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Chemotherapy

Terminology Adjuvant therapy - given in addition to standard therapy Consolidation therapy - given after induction therapy with multidrug regimens to further reduce tumor burden Induction therapy - initial dose of treatment to rapidly kill tumor cells and send the patient into remission Maintenance therapy - given after induction and consolidation therapies or after the initial standard therapy to kill any residual tumor cells and keep the patient in remission Neoadjuvant therapy - given before the standard therapy for a particular disease Remission - less than 5% tumor burden Salvage therapy - given when standard therapy fails Adjuvant therapies in various cancers Metastasis to bone - bisphosphonates (e.g. zoledronic acid) are given to prevent lytic lesions and pathologic fractures as well as malignant hypercalcemia. Bisphosphonates work by inhibiting osteoclasts and thereby preventing bone breakdown. Breast cancer Tamoxifen , a selective estrogen recep
Recent posts

Arsenic poisoning

Presentation Acute cases present with garlic breath, vomiting, watery diarrhea, and QTc prolongation. If severe, there can be pancytopenia and hepatitis.  Chronic cases present with: sensorimotor neuropathy -- stocking glove distribution with burning sensation, distal weakness, hyporeflexia skin changes -- 1. first there is a change in skin color (hypo/hyperpigmentaiton), 2. later hyperkeratosis (scaling of palms/ soles), 3. Mees lines (horizontal lines on fingernails)  Pathology Arsenic binds to sulfhydryl groups and disrupts cellular respiration and gluconeogenesis.  Sources of arsenic include pesiticides/ insecticides, contaminated water (e.g. well water), and pressure treated wood (e.g. antique furniture).  Diagnosis Urine arsenic levels Treatment Chelation therapy with: Dimercaprol (British anti-Lewisite, BAL) DMSA (meso-2,3-dimercaptosuccinic acid, succimer) Relevant Images Dimercaprol has sulfhydryl groups and arsenic binds to

Acute Intermittent Porphyria (AIP)

Presentation 30 to 40 year old patient has episodes of visceral autonomic dysfunction (typically results in abdominal pain ), sensorimotor neuropathy ( tingling, weakness ), and psychiatric symptoms . Episodes can last anywhere from a few days to weeks. For example 40 year old with acute onset of psychosis (delusions, insomnia, irritability), abdominal pain, and peripheral neuropathy (tingling in hands/ feet). There is usually a family history of mental illness e.g. schizophrenia. On physical exam, the abdomen is soft and usually non-tender or only minimally tender, this is because the abdominal pain is neuropathic. Patients may also have constipation, vomiting, anxiety, and mood changes. The onset is usually when patients are in their 30s and 40s . Pathology Partial deficiency of prophobilinogen deaminase , which is required for heme synthesis. Diagnosis  Elevated urinary porphobilinogen (dark red/ brown urine) Management Glucose in high doses can inhibit heme syn

Photosensitivity reactions

Drug-induced photosensitivity reactions Antibiotics - tetracyclines e.g. doxycycline Antipsychotics - chlorpromazine, prochlorperazine Diuretics - furosemide, hydrochlorothiazide Others - amiodarone, promethazine, piroxicam Photo toxic Reaction drug + ultraviolet radiation -> reactive oxygen species (ROS) produced -> damage cell membranes and DNA result is similar to a sunburn - redness, pain, bullae in sun exposed areas, but often worse.  Photo allergic Reaction drug + ultraviolet radiation -> change in drug structure -> delayed hypersensitivty reaction result is similar to eczema and requires sensitization (previous exposure)

Identifying cardiac auscultation murmurs & associated exam findings

Aortic regurgitation Murmur -- early diastolic murmur Exam findings -- hyperdynamic pulse, bounding or "water-hammer" peripheral pulses Detailed explanations blood regurgitates into the LV from the aorta --> even less blood in the aorta --> decreased DBP --> peripheral arteries "collapse". When the LV contracts the next time it has more blood to pump out -> increased stroke volume -> increased SBP -> peripheral arteries must accomodate this increased flow and pressure and they "expand". Net result "bounding" pulse Aortic stenosis Murmur --  Exam findings -- pulsus parvus et tardus (low amplitude and delayed upstroke) Mitral regurgitation Mitral stenosis Apical diastolic rumble Atrial septal defect Murmur -- widening and fixed splitting of S2, may have midsystolic pulmonary flow murmur Exam findings -- if large, tachypnea. Details ASD -> L to R shunting -> more blood in RA then RV

Hypertensive Complications

Terminology Severe hypertension = blood pressure >/= 180/120 mmHg Hypertensive urgency = severe hypertension without symptoms or acute end-organ damage Hypertensive emergency = severe hypertension with acute, life-threatening, end-organ complications. Malignant hypertension = hypertensive emergency where the end-organ damage presents as retinal hemorrhages, exudates or papilledema Hypertensive encephalopathy = hypertensive emergency where the end-organ damage presents as cerebral edema and non-localizing neurologic symptoms and signs. For example, headaches, nausea, vomiting, restlessness, confusion, agitation, seizures, and even coma. Management Blood pressure should be lowered slowly, 10-20% in the first hour then 5-15% over the next 23 hours. Cerebral ischemia can occur if blood pressure is lowered to fast, resulting in altered mental status and/or generalized seizures.

2 x 2 Contingency Table Calculations and Formulas

Positive predictive value = TP/ (TP + FP) Negative predictive value = TN/ (TN + FN) Sensitivity = TP / (TP + FN) Specificity = TN/ (TN + FP)