internal medicine EOR

kernig sign

"Make curved straight"-patient supine, bend leg holding at knee and straighten leg up. Severe pain in back and neck is positive

AKI

>0.3 increase in Cr in 48 hrs Initial imaging: -US labs: -BUN & Serum creatinine -reduced GFR causes: -pre-renal: low blood flow to kidneys (cardio shock, hemorrhage, sepsis, diuretics) -intra-renal: cellular damage (toxin, drug, infection, hypoperfusion) -post-renal: obstruction (large prostate, kidney stone, tumor, trauma, post-op, BPH) ESRD: MCC = DM & HTN

multiple sclerosis

disorder of the central nervous system that results from demyelination of the white matter in the brain and spinal cord, degeneration of axons and neurons, and astrocytic sclerosis. -20-50 y/o, women > men -Uhthoff phenomenon is a worsening of symptoms with high temperatures RF: -HLA-DR2 -increased distance from equator -1st degree relative = 7x risk -Vitamin D deficiency may be a risk factor for MS sx: -optic neuritis, monocular vision loss, bilateral internuclear ophthalmoplegia, fatigue, ataxia, tremor, and spasticity. -Lhermitte sign (an electrical sensation from the neck that radiates down the spine and into the extremities that occurs with neck flexion) -Charcot neurological triad: Nystagmus, intention tremor, and scanning speech -Bilateral internuclear ophthalmoplegia is pathognomonic types: The most common subtype of multiple sclerosis is relapsing-remitting.*** dx: -T2-weighted MRI*** -McDonald criteria (space & time)

Sjogren's syndrome

dryness of the mouth, eyes, and other mucous membranes due to lymphocytic infiltration of the exocrine gland and secondary gland dysfunction Salivary glands - xerostomia (dry mouth) Lacrimal glands - dry eyes (keratoconjunctivitis sicca) Parotid enlargement Diagnosis: + ANA (especially anti-SS-A (R0) and anti-SS-B (La) (+) Rheumatoid Factor (RF) (+) Schirmer Test (<5mm lacrimation in 5 min) -ESR/CRP Treat: with artificial tears, pilocarpine (cholinergic) for xerostomia -avoid wind/sun exposure to eyes Pilocarpine: a cholinergic drug that increased lacrimation and salivation (side effects include diaphoresis, flushing, sweating, bradycardia, diarrhea, N/V, incontinence and blurred vision) Cevimeline: stimulates muscarinic cholinergic receptors

thyroid cancer

staging: papillary - If the age is less than 45 years, then patients with any tumor size and any node metastasis without distant metastasis are classified as stage I. If there is distant metastasis, this group of patients would be classified as stage II.

bell's palsy

History of viral prodrome Waking up with unilateral facial nerve paralysis, hyperacusis, and taste disturbance PE will show CN VII palsy that does NOT spare the forehead*** Most commonly caused by HSV dx: -clinical tx: -Treatment is prednisone, -artificial tears, -patch/tape eyelid shut, -antivirals (for severe cases) acyclovir -cranial nerve decompression = last resort Bilateral: Lyme disease, infectious mononucleosis "if the pt can raise their eyebrows, so should you" (stroke)

subarachnoid hemorrhage

-nimodipine -ischemic = middle cerebral artery -hunt & hess severity scale Nonmodifiable risk factors of subarachnoid hemorrhage include older age, female sex, non-Caucasian ethnicity, posterior circulation aneurysms, and larger aneurysms. Modifiable risk factors include hypertension, tobacco use, and excessive alcohol use. Patient presents with abrupt onset of "worst headache of life" or thunderclap headache Diagnosis is made by noncontrast CT scan, blood will appear white on the CT If CT negative and suspicion high, lumbar puncture Most commonly caused by a ruptured aneurysm Hunt & Hess classifies severity of subarachnoid hemorrhage to predict mortality Treatment is supportive and nimodipine (decreases vasospasm)

Fibromyalgia

11 of 18 tender points -muscle biopsy - moth eaten appearance tx = supportive, exercise, PT, tx depression, 2nd line = TCA, (amytriptyline) Risk factors include -family history, chronic widespread pain, and aberrancies in serotonin or catecholamine signaling pathways. The patient's history will often include sleep and memory problems, fatigue, headaches and generalized pain especially in the mornings, and haziness often called "fibro fog." There may also be stiffness in the morning as well, which can be confused with spondyloarthropathies. On physical exam, tenderness in joints, muscles, and soft tissues will be observed. Diagnosis is clinical and should be suspected when patients have chronic pain without obvious cause for at least three months' duration. Laboratory studies are not helpful, as they are negative unless another condition is present, but a general rheumatologic workup should be performed to exclude other conditions. No specific radiological abnormalities will be found on imaging. Treatment for fibromyalgia can be complex and is often frustrating for patients. Aerobic exercise for at least 30 minutes per day, three days per week, while trying to reach target heart rate, should be prescribed first. If the patient does not respond well enough to only exercise, tricyclic antidepressants can be initiated, starting with low-dose amitriptyline. Low-dose cyclobenzaprine is an alternative. If none of those work, pregabalin or gabapentin, duloxetine, or milnacipran can be trialed, starting with a serotonin and norepinephrine reuptake inhibitor (SNRI) first. Fibromyalgia is a chronic and incurable condition that can be maintained at a tolerable level with interventions. Pharmacologic combination therapy is reserved for refractory cases and consists of low doses of duloxetine and amitriptyline, for example. Another option is duloxetine with pregabalin or gabapentin. Exercise can also be combined with physical therapy. It is important that combination therapy be monitored in consultation with specialists such as psychiatry or rheumatology. Opioids should be avoided in these patients, as they have not been shown to be effective. Common triggers of fibromyalgia include: Lyme disease, hypothyroidism, viral infections, and autoimmune disorders. Additionally, there is a correlation between fibromyalgia and emotional or physical trauma in childhood. Some patients with fibromyalgia have low levels of serotonin and norepinephrine, high levels of substance P, abnormalities in imipramine uptake receptor, low levels of growth hormone, and hypofunction of the hypothalamus-pituitary-adrenal axis The 2010 American College of Rheumatology criteria of fibromyalgia include the presence of the following features: -widespread pain index > 7, -symptom duration of at least three months, -and absence of an underlying disorder that would better explain the symptoms. Patients with fibromyalgia should avoid narcotics, nonsteroidal anti-inflammatory drugs, and steroids. What is the correct amount of pressure that is applied to tender points in a patient with fibromyalgia? Answer: 4 kg/cm, which can be quantified by pressing with a fingertip until the fingertip blanches.

bronchiectasis

A condition in which the lungs' airways become dilated and damaged, leading to inadequate clearance of mucus in airways Mucus builds up and breeds bacteria, causing frequent infections A common endpoint of disorders that cause chronic airway inflammation (CF, immune defects, recurrent pneumonia, aspiration, tumor)½ of cases are due to cystic fibrosis Symptoms include a daily cough that occurs over months or years and production of copious foul-smelling sputum, frequent respiratory infections DX: CXR = linear "tram track" lung markings, dilated and thickened airways - "plate-like" atelectasis; CT chest = gold standard Crackles, wheezes, purulent sputum TX: ambulatory oxygen, aggressive antibiotics for acute exacerbations, CPT (chest physiotherapy = bang on the back); eventual lung transplant a disorder of the large bronchi characterized by permanent dilation and destruction of the bronchial walls. About half of all diagnosed cases are secondary to cystic fibrosis. Common symptoms include a chronic productive cough with large amounts of mucopurulent, foul-smelling sputum, wheezing, shortness of breath, and pleuritic chest pain. Typically, the physical exam findings are nonspecific, and this condition is diagnosed with a high-resolution CT scan, which will show dilated and thickened bronchi. This finding is commonly referred to as "tram tracks." The treatment for an acute exacerbation of bronchiectasis consists of antibiotic therapy based on sputum smears or prior cultures. Ampicillin, amoxicillin, trimethoprim-sulfamethoxazole, ciprofloxacin, or levaquin can be used for empirical treatment. In order to prevent exacerbation recurrences, chest physiotherapy and daily bronchodilators are the primary treatment.

Pheochromocytoma

A noncontrast abdominal CT scan may detect adrenal tumors indicative of a pheochromocytoma. If an adrenal mass is present, a follow-up non-ionic contrast CT with a washout protocol is performed. Pheochromocytomas will often retain > 40% of the contrast after 15 minutes. An MRI may be used during pregnancy, in children, or for serial monitoring to avoid radiation. Surgical resection is the definitive treatment. An alpha-blocker (e.g., phenoxybenzamine, doxazosin) may be used prior to surgery to control the blood pressure. A calcium channel blocker (e.g., extended-release nifedipine, extended-release nicardipine) is usually used in addition to an alpha-blocker.

BPH

A prostate-specific antigen (PSA) level >1.5 ng/mL is indicative of BPH but is not a specific test. Patients with isolated BPH in the absence of other disease states will have a normal urinalysis. A prostatic ultrasound may detect an increased postvoid residual volume and may also be used to evaluate the size and shape of the prostate. Lifestyle modifications include the avoidance of antihistamines (which increases urinary retention), decreased fluid intake in the evening, and decreased alcohol and caffeine consumption. Additionally, a healthy diet with increased vegetable intake, exercise, and weight loss if overweight may help control BPH symptoms. First-line pharmacologic therapy includes the use of alpha-adrenergic receptor antagonists (e.g., prazosin, doxazosin, tamsulosin) and 5-alpha reductase inhibitors (e.g., finasteride, dutasteride). The 5-alpha reductase inhibitors block the conversion of testosterone to dihydrotestosterone, thereby inhibiting prostatic hyperplasia. Tadalafil is a phosphodiesterase-5 inhibitor that may be used second-line for BPH. Anticholinergic medications are adjunctive agents that are used in patients who fail alpha-adrenergic antagonists. Surgery is the definitive treatment for BPH, and the gold standard is a transurethral resection of the prostate.

CKD

A restricted protein intake to 0.6-0.8 g/kg/day is recommended as part of his dietary management to slow CKD progression. Salt intake > 3-4 g/day can result in hypertension and hypervolemia, while salt intake < 1 g/day can result in hypotension and hypovolemia. Therefore, a goal of less than 2 g/day of salt is ideal. In the presence of hypervolemia, fluid intake should be restricted to < 2 L/day. Potassium restriction to < 2 g/day is indicated if the glomerular filtration rate is < 10-20 mL/min/1.73 m2 or if the patient is hyperkalemic. Phosphate restriction to 600-800 mg/day is indicated in all patients with CKD. If the glomerular filtration rate is < 20-30 mL/min/1.73 m2, phosphorus binders are typically required in addition to dietary restrictions. Patients should be educated on foods that contain potassium (bananas, oranges, raisins, spinach, broccoli, potatoes, mushrooms, peas) and phosphorus (cola beverages, processed foods, eggs, dairy products, nuts, beans, meat). MCC = DM**

prostate cancer

A transrectal ultrasound-guided biopsy is the gold standard for detecting prostate cancer. MRI imaging may be used to evaluate regional lymph node involvement. A bone scan is useful for detecting bony metastases. The Gleason grading system assigns a score of 2-10 based on the architectural pattern of the biopsied specimen and determines the tumor size, pathologic stage, and prognosis. A score of 6 is considered low-grade cancer, a score of 7 is considered intermediate-grade cancer, and a score of 8-10 is considered high-grade cancer. The cancer stage, PSA level, Gleason score, age, and health of the patient are taken into account when determining treatment. Active surveillance (serial PSA levels, periodic digital rectal examinations, periodic prostate biopsies) is appropriate for patients with localized, low-grade prostate cancer and a life expectancy < 15 years. A radical prostatectomy is ideal for healthy patients with stage T1 or T2 prostate cancer. Radiation therapy is another option for patients with stage T1, T2, or select T3 prostate cancers. Patients with metastatic disease should receive androgen deprivation therapy with a gonadotropin-releasing hormone receptor agonist (e.g., leuprolide) or gonadotropin-releasing hormone receptor antagonist (e.g., degarelix). Bisphosphonates may be used to decrease the risk of androgen deprivation-associated osteoporosis. Prognostic prediction tools include the Kattan nomogram (incorporates cancer stage, grade, and PSA level) and the University of California San Francisco nomogram (incorporates cancer stage, PSA level, Gleason score, percent positive biopsies, and patient age). Patient will be an older man Obstructive uropathy and lower back pain Labs will show PSA > 10 ng/mL Diagnosis is made by needle-core biopsy Age is the most important risk factor Gleason score used to grade prognosis

metabolic disease

ATP III criteria (2001): need at least three of the following five traits Abdominal obesity (>35 in women, >40 in men) Serum triglycerides ≥ 150 mg/dL or drug treatment for elevated triglycerides Serum high-density lipoprotein (HDL) cholesterol < 40 mg/dL in men and < 50 mg/dL in women or drug treatment for low HDL cholesterol Blood pressure ≥ 130/85 mm Hg or drug treatment for HTN Fasting glucose ≥ 100 mg/dL (5.6 mmol/L) or drug treatment for elevated blood glucose

acromegaly

Acromegaly is most commonly caused by a pituitary macroadenoma but can occasionally be caused by ectopic secretion of growth hormone-releasing hormone or growth hormone that is secreted by a lymphoma, hypothalamic tumor, bronchial carcinoid, or pancreatic tumor. dx: The diagnosis of acromegaly is often made biochemically and does not require the presence of typical clinical features or the presence of a pituitary adenoma. The single best test for diagnosing acromegaly is the measurement of serum IGF-1. An unequivocal rise in serum IGF-1 confirms the diagnosis of acromegaly. A normal serum level of IGF-1 essentially excludes the diagnosis of acromegaly. When an equivocal serum level of IGF-1 is obtained, further testing using an oral glucose suppression test is required. Serum growth hormone is measured before and two hours after the ingestion of 75 g glucose. The criterion for the diagnosis of acromegaly is a growth hormone level > 1 ng/mL. tx: Treatment is transsphenoidal surgical resection of the tumor. Patients who have incomplete biochemical remission after surgery may benefit from dopamine agonists, somatostatin, tamoxifen, or pegvisomant. Diabetes insipidus can occur postoperatively but is usually mild and self-limiting. Hyponatremia can also occur postoperatively and should be treated with free water and hypotonic solution restriction.

AML/CML

Acute Myeloid Leukemia (AML): BLASTS + AUER RODS in ADULT PATIENT Population: Adults (80%) majority of patients > 50 y/o Anemia, thrombocytopenia, neutropenia. Splenomegaly, gingival hyperplasia and Leukostasis (WBC > 100,000) Aur Rods and > 20% blasts seen in bone marrow Chronic Myeloid Leukemia (CML): Strikingly Increased WBC count > 100,000 + hyperuricemia + Adult patient (usually > 50 years old) Population: Adults - patient usually > 50 y/o 70% asymptomatic until the patient has a blastic crisis (acute leukemia) Diagnostic studies: Philadelphia chromosome (translocation of chromosome 9 and 22) - "Philadelphia CreaM cheese", splenomegaly CML: a myeloproliferative neoplasm that is due to an acquired cytogenetic abnormality that involves a balanced translocation between the BCR gene on chromosome 9 and the ABL1 gene on chromosome 22, resulting in the abnormal fusion gene BCR-ABL1 gene located on chromosome 22 (known as the Philadelphia chromosome). -Patient will be 30-60 years old Most patients asymptomatic when diagnosed PE will show splenomegaly Labs will show Philadelphia chromosome t(9;22) (BCR-ABL) and low leukocyte alkaline phosphatase (LAP) Treatment is allogenic HSCT (curative), imatinib Phase determined by blast percentage

leukemias

Acute lymphocytic leukemia (ALL): CHILD + Lymphadenopathy + bone pain + bleeding + fever in a CHILD, bone marrow > 20% blasts in bone marrow Population: Children - most common childhood malignancy peak age 3-7 Highly responsive to chemotherapy (remission > 90%) ⇒ Chronic Lymphocytic Leukemia (CLL): Middle age patient, often asymptomatic (seen on blood tests), fatigue, lymphadenopathy, splenomegaly Population: Adults - most common form of leukemia in adults - peak age 50 y/o Diagnostic studies: SMUDGE CELLS on peripheral smear, mature lymphocytes Treatment with observation, if lymphocytes are > 100,000 or symptomatic, treat with chemotherapy What is the most common type of leukemia? Answer: Chronic lymphocytic leukemia.

essential tremor

Auto Dominant, improves with alcohol Tx: -1st line: Propranolol or primidone (or combo if doesn't work) -The third-line treatment involves using either gabapentin, topiramate, or alprazolam. There are two peaks of onset for essential tremor: during teenage years or in the sixth decade of life. Essential tremors are slow progressing and typically affect the upper extremities and head. An action tremor typically worsens in times of stress or high emotions and is present against gravity. This tremor improves with alcohol consumption. On a finger-to-nose test, the patient's tremor increases as the target approaches. Otherwise, the patient's neurological exam will have no other significant findings. Labs to be ordered include a TSH, TT4, and BMP. Before starting treatment, the patient should try to eliminate all unnecessary medications or stimulants and also try to make behavior changes prior to starting medication therapy. -dx: at least 3 yrs, absence of other neuro sx

Idiopathic Thrombocytopenic Purpura (ITP)

Autoimmune reaction to platelets usually after a viral illness (ITP is insidious and chronic) Diagnosis of exclusion Associated with HIV, HCV, SLE, CLL CBC normal except low platelets. (+ Direct Coombs Test) Treatment: Children supportive care (IVIG for refractory cases) Adults treat with Prednisone

Reactive Arthritis [Reiter's syndrome]

Autoimmune response to infection in another part of the body (Chlamydia +/- gonorrhea MC) ASYMMETRIC inflammatory arthritis CONJUNCTIVITIS, UVEITIS, URETHRITIS, and ARTHRITIS (can't see, can't pee, can't climb a tree!) Most commonly seen in Chlamydia (+/- gonorrhea and GI infections such as salmonella, Shigella, Campylobacter, Yersinia) Diagnosed by a history of infection, clinical exam, positive HLA-B27 (80%)*** Treatment: NSAIDs are the mainstay of therapy, antibiotics to treat the infection that triggered the disease (Chlamydia) an autoimmune inflammatory asymmetric peripheral oligoarthritis that develops as a reaction to an infection in another part of the body, most often the gastrointestinal or genitourinary systems. The most common organisms causing infection in the gastrointestinal system include Salmonella, Shigella, Yersinia, or Campylobacter. Chlamydia trachomatis is the most prevalent in the genitourinary system. Reactive arthritis occurs more frequently in men ages 20-50. Symptoms may be self-limited and typically present as acute, asymmetric pain of the large weight-bearing joints (usually knee or ankle), erythema, and swelling that occurs several weeks after the initial infection. Systemic symptoms of fever, fatigue, and weight loss may also be present. Mucocutaneous lesions may include balanitis and stomatitis. Fingernail involvement may resemble psoriatic changes. Mild conjunctivitis may occur early in the disease and anterior uveitis can develop any time. Carditis and aortic regurgitation may also occur. Isolation of the causative agent is not always necessary or required. The pattern of joint involvement and timing of onset of the arthritis following the infection is diagnostic. Treatment of choice is prescription NSAID therapy to ensure adequate anti-inflammatory and analgesic effects.

budapest criteria

CRPS: The Budapest criteria require the presence of at least one symptom in three of the following categories and one sign in two of the following categories: sensory, vasomotor, edema or sudomotor, and motor or trophic. Sensory signs and symptoms include hyperesthesia or allodynia. Vasomotor signs and symptoms include changes in skin color, temperature, or symmetry. Edema or sudomotor signs and symptoms include changes in edema or sweating. Motor or trophic signs and symptoms include decreased motor function, decreased range of motion, or trophic changes.

hypocalcemia

Calcium levels are regulated by parathyroid hormone secretion, calcitonin secretion by thyroid glands, and calcitriol secretion by the kidneys. -MCC = CKD Other causes of hypocalcemia include hypoparathyroidism, hypophosphatemia, and vitamin D deficiency. Hypoalbuminemia can cause pseudohypocalcemia since calcium is bound to albumin in the serum. Trousseau sign may also be induced by voluntary hyperventilation for one to two minutes after the cuff is removed and is more specific than Chvostek sign for hypocalcemia. Hypocalcemia is diagnosed when the corrected serum calcium is < 8.5 mg/dL. Ionized calcium, magnesium, phosphate, albumin, liver function test, and kidney function test should be measured. ECG may show prolonged QT interval and torsades de pointes in the setting of severe hypocalcemia. Oral replacement with calcium is the treatment of choice for asymptomatic hypocalcemia. For patients with severe hypocalcemia, intravenous supplementation using calcium gluconate is indicated. Magnesium deficits should be replaced prior to calcium supplementation -HYPER-reflexia What is the treatment for torsades de pointes? Answer: Intravenous magnesium sulfate

carcinoid tumor

Carcinoid syndrome (the hallmark sign) = Cutaneous flushing, diarrhea, wheezing and low blood pressure is actually quite rare and occurs in ~ 5% of carcinoid tumors and becomes manifest when vasoactive substances from the tumors enter the systemic circulation escaping hepatic degradation. The syndrome includes flushing, ↑ intestinal motility (diarrhea), itching and less frequently, heart failure, vomiting, bronchoconstriction, asthma, and wheezing ↑ Serotonin leads to collagen fiber thickening, fibrosis = heart valve dysfunction → tricuspid regurgitation, pulmonary stenosis/bronchoconstriction, and wheezing ↑ Histamine and bradykinin = vasodilation and flushing↑ serotonin synthesis → ↓ tryptophan → ↓ niacin/B3 synthesis = pellagra Chest X-Ray shows low-grade CA seen as pedunculated sessile growth in the central bronchi Bronchoscopy- pink/purple central lesion, well-vascularized Treatment is by surgical excision and carries a good prognosis The lesions are resistant to radiation therapy and chemotherapy Octreotide - a somatostatin analog that binds the somatostatin receptors and decreases the secretion of serotonin by the tumor -Niacin supplementation CT-Scan to locate the tumors Octreoscan → radiolabeled somatostatin analog (octreotide) binds to somatostatin receptors on tumor cells Urinalysis → elevated 5-hydroxyindoleacetic acid (5-HIAA) → is the main metabolite of serotonin and is used to determine serotonin levels in the body

myasthenia crisis

Cholinesterase inhibitors (e.g., neostigmine, pyridostigmine) are the mainstay of treatment. In patients with a thymoma who are < 65 years old, thymectomy is indicated unless muscle weakness is limited to the extraocular muscles. Corticosteroids, immunosuppressive agents, intravenous immunoglobulins, and plasmapheresis may be used in refractory disease or in patients with major disability. Life-threatening complications of myasthenia gravis are most often associated with respiratory difficulties and include aspiration pneumonia and myasthenic crisis. Myasthenic crisis is the most serious complication of myasthenia gravis and is characterized by extreme weakness of the respiratory muscles. Myasthenic crisis may be caused by pharmacologic noncompliance, respiratory infection, surgeries, or stress. Intravenous immunoglobulins and plasmapheresis are used to treat myasthenic crisis due to rapid treatment response.

Cushing's syndrome

Diagnosis of Cushing disease is made by high-dose dexamethasone suppression test, which will show ACTH suppression, ruling out other causes of increased ACTH or cortisol production. MRI of the brain can show a pituitary mass, which is suggestive of Cushing disease. Treatment is transsphenoidal surgery to remove the pituitary adenoma.

Thrombotic Thrombocytopenic Purpura (TTP)

Different from ITP (ITP is insidious and chronic) from TTP which is an acute febrile disease with multi-organ thrombosis (hence the name "thrombotic" thrombocytopenia) Thrombotic Thrombocytopenia (TTP): ↓ Platelets + anemia + schistocytes (RBC fragments) on smear Cause: After drugs: Quinidine, cyclosporine & pregnancy Inhibition of ADAMTS13 Presentation: Adults Purpura and "FAT RN"- Fever, Anemia, Thrombocytopenia, Renal failure, Neurological symptoms Diagnostic studies: CBC normal except low platelets. Schistocytes (RBC fragments) on the smear. (-) Coombs test Treatment: Steroids, plasmapheresis Causes of acquired TTP include pregnancy, cancer, HIV, lupus, and medications (such as desmopressin, quinine, cyclosporine, tacrolimus, mitomycin C, and gemcitabine). Congenital TTP often manifests in infancy and early childhood, while acquired TTP occurs in adulthood. Patient will be a woman Fever, confusion, difficulty speaking, headache, seizure, nausea, vomiting, diarrhea Labs will show elevated LDH, elevated indirect bilirubin, normal coagulation studies, microangiopathic hemolytic anemia, and thrombocytopenia Most commonly caused by severely decreased protease ADAMTS13 activity Treatment is plasma exchange with intravenous corticosteroids

Epididymis

E. coli characteristically grows on eosin methylene blue agar and has a metallic green sheen.

emphysema

Emphysema is a permanent enlargement of the terminal airspaces accompanied by the destruction of alveolar walls, which leads to "air trapping." These patients are known as "pink puffers" because they breathe through pursed lips. They are commonly very thin and cachectic males with a positive history of smoking. A chest X-ray shows a flattened diaphragm, an increase in anteroposterior diameter, and decreased vascular markings. The gold standard for diagnosis is a pulmonary function test, which would be consistent with obstructive disease. The patient's forced expiratory volume in one second (FEV1) would be decreased, however, the forced vital capacity (FVC) would stay the same, which causes a significant drop to the ratio of forced expiratory volume in one second to forced vital capacity (FEV1/FVC). In a patient with emphysema, this ratio would be less than 70%, which is diagnostic for obstructive pulmonary disease. Additional positive findings on a pulmonary function test include an increase in total lung capacity, an increase in expiratory reserve volume, and a decrease in the diffusing capacity of the lungs for carbon monoxide. What is the only genetic disease that is linked to chronic obstructive pulmonary disease? Answer: Alpha-1 antitrypsin deficiency. Patients with this disease will present prior to the age of 40 years and will have panlobular emphysema Excessive O2 → ↓ respiratory drive Patient will be older History of smoking Dyspnea PE will show pink skin, pursed-lip breathing, barrel chest, decreased breath sounds, and hyperresonance to percussion Diagnostics will show reduced FEV1 and increased TLC Most commonly caused by abnormal and permanent enlargement of airspaces and airspace wall destruction Emphysema in a young nonsmoker: think alpha-1-antitrypsin deficiency'

iron deficient anemia

Ferrous sulfate 325 mg given orally is the treatment of choice for iron deficiency anemia. Vitamin C may enhance the absorption of iron and should be given simultaneously. Iron should be supplemented during pregnancy and lactation. Parenteral iron is appropriate for patients who are intolerant to oral iron, those with gastrointestinal disease, and those who have continuing blood loss. In addition to supplementation with iron, patients should be encouraged to consume foods that are rich in iron, preferably foods rich in heme iron such as meats, poultry, and fish. Foods rich in heme iron are more readily absorbed than those rich in nonheme iron. Although all the foods in the vignette contain heme iron, only calf liver is considered a high-iron source. A serving of calf liver (2 ounces or 60 g) contains approximately 9 mg of iron.

hypertension

Hypertensive urgency is defined as blood pressure of greater than 180/110-120 mm Hg with no signs of acute target organ damage. Patients with hypertensive urgency may present with symptoms such as headache, atypical chest pain, epistaxis, and dizziness. Because hypertensive urgency likely represents moderate acute or chronic elevated blood pressure, the risk of morbidity and mortality is relatively low in the acute context. Hence, treatment in the ambulatory setting with oral agents, such as captopril, labetalol, clonidine, or prazosin, is recommended for hypertensive urgency. Recommendations indicate that follow-up in one to seven days is reasonable for these patients. Hypertensive emergency is defined as blood pressure greater than 180/110-120 mm Hg with evidence of acute target organ damage. Acute target organ damage includes hemorrhagic or ischemic stroke, acute coronary syndrome, aortic dissection, diffuse microvascular injury (i.e., malignant hypertension), and hypertensive encephalopathy. The presence of anemia, thrombocytopenia, acute kidney injury, or new-onset retinopathy is indicative of acute microvascular disease hypertensive emergency should be admitted to the ICU for blood pressure stabilization with IV antihypertensives due to the risk of significant morbidity and mortality associated with this syndrome. The rate in which blood pressure is lowered in patients with hypertensive emergency depends on concomitant end-organ damage. In general, current guidelines recommend lowering blood pressure by no more than 20-25% over one hour, then to 160/100 mm Hg within six hours, and then to target blood pressure in 48 hours in most patients. Judicious treatment of severe hypertension is recommended due to evidence of increased morbidity and mortality associated with rapidly lowering blood pressure. Patients with aortic dissection, pheochromocytoma, and eclampsia or preeclampsia require more aggressive treatment (i.e., reduction to systolic blood pressure to less than 140 mm Hg in the first hour and to less than 120 mm Hg in the case of aortic dissection). Choice of antihypertensive agents also depends on the etiology of acute end-organ damage. Dihydropyridine calcium channel blockers (e.g., nicardipine) and labetalol have been shown to be the most effective at lowering blood pressure in most clinical scenarios. Other agents, including beta-blockers (esmolol and metoprolol), nitroglycerine, nitroprusside, and hydralazine, are also appropriate in the correct clinical setting.

hyperkalemia

Insulin (B) and albuterol and sodium bicarbonate (D) can be used as the second step in management for patients with hyperkalemia. Both insulin and sodium bicarbonate facilitate the redistribution of potassium from the serum into the cells. Also dialysis. Before redistributing the potassium, it is important to stabilize the patient's cardiac function. Kayexalate (C) is the final step in treatment for hyperkalemia and will decrease the body's total potassium after the heart has been stabilized and the potassium has been redistributed. -1st = CALCIUM GLUCONATE*** History of kidney failure, DKA, rhabdomyolysis, tumor lysis Lethargy, weakness, paralysis PE will show bradycardia, hypotension, cardiac dysrhythmia ECG will show peaked T waves, prolonged PR, wide QRS Treatment is calcium gluconate, insulin, albuterol, bicarbonate sx: -peaked T, dropped P, sine wave, wide QRS HYPO-K causes: -Gastrointestinal losses due to vomiting, diarrhea, or laxative use and renal losses due to use of loop or thiazide diuretics.

anemia of chronic disease

Laboratory studies often show normocytic anemia with a hemoglobin level of 10-11 g/dL. Microcytic, hypochromic anemia may also be present in a minority of patients, in which case the mean corpuscular volume is rarely less than 70 fL. The mean corpuscular volume is normal or low in a subset of patients, while the red cell distribution width is normal or increased. The mean corpuscular hemoglobin concentration is always normal. (MCHC) The absolute reticulocyte count is frequently low, indicating an overall decrease in red cell production. More severe anemia with a hemoglobin level of < 8 g/dL may occur. The serum iron and transferrin levels (measured as the total iron-binding capacity) are low. The transferrin saturation is usually normal or low-normal. Hepcidin, an acute phase reactant, causes the sequestration of iron in its storage form (i.e., ferritin), thereby leading to a high ferritin in the serum. In some cases, a normal serum ferritin may be seen. Measurement of soluble transferrin receptor (a measure of total erythropoietic activity) is normal in patients with anemia of chronic disease. -HIGH FERRITIN***, normocytic anemia, low iron tx: The preferred initial therapy for anemia of chronic disease is the correction of the underlying disorder. Patients who have symptomatic anemia and who have not responded to treatment of the underlying disorder should receive erythropoietin (darbepoetin) if erythropoietin levels are < 500 mU/mL. Iron supplementation should be given to maintain a transferrin saturation of > 20% and ferritin level of > 100 ng/mL. Blood transfusion is indicated in the setting of symptomatic anemia if the clinician believes that there is insufficient time for the patient to respond either to the treatment of the underlying condition or to treatment with an erythropoiesis-stimulating agent. Treat with EPO analog (Epogen, Procrit) if Hgb <10 and stop when Hgb >11 d/t increased chance MI/stroke

Parkinson's disease

Lewy bodies in the substantia nigra and a decrease in dopaminergic neurons in the substantia nigra are postmortem findings in patients with Parkinson disease. Parkinson disease is the second most common neurodegenerative disorder after Alzheimer disease and is characterized by resting tremor, cogwheel rigidity, bradykinesia, shuffling gait, masked facies, micrographia, and postural instability. Cognitive impairment, depression, difficulty speaking or swallowing, balance problems, and sleep disturbances may also be present. Parkinson disease is more common in men and is mostly seen in adults > 50 years old. Exposure to pesticides and herbicides has been associated with an increased risk of developing Parkinson disease. tx: -Management is targeted at blocking acetylcholine with anticholinergic drugs or increasing dopamine levels to improve motor symptoms. -These medications include amantadine, levodopa (the precursor of dopamine), dopamine agonists (e.g., pramipexole, ropinirole), catecholamine-O-methyltransferase inhibitors (e.g., entacapone, tolcapone), monoamine oxidase inhibitors (e.g., rasagiline), anticholinergics, and antipsychotics. -Physical therapy, speech therapy, or electrical brain stimulation may benefit certain patients but has no effect on the disease course. dx: -myerson sign: blinking after tapping nose bridge

sarcoidosis

Lupus pernio (chronic, violaceous, raise plaques and nodules commonly found on cheeks, nose, eyes) = pathognomonic for sarcoid and most specific physical exam finding*** DX: Chest radiograph: Bilateral hilar lymphadenopathy. Reticular infiltrates Hypercalcemia; ACE levels 4x normal, elevated ESR Biopsy of peripheral lesions or fiber optic bronchoscopy for central pulmonary lesions Biopsy = non-caseating granulomas TX: Steroids = 90% respond to steroid Methotrexate, other immunosuppressive meds Serial PFTs to assess disease progression/guide treatment ACE-I for periodic HTN Prognosis depends on disease severity; spontaneous improvement common Pulmonary fibrosis = leading cause of death Labs will show hypercalcemia and elevated serum ACE It is more common in African American patients and presents approximately 10 years earlier in those individuals. Patients usually present with cough, dyspnea, fatigue, and general malaise. They may have chest pain, exercise intolerance, and muscle weakness may be present. A careful history should include questions about new skin lesions around tattoos or scars, dry mucous membranes, parotid swelling, arthralgias, and muscle weakness to rule out extrapulmonary manifestations. Peripheral lymphadenopathy is present in approximately 40 percent of patients. Testing should include a complete blood count, angiotensin-converting enzyme, liver and kidney function tests, erythrocyte sedimentation rate, and C-reactive protein levels. Tuberculosis testing should be completed to rule out tuberculosis as a cause of the granulomatous pulmonary changes. A chest radiograph will show hilar adenopathy that is typically symmetric bilaterally. Other changes such as reticular or ground-glass opacities and nodular scarring may also be present. A high-resolution computed tomography scan may be necessary to further evaluate pulmonary findings.

metformin

Metformin inhibits gluconeogenesis and increases glucose use after meals. Gluconeogenesis is inhibited by suppressing an enzyme that converts glycerophosphate to dihydroxyacetone phosphate. Most adults with type 2 diabetes are prescribed metformin as a first-line agent for glycemic control. The medication is typically well-tolerated and has a long-term positive safety profile. In addition, the medication may promote weight loss in some patients and does not cause any adverse cardiovascular events. The adverse effects that are associated with metformin include gastrointestinal upset, including diarrhea, nausea, a metallic taste in the mouth, and anorexia. These are the most common side effects associated with this medication, and patients should be aware of these before beginning this drug. These side effects are often transient in nature and can be controlled by reducing the dosage of the medication or discontinuing the drug if the side effects are intolerable. What laboratory testing should be reviewed before beginning metformin? Answer: Hemoglobin A1C, liver function tests, and serum creatinine. Lactic acidosis (C) is a serious but uncommon adverse event that can occur while taking metformin. This drug should not be administered to those at risk of developing lactic acidosis, including those with impaired kidney or liver function, a history of alcohol abuse, or a past history of lactic acidosis with metformin use. Vitamin B12 deficiency (D) can occur while taking metformin, however, this side effect is less common and is typically not severe enough to cause a megaloblastic anemia.

varicocele

On physical exam, there is a palpable collection of dilated veins, often referred to as a "bag of worms," to the superior aspect of the testicle. The collection of veins will worsen with Valsalva maneuver and when the patient is in an upright position. Varicoceles most commonly present on the left testicle. The diagnosis is primarily clinical, however, an ultrasound, which would be positive for retrograde blood flow to the scrotum, can confirm the diagnosis. The treatment for a varicocele is observation in most patients. For patients with severe varicocele or those at high risk for male infertility, a varicocelectomy or surgical repair can be done.

asthma

PFT's: Greater than 12% increase in FEV1 after bronchodilator therapy FEV1 to FVC ratio < 80% (You would expect the amount of air exhaled during the first second (FEV1) to be the greatest amount In asthma, since there is an obstruction (inflammation) you will have a decreased FEV1 and therefore a reduced FEV1 to FVC ratio Treatment guidelines: Mild Intermittent: Less than 2 times per week or 3-night symptoms per month Step 1: Short-acting beta2 agonist (SABA) PRN Mild Persistent: More than 2 times per week or 3-4 night symptoms per month Step 2: Low-Dose inhaled corticosteroids (ICS) daily Moderate Persistent: Daily symptoms or more than 1 nightly episode per week Step 3: Low-Dose ICS + Long-acting beta2 agonist (LABA) daily Step 4: Medium-Dose ICS +LABA daily Severe Persistent: Symptoms several times per day and nightly Step 5: High-Dose ICS +LABA daily Step 6: High-Dose ICS +LABA +oral steroids daily Acute treatment: Oxygen, nebulized SABA, ipratropium bromide, and oral corticosteroids

Paget's disease

Paget disease is more commonly seen in Caucasian patients and diagnosed in those >40 years of age. Paget disease typically affects multiple bones simultaneously with the pelvis, spine, femur, humerus, and cranium most affected. The first symptom of Paget disease is usually deep and aching pain that is worse at night. Paget disease often affects the proximal portion of long bones initially and advances distally. Spinal involvement can result in kyphosis. Bowed tibias are common, and "chalk stick" fractures may occur with mild trauma. Cranial involvement presents with patients reporting headaches and an increase in hat size. Dilated scalp veins may also be present with cranial involvement. Tinnitus, vertigo, and deafness may result from involvement of the petrous portion of the temporal bone. A markedly elevated serum alkaline phosphatase level is the most common lab abnormality associated with Paget disease.*** Calcium and phosphate levels are often normal, and osteolytic, sclerotic lesions are seen on radiographs. A "candle flame" or "blade of grass" sign in the long bones (as seen in the image above) is pathognomonic for Paget disease. Osteoporosis circumscripta, or focal radiolucencies in the cranium, is also consistent with Paget disease. Paget disease is treated with intravenous zoledronic acid (a bisphosphonate medication). Patients should be educated on the "first dose effect," which may cause an increase in pain upon initial administration that typically subsides with subsequent doses. Calcium and vitamin D are usually administered during the first two weeks of bisphosphonate therapy to prevent hypocalcemia. Oral bisphosphonates (e.g., alendronate) are inferior to the intravenous formulation for treatment of Paget disease. Patients taking oral bisphosphonates should take it on an empty stomach and remain upright for 30 minutes to prevent pill esophagitis. Labs will show increased serum alkaline phosphatase and bone-specific alkaline phosphatase X-ray will show bone thickening and enlargement with thickened cortices Most commonly caused by an increase in osteoclastic activity followed by an increase in osteoblastic activity Treatment is bisphosphonates

seizures

Partial seizures involve abnormal neuronal discharge in a specific area of the brain that spreads to nearby related cerebral areas. Partial seizures can be further differentiated into simple partial seizures (characterized by maintained awareness) and complex partial seizures (characterized by loss of consciousness). Patients with partial seizures often experience an initial motor or sensory manifestation known as an aura. The initial seizure manifestation then becomes more generalized as the seizure spreads to different areas of the cerebral cortex (Jacksonian march). Partial seizures can progress to generalized seizures in a process called secondary generalization. The two most common types of generalized seizures are tonic-clonic (grand mal) and absence (petit mal) seizures. In generalized seizures, abnormal neuronal discharge spreads diffusely throughout the cerebrum, resulting in loss of consciousness and generalized seizure manifestations. Tonic-clonic seizures begin with sudden loss of consciousness, after which the patient becomes rigid for 10-30 seconds (tonic phase). The tonic phase is followed by the clonic phase, which manifests as symmetric limb jerking. Often, relaxation of sphincters leads to bowel or urinary incontinence. Absence seizures are recurrent lapses of consciousness with no obvious motor or sensory manifestations. What antiepileptic agent is first line in patients with recurrent absence seizures? Answer: Ethosuximide. -hyponatremia <110, hypoglycemia, hypocalcemia, brain tumor, MC = seizure med non-compliance, ETOH w/d

PCKD

Patient presents with flank pain and hematuria PE will show hypertension Diagnosis is made by ultrasound Most commonly caused by autosomal dominant disorder Treatment is BP control: ACEIs, ARBs Associated with increased risk for berry aneurysm and intracerebral hemorrhage

diabetes insipidus (DI)

Patient presents with polyuria and polydipsia Labs will show increase in plasma osmolality and a decrease in urine osmolality Central DI: -most commonly caused by a decrease in ADH production -Diagnosis is made by vasopressin challenge test: >50% increase in urine osmolality and decreased urine volume -Treatment is intranasal DDAVP Nephrogenic DI: -history of taking lithium -Most commonly caused by kidney unresponsiveness to ADH -Diagnosis is made by water deprivation test: no change in urine osmolality -Treatment is HCTZ, amiloride, indomethacin

vitamin B-12 deficiency

Patient will most commonly be vegan Use of metformin can also cause B12 deficiency Fatigue, weakness, and peripheral neuropathy PE will show pallor and glossitis Labs will show MCV >100 fL, hypersegmented neutrophils, elevated homocysteine, elevated methylmalonic acid Treatment is parenteral vitamin B12 Neuropathy is much more common with vitamin B12 deficiency (as opposed to folate deficiency) Pernicious anemia: autoimmune destruction of cells that produce intrinsic factor (IF), resulting in vitamin B12 deficiency tx: Since 1% of vitamin B12 is passively absorbed, oral replacement with 1,000-2,000 µg of vitamin B12 once daily after parenteral loading is an alternative to monthly injections. Oral replacement is contraindicated in patients with neurologic symptoms, diarrhea, vomiting, or a previous bowel resection. The neurological abnormalities associated with vitamin B12 deficiency are due to subacute combined degeneration of the spinal cord, which is precipitated by the accumulation of methylmalonic acid. Vitamin B12 is a cofactor for the conversion of methylmalonic acid to succinyl CoA (which is important in fatty acid metabolism). As vitamin B12 becomes deficient, the levels of methylmalonic acid accumulate, which impairs spinal cord myelination, leading to poor proprioception, poor vibratory sense, and spastic paresis.

Hypernatremia

Patients with chronic hypernatremia are at risk for cerebral edema with rapid correction of sodium levels. Cerebral edema is more commonly seen in children than in adults, however, slower correction rates are needed for all patients with chronic hypernatremia. The goal for patients with chronic hypernatremia should be to lower serum sodium levels by 10 mEq/L in a 24-hour period, which is typically accomplished by administering 5% dextrose in water intravenously (at 1.35 ml/hour x the patient's weight in kilograms) Hyperglycemia, not hypoglycemia (B), is a potential risk of administering 5% dextrose in water intravenously. Blood glucose levels should be monitored frequently to prevent hyperglycemia from occurring. Osmotic demyelination syndrome (C) can occur with rapid correction of hyponatremia. Administering hypertonic saline solution intravenously can cause this syndrome to occur. How often should serum sodium and glucose levels be monitored during correction? Answer: Every two to three hours

Hemophilia

Patients with hemophilia will often present with recurrent prolonged bleeding, hematomas, hematuria, hemospermia, or hemarthrosis. The latter is a common presentation of patients with severe hemophilia and most commonly occurs in the ankles in children and the knee in adults and adolescents. Hemophilia disease severity depends on the quantitative lack of the associated clotting factors. Hence, individuals with minimal deficiencies will present with correspondingly milder disease manifestations and may, therefore, go undiagnosed until later in life. However, since hemophilia is due to an X-linked genetic mutation, disease manifestation almost always occurs in male children. Since hemophilia affects only the intrinsic pathway and spares the extrinsic pathway in the coagulation cascade, PT (which is a measure of the extrinsic pathway) will be within normal limits. Platelet count will also be normal in patients with hemophilia.

adrenal insufficiency

Patients with primary adrenal insufficiency will have decreased serum cortisol levels and elevated ACTH levels. If the test is equivocal, then an ACTH stimulation test can be ordered to see if the adrenal gland can mount a response to exogenous ACTH. In primary adrenal insufficiency, the patient will have decreased levels of cortisol despite exogenous ACTH stimulation. In patients who present in adrenal crisis, serum chemistries should be drawn and treatment with intravenous fluids and administration of hydrocortisone should be started promptly. Patients with chronic primary adrenal insufficiency are treated with daily oral glucocorticoids and mineralocorticoids. Dehydroepiandrosterone (DHEA) is used to supplement the loss of androgen production in some patients. Patient presents with abdominal pain, nausea, vomiting, diarrhea, fever, and confusion PE will show hyperpigmentation of skin and mucus membranes and hypotension Labs will show hyponatremia and hyperkalemia Most commonly caused by autoimmune destruction of the adrenal cortex Treatment is hydrocortisone

pulmonary nodules

Pulmonary nodules: < 3 cm = nodule; >3 cm = mass Found on CXR ⇒ get CT If suspicious ⇒ biopsy (ill-defined lobular or spiculated suggests cancer) Not suspicious ⇒ < 1 cm monitor at 3 mo, 6 mo, then yearly for 2 yr (calcification, smooth well defined edges = benign) Calcification suggests benign especially if central, concentric, popcorn Margins that are spiculated or irregular ⇒ CA Diameter < 1.5 cm strongly suggests benign; diameter > 5.3 cm strongly suggests CA Solitary pulmonary nodules are common and often discovered incidentally on chest X-ray or other imaging modalities. The majority of solitary pulmonary nodules are nonmalignant and arise from infectious, granulomatous, or vascular etiologies. The most common cause of a solitary pulmonary nodule is infectious granuloma. Solitary pulmonary nodules may also be malignant, and the risk factors for malignancy include older age, female sex, current or previous history of smoking, family history of lung cancer, and presence of emphysema. Certain nodule characteristics on chest X-ray that make the nodule more suspicious for malignancy include location in the upper lobe, larger nodule size, lower nodule count, spiculation, and part-solid characteristics. Nodules over 30 mm are much more likely to be malignant and should be biopsied. Nodules under 8 mm are very difficult to biopsy and not as likely to represent malignancy. For this reason, nodules under 8 mm should be examined via computed tomography of the chest with thin sections every six months to one year. Nodules that do not grow in size over a 24-month period are considered benign and need no further follow-up. Nodules between 8 mm and 30 mm should be assessed for risk of malignancy using a risk calculator or clinical judgment. -Part of the risk assessment involves a computed tomographic image of the nodule to better identify consistency and location. Patients who are current smokers with a 30 or more pack-year history and are between the ages of 55 and 80 years should receive serial low-dose computed tomography of the chest to screen for lung nodules. Lung nodules found during lung cancer screening are followed on a yearly or subyearly basis,

cor pulmonale

Right ventricular enlargement and eventually failure secondary to lung disorder that causes pulmonary artery HTN Etiology: COPD (most common), pulmonary embolism, vasculitis, asthma, ILD, acute respiratory distress syndrome Physical Exam: Lower extremity edema, neck vein distention, hepatomegaly, parasternal lift, tricuspid/pulmonic insufficiency, loud S2 DX: The diagnosis of cor pulmonale is usually made with an echocardiogram that shows evidence of increased pressure in the pulmonary arteries and right ventricle. Follow up tests can be done to identify the underlying cause, for example, spirometry can be done to look for chronic lung disease The gold standard diagnostic test to directly measure pulmonary pressures and assess for response to vasodilating medications is a right heart catheterization. TX: Diagnose and treat the underlying condition before cardiac structure change becomes irreversible Diuretics not helpful! May be harmful*** Cor pulmonale is the hypertrophy or dilation of the right ventricle with or without associated dysfunction, most commonly in the setting of pulmonary hypertension from chronic obstructive pulmonary disease (COPD) or hypoxemia. Other causes of pulmonary hypertension include pulmonary artery hypertension (group 1), left heart disease (group 2), pulmonary artery obstructions (group 4), and unclear or multifactorial mechanisms (group 5). Cor pulmonale does not include right ventricular dysfunction caused by left ventricular failure or congenital heart disease. Chronic is most commonly observed in patients with COPD or chronic hypoxemia, causing mean pulmonary arterial pressure to be greater than 25 mm Hg and causing remodeling of the right ventricle resulting in hypertrophy or dilation. In contrast, acute cor pulmonale is most commonly observed in the setting of large pulmonary embolism, causing acute dilation of the right ventricle. Symptoms of cor pulmonale are a prominent P2 sound, increased jugular venous pressure, peripheral edema, and ascites. ECG will show right ventricular hypertrophy, right axis deviation, right atrial enlargement, or a right bundle branch block. Echocardiogram will show an enlarged right ventricle with or without an enlarged right atrium. Right-sided heart catheterization is the definitive diagnosis of pulmonary hypertension and would show an elevated mean pulmonary arterial pressure of greater than 25 mm Hg at rest and greater than 30 mm Hg during exercise. *** Treatment of cor pulmonale is by treating the underlying disease to prevent progression of symptoms. Fluid overload can be managed with salt restriction and diuretics if required. Patient presents with peripheral edema, dyspnea, fatigue, and signs of right-sided heart failure PE will show pulmonary HTN + RVH Most common chronic cause: COPD Most common acute cause: PE Diagnosis is made by right heart catheterization***

nephrolithiasis

Risk factors for the development of renal calculi are: -acidic or alkaline urine, high urine calcium or uric acid, diuretic use, family history, dehydration, increased calcium or oxalate digestion, decreased potassium intake, hypertension, gout, and diabetes tx: -Stones measuring less than 5 mm are likely to pass spontaneously and can be managed outpatient with increased fluids and oral pain control. Stones measuring between 5-10 mm are less likely to pass and should be considered for elective lithotripsy or ureteroscopy as well as increased fluids and pain control. Stones greater than 10 mm are not likely to pass and are associated with increased risk of complications. These patients should be admitted, be given IV fluids and pain control, and undergo extracorporeal shock wave lithotripsy. If renal function is compromised, a urethral stent or percutaneous nephrostomy should be used.

Hypoglycemia

Risk factors that increase the odds of developing hypoglycemia are alcohol ingestion, older age, longer duration of diabetes, and erratic timing of meals. Symptoms of hypoglycemia include neurogenic manifestations such as tremor, palpitations, and anxiety. Neuroglycopenic symptoms occur as well, such as dizziness, delirium, and weakness. At profoundly low serum glucose concentrations, coma or death can occur. Typically, symptoms do not occur until blood glucose levels are less than 65 mg/dL. If they are able to, patients with symptomatic hypoglycemia should ingest 15 to 20 g of fast-acting carbohydrates. Typically, this ingestion of fast-acting carbohydrates is followed by a meal that will sustain the normal blood glucose levels. In cases of severe hypoglycemia, when the patient is unable to self-administer a fast-acting carbohydrate load, then glucagon can be administered intranasally, intramuscularly, or subcutaneously. Since the effect of glucagon is transient, this must be followed by intravenous glucose, or if the patient is able to eat, then they could be provided a meal. Usually glucose < 60 mg/dL Confusion, agitation, unresponsiveness Tachycardia, diaphoresis, tremulousness Focal neurologic deficit Dextrose, thiamine, glucagon

Thalassemia

Thalassemia is a microcytic anemia that is due to a genetic underproduction of alpha- or beta-globin chains, resulting in deficient hemoglobin synthesis and red blood cell hemolysis. When the underproduction of alpha-globin chains occurs, it is called alpha-thalassemia, which is more common in people of Southeast Asian or Chinese origin. Beta-thalassemia results from an underproduction of beta-globin chains and is more common in African or Mediterranean populations Alpha-thalassemia is due to gene deletion of one or more of the alpha genes that are present on chromosome 16. The deletion of two genes results in mild anemia and increased red blood cell count in trans deletion (when the deletions occur on different chromosomes) but causes an increased risk of severe thalassemia in the offsprings when the deletion is cis deletion (occurs on the same chromosome). When three alpha genes are deleted, severe anemia develops with the formation of tetramers of beta-chains (hemoglobin H) known as alpha-thalassemia H, which damages red cells. Deletion of four alpha genes result in hydrops fetalis and formation of tetramers of gamma-chains (hemoglobin Barts) that damage red blood cells. Beta-thalassemia occurs due to beta gene mutations (a point mutation in promoter or splicing genes) that are present on chromosome 11. Mutations often result in either absent (beta 0) or diminished production (beta +) of the beta-globin chains. Two clinically significant forms of beta-thalassemia exist, namely beta-thalassemia minor and major. Serum iron and ferritin levels are characteristically normal or elevated. Hemoglobin levels are usually between 3 and 6 g/dL. A peripheral smear typically shows microcytic, hypochromic red cells with the presence of target cells, acanthocytes, poikilocytes, nucleated red cells, and basophilic stippling depending on the type of thalassemia. Patients with alpha-thalassemia H should be given folic acid supplements. They should avoid iron supplements and oxidative drugs (such as dapsone, primaquine, quinidine, sulfonamides, and nitrofurantoin). Blood transfusions may be necessary when hemoglobin levels fall below 6 g/dL. Mediterranean, African, Asian origin Microcytic, hypochromic Mutations and deletions: severity Beta-thalassemia major: crew-cut skull X-ray, chipmunk facies, Frequent transfusions: Fe toxicity

salmonella

Salmonella is a gram-negative rod of the Enterobacteriaceae family that can cause typhoid (enteric) fever, acute enterocolitis, and bacteremia. All serotypes are members of the Salmonella enterica species. The three most common serotypes that infect humans (Salmonella serotype Typhi, Salmonella serotype Typhimurium, and Salmonella serotype Choleraesuis) belong to the subspecies Salmonella enterica enterica. S. Typhi is associated with typhoid fever, S. Typhimurium is associated with acute enterocolitis, and S. Choleraesuis is associated with bacteremia. Salmonella causes infection via fecal-oral transmission and is most commonly acquired through contaminated food (e.g., chicken, eggs, beef, fruit) or drink. Typhoid fever has an incubation period of 6-72 hours and is characterized by a gradual onset of malaise, headache, relative bradycardia, and gastrointestinal symptoms. Erythematous macules (Rose spots), abdominal distension and tenderness, and splenomegaly may be present on physical examination. Cultures of body fluids (e.g., blood, urine, stool) will be positive. Treatment for enteric fever depends on culture and sensitivity results but generally includes ciprofloxacin or ceftriaxone. The most common form of Salmonella is acute enterocolitis, which is characterized by bloody diarrhea, nausea, vomiting, fever, and cramping abdominal pain lasting less than one week. A diagnosis can be made with stool cultures. Treatment of uncomplicated cases of enterocolitis is symptomatic (e.g., hydration, antipyretics). Immunocompromised patients or patients with sickle cell disease should be treated with ciprofloxacin, ceftriaxone, trimethoprim-sulfamethoxazole, or azithromycin. Salmonella bacteremia tends to occur in immunocompromised patients and may affect the bones, joints, or organs. Patients with sickle cell disease are at increased risk of osteomyelitis caused by Salmonella. The treatment typically includes ciprofloxacin or ceftriaxone. Salmonella enterica serovar Typhi can colonize the gallbladder, resulting in an asymptomatic carrier state. Asymptomatic carriers can continuously spread Salmonella bacteria. High-dose ciprofloxacin or ampicillin may be used to treat carriers in the absence of gallstones but is not a definitive treatment. Cholecystectomy has a higher cure rate and is the preferred treatment in the presence of gallstones but is still not 100% effective at eliminating the carrier state. Enteric fever (salmonella typhi): a flu-like bacterial infection characterized by fever, GI symptoms, and headache. Transmitted via the consumption of fecally contaminated food or water GI symptoms may be marked constipation or "pea soup diarrhea" -Rose spots may be present (2-3 mm papule on trunk usually) -More common in the developing world (usually immigration cases) Gastroenteritis (Salmonella Typhimurium, Enteritidis, and Newport): results from improperly handled food that has been contaminated by animal or human fecal material It is estimated that 1 in 10,000 egg yolks is infected with Salmonella enteritidis Treat with Ceftriaxone or other medications based on the sensitivity

HIV patients

Screening for cardiovascular risk is recommended with more frequency in patients with HIV. Fasting lipid profile and glucose or hemoglobin A1C should be monitored at baseline and then every 6-12 months. Bone density testing is recommended in both men and women with HIV, with women being screened after menopause and men being screened after age 50 years. Cervical cancer screening in women with HIV is more frequent than in those without. There are some differences in vaccination recommendations for patients with HIV, especially those with a CD4 count less than 200 cells/microL who cannot receive live vaccinations. Tuberculosis screening after HIV diagnosis should be done in all patients. Those without a history of tuberculosis or positive screening are important to screen because tuberculosis can occur with any CD4 level. Screening is done with either a tuberculin skin test or interferon-gamma release assay. Patients with HIV who have tested negative for tuberculosis should have annual screening when there are risk factors present, such as living in communal settings, active drug use, or incarceration. Patients who initially tested negative with a CD4 cell count of < 200 cells/microL should repeat the tuberculosis screening once their CD4 count is above 200 cells/microL due to the possibility of false-negative results with this stage of the infection.

lung cancer

Small cell lung cancer is more aggressive, spreads early, and is less amenable to surgery. It originates in the central bronchioles. Non-small cell lung cancer is less aggressive, grows more slowly, is more amenable to surgery, and is broken down into three subtypes: squamous cell carcinoma, adenocarcinoma, and large cell carcinoma. Squamous cell carcinoma presents most commonly with a centrally located mass. Adenocarcinoma is the most common form of bronchogenic carcinoma and most commonly arises from the mucous glands in the periphery of the lung. Large cell carcinoma is an undifferentiated group of carcinomas that can present centrally or peripherally, and cytology shows large cells with rapid doubling time. It is typically a diagnosis of exclusion. Initial diagnosis of adenocarcinoma can be made using chest X-ray or CT scan. Sputum cytology can be used for definitive diagnosis of centrally presenting carcinomas, however, it has lower sensitivity for peripheral carcinomas. Bronchoscopy can be used to directly visualize centrally located tumors and obtain biopsies for definitive diagnosis. Tumors that originate in the periphery of the lung are more difficult to evaluate by bronchoscopy, therefore, transthoracic (percutaneous) needle aspiration and biopsy should be considered. Treatment of choice for non-small cell lung cancer is surgery with or without adjuvant or neoadjuvant chemotherapy and radiation. Which lung cancer complications make up the SPHERE acronym? Answer: Superior vena cava syndrome, Pancoast tumor, Horner syndrome, endocrine complications, recurrent laryngeal nerve compression, and effusions Small Cell (15% of cases) - 99% smokers, does not respond to surgery and metastases at presentation Location: (central mass), very aggressive Treatment: Combination chemotherapy needed Paraneoplastic syndromes: Cushing's, SIADH ⇒ Non-Small Cell (85% lung cancer cases) Adenocarcinoma - most common (peripheral mass), 35-40% of cases of lung cancer Most common Associated with smoking and asbestos exposure Location: Periphery Paraneoplastic syndrome: Thrombophlebitis Squamous cell (central mass) with hemoptysis, 25-35% of lung cancer cases Location: central May cause hemoptysis Paraneoplastic syndrome: hypercalcemia Elevated PTHrp Large cell - fast doubling rates - responds to surgery rare (only 5%) Location: Periphery 60% Paraneoplastic syndrome: Gynecomastia Carcinoid tumor (1-2%): lack glandular and squamous differentiation A tumor arising from neuroendocrine cells → leading to excess secretion of serotonin, histamine, and bradykinin GI tract carcinoid tumor may metastasize to lung (CA of appendix = MC; appendix → liver → lung) Presentation: hemoptysis, cough, focal wheezing, recurrent pneumonia Carcinoid syndrome = cutaneous flushing, diarrhea, wheezing, hypotension (telltale sign) Adenoma = MC type (slow-growing, rare)

Bacterial Meningitis

Streptococcus pneumoniae and Neisseria meningitidis are the most common causative agents in adults, or group B strep whereas Listeria monocytogenes can be present in patients over 50 years of age or those who have deficiencies in cell-mediated immunity. sx: Clinical presentation includes altered mental status, fever, headache, vomiting, and stiff neck, however, not all symptoms may be present. +/- rash Neisseria meningitidis infections can have a petechial rash and palpable purpura as well. Symptom onset is usually acute, within hours or one to two days of infection. -fever, AMS, nuchal rigidity = triad dx: Diagnosis is made via lumbar puncture as well as Gram stain and culture of the cerebrospinal fluid (CSF). -CSF will show a turbid color, elevated opening pressure, elevated lymphocytes, elevated protein, and low glucose (usually below 40 mg/dL). -Kernig (can't extend knees when hip flexed) and Brudzinski signs (flex of leg/thigh after flexed neck) -LP >1000, LOW GLUCOSE LEVELS, elevated protein & neutrophils -CT Scan 1st to r/o elevated pressures before LP***

Subacute thyroiditis (de Quervain's)

Subacute thyroiditis is typically associated with neck pain with a tender goiter and abnormal thyroid function tests. It affects women more often than it affects men and is an uncommon cause of hyperthyroidism. The etiology is thought to be a preceding viral infection, typically two to eight weeks prior to the thyroid inflammation. The inflammatory process releases large amounts of thyroxine and triiodothyronine into the serum, causing signs and symptoms of hyperthyroidism. After this initial hyperactive state, the stores of hormones are depleted and the patient reaches a state of euthyroidism before entering into a hypothyroid state. Eventually, recovery is complete and the thyroid begins to function normally again in most patients. Some patients will continue in a hypothyroid state and need chronic thyroid hormone supplementation. Subacute thyroiditis is typically a clinical diagnosis. Treatment includes supportive measures. Nonsteroidal anti-inflammatory medications, such as naproxen, or oral steroids can help decrease neck pain. Propranolol is used to help with transient symptoms of hyperthyroidism that some patients experience, such as palpitations and anxiety. How long do each of the stages of subacute thyroiditis last? Answer: Two to eight weeks.

Scleroderma (systemic sclerosis)

Systemic connective tissue disorder causing thickened skin (sclerodactyly), lung, heart, kidney, and GI tract Tight, shiny, thickened skin due to fibrous collagen buildup Limited cutaneous systemic sclerosis "CREST SYNDROME" - Calcinosis cutis, Raynaud's phenomenon, esophageal motility disorder, sclerodactyly (claw hand), telangiectasia affects the face, neck as well as distal to the elbow and knees Raynaud's phenomenon (60-70%) - worsens with smoking, gold, emotional stress. CCBs are the treatment of choice Diffuse cutaneous systemic sclerosis - skin thickening of the trunk and proximal extremities Laboratory studies specific to scleroderma (+) ANTI-CENTROMERE AB: associated with LIMITED crest disease and better prognosis (MOST SPECIFIC)** (+) ANTI-SCL-70 AB: associated with DIFFUSE disease and multiple organ involvement (+) ANA -anemia, proteinuria tx: -Acute management with DMARDs and steroids -Treat Raynaud's with vasodilators (CCBs and prostacyclin) -PPIs, cyclophosphamide -organ specific -refer to rheum dx: -PFTs, CT What is the most common and often the earliest symptom of scleroderma? Answer: Raynaud phenomenon. Endothelial and vascular injury, T lymphocyte infiltration in the skin, and collagen overproduction are the three main contributing factors to the pathophysiology of scleroderma and lead to extensive fibrosis. Scleroderma is most common in women and typically presents during the fifth and sixth decade of life. Risk factors include history of cytomegalovirus infection, exposure to certain toxins, and exposure to drugs such as bleomycin, cocaine, and paclitaxel.

bladder cancer

The diagnostic test of choice is a cystoscopy and biopsy. Staging of bladder cancer is based on the depth of penetration into the bladder wall and whether or not the cancer has metastasized. If the cancer is localized and superficial, a transurethral resection is the treatment of choice. However, if the cancer is invasive, then a radical cystectomy with chemotherapy and radiation is the treatment of choice. Most patients respond well to treatment, however, bladder cancer has the highest rate of recurrence of all cancers. -MC = urothelial (transitional cell) RFers: -SMOKING*** -dye, arsenic, exposure, chronic cystitis

coma

The etiology of coma can be structural (supratentorial lesions or subtentorial lesions) or metabolic. The latter is the most common cause of coma. Metabolic derangements causing coma include hepatic encephalopathy, electrolyte imbalances, hypoglycemia, hypoxemia, and intoxication (e.g., opioids, anticholinergics). The physical exam in patients with metabolic coma will reveal symmetric neurologic deficits since the disease state affects the whole brain. Other findings may indicate specific metabolic processes (e.g., pinpoint pupils indicating opioid intoxication). Structural causes of coma range from major strokes to masses causing herniation of the cerebrum into the brain stem. Lesions affecting the brain stem (subtentorial) will cause complete brainstem dysfunction, which typically manifests as fixed unreactive pupils and impaired or absent oculovestibular or oculocephalic reflexes. The most common etiology of subtentorial coma syndrome is brainstem stroke. Supratentorial lesions typically cause coma when the mass translates pressure inferiorly and causes herniation of the cerebrum through the tentorial notch. The increase in volume of the subtentorial compartment results in compression of the brainstem. This process can occur quickly or can be protracted (as is the case in slow-growing masses). The two most common herniation syndromes are central herniation (caused by a mass that directs a vertical vector of force toward the tentorial notch) and uncal herniation. Uncal herniation results from a unilateral mass causing a lateral force vector. This force vector pushes the temporal lobe over the edge of the tentorium and compresses the midbrain. Early transtentorial herniation will often present with a third cranial nerve palsy because the cranial nerve runs just inferior to the lateral edge of the tentorium. In the case of uncal herniation, only the ipsilateral eye will be affected, resulting in unilateral dilated and fixed pupil, Oculoceopahlic (doll's eyes) and oculovestibular (cold water reflex) assess the brainstem function. Unilateral motor deficits suggest supratentorial structural lesions, while symmetric motor impairment indicates subtentorial or metabolic causes. Diagnostic evaluation depends on the suspected etiology. It includes advanced imaging (CT or MRI), lumbar puncture (if concern for meningitis or subarachnoid hemorrhage), ECG, toxicology screening, chemistry panels, ABG, and a complete blood count. Treatment is focused on supportive measures (e.g., breathing and blood pressure) and correcting the underlying cause

CML

The laboratory findings associated with CML depend on the phase of the disease and the hallmark of CML is lymphocytosis, with a median WBC count of 150,000/microL. A peripheral blood smear in the chronic phase of CML demonstrates a left shift in granulocytes, with many immature granulocytes. An absolute basophilia and thrombocytosis will also be present. A bone marrow biopsy performed in the chronic phase will reveal a markedly hypercellular bone marrow with left-shifted granulocytic hyperplasia and basophilia. The blast count is typically less than 5% and megakaryocytes are small and hypolobated. In the acute phase of CML, the blast count in the bone marrow ranges from 10% to 20%, with significant basophilia in peripheral blood and bone marrow. Blast crisis is characterized by a blast count of greater than 20% in the bone marrow with the majority being myeloblasts, although lymphoblasts, erythroblasts, or undifferentiated blast cells may also be present. Tx: Tyrosine kinase inhibitors are the standard therapy for CML. They act by blocking the locus with tyrosine kinase function at the BCR-ABL1 transcript, thereby inhibiting the activity of tyrosine kinase. The ability to inhibit tyrosine kinase activity normalizes peripheral blood counts, eliminates the Philadelphia chromosome, and eradicates the BCR-ABL1 gene transcript at the molecular level. The selection of tyrosine kinase inhibitor depends on disease characteristics and drug tolerability. Imatinib mesylate is a first-generation drug that works by blocking the binding of adenosine triphosphate to the ABL tyrosine kinase domain. Adverse reactions of imatinib include nausea, diarrhea, fluid retention, hepatotoxicity, cardiotoxicity, and cytopenia. Second-generation drugs (such as dasatinib and nilotinib) were created to specifically target the point mutations in BCR-ABL1 genes. They are found to be more potent than imatinib and share similar side effect profiles. In addition, nilotinib causes QTc prolongation.

non-Hodgkin lymphoma (NHL)

The majority of malignant lymphomas are non-Hodgkin lymphomas, with the median age of diagnosis in the sixth decade of life. Non-Hodgkin lymphomas are tumors that originate from the lymph nodes. They can occur as a result of certain infections, chromosomal translocations, immunocompromised status and chronic inflammation as seen in autoimmune disorders such as Hashimoto thyroiditis or Sjögren syndrome, or environmental factors such as pesticides, hair dye, or chemotherapy. Clinical presentation varies based on the location of the lymphoma, speed of tumor growth, and function of the organ that is being affected by the malignancy. In patients with a low-grade lymphoma, painless peripheral adenopathy is the most common presenting symptom. More advanced stages of the disease present with weight loss, fatigue, weakness, night sweats, and unexplained fever.

hypercalcemia

The symptoms of hypercalcemia include anxiety, depression, cognitive dysfunction, nephrolithiasis, muscle weakness, and bone pain. Anorexia and nausea are gastrointestinal symptoms that are associated with moderate elevation in serum calcium. Treatment should be based on the severity of symptoms and the level of calcium excess. Patients with an albumin-corrected level of serum calcium of > 14 mg/dL typically require aggressive and immediate therapy. Hypovolemic states will prevent renal excretion of calcium, so volume expansion using intravenous saline is recommended. These patients should be treated with intravenous saline, calcitonin, and an intravenous bisphosphonate. Patients who have hypercalcemia secondary to malignancy typically require maintenance therapy with a bisphosphonate derivative. Patients with chronic granulomatous disease may have an overproduction of calcitriol. These patients typically benefit from glucocorticoids to decrease calcitriol production. ECG will show shortened QT interval Most common causes Malignancy (most common inpatient cause) Primary hyperparathyroidism (most common outpatient cause) Treatment is IV fluids, bisphosphonates, calcitonin

Post MI complications

The three most common types of post-MI mechanical complications are free wall rupture, ventricular septal rupture, and acute mitral valve regurgitation. Free wall rupture is a rare complication of MI that occurs within the first two weeks of initial symptom onset (it is most common at 24-48 hours after symptom onset) and carries a high mortality rate. Free wall rupture is caused by thinning of the myocardium and stress by asymmetrically contracting cardiac muscles that leads to a tear in the myocardium. Hemopericardium causing cardiac tamponade is often a sequela of the rupture. Hence, symptoms of cardiac tamponade (e.g., hypotension, elevated jugular venous pressure, muffled heart sounds [Beck triad], tachycardia, narrowed pulse pressures) seen in an individual within 24-48 hours of MI should raise suspicion for free wall rupture. Ventricular septal defect is a rare complication of MI within 10 days of symptom onset. Patients with ventricular septal defect due to MI will often present with a new holosystolic murmur and heart failure. Acute mitral valve regurgitation following MI is caused by papillary muscle rupture. Patients will present with a new systolic ejection murmur heard best at the cardiac apex and heart failure. Mural thrombosis, due to myocardial dyskinesis and subsequent hemodynamic stasis, is a known complication of MI that can result in the formation of emboli. Heart failure is a common complication of MI. It is caused by a cycle of decreased contractility from What medication classes are contraindicated in patients with right ventricular infarction? Answer: Nitrates and diuretics.

guillan barre

The three subtypes of Guillain-Barré are acute inflammatory demyelinating polyneuropathy (most common), axonal neuropathy (acute motor and acute motor sensory), and Miller Fisher syndrome. Guillain-Barré syndrome is a clinical diagnosis based on progressive, bilateral weakness of the extremities and areflexia. Autonomic symptoms, including diarrhea, constipation, hyponatremia, bradycardia, tachycardia, and urinary retention, may be present. In severe cases, respiratory muscles are affected, and breathing becomes difficult or impossible without respiratory support. Albuminocytologic dissociation (elevated protein levels with normal WBC count in the cerebral spinal fluid) is a classic finding in Guillain-Barré syndrome but may be absent in the first few days of symptom onset. MRI of the lumbosacral spine will show gadolinium enhancement of the nerve roots and is useful in ruling out other diagnoses. Hospitalization is required for treatment. Intravenous immunoglobulin and plasmapheresis are the most effective treatments. Supportive care is needed in the presence of respiratory, cardiac, or electrolyte abnormalities and includes intubation, mechanical ventilation, or electrolyte correction. Corticosteroids are not indicated and may delay recovery.*** Most patients fully recover within 12 months. About 3-5% of patients will die from Guillain-Barré complications (e.g., autonomic dysfunction, respiratory distress, pulmonary embolism, infection) even with treatment.

gout

Thiazide diuretics and aspirin should be avoided -acute attack don't start on allopurinol -older men & post-meno women -high purine foods (diuretics, salicylates, niacin) -warmth, swelling, erythema, 1st MTP (Podogra) -hyperuricemia, acute MONOarticular arthritis, dx: Diagnosis is by arthrocentesis - needle/rod-shaped negatively birefringent.*** Serum uric acid level >8.6 (not diagnostic) due to UNDER secretion of uric acid -arthrocentesis = monosodium urate crystals, biofringent NEGATIVE needle shaped -rat bites on XR tx: 1st = NSAIDs, ice if not then prednisone or triamcinolone if renal issues -prophylaxis = probenacid or allopurinol -C/I = ASA & loop or thiazide diuretics -low purine diets, increase water intake pseudogout: -rhomboid-shaped calcium pyrophosphate crystals - positively birefringent*** -large joints (knees)**, no tophi, LEs -same tx as NSAIDs dx: -lines of chondrocalcocenosis on imaging XR -arthrocentesis = calcium dihydrate rhomboid shaped POSITIVE BIFRINGENT*** tx: -Indomethacin (NSAIDs) = 1st line -intra-articular corticosteroids -colchicine = prophylaxis Drugs such as allopurinol, febuxostat, probenecid, and lesinurad will lower uric acid levels. Patients should be educated that sudden changes in uric acid levels may occur when taking these medications and may trigger gout attacks. Patients with asymptomatic hyperuricemia generally should not be treated. Other less common drugs for consideration include uricase, pegloticase, vitamin C, anakinra, and fenofibrate. Patients should be educated to avoid or restrict consuming foods that are high in purine (e.g., organ meats, sardines, mussels), avoid ingestion of alcoholic drinks (particularly beer) in excess, avoid beverages sweetened with high fructose corn syrup, and maintain adequate hydration. Gout has an excellent prognosis if treated early with good patient compliance.

Viral Encephalitis

West Nile virus is the most common cause of encephalitis in the United States. Other causes of viral encephalitis include arbovirus, herpes simplex virus type 1, varicella-zoster, Epstein-Barr virus, and HIV. Risk factors for West Nile encephalitis are being exposed to infected mosquitos, advanced age, immunosuppression, and infrequently blood transfusions from an infected donor. Most patients infected with West Nile virus are asymptomatic, however, symptoms of West Nile encephalitis include altered mental status ranging from subtle deficits to complete unresponsiveness. Focal neurologic deficits such as flaccid paralysis, coarse tremor, rigidity, postural instability, and bradykinesia can also be observed. Diagnosis is made via cerebrospinal fluid (CSF) examination using enzyme-linked immunosorbent assay (ELISA). Treatment of West Nile encephalitis is mainly supportive, with many patients regaining their baseline motor function in six to eight weeks after symptom onset. -temporal lobe = MC

SLE

Triad of joint pain + fever + malar (butterfly rash)*** - fixed erythematous rash on cheeks and bridge of nose sparing nasolabial folds*** (+) Anti-nuclear Ab (ANA): ANA best initial test (not specific) (+) Anti-double-stranded DNA and Anti-Smith Ab: 100% specific for SLE (not sensitive)*** -+ anti-histone antibody (drug induced - procainamide or hydralazine) Treatment is NSAIDs, steroids, immunosuppressants, hydroxychloroquine Drug-induced lupus: hydralazine, INH, procainamide, phenytoin, sulfonamides (HIPPS) Best contraception: LNG-IUS or POP dx: (4 of 11) -Malar rash (butterfly rash)*** -Discoid rash (chronic, can scar) -Photosensitivity (other rashes from sun exposure) -Mucosal involvement (ulcers, mouth, and nose) -Serositis (pleuritis, pericarditis) -Joint arthritis (2 or more) -Renal disorders (abnormal urine protein, diffuse glomerulonephritis) -Neurologic disorders (seizures, psychosis) -Hematologic disorders (anemia, thrombocytopenia, leukopenia) -ANA -multiple spontaneous abortions Other antibodies: Anti Smith, Anti-dsDNA, Anti-phospholipid (Anticardiolipin, Lupus anticoagulant, Anti-B2 Glycoprotein) tx: -Manage with sun protection, -hydroxychloroquine (for skin lesions), -NSAIDs, or acetaminophen for arthritis -Pulse dose steroids; -cytotoxic drugs (methotrexate, cyclophosphamide) An antinuclear antibody titer ≥ 1:40 is highly sensitive for SLE but not very specific. The presence of anti-Smith antibodies, anti-double-stranded DNA antibodies, and low levels of serum complement are more specific for SLE. Lifestyle modifications for patients with SLE include regular exercise, smoking cessation, and protection from sunlight. Pharmacologic management includes antimalarials (e.g., hydroxychloroquine), nonsteroidal anti-inflammatory drugs, and corticosteroids. Because hydroxychloroquine may cause retinal toxicity, patients should schedule an ophthalmologic examination within one year of treatment initiation. Corticosteroids may be administered orally, topically, intramuscularly, or intravenously. Belimumab, approved in 2011, is the newest SLE medication and is a monoclonal antibody that inhibits the B lymphocyte stimulator associated with the pathogenic effects of SLE. The 10-year survival rate for SLE has improved from 50% to > 90% over the last 70 years, which is likely due to earlier detection and treatment.

UTI

Tx: (uncomplicated) An uncomplicated urinary tract infection is best treated with either nitrofurantoin, trimethoprim-sulfamethoxazole, or a fluoroquinolone

SIADH

What cancer is syndrome of inappropriate antidiuretic hormone secretion (SIADH) most commonly associated with? Answer: Small cell carcinoma. a hypotonic, euvolemic hyponatremia common in hospitalized patients. SIADH may be caused by pulmonary conditions such as pneumonia or Legionnaires' disease, CNS disorders, malignancies, or certain drugs (e.g., chlorpromazine, theophylline, selective serotonin reuptake inhibitors). Hyponatremia is defined as a serum sodium level < 135 mEq/L. Hypotonicity is defined as a serum osmolality < 280 mOsm/kg. A urine sodium of 20-40 mEq/L indicates a euvolemic state. Symptoms of hypovolemia include nausea, vomiting, headache, lethargy, disorientation, and gait disturbances but may not occur until the serum sodium level is < 125 mEq/L. Severe hyponatremia may result in seizures, coma, or death. SIADH is a clinical diagnosis characterized by a hypotonic, euvolemic hyponatremia in the absence of cardiac, thyroid, hepatic, renal, and adrenal disease. Mild to moderate hyponatremia in asymptomatic patients with SIADH can typically be managed with fluid restriction, removal of offending agents, and treatment of infections, nausea, and pain. Oral sodium chloride tablets two to three times daily and low-dose furosemide may also be used in uncomplicated cases of SIADH. A cute, symptomatic hyponatremia (duration < 48 hours), as seen in the vignette above, should be corrected quickly with 3% hypertonic saline 100 mL over 10 minutes. Patients with severe chronic hyponatremia should be treated with a continuous infusion of 3% hypertonic saline with a goal correction rate of 4-6 mEq/L/24 hours. This slow rate of infusion decreases the risk of osmotic demyelination syndrome, patients with symptomatic or severe SIADH require close monitoring of their fluid intake, daily weight, and sodium levels, along with a nephrology consultation. Vasopressin 2 (V2) receptor antagonists (e.g., tolvaptan, conivaptan) may also be considered in severe SIADH as an alternative to 3% hypertonic saline.

giant cell arteritis

What findings are most common on eye exam for a patient with vision impairment due to temporal arteritis? Answer: Cotton-wool spots, a sign of impaired perfusion of the retina, are precursors of ischemic occlusion and appear as fluffy white patches on the retina.

hyperthyroidism

What is Jod-Basedow syndrome? Answer: Iodine-induced hyperthyroidism. Graves disease is more common in women, and the typical onset is between 20 and 40 years of age. Patients with a family history of thyroid disorders, including Graves disease and Hashimoto thyroiditis, are at an increased risk of developing autoimmune thyroid conditions. Graves disease is associated with other conditions, including atrial fibrillation, hypercalcemia, osteoporosis, and nephrocalcinosis. Amiodarone use increases the risk for developing Graves disease because it contains iodine. While Graves disease usually presents with hypermetabolic symptoms, including tachycardia, heat intolerance, weight loss, hyperreflexia, and diarrhea, patients on amiodarone may be bradycardic.*** Initial laboratory testing will include a thyroid panel, which will show decreased TSH levels and increased T3 and T4 levels. Thyroid receptor antibodies are the most specific test for Graves disease, although they may be occasionally present in other thyroid disorders (e.g., Hashimoto thyroiditis, toxic multinodular goiter). Antithyroglobulin and antiperoxidase antibodies are present in autoimmune thyroid disorders but are not specific to Graves disease

erectile dysfunction

What is the only FDA-approved medication for the treatment of Peyronie disease? Answer: Injectable collagenase Clostridium histolyticum. Antidepressant medications such as selective serotonin reuptake inhibitors (e.g., fluoxetine, paroxetine, sertraline), serotonin and norepinephrine reuptake inhibitors (e.g., duloxetine, venlafaxine), tricyclics (e.g., amitriptyline, nortriptyline), and older monoamine oxidase inhibitors (e.g., isocarboxazid, phenelzine) have the potential to cause erectile dysfunction. Other classes of medications that may cause erectile dysfunction include diuretics, certain beta-blockers, and opioids. Erectile dysfunction occurs in > 50% of men between 40-70 years of age. A detailed history of comorbid conditions and medications, physical exam, and laboratory testing are important to identify underlying risk factors of erectile dysfunction. Conditions associated with erectile dysfunction include increasing age, smoking, alcohol use, marijuana, dyslipidemia, hypertension, depression, stress, neurological conditions (e.g., stroke, spinal cord injury, multiple sclerosis), endocrine conditions (e.g., diabetes mellitus type 2, testosterone deficiency, hyperprolactinemia, thyroid disorders), and certain medications. Erectile dysfunction has a variety of etiologies. A patient with androgen deficiency will typically present with decreased libido. Neurogenic, arterial, venous, hormonal, psychogenic, and pharmacologic etiologies often cause a loss of erections. The most common cause of erectile dysfunction is a reduction in arterial flow secondary to progressive vascular disease

type 1 diabetes

Which serum test can be used to distinguish type 1 and type 2 diabetes mellitus? Answer: C-peptide protein, which is low or absent in type 1 diabetes. DKA: History of infection, ischemia (cardiac, mesenteric), infarction, insulin deficit (poor control), intoxication (five I's) Abdominal pain, vomiting, and fatigue PE will show fruity-smelling breath, dehydration, and AMS Labs will show hyperglycemia, ketonemia, and an anion gap metabolic acidosis Management Treat precipitating cause Correct volume depletion with NS, add dextrose to fluids once glucose is < 250 mg/dL Replete K+ deficit (usually falsely elevated), do not start insulin if K+ < 3.3 mEq/LIV insulin drip until anion gap closes Corrected sodium: add 1.6 mEq/L for each 100 mg/dL in serum glucose HHS = hyperglycemic hyperosmolar syndrome What lab abnormality in blood chemistries indicates an upper gastrointestinal bleeding source? Answer: An elevated blood urea nitrogen to creatinine ratio in the absence of renal dysfunction. Stage 1 hypertension is defined as a systolic pressure of 130-139 mm Hg and a diastolic pressure of 80-89 mm Hg. Stage 2 hypertension is defined as a systolic pressure of at least 140 mm Hg and a diastolic pressure of at least 90 mm Hg. Normal blood pressure is less than 120/80 mm Hg, and elevated blood pressure is defined as a systolic pressure of 120-129 mm Hg and a diastolic pressure of less than 80 mm Hg. modifications include weight loss, healthy diet, dietary sodium reduction, dietary potassium increase, increased physical activity, and limited alcohol intake. Pharmacotherapy should be considered for patients with stage 1 hypertension at high risk for cardiovascular disease, for patients with stage 2 hypertension, and for patients who have failed to reach target blood pressure despite nonpharmacologic therapy. When selecting the appropriate pharmacotherapy, careful consideration of the patient's comorbidities should be taken. For patients with a history of myocardial infarction, beta-blockers and angiotensin-converting enzyme (ACE) inhibitors are first-line therapy. Other drugs, such as dihydropyridine calcium channel blockers, thiazides diuretics, and mineralocorticoid receptor antagonists, may be added to achieve target blood pressure. ACE inhibitors are recommended for patients with diabetes mellitus or heart failure, -calcium channel blockers or thiazide diuretics are preferred in African-American patients, and losartan is preferred in patients with gout. -The goal of blood pressure therapy is a BP < 130/80 mm Hg. Refractory hypertension is defined as blood pressure that is not at goal even on three or more blood pressure medications. Cerebrovascular accident, dementia, myocardial infarction, heart failure, retinal vasculopathy, aortic dissection, and kidney disease are potential complications of hypertension. What class of antihypertensive medication has a side effect of constipation and peripheral edema? Answer: Calcium channel blockers.

MS

White matter plaques are most commonly seen in the ventricles as perpendicular projections (Dawson fingers) or ovoid lesions. Lesions in the dorsal column of the cervical spine are also commonly seen. Protein analysis of CSF fluid demonstrating oligoclonal bands is the most sensitive laboratory test and may be used to support the diagnosis. Elevated immunoglobulin G index and increased myelin basic protein are also indicative of multiple sclerosis. -CSF will show ↑ IgG protein, WBC pleocytosis tx: -Acute exacerbations of multiple sclerosis may be treated with high-dose intravenous corticosteroids (e.g., methylprednisolone), and plasma exchange may be used if the patient fails corticosteroid therapy. Symptomatic management includes gamma-aminobutyric acid agonists (e.g., baclofen) or benzodiazepines (e.g., diazepam) for spasticity and anticholinergics (e.g., oxybutynin) for urologic dysfunction. Disease-modifying agents such as beta-interferons and glatiramer acetate injections are used for long-term therapy. Unlike Guillain-Barré syndrome, multiple sclerosis presents with upper motor neuron spasticity and increased deep tendon reflexes***

rheumatoid arthritis

a chronic autoimmune disorder in which the joints and some organs of other body systems are attacked -MCP*** = MC JOINT INVOLVED -stiff >30-60 mins in AM** better with movement -fatigue, fever, ulnar deviation, nodules, swan neck (flex DIP & extended PIP) & buitoneire deformations (flex PIP and extend DIP) -T cell mediated, destruction by the pannus -women, smoker = RF dx: -Anti-CPP (MOST SPECIFIC) elevation -Initial test = rheumatoid factor -ESR/CRP -anemia of chronic dz -thrombocytosis ->3 joints -XR = soft tissue swell, joint effusion -MRI > tx: -DMARDs (methotrexate = 1st line) screen for HBV,HBV -pain = NSAIDs 1st line Leukocyte count on synovial joint fluid analysis is typically between 1,500 and 25,000/mm3, and levels of leukocyte count > 25,000/mm3 should increase the suspicion of coexisting infection. Laboratory studies demonstrate elevated ESR and CRP. Rheumatoid factor (RF) and anti-cyclic citrullinated peptide (anti-CCP) antibodies are positive in the majority of patients, although their presence is not specific for rheumatoid arthritis. Patients with positive RF or anti-CCP antibodies are considered to have seropositive rheumatoid arthritis. Plain radiographs are often normal in early disease but can reveal periarticular osteopenia, juxta-articular osteoporosis, joint space narrowing, and bone erosions as the disease progresses. MRI and ultrasonography are more sensitive than plain radiographs in detecting bone erosions, however, their clinical utility in the setting of rheumatoid arthritis is still under investigation. The treatment of rheumatoid arthritis requires an interdisciplinary approach, including the rheumatologist, physical and occupational therapists, and pharmacologist. At the time of initial diagnosis, all patients should be referred to a rheumatologist to initiate treatment and develop a long-term plan. Physical and occupational therapy should be implemented as soon as possible to improve the mechanics involved with performing activities of daily living and to improve the overall functioning of the patients. Pharmacologic management should be initiated early and should be aggressive to reduce pain, preserve function, and prevent deformity. The first-line therapy for rheumatoid arthritis is disease-modifying antirheumatic drugs (DMARDs). DMARDs prevent bone and joint destruction and slow the progression of the disease. Two forms of DMARDs exist: synthetic and biologic. Methotrexate is the first synthetic DMARD to be initiated. It is generally well tolerated and produces a beneficial effect within two to six weeks. The most common side effects include gastric irritation and stomatitis, although cytopenia (most commonly leukopenia or thrombocytopenia, or rarely pancytopenia), hepatotoxicity with fibrosis, and cirrhosis can also occur. Methotrexate is contraindicated in patients with chronic hepatitis, pregnant patients, and patients with significant kidney dysfunction (glomerular filtration rate < 30 mL/min). Heavy alcohol use should be discontinued, as it may exacerbate hepatotoxicity. Liver biochemical tests should be measured every 12 weeks along with CBC. Because methotrexate is a folate antagonist, patients should be supplemented with daily folate. Supplementation with folate reduces gastric irritation, stomatitis, cytopenia, and hepatotoxicity. Other synthetic DMARDs that can be used include sulfasalazine, leflunomide, antimalarials (hydroxychloroquine), and tofacitinib. Biologic DMARDs include tumor necrosis factor (TNF) inhibitors (etanercept, infliximab, adalimumab, golimumab, and certolizumab pegol), abatacept, rituximab, and tocilizumab. Combination DMARDs (for example, methotrexate plus a TNF inhibitor) are more efficacious than when either medication is used as monotherapy. Cervical changes may result in atlantoaxial instability or subluxation, necessitating cervical spine radiographs in patients with advanced rheumatoid arthritis who require intubation and sedation. Neck positioning required for intubation may be fatal in patients with undiagnosed atlantoaxial disease.

polymyositis

a muscle disease characterized by the simultaneous inflammation and weakening of voluntary muscles in many parts of the body Polymyositis is a chronic, idiopathic inflammatory DISEASE OF THE MUSCLE causing symmetrical, proximal, PAINLESS (versus polymyalgia rheumatica) muscle weakness -AAs, high risk of SMLC or bladder CA -C9-8 cells autoimmune -SYMMETRICAL, trunk/shoulder/hip pain gradual -NO SKIN MANIFESTATIONS ↑ Muscle enzymes: ↑ aldolase, elevated creatine kinase; ↑ ESR, (+) muscle biopsy, abnormal EMG (+) ANTI-JO 1 Antibodies***: Myositis-specific Antibody-associated with interstitial lung fibrosis"mechanical hands" hyperkeratotic cracked hands with a dirty appearance (+) Anti-SRP Ab: signal recognition particle Ab (+) Anti-Mi-2 Ab: specific for dermatomyositis Muscle biopsy: endomysial*** involvement with PM TX: corticosteroids and sometimes other immunosuppressants (methotrexate/azathioprine) Creatine kinase, which will be normal in polymyalgia rheumatica and elevated in polymyositis.***

ABCD2 score

age ≥ 60 years (1 point); systolic BP ≥ 140 mm Hg or diastolic BP ≥ 90 mm Hg (1 point); clinical features, including unilateral weakness with or without speech impairment (2 points) or speech impairment without unilateral weakness (1 point); duration of TIA ≥ 60 minutes (2 points), 10-59 minutes (1 point), or less than 10 minutes (0 points); and diabetes mellitus (1 point). Standard stroke protocol includes a noncontrast CT of the head (to differentiate between ischemic stroke, hemorrhagic stroke, and intracranial mass), complete blood count, complete metabolic panel, urinalysis, coagulation profile (PT, PTT), ECG monitoring, and serial cardiac enzymes. Patients presenting within 72 hours of TIA should be admitted if their ABCD2 score is greater than or equal to 4, if their ABCD2 score is less than 4 and there is uncertainty that outpatient evaluation can be completed within 48-72 hours, or if their ABCD2 score is less than 3 and there is evidence of cerebral infarction. 10% of TIA patients will have a stroke within 90 days Low-risk TIA (ABCD2 score < 4) or moderate to major ischemic stroke (National Institutes of Health Stroke Scale (NIHSS) > 3) Treatment with aspirin alone High-risk TIA (ABCD2 score ≥ 4) or minor ischemic stroke (NIHSS score ≤ 3) Begin with dual antiplatelet therapy (DAPT) for 21 days using aspirin plus clopidogrel ABCD2 score: predicts likelihood of subsequent stroke within 2 days

IgA nephropathy (Berger disease)

also known as Berger disease, is a cause of nephritic syndrome and is the most common primary glomerular disease worldwide, particularly in those of East Asian (e.g., Chinese, Taiwanese, Korean, etc.) and Caucasian descent. It is commonly seen in boys and young men. IgA nephropathy is a primary kidney disease of IgA deposition in the glomerular mesangium. The underlying pathophysiology is not entirely clear but may be linked to a deficiency in O-linked glycosylation of IgA subclass 1 molecules. Patients classically present with sudden onset of gross hematuria 1 to 2 days after an upper respiratory infection. This synpharyngitic presentation distinguishes IgA nephropathy from postinfectious glomerulonephritis. Serological tests are nonspecific. Serum complement levels are normal. Kidney biopsy will show a focal glomerulonephritis with mesangial proliferation. Immunofluorescence will show diffuse mesangial IgA and complement C3 deposits. About one-third of cases will resolve spontaneously. Another one-third of cases will have chronic microscopic hematuria and a normal serum creatinine. The remaining one-third will progress to end-stage renal disease. Treatment of IgA nephropathy depends on the course of the disease. Hypertension, proteinuria, and glomerular filtration rate should be monitored periodically. Blood pressure control with an angiotensin-converting enzyme inhibitor or angiotensin receptor blocker is appropriate. Corticosteroids may be indicated in patients with persistent proteinuria > 1 g/day or in adjunct with cyclophosphamide in patients with crescent formation on biopsy and a rapidly progressive clinical course. A kidney transplant may be indicated in patients with end-stage renal disease.

interstitial nephritis

an abrupt decline in kidney function due to damage or inflammation of the renal tubules and interstitium. It is an important cause of acute kidney injury and is usually caused by certain medications, infections (e.g., cytomegalovirus, Epstein-Barr virus, hepatitis C, herpes simplex virus, HIV, Mycobacterium, Rickettsia, syphilis, toxoplasmosis), or autoimmune conditions (kidney transplant rejection, lymphoproliferative disorders, systemic lupus erythematosus, glomerulonephritis). Some classes of medications associated with acute interstitial nephritis are antibiotics, nonsteroidal anti-inflammatory drugs (NSAIDs), sulfonamides, diuretics, and antituberculous drugs. NSAIDs (e.g., ibuprofen) are the most frequent cause of drug-induced acute interstitial nephritis, which is more common in older patients. Hematuria is rare with NSAID-induced acute interstitial nephritis, while nephrotic range proteinuria is common. The classic triad of fever, rash, and arthralgias associated with acute interstitial nephritis is seen in less than one-third of patients. Typically, laboratory testing will reveal eosinophiluria, and urinalysis will contain white blood cells, red blood cells, white cell casts, and occasionally eosinophils. Diagnosis is usually made from the clinical history, laboratory results, and response to treatment. Kidney biopsy is used for definitive diagnosis if the diagnosis is clinically unclear, and it will typically reveal an infiltration of inflammatory cells in the renal interstitium with interstitial edema that spares the glomeruli and blood vessels. Treatment of acute interstitial nephritis involves removing the offending agent, treating any infections, or managing the autoimmune disease. Most patients will recover within several weeks without additional treatment. Older patients and patients with prolonged oliguria may experience a more complicated course and may need a short course of corticosteroids or dialysis. Drugs - 5 Ps Pee (diuretics, especially sulfa ones) Pain-free (NSAIDs) Penicillins and cephalosporins Proton pump inhibitors rifamPin Immunologic and infectious disease: strep, SLE, CMV, Sjogren's, Sarcoidosis Urinalysis: WBC casts and eosinophils

Post-Strep Glomerulonephritis (PSGN)

an acute, immune-mediated inflammatory disorder of the glomerulus, typically occurring 1 to 3 weeks after a group A beta-hemolytic streptococcal infection. It is most commonly seen in patients who are 5-12 years of age, > 60 years of age, of low socioeconomic status, or of male gender. Patients typically present with hypertension, hematuria, and proteinuria. Patients may also present with oliguria and periorbital (more common in the morning), dependent (more common in the evening), or generalized edema. Diagnosis may be made on clinical presentation alone. A urinalysis will often show tea-colored or cola-colored urine, hematuria (> 3 RBCs/high-powered field), RBC casts, and proteinuria. Serum complement C3 is typically decreased. Antibodies associated with poststreptococcal glomerulonephritis include anti-streptolysin, anti-hyaluronidase, anti-streptokinase, anti-nicotinamide-adenine dinucleotidase, and anti-DNase B. Corticosteroids are not indicated for poststreptococcal glomerulonephritis, and treatment is supportive. Antihypertensive medications, salt and water restriction, and diuretics may be used as necessary. Children are likely to fully recover, while adults are at an increased risk of progression to chronic kidney disease. Other causes of glomerulonephritis include Henoch-Schonlein purpura, IgA nephropathy, hereditary nephritis, membranoproliferative glomerulonephritis, systemic lupus erythematosus, and vasculitis. Corticosteroids and immunosuppressive medications may be useful in non-streptococcal causes of glomerulonephritis. Dialysis is indicated in the presence of severe azotemia.

pyelonephritis

an infection of the kidney parenchyma and renal pelvis most commonly caused by gram-negative bacteria (e.g., E. coli, Proteus, Klebsiella, Enterobacter, and Pseudomonas). Gram-positive bacteria (e.g., Enterococcus faecalis, Staphylococcus aureus) may also cause pyelonephritis. Typical symptoms include fever, chills, flank pain, urinary urgency, urinary frequency, and dysuria. Patients may also present with gastrointestinal symptoms (e.g., nausea, vomiting, diarrhea). Fever, tachycardia, and pronounced unilateral costovertebral angle tenderness are common signs. Laboratory findings include leukocytosis and bandemia. Urinalysis may show pyuria, bacteriuria, hematuria, and white cell casts. Urine cultures and blood cultures may be positive. In patients with complicated pyelonephritis (e.g., pregnancy, immunocompromised, diabetic, anatomical renal abnormalities, kidney injury), Treatment is fluoroquinolone or TMP-SMX Inpatient or pregnant: ampicillin-gentamicin or third-gen cephalosporin

polymyalgia rheumatica

an inflammatory disorder of the muscles and joints characterized by pain and stiffness in the neck, shoulders, upper arms, and hips and thighs PAINFUL synovitis, bursitis, and tenosynovitis - aching STIFFNESS of PROXIMAL JOINTS (shoulder, hip, neck) in patients > 50 years old -ESR >50*** PMR is closely related to giant cell arteritis (temporal arteritis) - confirm w/ temporal artery biopsy Joint pain versus muscle pain in polymyositis STIFFNESS versus the weakness of polymyositis sx: -fever, malaise, weightloss -joint swell -clinical dx tx: -Patients respond quickly to low-dose corticosteroid therapy (prednisone), which may be required for up to 2 years and slowly tapered -Methotrexate may also be used -bilateral stiffness >30 mins a clinical diagnosis based on pain and stiffness around the shoulder, neck, and hip area. This disorder is more common in adults over 50 years of age, particularly women, and is seen more often in Caucasians than any other race. Pain and stiffness are worse after rest. Restricted shoulder range of motion is common, and patients often complain of pain and stiffness in the upper arms, hips, thighs, and upper and lower back. This restricted range of motion affects the patients' quality of life, and they may have trouble with daytime activities and sleeping at night. Patients may also experience joint swelling, fever, malaise, and weight loss. These nonspecific features may mimic other potential diagnoses, such as rheumatoid arthritis, giant cell arteritis, myositis, and fibromyalgia. Anemia and elevated ESR are present in most cases of polymyalgia rheumatica, and patients are treated with oral glucocorticoids with gradual tapering. Patients at high risk of relapse may benefit from a regular regimen of methotrexate. What is the most important difference between polymyalgia rheumatica and giant cell arteritis? Answer: Polymyalgia rheumatica does not cause blindness and will respond to a lower dose of prednisone therapy (10-20 mg/day). Giant cell arteritis can cause blindness and other large artery complications and is treated with a higher dose of prednisone therapy (40-60 mg/day).

sickle cell anemia

at 6 months of age, the onset of symptoms begins as fetal hemoglobin is replaced with HbS. Clinical manifestations of sickle cell anemia depend on the organ system affected but generally include severe pain and multiorgan damage. Life-threatening manifestations are common and include hemolytic anemia, acute chest syndrome, ischemic stroke, kidney injury, bone infarctions, avascular necrosis (commonly affecting humeral and femoral head), painful crisis, and splenic sequestrations. Individuals with sickle cell anemia are at an increased risk for cholelithiasis, splenomegaly, leg ulcers, aplastic crisis (in the setting of concurrent parvovirus B19 infection), infections with encapsulated organisms, priapism, retinopathy including blindness, and osteomyelitis. The definitive diagnostic study for sickle cell anemia is electrophoresis, which shows 50% or greater concentration of hemoglobin S precipitates. A peripheral blood smear may reveal target cells, nucleated red cells, and Howell-Jolly bodies. Laboratory studies may demonstrate hemolytic anemia (elevated reticulocyte count, elevated indirect bilirubin, elevated LDH), leukocytosis, and thrombocytosis. Chest radiographs may show new infiltrates. Arterial blood gas may demonstrate respiratory acidosis. tx: -Hydroxyurea is the only pharmacologic agent that has consistently demonstrated improvements in episodes of pain and survival rates for patients with sickle cell anemia. -It increases hemoglobin F and reduces the production of hemoglobin S, thereby reducing the number of red cells that are susceptible to sickling. -Although generally well-tolerated, side effects may occur and include abdominal pain, nausea, hyperpigmentation, and darkening of the nails. What is the most common cause of death in adults with sickle cell disease? Answer: Acute chest syndrome. S. pneumoniae sepsis: most common cause of death in children

testicular torsion

can occur at any age, it most commonly presents in prepubertal boys. Risk factors include undescended testicles at birth and genetic structural defects such as a bell clapper deformity. Testicular torsion is the rotation of the testicle around the spermatic cord within the tunica vaginalis, which can lead to testicular ischemia. Testicular torsion most commonly presents as sudden-onset severe scrotal pain and swelling. Patients may also present with nausea, vomiting, and lower abdominal pain. On physical exam, there will be a negative Prehn sign, meaning the patient will find no relief from pain with elevation of the affected testicle, and a negative cremasteric reflex. The initial diagnostic test includes a color Doppler ultrasound, which will show a decrease in blood flow to the affected testicle. Testicular torsion is a medical emergency, and the patient will need immediate surgery to detorse the affected testicle and possible orchiopexy

multiple myeloma

cancer of monoclonal plasma cells; MC primary tumor of bone/bone marrow in pt > 50 yo Older patient + bone and back pain refractory to treatments Presentation: "CRAB"- Calcium elevation, renal failure, anemia, and bone lesions DX: Urinalysis: Monoclonal proteinuria → Ig light chains (Bence Jones Protein) Blood smear: Rouleaux formation (stacked RBCs) Radiograph: X-ray showing lytic "punched-out" bone lesions of skull, spine, long bones Serum/Urine electrophoresis: Monoclonal (M protein) Spike (IgG or IgA) Bone marrow biopsy: > 10% clonal plasma cells Tx: bone marrow transplant = definitive Melphalan, steroids, thalidomide, bortezomib

emphysema continued

characterized by structural changes that occur distal to the terminal bronchioles. These structural changes include dilation and enlargement of the alveolar spaces without obvious fibrosis. This distinguishes emphysema from other types of chronic obstructive pulmonary disease such as chronic bronchitis or asthma. Patients with emphysema typically have moderate to severe airflow obstruction. There are varying subtypes of emphysema, including proximal acinar, panacinar, and distal acinar. Proximal acinar, or centrilobular emphysema, is associated with abnormal destruction of the bronchioles in the central portion of the acinus. Cigarette smoking is the most common cause. Panacinar emphysema involves all parts of the acinus. It is most commonly associated with alpha-1 antitrypsin deficiency. Distal acinar emphysema, or paraseptal emphysema, describes when the alveolar ducts are most heavily involved. This typically occurs in combination with proximal acinar or panacinar emphysema. Radiographic features of emphysema include flattening of the diaphragms, hyperinflation, increased radiolucency of the lungs, dilation of the distal bronchioles, and a long narrow heart shadow. Diagnosis is made after pulmonary function studies show an obstructive pattern that is not completely reversible after the administration of a bronchodilator.

myasthenia gravis

chronic autoimmune neuromuscular disorder caused by antibodies against acetylcholine receptors and muscle-specific tyrosine kinase. It is characterized by proximal muscle weakness (e.g., shoulders, thighs) and fatigability that improves with rest. Common initial symptoms include ptosis, diplopia, blurred vision, difficulty in chewing or swallowing, and respiratory muscle weakness. Sensation and reflexes are normal. A relapsing-remitting pattern is common. Young women who are HLA-DR3 positive and older men with a thymoma (as seen on the CT scan above) are at an increased risk of myasthenia gravis. A CT scan or MRI is useful for the detection of a thymoma. dx: diagnosis of myasthenia gravis may be made with a positive edrophonium (Tensilon. est) challenge. Edrophonium is a short-acting anticholinesterase that will transiently improve muscle weakness symptoms in patients with myasthenia gravis tx:Acetylcholinesterase inhibitor (pyridostigmine/neostigmine) = first line ⇒ stops breakdown of acetylcholine Immunosuppressive drugs (prednisone) ⇒ reduce the production of autoantibodies Thymectomy ⇒ reduces muscle weakness Myasthenic crisis: neuromuscular respiratory failure from dysphagia/aspiration (treat with plasma exchange, IVIG)

Dermatomyositis

chronic systemic immunological disease involving inflammation of the skin, connective tissue, and muscles -CD-4 cells involved -rashes -shawl sign -gottron papules What are some drugs that can cause myopathy? Answer: Hydroxychloroquine, colchicine, hydralazine, phenytoin, and angiotensin-converting enzyme inhibitors. Patient will be a woman Insidious, painless, proximal muscle weakness (polymyositis) and a rash PE Malar rash Heliotrope rash Gottron papules Labs will show ↑ CK and aldolase Diagnosis is made by EMG, muscle biopsy Treatment is steroids Increased risk for malignancy (in adults) Heliotrope rash (symmetric, confluent, purple-red macular eruption of the eyelids and periorbital tissue), Gottron papules, and a shawl sign when present are highly suggestive of dermatomyositis. Elevation in serum levels of aldolase and creatine phosphokinase is seen in both polymyositis and dermatomyositis. ANA may be routinely elevated, but it is not specific for polymyositis. Only anti-Jo-1 antibodies are a diagnostic marker for polymyositis and is associated with interstitial lung disease, arthritis, mechanic's hands, and Raynaud phenomenon. Nonspecific antibodies associated with polymyositis include anti-SRP and anti-Mi-2 antibodies. Electromyogram demonstrates supportive evidence of muscle inflammation such as increased insertional activity and spontaneous fibrillation, abnormal myopathic low amplitude, and short duration polyphasic motor unit potential. The definitive diagnosis of polymyositis is established by a muscle biopsy, which reveals muscle fiber necrosis, degeneration, and regeneration and inflammatory cell infiltrate. The first-line treatment is high-dose steroids for at least three months. If there is no significant improvement in three months, azathioprine or methotrexate may be added. For resistant disease, intravenous immune globulin, cyclosporine, or tacrolimus may be beneficial.

diabetes mellitus

goals: -The HbA1C goal for most nonpregnant adults with type 2 diabetes mellitus is less than 7%. HbA1C levels lower than this may be acceptable as long as the patient is not experiencing hypoglycemia, and levels higher than 7% but lower than 8% are appropriate in patients who are older, those who have a history of significant hypoglycemia, those with advanced macrovascular or microvascular complications, or those with significant comorbid conditions health maintenance: -These interventions include monitoring blood pressure, annual dental and dilated eye exams, assessment of hypoglycemic episodes, comprehensive foot examination, and laboratory testing, which should be addressed with the patient at their diabetes examinations. Patients with poor glycemic control should be seen at least quarterly, while those at goal may be seen every 6 months.

respiratory alkalosis

increased pH, a decreased PaCO2, and a decreased or normal bicarbonate are indicative of respiratory alkalosis. The most common cause of respiratory alkalosis is hyperventilation. Other pulmonary conditions (e.g., pneumonia, asthma, restrictive lung disease), sepsis, liver disease (e.g., cirrhosis), heart failure, and salicylate intoxication may also cause respiratory alkalosis. As a compensatory mechanism, hydrogen ions (H+) will shift from intracellular to extracellular and combine with bicarbonate (HCO3−) to form carbonic acid (H2CO3), resulting in a decrease of bicarbonate and pH. The body may also slow respirations to increase CO2 levels in order to decrease pH. In patients with chronic respiratory alkalosis, the compensatory mechanism is primarily renal excretion of bicarbonate and decreased renal H+ secretion. non-anion gap metabolic acidosis can be remembered by the acronym HARDUPS (hyperalimentation, acetazolamide, renal tubular acidosis, diarrhea, ureteropelvic shunt, posthypocapnia, spironolactone).

Frontotemporal Dementia

occurs as a result of a pathologic buildup of proteins in the frontal and temporal lobes of the brain. The usual onset is between 40-75 years of age. Frontotemporal dementia has two clinical subtypes: behavioral variant and primary progressive aphasia. Behavioral variant frontotemporal dementia is the most common subtype and presents with changes in the patient's behavior, personality, and social conduct. Patients may display impulsivity, engage in criminal behavior, make inappropriate sexual advances, revert to a child-like sense of humor, or fail to recognize social cues. Family members may notice the patient seems more withdrawn, apathetic, or emotionally disconnected. Patients can become uncaring, unsympathetic, and lash out at family members or pets. Hyperorality symptoms are common and include binge eating, excessive consumption of sugary products, placing inedible objects in the mouth, or eating only one type of food. dx: -MRI -definitive: post-mortem autopsy -worse prognosis/faster decline than Alz tx: There are no FDA-approved treatments for frontotemporal dementia. Supportive therapy for the patient and the patient's family includes counseling, the establishment of caretakers, financial planning, safety assessments, and occupational and speech therapy. The pharmacologic agents used in Alzheimer disease (e.g., donepezil, rivastigmine, memantine) are ineffective and may be detrimental if used in patients with frontotemporal dementia.***

bacterial prostatitis

infection of the prostate most commonly caused by gram-negative rods (e.g., Escherichia coli, Pseudomonas, Neisseria gonorrhoeae, Chlamydia trachomatis). The most likely route of infection is ascending urethral spread or reflux of urine into the prostatic ducts. Patients with acute bacterial prostatitis typically present with high fever, chills, dysuria, urinary retention, and lower back, perineal, sacral, or suprapubic pain. The prostate is warm, exquisitely tender, and boggy on digital rectal examination. Clinicians should be aware that the risk of septicemia is increased with vigorous prostate manipulation. A prostate massage is contraindicated in acute prostatitis. CBC results are consistent with bacterial infection and show leukocytosis with a left shift. Urinalysis will show pyuria, bacteriuria, or hematuria. A urine culture is the definitive diagnosis for the bacterial cause of prostatitis. N. gonorrhoeae and C. trachomatis are the most common causative agents in patients < 35 years of age. The treatment for N. gonorrhoeae and C. trachomatis is ceftriaxone or doxycycline. E. coli is the most common causative agent in patients ≥ 35 years of age and is treated with ciprofloxacin, levofloxacin, or trimethoprim-sulfamethoxazole. A pelvic CT or transrectal ultrasound for a prostatic abscess is indicated in patients who do not respond to antibiotics within 48 hours. Patients with a prostatic abscess or who display signs of sepsis should be admitted to the hospital and started on parenteral antibiotics (e.g., ampicillin and gentamicin) until culture and sensitivity results are available. Patients who are afebrile for 24-48 hours may be transitioned to an oral fluoroquinolone for 4 to 6 weeks.

Polyarteritis nodosa

inflammation of small and medium-sized arteries (vasculitis) RFers: -men in 40-50s -HBV/HCV dx: -tissue biopsy or angiogram -Biopsy of an affected artery (gold standard) demonstrates necrotizing arteritis ⇒ or arteriography showing the typical aneurysms in medium-sized arteries ↑ ESR, Most common in middle age men of 45 years old Classic PAN is ANCA negative (P-ANCA positive in < 20% of cases) Renal or mesenteric angiography: microaneurysms with abrupt cut-offs of small arteries) tx: -Steroids (prednisone) +/- cyclophosphamide if refractory -Plasmapheresis in patients with Hepatitis B virus Because the condition can relapse, patients must be monitored for relapse by blood pressure measurement, a review of systems, laboratory monitoring for drug toxicities, serum creatinine measurement, and urinalysis. Patients with polyarteritis nodosa should be screened for hepatitis B, as the illnesses can coexist.

complex regional pain syndrome

pain that occurs after an injury to an arm or a leg, a heart attack, stroke, or other medical problem ->6 MONTHS DURATION -women, 40 y/o -The pain is typically unilateral, severe, and out of proportion to any physical examination or diagnostic findings. -A previous history of a fracture, sprain or strain, soft tissue injury, or surgery is common. -Patients may present with sensations of burning, tingling, or myalgias. sx: -S.T.A.M.P (sensory, trophic, autonomic, motor, pain) -Patient will have a history of previous extremity injury or fracture -Light touch causes extreme pain and allodynia (pain felt from a nonpainful stimulus, such as clothes or bed sheets on the skin) tx: -a combination of psychological therapy, physical therapy, and pharmacologic treatments, sympathectomy (e.g., nonsteroidal anti-inflammatory drugs, gabapentin, corticosteroids, antidepressants, bisphosphonates, topical lidocaine, capsaicin cream). -Referral to a pain clinic may be necessary for patients who do not respond to initial treatments

Factor V Leiden

procoagulant clotting factor - amplifies the production of thrombin → clot formation Mutated factor V resistant to breakdown by activated Protein C - results in hyper-coagulability Symptoms/physical exam - Increased DVT and PE, especially in young patients Diagnosis with activated protein C resistance assay (factor V Leiden specific functional assay) - if positive, confirm with DNA testing. Normal PT/PTT Tx: LMWH bridge to warfarin; long term anti-thrombotic therapy not recommended protein C & S deficiency: -Tx: heparin / oral anticoagulation for life

guillan-barre

sudden-onset, rapidly progressing, bilateral ascending weakness that is characteristic of Guillain-Barré syndrome. Decreased or absent deep tendon reflexes is a characteristic finding on physical examination. Patients may experience muscle aches or cramping, cardiac dysrhythmias, BP instability, facial diparesis, or respiratory failure. Symptoms typically peak one month after onset. Campylobacter jejuni is a causative agent of gastroenteritis and is treated with erythromycin or azithromycin. C. jejuni causes 30-35% of Guillain-Barré cases. C. jejuni lipooligosaccharides are similar to human gangliosides, and infection with C. jejuni may result in antiganglioside antibodies that attack and destroy the myelin sheath and neurons due to molecular mimicry. Less common causes of Guillain-Barré syndrome include other gastrointestinal and respiratory infections such as Epstein-Barr virus, cytomegalovirus, Mycoplasma pneumoniae, and influenza virus. Guillain-Barré is slightly more common in men and is mostly seen in patients > 40 years of age.

neuropathy

sx: Neuropathy affecting the foot musculature may result in clawing of the toes and displacement of the submetatarsal fat pads anteriorly. This displacement results in altered gait and biomechanics that further increase the risk of ulcers over the metatarsal heads, joint subluxation, and periarticular fractures. Decreased or absent ankle jerk reflexes may also be seen on physical examination. -Charcot joint, also known as neurogenic arthropathy screening: All patients diagnosed with type 2 diabetes should be screened for neuropathy at the time of diagnosis. Patients with type 1 diabetes should be screened five years after their diagnosis.

headaches

tension HA: Patient presents with bilateral, nonpulsating, band-like pain PE will show neck muscle tenderness Most commonly caused by stress Treatment is NSAIDs (abortive), TCAs (preventive) Most common type of headache cluster HA: -Cluster headaches are severe, unilateral, periorbital headaches that last between 15-180 minutes. They may occur multiple times per day for several weeks or months. -Middle-aged men are most commonly affected. A family history of headaches or migraines is often absent. -During a cluster headache attack, patients may be restless or aggressive. -RF = CHRONIC SMOKER, worse w/ ETOH*** Ipsilateral lacrimation, conjunctival injection, rhinorrhea, miosis, ptosis, or eyelid edema may be present. The diagnosis for primary headaches is clinical. TX: -abortive treatment of choice for a cluster headache is 100% oxygen via nasal cannula. If 100% oxygen is not readily available, triptan medications (e.g., sumatriptan) or dihydroergotamine mesylate may be administered subcutaneously or intramuscularly as abortive treatment. -For prophylactic treatment of cluster headaches, a short-term corticosteroid along with a calcium channel blocker (e.g., verapamil) may be given. -The corticosteroid is then tapered as the calcium channel blocker takes full effect. migraine: -unilateral -pulsatile -+/- aura -better in dark room

diabetes continued

three diagnostic criteria exist for diabetes: symptomatic hyperglycemia, asymptomatic hyperglycemia, and prediabetes. Diabetes can be easily diagnosed when a patient is symptomatic (has polyuria, polydipsia, thirst, weight loss) and has a random blood glucose of ≥ 200 mg/dL. Both type 1 and type 2 diabetes can be diagnosed this way. In an asymptomatic patient, diabetes (often type 2) can be diagnosed by one of the following criteria: fasting blood glucose ≥ 126 mg/dL on more than one occasion (7.0 mmol/L), two-hour plasma glucose value of ≥ 200 mg/dL (11.1 mmol/L) during a 75 g oral glucose tolerance test (OGTT), or A1C values ≥ 6.5% (48 mmol/mol). In the absence of unequivocal symptomatic hyperglycemia, the diagnosis of diabetes must be confirmed by a repeat test on a subsequent day. The ADA criteria to diagnose prediabetes are as follows: impaired fasting glucose with fasting plasma glucose of 110-125 mg/dL (6.1-6.9 mmol/L), impaired glucose tolerance with two-hour glucose value after a 75 g OGTT of 140-199 mg/dL (7.8-11.0 mmol/L), and A1C values of 5.7 to < 6.5% (39-48 mmol/mol)

prolactinoma

tx: -The first-line treatment is dopamine agonists (bromocriptine, cabergoline). Surgical resection is indicated in adenomas that are refractory to first-line therapy, those with macroadenomas, or those with compressive features (bitemporal hemianopsia, headaches). can be functional (hormone-secreting) or nonfunctional (non-hormone-secreting) and microadenoma (< 1 cm in size) or macroadenoma (> 1 cm in size). A physical exam may show bitemporal hemianopsia. The diagnosis is generally made by elevated serum prolactin levels (> 200 ng/mL). A serum prolactin level > 200 ng/mL is typically associated with overt hypogonadism, subnormal estradiol secretion, and its consequences including amenorrhea, hot flashes, and vaginal dryness. MRI may show a sellar lesion. Serum prolactin can also be elevated in pregnancy, by several medications (estrogens, neuroleptics, opioids, antipsychotics, antidepressants), and nipple stimulation.

Hemolytic Uremic Syndrome (HUS)

↓ Platelets + anemia + renal failure (associated with E.coli O157: H7 and diarrheal illness in a child) Presentation: Post-infection: E.coli or Shigella Children Severe kidney problems