Insulin and normal saline
Based on lab changes, this patient with an increased anion gap metabolic acidosis was most likely suffering from DKA. Patients classically have fruity odor on breath & present with mental status changes, dehydration, abdominal pain, and tachypnea. Labs include hyperglycemia, ketosis, mild hyponatremia, normal or elevated serum K+ (despite a total body deficit), and increased plasma osmolality.
Insulin allows cells to use glucose for energy, decreasing lipolysis and production of ketone bodies. Ketones are the principal acid produced in DKA, so decreased ketones will increase serum bicarb. Insulin causes K+ to shift into cells, decreasing serum K+ level. Rehydration helps normalize Na+ and decrease osmolality.
In half of immunocompetent individuals, blastomycosis may present as a lung infection or cause flu like illness (fever, chills, myalgia, headache, nonproductive cough) or pneumonia (fever, cough, pleuritic chest pain). Pulmonary blastomycosis is diagnosed by finding typical yeast forms.
In immunocompromised patients, it can cause disseminated disease. Patients experience systemic systems (fever, weight loss, night sweats), lung involvement (cough, dyspnea), skin lesions (papule, pustules, ulcers, verrucous lesions) and bone bain (caused by lytic lesions)
Toxic renal injury
Ethylene glycol is rapidly absorbed from the GI tract and metabolized to glycolic acid (toxic to renal tubules) and oxalic acid which precipitates calcium oxalate crystals. Ethylene glycol is found in automobile antifreeze, engine coolants, and hydraulic brake fluids and may be used as a substitute for alcohol in alcohol abusers. Ethylene glycol ingestion leads to toxic, acute tubular necrosis with vacuolar degeneration and ballooning of the proximal tubular cells. Patients initially manifest with signs of ethanol intoxication and then signs of renal failure (anorexia, oliguria, flank pain) develops 24-72 hours later. Typical clinical findings induce high anion gap metabolic acidosis, increased osmoloar gap, and calcium oxalate crystals & tubular casts in the urine.
Note: prolonged hypotension & severe infection can lead to ischemic acute tubular necrosis which also presents with renal failure, oliguria, and anion gap metabolic acidosis, however, oxalate crystals in the tubular lumen aren't seen
Patient has latent TB and has lab values and a bone marrow aspirate consistent with sideroblastic anemia due to isoniazid use. Isoniazid directly inhibits the enzyme pyridoxine phosphokinase which normal concerts pyridoxine (B6) to its active form, pyridoxal 5' phosphate. Pyrodixal 5' phosphate is a cofactor for ALA-synthase, the enzyme that catalyzes the rate limiting step in heme synthesis. Inhibition of this enzyme causes microcytic hypo chromic anemia. Iron is transported to the developing erythrocytes that cannot form heme, and its granules accumulate circumferentially around the nucleus forming ring sideroblasts.
Causes of sideroblastic anemia: X-linked ALA synthase mutation, myelodysplastic syndrome, alcohol abuse, copper deficiency, medications (isoniazid, chloramphenicol, linezolid)
Since pyridoxal 5' phosphate is a cofactor for numerous enzymes, pyridoxine deficiency can also lead to dermatitis, stomatitis, neuropathy, and confusion.
Serotonin syndrome is characterized by confusion, agitation, tremor, tachycardia, HTN, clonus, myoclonus, muscle rigidity, hyperthermia, diaphoresis, and hyperreflexia. Any drugs that increase serotonin levels, including combinations of SSRIs, triptans, or MAO inhibitors and high doses of SSRIs can precipitate this syndrome. Tryptophan is a precursor for serotonin.
Cyproheptadine is an antihistamine with anti-serotonergic properties that can be used in the treatment of serotonin syndrome.
Mononucleosis like illness
CMV is typically associated with subclinical infection in the immunocompetent, with the occasional individual developing a mononucleosis like syndrome (fever, malaise, myalgia, atypical lymphocytosis, elevated liver transaminases) that is heterophiles antibody (mono spot) negative.
In the immunocompromised, primary or reactivated CMV infection can result in severe retinitis, pneumonia, esophagitis, colitis, or hepatitis.
24 year old presents for postpartum follow up 2 weeks after vaginal delivery. She is concerned as she has not yet lactated. Reports excessive fatigue and significant weight loss. Also reports nausea, loss of appetite, and postural dizziness. No headaches, visual problems, cold intolerance, constipation, or polyuria. Hemoglobin, sodium, cortisol, free T4, and TSH are all low. Pathologic process most likely responsible for patients symptoms? Thiamine
Branched chain alpha ketoacid dehydrogenase requires several coenzymes : thiamine, lipoate, coenzyme A, FAD, NAD. Some patients with MSUD improve with high dose thiamine, but most require lifelong restriction of leucine, isoleucine, and valine
Mutations in BCKDC results in accumulation of branched chain amino acids in serum and peripheral tissues resulting in neurotoxicity that includes seizures, irritability, lethargy, and poor feeding. A metabolite of isoleucine gives the urine a distinctive sweet odor. This disorder can be life threatening if untreated as brain swelling can lead to death
Cephalization of the pulmonary vessels, perihilar alveolar edema (batwing distribution), and blunting of the costophrenic angles due to pleural effusions. Kerley B lines (short horizontal lines perpendicular to the pleural surface that represent edema of the interlobular septa) may also be present. Cardiomegaly is also common.
Patients typically present with progressive cough, dyspnea, orthopnea, and/or LE edema. PE reveals tachycardia, tachypnea, accessory muscle use, and bilateral crackles or wheezing. Common precipitationg factors are myocardial ischemia/infarction, severe HTN, valvular heart disease, arrhythmias (afib), drug use (cocaine)
Membranous glomeulopathy is one of the most common causes of nephrotic syndrome in adults. It can occur secondary to underlying malignant tumors (lung and colon), DM, immunologic disorders (SLE), infections (HBV, HCV, malaria, syphilis), or certain mediations (gold, penicillamine, NSAIDs). Diffuse increased thickness of the glomerular basement membrane on LM (without increased cellularity), 'spike and dome' appearance on methanamine silver stain, and granular deposits on immunoflourecence are are diagnostic.
Patients with T1DM are prone to developing other autoimmune endocrinopathies including Hashimoto's thyroiditis, Graves' disease, and primary adrenal insufficiency (Addison's disease). Electrolyte abnormalities in patients with primary adrenal insufficiency include hyponatremia, hyperkalemia, hypercholeremia, and non anion gap metabolic acidosis. Autoimmune adrenalitis results from autoantibody production against all 3 zones of the adrenal cortex. Since the main defect is in the adrenal gland, ACTH doesn't increase serum cortisol. Since glucocorticoids increase insulin resistance, decreased cortisol levels lead to lower insulin requirements in patients with adrenal insufficiency. Decreased aldosterone leads to decreased Na, increased K+, and increased H+. The decreased H+ excretion causes a non anion metabolic acidosis with low HCO3- levels. This causes increased in Cl- retention which occurs in order to maintain electrical neutrality of ECF.
Note: exogenous serum cortisol increases with administration of ACTH in patients with secondary and tertiary adrenal insufficiency. These patients have an intact adrenal glans and can release aldosterone in response to angiotensin II so they don't develop mineralocorticoid deficiency, hyperkalemia, or metabolic acidosis.