This question is testing your knowledge on acute cystitis caused by Chlamydiae.

Chlamydial cell wall lacks classic peptidoglycan (due to reduced muramic acid), rendering β-lactam antibiotics ineffective.

Labs will demonstrate a (positive) leukocyte esterase. (positive) nitrites (indicates presence of Enterobacteriaceae). Sterile pyuria (pyuria with negative urine cultures) could suggest urethritis by Neisseria gonorrhoeae or Chlamydia trachomatis.

(FA 2021, Pg. 527)

This question is testing knowledge on the clinical reflexes, specifically the Achilles reflex.

One of the key things to pay attention to in the stem is that the patient has a left Achilles tendon reflex that is absent. The Achilles tendon reflex involves S1, S2 ("buckle my shoe").

This question is testing your knowledge on sarcoidosis.

It is not referenced in First Aid, but this is neurosarcoidosis. You can find a small amount of info on it in AMBOSS:

• Nervous system (neurosarcoidosis)
• Cranial nerve palsy (facial nerve palsy is the most common)
• Diabetes insipidus
• Meningitis
• Hypopituitarism
• Peripheral neuropathy
• Myopathy

Sarcoidosis can present in many other areas besides the lungs which is the typical question stem we are all used to seeing. One thing to note about it, is that where ever it implants it will cause symptoms in that region (e.g., CSF -> meningitis).

(FA 2021, Pg. 416)

This question is testing your knowledge on neutrophils.

In the stem patient has a right hand that is tender, erythematous, and edematous with an intact wooden splinter embedded in the soft tissue. Then the description of "white exudate" is given. This white exudate is pus and is generated by neutrophils. Additionally, neutrophils are the first responders to most insults to the skin.

Another very important thing to know is the neutrophil chemotactic agents: C5a, IL-8, LTB4, 5-HETE (leukotriene precursor), kallikrein, platelet-activating factor, N-formylmethionine (bacterial proteins). Make sure you know this, the test makers love to test this!

This question is testing your knowledge on gout.

In the question stem the examiners are showing you a picture of a hand with extensive tophus formations (often these appear on the external ear, olecranon bursa, or Achilles tendon).

Strongest risk factor for acquiring gout is hyperuricemia, which can be caused by:

• Underexcretion of uric acid (90% of patients)—largely idiopathic, potentiated by renal failure; can be exacerbated by certain medications (eg, thiazide diuretics).
• Overproduction of uric acid (10% of patients)—Lesch-Nyhan syndrome, PRPP excess, 􏰂 cell turnover (eg, tumor lysis syndrome), von Gierke disease.

Treatment:

• Acute: NSAIDs (eg, indomethacin), glucocorticoids, colchicine.
• Chronic (preventive): xanthine oxidase inhibitors (eg, allopurinol, febuxostat).

This question is testing your knowledge on microtubule inhibitors (all are M-phase specific).

Specifically, this question is asking you about Vinblastine. One important adverse effect to know about vinblastine (blasts the marrow): myelosuppression. Therefore, you would see a significant decrease in the numbers of neutrophils.

This question is testing your knowledge on T- and B-cell activation.

My specifically it is asking about B-cell activation and class switching. The following steps occur during this process, and step 4 is what you need to know in order to answer this question correctly:

1) Th-cell activation as above. 2) B-cell receptor–mediated endocytosis. 3) Exogenous antigen is presented on MHC II and recognized by TCR on Th cell. 4) CD40 receptor on B cell binds CD40 ligand (CD40L) on Th cell. 5) Th cells secrete cytokines that determine Ig class switching of B cells. 6) B cells are activated and produce IgM. They undergo class switching and affinity maturation.

This question is testing your knowledge on ovulation.

During ovulation there will be increased estrogen, increased GnRH receptors on the anterior pituitary. Estrogen will continue to rise and then eventually this will stimulate LH surge --> ovulation (rupture of follicle). Increased temperature will also occur and this is (progesterone induced).

Also, keep in mind that there are two phases of the ovarian cycle:

• Follicular phase
• Luteal phase

This is question is testing your knowledge on the pudendal nerve (S2-S4).

Is this patient the the motor component - external urethral and anal spincters. Injury such as stretch during child birth, prolonged cycling, and horseback riding could cause this. Patients will present with decreased sensation in the perineum and genital area; can cause fecal and/or urinary incontinence.

It is also important to know that the pudendal nerve can be blocked with local anesthetic during childbirth using ischial spine as a landmark for injection.

(FA 2021, Pg. 675)

This question is testing your knowledge on cryptorchidism.

This condition results in descent failure of one or both testes; impaired spermatogenesis (since sperm develop best at temperatures < 37°C); can have normal testosterone levels (Leydig cells are mostly unaffected by temperature); associated with increased risk of germ cell tumors. Prematurity increases risk of cryptorchidism. Decreased inhibin B, increased FSH, increased LH; testosterone decreased in bilateral cryptorchidism, normal in unilateral. Most cases resolve spontaneously; otherwise, orchiopexy performed before 2 years of age.

This question is testing your knowledge on Candida albicans. When CD4+ is lower than 100/mm3 then the patient is at risk for a normal flora candida skin infection.

This question is testing your knowledge of being aware that when a patient is experiencing symptoms/pain that it may be due to a depression or a major depressive episode. This patient is experiencing symptoms but there is no apparent medical evidence for those symptoms.

This question is testing your knowledge on Lyme disease. The stem describes the patient as having a rash and flu-like illness 2 months ago, and now he is presenting with pain in multiple joints and fatigue. The stem is describing Stage 1 and 2 of Lyme disease.

• Stage 1—early localized: erythema migrans (typical “bulls-eye” configuration B is pathognomonic but not always present), flu-like symptoms.

• Stage 2—early disseminated: secondary lesions, carditis, AV block, facial nerve (Bell) palsy, migratory myalgias/transient arthritis.

There us also a Stage 3 which was not described in the stem:

Stage 3—late disseminated: encephalopathy, chronic arthritis, peripheral neuropathy.

Also, when it comes to treatment know that doxycycline is 1st line, and if you have a pregnant patient then you would prescribe amoxicillin or to patients who are under 8 years old. Additionally, IV ceftriaxone is required.

This question is testing your knowledge on the respiratory/conducting zone. The bronchioles are comprised of the (bronchioles, terminal bronchioles, and respiratory bronchioles) which all contain smooth muscle, the respiratory bronchioles have the most "sparse" amount of smooth muscle though. Together, these comprise the largest amount of smooth muscle in the respiratory tract and therefore would be most susceptible to flow limitation due to smooth muscle contraction during an asthma attack.

This question is testing your knowledge on tetracyclines. The patient in the stem is taking tetracyclines and had spent the day at the beach (a big no no) while on these meds. One adverse effect with tetracyclines is that they cause photosensitivity.

Make sure you know all of the adverse effects of tetracyclines and many of them have very bad outcomes.

This question is testing you knowledge on skeletal muscle adaptations (specifically atrophy). The patient is described to have cachexia and significant muscle wasting, these are manifestations of atrophy. Atrophy occurs via:

• Decreased myofibrils (removal via ubiquitin-proteosome system)
• Decreased myonuclei (selective apoptosis)

It is important to know the molecular mechanisms of atrophy above as these are what the test makers love to test your cellular and molecular knowledge on many concepts.

This question is testing your knowledge on Severe Combined Immunodeficiency (SCID). When considering a SCID diagnosis consider these aspects:

Defect:

• IL-2R gamma chain (most common, and x-linked recessive).
• Adenosine deaminase deficiency (Autosomal recessive)..
• RAG mutation --> VDJ recombination defect.

Presentation:

• Patients will present with features such as failure to thrive, chronic diarrhea, and thrush.
• Patients will present with recurrent viral, bacterial, fungal, and protozoal infections.

Findings:

• Decreased T-cell receptor excision circles (TRECs)
• Part of newborn screening for SCID
• Absence of a thymic shadow (CXR), germinal centers (on lymph node biopsy), and T cells (flow cytometry)

I believe this question is just testing your knowledge on type I pneumocytes and is you know that these are what comprise a majority of the alveolar surface area.

To be more specific, type I pneumocytes are of squamous cell origin and they cover 97% of alveolar surfaces. It makes sense that they would be made of thin "squamous" tissue as this is what makes them optimal for gas exchange.

This question is asking you about one very peculiar fact about Hepatitis E, and that is that is can cause fulminant hepatitis in expectant (pregnant) patients. This leads to a high mortality in pregnant patients.

Some other important things to know about Hepatitis E is that it is enteric and epidemic (e.g. in parts of Asia, Africa, Middle East), and that there is no carrier state.

This question is testing your knowledge of neuraminidase inhibitors (e.g. Oseltamivir, Zanamivir) which are commonly used to treat influenza or aka "the flu". Neuraminidase inhibitors decrease the release of progeny virus.

One important thing to know is that this therapy needs to be done within 48 hours of symptom onset. If this is done it isn't guaranteed but it (may) shorten the duration of the illness with influenza.

(FA 2021, Pg. 338)

This question is testing your knowledge of dopamine antagonist (e.g. antipsychotics, metoclopramide). Dopamine antagonists and estrogens (e.g. OCPs, pregnancy) stimulate prolactin secretion).

What really important this though is to know and I think a lot of people get confused is that when prolactin production is blocked off via the dopamine pathway, the hypothalamus re-routes through thyroid releasing hormone (TRH) and then back through the anterior pituitary to stimulate prolactin secretion which then causes the galactorrhea in the patient.

This patient is experiencing one of the most feared complications of alcohol withdrawal, which is delirium tremens. This is typically seen about 2-4 days after the patients last drink. Classically seen in a situation where the patient has to stay in the hospital for an extended amount of time (becomes an inpatient) and cannot drink alcohol.

Clinical features:

• Altered mental status, hallucinations, autonomic hyperactivity, anxiety, seizures, tremors, psychomotor agitation, insomnia, and nausea.

Treatment:

• Longer-acting benzodiazepines (e.g. diazepam).

(FA 2021, Pg. 538)

This question is eluding to the genetic concept of "anticipation" which is seen in the condition being described in this stem (Huntington disease).

Huntington disease is the result of a triple repeat expansion (a CAG repeat to be specific). When younger family members present with the disease earlier then the previous generations then we can suspect that they have MORE of these triple repeat expansions (e.g. Son has 1000 CAG repeats and the father has only 100 CAG repeats). Ultimately this leads to an earlier manifestation of the disease.

(FA 2021, Pg. 538)

This patient has Parkinson disease. This question is asking you to identify where the problem in the brain occurs which is in the basal ganglia. Within the basal ganglia is the dopaminergic neurons of the substantia nigra. It is these neurons the become lost slowly over time and grossly (depigmentation)occurs at the substantia nigra pars compacta specifically.

Also, make note that histologically you will see Lewy bodies. These are composed of alpha-synuclein (intracellular eosinophilic inclusions).

A good memory anchor for this one is to know that this is what Robin Williams is said to have died from.

(FA 2021, Pg. 513)

Another small detail that the test makers could test, make sure that you know the area of postrema is found in the (dorsal medulla). This is the area in which it responds to anti-emetics (e.g. Ondansetron).

(FA 2021, Pg. 369)

Patient has hypertrophic pyloric stenosis. This is the most common cause of gastric outlet obstruction in infant (1:600).

Clinical features:

• Palpable olive-shaped mass in the epigastric region
• Visible peristaltic waves
• Non-bilious projectile vomiting (make sure you can differentiate this with intestinal atresia which presents with bilious vomiting)
• Appears around 2-6 of age
• More common in first born males
• Associated with macrolide exposure

Imaging (ultrasound): Will demonstrate a thickened and lengthened pylorus

Treatment: Surgical incision of the pyloric muscles (pyloromyotomy)

(FA 2021, Pg. 69). This patient has vitamin B12 deficiency. The patient has been consuming a vegetarian diet for 12 years...so that is plenty of time for them to run out of their B12 stores. Vegetarians are particularly at risk for this deficiency because they do not consume animal products which contain a good amount of B12.

(FA 2021, Pg. 320) This is hypovolemic shock. This type of shock is caused by hemorrhage, dehydration, and burns. The patients skin will present as cold and clammy. PCWP (preload) will be decreased, CO decreased, SVR (after load) will be increased. First line treatment will be to administer IV fluids promptly.

(FA 2021, Pg. 320) This is hypovolemic shock. This type of shock is caused by hemorrhage, dehydration, and burns. The patients skin will present as cold and clammy. PCWP (preload) will be decreased, CO decreased, SVR (after load) will be increased. First line treatment will be to administer IV fluids promptly.

(FA 2021, Pg. 320) This is hypovolemic shock. This type of shock is caused by hemorrhage, dehydration, and burns. The patients skin will present as cold and clammy. PCWP (preload) will be decreased, CO decreased, SVR (after load) will be increased. First line treatment will be to administer IV fluids promptly.