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.
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)
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.
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!
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.
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)
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.
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.
Cold temperature: Causes peripheral vasoconstriction and central vasodilation
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!
Pg 391, FA 2020
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.
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]
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.
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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
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.
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.
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 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
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]
Pg 366 FA 2020.
Hemorrhoids are dilatations of arteriorvenous plexuses in the rectum. Blockages on the arterial side will not cause the plexus to fill while venous thromboses will cause a back up of fluid.
Clues for hinting which vein are the location at the anal margin and that he was in extreme pain. External hem's will be painful, pointing towards inferior rectal as the answer since it drains below the pectinate line where external hem's are found.
What you can see is
1.Hyperkeratosis (thickened stratum corneum) 2.Parakeratosis (you can see the nuclei very clearly in the stratum corneum) 3.Dysplasia (notice keratinocytes hyperchromatic and large nuclei go up almost all the way to the top. This isnt so in normal skin)
all this fits actinic keratosis
The best way to explain this:
Firstly, the only possible combinations for the child are 1,2 or 2,3, one from each parent (that eliminates A, C & D)
They are looking for the genotype for III if he is unaffected by the disease. In I, we see that the male is affected, and the female is not. In II, both the female and male are affected.
If II female is 1,1 one of each 1 alleles comes from each parent, II male, we recognize that the 3 allele has to come from I female, and 1 allele HAS to come from I male. Therefore, one can infer that it is the one of the 1 genes from the I male causing the disease. If III is unaffected, the only option would be 3,2.
FA 2020 pg 425
Porphyria cutanea tarda-- defect in UROD in the heme synthesis pathway that causes photosensitivity and blistering
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
I think inhalants are a new add to FA2020 (at least they weren't in Zanki), so I go to this one by elimination:
eliminated Meth + PCP + Cocaine because they're Stimulants.
eliminated EtOH b/c it would take a long time for cerebellar atrophy to manifest and I doubt a 14yo has been drinking since birth.
Uterine conditions FA2020 p648
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!
Looking at the symptoms, they fit with cerebellar issue, as the cerebellum is responsible for modulating movement and aiding in coordination and balance. [FA2020 p499]
She does not have paralysis or parasthesia but rather lack of control of movement, making injury to the cerebrum less likely. Further, her issues are not localized to the upper or lower extremity and do not fit with any syndrome of spinal cord. Ataxia is also typically a buzzword for associations with the cerebellum. In this case, her limb ataxia is likely from a metastasis to the left cerebellar hemisphere.
If you want to review:
Common brain lesions can be found FA2020 p511.
Spinal lesions can be found FA2020 p530.
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)
Patient with Primary Hypothyroidism (problem with the gland itself ) treated with T3
So what happens when we give our Patient T3.
- firstly , we inhibit secretion of TSH from the pituitary gland . ( TSH decreases ).
This means less stimulation of the Thyroid and less hormone production . The Throid hormone it primarily makes and releases is T4 , ( and so T4 decreases ) . Naturally you would also expect a decrease in T3 but patient is taking exogenous T3( and so T3 increases )
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.
I was thrown off because Pathoma/Dr. Sattar and pixorize say it is critical to start steroids ASAP to avoid permanent damage to the ophthalmic artery and blindness in patients suspected of having Giant Cell (Temporal) Arteritis.
This means not waiting for diagnostic confirmation.
However a 99% sensitivity does not equate to a 99% certainty of GCA/TA. So additional testing is the best answer choice even though her elevated ESR gives us strong suspicion of GCA/TA.
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
According to FA2019, pg. 468:
Rosacea is a facial disorder characterized by erythematous papules and pustules, but no comedones (hence this patients erythema over the nose and cheeks, with scattered telangiectasias and a few papules); may be associated with facial flushing in response to external stimuli (hence, blushing easily, spicy foods precipitating a flushing reaction).
Acne vulgaris would present with comedones.
Carcinoid syndrome can also present with episodic flushing triggered by foods, alcohol, or stress. But, this would also present with systemic symptoms--diarrhea, weakness, SOB, sweating, etc.
Pityriasis rosea is a viral rash that lasts between 6-12 weeks and would not be expected as the cause based on this patient's 3-yr history.
Seborrheic dermatitis causes an itchy rash with flaky scales (no flaking present in our patient here),
She has a craniopharyngioma, the most common childhood supratentorial tumor which is derived from remnants of Rathke's pouch (FA2020 p528). Craniopharyngiomas commonly have calcification and can cause hypopituitary issues (like low HGH). Suprasellar is also the location of the pituitary, and pituitary tumors in general cause bitemporal hemianopsia due to compression of the optic chiasm.
Rathke's pouch (where craniopharyngiomas and anterior pituitary are derived from) is derived from the surface ectoderm of the oral cavity.
Note that the neurohypophysis (posterior pituitary) is derived from neural ectoderm while the adenohypophysis (anterior pituitary) is derived from surface ectoderm of the oral cavity.
This woman likely has endometriosis, characterized by cyclic pelvic pain, bleeding, and associated with infertility (FA2020 p648). It is associated with "chocolate cysts" on the ovaries. Proliferative endometrial tissue would be found on biopsy
Endometriosis scar tissue/adhesions can cause the uterus to stick in a backwards position (retroverted) according to https://www.healthline.com/health/womens-health/tilted-uterus
Polycystic ovarian syndrome is associated with obesity would also likely have symptoms of hisutism and acne as well as infertility. It also presents with amenorrhea or oligomenorrhea. [FA2020 p645]
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.
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Aplastic anemia: anemia, leukopenia, thrombocytopenia
CML, i.e. leukemias: anemia, ↓ mature WBC, ↓ plt, peripheral blood smear shows mature & maturing granulocytes (FA 2020, p. 432)
β-thalassemia major: microcytic, hypochromic anemia with target cells and anisopoikilocytosis, skeletal deformities, etc. (FA 2020, p. 418)
Cobalamin deficiency: d/t malabsorption, pancreatic insufficiency, gastrectomy, or insufficient intake, neurological Sx
Personally, I got this wrong, because to me, the RBCs in that smear looked both larger and more irregularly shaped, so in hindsight, I really should've honed in more on the HPI, i.e. the patient really has anemia and no other relevant PMx.
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.
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:
First step to approach this problem is to eliminate Listeria monocytogenes (it is a gram positive ROD) and both staphylococcal species (Staph is always catalase positive), which leaves us with Streptococcus pneumoniae and Enterococcus faecalis.
Strep pneumoniae is an alpha hemolytic strep while enterococcus is typically gamma hemolytic, so seeing as there is no hemolysis on blood agar (meaning gamma hemolytic), Enterococcus is the correct answer. VRE (vancomycin resistant enterococcus) are also an important cause of nosocomial infections such as from his venous catheter.
Here is a good algorithm/flow chart for gram positive identification!