection pathologies from FA 2020.
Chronic allograft rejection of a transplanted organ occurs over months to years (the question was in the timeline of weeks). It is secondary to a CD4+ T lymphocyte response against donor peptides such as MHC. T cell activation leads to cytokine production and humoral and cellular hypersensitivity reactions (type II and IV). When you think Chronic rejection, you should be thinking VESSELS because this often leads to vascular arteriosclerosis and smooth muscle proliferation with parenchymal fibrosis and atrophy.
With acute rejection, you should be thinking of INFILTRATION, that is T-lymphocytes in the vasculature of the tubules and arterial walls leading to endothelitis. The primary histologic changes include interstitial infiltration with lymphocytic cells, in addition to the obliteration of the tubular basement membranes (as in this question with a kidney transplant).
See pages from FA 2020 and other resources.
The moment we see HepB seropositivity, cutaneous eruptions, and different stages of TRANSMURAL INFLAMMATION WITH FIBRINOID NECROSIS, we should be thinking Polyarteritis nodosa (PAN). It is treated with corticosteroids and cyclophosphamide.
This patient had segmental transmural necrotizing arteritis making PAN the best answer.
Recall that for Giant cell arteritis or temporal arteritis, one would see a headache, temporal tenderness, jaw claudication, and fever.
See this question in NBME 27.
Antiphospholipid syndrome is diagnosed based on recurrent venous thromboses (hypercoagulability), frequent miscarriages, thrombocytopenia, and a false-positive rapid plasma reagin test. It is associated with clinical criteria including a history of thrombosis (arterial or venous) or spontaneous abortion along with laboratory findings of lupus anticoagulant, anticardiolipin, anti-ฮฒ2 glycoprotein I antibodies.
See this question from the same block asking about Kawasaki syndrome (but related to hepatic encephalopathy).
Systemic ammonia absorption is prevented by the administration of lactulose, which is degraded by gut bacteria to create an acidic environment (via conversion to lactic and acetic acid) that facilitates the conversion of ammonia to ammonium, trapping it in the lumen of the bowl for subsequent excretion in the stool.
Recall that you can also give rifaximin or neomycin to decrease the levels of ammoniagenic bacteria.
Target cells have 4 possible associated pathologies HALT:
"HALT," the hunter said to his target.
Thalassemias can also present with basophilic stippling, where an erythrocyte is just muddled with darkly staining granules (that do NOT contain iron). This is also seen in sideroblastic anemia. Note that in sideroblastic anemia you would see Pappenheimer bodies (iron-containing basophilic granules).
Thalassemias are diseases of defective globin chains, either in the alpha or beta globin chain. The moment you see HbA2 mentioned, you should be thinking of beta-thalassemias. To differentiate between major and minor beta-thalassemias, you need to look at the amount of HbA2 and HbF replacing HbA.
beta-thalassemia minor is primarily an asymptomatic disease with mild microcytic anemia. Hb electrophoresis shows a small amount of HbA2 and HbF and near normal (90%) concentrations of HbA.
This person has NO HbA (an absence of HbA) and increased concentrations of HbA2 and HbF so it must be major beta thalassemia.
This page from FA2020 and other resources show that certain lab values in pregnancy screening are diagnostic for Trisomy 21.
The easy thing to remember is that in all autosomal trisomies PAPP-A is decreased. (In trisomy 21 Down, 18 Edwards, and 13 Patau, PAPP or pregnancy-associated plasma protein is decreased).
For Down syndrome specifically, first-trimester ultrasound commonly shows increased nuchal translucency and hypoplastic nasal bone.
Finally, in trisomy 21 Down syndrome, the markers are HI up, as in
In other trisomies, these values are decreased.
These are usually what they teach in school I think:
Midclavicular line between 6th & 8th ribs -> 7th intercostal space
Midaxillary line between 8th & 10th ribs -> 9th intercostal space (or the midscapular line if the patient is upright)
Paravertebral line between 10th and 12th ribs ->10th intercostal space
In general, you want to do it above a rib because the intercostal arteries, veins, and nerves run along the bottom of a rib. You're aiming for the costodiaphragmatic recess which is usually found between the 8th and 10th ribs. The correct position for a thoracocentesis is above the 9th rib on the affected side, along the midaxillary line if the patient is supine, or the posterior midscapular line if the patient is upright.
I answered this question using the fact that HMG-CoA reductase inhibitors or statins greatly decrease LDL concentrations by upcycling LDL receptors on hepatocytes. It must be that the primary mechanism of serum LDL cholesterol accumulation is then decreased clearance by the liver.
I thought this question was difficult because I tunnel-visioned on the diagnosis being hepatic encephalopathy (which it somewhat is), but it is hepatic encephalopathy secondary to Reye syndrome.
Mitochondrial dysfunction is associated with the pathogenesis of Reye syndrome, which is associated with salicylate use (such as aspirin) in children preceding viral infection. Usually, a VZV or influenza infection is treated with aspirin, and aspirin metabolites decrease beta-oxidation by reversibly inhibiting MITOCHONDRIAL enzymes. These mitochondrial abnormalities are associated with SHINE:
You want to avoid aspirin in children, except in those with Kawasaki (mucocutaneous lymph node syndrome) disease.
Cat scratch disease is caused by infection with the gram-negative coccobacillus Bartonella henselae*. Infection is acquired via scratches or bites from domestic or feral cats, which can most commonly cause local lymphadenitis in the lymphatic drainage pattern of the scratch location. Because people get scratched on their arms, the most common locations are the axillary nodes. Histological examination shows NECROTIZING GRANULOMAS WITH STELLATE MICROABCESSES.
Recall that red infarcts happen not only when there is venous occlusion and ischemia in organs with multiple blood supplies (such as the liver, lung, intestine, and testes) BUT ALSO WHEN there is reperfusion injury, mainly after angioplasty. Reperfusion injury is due to the production of free radicals and peroxides. Reperfusion injury can also happen after thrombolytic therapy. This is also seen in the first 0-24 hrs of myocardial infarction where reperfusion injury can cause free radicals and increased Calcium influx.
So why then is E) Protease inactivation by cytoplasmic free calcium ions incorrect? Although altered membrane permeability as a result of oxidative damage leads to changes in calcium flux and a rise in intracellular calcium, this intracellular calcium leads to ACTIVATION, rather than inactivation.
I saw the government building/employees being affected and I instantly picked Anthrax because of that incident where people sent Anthrax-laced letters to people in the US through the mail as a form of bioterrorism. If I had read the question more clearly, the symptoms of organophosphate (or anticholinesterase) poisoning were evident (DUMBBELSS).
The easiest way to remember these is just know that acetylcholine or cholinergic tone in general is usually parasympathetic or "rest-and-digest". So you can urinate and defecate, you can keep your pupils closed, slow your heart rate down, and salivate to eat. Though organophosphate poisoning through something like parathion or malathion is commonly seen in insecticides (where the poisoned victim is usually a farmworker or someone in an agricultural setting), I guess it can also happen as a form of bio-terrorism.
You can reverse this poisoning through Atropine, a muscarinic antagonist, a competitive inhibitor that can cross the BBB. Pralidoxime is also given to regenerate AChE.
Sometimes in pathology, a term will be used exclusively for one situation, and thatโs it. Two phrases that come to mind are โstarry sky patternโ (Burkitt lymphoma) and โcerebriform nucleusโ (mycosis fungoides/Sezary syndrome). ... โOwlโs eyeโ belongs to the latter category of patterns in pathology images that are seen in multiple diseases. It can be used to describe the nuclei of cells infected by CMV (as in this question), and it can also be used to describe the nuclei of Reed-Sternberg cells in Hodgkin lymphoma (CD15+ and CD30+ B-cells) (taken from this blog).
This clip from Family Guy always sticks with me for some reason. Some people can become addicted to Phenylephrine or Oxymetazoline (alpha-1-receptor agonists) nasal sprays (like Afrin).
The difficult aspect of this question was making the jump from noting he has asthma (which was not obvious to me) and then that he might be hyperventilating and then the final jump to respiratory alkalosis (due to low CO2 from the hyperventilation). If you can make those jumps, you just pick the answer with the high pH, and low CO2 (of which there is only one option).
I guess the acute onset and the high minute ventilation do indicate asthma but it is hard to catch. Dyspnea and hypoxia stimulate an increase in respiratory drive, which in turn leads to tachypnea or increased tidal volume; hyperventilation occurs leading to respiratory alkalosis as acidic CO2 is eliminated.
Dipeptides and tripeptides are produced by the activity of trypsin and chymotrypsin within the lumen of the duodenum. Free amino acids are produced upon further digestion of these small peptides within the brush border of the intestinal mucosa.
The lumen of the duodenum is wrong because that is where larger complex polypeptides are broken down to di- and tripeptides but the action of taking di- and tripeptides down to individual amino acids happens in the intestinal mucosa.
Polyhydramnios is almost always associated with an issue with the baby's ability to swallow amniotic fluid, preventing its recycling and resulting in the overproduction of amniotic fluid. Inability to swallow may be due to esophageal or duodenal atresia or anencephaly. It can also be associated with maternal diabetes, fetal anemia, and multiple gestations.
Increased concentrations of fetal hemoglobin results in a left shift of the oxygen dissociation curve with the maintenance of the sigmoidal cooperative binding characteristics.
I like to remember the "CADET!, stand RIGHT" mnemonic:
Factors that move the oxygen dissociation curve to the right are those physiological states where tissues need more oxygen. For example, during exercise, muscles have a higher metabolic rate, and consequently need more oxygen, produce more carbon dioxide and lactic acid, and their temperature rises (from Wikipedia on the O2-Hb dissociation curve).
Total blood volume can be calculated by the following equation:
Total blood volume = Erythrocyte stuff + Plasma stuff
TBV = hematocrit% * TBV + plasma% * TBV
(where hematocrit% + plasma% = 100%)
TBV = hematocrit% * TBV + plasma volume
and in this question
TBV = 0.4*TBV + 3L
0.6*TBV = 3L
TBV = 5 L
I-cell disease is an AR lysosomal storage disease that results from a defect in N-acetylglucosaminyl-1-phosphotransferase enzymes. This results in the failure of phosphorylation of lysosomal hydrolases, which subsequently leads to their exocytosis from the cell instead of routing to their normal site of action within the lysosome.
One way to have answered this question, if you didn't have the ion values memorized for metabolic alkalosis caused by vomiting is to remember what happens in BULIMIA NERVOSA.
Bulimia nervosa consists of recurring episodes of binge eating with compensatory purging behaviors at least weekly over 3 months. The electrolyte disturbances seen in that disease (which are high-yield and tested often) are
Vomiting and Bulimia both lead to hypochloremic hypokalemia and metabolic alkalosis.
See this question in NBME 25.
See this question in NBME 25.
While EBV infects B cells through CD21,
the atypical lymphocytes in on peripheral blood smear are cytotoxic CD8+ T lymphocytes reacting to the viral infection.
Region of consolidated parenchyma in pneumonia
demonstrates impaired gas exchange and may cause hypoxia.
Congenital neutropenia is defined as neutropenia that is present at or around the time of birth, is not related to a secondary cause, and persists.
In cases of mild neutropenia, symptoms are less common, although patients may eventually develop stomatitis and gastrointestinal ulceration.
In severe cases, there is a substantially heightened risk for invasive bacterial infection.
AML is an aggressive malignancy of myeloid cells and commoniy presents in adults with pancytopenia and circulating blasts on peripheral smear.
Gingival hypertrophy is not an uncommon finding and represents infiltration of the gingiva by malignant cells.
Depending upon the types of mutations present, patients are divided into good, intermediate, or poor risk subcategories. Those with poor risk disease invariably go on to stem ceil transplant after induction and consolidation chemotherapy.
Infertile patient with autoantibodies to sperm on Labs = dysfunctional Sertoli cells.
The CBFA1 gene mutation in cleidocranial dysplasia results in impaired osteoblast differentiation with resultant impaired ossification in membranous bone.
Features include frontal bossing, facial bone malformations, supernumerary teeth, and absent or diminutive clavicles.
Oxygenation of mechanically ventilated patients in the setting of acute lung injury is challenging because of reduced lung compliance and absorptive atelectasis from fluid in the alveolar space.
Positive end-expiratory pressure (PEEP) can reduce the amount of alveolar collapse and atelectasis.
Renal papillary necrosis (RPN) occurs following Ischemic, inflammatory, infectious, or toxin-mediated damage to the renal papilla and describes the sloughing and loss of the papillae including substructures such as the distal collecting tubule.
RPN can be triggered by infections (eg. acute pyelonephritis), diabetes mellitus, sickle cell disease, or NSAIDs.
It typically presents with gross hematuria and proteinuria on urinalysis.
Nevocellular nevus = Nevus.
DDX:
seborrheic keratosis= benign proliferation of the epidermis. Greasy, adherent appearance. Associated with some GI malignancies.
Actinic keratosis= premalignant lesion that may progress to squamous cell carcinoma. Rough, scaly patches of skin in sun exposed areas.
Epithelial cell connections include tight junctions, adherens junctions, desmosomes, and gap junctions.
Tight junctions are responsible for creating a tight seal to prevent the paracellular movement of solutes or water through an epithelial or endothelial lining.
Inflammation often impairs the efficacy of tight junctions.
The physician should respond that cancer is a possibility!!
Allosteric activators influence enzymes by inducing conformational change at the active site, which increases binding affinity for the substrate. This is reflected by a decreased Km.
AMP a breakdown product of adenosine triphosphate, is generated in states of fasting and thus upregulates glycogen phosphorylase to liberate stored glucose and supply the cells with a substrate for glycolysis when none is nutritionally available.
Acromegaly is associated with excessive growth hormone and IGF-1 concentrations, which lead to deranged glucose homeostasis.
This is done by increasing peripheral insulin resistance, impairing muscle and adipose uptake of glucose, and increasing lipolysis and hepatic gluconeogenesis.
Patients with acromegaly experience increased rates of DM and hypertriglyceridemia.
Glucose-dependent insulinotropic peptide (GIP) is secreted by K cells in the duodenum and jejunum, and it functions to decrease gastric acid production and stimulate insulin release from the pancreas.
Insulin promotes the peripheral tissue uptake of glucose and hepatic glucose storage, resulting in a decreased glucose concentration in the serum.
vs.
Motilin: is secreted by the small intestine and stimulates intestinal peristalsis. Motilin receptors are targeted by erythromycin and metoclopramide, used therapeutically in gastroparesis.
Secretin: secreted by duodenal S cells. Increases release of bicarb Rich pancreatic secretions and inhibits gastric acid.
Somatostatin: regulatory peptide secreted by D cells of the pancreas and gastrointestinal mucosa that inhibits gastric acid and pepsinogen secretion, gallbladder contraction, and insulin and glucagon release. Somatostatin would have an indirect effect on glucose through counterregulatory action of both insulin and glucagon.
The volume of distribution is a theoretical volume in which a drug exists based on its plasma concentration.
It is altered by changes in volume of the intravascular, interstitial, and intracellular compartments.
Increases in volume of distribution are exhibited by a slower rate of increase in plasma drug concentration and a prolonged period before reaching steady-state concentration. (slower to reach the plateau)
Regional Auto registration is mediated by the delivery of filtered sodium to the macula densa.
decrease in BP --> Hypo-perfusion of the glomerulus leads to decrease sodium filtration, and activation of RAAS by the macula densa, which causes AT-2 mediated constriction of the glomerular efferent arteriole, and consequent increase in intraglomerular pressure/GFR.
The kidneys relatively low metabolic demands compared with high blood flow result in a small difference in renal arterial and venous po2.
The po2 in the renal vein is relatively High compared to other organs that depend on blood flow to meet local metabolic demands.
kidneys are small, and receive almost one-fourth of total cardiac output, getting the largest blood flow per gram of tissue. Blood flow in the kidneys is excessive because it's more for filtration purposes. Thus there will be a small difference in arterial and venous po2.
Waardenburg Syndrome
Most children between the ages of three and five years old will he death is temporary and reversible. Further, preschool-age children are frequently unaware of the inevitability of death.
The cut point of a test should be set to optimize sensitivity, specificity, or both depending on the clinical utility of the test.
A more sensitive test should be employed when ruling out a significantly mortal or morbid diagnosis.
There is overlap between the two, suggesting that some patients will test equivalently on the test but may or may not have the disease. Setting the cut point to point B would permit all patients within the area under the infected curve to be identified as positive, which maximizes sensitivity, while minimizing the number of false positives, and therefore optimizing specificity while prioritizing sensitivity.
Alcohol leads to the induction of P450 enzymes that convert acetaminophen to N-acetyl-p-benzoquinoneimine (NAPQI), a toxic metabolite that causes hepatotoxicity in the setting of acetaminophen overdose.
M. Acidosis or decreased NAD+ and increased NADH do not play a direct role in acetaminophen-mediated hepatotoxicity!
Examination during an open fung biopsy shows a thick: firm, white pleural tumor that ensheathes the right lung. = Mesothelioma.
Asbestosis is a chronic progressive pulmonary disorder associated with interstitial fibrosis and an increased risk for both primary bronchogenic carcinoma and malignant mesothelioma. Occupational risk factors for asbestos exposure include shipbuilding, roofing, and plumbing.
The round ligament of the uterus is a fibromuscular band of tissue that extends from the superolateral part of the uterus where the fallopian tubes insert, passes through the inguinal canal, and ends in the labia majora. Stretching of the round ligament commonly leads to pain during pregnancy.
The postsynaptic membrane potential (Choice D) may be decreased in LEMS secondary to the decreased presynaptic release of acetylcholine. = WRONG ANS.
During pregnancy, progesterone is produced by the:
corpus Luteum for the first 7-10 weeks of gestation, secondary to stimulation by human chorionic gonadotropin from the placental syncytiotrophoblast.
after 7+ weeks, it is primarily produced by the placenta.
Brief psychotic disorder Is characterized by at least one acute psychotic symptom (eg. delusions, hallucinations, disorganized speech, disorganized behavior) lasting less than one month.
I-cell disease is an autosomal recessive inherited lysosomal storage disease that results from a defect in N-acetylglucosaminyl-1-phosphotransferase enzymes.
results in a defect of addition of mannose phosphate to lysosomal enzymes.
This results in the failure of mannose residue phosphorylation of lysosomal hydrolases, which subsequently leads to their abnormal expulsion from the cell instead of to their normal site of action within the lysosome.
Presents with coarse facial features, generalized hypotonia, bilateral hip dislocation, and inguinal hernias. Also presents with developmental delay and delayed growth.
increase serum activity of lysosomal enzymes.
*results in a defect of addition of mannose phosphate to lysosomal enzymes.
This results in the failure of mannose residue phosphorylation of lysosomal hydrolases, which subsequently leads to their abnormal expulsion from the cell instead of to their normal site of action within the lysosome.
Presents with coarse facial features, generalized hypotonia, bilateral hip dislocation, and inguinal hernias. Also presents with developmental delay and delayed growth.
increase serum activity of lysosomal enzymes.
Anticipation is a genetic phenomenon in which disease traits are more severe and/or appear at earlier ages in later generations. Anticipation typically results from trinucleotide repeat expansions. Myotonic dystrophy, which features intergenerational anticipation, results from a trinucleotide repeat expansion of the DMPK gene in skeletal muscle cells that leads to progressive muscle dysfunction.
Struvite precipitates as renai calculi in alkaline urine, which can be caused by urinary tract infections with urease-producing organisms such as Proteus. Urease catalyzes the conversion of urinary urea to ammonia and carbon dioxide, which results in alkalinization. Struvite calculi may be large and branching, often requiring surgical removal
(image with large staghorn stone)
Next step: colonoscopy to rule out CRC.
Protein-calorie malnutrition, or failure to thrive, characterizes the terminal stage of dementia, Alzheimer type.
Signs of protein-calorie malnutrition include weight loss, muscle wasting, hypoalbuminemia, and signs of vitamin deficiencies.
Central diabetes insipidus may result from head trauma and is characterized by inadequate secretion of ADH.
Lack of ADH leads to decreased free water reabsorption from collecting tubules, resulting in an abnormally increased serum osmolality.
Brain Stem Gliomas are the most common pediatric brain tumor and are typically low-grade pilocytic astrocytomas that may occur in the cerebellum or brain stem.
DDX: Arnold-Chiari malformations:
Deficiencies in the enzymes required to synthesize or recycle BH4 result in a clinical syndrome that is largely indistinguishable from PKU, as BH4 is a necessary cofactor in the reactions catalyzed by PAH.
These disorders are inherited in an autosomal recessive fashion and treatment ES with oral replacement of BH4.
Metabolism of tetrahydrobiopterin (BH4) is deficient in a small subset of patients with phenylketonuria (PKU). The majority of patients with PKU have a deficiency in the enzyme phenylalanine hydroxylase (PAH) that converts phenylalanine to tyrosine. Deficiency results in accumulation of phenylalanine and its metabolites phenylacetate and phenyllactate.
However defects in enzymes that either produce or recycle BH4 can have similar clinical manifestations since BH 4 is a required cofactor for the function of PAH. It is also used as a cofactor for the enzymes tyrosine hydroxylase and tryptophan hydroxylase.
Autosomal recessive mutations in these enzymes result in impaired metabolism and recycling of BH4.
Clinical manifestations include neurotransmitter deficiency in addition to symptoms normally associated with PKU: microcephaly, skin disease, seizures, and intellectual disability.
The introduction of pathogenic bacteria into the normally sterile environment of the peritoneum induces a robust inflammatory response, with the secretion of fibrin that subsequently traps and encases bacteria.
While important in limiting the spread of infection, it can also predispose to the formation of abscesses.
Colonic malignancy has a long latency period, which suggests that any study intended to detect the difference in risk factors and exposures should also have a similarly long evaluation period.
An absence of sufficient duration may limit internal validity and limit the ability to conclude the presence or absence of an association between the exposure and outcome in question.
DDX:
DDX:
Patent ductus arteriosus: results in a continuous, machine-like murmur best heard at the left second intercostal space radiating to the clavicle.
Pulmonic stenosis: a systolic murmur best heard at the second left intercostal region; it is also often crescendo-decrescendo, though it is quieter and radiates less to the lower neck than aortic stenosis because of the lower pressure in the pulmonary circulation. Pulmonic stenosis is typically seen in tetralogy of Fallot.
Tricuspid regurgitation: a holosystolic murmur best heard at the left lower sternal border; it may result from severe pulmonary hypertension or infective endocarditis in IVDU.
DDX:
Atrial septal defect: results in a left-to-right shunt with abnormal flow of blood from the left atrium to the right atrium. This causes relative volume overload of the right atrium and ventricle, which presents as a fixed, split and low-grade physiologic ejection murmur.
Coarctation of the aorta: narrowing of the aorta. Associated with a bicuspid aortic valve and Turner syndrome. It typically presents with a systolic murmur along with differential pulses and blood pressures between extremities.
Mitral regurgitation: a holosystolic murmur best heard at the left fourth or fifth intercostal space along the midclavicular line and radiates to the left axilla. It is commonly a/w: mitral valve prolapse, endocarditis, acute rheumatic fever, and prior myocardial infarction.
Mitral stenosis: classically heard as an opening snap followed by a diastolic rumble, loudest over the cardiac apex and radiates to the axilla. If severe enough, it can result in left atrial enlargement, cardiogenic pulmonary edema, and arrhythmias such as atrial fibrillation and flutter.
Do session tokens invalidate? If I try to submit this comment later is it invalidated? Try later.