D- This patient experienced symptoms of hypoglycemia (e.g., restlessness, sweating, and confusion) due to over-supplementation of exogenous insulin. Mistakes in calculating the necessary insulin dosage after a high-carbohydrate meal are common. When adjusting insulin doses for a specific meal, typically the shorter-acting insulin formulation is adjusted while the basal insulin formulation is left the same. This patient’s father increased the doses of both of her insulin formulations around a high-carbohydrate meal with good intent to prevent hyperglycemia. This adjustment most likely led to overcompensation of this child’s carbohydrate intake, causing a brief period of symptomatic hypoglycemia. These symptoms are multifactorial, including autonomic (e.g., sweating, restlessness) and neuroglycopenic (e.g., confusion) in nature.

B- This patient is experiencing symptoms of cardiac obstruction (e.g., fainting). She is subsequently found to have S3 and S4 heart sounds and a pedunculated intracardiac mass, pathognomonic for a cardiac myxoma. Biopsy findings of scattered mesenchymal cells surrounded by gelatinous material (composed of glycosaminoglycans) further support this diagnosis. Cardiac myxomas are most commonly found in the left atrium. These tumors act as a ball-valve obstruction, causing intermittent symptoms, including dizziness, palpitations, and syncope. Weight loss, fever, pallor, chills, fatigue, and other constitutional symptoms are also possible as these tumors frequently secrete IL-6.

A- This infant has polycystic kidney disease leading to Potter’s sequence. Since genetic testing reveals two copies of a genetic mutation, that suggests this is an autosomal recessive condition. The Hardy-Weinberg principle states that in a population at equilibrium, the genotypic proportions will follow the formula p2+2pq+q2=1, where p2 is the frequency of homozygous dominants, 2pq is the frequency of heterozygotes, and q2 is the frequency of homozygous recessives. The frequency of each allele occurring in the population will follow p+q=1, where p is the frequency of the dominant allele, and q is the frequency of the recessive allele. Since this is an autosomal recessive condition, only homozygous recessive individuals will have the disease, so the disease frequency and the q2 is 1/10,000. The mutation rate, which is the same as the frequency of recessive alleles in the population, can be calculated by taking the square root of 1/10,000, which comes out to q = 1/100. For additional information check out MedSchool Bootcamp's video on Hardy-Weinberg Genetics.

B- This elderly female has evidence of worsening osteoarthritis involving her wrists and hands that causes her significant pain and loss of function, especially when buttoning her coat. The image of her hand reveals Heberden and Bouchard nodes (especially of the 3rd PIP). Osteoarthritis occurs due to chronic mechanical forces translated across joints and age-related decreases in proteoglycan synthesis. This process leads to the loss of cartilage elasticity and subsequent degeneration and inflammation of the cartilage. This can be seen as subchondral sclerosis and joint space narrowing, especially on imaging.

D- This previously health patient has developed severe left-sided flank pain, tachycardia, and hypertension (likely from pain). Further evaluation reveals microscopic hematuria and a small ureteric calculus (kidney stone) composed of uric acid. Uric acid stones are a relatively uncommon finding of nephrolithiasis, as most are calcium based. Patients with underlying impairments in uric acid metabolism (underexcretion or overproduction) are more likely to develop nephroliths composed of uric acid. Conditions associated with these stones include gout, high cell turnover (e.g., tumor lysis syndrome, myelodysplastic syndromes), hyperuricemia, and hyperuricosuria. Out of the listed choices, an impairment in purine metabolism (adenine, guanine) is the most likely cause of his presenting illness. (E) Urea cycle abnormalities include ornithine transcarbamylase deficiency, arginase deficiency, carbamoyl phosphate synthetase 1 deficiency, and N-acetylglutamate synthase deficiency. These disorders involve dysfunction of ammonia conversion into urea for excretion. They are not involved in purine metabolism and/or uric acid production. For additional information check out MedSchool Bootcamp's video on Purine Metabolism.

A- This patient has developed worsening symptoms of hypothyroidism (e.g., cold intolerance, constipation, and severe fatigue) after beginning calcium carbonate supplementation for lumbar spine osteopenia. Lab studies reveal elevated TSH and decreased free T4 concentrations, confirming worsening hypothyroidism. This is most likely due to nonspecific complex formation between calcium and levothyroxine within the intestinal lumen. It is known that taking these two medications within a four hour window can significantly decrease the absorption and bioavailability of levothyroxine.

A- This elderly patient presenting with a 5-day history of a painful rash that does not cross the midline likely is suffering from herpes zoster (shingles). Herpes zoster classically presents in a dermatomal distribution that does not generally cross the midline. Lesions are often vesicular and painful in nature. Reactivation of varicella-zoster virus is thought to contribute to the development of shingles in immunocompromised individuals secondary to deficiencies in cellular immunity. Cellular immunity is essential in the identification and destruction of intracellular pathogens, such as viruses, through the use of MHC class I proteins on host tissue. For additional information check out MedSchool Bootcamp's video on Herpes Simplex and Varicella Skin Infections.

E- This patient is found to have accessory spleens after suffering crush injuries in a motor vehicle collision. The most likely origin of this congenital anomaly is a thickening of the dorsal mesogastrium. This occurs due to an incomplete fusion of mesenchymal buds during development. During the fifth week of development, a primitive spleen forms in the midline from the mesoderm of the dorsal mesogastrium (in the midline). This rotates to the left side as the foregut develops. The unfused mesenchymal buds can form accessory spleens in any position between the original primitive spleen formation and the final site of the spleen (LUQ). Of note, accessory spleens can also be formed by the descent of the gonads during development—the spleen initially forms near the urogenital ridge. Due to this physical proximity, it is possible for the primitive gonadal tissue to become fused to some of the mesenchymal buds. As the gonads develop and descend, they can drag accessory splenic tissue with them; this leads to the placement of accessory spleens in the pelvis or groin.

C- Benzodiazepines are the first-line agents in the management of alcohol withdrawal. Longer acting agents (e.g., chlordiazepoxide, diazepam) are classically preferred in most patients, but shorter acting agents (e.g., lorazepam, temazepam) are preferred in patients with altered drug metabolism (e.g., liver disease, elderly). These agents are indirect GABA-A receptor agonists that increase the action of GABA binding by increasing the frequency of chloride channel opening. This leads to postsynaptic membrane hyperpolarization and decreased symptoms associated with neuronal excitability (e.g., anxiety, insomnia, tremor, palpitations, sweating, seizures). For additional information check out MedSchool Bootcamp's video on Alcohol Withdrawal.

B- This patient has poorly controlled type II diabetes mellitus. This is most likely due to her travel and work situation, leading her to eat excessive amounts of “fast” food (e.g., overly processed, high-carbohydrate density foods) and forget to measure her blood glucose concentration. The best action by the physician would be to further explore and inquire about the barriers this patient is experiencing when it comes to diet adherence (e.g., financial ability, time requirement, food macronutrient knowledge). (C, D, G) Increasing this patient’s medications may be necessary but is likely to be less effective if the patient’s dietary adherence is the primary issue. Referral to a nutritionist could be helpful if a lack of macronutrient knowledge and healthy food choices is a source of this patient’s problem. (E) Measuring the blood glucose concentration is unlikely to be helpful as it is more than likely elevated. This patient displays no signs of HHS or DKA so this is unwarranted. (F) Though monitoring of renal function is essential in patients with diabetes mellitus, this is unlikely to help improve her level of disease control. (A) Creating an exercise regimen for a patient who already feels time constraints and cannot handle the current level of intervention is unlikely to be helpful.

D- This young male presents with bilateral parotid gland swelling, fever, malaise, and decreased appetite. This presentation is classic for an infection with Mumps virus—a highly contagious viral infection transmitted via airborne droplets, contaminated saliva and/or respiratory secretions. Mumps classically effects the salivary glands (especially the parotid gland) before disseminating to lacrimal, thyroid, mammary glands, ovaries, testes, pancreas and/or central nervous system. This can be differentiated by other causes of parotid gland swelling due to its bilateral nature, painful presentation, and fever. Sialadenitis is typically unilateral and painful, sialolithiasis is unilateral and partial with prandial pain, and salivary gland tumors are typically unilateral, painless +/- signs of invasion (e.g., facial nerve compression and palsy), systemic signs (e.g., weight loss, fatigue.

A- This patient has developed multiple episodes of angioedema (e.g., throat tightness and swelling of the face, lips, and tongue) six weeks after beginning an ACE inhibitor. She has no signs of urticaria (hives). This is most likely due to increased levels of bradykinin caused by impaired catabolism in the presence of an ACE inhibitor. ACE inhibitors prevent the conversion of angiotensin I to angiotensin II in the treatment of hypertension; they also prevent the inactivation of bradykinin into physiologically inactive peptides. A buildup of bradykinin leads to overactivation of B2 receptors, causing the release of prostacyclin, NO, and other endothelium-derived relaxing and hyperpolarizing factors. This leads to vasodilation and possible hypotension, seen clinically as angioedema. For additional information check out MedSchool Bootcamp's video on Antihypertensives.

B- This patient has a left-sided varicocele, due to an abnormal enlargement, tortuosity, and distention of the scrotal pampiniform plexus—network of small veins that runs in the spermatic cord, providing testicular venous drainage. This is most commonly due to proximal obstruction of the testicular vein. The left side is more commonly affected as the left testicular vein enters the left renal vein at a ~90° angle. The right testicular vein enters the IVC directly. The left renal vein passes between the superior mesenteric artery and the aorta, leaving it susceptible to period compression (nutcracker syndrome). The increased pressure within the left renal vein transmits to the left testicular vein, leading to scrotal pampiniform plexus distension—over time this leads to enlargement and tortuosity. This can be exacerbated by increased intraabdominal pressure (e.g., Valsalva) and observed with doppler ultrasound of the affected testicle. For additional information check out MedSchool Bootcamp's video on Male Reproductive Anatomy.

B- This patient has developed chronic myelogenous leukemia with the presence of the Philadelphia chromosome. This is due to a translocation between chromosomes 9 and 22, t(9;22). Fusion of the ABL1 gene from chromosome 9 with the BCR gene from chromosome 22 leads to the formation of a BCR-ABL gene. This encodes for a non-receptor tyrosine kinase that has enhanced enzymatic activity. The results of the translocation include inhibition of apoptosis and increased baseline mitotic activity. Translocations represent the recombination of chromosomal regions between nonhomologous chromosomes. For additional information check out MedSchool Bootcamp's video on Chronic Myeloid Leukemia.

A- This patient presents with signs and symptoms of cystic fibrosis, an autosomal recessive disease due to a defect in the CFTR gene on chromosome 7. This gene encodes the cystic fibrosis transmembrane conductance regulator—a chloride and bicarbonate channel responsible for fluid secretions nd extracellular alkalinization. Patients with cystic fibrosis are unable to secrete bicarbonate adequately, leading to organ specific manifestations (e.g., pancreatic insufficiency, dental caries, impaired gastrointestinal mucous secretion, cervical mucous thickening, impaired fertility). Kunzelmann K, Schreiber R, Hadorn HB. Bicarbonate in cystic fibrosis. J Cyst Fibros. 2017;16(6):653-662. doi:10.1016/j.jcf.2017.06.005. For additional information check out MedSchool Bootcamp's video on Cystic Fibrosis.

C- This patient has suffered damage to the upper trunk due to right clavicular fracture. His current deficits include decreased DTRs in the biceps (C5-6) and brachioradialis (C5-6) and decreased sensation over the right shoulder (Axillary nerve- C5-6). Out of the listed options, impaired shoulder abduction (due to impaired axillary nerve transduction) is the most likely. (A) Elbow extension is maintained by the extensor compartment innervated by an intact radial nerve (C5-T1). (B) Finger abduction is maintained by the dorsal interossei innervated by an intact ulnar nerve (C8-T1). (D) Thumb flexion is maintained by flexor pollicis longus (median nerve and brevis (superficial: median, deep: ulnar) innervated by intact median nerve (C6-T1) and ulnar nerves (C8-T1). Wrist flexion is also maintained by intact ulnar and median nerves via multiple muscles of the anterior compartment.

C- This patient presents with signs of platelet dysfunction (e.g., nosebleeds, easy bruisability, gingival bleeding) in the presence of a family history, normal platelet count, normal ristocetin cofactor response assay, and impaired thrombin-mediated platelet aggregation. This is most likely due to Glanzmann thrombasthenia—an aggregation disorder due to an autosomal recessive deficiency in platelet receptor GpIIb-IIIa. Most affected patients are asymptomatic or develop minor bleeding (e.g., petechiae, menorrhagia, epistaxis, purpura, gingival bleeding). Lab findings include increased bleeding time, normal platelets, and impaired platelet aggregation studies (impaired thrombin-mediated platelet aggregation). PT/INR, aPTT, D-dimer, and fibrin degradation products will all be within normal limits. For additional information check out MedSchool Bootcamp's video on Platelet Disorders.

E- This patient has developed new-onset shortness of breath after living at high-altitude for a period of 2 years. Findings include jugular venous distention and lower extremity pitting edema. This is most likely due to group 3 pulmonary hypertension—high altitude. High altitude exposure is associated with decreased PiO2 (atmospheric oxygen). Along with tachypnea, and renal bicarbonate excretion that occurs acutely, pulmonary vascular resistance increases (D) in response to hypoxic pulmonary vasoconstriction. Over time, this leads to pulmonary hypertension and eventual concentric right ventricular hypertrophy (F). As the wall of the right ventricle thickens, diastolic compliance decreases. As a result, the height of the P waves in lead I increase (P pulmonale, right atrial enlargement) (A), height of R waves in lead V1 increase (increased right ventricular mass) (B). Compensation to chronic hypoxia also includes erythroid expansion (erythropoiesis), increased erythrocyte mass, and increased hematocrit (C). For additional information check out MedSchool Bootcamp's video on Pulmonary Hypertension.

E- This patient has primary pulmonary tuberculosis. The typical treatment regimen consists of two months of rifampin, isoniazid, pyrazinamide, and ethambutol followed by four months of rifampin and isoniazid. Rifampin inhibits bacterial DNA-dependent RNA polymerase, preventing transcription and mRNA synthesis. This leads to impaired bacterial protein synthesis and cell death.

D- This patient is found to have a large hepatic laceration involving the right and left lobes. Hepatic bleeding is often controlled via the Pringle maneuver—temporary occlusion of the hepatoduodenal ligament via vascular clamp or surgeon’s hand in order to decrease blood flow to the liver through the hepatic artery and portal vein. For additional information check out MedSchool Bootcamp's video on GI Gross Anatomy.

C- This 1-month-old male has developed signs and symptoms of bronchiolitis (e.g., fever, cough, intercostal retractions, diffuse wheezing). He is subsequently found to have blood cultures growing coagulase-negative, catalase-positive, gram-positive cocci in clusters. This is representative of Staphylococcus epidermidis. Bronchiolitis is most commonly caused by respiratory syncytial virus (RSV) and occasionally with parainfluenza virus. This blood culture result is most likely due to contamination of blood culture vials with normal skin flora.

C- Increases in trans-fatty acid intake are known to adversely affect serum lipid studies, owing to a greater risk of atherogenesis and coronary artery disease. Trans-fatty acid intake is linked with reduced HDL, increased total cholesterol and increased LDL.                

D- Clearance of a drug is defined as the volume of plasma cleared of a drug in a unit of time (typically hours). It can be calculated by dividing the rate of elimination of a drug by the plasma drug concentration. The rate of elimination of this drug is unknown, necessitating another equation to be used. Infusion rate = Clearance x Steady state concentration. In this case, 100mg/hr = Clearance x 50 mg/L. Solving for clearance = 100mg/hr divided by 50 mg/L = 2 L/hr. 

D- This patient has developed acute tubular necrosis (e.g., muddy brown casts, acute kidney injury, elevated creatinine) in the setting of E. coli sepsis. This is most likely due to decreased renal blood flow caused by hypotension and renal ischemia. The most likely areas of the kidney to be affected by ischemia include the proximal convoluted tubular and the thick ascending limb due to greater levels of metabolic activity and oxygen consumption.

E- This patient with a past medical history of myasthenia gravis has developed increasing weakness, shortness of breath, and abdominal cramping. Further evaluation reveals bradycardia, tachypnea, weak cough, impaired inspiratory force, hyperactive bowel sounds, myogenic fasciculations, and decreased deep tendon reflexes. In the context of this patient’s medical history of medication use (prednisone and pyridostigmine), this is most likely due to an overdose of pyridostigmine. This agent is an acetylcholinesterase inhibitor used in patients with myasthenia gravis to improve synaptic ACh levels and decrease neuromuscular symptoms. In excess, this can lead to multiple cholinergic side effects, including bradycardia, hypotension, nausea, abdominal pain, diarrhea, hypoventilation, lethargy, weakness, paralysis, bronchospasm, etc. For additional information check out MedSchool Bootcamp's video on Myasthenia Gravis.

B- Paracentric chromosomal inversions involve two breaks in one chromosome to create an intervening segment. This segment does not contain the centromere. The segment is then inverted (180 degrees) and re-inserted. These inversions can survive for long periods of time, through multiple generations. Normally, during prophase I, each pair of chromosomes come together and exchange genetic material (crossing over). A single chromosome containing a paracentric inversion may present structural challenges to crossover events, requiring the chromosomes to form a loop, allowing the inverted segment of one chromosome to align its genes accordingly with the normal segment of the other corresponding chromosome. If a crossover event occurs within the loop formed, two disproportionate chromosomal segments are produced. One chromosome may contain 2 centromeres, whereas the other may contain none. If a fetus is conceived with either of these two formed chromosomes, the pregnancy would be at risk for early spontaneous abortions. A liveborn child, would likely be the result of a crossover event occurring outside of the loop, in which case, two structurally similar chromosomal segments would be produced, and thus not be associated with aneuploidy. 

D- This young boy has a family history significant for Huntington disease in a maternal grandfather, colon cancer in paternal grandfather, numbers colonic polys in father necessitating colectomy, and a confirmed heterozygous APC frameshift gene mutation in his father. Based on this patient’s current risk for genetic disease, investigating his risk of familial adenomatous polyposis (APC gene-adenomatous polyposis coli) is most appropriate. Since this patient’s father has a frameshift mutation it is appropriate to look for this directly. Though he may be at risk of Huntington disease, this is less important to test for as there is no preventative or curative treatment available. For additional information check out MedSchool Bootcamp's video on Single Stranded DNA Repair.

A- This 53-year-old female presents with six years of stiffness and pain in her hands that causes her difficulty buttoning her clothes. She is subsequently found to have multiple Swan Neck deformities (PIP hyperextension, DIP flexion). This is most likely representative of rheumatoid arthritis (RA). RA is associated with anti-citrullinated peptide antibodies ( > 90% specificity), rheumatoid factor (less specific, elevated in infectious disease, other autoimmune diseases, some healthy individuals), and antinuclear antibodies. RA is also associated with a genetic disposition with HLA-DR4 an HLA-DR1 proteins. 

F- This patient is a known amphetamine drug abuser presenting with irritability, restlessness, tremor, palpitations, tachycardia, tachypnea, and hypertension. This is most likely due to recent amphetamine use. Amphetamines cause these symptoms via the increased synaptic release and inhibited reuptake of biogenic amines (epinephrine, norepinephrine, serotonin, and dopamine). This leads to sympathetic overstimulation and hallucinogenic effects. For additional information check out MedSchool Bootcamp's video on Amphetamines.

B- This young female has developed dysentery (blood diarrhea), acute kidney injury (oliguria, elevated creatinine), anemia, and thrombocytopenia, representing hemolytic uremic syndrome. This is most likely due to infection with the O157:H7 serotype of enterohemorrhagic Echerischia coli. Gastrointestinal inflammation facilitates the systemic circulation of bacterial toxins (Shiga-like toxin, verotoxin). This toxin preferentially causes endothelial damage, especially in the glomerulus (due to Gb3 receptor expression). Once damage, endothelial cells release cytokines that promote further damage, vasoconstriction, microthrombi formation and microangiopathic hemolytic anemia (MAHA). This leads to end-organ ischemia and damage, most commonly in the kidneys (large percentage of total blood flow), leading to acute kidney injury (e.g., decreased GFR, azotemia). 

D- In healthcare settings, a professional interpreter must be used whenever a patient is not fluent in English. It would not be appropriate to delay care or communications with the patient and their family to wait for the hospital interpreter, so using a telephone interpreter service is the most appropriate option in this scenario.

E- This patient has developed neutropenic fever, a common oncologic emergency in patients receiving chemotherapy. This is caused by a severe decrease in absolute neutrophil count (ANC < 500 or expected to decrease to that level based on trends) that can lead to life-threatening infections. Though these infections can be severe (gram-negative rod bacteremia), patients often present with mild symptoms (e.g., low grade fever, tachycardia, lack of erythema) due to lack of neutrophil-mediated inflammation. Patients should receive early empiric antibiotic therapy and investigation for source should be rapid and thorough (e.g., central line associated blood stream infection workup, blood cultures, imaging). For additional information check out MedSchool Bootcamp's video on Cell Cycle Dependent Drug Targets.

B- This patient with distant right colon resection and chemotherapy presents with fatigue on follow-up examination. CT imaging reveals multiple new hepatic and pulmonary masses, consistent with cancer recurrence and metastasis. This patient’s primary gastrointestinal malignancy most likely traveled through the right-sided mesenteric venules into the superior mesenteric vein and into the portal vein, through the liver (depositing hepatic metastases), and into the inferior vena cava before reaching the lungs. For additional information check out MedSchool Bootcamp's video on Veins, Anastomoses, and Hemorrhoids.

A- This patient with a past medical history of acute lymphoblastic leukemia is seen for follow-up. The physician adds an agent to decrease the toxicity of high-dose methotrexate on his normal cells. This agent is most likely folinic acid, also known as leucovorin or active folic acid. This bypasses the requirement for normal healthy cells to activate folic acid via dihydrofolate reductase—the enzymatic target of methotrexate. This “rescues” the normal cells from methotrexate’s adverse effects. This is known as salvage therapy or leucovorin rescue therapy. For additional information check out MedSchool Bootcamp's video on Clinical Applications of Pyrimidine Pathway.

C- This newborn male is found to have a small blind pit at the midline of the tongue at the intersection of the anterior two-thirds and posterior-one third and a mass adhered to the hyoid bone. This small blind pit represents the foramen cecum of the tongue—this serves as the embryonic origin of the thyroglossal duct. During embryogenesis, the thyroid normally descends through the thyroglossal duct into its adult anatomical position in the neck. In some cases, the thyroid fails to descend completely, leading to a lingual thyroid, as seen in this patient. The cells within the thyroid produce tetraiodothyronine (T4) and triiodothyronine (T3) that have many physiologic effects, including CNS development, metabolism regulation, catecholaminergic receptor expression, respiratory center stimulation, musculoskeletal system maturation, bone growth, and many others. Thyroid hormones (mainly T3) enter target cells, binds to nuclear thyroid hormone receptors (TR) that are heterodimerized with RXR. This leads to disruption of nuclear corepressor binding and promotion of coactivator binding, which causes recruitment of polymerases and initiation of gene transcription. For additional information check out MedSchool Bootcamp's video on the Pharyngeal Apparatus.

C- This receptor has found that are deficient in a specific eosinophil protein are more susceptible to filarial parasitic infections. This is most likely representative of a major basic protein deficiency. Major basic protein is an eosinophilic protein that is involved in host defense against parasites. It is produced in response to IgE antibody-dependent cell-mediated cytotoxicity. Release leads to destruction of pathogens via cytotoxic mechanisms as well as the release of histamine from mast cells and basophils, and the recruitment of neutrophils and macrophages. For additional information check out MedSchool Bootcamp's video on Eosinophils.

D- Keratosis pilaris (KP) is a common dermatologic condition characterized by keratinized hair follicles that are most commonly found on the extensor surfaces of the arms and thighs. KP is a benign condition that is sometimes associated with atopic dermatitis. It typically consists of nonpruritic and nonpainful erythematous bumps but, as in this patient, is sometimes a source of social embarrassment. There is typically no need to treat KP but keratolytic medications are sometimes prescribed if patient’s develop worry or social impairment. For additional information check out MedSchool Bootcamp's video on Dermatologic Histopathology.

B- This patient with a known history of obstructive sleep apnea (OSA) on continuous positive airway pressure device has developed increasing daytime somnolence and signs of cyanosis (e.g., blue lips, earlobes, and nail beds). Arterial blood gas reveals a hypercarbic, hypoxic respiratory acidosis. OSA is a common cause of increased hemoglobin concentration, termed appropriate absolute polycythemia. This is due to appropriate increase in erythryocyte mass due to increased erythropoietin stimulation from chronic oxygen desaturation. (A) Serum bicarbonate is most likely to be increased as a renal compensation for chronic respiratory acidosis. (C) Total lung capacity is most likely decreased in the morbidly obese patient due to musculoskeletal restriction. (D) OSA is a likely cause of group 3 pulmonary hypertension (chronic-lung disease etiology) that can lead to right ventricular hypertrophy (cor pulmonale). For additional information check out MedSchool Bootcamp's video on Sleep Apnea.

F- This patient with chronic kidney disease is found to have elevated creatinine and hyperphosphatemia. This is most likely due to impaired renal function. Patients with severely impairred renal dysfunction are unable to secrete phosphate. This retained phosphate deposits within the vasculature and organs as calcium-phosphate products, depleting the serum calcium level. This is sensed by the parathyroid glands, stimulating the release of parathyroid hormone in attempt to raise serum calcium. The damage kidneys are unable to upregulate 1-alpha-hydroxylase to form active 1,25 vit D. This leads to an inability to increase renal calcium reabsorption and phosphate secretion as well as impaired gastrointestinal calcium and phosphate absorption. Over time, the continued PTH secretion can lead to bone pain and increased risk of fractures (renal osteodystrophy)

E- This patient has congestive heart failure insufficiently treated with an ACE inhibitor. Because of continued symptomatology, her physician adds a potassium sparing diuretic (e.g., spironolactone, eplerenone, triamterene, amiloride). These agents work within the late distal convoluted tubule and collecting tubule, leading to decreased sodium reabsorption and potassium excretion. This patient was most likely prescribed spironolactone as it has been shown to reduce mortality in heart failure with reduced ejection fraction. Amiloride and triamterene are more commonly co-prescribed with thiazide diuretics to maintain a normal potassium level. Eplerenone is rarely used as an initial agent.