I don't like how they are asking this, but I think what they are getting at is that after the stent placement ("subsequent to the stent placement") there will be reperfusion injury to the myocardial tissue which occurs through free radical injury and therefore membrane lipid peroxidation is the best answer (FA2020 p210 mentions membrane lipid peroxidation as a mechansism of free radical damage and lists reperfusion injury after thrombolytic therapy as a type). Elevations in the cardiac enzymes I assume are because of the injury to the cells.
Pelvic splanchnic nerves carry the parasympathetic fibers that are responsible for hindgut intestinal motility including voiding (image). [FA2020 p364].
Diabetes mellitus can cause nerve damage and gastroparesis, treated with metoclopromide (FA2020 p400).
The question stem is referring to a conjugate vaccine. This is because conjugate vaccines convert T-independent antigens (polysaccharides) into T-dependent antigens by conjugating them with a protein. [FA2020 p127]
Remember that in order for a T-cell to be able to respond to an antigen via MHC, it MUST be a protein. Thus, T-dependent (dependent on T-cells) responses are to proteins. T-dependent responses are overall better because then B-cells can then undergo affinity maturation and class switching through interaction with T-cells. So, by conjugating bacterial polysaccharides to proteins, the immune response will be a more robust T-dependent reaction and will yield better protection. [FA2020 p103]
Conjugate vaccines exist for encapsulated bacteria (as the capsules are polysaccharide and would need to be conjugated to protein to improve response). These are Neisseria meningitidis, Haemophilus influenzae, and Streptococcus pneumoniae
You can remember these encapsulated organisms and their conjugate vaccine because they are THE SAME organisms that you become susceptible to when you have a splenectomy and which necessitate vaccination.
DISTRIBUTIVE SHOCK (I.E. SEPTIC OR ANAPHYLAXIS) ARE THE ONLY SHOCKS WITH INCREASED CARDIAC OUTPUT!
This man presents with hypothermia (septic shock can present with hyper or hypothermia), tachycardia, and low blood pressure with increased cardiac output, characteristic of septic shock. Further distributive shock is associated with severe decrease in systemic vascular resistance while other forms of shock have increased systemic vascular resistance.
Just to add to the explanation here is what you would see in the others (most on FA2020 p484)
This has to do with the algorithm of treating shock. Septic (a type of distributive) shock as well as hypovolemic shock are treated with IV fluid resuscitation (FA2020 p310). Crystalloid fluids are first-line choice, and normal saline (0.9%, isotonic) is first-line specifically in cases of shock.
5% dextrose in water and 0.45% saline is hypertonic and not useful here.
5% dextrose alone is isotonic in the bag but physiologically hypotonic. It is more often given for fluid replacement after severe dehydration.
0.45% saline only is hypotonic and not useful here.
3% saline is hypertonic and not useful here.
Hormone sensitive lipase (HSL) is the enzyme which degrades triglycerides stored within adipocytes (FA2020 p93). Thus, it makes sense that it is activated in times of fasting and suppressed in the fed state.
Insulin would inhibit HSL, as insulin is a fed state enzyme secreted by the pancreas and would want to trigger storage of triglycerides.
In contrast glucagon is secreted in response to hypoglycemia by the pancreas and will trigger fasted state activation. In terms of the fed/fast state I always think of glucagon and epinephrine kind of like a superhero and their side kick, because they usually work together in the fasting state on similar targets to ensure the body has enough energy (this helps me remember that epinephrine and glucagon are fasting state hormones). Here though is epinephrine's big action away from glucagon, where glucagon has minimal effect and epinephrine has the big action of activating HSL! Glucagon has a minor role and other catecholamines and ACTH can also serve to activate HSL as well.
Another example of the synergistic work of glucagon and epinephrine is in glycogen breakdown (FA2020 p85). Both will trigger cAMP increase and protein kinase A activation which will phosphorylate glycogen phosphporylase and activate it (FAST PHOSPHORYLATE! Hormone sensitive lipase is actually phsophorylated to activate it as well).
FUN FACT: Hormone sensitive lipase actually got its name because it was sensitive to epinephrine!
In agreement with the other post: (see FA2020 p331)
You would want to check FREE T4 because pregnancy increases Thyroid binding globulin. It is possible she might have increased overall T4, but NOT have hyperthyroidism because the free T4 is normal (i.e. her increases amount of thyroid binding globulin has bound more T4, and since our bodies respond to the concentration of free T4 only, the hypothalamus should ensure that the free T4 is kept constant; this would appear as increased overall T4)
Another way of thinking of this:
If we increase bound T4 and keep free T4 the same, we would still increase overall T4. Thus to know if she truly has hyperthyroidism we must look at free T4 concentration.
From FA2020, pg. 381:
Tubular adenoma--> neoplastic; tubular histology has less malignant potential than villous; tubulovillous has intermediate malignant potential; usually asymptomatic, may present with rectal bleeding. Hence our patient who has been undergoing evaluation for fecal occult blood.
Hyperplastic polyp--> most common, generally smaller and in rectosigmoid region. I'm guessing the picture attached to this question is trying to clue us into this not being a small lesion.
Inflammatory pseudopolyps--> due to mucosal erosion in inflammatory bowel disease. There is no appreciable erosions in this picture, also the mass appears pedunculated, so we know it's not a spot of normal mucosa that just looks raised compared to surrounding erosion.
Juvenile polyp and Peutz-Jeghers syndrome--> these are both genetic disorders with numerous hamartomatous polyps seen in the colon. Peutz-Jeghers also associated with increased risk of breast and other GI cancers. It is unlikely that our patient had either of these b/c he is 70 y/o; therefore, if he had one of these, he would likely have more than one colon lesion and may also present with a history of other cancers at his age.
Yellow nodules (cholesterol deposits) on the achilles tendons have a very high association with Type II familial dyslipidemia, or familial hypercholesterolemia. This is caused most often by a defect in the LDL receptor function. (FA2020 p94)
FA2019, pg. 666:
Based on the findings of decreased breath sounds, dull percussion, and decreased tactile fremitus, pleural effusion is your answer.
This was more of a rule-out question than a remember-the-arrows-on-a-page-in-FA question for me!
Breath sounds are decreased, so you can rule out asthmatic bronchitis (wheezing) and pulmonary embolism (normal breath sounds, but tachypneic). Bronchiectasis can have a number of findings--crackles, rhonchi, wheezing, mid-inspiratory squeaks, etc.
Emphysema (loss of alveolar septal tissue) and pneumothorax have increased air in the lungs, therefore, they will be hyperresonant on percussion, so rule those out too.
Tactile fremitus decreases with most everything, but consolidation--low frequency sounds travel well in dense material (lobar pneumonia), but travel poorly through liquid (pleural effusion). Therefore, based on decreased fremitus, rule out pneumonia.
So...you're left with pleural effusion as your answer!
The classic triad of a renal cell carcinoma is: 1) hematuria; 2) flank pain; and 3) a palpable flank mass. The classic RCC comes from a VHL mutation. No VHL means you can't inhibit HIF (hypoxia inducible factor). This leads to uncontrolled activation of VEGF, leading to the hypervascular mass.
Here is a great image showing the timeline for the different pubertal changes in males and females. Tanner stages are found in FA2020 p673.
In females, the earliest detectable sign of pubertal change is breast bud development which only slightly precedes pubic hair development. In males, testicular enlargement is the first detectable sign.
My reasoning for this question:
Pg 391, FA 2020
Frankly pretty floored that anybody thought that this question contained enough information for someone to confidently answer it.
The question has you assume that both parents are heterozygotes at the locus. Why? I assume I'm missing some esoteric fact about P450 allele frequencies.
This child likely has a meningomyelocele (neural tube defect caused by failure of the neuropores to fuse in week 4, FA2020 p491). Neural tube development in general occurs weeks 3-8 (FA2020 p612) which corresponds most closely to days 15-40. Organogenesis and most vital development also occurs during this period.
Days 1-10 are typically "all or nothing" in that a defect would cause fetal demise.
Days 60-75 (~weeks 8-10) are associated with external genital development, palate and teeth.
The most critical periods are typically over by week 10 (see this chart)
This individual is suffering from hypocalcemia, which explains the seizures, twitching (reason for Chvostek sign - tapping of the facial nerve causing contraction of the muscles), and spasms (similar to Trousseau sign - inflation of the blood pressure cuff causing carpal spasm). It also may present with QT prolongation and numbness and tingling (as described). It is also important to note that though mild hypocalcemia causes hyporeflexia, extreme hypocalcemia can lead to hyperreflexia, tetany, parasthesias, and seizures (see here). Basically you cannot bank on the reflexes.
Hypercalcemia would present with stones (renal), bones(pain), groans(abdominal pain), thrones( urinary frequency), psychiatric overtones(anxiety, altered mental status).
The others answers are incorrect because:
Electrolyte Disturbances: FA2020 p591
Just to clarify, complete resolution after injury can only occur if the basement membrane remains intact as this below this is where the stem cells are located. If there is damage to the basement membrane, you will have incomplete resolution and scar formation. The best example of this is skin injury.
Osteomyelitis is a common complication of sickle cell disease and can be distinguished here because of the elevated WBC/neutrophil (indicating bacterial infection). It is important to note the most common cause of sickle cell osteomyelitis is Salmonella or Staph aureus (in a healthy individual the most common cause is Staph aureus). [FA2020 p180 and 422]
Lichen sclerosus is a vulvular pathology involving thinning of the epidermis with fibrosis/sclerosing dermis, most commonly presenting with skin fragility (paper-thin) in post-menopausal women (FA2020 p644)
The other answers do not fit:
Changes that happen in aging:
Stays the same: TLC (very important to know this)
Increased: lung compliance, residual volume, V/Q mismatch, A-a gradient
Decreased: chest wall compliance, FVC, FEV1, respiratory muscle strength, ventilatory response to hypoxia/hypoxemia
AKA don't get old
Cold temperature: Causes peripheral vasoconstriction and central vasodilation
Metabolic acidosis because the arterial pH goes in the same direction as the bicarb and pCO2 (i.e. both pH and bicarb/pCO2 are decreased from normal); in primary respiratory acidosis/alkalosis the arterial pH goes in the opposite direction as the bicarb and pCO2.
Once you know that it is a primary metabolic acidosis, you have to check for concomitant respiratory disorders. Do this with Winter's formula:
expected pCO2 = 1.5(HCO3) + 8 +/- 2
so... expected pCO2 = 1.5(11) + 8 +/- 2 --> pCO2 = 24.5 +/- 2 = expected pCO2 is between 22.5-26.5, therefore, 23 is in the expected range, no concomitant respiratory process
Ligation of the internal iliac artery is used to stop postpartum uterine bleeding while preserving fertility as the ovarian arteries provide collateral circulation (FA2020 p640).
Here is an image showing the uterine artery coming off the internal iliac with the ovarian artery collateral.
He has an upper motor neuron lesion which is causing paralysis on his left lower side, so he will have hyperreflexia on this side. Thus the deep tendon reflex will actually be increased/strongest in his left achilles tendon initially after the accident. [FA2020 p529]
Loratadine is a second generation antihistamine and thus would be preferred in this patient as it does not cause sedation. [FA2020 p686]
Since he works operating heavy machinery, it would be preferred to put him on a second generation antihistamine. Bropheniramine, hydroxyzine, and diphenhydramine are first generation antihistamines which cause sedation.
Ranitidine is a histamine H2 blocker used to decrease secretion by parietal cells in peptic ulcer disease, gastritis, and gastric reflux [FA2020 p399]
Differential Diagnosis of Newborn/Neonatal Vomiting
-Benign gastroesophageal reflux ( i.e immature lower esophageal sphincter )
regurgitation of food shortly after feeding .
No further symptoms , healthy children with normal development
-Hypertrophic pyloric stenosis
Regurgitation - projectile nonbilious vomiting electrolyte imbalances ( alkalosis and hypokalemia ) * physical examination may reveal an olive mass on palpation of epigastrium
*typically starts from between 2nd and 7th week of age
-Midgut volvulus /Malrotation /Duodenal atresia * bilious vomiting * abdominal distention * Imaging may reveal signs like the double bubble sign ( duodenal atresia ) etc
Note: The list is not exhaustive as there are many more causes associated with newborn vomiiting
First aid 2020 pg 511-- brain lesion in the subthalamic nucleus = contralateral hemiballismus
FA 2020 pg 425
Porphyria cutanea tarda-- defect in UROD in the heme synthesis pathway that causes photosensitivity and blistering
This would be a prospective cohort as they are looking at two groups with and without risk factors and assessing disease incidence.
UWorld has a super pretty picture which helps visually explain the differences (Copyright UWolrd, blah blah buy UWorld)
This is a Congenital Diaphragmatic Hernia (FA2020p370).
Conginital diaphragmatic hernias are caused by a congenital defect of the pleuroperitoneal membrane which allows contents of the abdominal cavity to herniate upward, and displace the contents of the thorax (hence why our baby has displacement of the mediastinal contents to the right). This also leads to lung malformation and respiratory distress (hence the low apgar scores). Because the stomach is likely herniates upward, a nasogastric tube placed would appear in the left mediastinum (because that is where the stomach is). Further, there is an absence of bowel gas in the abdomen likely because the bowels are herniated into the thorax.
Splenectomy is indicated for hereditary spherocytosis because it is an intrinsic hemolytic anemia where the spleen is destroying the red cells even though they could technically function fine. Thus splenectomy will prevent premature removal by the spleen (FA2020 p422).
Sickle cell disease causes autosplenectomy/splenic infarct/sequestration but splenectomy is not indicated because the spleen is not contributing to the symptoms of sickle cell, the symptoms are caused by the vasoocclusive disease.
Mycobacterium leprae likes cool temperatures (FA2020 p141)
Mycobacterium leprae is an acid-fast bacteria which can cause two skin manifestations:
Leprosy likes cool temperatures so it infects skin and superficial nerves. Even without knowing the organism, the link could also be potentially inferred!
Maxillary nerve injury (specifically the infraorbital nerve) is an important potential complication of orbital rim fractures (e.g. blow out fractures) [See here]
Here is a picture of the territories of the different branches of the trigeminal nerve for sensation which could help you answer this question as he has numbness under the eye to the upper lip.
Orbital floor fractures can lead to entrapment of the inferior rectus, which can be a cause of pain on upward gaze and diplopia when asked to look upward. This is an ophthalmologic emergency (https://emedicine.medscape.com/article/825772-overview).
This mainly has to do with the location of the SA node (see here). The SA node is located in the atrial wall at the junction of the superior vena cava and right atrium.
The AV node lies near the back of the intraventricular septum near the opening of the coronary sinus (the triangle of Koch defines the AV node location)
Other fun facts from UWorld about ablation and different sites of origin, etc:
Gluconeogenesis primarily occurs in the liver, but enzymes for gluconeogenesis are also found in kidneys and intestinal epithelium. FA2019 p. 78
This protein is an uncoupling agent (likely thermogenin which is found in brown adipose and serves to increase heat production. Uncoupling agents will cause increased permeability of the mitochondria membrane, necessitating more oxygen consumption in order to generate the same ion gradient. Since more oxygen is consumed to generate the same gradient, more oxygen would be consumed to generate the same amount of ATP, so the ratio of oxygen consumption to ATP generation increases. (FA2020 p78)
Another way of thinking about this is that oxygen will continued to be consumed to attempt to generate the gradient, but the leaky membrane will prevent the gradient from being formed properly and therefore prevent ATP from being formed. Thus there is the same amount of oxygen consumed for little to no ATP being made so again the ratio of oxygen consumption to ATP generation increases. This is closer to what actually happens in the body but I found it easier to think about it the first way.
Below are links to pictures of what each organism would look like on a stain:
Pg 366 FA 2020.
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Cyclophosphamide is an alkylating agent which cross-links DNA at guanine and interferes with DNA replication (FA2020p441)
Other alkylating agents that interfere with DNA replication include busulfan, isofosfamide, nitrosureas and procarbazine (procarbazine is nonspecific).
The pt has sarcoidosis via the classic demographic association and the b/l hilar adenopathy
in sarcoid you get increased ACE and you also get hypercalcemia due to increased 1-alpha-hydroxylase (via acitvated macrophages) which leads to increased vitamin D
FA2020 pg 676
This question is essentially asking what happens to sympathetic and parasympathetic efferents in the setting of hypovolemia/dehydration. In this setting, there would be lower blood pressure and thus this would cause reduced firing of the carotid baroreceptors, ultimately leading to feedback which stimulates the sympathetic nervous system (to increase heart rate and cause peripheral vasoconstriction in order to compensate for hypovolemia) while also inhibiting the parasympathetics.
Cyclosporine is an immunosuppressant that blocks T-cell activation by preventing IL-2 transcription (FA2020 p120)
Even without remembering the mechanism of cyclosporine, the answer could be inferred as most medications used after kidney transplant (cyclosporine, tacrolimus, sirolimus, basiliximab) block T-cell activation. This mechanism MAKES LOGICAL SENSE because T-cells are the primary mediators of acute rejection, which is what we are trying to prevent directly after a kidney transplant.
Answering this question requires general knowledge of the catecholamine synthesis pathway (FA2020 p83).
The approach I took to this question was mainly elimination of wrong answers:
This leaves the answer, dopamine beta-hydroxylase.
FA 2019, pg. 556. Stages of change model.
Precontemplation --> denying the problem (i.e. if this patient didn't think that he needed insulin to control his blood sugar)
Contemplation --> acknowledges the problem, but is unwilling to change (i.e. our patient here, knows that he needs insulin, but not ready to take it b/c it made people in his family sick)
Preparation/determination --> preparing for behavioral change (i.e. patient asking the doctor to prescribe insulin to control his blood sugar)
Action/willpower --> changing behaviors (i.e. patient is taking insulin)
Maintenance --> maintaining changes (i.e. patient has taken his insulin for last 5 years with fidelity)
Relapse --> returning to old behaviors and abandoning changes
6-month history of exertional chest pain that is relieved by rest = stable angina. Per FA2019, pg. 301--stable angina is usually secondary to atherosclerosis with more than 70% occlusion.
Contrary to what you might think (or at least this is doublethink for me!), plaques that occlude a larger percentage of the lumen are usually older and more stable (i.e. calcified) and this makes them less dangerous. These larger, older occlusions usually have a well-developed fibrous cap that makes them less likely to rupture and cause unstable angina/NSTEMI or STEMI.
B/c this guy has had symptoms that are not increasing in intensity over the past 6 months, he likely has a calcified, lg. plaque.