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 +0  (free120#33)

Fragile X syndrome X-linked dominant inheritance. Trinucleotide repeat in FMR1 gene = hypermethylation = Increased expression.

Most common inherited cause of intellectual disability (Down syndrome is the most common genetic cause, but most cases occur sporadically).

Findings: post-pubertal macroorchidism (enlarged testes), long face with a large jaw, large everted ears, autism, mitral valve prolapse, hypermobile joints.

Trinucleotide repeat expansion [(CGG) n ] occurs during oogenesis.

melanoma  decreased expression

 +0  (free120#14)

Larva currens (Latin for racing larva) is an itchy, cutaneous condition caused by infections with Strongyloides stercoralis. It is caused by the intradermal migration of strongyloides and distinguished from cutaneous larva migrans (caused by hookworms Ancylostoma and Necator) by its rapid migration, perianal involvement and wide band of urticaria.

 +0  (nbme24#7)
  1. Phase I Small number of either healthy volunteers or patients with disease of interest. “Is it Safe?” Assesses safety, toxicity, pharmacokinetics, and pharmacodynamics.

  2. Phase II Moderate number of patients with disease of interest. “Does it Work?” Assesses treatment efficacy, optimal dosing, and adverse effects.

  3. Phase III Large number of patients randomly assigned either to the treatment under investigation or to the standard of care (or placebo). “Is it as good or better?” Compares the new treatment to the current standard of care (any Improvement?).

  4. Phase IV Postmarketing surveillance of patients after treatment is approved. “Can it stay?” Detects rare or long-term adverse effects (eg, black box warnings). Can result in treatment being withdrawn from Market.

 +0  (nbme24#3)

Bone marrow suppression (can be reversed with granulocyte colony-stimulating factor [G-CSF] and erythropoietin), peripheral neuropathy, lactic acidosis (nucleosides), anemia (ZDV), pancreatitis (didanosine).

abhishek021196  Adverse effects of NRTIs

 +1  (nbme24#45)

COPS: CNS = Oligodendrocytes, PNS = Schwann cells.

Neuroepithelia in neural tube—CNS neurons, ependymal cells (inner lining of ventricles, make CSF), oligodendrocytes, astrocytes. Neural crest—PNS neurons, Schwann cells, glia, melanocytes, adrenal medulla.

In CNS (including CN II), myelin is synthesized by oligodendrocytes; in PNS (including CN III-XII), myelin is synthesized by Schwann cells.

Since CP angle mass is a vestibular schwannoma, it arose from Neural Crest cells.

 +0  (nbme24#17)

Homeobox (Hox) genes are in multiple locations and perform segmental organization in cranial-caudal direction, transcription factor coding. Mutations = appendages in wrong locations. Isotretinoin increases Hox gene expression.


Sonic hedgehog (SHH) gene present in the Zone of polarizing activity at base of limb buds and perform the function of anterior-posterior axis patterning, CNS development. Mutations = holoprosencephaly

abhishek021196  FA20 - 612

 +1  (nbme24#14)

Null (H 0 ) Hypothesis = Hypothesis of no difference or relationship (eg, there is no association between the disease and the risk factor in the population).

If the 95% CI for odds ratio or relative risk includes 1, H 0 is not rejected.

Since the CI here includes 1, it means that its not significant and therefore p value should not be < 0.5. Therefore p = 0.5-1.

 +0  (nbme24#18)

Posterior inferior cerebellar artery [PICA] supplies

  1. Lateral medulla
  2. Nucleus ambiguus (CN IX, X, XI)
  3. Vestibular nuclei
  4. Lateral spinothalamic tract, spinal trigeminal nucleus
  5. Sympathetic fibers
  6. Inferior cerebellar peduncle

Damage to PICA causes Lateral medullary (Wallenberg) syndrome.

Dysphagia, hoarseness, decreased gag reflex, hiccups. Vomiting, vertigo, nystagmus decreased pain and temperature sensation from contralateral body, ipsilateral face. Ipsilateral Horner syndrome. Ipsilateral ataxia, dysmetria.

Nucleus ambiguus effects are specific to PICA lesions.

“Don’t pick a (PICA) horse (hoarseness) that can’t eat (dysphagia).” Also supplies inferior cerebellar peduncle (part of cerebellum).

 +0  (nbme24#23)

Vitamin E Deficiency - Hemolytic anemia, acanthocytosis, muscle weakness, demyelination of posterior columns (Decreased position and vibration sensation) and spinocerebellar tract (ataxia).

Neurologic presentation may appear similar to vitamin B 12 deficiency, but without megaloblastic anemia, hypersegmented neutrophils, or increased serum methylmalonic acid levels.

 +0  (nbme24#33)


Characterized by dysuria, frequency, urgency, low back pain. Warm, tender, enlarged prostate.

Acute bacterial prostatitis—in older men most common bacterium is E coli; in young men consider C trachomatis, N gonorrhoeae.

Chronic prostatitis—either bacterial or nonbacterial (eg, 2° to previous infection, nerve problems, chemical irritation).

 +0  (nbme24#28)

Remember that ⊕ stranded RNA viruses are: I went to a retro (retrovirus) toga (togavirus) party, where I drank flavored (flavivirus) Corona (coronavirus) and ate hippie (hepevirus) California (calicivirus) pickles (picornavirus).

Since Measles virus is not a part of this list, it's a negative sense virus.

 +0  (nbme24#22)

Peroxisome = Membrane-enclosed organelle involved in β-oxidation of very-long-chain fatty acids (VLCFA) (strictly peroxisomal process).

Zellweger syndrome

Autosomal recessive disorder of peroxisome biogenesis due to mutated PEX genes.

Hypotonia, seizures, hepatomegaly, early death.

 +0  (nbme24#2)

Sleep apnea

Repeated cessation of breathing > 10 seconds during sleep = disrupted sleep = daytime somnolence.

Diagnosis confirmed by sleep study.

Nocturnal hypoxia = systemic/pulmonary hypertension, arrhythmias (atrial fibrillation/flutter), sudden death.

Hypoxia = More EPO release = More erythropoiesis.

 +0  (nbme24#15)

Free radicals damage cells via membrane lipid peroxidation, protein modification, DNA breakage. Initiated via radiation exposure (eg, cancer therapy), metabolism of drugs (phase I), redox reactions, nitric oxide (eg, inflammation), transition metals, WBC (eg, neutrophils, macrophages) oxidative burst.

euchromatin69  fa19 pg 210

 +0  (nbme24#29)

Main causes of renal artery stenosis:

  1. Atherosclerotic plaques—proximal 1/3 of renal artery, usually in older males, smokers.

  2. Fibromuscular dysplasia—distal 2/3 of renal artery or segmental branches, usually young or middle-aged females.

 +0  (nbme24#27)

Calcium Pyrophosphate [Pseudogout] Crystals are rhomboid and weakly ⊕ birefringent under polarized light (blue when parallel to light).

Gout [Monosodium urate] Crystals are needle shaped and ⊝ birefringent under polarized light (yellow under parallel light, blue under perpendicular light

 +0  (nbme24#49)

Androgen insensitivity syndrome

Defect in androgen receptor resulting in normal-appearing female (46,XY DSD); female external genitalia with scant axillary and pubic hair, rudimentary vagina; uterus and fallopian tubes absent due to persistence of anti-MĂźllerian hormone from testes.

Patients develop normal functioning testes (often found in labia majora; surgically removed to prevent malignancy). High testosterone, estrogen, LH (vs sex chromosome disorders).

Paramesonephric (Müllerian) duct develops into female internal structures— fallopian tubes, uterus, upper portion of vagina (lower portion from urogenital sinus). Male remnant is appendix testis.

Müllerian agenesis (Mayer-Rokitansky- Küster-Hauser syndrome)—may present as 1° amenorrhea (due to a lack of uterine development) in females with fully developed 2° sexual characteristics (functional ovaries).

 +0  (nbme24#16)

According to FA 2020 Pg175, AIDS diagnosis: ≤ 200 CD4+ cells/mm3 (normal: 500–1500 cells/mm3). This patient has 5% lymphocytes out of 2000 overall = 100 cells = AIDS.

 +0  (nbme24#4)

Acute hemolytic transfusion reaction

Type II hypersensitivity reaction

Typically causes intravascular hemolysis (ABO blood group incompatibility)

During transfusion or within 24 hr (due to preformed antibodies)

Fever, hypotension, tachypnea, tachycardia, flank pain, hemoglobinuria (intravascular), jaundice (extravascular)

Donor RBC with A and/ or B group antigens react with Host anti-A, anti-B IgG, IgM.

 +0  (nbme24#3)

Urine anion gap = Urine Na + K − Cl

In a metabolic acidosis without a serum anion gap:

A positive urine anion gap suggests a low urinary NH4+ (e.g. renal tubular acidosis).

A negative urine anion gap suggests a high urinary NH4+ (e.g. diarrhea).

 +0  (nbme24#46)

Location - Dorsal midbrain.

Parinaud syndrome—vertical gaze palsy, pupillary light-near dissociation, lid retraction, convergence-retraction nystagmus.

Causes - Stroke, hydrocephalus, pinealoma.

 +0  (nbme24#8)

Ornithine transcarbamylase deficiency. Most common urea cycle disorder. X-linked recessive (vs other urea cycle enzyme deficiencies, which are autosomal recessive).

Interferes with the body’s ability to eliminate ammonia.

Often evident in the first few days of life, but may present later. Excess carbamoyl phosphate is converted to orotic acid (part of the pyrimidine synthesis pathway).

Findings: Increased orotic acid in blood and urine, Decreased BUN, symptoms of hyperammonemia. No megaloblastic anemia (vs orotic aciduria).

passispass  Can it be an X-linked disease if both females are affected and boy is not? I think unlikely

 +1  (nbme24#28)

Type II error (β) Stating that there is not an effect or difference when one exists (null hypothesis is not rejected when it is in fact false).

β is the probability of making a type II error. β is related to statistical power (1 – β), which is the probability of rejecting the null hypothesis when it is false.

Increase power and Decrease β by: Increased sample size Increased expected effect size Increased precision of measurement

Also called false-negative error. β = you blindly let the guilty man go free.

If you increase sample size, you increase power. There is power in numbers.

 +0  (nbme23#22)

Bortezomib, carfilzomib

Mechanism = Proteasome inhibitors, induce arrest at G2-M phase and apoptosis.

Use = Multiple myeloma, mantle cell lymphoma.

Adv Effects = Peripheral neuropathy, herpes zoster reactivation

tyrionwill  under Bortezomib, the proteasome cannot digest viral Ag and presents it to the membrane-bonded MHC-I. Therefore CD8-Tc cannot recognize the host cells containing relapsed VZV. That is probably why shingles is one of the popular side effect of Bortezomib.

 +0  (nbme23#21)


Mechanism = Monoclonal antibody against CD20, which is found on most B-cell neoplasms.

Use = B-cell Non-Hodgkin lymphoma, CLL, ITP, rheumatoid arthritis, TTP, AIHA, MS.

Adv effects = Increased risk of progressive multifocal leukoencephalopathy in patients with JC virus.

tyrionwill  low IgG in response to infection/vaccination leads to broad bacteria and virus infection or reactivation. bacteria: strep pneumonia, Hib virus: JC, HBV, CMV...

 +0  (nbme23#23)

One of the tx strategies for drug induced Parkisonism or otherwise is to Curb excess cholinergic activity. Done by Benz-tropine, trihexyphenidyl (Antimuscarinic; improves tremor and rigidity but has little effect on bradykinesia in Parkinson disease). Park your Mercedes-Benz.

 +1  (nbme23#6)

Borderline = Unstable mood and interpersonal relationships, fear of abandonment, impulsivity, self- mutilation, suicidality, sense of emotional emptiness.

Females > males.

Splitting is a major defense mechanism.

Treatment: dialectical behavior therapy.

 +0  (nbme23#37)

Dorsal column (pressure, vibration, fine touch, proprioception)


• Fasciculus graciLis (Lower body, legs) • Fasciculus cUneatus (Upper body, arms)

Dorsal columns are organized as you are, with hands at sides. “Arms outside, legs inside.”

 +0  (nbme23#31)

Male child, recurrent infections, no mature B cells = Bruton disease (X-linked agammaglobulinemia)

Common variable immunodeficiency - Defect in B-cell differentiation. Cause unknown in most cases. May present in childhood but usually diagnosed after puberty. Increased risk of autoimmune disease, bronchiectasis, lymphoma, sinopulmonary infections Decreased plasma cells, Decreased immunoglobulins

 +1  (nbme23#40)

Spleen—arises in mesentery of stomach (hence is mesodermal) but has foregut supply (celiac trunk -> splenic artery.

Splenorenal ligament = Connects Spleen to left pararenal space. It contains Splenic artery and vein, tail of pancreas. It is a derivative of dorsal mesentery.

 +0  (nbme23#46)

Rough endoplasmic reticulum Site of synthesis of secretory (exported) proteins and of N-linked oligosaccharide addition to lysosomal and other proteins. Nissl bodies (RER in neurons)—synthesize peptide neurotransmitters for secretion. Free ribosomes—unattached to any membrane; site of synthesis of cytosolic, peroxisomal, and mitochondrial proteins. Mucus-secreting goblet cells of the small intestine and antibody-secreting plasma cells are rich in RER. Proteins within organelles (eg, ER, Golgi bodies, lysosomes) are formed in RER.

Smooth endoplasmic reticulum Site of steroid synthesis and detoxification of drugs and poisons. Lacks surface ribosomes. Location of glucose-6-phosphatase (last step of glycogenolysis). Liver hepatocytes and steroid hormone– producing cells of the adrenal cortex and gonads are rich in SER.

 +0  (nbme23#23)

I-PRA-tropium, tiotropium Use - COPD, asthma (“I pray I can breathe soon!”).

Muscarinic antagonists competitively block muscarinic receptors, preventing bronchoconstriction. Tiotropium is long acting.

 +0  (nbme23#9)

Q fever Coxiella burnetii, no arthropod vector. Spores inhaled as aerosols from cattle/sheep amniotic fluid. Presents with headache, cough, influenza-like symptoms, pneumonia, possibly in combination with hepatitis. Common cause of culture ⊝ endocarditis. Q fever is caused by a Quite Complicated Bug because it has no rash or vector and its causative organism can survive outside in its endospore form. Not in the Rickettsia genus, but closely related.

 +0  (nbme23#19)

Regulatory T cells Help maintain specific immune tolerance by suppressing CD4 + and CD8 + T-cell effector functions. Identified by expression of CD3, CD4, CD25, and FOXP3.

Activated regulatory T cells (Tregs) produce anti-inflammatory cytokines (eg, IL-10, TGF-β).

IPEX (Immune dysregulation, Polyendocrinopathy, Enteropathy, X-linked) syndrome— genetic deficiency of FOXP3 = autoimmunity. Characterized by enteropathy, endocrinopathy, nail dystrophy, dermatitis, and/or other autoimmune dermatologic conditions. Associated with diabetes in male infants.

 +1  (nbme23#24)

Primary polycythemia = Disorder of Increased no of RBCs, usually due to acquired JAK2 mutation. May present as intense itching after shower (aquagenic pruritus). Rare but classic symptom is erythromelalgia (severe, burning pain and red-blue coloration) due to episodic blood clots in vessels of the extremities. There is DECREASED EPO (vs 2° polycythemia, which presents with endogenous or artificially raised EPO). Treatment: phlebotomy, hydroxyurea, ruxolitinib (JAK1/2 inhibitor).

 +0  (nbme23#40)

Early PCT—contains brush border. Reabsorbs all glucose and amino acids and most HCO 3 – , Na + , Cl – , PO 4 3– , K + , H 2 O, and uric acid. Isotonic absorption. Generates and secretes NH 3 , which enables the kidney to secrete more H + . PTH—inhibits Na + /PO 4 3– cotransport = Increased PO 4 3– excretion

 +0  (nbme23#11)

Ingested—Enterobius, Ascaris, Toxocara, Trichinella, Trichuris You’ll get sick if you EATTT these!

Cutaneous—Strongyloides, Ancylostoma, Necator These get into your feet from the SANd

Bites—Loa loa, Onchocerca volvulus, Wuchereria bancrofti Lay LOW to avoid getting bitten

 +0  (nbme23#47)

Shoulder muscles that form the rotator cuff: Supraspinatus (suprascapular nerve)— abducts arm initially (before the action of the deltoid); most common rotator cuff injury (trauma or degeneration and impingement; tendinopathy or tear [arrow in A ]), assessed by “empty/full can” test

Infraspinatus (suprascapular nerve)—externally rotates arm; pitching injury

teres minor (axillary nerve)—adducts and externally rotates arm

Subscapularis (upper and lower subscapular nerves)—internally rotates and adducts arm

 +0  (nbme22#13)

The encounter should begin with the teen and parents discussing the teen's past medical history and parents' concerns

Parents should be asked to wait in the waiting room and be reassured that they will be invited back in to discuss any remaining issues

Once alone with the teen, establish ground rules for confidentiality

The teen's history yields far more information than the physical examination and results of diagnostic tests

 +0  (nbme22#43)

Therapeutic effect of danazol may have two mechanisms of action: (1) promotion of C4 synthesis by anabolic effect resulting in an improvement of the complement system with the disappearance of CIC and (2) a minor increase in C1 inh level primarily due to the lack of its consumption.

Most cases of HAE are caused by mutations of the SERPING1 gene, which contains the information necessary to generate a protein called C1 esterase inhibitor (C1INH). People with HAE produce nonfunctional or insufficient amounts of C1INH, leading to spontaneous swelling in the body. As a consequence of C1INH deficiency, C4 protein levels are also almost always low in HAE patients.

Winstrol = Stanozolol increases levels of C1INH and C4 protein in the blood by enhancing their production. Elevating levels of the two proteins close to the normal range helps prevent HAE attacks. Although the exact mechanism of how it acts on protein production is not fully understood, Winstrol is a well-established treatment for managing HAE.

 +0  (nbme22#43)

There are three main types of HAE.[3] Type I and II are caused by a mutation in the SERPING1 gene that makes the C1 inhibitor protein while type III is often due to a mutation of the factor XII gene.[3] This results in increased amounts of bradykinin which promotes swelling.[3] The condition may be inherited from a person's parents in an autosomal dominant manner or occur as a new mutation.[3] Triggers of an attack may include minor trauma or stress, but often occurs without any obvious preceding event.[3] Diagnosis of type I and II is based upon measuring C4 and C1-inhibitor levels.

 +0  (nbme22#17)

A better way to visualize this is the two hands of a clock, with one hand facing 12 and the other facing 6. The vertical line they form represents the fibula of the person's right leg. The lateral force approaches from 3 o'clock, sending the lower hand snapping outwards to point at 5 o'clock.

Pott's fracture, also known as Pott's syndrome I and Dupuytren fracture, is an archaic term loosely applied to a variety of bimalleolar ankle fractures.[1] The injury is caused by a combined abduction external rotation from an eversion force. This action strains the sturdy medial (deltoid) ligament of the ankle, often tearing off the medial malleolus due to its strong attachment. The talus then moves laterally, shearing off the lateral malleolus or, more commonly, breaking the fibula superior to the tibiofibular syndesmosis.

 -1  (nbme22#24)

This question in it's essence is asking that after inserting the catheter in the femoral artery, which landmark should we use beyond which superiorly lies the renal artery, and the answer is the origin of the testicular artery. What a weirdly worded question though. :?

makinallkindzofgainz  I don't think it's worded that weirdly. The guide wire should be advanced superiorly just beyond the testicular artery to approach the right renal artery.

 +1  (nbme22#42)

Disseminated intravascular coagulation (DIC) involves abnormal, excessive generation of thrombin and fibrin in the circulating blood. During the process, increased platelet aggregation and coagulation factor consumption occur. DIC that evolves slowly (over weeks or months) causes primarily venous thrombotic and embolic manifestations; DIC that evolves rapidly (over hours or days) causes primarily bleeding. Severe, rapidly evolving DIC is diagnosed by demonstrating thrombocytopenia, an elevated partial thromboplastin time and prothrombin time, increased levels of plasma D-dimers (or serum fibrin degradation products), and a decreasing plasma fibrinogen level. Treatment includes correction of the cause and replacement of platelets, coagulation factors (in fresh frozen plasma), and fibrinogen (in cryoprecipitate) to control severe bleeding. Heparin is used as therapy (or prophylaxis) in patients with slowly evolving DIC who have (or are at risk of) venous thromboembolism.

 +0  (nbme22#4)

The right ventricle (RV) receives its arterial blood supply primarily from the right coronary artery (RCA), which arises from the right coronary cusp of the aorta. The division produces the conus artery which supplies blood flow to the right ventricular outflow tract. The sinoatrial node (SA) is also supplied by the RCA from the second division. Coursing in the atrioventricular groove, the RCA then gives off multiple, small branches to supply the anterior RV before dividing terminally into the acute marginal branch (AM) that runs anteriorly along the diaphragm, and the posterior descending artery (PDA) that runs posteriorly. The PDA also supplies the atrioventricular node (AV) in 90% of patients, with a branch of the left circumflex artery providing flow in the remainder of patients. The PDA supplies the inferior wall of both ventricles, and is a terminal branch of the RCA in 85% of patients, but may arise from the left coronary circulation in 15% of the population.

The primary effects of RV ischemia and infarction result from decreased RV contractility. This leads to a reduction in blood flow from the venous system to the lungs, and finally to the left side of the heart. The clinical signs of this are increased right sided heart pressures, increased pulmonary artery (PA) systolic pressures, and decreased left ventricular preload. Symptoms may include peripheral edema especially distention of the jugular vein, hypoxemia, and hypotension.

Additionally, as the RV dilates the motion and function of the interventricular septum is altered. If the RV is dilated secondary to overload or if the septal myocardium is jeopardized by simultaneous left ventricle (LV) ischemia the symptoms of hypotension and cardiac failure may be pronounced. If the septum shifts leftward during diastole it impedes left ventricular filling and as a result cardiac output is decreased. This is termed loss of biventricular interdependence.

 +2  (nbme22#9)

acute hemolytic transfusion reaction (AHTR), also called immediate hemolytic transfusion reaction, is a life-threatening reaction to receiving a blood transfusion. AHTRs occur within 24 hours of the transfusion and can be triggered by a few milliliters of blood. The reaction is triggered by pre-formed host antibodies destroying donor red blood cells. AHTR typically occurs when there is an ABO blood group incompatibility, and is most severe when type A donor blood is given to a type O recipient.Antibodies against A and B blood groups (isohemagglutinins) present in the recipient's blood destroy the donor red blood cells.They also activate the coagulation cascade (blood clotting system) via factor XII, which can lead to disseminated intravascular coagulation and kidney damage. Isohemagglutinins also activate the complement cascade via C3a and C5a, which then promote inflammatory cytokine release from white blood cells. These inflammatory cytokines include IL-1, IL-6, IL-8, and TNF-alpha, which cause symptoms of low blood pressure, fever, chest pain, nausea, vomiting, and wheezing

 +0  (nbme21#19)

Hereditary angioedema (HAE) caused by C1-esterase inhibitor deficiency is an autosomal-dominant disease resulting from a mutation in the C1-inhibitor gene. HAE is characterized by recurrent attacks of intense, massive, localized subcutaneous edema involving the extremities, genitalia, face, or trunk, or submucosal edema of upper airway or bowels. Routine long-term prophylaxis with either attenuated androgens or C1-esterase inhibitor has been shown to reduce the frequency and severity of HAE attacks.

 +0  (nbme21#13)

Hypoxic pulmonary vasoconstriction (HPV), also known as the Euler-Liljestrand mechanism, is a physiological phenomenon in which small pulmonary arteries constrict in the presence of alveolar hypoxia (low oxygen levels). By redirecting blood flow from poorly-ventilated lung regions to well-ventilated lung regions, HPV is thought to be the primary mechanism underlying ventilation/perfusion matching.[1][2] The process might initially seem counterintuitive, as low oxygen levels might theoretically stimulate increased blood flow to the lungs to increase gas exchange. However, the purpose of HPV is to distribute bloodflow regionally to increase the overall efficiency of gas exchange between air and blood. While the maintenance of ventilation/perfusion ratio during regional obstruction of airflow is beneficial, HPV can be detrimental during global alveolar hypoxia which occurs with exposure to high altitude, where HPV causes a significant increase in total pulmonary vascular resistance, and pulmonary arterial pressure, potentially leading to pulmonary hypertension and pulmonary edema. Several factors inhibit HPV including increased cardiac output, hypocapnia, hypothermia, acidosis/alkalosis, increased pulmonary vascular resistance, inhaled anesthetics, calcium channel blockers, positive end-expiratory pressure (PEEP), high-frequency ventilation (HFV), isoproterenol, nitric oxide, and vasodilators.

Subcomments ...

Swallowing amniotic fluid is a critical component of lung development. Fetuses with severe oligohydramnios are plagued by pulmonary hypoplasia, which is the cause of death in fetuses born with Potter syndrome (renal agenesis).

mambaforstep  this is the second explanation that makes sense to me that I see downvoted. if you see something wrong and downvote, please explain! I want to know what im missing +2  
abhishek021196  Maybe someone downvoted because in this question, there wasnt a mention of renal agenesis but rather urethral obstruction although that would lead to Potter sequence as well. +  

Codeine is a prodrug with basically no analgesic effects by itself. It instead must be metabolized (mostly by the liver via CYP2D6) into morphine in order to provide analgesia. Some folks convert more, some less.

abhishek021196  Just a side note, CYP2D6 is responsible for metabolism of cardiovascular drugs. The dirty mnemonic is that since a 2D Echo is used to image the heart, CYP2D6 metabolizes CV drugs. +  

submitted by drmohandes(53),
  • total T4 (or T3) = free + TBG-bound
  • pregnancy → TBG increase → TBG-bound T4 increase → free decrease → less negative feedback → more TSH → restore free T4 levels
abhishek021196  Very simple explanation. Thank you +  

submitted by neonem(452),

Sotalol is a type III antiarrhythmic (K+ channel-blocking) that also has beta-blocker activity (Type II antiarrhythmic). This explains the decreased heartrate and blood pressure (beta-1 blocking activity), with the QT prolongation - all type III AADs cause QT prolongation.

abhishek021196  Would like to add that the IA antiarrythmics = Quinidine, Disopyramide, Procainamide also prolong QT interval and can lead to tosades de Pointes and they would most likely present with Cinchonism (headache, tinnitus with quinidine), reversible SLE-like syndrome (procainamide), HF (disopyramide), thrombocytopenia. The decreased HR and BP point towards Sotalol. +  

submitted by m-ice(237),

This woman has a lot of signs that point toward an intestinal parasitic infection: recent travel to Papua New Guinea, cough and alveolar infiltrates, high eosinophil count, and a stool sample that has a worm in it. Most likely the patient has a Strongyloides infection, as this is the intestinal parasite that shows larva on stool sample. Basically all intestinal parasites can be treated with Bendazole drugs, such as Thiabendazole. Praziquantel would be more appropriate for a worm or liver fluke infection.

fulminant_life  just to add to the explanation above," cutaneous larva currens" is a specific finding for strongyloides. Also the picture they used is the exact same one on wikipedia lol +6  
yb_26  they really should add Wikipedia in the list of top-rated review resources with A+ level of recommendation in FA2020))) +6  
usmile1  also a side note: cutaneous larva CURRENS is pathognomonic for strongyloides whereas Cutaneous larva MIGRANS is for ancylostoma braziliense or nectar Americanus +4  
solgabrielamoreno  FA 2019 pg 159 . Bendazoles because worms are bendy. (Treatment for roundworms) Praziquantel is for Cysticercosis (Taenia Solium) and Diphyllobothrium Latum Mefloquine : treats malaria Hydroxycloroquine: treats Malaraia, also RA & Lupus (immunisuppresive & anti-parasite) Dexamethasone: Steroid for inflammation +  
abhishek021196  FA20 says Ivermectin OR Bendazoles for Strogyloides, so in a future question, if Ivermectin is listed, that could be the right answer for this as well. +  

Bone marrow suppression (can be reversed with granulocyte colony-stimulating factor [G-CSF] and erythropoietin), peripheral neuropathy, lactic acidosis (nucleosides), anemia (ZDV), pancreatitis (didanosine).

abhishek021196  Adverse effects of NRTIs +  

submitted by m-ice(237),

The patient states that she does not want a hormonal form of birth control. So, the question is really asking which of the non-hormonal options is most effective. The tricky part here, I think, is that the question makes you want to not pick IUD, because many IUDs are hormonally based. However, a non-hormonal IUD, like a copper IUD, is still more effective than the other options listed.

bullshitusmle  copper intrauterine devices are hormon free FA2017 page 622 +1  
medguru2295  they needed to specifiy. I eliminated IUD bc patient states no hormones. +  
abhishek021196  The question doesnt make sense. IUDs are typically contraindicated in nullipara because of increased risk of expulsion and intractable abdominal pain, among other things such as perforation. The pt is 22, likely to be a nullipara. Why cant we prescribe a diaphragm instead which is a non hormonal method too, and remove the vaguity of hormonal vs non hormonal IUD? :/ +  
123ojm  in practice many nullparious women have IUDs. I think this question was seeing whether you knew that some forms of IUDs are non-hormonal and that the other methods are far less effective, +  

Homeobox (Hox) genes are in multiple locations and perform segmental organization in cranial-caudal direction, transcription factor coding. Mutations = appendages in wrong locations. Isotretinoin increases Hox gene expression.


Sonic hedgehog (SHH) gene present in the Zone of polarizing activity at base of limb buds and perform the function of anterior-posterior axis patterning, CNS development. Mutations = holoprosencephaly

abhishek021196  FA20 - 612 +  

submitted by susyars(13),

Is it me or this question is worded weird?

“this cells are most likely to closely resemble which of the following types of normal respiratory tract cells“

Like, you dont have normally neuroendocrine cells in the lung

Maybe i miss understood this question, i knew exactly what they were talking about, but the way they set the last sentence really drives me LOCA

abhishek021196  They are talking about Kulchitsky cells = pulmonary neuroendocrine cells (PNEC). These are the cells from which NE tumors of the lung i.e. small cell ca arise from. +2  

submitted by dr_ligma(24),

If NBME asks about a kid with suspicious rash under his nose + lightheaded/dumber in class, that kid's huffing glue

abhishek021196  Inhalants intoxication causes disinhibition, euphoria, slurred speech, disturbed gait, disorientation, drowsiness. Withdrawl leads to irritability, dysphoria, sleep disturbance, headache. +  

submitted by sajaqua1(390),

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

abhishek021196  SCHIZOTYPAL = Included on the schizophrenia spectrum. Pronounce schizO-TYPE-al: Odd-TYPE thoughts. +  

submitted by nwinkelmann(219),

I literally just realized why this question confused me so much (and I've tried to figure it out a couple of times, lol). I let the colloquial definition of bulimia (i.e. vomiting) stick in my mind, that I forgot the actual medical definition = normal BMI (>18) + binge eating and purging (where purging could be induced vomiting or diuretic use or laxative use or/and excessive exercise). So really, what this question was asking is simply what is the electrolyte balance of excessive diarrhea? GEEZ! I made it so much harder in my head when trying to answer it originally.

Diarrhea causes non-anion gap (i.e. hyperchloremic) metabolic acidosis. Stool predominantly contains HCO3- and K+, so excessive diarrhea = excessive loss of HCO3- and K+. Chloride levels in the serum will be increased due to the normal HCO3-/Cl- equilibrium, so as negative charge dissipates due to loss of HCO3-, Cl- will increase correcting the anion-gap.

drdoom  Bulimia comes from Greek "ravenous hunger"; the term is a literal concatenation of the words for ox (bous) + hunger (limos). So, in Greek, bou-limia is literally "ox hunger", which is a nod to how the word is used in medicine = perpetual and insatiable appetite for food (the very "opposite" of vomiting). +1  
abhishek021196  I agree with your reasoning but the classic case description of Bulima lists electrolyte disturbance of HypOkalemia, HypOchloremia, and Metabolic Alkalosis, along with other things like parotid hypertrophy and dorsal hand calluses due to the induced vomiting. I tripped up there. :/ FA 20 Pg 567 +  
llamastep1  Take home lesson: reasoning > memorizing +  

submitted by smc213(96),

To be completely clear!

This patient has Cystinosis a rare autosomal recessive lysosomal storage disorder and most common cause of Fanconi syndrome in children. Cystinosis is systemic and leads to cystine crystal deposits in cells and tissues throughout the body.

Although Wilsons disease can lead to FS, the crystals in the corneas does not correlate with Wilsons disease.
More info: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4841061/

highyieldboardswards  Thank you! You are a legend for figuring this out! +  
paulkarr  Appreciate you. +  
drzed  And even if it was Wilson disease, it would have the exact same consequence leading to Fanconi syndrome. +1  
abhishek021196  Fanconi syndrome Generalized reabsorption defect in PCT = Increased excretion of amino acids, glucose, HCO 3 – , and PO 4 3– , and all substances reabsorbed by the PCT May lead to metabolic acidosis (proximal RTA), hypophosphatemia, osteopenia Hereditary defects (eg, Wilson disease, tyrosinemia, glycogen storage disease), ischemia, multiple myeloma, nephrotoxins/drugs (eg, ifosfamide, cisplatin), lead poisoning. Polyuria, renal tubular acidosis type II, growth failure, electrolyte imbalances, hypophosphatemic rickets = Fanconi syndrome (multiple combined dysfunction of the proximal convoluted tubule). +  

submitted by lfsuarez(118),

This question asks about the mechanism of phototherapy as it relates to neonatal jaundice. With phototherapy, bilirubin is simply converted to water soluble isomers that are then able to be excreted by the kidney. This however does not conjugate the bilirubin.

almondbreeze  FA 2019 pg 387 +  
abhishek021196  Physiologic neonatal jaundice At birth, immature UDP-glucuronosyltransferase = unconjugated hyperbilirubinemia = jaundice/ kernicterus (deposition of unconjugated, lipid-soluble bilirubin in the brain, particularly basal ganglia). Occurs after first 24 hours of life and usually resolves without treatment in 1–2 weeks. Treatment: phototherapy (non-UV) isomerizes unconjugated bilirubin to water-soluble form. +  

submitted by sajaqua1(390),

Wouldn't total AV nodal ablation destroy to autorhythmicity of the pacemaker? That would mean that below the AV node the rhythm would be provided by a ventricular foci, and those usually create wide QRS complexes.

haliburton  that was my reasoning as well. guess not. +  
yotsubato  Shitty NBME grammar strikes again. +1  
charcot_bouchard  No. No guys. Bundle of his located below AV node and it can generate impulse. it calls junction escape rhythm and narrow complex. Below this is purkinje, bundle branch & ventricular muscle. those are wide complex +5  
abhishek021196  Third-degree (complete) AV block The atria and ventricles beat independently of each other. P waves and QRS complexes not rhythmically associated. Atrial rate > ventricular rate. Usually treated with pacemaker. Can be caused by Lym3 disease +1  

submitted by sajaqua1(390),

The marrow shows precursors to erythrocytes, as well as megakaryocytes. This is to show you that the issue isn't underproduction, which means that we are losing RBC and platelets somewhere ie destruction. That rules out D and E. There is nothing to indicate tha the child has disseminated tuberculosis (B). At this point we are left with A or C. A would indicate Disseminated Intravascular Coagulation (DIC) or something similar, which would result in low platelets and RBC but we would also see abnormal RBC like schistocytes ("helmet" cells). We are explicitly told that the erythrocytes are normochromic and normocytic. However, immune destruction of platelets explains it all- the destruction of platelets leads to some hemorrhaging and so a drop in RBC, and ITP classically arises after a recent upper respiratory tract viral infection.

meningitis  Just in case anyone is wondering like I did, the low platelet count explains thethose multinucleated cells. They are Megakaryocytes in Bone Marrow Biopsy. +9  
nwinkelmann  Also, don't forget that autoimmune thrombocytopenia purpura has 2 demographics: young kids, which generally resolves spontaneously fairly quickly, and then young adult females which is a true autoimmune condition that doesn't resolve. Patient's age + thrombocytopenia + essentially normal rest of heme pannel = autoimmune thrombocytopenia purprua in child. +4  
abhishek021196  That is exactly how I approached this question. Normal heme panel and a decreased Platelet count in a young boy after an infection just made me intuitively select ITP. +  

submitted by sajaqua1(390),

This patient has widespread destruction of both adrenal glands, which means that she will lose both her mineralocorticoids and her glucocorticoids. The loss of the mineralocorticoids and the effect on the kidneys is what is being tested here. When aldosterone is functioning and abundant, it has several critical functions on the nephron. First, it upregulates Na+/K+ ATPase expression on the basolateral membrane, establishing a strong electrochemical gradient that better absorbs Na+, while the increased intracellular K+ concentration makes it easier to lose K+ from the cell into the lumen. Aldosterone also upregulates the expression of epithelial sodium channels (ENaC) on the collecting duct, reabsorbing more Na+. Finally, aldosterone increases expression of H+ ATPases on alpha-intercalated cells of the collecting duct, which are responsible for secreting H+ (this is part of contraction alkalosis).

With the loss of aldosterone, we will see a decreases Na+/K+ gradient and decreased Na+ reabsorption; this leads to decreased serum sodium and increased serum potassium. At the same time, not expressing H+ ATPases will lead to H+ not being secreted, creating a more acidic environment (pH will decrease).

abhishek021196  Very well written explanation. Bravo +1  

submitted by sugaplum(157),

This is ridiculous but I could never keep these straight so meet my family:
Achey grandpa Meynert
Dope cousin VT with a side Ho* (who's names are just initials) SNc
Uncle and aunt Raphe and sara Cousin Gabby always screaming Na-Na-Na
norepi reminds me of the color blue, so locus ceruleus

paulkarr  LOL. Achey Granpa Meynert. I'm gonna steal this from you. +  
abhishek021196  Achey grandpa Meynert = ACh / Basal Nucleus of Meynert Dope Cousin VT = Dopamine / Ventral tegmentum, SNc Uncle and aunt Raphe and Sara = Serotonin / Raphe nuclei(medulla, pons) Cousin Gabby always screaming NA-NA-NA = GABA / Nucleus Accumbens Norepi = Locus ceruleus. +  
llamastep1  Amazing +  
mnemonicsfordayz  ACHey GRANDPA MEYNERT TREMBLES in the BASEment; DOPE cousin VT SNaCks DOWNstairs by the kitchen TAP; NANA GABBY ROCKS and ANXIOUSLY cooes...; "NENENENE... NENENENE...NENENE...NENE" to CRYING BLUE-eyed baby ELSIE; aunt SERO and uncle RAPHE DULLY PARK in the DOWNpour. CAPS = relevant info, lowercase = irrelevant. Includes diseases: DOWN, ANXIOUSLY, CRYING, DOWN = anxiety/depression; TREMBLES, TAP, ROCKS, PARK = movement disorder; GRANDPA = Alzheimer's. Note: ELSIE = LC = Locus ceruleus +  
mnemonicsfordayz  The extended "NENE" series is just for humor - shorten if you like ;) Also, ANXIOUSLY applies to both NTs in that sentence: GABA and NE. +  

submitted by usmleuser007(280),

1) Superficial (first-degree) = Epidermis ~ presents as red skin without blisters

2) Superficial partial thickness (second-degree) = Extends into superficial (papillary) dermis ~ Presents with redness with clear blister & blanches with pressure

3) Deep partial thickness (second-degree) = Extends into deep (reticular) dermis ~ presents as yellow or white skin with less blanching. May be blistering.

4) Full thickness (third-degree) = Extends through entire dermis ~ presents as stiff and white/brown skin. No blanching.

5) Fourth-degree = Extends through entire skin, and into underlying fat, muscle and bone ~ presents as black skin; charred with eschar

endochondral1  what is rhus dermis? +2  
endochondral1  nvm its urshiol +  
btl_nyc  Allergic contact dermatitis because of contact with poison ivy. +  
abhishek021196  Urushiol-induced contact dermatitis (also called Toxicodendron dermatitis or Rhus dermatitis is a type of allergic contact dermatitis caused by the oil urushiol found in various plants, most notably species of the genus Toxicodendron: poison ivy, poison oak, poison sumac, and the Chinese lacquer tree. +1  

submitted by seagull(846),

! I hate these with a burning F***ing passion. Thumbs up if you agree

mcl  Amen brother +1  
praderwilli  Every morning: "I think i'll go over glycogen storage diseases, lysosomal storage diseases, and dyslipidemias after questions this afternoon." Every afternoon: Nah +21  
mcl  oh my god are you me +1  
praderwilli  I recently found a program called Pixorize. It's pretty much Sketchy for biochem. Wish I discovered it sooner cuz it has helped for a lot of the painful things like this! +5  
tentorium  [special] +  
tentorium  [special] +1  
tentorium  [special] +  
drhello  hello +  
burak  Cherry red spot basically means niemann-pick or tay sachs. Two differences between is: 1- No HSM in Tay Sachs, HSM in niemann-pick. 2- Both of them has muscle weakness but there is hyperreflexia in Tay Sachs, but areflexia in niemann pick disease. In stem cell HSM is not described and hyperreflexia noted. +2  
abhishek021196  What is HSM? +  
mysticsoul  HSM - HepatoSplenoMegaly. Cherry red spots think of Tay Sachs, deficient enzyme - HeXosaminidase A, accumulated substrate GM2 ganglioside. Niemann-Pick - Spingomyelinase, Spingomyelin <- which is not even a choice. FA18 Pg 88 +  

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