First question : They tell us its a lymphocytic leukemia

Second question : Deciphering whether it is a B cell or T cell.

The cells have no surface bound Ig M ,Ig G or cytoplasmic chains for these antibodies , but have a rearranged gene segment( meaning active ) for the T cell Receptor . So the Cells are T Cells

Third question : Now that we know that they are T Cells , we want to know whether they are CD4 or CD 8 positive

The cells in the clinical vignette lack both CD4 and CD 8 ( double negative ) According to how T cells normally develop - They start of as being double negative ( i.e not expressing CD4 or CD 8) in the subcapsular region and progressively become
- positive for both CD 4 and CD 8 in the cortex
- and eventually acquire the TCR and CD3 by the time they get to the medulla

These cells therefore must T lymphocyte thymocytes localised to the cortex

Here is my take: a ventricular septal defect in infancy allows for left to right shunting of blood in the ventricles. This causes an increased pressure in the right ventricle (due to more blood being pushed into it) and a decreased pressure in the left ventricle. Because there is more blood in the pulmonary circulation from the shunt, I think the left atrial pressure would also be increased in an early VSD.

SO when you repair the VSD, the left ventricle pressure will be increased compared to when the shunt was present (it is no longer losing blood), the right ventricle pressure will be decreased (it is no longer getting blood from the shunt), and the left atrial pressure will be decreased (there is no longer overload of the pulmonary system returning to the left atrium).

FA2020 p298

Deoxyhemoglobin has a higher pKa than oxyhemaglobin and thus will accept hydrogen ions more readily. This is important in the ability to "carry" CO2 as the main mechanism of CO2 transport is actually conversion of CO2 to HCO3- (CO2 + H2O -> HCO3- + H+), thus deoxyhemaglobin carries the H+ while HCO3- is transported in the plasma to the lungs. Carbaminohemaglobin is actually only about 20% of the CO2 trasnport and CO2 dissolved as CO2 is 10%; trasnport as HCO3- is around 70% of the CO2 transport.

Here is another image of the process.

Another important aspect of the process to take note of that they like to ask about is the chloride shift. Chloride moves the opposite direction as HCO3- in the RBC. Thus at tissues where we are generating HCO3- from CO2 and need to pump it out of the cell, chloride moves into the cell.At the alveoli where we need to pump HCO3- back into the RBC to turn it into CO2, chloride moves out of the cell.

Other answers:

• 2,3BPG will bind and stabilizes deoxyhemaglobin making it less attracted to oxygen, shifting the hemaglobin dissosiation curve right.
• Deoxyhemaglobin has a higher capacity to form carbanimohemaglobin
• Deoxyhemaglobin has a higher pKA than oxyhemaglobin (this is why it can accept hydrogen ions more readily)
• Competition for binding site is not a major mechanism for the ability to carry CO2 as most CO2 is "carried" by conversion to HCO3-
• Nitric oxide binding is not a mechanism of CO2 carry.

The description points to pancreatic insufficiency due to steatorrhea (fat in the stool, likely due to insufficiency of pancreatic lipase) and muscle fiber in the stool (which points to incomplete protein digestion, likely due to insufficiency of pancreatic proteases).

Further, he has no deficiency in carbohydrate absorption as evidenced by the D-xylose test (which indicates an intact mucosa for absorption and does not require digestive enzymes, FA2020 p373); and he has no abnormalities on biopsy of the intestine.

Thus, the primary issue is pancreatic insufficiency and supplementation of pancreatic enzymes is most helpful.

NFKB is in its inactive state bound to IKB. As a part of the classical pathway, bacterial antigens bind to TLR and activate IKB kinase, (kinase phosphorylates)

• IKB is ubiquinated and degraded

• NFKB enters nucleus and synthesises the inflammatory stuff

Uw QID: 11955

First step is to make the presumptive diagnosis of osteoporosis from the clinical vignette . ( The supposed subtype in our patient is postmenopausal osteoporosis)

After this the next step is to make an association with the lab findings The primary defect is a deficiency of estrogen . Normally estrogen decreases osteoclast activity by

1. inducing apoptosis
2. increased formation of osteoprotegerin a decoy molecule which inhibits activation of RANK receptors

Net effect of losing estrogen is increased osteoclast activity ,and in this question by extension RANK L concentration .

NOTE : ALP which is an indicator of osteoblast activity does not change/ increase in osteoporosis , as such avoid all options with an increase in osteoblast activity

FA2020 p 612 has early fetal development. Here are the explanations for the answers:

• The syncytiotrophoblast mediates early implantation in the first week and this is when hCG secretion begins. Further, it forms concuttently with the cytotrophoblast from the trophoblast.
• The bilaminar disc (two layers) is present during week two, and gastrulation occurs during week 3 and 3 germ layers are the product.
• The neural tube is not fully formed until day 21 but the neural plate is formed on day 18 (FA2020 p490)
• The embryo is NOT resistant to teratogens here, neural tube defects can occur if the embry is exposed to teratogens in week 3. Earlier than this the embryo is in an "all or nothing" stage and death of the embryo is more likely to occur if the embryo is exposed.
• The somites form adjacent to the neural groove prior to sclerotome migration.

Basically, even without knowing all the exact days of development, most answers can be eliminated based on having the events in the incorrect order or having an incorrect aspect about development (i.e. the syncytiotrophoblast forms concurrent with the cytotrophobast, 3 germ layers are present after gastrulation, the embryo is never truly resistant to teratogens after implantation, the sclerotome forms from somites so somites have to come first).

Here is a general overview of the first three weeks of development after fertilization.

Here is another one if that doesn't do it for ya.

I definitely did not know this, but apparently smoking can worsen GERD due to tendency of nicotine to cause relaxation of the lower esophageal sphincter. Smoking is also linked to stomach ulcers due to interference with gastric mucosa and acid production. Just don't smoke kids. Don't do drugs. Stay in school forever like med students.

A note to self : Creatine phosphate is a short term energy source in muscle . Acts by donating phosphate groups to regenerate ATP .

*Creatine is derived from Arginine and metabolised to Creatinine ( which is excreted by the kidneys )

This is likely Herpes Simplex Virus 1 (based on the vesicular lesions on the lip) which remains dormant in sensory ganglia, most commonly the trigeminal ganglion (FA2020 p164).

Important aspects of volatile (gas) anesthetics: (FA2020 p549):

• MAC (minimum alveolar concentration): essentially the ED50 for inhaled anesthetics, this is the minimum concentration of anesthetic that causes a response in 50% of patients
• LOW MAC means HIGH potency - more potent drugs would have a lower minimum amount needed to be present in the alveoli in order to exert their effect.
• LOW MAC is related to HIGH lipid solubility (higher oil/gas partition coefficient) - more lipid soluble agents tend to be more potent because of their increased ability to cross the BBB
• MACs are additive (i.e. one gas at 1.5 MAC = two gases at 0.75 their respective MACs)
• Blood/gas partition coefficient: an expression of solubility; anesthetics with a low blood gas partition coefficient have a rapid onset/offset
• i.e. LESS plasma solubule anesthetic = FASTER onset/offset
• This is because less plasma soluble agents will "fill up" their maximum amount in the blood reservoir quicker and thus are pushed down their concentration gradient into the brain quicker; i.e. they quickly saturate the blood and will move on to affecting the brain quicker
• MAC and blood/gas partition coefficient also tend to be inversely related -- higher MAC = lower blood/gas partition coefficient and vice versa; thus many of the more potent anesthetics have a longer time for onset/offset

Here, we want to know loading dose which is equal to the volume of distribution x target concentration in plasma.

So our loading dose = 1.81L/kg x 10mg = 18.1mg/kg

She is a 55kg person so 18.1mg/kg x 55kg = 995.5 mg which approximates to 1000mg total loading dose.

Important Pharm Equations to Remember

Uterine atony is the most common cause postpartum hemorrhage due to failure of the uterus to effectively contract and retract after delivery. It is treated with uterine massage and oxytocin.

Botulism toxin acts via proteases that cleave SNARE and prevent acetylcholine release at the neuromuscular junction (FA2020 p132). Thus, it does not directly affect the post-synatpric muscle cell. If you add external acetylcholine, you would still have a completely normal response. This eliminates all but two answers.

The end plate potential (EPP) would be affected by botulism toxin because the end plate potential is the change in voltage that occurs at the postsynaptic muscle motor endplate after an action potential in the motor neuron axon triggers release of many acetylcholine vesicles. Normally, an action potential in the motor neuron will cause influx of calcium that leads to fusion of Ach vesicles (requiring SNARE) and exocytosis, releasing large quantities of Ach into the synapse which can then bind and trigger an EPP in the muscle. With botulism, fusion of the Ach vesicles is inhibited so less Ach is released and the EPP is blunted. Notably, the voltage is the same as the mEPP which is the voltage after random occurrence of Ach release (see below).

A miniature end plate potential (mEPP) is the voltage change that occurs when one vesicle of acetylcholine is released. These occur randomly. mEPP would not be affected by botulism toxin because it is the produce of random fusion of a vesicle which could still occur after administration of botulism toxin.

Here is an image reminding the difference between EPP and mEPP.

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The primary mechanism of inflammation "tumor" or swelling is increased permeability of the endothelium which leads to leakage of fluids (FA2020 p213)

• Arterial: Pco2 30 mm Hg, Po2 96 mm Hg
• Arterial O2 content: 12 vol% (N=17%–21%)
• Mixed venous Po2 36 mm Hg

• Mixed venous O2 content 8 vol% (N=10%–16%)

• A) Anemia - Patient has nl PaO2 and decreased O2 content. Also patient is hyperventilating and CO2 is thus low.

• B) Drug-induced alveolar hypoventilation - Arterial PO2 would be low&CO2 high
• C) Residence at a high altitude - Arterial PO2 would be low
• D) Severe regional mismatching of alveolar ventilation and pulmonary capillary perfusion - Pulmonary Embolus would cause a decrease in arterial PO2 E) Voluntary hyperventilation - Arterial O2% content would be nl

Anemia causes hypoxia without hypoxemia. Meaning low O2 delivery to tissues but not low O2 saturation of the blood. The lungs can adequately deliver O2 to the arterials so PaO2 is normal. Anemia causes low O2 content because you have relatively low amounts of Hb to carry oxygen.

O2 content = (1.34 × Hb × Sao2) + (0.003 × Pao2)

Based on the history (consumption of large amounts of alcohol and elevated serum amylase/lipase with hypocalcemia), this man likely has acute pancreatitis (FA2020 p397). One of the major complications is autodigestion of tissues, such as what is seen in the image.

Lentigo maligna is a type of melanoma (FA2020 p484), hence why it is important the lesion is brown/black with irregular borders and enlarging (all hallmarks of melanoma). The biopsy description also fits lentigo maligna, but even if you are not a pathologist the description that fits cancer and and "atypical melanocytes" should point you to lentigo maligna.

• Acanthosis nigricans is thickening (acanthosis means epidermal hyperplasia) and darkening of skin in folds and creases associated with insulin resistance
• Actinic keratosis is a premalignant lesion that is a small, rough, erethematous or brownish papule/plaque
• Compound nevus is a type of mole that is slightly elevated, brown or light brown, and has regular borders. It is not fast-growing.
• Sebhorreic keratosis are "stuck-on" flat, greasy, pigmented squamous epithelial proliferation of immature keratinocytes with keratin-filled cysts. Rapid onset of multiple indicates possible GI malignancy.

FA2020 p482, 477 and 484

This man likely has diabetic neuropathy and thus would have neuropathic pain. Neuropathic pain is described as a burning pain as compared to the other kinds of pain.

Here are some differences between nocioceptive and neuropathic pain.

Here is a chart of descriptors used for neuropathic v nocioceptive pain.

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I don't like this question for many reasons, but basically he has sarcoidosis (noncaseating granulomas with no pathogen found on biopsy) which according to First Aid is more common in African-American females. Since he is African-American that is his risk factor (FA2020 p676).

In hypothesis testing, the alpha value is the probability of making a Type I error. This is the type of error mentioned in the question.

• Type I error - you find a difference when a difference doens't really exist.
• One way of remembering this is that this is what scientists "want" to make: they want to find a significant difference in their data, thus it is the "first mistake" they'd make.
• Alpha is the probability you are willing to accept that you could have made a type I error (i.e. an alpha value of 0.05 means there is a 5% probability you could make a type I error and reject the null hypothesis when you should not)


• Type II error - you do not find a difference when you should have because a true difference really exists
• Beta is the probability that you make a type II error
• Power is equal to (1 - beta)
• Power can be increased by increasing sample size, and thus with a larger sample you have a lower probability of making a Type II error
• Power can also be increased by increasing expected effect size or increasing precision. It is interesting to note accuracy has no effect on power.

FA2020 p263

In this study, a placebo is not used on the control group. The experimental group gets dextromethorphan while the control group gets "no treatment". This results in procedure bias, as subjects in different groups are not treated the same. Blinding and use of a placebo reduce the influence of participants and researchers on procedures and interpretation of outcomes as neither are aware of group assignments.

See table on bias and study errors in FA 2019 p 260.

TL;DR: Even with Type I or II renal tubular acidosis the ammoniagenesis from glutamine is not impaired and thus is the main source of ammonia.

Here is my take: Based on her history and measured plasma values, this girl likely has one of the "low potassium" renal tubular acidoses, either Type I or Type II (see this chart for reasoning based on measured values or this image for fun colorful renal tubular acidosis and FA2020 p593)

Then, we are told that she has a defect in "ammoniagenesis". In the renal tubules, ammonia is generated in two primary ways: via direct conversion of glutamine to ammonia in the proximal tubule which is then secreted into the tubule, or by NH3 combining with with H+ in the collecting tubules (which I guess they are considering a separate ammoniagenesis pathway even though its all kinda related?). See this diagram or this diagram

Assuming our girl has Type I renal tubular acidosis, there will be decreased availability of hydrogen ions in the renal tubules to combine with NH3. Thus, the primary source of ammonia production in this patient will be glutamine (which is the major source of ammoniagenesis in a normal person anyways).

Further reasoning - Type I is impaired secretion of hydrogen ions into the lumen, so there will be less hydrogen ions available. She likely has type I because this is primarily treated with potassium citrate (both to buffer and to prevent renal stones which are a common complication). Even if she had Type II the increased excretion of bicarb would also buffer more H+ leaving less for ammoniagenesis in the NH3/H+ combination fashion.

Contrarily, Type 4 renal tubular acidosis (hyperkalemic) results in decreased synthesis of ammonia in the proximal tubules, which we know she does not have because of her low potassium.

Key aspects of the question:

• Hypokinesis of the posterior left ventricle with increasing activity levels - in my opinion this is the primary clue to stenosis of the right coronary artery. This is because the posterior heart is supplied by the posterior descending artery, which in most people who have right dominant coronary circulation is a branch of the right coronary artery.
• "When climbing stairs" and the hypokinesis being present on stress testing - this helps you to know the condition is only exacerbated in exercise, and stenosis of the RCA generates symptoms in exercise because in excersise the increase in oxygen demand typically causes dilation of the coronary vessels to accomadate. When there is stenosis, the vessel cannot dilate and thus there is transient ischemia of the area the vessel supplies (this is potentially exacerbated by the coronary steal phenomenon in a stress test which can occur with administration of vasodilators) FA2020 p304

Increase in oxygen consumption is the normal response to exercise and alone is not pathologic. Extravascular compression of the coronary arteries is also considered normal and nonpathologic; this is why most coronary blood flow occurs during diastole and why the endocardium is most susceptible to ischemia.

This woman has the classic signs of vitamin C deficiency, or scurvy: easy bruising, petichiae, perifollicular hemorrhages, gum disease, and slow wound healing. Vitamin C is necessary for proper hydroxylation of proline and lysine in collagen. (FA2020 p69 [nice])

Immunohistochemistry uses fluorescently tagged antibodies to bind specific antigens on tissues. In this case, an antibody could be directed against CD44v10 variant protein used to tag the cells in the samples that express the variant. This is also useful because it can be done on slides of paraffin embedded tissue.

• Affinity column chromatography is used to separate a biochemical mixture based on interaction between antigen/antibody, enzyme/substrate, receptor/ligand, etc. but would not be useful in pre-embedded tissues or this case
• Density gradient centrifugation is used on mixtures to separate them into components and is particularly useful in separating cell suspensions, such as in separating blood into layers to get the buffy coat with WBCs
• Northern blot is for RNA and fluorescently tags a piece of RNA present in a sample
• PCR is for identifying/anplifying a DNA segment
• Reverse transcriptase (RT) PCR is typically used to measure expression levels of an mRNA
• Southern blot is for identifying a DNA segment in a digest

The burnt almond smell and noncyanotic dyspnea is characteristic of cyanid poisoning. Cyanide poisoning is treated with nitrites because nitrites oxidize hemoglobin to form methamoglobin which binds cyanide, allowing less toxicity. Thiosulfate is often added to increase renal excretion as thiocyanate. Cyanide toxicity may also be treated with hydroxycobalmin, which binds cyanide.

FA2020 p667 has differentiation of cyanide from CO poisoning.

Tuberous sclerosis is characterized by HAMARTOMASS [Hamartomas in CNS and skin, Angiofibromas , Mitral regurgitation, Ash-leaf spots , cardiac Rhabdomyoma, (Tuberous sclerosis), autosomal dOminant; Mental retardation (intellectual disability), renal Angiomyolipoma , Seizures, Shagreen patches, FA2020 p525]

If you didn't know what hamartomas look like (i.e. me), here is a picture of what they were describing. They also describe seizures, subependymal calcified nodules (likely hamartomas of the CNS), and a cardiac mass, which is likely a rhabdomyoma. These are characteristic of Tuberous Sclerosis.

Wrong answer explanations:

• Familial hypertrophic cardiomyopathy is associated with sudden death in athletes, not seizures and hamartomas.
• Gardner Syndrome is also called familial colorectal polyposis and is a form of familial adenomatous polyposis.
• Glycogen storage disease Type I is Von Gierke disease, which presents with hepatosplenomegaly and severe fasting hypoglycemia typically in infancy.
• Multiple Endocrine Neoplasia Type I is associated with all the P's -> Pancreatic, Parathyroid, and Pituitary (pancreatic endocrine tumors, parathyroid adenomas, and pituitary tumors)

Note: IL-12 receptor deficiency, or a defect in the Interferon Gamma receptor
Think Disseminated Mycobacterial and Fungal Infections . Also salmonella *

This woman's cardiac arrest caused a period of loss of blood flow and ischemia in the kidney that has led to acute tubular necrosis. In ATN there is an inciting event then an oliguric phase. In ATN, there is death of renal tubular epithelial cells that slough off and form muddy brown granular casts. Keep in mind the proximal tubule and thick ascending limb are the part of the kidney most susceptible to hypoxic injury. [FA2020 p602]

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Lipopolysaccharide, or LPS, is the primary endotoxin mediator of gram(-) sepsis leading to septic shock. This woman likely has sepsis from E. coli, a gram negative bacterium which produces LPS, based on her history indicating a UTI. E.coli are the most common cause of UTI. (FA2020 p133)

Based on the question stem and the autoanitbodies given (butterfly rash combined with anti-dsDNA/anti-Sm/antiphospholipid), this woman has classic lupus. SLE is associated with cytopenias, so thrombocytopenia is the best choice of the available answers. Thrombocytopenia is common in lupus (FA2020 p470)

• HUS is associated with E.coli or Shigella infection and not Lupus. Lupus kidney disease is diffuse proliferative glomerulonephritis.
• Macrocytic anemia is typically caused by B12 or folate deficiency and not associated with lupus. Lupus anemia is typically anemia of chronic disease, which is normocytic, or due to inadequate RBC production or iron deficiency, which is microcytic.
• Multiple nucleated erythrocytes are found in leukemias when the RBCs are being "pushed" out of the bone marrow, or in diseases where the bone marrow is highly stressed. Lupus does not typically cause this.
• I am not 100% sure why rouleax formation is wrong, because as far as I understand any condition that increases monoclonal Abs can cause rouleaux formation, but I am assuming it is just not as common/likely, hence thrombocytopenia which is very common is the better answer

From what I can tell, the gist of this question is that he has SCID and since the SCID child has basically no immune system (particularly because the lack of T-cell immunity) there is a higher chance of transfusion-associated graft versus host disease (TA-GVHD) so blood products have to be irradiated.

Here is a medscape reference with who requires irradiated RBCs due to increased risk of TA-GVHD for your perusing.

This woman has Polycystic ovarian syndrome. This can be deduced because of the high LH:FSH ratio (>2), high BMI, and presence of withdrawal bleeding in a progesterone withdrawal test. In polycystic ovarian syndrome, there is increased release of androgens from theca interna cells. These androgens can cause symtoms commonly associated with PCOS (hirsutism, acne) but can also be aromatized to estrogen in adipose tissue. The presence of estrogens in this form causes constant negative feedback on the hypothalamus and dysregulation in the appropriate levels of the gonadotropins (see here and here)

Here is a comparison graph of the hormone levels in a normal menstrual cycle to PCOS.

A progesterone withdrawal test is used to help determine the cause of amenhorria. If withdaral bleeding occurs, it means the patient has sufficient estradiol and the amenorrhia is due to anovulation. If no withdrawal bleeding occurs, it means the patient either has chronic anovulation without estrogen, a nonreactive endometrium, or a problem with uterine outflow. In our patient's case, she has withdrawal bleeding so she has anovulation, a common symptom of polycystic ovarian syndrome.

This is left homonomous hemianopia, which is caused by lesion to the contralateral optic tract (D). This occurs because the nasal retinal fibers (temporal visual field) cross at the optic chiasm while the temporal retinal fibers (nasal visual field) do not. See FA2020 p542 or here for image.

Lesion of the optic nerve (A or C) would cause complete blindness in either eye.

Lesion of the optic chiasm (B) causes bitemporal hemianopia.

Lesion to the left optic tract (E) would cause right homonomous hemianopia.

F and G are the oculomotor nerves.

This woman has a carcinoid tumor, associated with carcinoid syndrome characterized by flushing, wheezing, and diarrhea. (FA2020 p 352) Based on her CXR I'd say she probably has a bronchial carcinoid tumor. Tumor cells would be chromogranin(+).

Carcinoid syndrome is a paraneoplastic syndrome caused by secretion of serotonin (5-HT). It is treated with a somatostatin analog like octreotide and the presence of 5-HIAA in the urine can be a marker (5-HIAA is a serotonin breakdown product).

This is a partial mole because of the presence of fetal parts. Complete moles have no fetal parts, partial moles have fetal parts(PARTial = fetal PARTs). (FA2020 p642)

Oseltamivir and zanamivir are influenza neuraminidase inhibitors. Typically, neuraminidase allows influenza particles to bud off host cells. Without the functioning enzyme, the virion buds cannot detach from the host cell membrane.

The uneven distribution of ADHD based on gender(more cases of ADHD among boys ) is a potential confounder , and so STRATIFICATION addresses this

Although botulism blocks ACh release, it wouldn't have effects on mpp and the response to exogenous ACh provided to the synaptic junction. The potentials would be the same as it would normally be. The epp difference was disclaimed in the question stem.

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Acute MI and mitral regurg from the murmur leads to LV failure and backflow of blood into the lungs.

This leads to increased pulmonary hydrostatic capillary pressure. This will lead to excess volume leaking from the pulmonary capillaries into the interstitial and this will manifest as pulmonary edema (crackles).

Pulmonary edema will interfere with gas exchange leading to hypoxemia.

pregnancy causes hypervolemia, and higher blood volume/flow through the heart will increase murmurs (aortic regurg.)