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Patients with chronic severe mitral regurgitation have what type of pulse and what hapens to the amplitude

(Choice B) Patients with chronic severe mitral regurgitation have a bounding pulse with a brisk upstroke due to increased LV ejection volumes. Arterial pulses are overall reduced in amplitude in patients with mitral stenosis due to reduced stroke volume.

Sotalol what is it?

(Choice E) Sotalol is a class III antiarrhythmic drug with beta blocker properties and is primarily used for the treatment of atrial and ventricular arrhythmias. It would not be indicated in a patient with a recent myocardial infarction who is in sinus rhythm.

A 75-year-old man is brought to the emergency department due to acute-onset profuse vomiting of large amounts of bright red blood. He has had intermittent, dull epigastric pain for the last 3 months. Medical history is significant for chronic obstructive pulmonary disease with multiple exacerbations and lumbar spinal stenosis. The patient has smoked 1 pack of cigarettes daily for 40 years.Blood pressure is 70/40 mm Hg and pulse is 120/min. Examination shows epigastric tenderness. The patient dies an hour after admission despite resuscitation efforts. Autopsy shows a deep peptic ulcer localized proximally on the lesser curvature of the stomach. The ulcer most likely penetrated which of the following arteries?

- left gastric. Massive hemorrhage with hypovolemic shock is a potential life-threatening complication of peptic ulcer disease (PUD). Most cases of PUD are due to Helicobacter pylori infection or nonsteroidal anti-inflammatory drug use. Other risk factors include smoking, glucocorticoid use, and older age. The resultant inflammation leads to mucosal atrophy and ulcer formation. The left and right gastric arteries run along and perfuse the lesser curvature of the stomach, and are a common source of hemorrhage from penetrating gastric ulcers.

Phenoxybenzamine

-Nonselective α-blocker -Irreversible -Used preoperatively for pheochromocytoma to prevent catecholamine (hypertensive) crisis -Toxicity: orthostatic hypotension, reflex tachycardia

A bifid carotid pulse with brisk upstroke ("spike-and-dome") is characteristic of?

A bifid carotid pulse with brisk upstroke ("spike-and-dome") is characteristic of hypertrophic cardiomyopathy, a condition with dynamic left ventricular outflow tract obstruction during systole. SpO2 in the cardiac chambers remains normal.

A decreased femoral-to-brachial blood pressure ratio is found in?

A decreased femoral-to-brachial blood pressure ratio is found in coarctation of the aorta, which does not alter right ventricular SpO2.

Describe mitral stenosis, what will happens to left atrial cavity, left ventricular cavity size, left ventricular wall thickness, left ventricular relaxation?

A dilated left atrial cavity with normal LV parameters is indicative of mitral stenosis. Patients typically have pulmonary edema in addition to symptoms of right-sided heart failure. Accumulation of amorphous extracellular material is not expected on autopsy. left atrial cavity-dilated, left ventricular cavity size-not dilated, left ventricular wall thickness-normal, left ventricular relaxation-normal

Describe the granulomatosis with polyangitiitis manifestations?

A patient will have chronic constitutional and pulmonary symptoms associated with patchy lung infiltrates/cavitation and laboratory findings of glomerulonephritis (hematuria, increased creatinine). These findings are suggestive of granulomatosis with polyangiitis (GPA), a small vessel vasculitis associated with antineutrophilic cytoplasmic antibodies (ANCA). Patients with GPA generally present with weeks or months of constitutional symptoms (eg, arthralgias, fatigue, low-grade fever, weight loss) and manifestations in the following areas: Upper airway: otitis media, nasal crusting/ulcers, rhinorrhea Lower airway: hoarseness, cough, stridor, hemoptysis, pulmonary infiltrates Kidney: rapidly progressive glomerulonephritis Laboratory evaluation frequently shows anemia of chronic disease due to elevated levels of inflammatory cytokines and renal insufficiency due to glomerulonephritis (eg, microscopic hematuria, red cell casts, negative nitrate/bacteriuria). Chest imaging often reveals patchy lung infiltrates, nodules, and/or cavitations.

A precordial continuous, machine-like murmur indicates? What happens to the pulmonary arterySpO2?

A precordial continuous, machine-like murmur indicates patent ductus arteriosus, which produces isolated pulmonary artery SpO2 elevation.

What is a rectocele and who does it effect?

A rectocele, which occurs when the rectum prolapses into the posterior vaginal wall, usually develops in elderly, multiparous women. Although constipation is common, patients usually describe pelvic pressure and the need to manually push on the vagina or rectum to defecate.

A 44-year-old man is brought to the hospital after being found unresponsive. Temperature is 35.6 C (96.1 F), blood pressure is 120/80 mm Hg, and pulse is 110/min. He is responsive only to pain and has dry mucous membranes. The patient's condition is initially treated with intravenous fluids, and his mental status slowly improves, but urine output decreases and flank pain develops. A renal biopsy reveals marked ballooning andvacuolar degeneration of proximal renal tubules; multiple oxalate crystals are observed in the tubular lumen. Which of the following is most likely responsible for this patient's acute kidney injury? A. Direct tubular injury due to exogenous toxin ingestion B. Direct tubular injury from filtered monoclonal light chains C. Increased endogenous parathyroid hormone production D. Microthrombosis of the glomerular capillaries E. Prerenal azotemia due to splanchnic vasodilation

A. Direct tubular injury due to exogenous toxin ingestion

A 52-year-old postmenopausal woman comes to the office for evaluation of several months of episodic abdominal discomfort and nausea, especially after a fatty meal. She has no past medical history and does not use tobacco, alcohol, or illicit drugs. Her BMI is 33 kg/m2. Physical examination shows a soft, nontender abdomen with normal bowel sounds. Liver span is 8 cm. Murphy sign is negative. Abdominal x-ray reveals no calcifications, but abdominal ultrasound shows a small, non-obstructing gallstone. The patient prefers nonoperative management. Which of the following would best treat this patient's condition? A. bile acid supplements B. cholestyramine therapy C. Estrogen replacement therapy D. Fenofibrate therapy E. Iron chelation therapy F. Phosphate-binding agent G. Rapid weight loss

A. bile acid supplements Medical therapy to dissolve cholesterol gallstones is an option in patients refusing cholecystectomy or with high surgical risk. Hydrophilic bile acids (eg, ursodeoxycholic acid) improve cholesterol solubility by reducing the amount of cholesterol secreted into the bile and increasing biliary bile acid concentration.

ACE inhibitors and angiotensin II receptor antagonists (eg, valsartan) how does it affect the RAAS pathway?

ACE inhibitors and angiotensin II receptor antagonists (eg, valsartan) block the RAAS pathway, causing a feedback increase in serum renin levels.

Mitochondrial vacuolization reduces the cellular capacity for? and it is associated with?

ATP generation and is associated with irreversible injury.

Describe how abciximab works?

Abciximab is a monoclonal antibody that inhibits platelet aggregation by targeting the platelet IIb/IIIa receptor. Heparin is an anticoagulant that potentiates antithrombin III, resulting in the inactivation of thrombin and other factors. Tissue plasminogen activator (alteplase) converts plasminogen to plasmin and causes fibrinolysis. These agents are used in the acute management of cardiovascular events but are not useful for long-term management.

Acetaminophen overdose can cause acute liver failure how?

Acetaminophen overdose can cause acute liver failure through the depletion of intracellular glutathione, leading to an overabundance of hepatotoxic metabolites (eg, N-acetyl-p-benzoquinone imine). Salicylates do not deplete intracellular glutathione like acetaminophen does.

Describe what is achalasia?

Achalasia results from ganglionic degeneration within the esophageal myenteric plexus, leading to the inability to relax the lower esophageal sphincter. It typically causes dysphagia of both solids and liquids and is rare in children. There are no specific endoscopic findings; however, a barium swallow demonstrating a bird-beak appearance of the esophagus is characteristic.

What is acute choleocystitis? Describe what happens? What are the potential complications ?

Acute cholecystitis is caused by gallstone obstruction of the cystic duct in more than 90% of cases. Ingestion of fatty foods then stimulates contraction of the gallbladder against the impacted stone, resulting in severe colicky pain. Mechanical disruption of the gallbladder mucosa and release of inflammatory mediators (eg, lysolecithin, prostaglandins) cause the obstructed gallbladder to become inflamed and edematous. As blood supply to the distended organ becomes compromised, secondary bacterial infection frequently develops. Potential complications include gangrene and perforation, with subsequent formation of a pericholecystic abscess or generalized peritonitis

What does acute respiratory distress syndrome due to? What would the chest xray look like?

Acute respiratory distress syndrome (ARDS), or noncardiogenic pulmonary edema, results from endothelial injury and pulmonary capillary fluid leakage; it is typically preceded by a precipitating event such as aspiration, sepsis, pneumonia, or trauma. The appearance on chest x-ray is similar to ADHF, but pleural effusions are typically less prominent with ARDS (mostly alveolar opacification is seen), and ADHF is more likely in the absence of a recent inciting event for ARDS.

What are additional symptoms due to differential in blood pressure?

Additional symptoms due to this differential in blood pressure include headache, epistaxis, chest pain, and lower extremity claudication.

D. Proliferation of irregularly shape glands and pleomorphic cells

Adenocarcinoma of the lung is generally marked by the proliferation of irregular glands and pleiomorphic cells. Although this condition can cause normocytic anemia, cough, shortness of breath, and weight loss, it is not strongly associated with renal insufficiency or cavitary lung lesions (cavitary lesions are more common with squamous cell carcinoma). In addition, most cases arise in older patients.

What can adenosine be used for?

Adenosine is used as a vasodilator in chemical cardiac stress tests and as a fast acting antiarrhythmic for stopping acute supraventricular tachycardias. Adenosine has an extremely short half-life, and its immediate adverse effects include chest burning, flushing, and transient hypotension.

How does adenosine work?

Adenosine stimulates A1 receptors on the surface of cardiac cells, activating potassium channels and increasing potassium conductance, which causes the membrane potential to remain negative for a longer period. This results in transient slowing of the sinus rate and increased atrioventricular (AV) nodal conduction delay.

Adults with coarctation of the aorta have what and can put them at risk for?

Adults with coarctation of the aorta often have chronic hypertension and are at increased risk of developing life-threatening aneurysms of the aorta (eg, dissection, rupture) and cerebral vessels (ie, intracranial hemorrhage).

How does advanced liver disease lead to renal failure, what are the hallmarks?

Advanced liver disease with portal hypertension and splanchnic vasodilation may lead to renal failure (hepatorenal syndrome). The hallmark of this condition is renal vasoconstriction, resulting in prerenal azotemia. The kidneys are histologically normal and resume function following liver transplantation.

In anemia of chronic disease what are the cytokines and the main predicament?

Although ACD is mediated by a wide range of inflammatory cytokines (eg, IL-1, IL-6, tumor necrosis factor-alpha, interferon gamma), the major player is hepcidin, a small peptide released by the liver in response to inflammation. Hepcidin binds to and inhibits iron channels on enterocytes and reticuloendothelial macrophages, leading to reduced iron absorption in the gut and reduced iron recycling in the reticuloendothelial system (the site of senescent erythrocyte destruction). This significantly reduces circulating serum iron, which limits iron availability for erythropoiesis.

How can you tell PAN from GPA?

Although PAN often affects the kidney, the lung is generally spared. In contrast to GPA, PAN is not associated with ANCA.

Alveolar hemosiderin-laden macrophages are indicative of and what is the cause of them?

Alveolar hemosiderin-laden macrophages indicate alveolar hemorrhage. They most commonly result from chronic elevation of pulmonary capillary hydrostatic pressure in the setting of left-sided heart failure. This patient most likely had heart failure due to left ventricular dysfunction. Impaired forward pumping by the left ventricle causes increased pulmonary capillary pressure that can lead to pulmonary edema and dyspnea. The rise in hydrostatic pressure also disrupts the integrity of the pulmonary capillaries, leading to extravasation of red blood cells and alveolar hemorrhage. The red blood cells are eventually phagocytosed by macrophages, and the iron from hemoglobin is converted to hemosiderin.

Desribe amiodarone?

Amiodarone (and other class III and class IA antiarrhythmic agents) causes lengthening of the cardiac action potential, which manifests as QT interval prolongation on ECG. QT prolongation caused by amiodarone, in contrast to other drugs, is associated with a very low risk of torsades de pointes.

How does amiodarone work?

Amiodarone is a class III antiarrhythmic drug used for the management of a variety of supraventricular and ventricular arrhythmias. Class III drugs predominantly block potassium channels and inhibit the outward potassium currents during phase 3 of the cardiac action potential, prolonging repolarization and total action potential duration (APD). Amiodarone (and other class III and class IA antiarrhythmic agents) causes lengthening of the cardiac action potential, which manifests as QT interval prolongation on ECG. QT prolongation caused by amiodarone, in contrast to other drugs, is associated with a very low risk of torsades de pointes.

What is amlodipine use for and the adverse effects?

Amlodipine is a dihydropyridine CCB that has a predominant vasodilator effect with minimal negative effect on cardiac conduction and contractility. Major adverse effects include lightheadedness, flushing, and peripheral edema.

Describe amyloid cardiomyopathy, what will happens to left atrial cavity, left ventricular cavity size, left ventricular wall thickness, left ventricular relaxation?

Amyloid cardiomyopathy, caused by the accumulation of misfolded amyloid fibrils, appears as pink, amorphous extracellular material on light microscopy. The ventricular walls become stiff and uniformly thickened, leading to impaired diastolic relaxation, a dilated left atrial cavity, and progressive left- and right-sided heart failure. Left ventricular cavity size is typically normal or decreased. left atrial cavity-dilated, left ventricular cavity size- not dilated, left ventricular wall thickness-increased, left ventricular relaxation-impaired

Angiosarcomas are derived from ______. In the liver, they appear grossly as poorly circumscribed, hemorrhagic lesions. Microscopic examination typically shows vascular structures lined by atypical (eg,________) cells that express CD31 which is? ____ is expressed on the surface of endothelial cells and functions in leukocyte migration through the endothelium.

Angiosarcomas are derived from endothelial cells. In the liver, they appear grossly as poorly circumscribed, hemorrhagic lesions. Microscopic examination typically shows vascular structures lined by atypical (eg, hyperchromatic, pleomorphic) cells that express CD31 (ie, platelet endothelial cell adhesion molecule [PECAM1]). PECAM1 is expressed on the surface of endothelial cells and functions in leukocyte migration through the endothelium.

Describe ankylosing spondylitis? What can it incrase risk of?

Ankylosing spondylitis is a chronic inflammatory disease of the axial skeleton characterized by progressive pain and stiffness of the spine, sacroiliitis, and increased risk of aortic regurgitation.

What are the two toxins and what do they cause for C diff?

Antibiotic therapy is the most important risk factor for C difficile infection (CDI) as it can alter the microbiome, leading to a potential overgrowth of pathogenic strains and clinical disease. The organism causes disease by releasing 2 toxins that damage the mucosal lining of the large intestine, leading to diarrhea (toxin A) and necrosis (toxin B) with pseudomembrane formation.

What happens to Aortic compliance as you age?

Aortic compliance progressively decreases with age, especially in those age >65. This leads to an increase in pulse pressure, a slight decrease in diastolic pressure, and the characteristic isolated systolic hypertension commonly seen in the elderly population.

What is the intensity, and the characterized

Aortic regurgitation causes a decrescendo diastolic murmur with maximal intensity occurring just after closure of the aortic valve, when the pressure gradient between the aorta and left ventricle is the highest. The pressure tracing for aortic regurgitation is characterized by loss of the aortic dicrotic notch, steep diastolic decline in aortic pressure, and high-peaking systolic pressures.

Describe how argatroban works?

Argatroban is a direct thrombin inhibitor primarily used in the treatment of heparin-induced thrombocytopenia.

What happens in asthma and chronic obstructive pulmonary disease (COPD) exacerbation are the most frequent causes of? What can you give for acute for acute asthma or COPD?

Asthma and chronic obstructive pulmonary disease (COPD) exacerbation are the most frequent causes of pulsus paradoxus in the absence of significant pericardial disease. Beta-adrenergic agonists control acute asthma and COPD exacerbations by causing bronchial smooth muscle relaxation via increased intracellular cAMP.

Atrial and ventricular septal defects initially involve in what type of shunting and are they cyanotic or acyantotic? What are large septal defects at risk for?

Atrial and ventricular septal defects initially involve left-to-right intracardiac shunting and are therefore acyanotic at birth. Large septal defects are at risk for shunt reversal and Eisenmenger syndrome; however, since the right-to-left shunt is intracardiac, cyanosis and clubbing affect the upper and lower extremities equally.

Describe the location for Atrial fibrillation (most common)?

Atrial fibrillation is recognized by an irregularly irregular rhythm with variable R-R intervals and absence of P waves on ECG. The development of AF most commonly involves ectopic electrical foci in the pulmonary veins that trigger fibrillatory conduction in abnormal (remodeled) atrial tissue.

What are the symptoms of autoimmune hepatitis and what is the histology of it?

Autoimmune hepatitis can cause fatigue, pruritus, and jaundice but is characterized histologically by portal and periportal lymphoplasmacytic infiltration. It is usually diagnosed in women with other autoimmune conditions (eg, celiac disease).

A 52-year-old man comes to the office due to a chronic cough for the last 3 weeks. The patient says, "I haven't been coughing up phlegm, but sometimes I notice some blood on the tissue when I cough particularly hard." He has smoked 2 packs of cigarettes daily for the past 30 years and drinks 3 or 4 cans of beer on weekends. He works as a welder on an assembly line and says his father died of lung cancer at age 70. Physical examination shows right-sided face and arm swelling and engorgement of subcutaneous veins on the same side of the neck. Which of the following veins is most likely obstructed in this patient? A. Axillary B. Brachiocephalic C. External Jugular D. Internal Jugular E. Subclavian F. Superior vena cava

B. Brachiocephalic This patient has symptoms consistent with an obstructed right brachiocephalic (innominate) vein. This may be the result of external compression by an apical lung tumor or thrombotic occlusion as can occur when a central catheter has been in place for an extended period.

A 15-month-old boy is brought to the office by his parents for poor weight gain. The parents have also noticed frequent, large, foul-smelling stools. He was admitted to the hospital for a prolonged bout of bacterial pneumonia 6 months ago. Both parents are healthy and have no similar symptoms. The child was born at term at home. He is at the 20th percentile for length and 3rd percentile for weight. Vital signs are normal. On examination, the child appears thin and has a nontender, nondistended abdomen. Which of the following is most likely present in this patient? A. Decreased fecal calcium content B. Decreased fecal elastase C. Increased fecal calprotectin D. Increased fecal chymotrypsin E. Increased pancreatic bicarbonate

B. Decreased fecal elastase

A 68-year-old woman comes to the office due to recurrent syncopal episodes. The most recent incident occurred 3 days ago while she was walking to her car and lasted about 1 minute. She was able to resume her normal activities afterward although she felt tired. She had no preceding chest pain or palpitations. The patient has had 2 similar syncopal episodes in the past 2 months, along with frequent episodes of intermittent dizziness. Medical history includes hypertension and chronic kidney disease. She takes lisinopril, amlodipine, and clonidine daily. Blood pressure is 155/85 mm Hg and pulse is 44/min. Heart and lung sounds are normal. After the offending medication is discontinued, she has no further syncopal episodes. The drug responsible for this patient's episodes most likely functions through which of the following mechanisms? A. Decreaseing presynpatic release of acetylcholine B. Decreasing presynpatic release of norepinephrine C. Blockade of beta 1 receptors in sinoatrial node D. Blockade of calcium channels in the atrioventricular node E. Blockade of potassium channels in the atrioventricular node

B. Decreasing presynpatic release of norepinephrine

A 35-year-old previously healthy woman comes to the hospital due to increasing shortness of breath and cough. Over the past few months, she has had arthralgias, fatigue, low-grade fever, and weight loss. Laboratory results are as follows: Complete blood count Hemoglobin10.4 g/dL Leukocytes8,000/mm3 Serum chemistry: Blood urea nitrogen28 mg/dL Creatinine 2.7 mg/dL Urinalysis Nitrites-negative Bacteria none Red blood cells 20-30/hpf CT scan of chest is shown in the exhibit. Histologic examination of the lung would most likely reveal which of the following findings? A. Fibrinoid degeneration of the vessel wall with luminal narrowing B. Necrotizing arteritis and focal collections of epithelioid histiocytes C. Necrotizing granuloma with a predominance of eosinophils D. Proliferation of irregularly shape glands and pleomorphic cells

B. Necrotizing arteritis and focal collections of epithelioid histiocytes This patient has chronic constitutional and pulmonary symptoms associated with patchy lung infiltrates/cavitation and laboratory findings of glomerulonephritis (hematuria, increased creatinine). These findings are suggestive of granulomatosis with polyangiitis (GPA), a small vessel vasculitis associated with antineutrophilic cytoplasmic antibodies (ANCA). Patients with GPA generally present with weeks or months of constitutional symptoms (eg, arthralgias, fatigue, low-grade fever, weight loss) and manifestations in the following areas: Upper airway: otitis media, nasal crusting/ulcers, rhinorrhea Lower airway: hoarseness, cough, stridor, hemoptysis, pulmonary infiltrates Kidney: rapidly progressive glomerulonephritis Laboratory evaluation frequently shows anemia of chronic disease due to elevated levels of inflammatory cytokines and renal insufficiency due to glomerulonephritis (eg, microscopic hematuria, red cell casts, negative nitrate/bacteriuria). Chest imaging often reveals patchy lung infiltrates, nodules, and/or cavitations. Although ANCA is positive in >85% of patients with GPA (c-ANCA in particular), it is a non-specific marker. Therefore, tissue biopsy is generally required for diagnosis; histopathology will show a necrotizing arteritis with granulomatous inflammation (eg, epithelioid histiocytes, multinucleated giant cells) and a mixture of surrounding inflammatory cells. Veins and capillaries are also frequently affected.

Describe what BCL2 does? What does the mutation do? How does it present?

BCL2 produces a protein that sits on the outer membrane of mitochondria and controls cell survival and apoptosis. BCL2-activating mutation is common in follicular lymphoma. Although patients with follicular lymphoma often have large abdominal masses, almost all cases are marked by significant peripheral lymphadenopathy and B symptoms (eg, night sweats)

What is BRAF and what does the mutation cause?

BRAF is a protooncogene that produces a protein involved in growth signal transduction from the cell membrane to the interior of the cell. BRAF mutations are most strongly associated with malignant melanoma.

Which drugs provide long term survival in patients with systolic HF?

Beta blockers after stabilization Other drugs that improve long-term survival in patients with systolic HF include ACE inhibitors, angiotensin II receptor blockers, and aldosterone antagonists (eg, spironolactone, eplerenone).

In acute myocardial infarction what is beta blockers used for?

Beta blockers are used in AMI to reduce myocardial oxygen demand by lowering heart rate, cardiac contractility, and afterload. They have been shown to reduce short-term morbidity (eg, recurrent symptoms or reinfarction), minimize infarct size, and improve long-term survival.

How do bile acid resins (bile acid sequestrants work)

Bile acid-binding resins (ie, bile acid sequestrants) work by binding bile acids in the gastrointestinal tract, thereby interfering with the enterohepatic circulation of bile acids and causing increased bile acid excretion. This results in hepatic synthesis of new bile acids, a process that consumes liver cholesterol stores. Hepatic uptake of LDL from the circulation is increased for continued bile acid synthesis. Bile acid production and secretion are increased by 10-fold due to this interruption of the enterohepatic circulation of bile acids. Hepatic cholesterol reduction is an activating factor for HMG CoA reductase and subsequently results in increased hepatic cholesterol synthesis. This effect can be blocked with the addition of a statin drug to the treatment regimen, leading to a greater reduction in LDL levels than with use of either drug alone (synergistic action).

Tetrodotoxin (puffer fish) what is the mechanisms?

Binds to Na+ channels, inhibiting Na+ influx and preventing action potential conduction

Batrachotoxin (South American frogs) what is the mechanisms?

Binds to the Na+ channel, keeping it open and causing persistent depolarization

Ciguatoxin (exotic fish, Moray eel) what is the mechanisms?

Binds to the Na+ channel, keeping it open and causing persistent depolarization

Describe black pigmented stones and what do you they increase and how can you get them?

Black pigment stones arise from conditions that increase the amount of unconjugated bilirubin in bile, which promotes calcium bilirubinate precipitation. This may occur in the setting of chronic hemolysis (eg, sickle cell anemia, β-thalassemia, hereditary spherocytosis) and increased enterohepatic cycling of bilirubin (eg, ileal disease).

How does breat cancer effect the heart?

Breast cancer is one of the most common malignancies to metastasize to the heart, typically causing pericardial effusion that may gradually progress to cardiac tamponade. However, tamponade predominantly affects diastolic filling of the right-sided heart chambers and does not decrease left ventricular ejection fraction.

Describe brugada syndrome?

Brugada syndrome is an autosomal dominant condition that can be associated with mutations in cardiac sodium or L-type calcium channels, leading to characteristic ECG changes (eg, pseudo right bundle branch block, ST-segment elevation in leads V1-V3) and an increased risk of ventricular tachyarrhythmias and sudden cardiac death.

A 34-year-old man is found to have dyslipidemia. His other medical problems include a myocardial infarction 1 week ago. His father died of myocardial infarction at the age of 48 years. Several other family members have had myocardial infarctions and hypertension. The patient smoked cigarettes and drank alcohol occasionally but quit after his myocardial infarction. He is started on simvastatin and cholestyramine. Which of the following best describes the independent effects of simvastatin and cholestyramine, respectively, on hepatic cholesterol synthesis? A. increased and increase B. Increase and decrease C. Decrease and increase D. Decrease and Decrease E. Increase and no change

C. Decrease and increase

This patient with failure to thrive, steatorrhea, and a hospitalization for pneumonia most likely has cystic fibrosis (CF). Is it autosomal or x linke dominant or recessive CF is an autosomal recessive disorder? What does it cause? in

CF is an autosomal recessive disorder in which a defective chloride channel causes the accumulation of thick, dehydrated secretions in multiple organs. In the pancreas, viscous mucus obstructs small ducts and acini, preventing digestive enzymes from reaching the intestinal lumen and leading to progressive pancreatic inflammation and fibrosis. This ultimately causes pancreatic insufficiency, which may be present at birth in patients with CF and typically progresses throughout childhood. Elastase is a pro-enzyme (ie, zymogen) produced by pancreatic acinar cells and activated by trypsin within the duodenal lumen. Because elastase production and secretion are decreased in patients with pancreatic insufficiency, fecal elastase levels are also decreased; the presence of low fecal elastase is an accurate and noninvasive method for diagnosing pancreatic insufficiency of any cause (eg, CF, chronic pancreatitis).

Calcific AS is caused by?

Calcific AS is caused by chronic hemodynamic stress or atherosclerotic inflammation that eventually leads to progressive aortic valve leaflet thickening, calcification, and stenosis.

Describe the effects of calcium channel blockers?

Calcium channel blockers are frequently used in the treatment of several cardiovascular disorders, including hypertension, angina pectoris, and certain cardiac arrhythmias. They inhibit the L-type calcium channel on vascular smooth muscle and cardiac cells and are divided into 2 major categories based on their predominant actions: Dihydropyridines (nifedipine, amlodipine, felodipine) primarily affect arterial smooth muscle, causing vasodilation with little or no effect on cardiac conduction or contractility. Nondihydropyridines (verapamil, diltiazem) affect the myocardium, slowing heart rate (negative chronotropic effect) and reducing contractility (negative inotropic effect).

Describe using Dihydropyridines (eg, nifedipine, amlodipine) vs Nondihydropyridines (eg, verapamil, diltiazem)?

Calcium channel blockers inhibit the L-type calcium channel on vascular smooth muscle and cardiac cells. Dihydropyridines (eg, nifedipine, amlodipine) primarily affect peripheral arteries and cause vasodilation. Nondihydropyridines (eg, verapamil, diltiazem) affect the myocardium and can cause bradycardia and slowed atrioventricular conduction

What is calprotectin?

Calprotectin is a protein derived from neutrophils that is released into the stool of patients with inflammatory diarrhea (eg, ulcerative colitis, Crohn disease).

Carbamoyl phosphate is a in which cycle? what is it synthesized by?

Carbamoyl phosphate is a urea cycle intermediate synthesized by carbamoyl phosphate synthetase I, which transfers an ammonia molecule from glutamine or glutamate to a phosphorylated bicarbonate. Carbamoyl phosphate production is decreased in patients with advanced liver disease.

When are beta blockers contraindicated?

Cardioselective beta blockers with predominant action on beta-1 receptors (eg, metoprolol, atenolol, bisoprolol, nebivolol) are safe in patients with stable obstructive lung disease and are the beta blocker of choice in these patients. Combined beta and alpha receptor blockers (eg, carvedilol, labetalol) are also well tolerated and have been used safely in patients with COPD.

Carotid sinus hypersensitivity what is it?

Carotid sinus hypersensitivity is most commonly seen in elderly men and involves an exaggerated vasovagal response to tactile stimulation of carotid sinus baroreceptors (eg, adjusting a shirt collar or necktie). The resulting increase in parasympathetic output leads to a prolonged sinus pause that contributes to the excessive drop in blood pressure, leading to transient loss of cerebral perfusion that manifests as presyncope (eg, lightheadedness) or syncope.

What is cast nephropathy common seen?

Cast nephropathy is usually seen in multiple myeloma and is due to large amounts of monoclonal free chain deposition in the kidney. Interstitial nephritis (inflammation in the area surrounding the renal tubules) is most commonly due to drugs (eg, analgesics, antibiotics), recent infection, or systemic conditions (eg, sarcoidosis).

Describe how resins work?

Cationic exchange resins (eg, cholestyramine) decrease LDL cholesterol by interfering with the enterohepatic circulation of bile acids. Bile acid binding resins can significantly increase triglyceride levels in patients with pre-existing hypertriglyceridemia. In addition, cationic exchange resins have not been proven to prevent cardiac events.

What is celiac disease and what do you see on biopsy?

Celiac disease is a chronic malabsorptive disorder caused by a hypersensitivity to gluten, a protein found in wheat, barley, and rye. Gliadin (a gluten component) triggers an immune-mediated reaction causing villous atrophy, crypt hyperplasia, and intraepithelial lymphocyte infiltration. The atrophy in celiac disease causes impairment of nutrient absorption in the duodenum and proximal jejunum, regions where the concentration of gluten is the highest. (Choice A)

describe il-12

Cell-mediated immunity is stimulated by production of IL-12 from activated antigen-presenting cells. IL-12 stimulates CD4+ helper T cells to differentiate into the Th1 subtype. Th1 cells then secrete IL-2 and interferon-γ (IFN-γ). IL-2 stimulates the autocrine proliferation of Th1 cells and furthers Th1 recruitment. IFN-γ activates macrophages and promotes granuloma formation. Activated macrophages and T cells also produce tumor necrosis factor-alpha, further assisting in leukocyte recruitment and granuloma maintenance. ex sarcoidoisis

What is the characteristic histopathology of takayasu arteritis?

Characteristic findings on histopathology include mononuclear infiltrates and granulomatous inflammation of the vascular media, leading to arterial wall thickening and occlusion.

chordal ruputure would lead to?

Chordal rupture would lead to flail mitral leaflet with mitral valve prolapse and mitral regurgitation. Mitral regurgitation associated with chordal rupture would lead to a holosystolic decrescendo murmur.

When would you have a widened pulse pressure?

Chronic aortic regurgitation (AR) causes a reduction in diastolic blood pressure and a compensatory increase in left ventricular stroke volume. These changes create a high-amplitude, rapid rise-rapid fall pulsation (ie, widened pulse pressure) and the other characteristic findings of AR (eg, head bobbing, "pistol-shot" femoral pulses).

What happens to the kidney when you have chronic hemolysis?

Chronic hemolysis with breakdown of iron-containing erythrocytes can also lead to iron deposition in the kidney (hemosiderosis), which can interfere with proximal tubule function and cause interstitial scarring and cortical infarcts. The hemosiderosis combined with microvascular thrombosis can increase the risk of chronic kidney disease.

Which drug provides direct dilation of arteries and inhibition of platelet aggregation?

Cilostazol reduces platelet activation by inhibiting platelet phosphodiesterase, the enzyme responsible for the breakdown of cAMP. It is also a direct arterial vasodilator. The net effect is a decrease in claudication symptoms and an increase in pain-free walking distances in patients with peripheral arterial disease (PAD). Patients with PAD should be initiated on a graded exercise program, which has also been shown to improve symptoms.

Describe and name class IA drugs?

Class IA (procainamide, quinidine), IB (lidocaine), and IC (flecainide) antiarrhythmic drugs inhibit sodium-dependent (phase 0) depolarization and slow conduction. Class IA and IC agents also have some potassium-blocking activity and can cause prolongation of the action potential (seen mostly with class IA agents). However, all class I drugs have prominent sodium channel-blocking activity, which would blunt the blue tracing in the above graph.

Class III antiarrhythmics predominantly work how?

Class III antiarrhythmic drugs (eg, amiodarone, sotalol, dofetilide) predominantly block potassium channels and inhibit the outward potassium currents during phase 3 of the cardiac action potential, thereby prolonging repolarization and total action potential duration.

Describe what class III antiarrhythmics drugs, name and describe what they do?

Class III antiarrhythmics (eg, dofetilide) bind to and block the potassium channels responsible for phase 3 repolarization of the cardiac action potential, which can put at risk and increase risk of?

Class III antiarrhythmics (eg, dofetilide) bind to and block the potassium channels responsible for phase 3 repolarization of the cardiac action potential. can prolong the QT interval and increase the risk of polymorphic ventricular tachycardia (ie, torsade de pointes), a serious cause of cardiac syncope.

What is the classical presentation of celiac disease?

Classic celiac disease presents after introduction of gluten into the diet (between age 6-24 months) with symptoms of malabsorption (eg, diarrhea, steatorrhea, flatulence, nutrient deficiencies, weight loss). Other manifestations include delayed puberty and short stature in children and anemia in adults.

What are the classical endoscopic findings for

Classic endoscopic findings include stacked, circular, ringlike indentations; linear furrowing; and scattered, small, whitish papules (ie, eosinophilic microabscesses). Biopsies demonstrate eosinophilic mucosal infiltration.

Classically, the stimulation of acid secretion within the stomach is separated into three phases, what are they and describe them?

Classically, the stimulation of acid secretion within the stomach is separated into three phases: cephalic, gastric, and intestinal. The cephalic phase is mediated primarily by cholinergic and vagal mechanisms, and is triggered by the thought, sight, smell, and taste of food. The gastric phase is mediated by the presence of gastrin (which stimulates histamine secretion and therefore, indirectly, acid secretion), and is triggered by the chemical stimulus of food and distension of the stomach. The intestinal phase is initiated when protein-containing food enters the duodenum, but this phase plays only a minor role in stimulating gastric acid secretion.

Common adverse effects of nondihydropyridine calcium channel blockers (eg, diltiazem, verapamil) include?

Common adverse effects of nondihydropyridine calcium channel blockers (eg, diltiazem, verapamil) include constipation, bradycardia, atrioventricular block (negative chronotropic effect), and worsening of heart failure in patients with left ventricular systolic dysfunction (negative inotropic effect).

What are complications of aortic coarctation include cerebral and aortic aneurysm.

Complications of aortic coarctation include cerebral and aortic aneurysm. Cerebral aneurysm with life-threatening rupture causing subarachnoid hemorrhage is likely due to chronic hypertension. Aortic aneurysms usually develop near the site of coarctation due to embryologic vessel wall abnormalities and may lead to dissection or fatal rupture.

When is coarctation critcal and when is it less severe?

Critical coarctation (severe narrowing) often presents in the neonatal period with heart failure and cardiogenic shock. However, less severe narrowing allows for distal (but decreased) perfusion to the lower extremities and may present with only asymptomatic upper extremity hypertension in children or adults.

Cromolyn sodium what does help to manage and how?

Cromolyn sodium inhibits mast cell degranulation and release of histamine and leukotrienes. It is used occasionally for management of chronic asthma but is not effective for immediate relief of acute asthmatic or COPD exacerbations.

Cystic medial necrosis predisposes to the formation?

Cystic medial necrosis predisposes to the formation of thoracic aortic aneurysms with an increased risk of aortic dissection. It can also cause dilation of the aortic root leading to aortic regurgitation.

A 34-year-old woman who recently emigrated from Russia comes to the physician due to weakness, exertional dyspnea, and orthopnea. On cardiac auscultation, a snap followed by a rumbling diastolic murmur is heard over the cardiac apex. The snap most likely occurs nearest to which of the following points on the cardiac pressure-volume loop? A. B. C. D. E. F.

A 48-year-old man comes to the office for a follow-up visit. He was diagnosed with hypercholesterolemia 6 months ago and has been strictly following dietary and lifestyle modifications as advised. The patient has no other medical problems. He does not use tobacco, alcohol, or illicit drugs. His father has diabetes mellitus and coronary artery disease. The patient's blood pressure is 126/70 mm Hg and BMI is 33.1 kg/m2. Physical examination is normal. Laboratory studies show a current LDL level of 190 mg/dL. Which of the following should be obtained before starting statin therapy in this patient? A. Apolipoprotein-B level B. Complete blood count C. Lipoprotein lipase activity assay D. Liver transaminase levels E. Serum cortisol level F. Serum creatinine?

D. Liver transaminase levels This patient has a severe elevation in his LDL level. This degree of hyperlipidemia, especially with a family history of coronary artery disease, suggests familial hypercholesterolemia and confers a very high risk for cardiovascular events. HMG-CoA reductase inhibitors (statins) are the first-line therapy for most patients with hypercholesterolemia and have been proven to reduce the risk of cardiac events. The statins are structural analogs of HMG-CoA and competitively inhibit HMG-CoA reductase, the enzyme responsible for the rate-limiting step in cholesterol synthesis. Serious side effects of statins include myopathy and hepatitis. Although mild elevations of liver enzymes are common, significant liver injury (aspartate transaminase/alanine transaminase levels more than 3 times the upper limit of normal) is seen in less than 1% of patients and is usually reversible if the medication is discontinued. Liver function tests are recommended before starting statin therapy; otherwise, routine monitoring is not necessary unless symptoms of hepatic injury develop (eg, fatigue, malaise, anorexia). (Choice A) Apolipoprotein-B (Apo-B) is a structural protein found in atherogenic lipoprotein particles. Each lipoprotein particle contains only a single Apo-B molecule, so measurement of Apo-B levels can quantify the LDL particle count. Patients with increased LDL particle counts are at greater risk for cardiovascular events. However, measurement is of limited clinical utility and would not change management in this case. (Choice B) Statin medications do not cause any significant hematologic toxicity. (Choice C) Lipoprotein lipase deficiency can cause familial hypertriglyceridemia (heterozygous deficiency) and chylomicronemia (homozygous deficiency) syndromes. These conditions present with elevated serum triglyceride levels but do not cause elevation in LDL levels. (Choice E) Because cholesterol is a precursor in the synthesis of adrenocortical and gonadal steroid hormones, statin medications can, in theory, cause hypogonadism or hypoadrenalism. Clinically, however, there are no significant alterations in serum cortisol or gonadal steroid levels unless patients are also on other adrenal enzyme inhibitors (eg, ketoconazole, aminoglutethimide). (Choice F) Statins have no significant renal side effects. In rare instances, they can cause rhabdomyolysis, which can precipitate acute renal failure; however, this occurs less commonly than hepatic dysfunction and would be associated with myalgias and myoglobinuria.

A 62-year-old woman comes to the office due to a change in bowel habits. For 2 months, she has had bowel movements once every 5 or 6 days. The patient describes her stools as hard and lumpy and of small volume; defecation is uncomfortable. She has no trouble passing gas and has no other symptoms, including no nausea, vomiting, or weight changes. The patient was admitted to the hospital 3 months ago for acute diverticulitis, and her hospital course was complicated by new-onset atrial fibrillation. Colonoscopy a month after hospitalization revealed sigmoid diverticulosis but no masses or polyps. The patient takes fiber supplements, diltiazem, and apixaban. She does not use tobacco or alcohol. Vital signs are within normal limits. Cardiac auscultation reveals an irregular heart rhythm but no murmurs. Abdominal examination is significant for mild distension. Which of the following best explains this patient's symptoms? A. Alterations in colonic microbiome B. Gastrocolic reflex impairement C. Inappropriate contraction of pelvic floor muscles D. Medication adverse effects E. Posterior vaginal wall prolapse F. Sigmoid volvulus

D. Medication adverse effects Constipation is an exceedingly common gastrointestinal condition with a wide variety of underlying etiologies (eg, autonomic neuropathy, hypothyroidism, electrolyte abnormalities). In this patient who developed constipation after new-onset atrial fibrillation, the most likely etiology is a drug effect related to diltiazem. Diltiazem and verapamil are non-dihydropyridine calcium channel blockers that decrease conduction velocity in the sinoatrial and atrioventricular nodes and are often used in the management of atrial fibrillation. Constipation, a common adverse effect, occurs due to inhibition of the colonic migrating motor complex, resulting in slowed contractions of colonic smooth muscle. This is not typically seen with dihydropyridine calcium channel blockers (eg, amlodipine, nifedipine).

A 62-year-old man comes to the emergency department due to acute-onset constipation. His last bowel movement was 4 days ago; before that time, his stools were always regular. Review of systems is positive for dry cough, increasing low back pain, a 9-kg (20-lb) weight loss in the past month, and increasing difficulty with urination. He has smoked 2 packs of cigarettes daily for 30 years. Vital signs are within normal limits. Point tenderness is elicited with palpation over the lower spine. Bilateral lower extremity weakness is present, and sensation is impaired in the perineal region. Chest x-ray reveals a right lung mass. Dysfunction of which of the following nerves best explains this patient's constipation? A. Greater splanchnic nerve B. Ilioinguinal nerve C. Lesser splanchnic nerve D. Pelvic splanchnic nerves E. Vagus nerve

D. Pelvic splanchnic nerves This patient with a lung mass has progressive low back pain, bilateral lower extremity weakness, bowel/bladder dysfunction, and impaired perineal sensation; this presentation is highly concerning for cauda equina syndrome. The cauda equina is formed from lumbosacral nerve roots which can be compressed by epidural metastasis (most commonly from lung cancer), trauma, or disc herniation. The symptoms of cauda equina syndrome result from disruption of nerve roots to the sciatic nerve (eg, lower extremity weakness, radicular low back pain), pudendal nerve (eg, saddle anesthesia), and/or pelvic splanchnic nerves. The pelvic splanchnic nerves (S2-S4) provide parasympathetic innervation to the hindgut, bladder, and urinary sphincters that promotes peristalsis, bladder emptying, and pelvic floor relaxation during defecation. Constipation and difficulty urinating are prominent symptoms in cauda equina syndrome due to loss of parasympathetic input to the bowel and bladder.

A 67-year-old man comes to the emergency department due to progressive shortness of breath and chest tightness. He has had no lightheadedness or syncope. The patient takes lisinopril for hypertension and metformin for type 2 diabetes mellitus. He has smoked a pack of cigarettes daily for the last 40 years. The blood pressure cuff is inflated to 140 mm Hg and the pressure is released very slowly. At 120 mm Hg, intermittent Korotkoff sounds are heard only during expiration. At 100 mm Hg, Korotkoff sounds are heard throughout the respiratory cycle. Item 1 of 2 This physical examination finding can be seen in which of the following conditions? A. Aortic valve disease B. Mitral valve disease C. Myocardial ischemia D. Pericardial disease E. Peripheral valvular disease

D. Pericardial disease Systemic arterial pressure normally falls by <10 mm Hg during normal inspiration. Pulsus paradoxus refers to an exaggerated drop (>10 mm Hg) in systolic blood pressure during inspiration. It is detected by inflating a blood pressure cuff above systolic pressure and gradually deflating it. The difference between the systolic pressure at which Korotkoff sounds first become audible during expiration and the pressure at which they are heard throughout all phases of respiration quantifies pulsus paradoxus (20 mm Hg in this patient). Inspiration causes an increase in systemic venous return, resulting in increased right heart volumes. Under normal conditions, this results in expansion of the right ventricle into the pericardial space with little impact on the left side of the heart. However, in conditions that impair expansion into the pericardial space (eg, acute cardiac tamponade), the increased right ventricular volume occurring with inspiration leads to bowing of the interventricular septum toward the left ventricle. This leads to a decrease in left ventricular (LV) end-diastolic volume and stroke volume, with a resultant decrease in systolic pressure during inspiration.

A 34-year-old man comes to the office to establish medical care. The patient recently emigrated from Eastern Asia. He has no chronic medical conditions but reports intermittent abdominal discomfort and episodic diarrhea over the past several months. He has also had occasional dry cough and throat irritation. Physical examination shows no abnormalities. Serologic testing for Strongyloides stercoralis IgG is positive. Detection of which of the following is most suggestive of active infection by the pathogen in this patient? A. multioculated liver cyst B. Perianal egg deposition C. Proglottids in the stool D. Rhabditiform larvae in the stool E. Trophozoites and cysts in the stool

D. Rhabditiform larvae in the stool Strongyloides stercoralis infection occurs when filariform (infective) larvae in contaminated soil penetrate human skin, travel to the lungs through the bloodstream/lymphatics, and ascend the tracheobronchial tree to be swallowed. They then enter the small intestine, mature, and reside in the mucosa. Rhabditiform (noninfective) larvae are excreted into the stool and can be detected on stool microscopy, which is diagnostic.

A 72-year-old man comes to the clinic due to episodic lightheadedness. The episodes typically occur in the morning when the patient adjusts his shirt collar or tightens his tie and he briefly feels like he is going to pass out. The patient had a thyroidectomy 5 years ago for a large benign tumor. He also has hypertension and takes amlodipine. Blood pressure is 135/78 mm Hg and pulse is 78/min. Physical examination reveals no heart murmurs or carotid bruits. ECG shows normal sinus rhythm. The patient is given an ambulatory ECG monitoring device. During symptomatic episodes, the device is most likely to show which of the following? A. Atrial Fibrillation B. Mobitz type II second-degree heart block C. Paroxysmal supraventricular tachycardia D. Sinus Pause E. Ventricular tachycardia

D. Sinus Pause This patient with episodes of presyncope (eg, lightheadedness, feeling of impending loss of consciousness) that occur when he adjusts his shirt collar or necktie most likely has carotid sinus hypersensitivity (CSH). The condition results from overly sensitive carotid baroreceptors that stimulate an excessive vasovagal response to tactile stimulation. CSH is most commonly seen in elderly men; underlying carotid atherosclerotic disease and prior neck surgery (eg, thyroidectomy) are risk factors.

Having a decreased RAP and LVEDP can occur in what setting?

Decreased RAP and LVEDP can occur in the setting of intravascular volume depletion.

Describe diastolic blood pressure and systolic blood pressure.

Diastolic blood pressure is the baseline hydrostatic pressure in the arterial system and is directly related to systemic vascular resistance (SVR) and arterial blood volume. Systolic blood pressure is the summation of diastolic pressure and pulse pressure

Describe the difference between the transposition of great arteries vs patent ductus arteriosus presents?

Differential clubbing and cyanosis can occur with uncorrected transposition of the great arteries when there is extracardiac shunting through a PDA to allow mixing between the two parallel blood circuits. However, the cyanosis will be present in the upper extremities and not the lower extremities, as oxygenated blood will flow across the PDA into the descending aorta (ie, postductal oxygen saturation is higher).

Differential cyanosis (ie, postductal < preductal oxygen saturation) in a neonate suggests?

Differential cyanosis (ie, postductal < preductal oxygen saturation) in a neonate suggests right-to-left shunting across a patent ductus arteriosus, such as in persistent pulmonary hypertension of the newborn (PPHN). Patients with PPHN typically have an underlying pulmonary disorder with respiratory distress and strong femoral pulses.

How does Digoxin work?

Digoxin inhibits the Na+-K+-ATPase pump in myocardial cells, resulting in an increase in intracellular sodium, which leads in turn to a rise in intracellular calcium concentration. Digoxin does not affect potassium channels and has minimal effect on potassium efflux from myocardial cells during the action potential.

Dilated cardiomyopathy what chemo drugs can cause it and how does it compensate for increase in ventricular volume?

Dilated cardiomyopathy results from a direct insult to cardiomyocytes that impairs their contractile function. There is an increase in left ventricular volume that is initially compensated for by the Frank-Starling mechanism and later by eccentric hypertrophy to maintain cardiac output. However, overwhelming wall stress eventually leads to marked impairment in myocardial contractile function, reduced cardiac output, and symptomatic decompensated heart failure. The elevated left ventricular end-diastolic pressure (LVEDP) is transmitted backward to the pulmonary veins and capillaries, leading to pulmonary edema (evidenced by crackles on lung auscultation).

Describe dilated cardiomyopathy, what will happens to left atrial cavity, left ventricular cavity size, left ventricular wall thickness, left ventricular relaxation?

Dilated left atrial and ventricular cavities with normal LV wall thickness is consistent with dilated cardiomyopathy, which results from contractile dysfunction after direct myocardial insult (eg, infection, chronic alcohol toxicity). LV relaxation may be normal or impaired depending on the disease progression and underlying etiology. Interstitial fibrosis would be prominent on microscopy in addition to findings specific to the underlying cause (eg, inflammatory cells in viral myocarditis). left atrial cavity-dilated, left ventricular cavity size-dilated, left ventricular wall thickness-normal, left ventricular relaxation-impaired

name non-dihydropyridine calcium channel blockers and what do they do?

Diltiazem and verapamil are non-dihydropyridine calcium channel blockers that decrease conduction velocity in the sinoatrial and atrioventricular nodes and are often used in the management of atrial fibrillation.

When you lose alot of fluid from diuretics what does that lead to?

Diuretic-induced hypovolemia leads to decreased renal blood flow, which also increases renin levels and activates RAAS.

Dobutamine how does it work?

Dobutamine is a beta adrenergic agonist with predominant activity on beta-1 receptors, weaker activity on beta-2 receptors, and minimal activity on alpha-1 receptors. It is used for management of refractory heart failure associated with severe left ventricular systolic dysfunction and cardiogenic shock. Stimulation of beta adrenergic receptors results in increased production of cAMP in target cells and causes the following effects: Positive inotropy and chronotropy: Increased cardiac contractility (potent effect) and heart rate (weaker effect), leading to increased cardiac output (improves end-organ perfusion) and decreased left ventricular filling pressures (improves pulmonary congestion/edema) Mild vasodilation: Decreased systemic vascular resistance that often causes a slight reduction in blood pressure; this avoids the increase in afterload seen with other vasopressor/inotropic agents (eg, norepinephrine) but limits its usefulness in severely hypotensive patients The strong inotropic effect of dobutamine significantly increases myocardial oxygen consumption, which can trigger or exacerbate myocardial ischemia. As such, dobutamine should not be used routinely in patients with decompensated heart failure. However, in patients with cardiogenic shock, this drawback is often outweighed by improvement in cardiac output and end-organ perfusion.

Drug-induced renal interstitial inflammation can be seen to cause acute kidney injury when?

Drug-induced allergic interstitial nephritis is an eosinophilic AKI usually triggered by beta-lactam antibiotics and nonsteroidal anti-inflammatory drugs. It occurs after continual exposure (eg, several days), and eosinophiluria is usually present.

Drug induced glomerular injury due to immune complex formation can be seen to cause acute kidney injury when?

Drug-induced lupus, a rare adverse effect of hydralazine, causes acute kidney injury (AKI) due to immune complex-mediated glomerulonephritis. However, an active urine sediment (eg, red cells, white cells, casts) and other systemic signs of lupus (eg, rash, pleuritis) would be expected.

What is dubin- johnson syndrome?? What do you expect to happen to bilrubin conjugation, bilirubin storage and excretion?

Dubin-Johnson syndrome is a benign, inherited disorder of bilirubin metabolism characterized by defective hepatic excretion of bilirubin into the biliary system. Bilirubin conjugation is normal, but defective excretion results in increased hepatocyte storage of bilirubin, resulting in dense liver pigmentation.

Duchenne muscular dystrophy, describe disorder?

Duchenne muscular dystrophy is an X-linked disorder caused by mutations in dystrophin, a structural membrane protein that stabilizes the plasma membrane of myocytes. Patients typically present with progressive proximal muscle degeneration and weakness. Additional features may include cardiomyopathy and conduction abnormalities.

A 6-month-old boy is brought to the emergency department due to lethargy for several hours. His mother says he is usually a "very active baby," and she is afraid that he is "coming down with something." The patient's birth history is unremarkable, and he was born at 38 weeks gestation. He is afebrile. Blood pressure is 70/44 mm Hg, pulse is 240 beats/min, and respirations are 52/min. The patient appears pale and is perspiring. Capillary refill time is less than 2 seconds. The lungs are clear to auscultation. No murmurs are heard. An ECG shows a regular heart rate of 240/min with narrow QRS complexes and no identifiable P waves. Which of the following is the most likely cause of this patient's hypotension? A. Decreased effective intravascular volume B. Decreased myocardial contractility C. Decreased peripheral vascular resistance D. Left to right intracardiac shunting E. Shortening of ventricular diastole

E. Shortening of ventricular diastole This patient is pale, lethargic, and diaphoretic with ECG findings consistent with supraventricular tachycardia (SVT), the most common pediatric arrhythmia. Normally, depolarization impulses originate at the sinoatrial node and travel through the atrial myocardium to the atrioventricular (AV) node, where the signal pauses to allow ventricular filling following atrial contraction. The impulse then continues through the His-Purkinje system to the ventricular myocardium. SVT occurs when an impulse originates at an abnormal focus above the ventricles, most commonly a reentrant circuit within the AV node (ie, AV nodal reentry tachycardia). Heart rate is elevated (usually >150/min in adults or >220/min in infants), but rhythm is usually regular. QRS complexes are narrow, and P waves are generally buried within the QRS complex due to retrograde atrial depolarization occurring in conjunction with anterograde ventricular depolarization. With persistent tachycardia, ventricular diastole shortens, allowing less time for ventricular relaxation and filling. Stroke volume and cardiac output decrease, leading to hypotension and poor peripheral perfusion. Infants may become altered (eg, lethargic, poor feeding) and develop signs of heart failure (eg, tachypnea, crackles, hepatomegaly).

A 64-year-old man comes to the emergency department due to chest discomfort and shortness of breath. Medical history includes hypertension, type 2 diabetes mellitus, and severe osteoarthritis of the left knee. The patient is an active smoker with a 20-pack-year smoking history. He undergoes dobutamine infusion with simultaneous cardiac imaging. The following is seen: Before infusion: normal left ventricular contractility, ejection fraction 60% During infusion: decreased apical contractility, ejection fraction 45% Five minutes after infusion: normal left ventricular contractility, ejection fraction 60% Which of the following best explains the observed findings? A. Coronary artery occlusion due to plaque thrombosis (9%) B. Coronary artery vasospasm (10%) C. Focal myocardial fibrosis (3%) D. Normal myocardial contractile response (18%) E. Supply-demand mismatch due to fixed coronary stenosis (57%) A. Coronary artery occlusion due to plaque thrombosis B. Coronary artery vasospasm C. Focal myocardial fibrosis D. Normal myocardial contractile response E. Supply-demand mismatch due to fixed coronary stenosis

E. Supply-demand mismatch due to fixed coronary stenosis Stable angina results from fixed coronary artery stenosis in the setting of atherosclerotic coronary artery disease (CAD). Such a stenosis limits blood supply to the downstream myocardium, which, during periods of increased myocardial oxygen demand (eg, exercise), can cause a mismatch of oxygen supply and demand that manifests as anginal symptoms (eg, chest pain, shortness of breath). Pharmacologic stress testing can be useful in diagnosing atherosclerotic CAD. Dobutamine, a beta-1 agonist, increases heart rate and contractility to mimic the increase in myocardial oxygen demand that occurs with exercise. Myocardium that is unable to obtain sufficient blood flow to meet the increased oxygen demand typically demonstrates a transient decrease in contractility (ie, wall motion defect), often leading to reduced ejection fraction. This patient with a transient wall motion defect localized to the cardiac apex most likely has a fixed atherosclerotic lesion that limits blood flow to that area of myocardium. (Choice A) Coronary artery occlusion due to plaque rupture and thrombosis leads to acute myocardial infarction (MI). Because of total coronary artery occlusion and a completely blocked myocardial oxygen supply, a persistent (before, during, and after dobutamine infusion), rather than transient, wall motion defect would be expected. (Choice B) Vasospastic angina is due to coronary artery vasospasm and can mimic stable angina that results from atherosclerotic CAD; however, vasospastic angina typically occurs in relatively young patients (age <50). In addition, dobutamine has only a small agonistic effect on alpha-1 receptors and is unlikely to trigger coronary vasospasm. (Choice C) Focal myocardial fibrosis typically results from previous MI. Contractility is impaired in the fibrosed myocardium, leading to a persistent wall motion defect similar to that expected with acute MI. (Choice D) In the normal state, dobutamine boosts myocardial contractility, and the rise in myocardial oxygen demand is met by increased myocardial oxygen supply via increased blood flow. Therefore, the normal response to dobutamine infusion is a transient increase in ejection fraction.

Eosinophilic esophigitis (EOE) is common in here and what do they have a history of? What symptoms do they have?

EOE is most common in males with a history of atopic conditions (eg, eczema, asthma). Patients often have intermittent solid food dysphagia. Other symptoms include vomiting, reflux, and chest and upper abdominal pain. When EOE is severe, food can become trapped in the esophagus (ie, esophageal food impaction), requiring urgent upper endoscopy to remove the impacted food bolus.

Who is

Describe how enterobius vermicularis migrate? How can you make a diagnosis and what are the symptomes?

Enterobius vermicularis (pinworms) migrate out of the anus at night to deposit eggs on the surrounding perianal folds. Eggs can be detected by examining a piece of adhesive tape briefly applied to the perianal region shortly after the patient awakens. Perianal itching usually occurs.

corticosteroids what does help to manage and how

Eosinophil degranulation would be impaired by corticosteroids, which play an important role in treatment of acute asthma or COPD exacerbations. However, beta agonists provide immediate relief, whereas corticosteroids would take several hours to a few days to take effect.

What is the pathogenesis of eosinophili esophaitis?

Eosinophilic esophagitis Pathogenesis Chronic Th2 cell-mediated disorder triggered by food antigens Eosinophilic infiltration of the esophageal mucosa - This patient with a history of solid food dysphagia has an esophageal food impaction due to eosinophilic esophagitis (EOE). EOE is a chronic Th2 cell−mediated disorder triggered by food antigen exposure. When activated, Th2 cells release chemokines (eg, IL-13, IL-5) that stimulate eosinophilic recruitment to the esophageal mucosa.

Necrotizing granuloma with a predominance of eosinophils

Eosinophilic granulomatosis with polyangiitis (Churg-Strauss) is marked by the formation of necrotizing granulomas with a predominance of eosinophils. Although renal insufficiency and glomerulonephritis occur in a minority of patients, almost all patients have years of preceding asthma. In addition, cavitary lesions are uncommon.

What are the epidemiology and clinical features of eosinophilic esophagitis?

Epidemiology Men > women History of atopic conditions Clinical features Intermittent dysphagia Reflux, vomiting, chest or abdominal pain Esophageal food impaction

Esmolol how does it work?

Esmolol is a rapid-acting, short-duration beta blocker (class II antiarrhythmic) that slows the rate of discharge of sinus or ectopic pacemakers and increases the refractory period of the AV node. It has no effect on potassium efflux from myocardial cells.

Esmolol what does it do?

Esmolol is a rapidly acting, short-duration beta blocker (class II antiarrhythmic) that slows the rate of discharge of sinus or ectopic pacemakers and increases the refractory period of the AV node. It has no effect on QT interval

Esmolol is used in IV fusion for?

Esmolol is a selective beta-1 receptor blocker that is given by intravenous infusion. It is first-line therapy for acute aortic dissection as it has a short half-life (allowing for easy dose titration) and reduces shear stress in 2 ways: Negative inotropy decreases LV contraction velocity. This decreases the rate of blood ejection and reduces stroke volume (Choice E) to decrease the rise in blood pressure with each contraction (ie, decreased rate and magnitude of blood pressure change). Negative chronotropy decreases heart rate, subjecting the aortic wall to fewer LV contractions per minute (ie, decreased number of blood pressure changes).

What is the presentation of esophageal SCC?

Esophageal SCC typically presents with progressive solid-food dysphagia and weight loss. Chronic gastrointestinal blood loss may result in iron deficiency anemia.

What effect does estrogen and progesterone have on cholesterol and gall stone formation?

Estrogen increases cholesterol secretion and progesterone reduces bile acid secretion, ultimately causing bile to become supersaturated with cholesterol. Progesterone also slows gallbladder emptying, which causes bile stasis and further promotes gallstone formation.

Ethylene glycol itself is relatively nontoxic; however, it is metabolized to glycolic acid and oxalic acid, resulting in its various toxicities. Acute kidney injury occurs due to both glycolic acid, and oxalic acid, how?

Exaggerated vascular smooth muscle contraction is the cause of and with what other symptoms?

Exaggerated vascular smooth muscle contraction (eg, in response to cold or vibration) causes Raynaud phenomenon. Symptoms are typically acute and episodic and manifest as a triphasic color change (pallor, cyanosis, erythema) in the distal extremities.

What are examples of intracardiac right-to-left shunts ?

Examples of intracardiac right-to-left shunts include a patent foramen ovale in PPHN and a ventricular septal defect in tetralogy of Fallot. Because the mixing of deoxygenated and oxygenated blood occurs within the heart in these cases, preductal and postductal saturations would be equally low.

Describe how ezetimibe works?

Ezetimibe inhibits cholesterol absorption from the gastrointestinal tract, but evidence for reduction in cardiovascular events is mixed, and benefits over statin monotherapy are likely minimal. It may be considered for patients who cannot take statins due to significant hepatotoxicity or myopathy, or who have very high LDL levels despite statin therapy.

What are factor development of edema include:

Factors that favor development of edema include: Elevated capillary hydrostatic pressure: Higher capillary pressures increase plasma filtration into the interstitium, particularly in dependent tissues. Causes include arteriolar dilation (eg, dihydropyridine calcium channel blockers) and impaired venous return (eg, high central venous pressure, venous thrombosis). Decreased plasma oncotic pressure: Plasma proteins (eg, albumin) generate oncotic pressure that pulls interstitial fluid back into the capillary bed venules. Edema develops in conditions with decreased albumin levels (eg, nephrotic syndrome, cirrhosis, malnutrition). Sodium and water retention: Increased intravascular volume raises capillary hydrostatic pressure and decreases plasma oncotic pressure (dilutes plasma proteins). Causes include kidney disease and heart failure. Lymphatic obstruction: Decreased lymphatic return impairs removal of excess interstitial fluid. Common causes of lymphatic obstruction include filariasis, invasive malignancies, and iatrogenic etiologies (eg, surgical lymph node dissection and radiation therapy).

What is Familial hypocalciuric hypercalcemia?

Familial hypocalciuric hypercalcemia is a benign disorder caused by mutations in the calcium-sensing receptor in the parathyroid gland and kidneys. Higher calcium levels are required to suppress secretion of PTH, leading to mild hypercalcemia and hypocalciuria. PTH is high-normal or mildly elevated.

What do fibrates do?

Fibrates activate peroxisomal proliferator-activated receptor alpha, a transcription factor that increases lipoprotein lipase activity. Fibrates decrease triglyceride levels and raise HDL levels. However, fibrates are inferior to statins for reducing cardiovascular events and are primarily used to prevent pancreatitis in patients with very high triglyceride levels.

What effect does fibrates have on bile and therefore gallstones?

Fibrates increase cholesterol content in bile, which increases the risk of gallstones.

Fixed LV outflow tract obstruction what happens to the pulse and ejection?

Fixed LV outflow tract obstruction (eg, valvular aortic stenosis) can cause pulsus parvus et tardus, which is palpable as a slow-rising, low-amplitude pulse due to diminished stroke volume (pulsus parvus) and prolonged LV ejection time (pulsus tardus).

Fixed splitting of S2 occurs with? what happens to SpO2?

Fixed splitting of S2 occurs with an atrial septal defect (ASD), which causes increased SpO2 in the right atrium compared with the vena cava but identical right atrial and ventricular SpO2. VSD may result in wide splitting of S2 due to increased right ventricular volume causing delayed closure of the pulmonary valve; however, fixed splitting of S2 is more indicative of an ASD, as equalization of left and right atrial pressures minimizes the respiratory variation in ventricular blood flow.

Describe focal aware seizures?

Focal aware seizures (previously simple partial seizure): Patients are aware and interactive but have symptoms corresponding to the involved area of the brain (eg, face or limb twitching/jerking - frontal lobe motor cortex, auditory/olfactory hallucinations - temporal lobe, visual phenomena - occipital lobe).

Describe focal impaired awareness seizures? What are the symptoms?

Focal impaired awareness seizures (previously complex partial seizures): Patients appear awake but do not interact appropriately (eg, blank stare) and frequently engage in repetitive, stereotyped automatisms (eg, lip smacking, hand wringing, repeating words).

Focal seizures with imparired awareness are typical manifestations of what types of epilepsy? What are they preceded?

Focal seizures with impaired awareness are the typical manifestation of temporal lobe epilepsy, the most common type of recurrent seizure disorder. Seizures are often preceded by a distinctive aura (eg, uneasy epigastric sensation, unpleasant olfactory hallucinations) that localizes the origin of the epileptiform discharges to the mesial temporal lobe (eg, hippocampus, amygdala, parahippocampal gyrus). The disorder is usually due to underlying hippocampal sclerosis (ie, mesial temporal sclerosis), which is associated with childhood febrile seizures.

A 15-year-old boy comes to the office for a follow-up appointment. Since early childhood, he has suffered from recurrent respiratory infections and chronic diarrhea. The patient has been hospitalized several times for parenteral antibiotic treatment. Current prescribed medications include pancreatic enzyme therapy and a number of dietary supplements. Physical examination shows decreased proprioception and hyporeflexia in the lower extremities. Laboratory findings are suggestive of mild hemolytic anemia. Which of the following conditions is the most likely cause of these findings? A. Niacin deficiency B. Riboflavin deficiency C. Thiamine deficiency D. Vitamin A deficiency E. Vitamin C over use F. Vitamin D deficiency G. Vitamin E deficiency H. Vitamin K deficiency

G. Vitamin E deficiency

A 44-year-old woman comes to the office due to indigestion. The patient says she often develops right upper quadrant abdominal discomfort and nausea with fatty meals, which subside spontaneously after several hours. She does not use tobacco, alcohol, or illicit drugs. The patient immigrated to the United States from Nepal 10 years ago. Abdominal ultrasound reveals numerous gallstones, and she undergoes elective laparoscopic cholecystectomy. The stones in her gallbladder have very low cholesterol content and appear small, dark, and spiculated. Which of the following conditions most likely predisposed this patient to gallstone formation? A. Chronic hemolysis B. metabolic syndrome C. multiparity D. oral contraceptive use E. rapid weight loss

Gallstones are formed by the aggregation of bile constituents and are categorized as cholesterol stones, pigment stones, or mixed stones. Pigment gallstones, which account for only 10%-25% of gallstone cases in the United States, are most common in rural Asian populations. These stones can be brown to black and arise from conditions that increase the amount of unconjugated bilirubin in bile, which promotes calcium bilirubinate precipitation. Brown pigment stones are associated with biliary tract infections (microbes producing β-glucuronidases), whereas black stones occur in the setting of chronic hemolysis (eg, sickle cell anemia, β-thalassemia, hereditary spherocytosis) and increased enterohepatic cycling of bilirubin (eg, ileal disease). Grossly, black pigment stones are usually present in significant numbers and are small, spiculated, and friable. Because these stones contain high amounts of calcium carbonates and phosphates, they are often radiopaque and appear on x-ray. (Choices B, C, D, and E) Obesity/metabolic syndrome, multiparity, oral contraceptive use, and rapid weight loss are significant risk factors for development of cholesterol gallstones. Educational objective:Black pigment stones arise from conditions that increase the amount of unconjugated bilirubin in bile, which promotes calcium bilirubinate precipitation. This may occur in the setting of chronic hemolysis (eg, sickle cell anemia, β-thalassemia, hereditary spherocytosis) and increased enterohepatic cycling of bilirubin (eg, ileal disease).

Which Germline mutations is associated with familial adenomatous polyposis?

Germline mutations in the adenomatous polyposis coli (APC) tumor suppressor gene are associated with familial adenomatous polyposis (FAP). FAP causes innumerable colon polyps and colon cancer. Patients typically have hematochezia.

This patient had self-resolving scleral icterus and isolated indirect hyperbilirubinemia associated with a period of stress. These findings are consistent with?

Gilbert syndrome, the most common inherited disorder of bilirubin metabolism.

Alteration of the blood pressure-flow relationship in renal arterioles happens when?

Giving a drug like hydralazine to a chronic hypertensive

Necrotizing arteritis and focal collections of epithelioid histiocytes is indicative of?

Granulomatosis with polyangiitis is an ANCA-associated systemic vasculitis that typically presents with upper (eg, purulent nasal discharge) and lower (eg, cavitary lung lesion) respiratory manifestations and renal insufficiency due to glomerulonephritis. Biopsy typically reveals a necrotizing arteritis with granulomatous inflammation (eg, epithelioid histiocytes, multinucleated giant cells) and lack of immunoglobulin/complement deposition.

Where does granulomatous inflammation of the media occur in large vessels?

Granulomatous inflammation of the media occurs in the large vessel vasculitides Giant cell arteritis (temporal arteritis) and Takayasu arteritis. Giant cell arteritis typically affects patients age >50 and presents with unilateral headache, jaw claudication, and transient vision loss. Takayasu arteritis usually affects young women of Asian descent and presents with diminished pulses often accompanied by angina and/or carotid artery pain

A 74-year-old man comes to the office for a follow-up visit for hypertension. His last visit was a year ago. He has no chest pain, shortness of breath, leg swelling, or dizziness. The patient is compliant with his medications and can tolerate a moderate level of physical activity. Blood pressure is 145/75 mm Hg and pulse is 67/min and regular. Auscultation findings at the base of the heart are depicted in the exhibit below. A. Ankylosing spondylitis B. Chordal rupture C. Coronary artery disease D. Cystic medial necrosis E. Infective Endocarditis F. Rheumatic Fever G. Right Ventricular failure H. Valvular calcification

H. Valvular calcification The diagram above depicts a crescendo-decrescendo systolic murmur peaking in midsystole, characteristic of aortic or pulmonic stenosis. The most common cause of aortic stenosis (AS) in elderly patients (age >70) is degenerative calcification of the aortic valve leaflets.

What is hemochromatosis? What is it typically associated with?

Hemochromatosis leads to excessive hepatic iron storage, which results in visible iron deposits within hepatocytes. It is typically associated with diabetes, skin hyperpigmentation, arthralgias, and cardiomyopathy.

Hepatic cavernous hemangiomas are common benign vascular lesions. What does it show on microscopy?

Hepatic cavernous hemangiomas are common benign vascular lesions. Microscopy shows a well-circumscribed proliferation of dilated vascular structures that are lined by endothelial cells lacking atypia.

Herpes simplex virus esophagitis is characterized histologically by? Who does it typically occur in? What do you see on endoscopy?

Herpes simplex virus esophagitis is characterized histologically by eosinophilic intranuclear inclusions within esophageal squamous cells. It typically occurs in immunocompromised patients and results in severe odynophagia. Endoscopy demonstrates ulcerations with a volcano-like appearance.

the direct effect of norepinephrine on heart rate--what happens?

However, the direct effect of norepinephrine on heart rate is counteracted by an indirect, baroreceptor-mediated reflex bradycardia that occurs following the increase in peripheral resistance. The combined result of these effects is often an unchanged or even decreased heart rate.

What drugs caueses drug induced lupus?

Hydralazine Isoniazid Procainamide Minocycline Quinidine

hyperammonemia is due to?

Hyperammonemia in advanced liver failure occurs as a direct result of the cirrhotic liver's inability to metabolize nitrogenous waste products. Ammonia crosses the blood-brain barrier and causes excess glutamine to accumulate within astrocytes. This decreases the amount of glutamine available for conversion to glutamate in the neurons, resulting in disruption of excitatory neurotransmission.

Hyperparathyroidism causes hypercalcemia, causes?

Hyperparathyroidism causes hypercalcemia, which predisposes patients to calcium stone (eg, calcium oxalate) formation.

Where do you see onion skin appearing, concentric thickening of the arteriolar wall?

Hyperplastic arteriolosclerosis is characterized by thickening of the arteriolar wall due to the concentric proliferation of smooth muscle cells and reduplicated basement membranes, giving the arterioles an onion-skin appearance. These changes occur as an adaptive response of arterioles to severe (malignant) hypertension.

For asthma what do you expect to see histologically/

Hyperreactivity of airways to environmental allergens occurs in asthma. Microscopic analysis of sputum may reveal Curschmann spirals, which represent spiral-shaped mucus plugs.

This patient died from an intracranial hemorrhage due to a ruptured cerebral aneurysm. What increases a risk of aneurysm?

Hypertension, genetic conditions (eg, Ehlers-Danlos syndrome), and lifestyle factors (eg, cigarette smoking) increase the risk of aneurysm development.

how can hyperthyroidism lead to hypercalcemia?

Hyperthyroidism can cause hypercalcemia due to increased osteoclastic bone resorption, but serum calcium in hypothyroidism is usually normal.

IL-10 is a cytokine involved in

IL-10 is a cytokine involved in the downregulation of immune responses.

IL-5 is a product of?

IL-5 is a product of Th2 cells

Ibutilide what is it?

Ibutilide is a class III antiarrhythmic drug (potassium channel blocker) used for acute termination of atrial flutter or atrial fibrillation. Like other class III antiarrhythmics, ibutilide causes prolonged QT interval that can precipitate a deadly arrhythmia (torsade de pointes).

Describe what triggers Gilbert syndrome? What happens to bilirubin conjugation, hepatocyte bilrubin storage, and excretion?

In Gilbert syndrome, a genetic mutation results in reduced enzymatic activity of UDP glucuronosyltransferase and therefore decreased bilirubin conjugation . Triggers associated with increased bilirubin production (eg, stress, illness, hemolysis) result in episodic exacerbations of indirect hyperbilirubinemia, as seen in this patient. Because bilirubin excretion into the bile duct is normal in Gilbert syndrome, hepatocyte bilirubin storage is also normal, as is liver histology (

Where do you see lipid filled intimal plaques ?

In atherosclerosis Lipid-filled intimal plaques that bulge into the arterial lumen are seen in patients with atherosclerosis.

What happens to a radiotracer if a patient has acute choleocytisis?

In patients with a patent cystic duct, the gallbladder will be seen as the radiotracer accumulates and concentrates within (image C). In acute or chronic cholecystitis, the radiotracer will be taken up by the liver with progressive excretion into the common bile duct and proximal small bowel, but the gallbladder will not be visualized due to the obstruction (image A and B).

What happens to the patient with chronic hypertension has a hypertensive urgency given hydralazine?

In patients with long-standing hypertension, a chronic autoregulatory shift in the blood pressure-flow relationship occurs, affording less perfusion (flow) at any given pressure. Therefore, excessively rapid correction of blood pressure toward normal may induce relative ischemia.

In severe in tetraology of fallot , what happens to keep circulation?

In severe TOF, critical pulmonary stenosis or atresia limits blood flow from the right side of the heart to the pulmonary circulation for oxygenation. Instead, blood reaches the pulmonary vascular bed via retrograde flow from the aorta through the DA. Without flow through the DA, affected neonates are unable to oxygenate blood. These patients are cyanotic after birth, as in this neonate, and require immediate administration of prostaglandin E1 to maintain patency of the DA.

most gallstones are due to the ________, which usually precipitates out of bile with calcium salts and mucin, forming _______, as seen in this patient.

In the United States, most gallstones are due to the supersaturation of cholesterol, which usually precipitates out of bile with calcium salts and mucin, forming white or yellow cholesterol stones, as seen in this patient. Cholesterol stone formation occurs due to the following: Increased cholesterol synthesis: Hypercholesterolemia, caused by diet, genetics, diabetes mellitus, medications (eg, oral contraceptives), or obesity (increased HMG-CoA reductase activity), results in hypersecretion of cholesterol into the bile. Gallbladder hypomotility: Pregnancy, medications (eg, somatostatin), prolonged fasting, parenteral nutrition, and spinal cord injury lead to gallbladder stasis, which promotes excessive water resorption from bile and concentration of cholesterol. Decreased bile acid synthesis (or recirculation): Fibrates (eg, fenofibrate) inhibit bile acid synthesis, increasing cholesterol concentration within the bile. Decreased bile acid resorption at the ileum (eg, due to Crohn disease) also promotes cholesterol concentration. Increased calcium or mucin concentration: Rapid weight loss (eg, gastric bypass) promotes increased calcium and mucin concentrations in the bile, which trap cholesterol crystals and promote stone formation.

How does HDL removed cholesterol?

In the direct pathway, HDL delivers cholesterol esters directly to the liver via a scavenger receptor (SCARB1) on the hepatocyte cell membrane. In the indirect pathway, the cholesterol in HDL is transferred to low-density lipoprotein (LDL) and very low-density lipoprotein (VLDL) by the cholesteryl ester transfer protein.

What are the two ways the kidneys do blood flow autoregulation?

In the kidneys, blood flow autoregulation involves 2 key mechanisms: Myogenic response: Afferent glomerular arterioles reflexively constrict when they sense greater stretch forces (high BP). Tubuloglomerular feedback: High arterial pressure causes hyperfiltration (↑ glomerular filtration rate), increasing sodium and chloride delivery to the macula densa, which secretes vasoactive mediators (eg, adenosine) to constrict the afferent arterioles

what is the histopathology for thromboangitis obliterans describe what happens or cause of it?

In thromboangiitis obliterans, chronic exposure to tobacco products is thought to cause direct endothelial injury or trigger a delayed-type hypersensitivity reaction against the endothelium. Histopathology shows highly cellular, inflammatory intraluminal thrombi (ie, containing neutrophils, multinucleated giant cells) in the arteries and veins with sparing of the vessel wall and internal elastic lamina. This segmental, thrombosing vasculitis often extends contiguously into veins and nerves, a feature rarely seen in other types of vasculitis.

Describe the patients with VSD the transition from in utero to birth

In utero, vascular resistance against left- and right-sided cardiac outflow is nearly equal. At birth, once the placenta is no longer responsible for oxygenation, pulmonary vascular resistance drops and systemic vascular resistance increases.In patients with VSD, this transition causes shunting of blood from the LV to the RV due to increased left-sided cardiac pressure relative to right-sided pressure. The unrestricted blood flow to the RV causes increased pressure in the RV (Choices B and D) and allows a large volume of blood from the LV to reenter the pulmonary circulation; this high volume of recirculating blood leads to left-sided volume overload with increased pressure in the LV and left atrium (Choices A and C). Right atrial pressure is unchanged.

Increased LV mass with a dilated LV cavity, decreased LV ejection fraction, and normal LV relaxation are consistent with

Increased LV mass with a dilated LV cavity, decreased LV ejection fraction, and normal LV relaxation are consistent with dilated cardiomyopathy. Normal LV mass and cavity size with preserved ejection fraction and impaired LV relaxation describe restrictive cardiomyopathy; the LV walls are stiffened but are not typically thickened. Both conditions are likely to lead to symptomatic heart failure with jugular venous distension and pulmonary edema (evidenced by crackles on lung auscultation).

Increased LV mass with normal LV relaxation and normal (or somewhat increased) LV cavity size and ejection fraction are consistent with?

Increased LV mass with normal LV relaxation and normal (or somewhat increased) LV cavity size and ejection fraction are consistent with athlete's heart, which describes physiologic cardiac changes (eg, LV cavity enlargement and wall thickening) that improve cardiac function in response to intense endurance training. A murmur consistent with HCM is not expected in athlete's heart.

Increased LV mass with small LV cavity size, decreased ejection fraction, and impaired ventricular relaxation occurs in ?

Increased LV mass with small LV cavity size, decreased ejection fraction, and impaired ventricular relaxation occurs in severe aortic stenosis. The fixed obstruction created by the stenotic valve leads to pressure overload and concentric LV hypertrophy, and also restricts stroke volume to decrease ejection fraction. The murmur of aortic stenosis is similar to that of HCM but is differentiated by a decrease in intensity with maneuvers that decrease (rather than increase) LV preload (eg, abrupt standing, Valsalva strain phase).

Increased blood oxygen saturation between 2 right-sided vessels or chambers indicates the presence of?

Increased blood oxygen saturation between 2 right-sided vessels or chambers indicates the presence of a left-to-right shunt. If the abnormal oxygen increase occurs between the right atrium and the right ventricle, a ventricular septal defect (VSD) is likely present. Small VSDs produce a holosystolic murmur that is loudest over the lower left sternal border.

Infectious endocarditis can cause what valvular disease?

Infectious endocarditis of the aortic or mitral valve typically causes aortic or mitral regurgitation, respectively. Aortic regurgitation leads to an early diastolic murmur, best heard over the lower left sternal border or right second interspace with the patient sitting and leaning forward with breath held in full expiration. Mitral regurgitation causes a holosystolic murmur best heard at the cardiac apex in the left lateral decubitus position.

Intestinal tapeworms are made of?

Intestinal tapeworms (eg, Taenia solium, Taenia saginata, Diphyllobothrium latum) are flatworms made up of multiple segments (proglottids). These are shed from the distal end of the worm and can be detected in the stool of infected individuals. Most cases are asymptomatic.

The major genomic abnormality in pancreatic ductal adenocarcinoma is? What other cancers can have KRA activating mutations?

KRAS-activating mutation, which allows tumor cells to grow and divide without input from the cellular milieu due to aberrant activity that relays a continuous growth signal to the nucleus. Because KRAS mutations are one of the earliest oncogenic mutations in pancreatic adenocarcinoma, tests for KRAS abnormalities are being developed to help with early detection. Many colorectal cancers and non-small cell lung cancers also have KRAS-activating mutations.

Left-to-right shunts through septal defects and PDAs are characterized

Left-to-right shunts through septal defects and PDAs are characterized by oxygenated blood crossing back into the right-sided circulation. Therefore, cyanosis does not occur. (Choices D and F)

Leuprolide is used in management of? .

Leuprolide is a synthetic analog of gonadotropin-releasing hormone (GnRH). Continuous administration suppresses release of LH and FSH. Leuprolide is used in management of prostatic cancer, precocious puberty, and endometriosis.

Lidocaine what does it do?

Lidocaine is a class IB antiarrhythmic drug that acts by blocking sodium channels and inhibiting phase 0 depolarization. It does not prolong the QT interval.

Lidocaine is occasionally used for?

Lidocaine is occasionally used in the management of symptomatic ventricular arrhythmias, usually in the setting of acute myocardial infarction. It is not used to treat atrial arrhythmias.

What are lower airway manifestations?

Lower airway: hoarseness, cough, stridor, hemoptysis, pulmonary infiltrates

What is the difference between large patent ductus arteriosus complicated by Eisenmenger syndrom vs large septal defcts and tetraology of fallot?

Lower extremity differential clubbing and cyanosis without pulse discrepancy is caused by a large patent ductus arteriosus complicated by Eisenmenger syndrome (reversal of shunt flow from left-to-right to right-to-left). In contrast, intracardiac right-to-left shunting in patients with large septal defects and Tetralogy of Fallot results in whole-body cyanosis.

What do you expect to see in squamous cell carcinoma of the lungs?

Malignant transformation of bronchial epithelial cells underlies the development of most types of lung cancer. Histopathology typically shows hyperchromatic nuclei and poorly organized cell structure, such as in squamous cell carcinoma of the lung.

What are manifestations of PNH?

Manifestations of PNH include the following: Fatigue and jaundice due to hemolytic anemia (elevated bilirubin and lactate dehydrogenase, low haptoglobin, hemoglobinuria [which may be nocturnal]) Thrombosis at atypical sites (eg, hepatic, portal, or cerebral veins) possibly due to the release of prothrombotic factors from lysed red blood cells and platelets (mesenteric vein thrombosis may explain this patient's abdominal pain) Pancytopenia due to stem cell injury

What is the most common arrythmia in wolff-parkinson white syndrome?

Many patients with an accessory conduction pathway can be asymptomatic and are diagnosed only when a WPW pattern is incidentally recognized on ECG. However, some patients will develop symptomatic arrhythmias. Atrioventricular reentry tachycardia (AVRT), a type of paroxysmal supraventricular tachycardia, is the most common arrhythmia that occurs with WPW. AVRT results from a rapid reentrant circuit that typically travels down the AV node to the ventricles and back up the accessory pathway, with patients often experiencing palpitations and a racing heart.

What is octeotride, what's it used for?

Medical therapy with octreotide can be used to control symptoms. Octreotide is a synthetic analog of somatostatin with a longer half-life. It acts on somatostatin receptors and inhibits secretion of many hormones and hormone-like substances. Octreotide is also used to inhibit secretory diarrhea in VIPomas (pancreatic endocrine tumors).

Membranous glomerulonephritis can be associated with?

Membranous glomerulonephritis can be associated with systemic lupus erythematosus, drugs (eg, nonsteroidal anti-inflammatory drugs [NSAIDs]), hepatitis B and C, or solid tumor malignancies (eg, lung, prostate, gastrointestinal).

Minimal change disease can be associated with ?

Minimal change disease can be associated with drugs (eg, NSAIDs), hematologic malignancies (eg, lymphoma, leukemia), or allergens (eg, fungi).

How do you characterize the sound from mitral stenosis?

Mitral stenosis is characterized by an opening snap followed by a rumbling diastolic murmur that is best heard over the cardiac apex.

Ventricular tachycardia most commonly originates from ? What would you see on ECG?

Monomorphic ventricular tachycardia most commonly originates from areas of ischemic myocardium; however, it can sometimes originate from nonischemic sites in the papillary muscles or right ventricular outflow tract. ECG of ventricular tachycardia typically demonstrates regular R-R intervals and wide QRS complexes.

Mucosal cyanosis and fingernail clubbing may be observed in?

Mucosal cyanosis and fingernail clubbing may be observed in cyanotic congenital heart disease or as late features of ASDs or VSDs (eg, Eisenmenger syndrome). Blood flow across the VSD in Eisenmenger syndrome is right to left due to elevated pulmonary vascular resistance, resulting in decreased SpO2 in the left ventricle.

For multiple myeloma nephropathy, what can it cause. What is the presentation? What would you see on biopsy?

Multiple myeloma can cause light-chain cast nephropathy due to obstruction of the proximal tubules. This causes ATN, but biopsy demonstrates eosinophilic (light-chain) casts. It also typically occurs in older patients and presents with hypercalcemia and anemia; altered mentation is unexpected

When there is an MI what happens to the right ventricle?

Myocardial infarction (MI) involving the left ventricle (LV) commonly leads to scarring and a sustained reduction in contractile function; however, contractile function of the right ventricle (RV) almost always returns to normal following MI. Some of the reasons for protection of the RV from infarction include: The relatively small muscle mass and afterload of the RV create less oxygen demand and necessitate lower oxygen extraction at rest. This allows for a large capacity to increase oxygen extraction during periods of ischemia. The relatively low systolic pressure of the RV (eg, ≤25 mm Hg) allows for coronary perfusion throughout the cardiac cycle; during MI, this enables the RV to pull blood flow from collateral vessels during both systole and diastole. In contrast, the high systolic pressure of the LV (eg, 120 mm Hg) blocks coronary blood flow of the LV walls during systole, allowing for perfusion during diastole only.

Myocardial ischemia or infarction can lead to what happening to pressure?

Myocardial ischemia or infarction can lead to decreased systemic blood pressure or hypotension due to reduced cardiac output

Describe what determins myocardial oxygen demand vs supply?

Myocardial oxygen demand is determined by heart rate, blood pressure (afterload), left-ventricular end-diastolic volume (preload), and cardiac contractility, whereas myocardial oxygen supply is determined by coronary blood flow.

Describe myoxomas?

Myxomas are the most common primary cardiac neoplasm and usually arise within the left atrium. The tumors typically cause position-dependent obstruction of the mitral valve, leading to a mid-diastolic murmur and symptoms of decreased cardiac output (eg, dyspnea, syncope). Constitutional symptoms (eg, fever, weight loss) may also be present. Histologically, the tumors demonstrate scattered cells within a mucopolysaccharide stroma and blood vessels with hemorrhage.

Nectrotizing inflammation of medium-sized arteries with systemic manifestations is seen in?

Necrotizing inflammation of medium-sized arteries is seen in polyarteritis nodosa, which is characterized by multisystem involvement (eg, glomerulonephritis, skin lesions, neuropathy, bowel ischemia, myositis).

Neutrophil elastase-mediated alveolar septal destruction is indicative of and what would you see histologically?

Neutrophil elastase-mediated alveolar septal destruction underlies the pathogenesis of emphysema, which can occur with smoking or alpha-1 antitrypsin deficiency. Microscopy shows cystic enlargement of the airspaces with loss of the normal lobular architecture.

Describe how niacin works?

Niacin (vitamin B3) given in pharmacologic doses is the most effective agent for raising HDL levels, but does not reduce the risk of cardiovascular events and is associated with adverse effects (eg, flushing, hyperglycemia). It is primarily used for patients who have failed other lipid-lowering drugs.

Nondihydropyridine CCBs exert their primary action by?

Nondihydropyridine CCBs exert their primary action by blocking the L-type calcium channels, thereby decreasing phase 0 depolarization and conduction velocity in the sinoatrial and AV nodes. This leads to slowing of the sinus rate and slowing of conduction through the AV node, which can cause bradycardia and varying degrees of AV block. The drugs also have a negative inotropic effect and are relatively contraindicated in patients with left ventricular systolic dysfunction. Constipation, which is typically more prominent with verapamil than diltiazem, likely occurs due to reduced contraction of colonic smooth muscle.

What is the preferred pharmacologic treatment for septic shock?

Norepinephrine, an adrenergic agonist, is the preferred pharmacologic treatment for septic shock as it predominately stimulates a1, a2, and B1 receptors, with little influence on B2 receptors.

What happens in normal bilirubin metabolism?

Normal bilirubin metabolism begins with hepatic uptake of unconjugated bilirubin produced from red blood cell turnover. Within the liver, UDP glucuronosyltransferase conjugates bilirubin with glucuronic acid, after which conjugated bilirubin is excreted into bile canaliculi.

Nuclear shrinkage (pyknosis), fragmentation, and dissolution characterize what state of a injury to the cell?

Nuclear shrinkage (pyknosis), fragmentation, and dissolution characterize irreversible injury of the cell.

Obstructive pulmonary diseases are associated with for xray?

Obstructive pulmonary diseases (eg, chronic obstructive pulmonary disease) are associated with hyperinflated lungs and a flattened diaphragm. Asthma is an exception as the chest x-ray is typically normal between exacerbations.

Describe how omega-3 work?

Omega-3 essential fatty acids are sometimes used for hyperlipidemia treatment. They cause a decrease in serum triglycerides and a slight increase in HDL concentration but do not appear to significantly reduce cardiovascular events.

What does a chest xray look like for pneumothorax?

On chest x-ray, pneumothorax is demonstrated by a white, visceral pleural line with an absence of peripheral pulmonary markings. The mediastinum is often shifted away from the affected side in tension pneumothorax.

If given a pressure volume loop where would you identify the opening snap?

On the left ventricular pressure-volume loop, the opening snap occurs during mitral valve opening at the end of isovolumetric relaxation, and it is followed by a diastolic rumble during diastolic filling.

Describe what and pathogenesis of osler nodes?

Osler nodes are tender, violaceous nodules typically located in the pulp of fingers and toes. The pathogenesis of Osler nodes is immune-complex deposition in the skin.

What are other potential complications of PUD (Peptic ulcer disease)

Other potential complications of PUD include penetration into other adjacent structures (eg, biliary tract, colon), gastric outlet obstruction, and free wall perforation with peritonitis.

Why do patients with pancreatic insufficiency?

Pancreatic insufficiency is common in cystic fibrosis because thick, viscous secretions in the pancreas block digestive enzymes, leading to malabsorption (eg, steatorrhea, failure to thrive). The presence of low fecal elastase is an accurate and noninvasive method for diagnosing pancreatic insufficiency.

What is the triad for Paroxysmal nocturnal hemoglobinuria?

Paroxysmal nocturnal hemoglobinuria is due to a gene defect that leads to uncontrolled complement-mediated hemolysis. The classic triad includes hemolytic anemia (hemoglobinuria), pancytopenia, and thrombosis at atypical sites. Chronic hemolysis can cause iron deposition in the kidney (hemosiderosis).

Describe which congenital heart diseases causes left to right intracardial shunt? If left untreated what could happen?

Patent ductus arteriosus and atrial and ventricular septal defects create a left-to-right intracardial shunt that, if untreated, may lead to right-to-left shunting (ie, Eisenmenger syndrome) due to pulmonary hypertension. This may increase risk of a paradoxical thromboembolism from the venous to arterial circulation directly to the brain, causing an ischemic stroke

Patients with anemia of chronic disease cause what type of anemia and what labs will be elevated and reduced?

Patients with ACD typically develop normocytic or slightly microcytic anemia with a low reticulocyte response. Total iron-binding capacity is generally reduced due to cytokine-mediated suppression of transferrin. Treatment of the underlying condition (eg, antiretroviral therapy) often ameliorates or resolves ACD.

Describe AVNRT?

Patients with AVNRT have 2 distinct AV nodal conduction pathways: a fast pathway with a long refractory period and a slow pathway with a short refractory period. During normal conduction, an impulse from the atria travels down both the fast and slow pathways, and the impulse from the slow pathway is blocked by the long refractory period of the fast pathway, allowing organized conduction of one impulse to the ventricles. On occasion, an impulse from the atria (eg, premature atrial contraction) occurs while the fast pathway is still refractory, traveling down only the slow pathway. If the fast pathway is no longer refractory by the time the impulse reaches the bottom of the slow pathway, the impulse may travel back up the fast pathway, creating a reentrant circuit with rapid conduction of impulses to the ventricles. On ECG, retrograde conduction up the fast pathway creates a retrograde P wave; however, because this conduction is usually simultaneous with anterograde conduction to the ventricles, the P wave is often buried within the QRS complex and is not visible

Why do patients with chrohns disease get gallstones and what is the most common location for crohn disease?

Patients with Crohn disease affecting the terminal ileum (most common site of involvement) are prone to developing gallstones. Decreased bile acid reabsorption by the inflamed terminal ileum promotes cholesterol supersaturation of the bile, resulting in gallstone formation.

Describe the pathophysiology, clinical features and treatment for Reyes syndrome?

Patients with Reye syndrome typically have vomiting and encephalopathy (eg, lethargy, altered mental status) related to the buildup of ammonia from liver failure. Seizures and coma may also occur. In addition to hyperammonemia, laboratory analysis typically shows markedly elevated aminotransferases, as seen in this patient. In addition, PT and PTT are often prolonged due to impaired hepatic synthetic function, but bilirubin is generally normal to slightly elevated. There is no specific treatment for Reye syndrome other than supportive care.

People with advanced heart failure also develop elevated RAP--why?

Patients with advanced heart failure also develop elevated right atrial pressure (RAP). RAP is representative of central venous pressure and elevation is indicative of underlying volume overload and possible right-sided heart failure (which most commonly occurs secondary to left-sided heart failure due to backward transmission of elevated pressure overloading the right ventricle). In addition, since the underlying insult in dilated cardiomyopathy often directly affects the right ventricular myocardium, concomitant right ventricular failure is particularly likely in these individuals.

In chronic heart failure how does edema?

Peripheral edema results from the accumulation of fluid in the interstitial spaces. Factors that promote edema include elevated capillary hydrostatic pressure, decreased plasma oncotic pressure, sodium and water retention, and impaired lymphatic drainage. In chronic heart failure, increased lymphatic drainage initially offsets factors favoring edema, whereas acute changes (eg, venous thrombosis, heart failure decompensation) are more likely to produce edema. Increased capillary fluid transudation raises interstitial hydrostatic pressure, resulting in increased lymphatic drainage. This compensatory response can delay the development of clinically apparent edema. However, progressive heart failure, cirrhosis, or renal failure can eventually overwhelm lymphatic return capacity and produce significant edema.

What does peripheral vascular disease cause

Peripheral vascular disease causes decreased pulse amplitude within the affected extremities. This is most commonly observed in the lower extremities, which will have diminished or absent distal pulses caused by widespread peripheral arterial disease.

What is Eisenmenger's syndrome?

Phenomenon that occurs from long-standing L to R shunt that leads to Pulmonary Vascular Resistance...eventually the magnitude of the shunt become "equal" and then reversed with a net R to L shunt (increase pulmonary arterial pressure leads to intimal and medial hyperplasia)

Phosphate binding agents are used for?

Phosphate-binding agents can lower serum phosphate in chronic kidney disease and dialysis patients but do not significantly affect gallstones.

Plasma renin activity is useful in measuring?

Plasma renin activity (PRA) is measured as the amount of angiotensin I generated per unit of time and is a useful tool for assessing the function of the renin-angiotensin-aldosterone (RAAS) axis.

Fibrinoid degeneration of the vessel wall with luminal narrowing is indicative of?

Polyarteritis nodosa (PAN) is marked by transmural segmental inflammation of medium-sized muscular arteries with fibrinoid necrosis, which causes lumen narrowing, thrombosis, and organ ischemia.

What can Potassium-sparing diuretics be used in conjunction with another med for?

Potassium-sparing diuretics are often added to loop or thiazide diuretics to prevent hypokalemia. Amiloride and triamterene directly inhibit the epithelial sodium channel, preventing sodium from entering the principal cell, which reduces the electrochemical gradient (ie, negative luminal charge) that helps drive potassium secretion.

When do you usually get primary hyperparathyroidsm?

Primary hyperparathyroidism is caused by parathyroid hyperplasia or adenoma; it is characterized by hypercalcemia with elevated or inappropriately normal PTH levels.

What is primary sclerosing cholangitis?

Primary sclerosing cholangitis is characterized by inflammation, fibrosis, and stricture of intrahepatic and extrahepatic bile ducts. Histologic findings include fibrous obliteration of bile ducts and concentric periductal connective tissue deposition (eg, onion skin-like pattern). Manifestations reflect cholestasis and include jaundice, pruritus, fatigue, and a cholestatic injury pattern (ie, elevated alkaline phosphatase, direct hyperbilirubinemia).

What is pulse pressure?

Pulse pressure is the amount that arterial pressure increases above diastolic pressure during left ventricular contraction; it is directly related to stroke volume and inversely related to aortic compliance.

What is pulsus paradoxsus and how do detect it?

Pulsus paradoxus refers to an exaggerated drop (>10 mm Hg) in systolic blood pressure during inspiration. It is detected by inflating a blood pressure cuff above systolic pressure and gradually deflating it.

Draw out and describe the pathway of RAAS system?

Renin converts angiotensinogen to angiotensin I, which is then converted in the lung to angiotensin II, a potent vasoconstrictor that stimulates aldosterone secretion. Plasma renin activity (PRA) is measured as the amount of angiotensin I generated per unit of time and is a useful tool for assessing the function of the renin-angiotensin-aldosterone (RAAS) axis.

Reperfusion after ? What does it cause?

Reperfusion after ischemic insult to the liver can create hepatotoxic reactive oxygen species, such as superoxide. Reperfusion injury occurs in the setting of profound hypotension (eg, septic shock), which is not present in this patient

Why does Reyes syndrome occur?

Reye syndrome most commonly occurs in children who are given salicylates (eg, aspirin) during a viral infection (eg, influenza). In susceptible patients, salicylates can damage mitochondria within hepatocytes and inhibit enzymes involved in fatty acid beta-oxidation, the primary metabolic pathway hepatocytes depend on to maintain normal cellular function. Salicylate-induced hepatic injury prevents the liver from keeping up with metabolic demands, which often increase in the setting of a viral infection and predisposes patients to the development of acute liver failure.

Rituximab is a what type of drug and treats what?

Rituximab is a CD20 monoclonal antibody used to treat multiple myeloma, leukemia, and multiple autoimmune disorders

What is the presentation of Small intestinal bacterial overgrowth (SIBO)?

SIBO presents with chronic watery diarrhea due to mucosal inflammation, damage to brush border enzymes, and deconjugation of bile acids (the free bile acids are a direct enterocyte irritant). Bacterial fermentation of unabsorbed carbohydrates produces excessive gas (eg, hydrogen, methane, carbon dioxide) manifesting as bloating and flatulence. In severe cases, fat malabsorption can lead to deficiency of several fat-soluble vitamins (eg, A, D, E)

Sarcoidosis is due to?

Sarcoidosis is thought to result from a dysregulated cell-mediated immune response to an unidentified antigen, which causes the formation of granulomas.

How do you screen for celiac disease?

Screening is with serology testing for elevated IgA anti-endomysial and anti-tissue transglutaminase antibodies; diagnosis is confirmed by endoscopic biopsy. With strict adherence to a gluten-free diet, symptom resolution occurs within weeks and is followed by normalization of histology and antibody levels.

When do you usually get secondary hyperparathyroidsm?

Secondary hyperparathyroidism is usually seen in patients with chronic kidney disease and is due to phosphate retention and decreased production of 1,25-dihydroxyvitamin D; these disturbances lead to decreased intestinal calcium absorption, hypocalcemia, hyperphosphatemia, and a compensatory increase in PTH secretion.

What are kerley B lines?

Seen in acute decompensated heart failure. The chest x-ray may also show Kerley B lines—short, horizontal lines perpendicular to the pleural surface that represent edema of the interlobular septa. Cardiomegaly (cardiac-to-thoracic width ratio >50%) is also common in heart failure, but it is difficult to assess on anteroposterior view due to magnification of the heart.

What would you see on biopsy with polyarteritis nodosa?

Segmental fibrinoid necrosis (amorphic, eosinophilic areas) of the vessel wall Infiltration of the vessel wall with mononuclear cells and neutrophils Internal and external elastic laminae damage, which may cause microaneurysms XX most other vaculitis don't have granulomaous inflammation--> makes it unique

What is sigmoid volvulus and how does it present?

Sigmoid volvulus typically presents with progressive abdominal pain, nausea, and constipation and eventually results in bowel obstruction (eg, failure to pass gas, obstipation, possible perforation). Symptoms occur over the course of days, not months.

Signs of fat and protein malabsorption due to pancreatic insufficiency include?

Signs of fat and protein malabsorption due to pancreatic insufficiency include steatorrhea (bulky, foul-smelling stools), failure to thrive, and fat-soluble vitamin deficiencies (A, D, E, and K).

For Silicosis what would you expect to see on histology?

Silicosis results from chronic inflammation triggered by inhaled particles of crystalline silica. Histopathology typically shows silicotic nodules consisting of whorls of concentric collagen fibers. As with other causes of interstitial lung disease, excessive deposition of extracellular collagen eventually leads to pulmonary fibrosis.

Why would you give someone both simvastatin and cholestyramine work together and what do they work together to do?

Simvastatin decreases hepatic cholesterol production, while cholestyramine increases hepatic cholesterol and bile acid synthesis. Combination therapy results in a synergistic reduction in plasma LDL level.

A 32-year-old woman comes to the clinic due to 6 weeks of bloating and diarrhea. She has multiple watery bowel movements a day without visible blood. The patient underwent Roux-en-Y gastric bypass surgery for morbid obesity 3 years ago and has no other medical conditions. Vital signs are within normal limits. Physical examination is unremarkable. A jejunal aspirate shows a bacterial count of >105/mL, consistent with small intestinal bacterial overgrowth. Which of the following serum levels is most likely to be increased in this patient? A. Cobalamin B. Folate C. Vitamin D D. Zinc

Small intestinal bacterial overgrowth (SIBO) is characterized by the proliferation of colonic or oral organisms in the small bowel. It is a common complication of Roux-en-Y gastric bypass surgery; this procedure creates a small gastric pouch, which is removed from the remainder of the stomach and attached to the jejunum via a gastrojejunal anastomosis. The larger bypassed portion of the stomach and duodenum is reattached to the jejunum distally. This results in a closed-ended gastroduodenal limb, in which bacteria can proliferate and ferment any food that may be diverted into this segment. SIBO presents with chronic watery diarrhea due to mucosal inflammation, damage to brush border enzymes, and deconjugation of bile acids (the free bile acids are a direct enterocyte irritant). Bacterial fermentation of unabsorbed carbohydrates produces excessive gas (eg, hydrogen, methane, carbon dioxide) manifesting as bloating and flatulence. In severe cases, fat malabsorption can lead to deficiency of several fat-soluble vitamins (eg, A, D, E) (Choice C). In addition, the enteric bacteria in SIBO produce increased quantities of folate and vitamin K. As a result, serum folate levels may be elevated; vitamin K levels are often normal or only slightly increased because fat malabsorption offsets the increased production. (Choice A) SIBO typically causes cobalamin (vitamin B12) deficiency due to decreased intestinal absorption of both free and intrinsic factor-bound vitamin B12. In addition, the bacteria compete for the uptake and use of vitamin B12. (Choice D) Patients with SIBO often develop zinc deficiency due to malabsorption and nonspecific losses from chronic diarrhea. Educational objective:Small intestinal bacterial overgrowth is a common complication of Roux-en-Y gastric bypass due to excessive bacterial proliferation in the blind-ended gastroduodenal segment. The associated malabsorption can lead to deficiency of many vitamins (eg, A, B12, D, E) but increased production of folate and vitamin K.

Prerenal azotemia due to global reduction in cardiac output can be seen to cause acute kidney injury when?

Some drugs (eg, acyclovir, indinavir) can precipitate in the urine, causing AKI due to crystalluria. Urine sediment may show tubular necrosis (eg, granular casts), but crystals are usually also seen.

What can be used during a stress test in stead of doing a stress test?

Stable angina results from fixed coronary artery stenosis that limits blood flow to downstream myocardium, preventing the myocardial oxygen supply from increasing during exertion. Dobutamine mimics the effects of exercise and increases myocardial oxygen demand; it can be used during stress testing to provoke areas of ischemic myocardium, which can be recognized on imaging by a localized and transient decrease in contractility (ie, wall motion defect).

Describe statin and what they do to?

Statins are the first-line therapy for most patients with hypercholesterolemia. These drugs competitively inhibit HMG CoA reductase, the enzyme responsible for the conversion of HMG CoA to mevalonate (ie, the rate-limiting step in hepatic cholesterol synthesis). This inhibition decreases hepatic cholesterol synthesis. The resulting upregulation of LDL receptors causes increased uptake of LDL from the circulation. Statins are very effective in reducing LDL cholesterol. Statins' effects on triglyceride and HDL levels are comparatively modest.

A 58-year-old woman comes to the emergency department complaining of lightheadedness and urinary retention over the past day. She has a history of depression and of urinary incontinence, for which she takes medication. She recently was started on a new antidepressant due to lack of response to previous therapy. Her pulse is 110/min. She appears flushed and her skin is warm and dry. Which of the following findings would help confirm the most likely diagnosis? A. Alogia B. Blurry vision C. Jaundice D. Muscle rigidity E. Tremor

Step 1: Disease DiagnosisThis patient has likely anticholinergic toxicity based on her tachycardia, flushed warm skin, and urinary retention in the setting of starting a new antidepressant drug. Based on the history and presenting symptoms of this patient, it is likely the new medication was a tricyclic antidepressant (TCA). TCAs are known to produce anticholinergic adverse effects and also may cause fatal arrhythmias, which is why they are used more commonly as second- or third-line antidepressants when other agents fail. She also likely is taking an anticholinergic agent such as oxybutynin to treat her incontinence. This would increase the likelihood of anticholinergic adverse effects of an antidepressant drug.Step 2: History and Physical ExamPatients with anticholinergic toxicity most likely would present with blurry vision, which is a symptom of toxicity along with mydriasis, urinary retention, tachycardia, dry mucous membranes, warm and flushed skin, and sometimes delirium.The other choices are incorrect: Muscle rigidity is an adverse effect of antipsychotic or antidopaminergic medications, which also can cause neuroleptic malignant syndrome or malignant hyperthermia. Jaundice is usually a sign of liver dysfunction, which can be caused by many drugs. Alogia, or complete lack of speech, can be associated with a severe injury to the language center or frontal lobe of the brain. Tremor may be treated by anticholinergics, not caused by them.

Stimulation of α1 adrenoreceptors leads?

Stimulation of α1 adrenoreceptors leads to vasoconstriction in the skin and viscera, resulting in increased systolic and diastolic blood pressure with decreased renal and hepatic blood flow. α1-mediated vasoconstriction occurs via the IP3-second messenger pathway.

Stimulation of α2 adrenoreceptors causes?

Stimulation of α2 adrenoreceptors causes a decrease in cAMP in pancreatic β cells and in the intestines, resulting in decreased insulin secretion and reduced intestinal motility. Central α2 adrenoreceptors are not stimulated by intravenous administration of norepinephrine as the molecule does not cross the blood-brain barrier.

Stimulation of β1 adrenoreceptors within leads to?

Stimulation of β1 adrenoreceptors within the heart increases cAMP concentrations through Gs-mediated receptor coupling, which leads to increased cardiac contractility, conduction, and heart rate. However, the direct effect of norepinephrine on heart rate is counteracted by an indirect, baroreceptor-mediated reflex bradycardia that occurs following the increase in peripheral resistance. The combined result of these effects is often an unchanged or even decreased heart rate.

Stimulation of β2 adrenoreceptors in bronchial smooth muscle cells leads to?

Stimulation of β2 adrenoreceptors in bronchial smooth muscle cells leads to increased, rather than decreased, cAMP synthesis, resulting in bronchodilation. Regardless, norepinephrine does not significantly stimulate β2 adrenoreceptors.

What are strongyloides stercoralis? Wat are their life cycles?

Strongyloides stercoralis is a roundworm endemic to tropical and subtropical areas of Southeast Asia, Africa, and Western Pacific nations. It is transmitted when filariform larvae (infective) in soil contaminated with human feces come into direct contact with skin (eg, walking barefoot on the beach). The larvae penetrate the site of contact, migrate through the bloodstream/lymphatics to the lungs, and enter the alveoli. They then ascend the tracheobronchial tree and are swallowed. In the duodenum and jejunum, the larvae mature into adult worms, enter the intestinal mucosa, and secrete rhabditiform larvae (noninfective) that are excreted in stool. A minority of rhabditiform larvae mature to filariform larvae and reinfect the host through the intestinal mucosa or perianal skin (autoinoculation).

Patient's presentation (fever, dyspnea, and a new blowing holosystolic murmur best heard at the cardiac apex) is. Patients with can develop several peripheral cutaneous or mucocutaneous stigmata of endocarditis including petechiae, splinter hemorrhages, Roth spots, Janeway lesions (see above Image), and Osler nodes. What could it be?

Suggestive of mitral regurgitation likely due to infective endocarditis (IE) These are Janeway lesions

Symptomatic management of peripheral artery disease (PAD) ?

Symptomatic management of peripheral artery disease (PAD) includes a graded exercise program and cilostazol. Cilostazol is a phosphodiesterase inhibitor that inhibits platelet aggregation and acts as a direct arterial vasodilator. Patients with PAD should also receive an antiplatelet agent (aspirin or clopidogrel) for secondary prevention of coronary heart disease and stroke.

Systemic sclerosis may result in what kind of esophogeal problem?This can cause?

Systemic sclerosis may result in esophageal dysmotility and incompetence of the lower esophageal sphincter due to atrophy and fibrous replacement of the esophageal muscularis. This can cause gastroesophageal reflux with an increased risk of Barrett's esophagus and stricture formation.

What do you plan to see on endoscopy with a patient with systemic sclerosis?

Systemic sclerosis results in esophageal smooth muscle fibrosis, leading to severe gastroesophageal reflux. It occurs more commonly in adult women and usually presents with thickened skin and Raynaud phenomenon. Endoscopy typically demonstrates a dilated esophagus.

Asian women of reproductive age with lower extremeity claudication (exertional pain due to limited blood flow reserve) and constitiutional symptoms is typical features of what vasculitis disease; describe what vessels it may involve ?

Takayasu arteritis (TA). TA is a chronic, large-artery vasculitis that primarily involves the aorta and its branches. TA predominantly

Granulomatous inflammation of the vascular media is indicative of which vasculities?

Takayasu arteritis is a chronic, large-artery vasculitis that primarily involves the aorta and its branches. It presents with constitutional (eg, fever, weight loss) and arterio-occlusive (eg, claudication, blood pressure discrepancies, pulse deficits) findings in patients age <40. Histopathology shows granulomatous inflammation of the vascular media.

What does granulomatous inflammation of large arteries indicative of what disease?

Takayasu disease

Terazosin is what type of drug and used for and major adverse effects?

Terazosin is an alpha-1 adrenergic antagonist used in the treatment of benign prostatic hyperplasia and hypertension. Major adverse effects include lightheadedness and orthostatic hypotension.

Th1 cells are

Th1 cells are central to cell-mediated immunity. However,. Moreover,

Asthma is driven by what cell? What cytokines are involved?

Th2 cells are involved in humoral immunity and defense against extracellular parasites. Asthma, a Th2-driven disease, Cytokines involved with asthma include IL-4 and IL-5, which are secreted by Th2 cells. IL-4 promotes B-cell class switching to form IgE antibodies, and IL-5 promotes eosinophil production and activation. IL-3 is also involved in asthma (as it promotes survival of mast cells) but mainly supports the growth and differentiation of bone marrow stem cells.

Describe QT inerval and prolongation with a drug like amidarone?

The QT interval represents the time required for ventricular depolarization and repolarization; it can be regarded as a rough estimate of the APD. Drugs that significantly prolong the cardiac action potential (eg, class IA and III antiarrhythmics) cause prolongation of the QT interval. Prolonged QT is associated with a form of ventricular tachycardia called torsades de pointes (polymorphic ventricular tachycardia). However, unlike other drugs that cause QT prolongation, amiodarone has very little risk of inducing torsades de pointes. This effect is thought to be due to it having a more homogeneous effect on ventricular repolarization compared to other drugs (ie, less QT dispersion).

The action potential of ventricular and non-nodal conduction cells within the heart consists of four phases describe them?

The action potential of ventricular and non-nodal conduction cells within the heart consists of four phases. Phase 4: Resting potential (diastole). Resting potential is determined largely by membrane permeability to K+ ions when in the resting state. The resting potential of cardiac myocytes is approximately -90mV, while the resting potential of skeletal myocytes is approximately -75mV. The highly negative resting potential of cardiac myocytes reduces the risk of arrhythmias, as a larger stimulus is needed to excite the cells. Phase 0: Rapid depolarization. As in skeletal myocytes, the action potential onset occurs when voltage-gated Na+ channels open and Na+ ions rush into the cell. Phase 1: Initial rapid repolarization. This phase is associated with the rapid closure of Na+ channels. Phase 2: Plateau. This phase is a distinctive feature of the cardiac action potential not seen in other tissues. It is characterized by the opening of L-type dihydropyridine-sensitive Ca++ channels and the closure of some K+ channels. Consequently, the membrane becomes highly permeable to Ca++ ions and minimally permeable to K+ ions. Phase 3: Late rapid repolarization. This phase features closure of Ca++ channels and the opening of K+ channels. Efflux of K+ from the cell restores the membrane resting potential.

Explain why a person with chronic hypertension in a hyptensive urgency should be slowly given medications to bring it down?

The autoregulation response protects organs from dangerous, persistent BP elevations. In chronic hypertension, there is baseline constriction of afferent glomerular arterioles. This causes the entire renal autoregulation curve to be shifted to the right: a hypertensive patient's kidneys receive less blood flow at any given BP relative to those of a healthy patient without hypertension. Quickly lowering the BP to normal (eg, 145/95 mm Hg) causes a steep drop in blood flow, leading to ischemic ATN; as a result, BP should be lowered gently, targeting above-normal values (eg, 25% reduction over several hours).

What happens carotid sinus hypersenstitivity?

The baroreceptor response in CSH mimics the normal response to increased blood pressure but is more exaggerated; increased parasympathetic output leads to a prolonged sinus pause (eg, 3-5 seconds) and decreased sympathetic outflow causes marked peripheral vasodilation. The resulting delay in ventricular contraction and decreased systemic vascular resistance leads to a profound reduction in blood pressure and transient loss of cerebral perfusion that manifests as presyncope or syncope.

Describe noncaseating granulomas? What does it look like?

The biopsy specimen with multiple, noncaseating granulomas—characterized by a central collection of tightly clustered epithelioid macrophages with abundant pink cytoplasm surrounded by a rim of mononuclear cells—confirms the diagnosis. Multinucleated giant cells, formed by macrophage fusion, are discernable at higher magnification.

The cephalic and gastric phases _______ gastric acid secretion, while intestinal influences tend to ______ gastric acid secretion.

The cephalic and gastric phases stimulate gastric acid secretion, while intestinal influences tend to reduce gastric acid secretion.

Describe the chest xray for idiopathic interstitial fibrosis ?

The chest x-ray in idiopathic interstitial fibrosis shows diffuse, reticular opacities typically associated with decreased lung volumes. Most patients have slowly progressive dyspnea and a nonproductive cough.

The chest x-ray in pulmonary arterial hypertension reveals ?

The chest x-ray in pulmonary arterial hypertension reveals enlargement of the pulmonary arteries and right ventricle and absence of pulmonary edema.

The combination of wheezing, diarrhea, and facial flushing in association with an ileal tumor with hepatic metastasis is suggestive of?

The combination of wheezing, diarrhea, and facial flushing in association with an ileal tumor with hepatic metastasis is suggestive of carcinoid syndrome. Carcinoid tumors (most common ileal tumors) secrete a number of biologically active substances including serotonin and can cause symptoms when they metastasize. Common manifestations of carcinoid syndrome include flushing, asthma-like symptoms (wheezing, dyspnea), diarrhea, and syncope (due to low blood pressure). Long-standing carcinoid syndrome can cause right-sided valvular heart disease.

What does hte common hepatic artery perfuse?Where does it come from?

The common hepatic artery perfuses the liver, gallbladder, pylorus, duodenum, and pancreas. It arises from the celiac trunk and ends when it bifurcates into the proper hepatic and gastroduodenal arteries.

The diagram above depicts a crescendo-decrescendo systolic murmur peaking in midsystole, characteristic of ?

The diagram above depicts a crescendo-decrescendo systolic murmur peaking in midsystole, characteristic of aortic or pulmonic stenosis. The most common cause of aortic stenosis (AS) in elderly patients (age >70) is degenerative calcification of the aortic valve leaflets.

What is gastrocolic reflex and when is it defective?i

The gastrocolic reflex is a neurogenic reflex triggered by gastric distension from food, leading to colonic contractions; impairment of the reflex can cause constipation. However, this typically occurs in patients with diabetic neuropathy and gastroparesis.

When can you have an ulcer at the posterior duodenal bulf, which artery is involved?

The gastroduodenal artery supplies blood to the pylorus and proximal duodenum. Ulcers in the posterior duodenal bulb can erode into the gastroduodenal artery, but a gastric ulcer at the lesser curvature would not involve these arteries.

What are the risk factors for esophageal scc?

The incidence of esophageal SCC is decreasing in the United States, with the highest incidence occurring in middle-aged and older individuals (age >50). The most significant risk factors for SCC in the United States include cigarette smoking and alcohol intake. In Asia, the chewing of betel nuts and consumption of foods containing N-nitroso compounds (often found in preserved or pickled vegetables) are commonly associated with SCC. Other risk factors include preexisting esophageal disease (eg, achalasia, caustic injury) and ingestion of high-temperature liquids

Draw out and describe the pressure volume loop?

The left ventricular (LV) pressure-volume loop follows the cardiac cycle through left ventricular contraction, ejection, relaxation, and refilling, as follows: Isovolumetric contraction: The cardiac cycle begins with initiation of left ventricular contraction and closure of the mitral valve at point 1; an S1 is heard at this time, marking the end of diastole (Choice A). Although intraventricular pressure increases after point 1, initially, no blood leaves the ventricle because both the aortic and mitral valves are closed. At point 2, LV pressure overcomes systemic diastolic pressure and the aortic valve opens (Choice B). Ventricular ejection: LV volume decreases as blood is ejected into the aorta. The peak of the ejection curve denotes systolic blood pressure and represents the high point of LV afterload (Choice E). LV ejection ends at point 3 with aortic valve closure and an S2 is heard (Choice C). The horizontal distance between point 2 (or point 1) and point 3 represents the stroke volume. Isovolumetric relaxation: LV pressure rapidly falls from point 3 to point 4. No blood leaves or enters the left ventricle during this time because both the aortic and mitral valves are closed. Ventricular filling: The mitral valve opens at point 4 and diastolic filling of the left ventricle begins. LV volume and pressure gradually increase until mitral valve closure occurs again at point 1 and the cycle begins anew. Extra heart sounds (ie, an S3 or S4) may be heard during diastolic filling between point 4 and point 1 (Choice F).

Vitamin E deficiency presents as?

The most common clinical manifestations of vitamin E deficiency are neuromuscular disease (eg, skeletal myopathy, spinocerebellar ataxia, polyneuropathy) and hemolytic anemia. Involvement of the dorsal column in the spinal cord is associated with the loss of proprioception and vibratory sense. Spinocerebellar tract involvement causes ataxia, and peripheral nerve dysfunction results in hyporeflexia.

Where would you hear valvular aortic stenosis?

The murmur of valvular AS is best heard over the right second interspace (where the aorta leaves the base of the heart) with radiation to neck and carotid arteries. A longer and late-peaking murmur usually indicates severe AS, whereas a brief and early-peaking murmur indicates less severe stenosis. However, the intensity of the murmur does not correlate with the severity of stenosis.

What are other signs of cauda equina?

The pelvic splanchnic nerves (S2-S4) provide parasympathetic innervation to the bowel and bladder, and their impairment in cauda equina syndrome can cause constipation and difficulty urinating. Other signs of cauda equina syndrome include radicular low back pain and leg weakness (sciatic nerve) as well as saddle anesthesia (pudendal, ilioinguinal nerves).

Describe the anatomy and connections of brachiocephalic?

The right brachiocephalic vein is formed by the union of the right subclavian vein and the right internal jugular vein. The right external jugular vein drains into the right subclavian vein, so obstruction of the right brachiocephalic vein will also cause venous congestion of structures drained by the external jugular vein. It is important to note that the right brachiocephalic vein also drains the right lymphatic duct, which drains lymph from the right upper extremity, the right face and neck, the right hemithorax, and the right upper quadrant of the abdomen.

Where does the right gastroepiploic artery arise from and supply?

The right gastroepiploic artery arises from the gastroduodenal artery and perfuses the distal greater curvature of the stomach. Gastric ulcers do not commonly occur in the greater curvature.

Where does the splenic artery arise from and supply?

The splenic artery arises from the celiac trunk and supplies blood to the spleen. It is separated from the posterior wall of the stomach by the pancreas and is only rarely penetrated by gastric ulcers.

The systolic hypertension induced by aortic stiffening likely contributes

The systolic hypertension induced by aortic stiffening likely contributes to mild concentric left ventricular hypertrophy, another common finding in elderly individuals.

This patient has progressive dyspnea and orthopnea (cough when lying down), along with chest x-ray findings of prominent pulmonary vessels, patchy bilateral airspace opacities, blunting of the costophrenic angles (pleural effusions), and a fissure sign (created by fluid trapped between the right upper and middle lobe). What are these symptoms from?

These findings are consistent with acute decompensated heart failure (ADHF); chronic hypertension is a common cause of heart failure due to concentric left ventricular hypertrophy and resulting diastolic dysfunction. In ADHF, increased atrial and ventricular filling pressures are transmitted to the pulmonary vasculature, causing fluid transudation into pulmonary interstitial and alveolar spaces (cardiogenic pulmonary edema). The chest x-ray may also show Kerley B lines—short, horizontal lines perpendicular to the pleural surface that represent edema of the interlobular septa. Cardiomegaly (cardiac-to-thoracic width ratio >50%) is also common in heart failure, but it is difficult to assess on anteroposterior view due to magnification of the heart.

A 54-year-old man comes to the office due to new-onset muscle cramps. The patient has a history of hypertension and was started on hydrochlorothiazide 4 weeks ago. Blood pressure is 138/86 mm Hg and pulse is 78/min. Examination shows no abnormalities. Based on his most recent laboratory results, triamterene is added to the current therapy. Which of the following best describes the mechanism of action of this medication? A. Blocking renal tubular epithelial sodium channels B. Decreased aldosterone production C. Increased intestinal absoption of potassium D. Inhibiting aldosterone receptor activity in renal collecting duct E. Inhibiting Na/K ATPase activity in skeletal muscle.

Thiazide diuretics lower blood pressure by inhibiting Na+/Cl− cotransporters in the distal convoluted tubules, thereby decreasing reabsorption of Na+ and Cl−. Both thiazides and loop diuretics induce volume loss with subsequent activation of the renin-angiotensin-aldosterone system. Aldosterone increases renal sodium resorption in exchange for potassium by upregulating the synthesis and activity of the following: Epithelial sodium channels: Found on the apical membrane of principal cells, it absorbs Na+ from the tubular lumen Na+/K+-ATPase pump: Located on the basal membrane of principal cells, it extrudes Na+ into the interstitial space in exchange for potassium Because of these effects, increased aldosterone levels commonly result in hypokalemia, which can lead to muscle cramps, weakness, and (when severe) cardiac arrhythmias. Potassium-sparing diuretics may be added to prevent hypokalemia. These weak diuretic medications act in the distal nephron, where they reduce potassium excretion via the following mechanisms: Triamterene and amiloride directly inhibit the epithelial sodium channel, preventing sodium from entering principal cells. This reduces the electrochemical gradient (ie, negative luminal charge) that helps drive potassium secretion. Aldosterone antagonists (ie, spironolactone, eplerenone) directly inhibit the mineralocorticoid receptor, resulting in decreased formation and activity of epithelial sodium channels and Na+/K+-ATPase pumps (Choice D).

What mechanism is the way that leads to hypercalcemia and hypocalciuria?

Thiazides increase renal Ca2+ reabsorption, leading to hypercalcemia and hypocalciuria. This occurs through 2 major mechanisms: Thiazides inhibit the Na+/Cl− cotransporter on the apical side of distal convoluted tubule cells, which decreases intracellular Na+ concentration. This activates the basolateral Na+/Ca2+ antiporter, which pumps Na+ into the cell in exchange for Ca2+. The resulting decrease in intracellular Ca2+ enhances luminal Ca2+ reabsorption across the apical membrane. Hypovolemia induced by thiazides increases Na+ and H2O reabsorption in the proximal tubule, leading to a passive increase in paracellular Ca2+ reabsorption. The increase in circulating calcium suppresses parathyroid hormone (PTH) release, leading to a new steady state with a mildly elevated serum calcium concentration and low serum PTH.

What is the cause of the head bobbing and pulsations in aortic regurgitation?

This high-amplitude pulsation with rapid diastolic collapse is responsible for the unusual pulsation findings in AR

Describe how How is that accomplished autoregulation is maintained?

This is accomplished mostly by automated alterations in vascular resistance via the release of locally acting mediators, namely adenosine (released from cardiomyocytes as ATP is broken down for energy) and nitric oxide (synthesized by endothelial cells in response to chemical mediators and mechanical stress).

What is the peak intensity would you expect for aortic stenosis?

This is the peak systolic pressure produced by the left ventricle during systole; the peak intensity of the crescendo-decrescendo murmur of aortic stenosis is heard here.

A 38-year-old man comes to the emergency department because he has been vomiting blood. After appropriate resuscitation measures, he undergoes upper gastrointestinal endoscopy, which reveals a bleeding duodenal ulcer. During hospital day 2, the patient develops decreased urine output. Serum creatinine rises to 3.0 mg/dL from a baseline of 1.2 mg/dL. Renal biopsy shows patchy epithelial necrosis of the tubules, tubulorrhexis, and intratubular casts. On hospital day 8, urine output significantly increases and serum creatinine levels decline. Over the next few days, this patient is at highest risk for which of the following complications? A. Hyperphosphatemia B. Hypokalemia C. Metabolic acidosis D. Urinary protein loss E. Volume overload

This patient developed acute renal failure after gastrointestinal hemorrhage; renal biopsy showing epithelial necrosis of the tubules, tubulorrhexis, and intratubular casts is consistent with acute tubular necrosis (ATN). ATN is characterized by tubular injury due to renal ischemia (eg, shock, hemorrhage) or direct cytotoxicity (eg, radiologic contrast agents, aminoglycosides). The clinical course of ATN can be broken into 3 stages. The initiation stage is marked by the inciting event (eg, hemorrhage, as in this patient) and the onset of tubular injury. If significant tubular damage occurs, the maintenance stage (oliguric stage) follows in 24-36 hours. During this stage, urine output decreases and patients may develop volume overload. Renal tubular dysfunction results in the characteristic low urinary osmolality (<350 mOsm/kg), high urinary sodium (>30 mEq/L), and high urinary fractional sodium excretion (>1%).

This patient has altered mental status and acute renal failure. In conjunction with the oxalate crystals noted on renal biopsy, this presentation is consistent with? Describe the course of this?

This patient has altered mental status and acute renal failure. In conjunction with the oxalate crystals noted on renal biopsy, this presentation is consistent with ethylene glycol poisoning. Ethylene glycol is a toxic alcohol found in antifreeze, engine coolants, and brake fluids and may be accidentally or intentionally ingested (used as a substitute for alcohol). Patients initially have symptoms of ethanol intoxication; signs of acute renal failure (oliguria, flank pain) develop approximately 24-72 hours after ingestion. Ethylene glycol itself is relatively nontoxic; however, it is metabolized to glycolic acid and oxalic acid, resulting in its various toxicities.

Patient with marfans syndrome

This patient has clinical features of Marfan syndrome, an autosomal dominant disorder caused by mutations in the FBN1 gene encoding fibrillin-1, a main component of extracellular matrix microfibrils. Fibrillin-1 provides support to elastic fibers and helps maintain connective tissue integrity. It also regulates extracellular matrix remodelling by binding to and sequestering transforming growth factor-beta (TGF-beta). In Marfan syndrome, defective fibrillin-1 is unable to bind TGF-beta. The resulting overexpression of free, active TGF-beta leads to increased production of matrix metalloproteinases, which cleave elastic fibers and other components of the extracellular matrix, reducing tissue integrity. Within the mitral valve, this process results in fragmentation of elastic fibers and decreased collagen density with pooling of glycosaminoglycans (myxomatous mitral degeneration). The elongated, floppy mitral valve leaflets prolapse into the atrium, which causes a midsystolic click on auscultation and allows for mitral valve regurgitation. This regurgitant flow is characterized by a mid-to-late systolic apical murmur, as seen in this patient; severe regurgitation may produce a holosystolic murmur.

A 35-year-old woman comes to the clinic due to severe heartburn that is resistant to over-the-counter antacids. The patient has no known medical problems and takes no other medications. She occasionally has a glass of wine with dinner but does not use tobacco or illicit drugs. Physical examination shows scattered telangiectasias on the face, several ulcers at the tips of the fingers, and small calcium deposits in the soft tissues of the hands and elbows. Which of the following processes is the most likely cause of this patient's heartburn?

This patient has features consistent with CREST syndrome (ie, Calcinosis, Raynaud phenomenon, Esophageal dysmotility, Sclerodactyly, Telangiectasia), a limited variant of systemic sclerosis with skin disease that primarily affects the face, forearms, and fingers. The pathogenesis of systemic sclerosis involves chronic autoimmune inflammation, vascular endothelial injury resulting in chronic ischemic tissue damage (eg, fingertip ulcers), and excessive activation of fibroblasts leading to progressive tissue fibrosis. Esophageal dysmotility is a result of atrophy and fibrous replacement of the muscularis in the lower esophagus. The esophageal body and the lower esophageal sphincter become atonic and dilated, resulting in symptoms of gastroesophageal reflux (eg, heartburn, regurgitation, dysphagia). This increases the risk of Barrett's esophagus and fibrous stricture formation. (Choice A) A sliding hiatal hernia is characterized by herniation of the gastroesophageal junction and a portion of the stomach through the esophageal hiatus, which predisposes patients to gastroesophageal reflux. (Choice C) Increased gastric acid production occurs with gastrinomas, gastrin-secreting neuroendocrine tumors of the small intestine/pancreas that often present with multiple or medically refractory peptic ulcers. (Choice D) Achalasia is an esophageal motility disorder characterized by failed relaxation of the lower esophageal sphincter resulting in food retention, dilation of the esophageal body, and symptoms of solid/liquid dysphagia. (Choice E) Diffuse esophageal spasm is characterized by periodic, uncoordinated, simultaneous contractions of the lower esophagus due to impaired inhibitory innervation within the esophageal myenteric plexus. Patients typically have liquid/solid dysphagia and chest pain due to inefficient propagation of food into the stomach.

Squamous cell carcinoma can be identified as?

This patient has squamous cell carcinoma (SCC), which is characterized by flattened polyhedral or ovoid epithelial cells with eosinophilic cytoplasm, keratin nests or pearls within or between cells, and intercellular bridging.

Describe what sodium nitroprusside can be used for in heart failure. And how it works?

This patient most likely has acute heart failure due to systemic hypertension, which can be treated with an infusion of sodium nitroprusside. Sodium nitroprusside is a short-acting agent that causes balanced vasodilation of the veins and arteries; as such, it decreases left ventricular (LV) preload and afterload, allowing for maintenance of cardiac output (unchanged stroke volume) at a lower LV pressure (decreased LV work). LV contractility is essentially unchanged. Sodium nitroprusside is a short-acting agent that causes balanced vasodilation of the veins and arteries to decrease both left ventricular (LV) preload and afterload. The balanced vasodilation allows for maintenance of stroke volume and cardiac output at a lower LV pressure (lower cardiac work).

What kin of murmur do you expect to see and what maneuvers do you expect to decreased with someone with hypertrophic cardiomyopathy?

This patient with a systolic murmur along the left sternal border that decreases in intensity with maneuvers that increase left ventricular (LV) blood volume likely has hypertrophic cardiomyopathy (HCM). HCM is characterized by increased LV muscle mass and a small LV cavity. Because LV contractility is typically intact and outflow obstruction is dynamic and commonly only present with exercise, there is usually preserved ejection fraction. However, impaired relaxation of the hypertrophied LV wall typically leads to diastolic dysfunction.

Patient with an audible snap followed by a rumbling diastolic murmur over the cardiac apex likely has what type of

Where are you most likely to hear an audible snap followed by a rumnbling diastolic murmur heard over the cardiac apex?

This patient with an audible snap followed by a rumbling diastolic murmur over the cardiac apex likely has mitral stenosis, which is most commonly seen due to underlying rheumatic heart disease in patients emigrating from Latin America, Africa, or Asia. The audible snap observed with mitral stenosis is created by the stenotic and calcified valve snapping open (ie, opening snap) and is heard during mitral valve opening at point 4.

A 10-year-old boy who recently immigrated from overseas with his family is brought to the office due to exertional dyspnea and fatigability. The boy tires easily when walking and cannot keep up with his peers at the playground. According to his parents, he was diagnosed with congenital heart disease in infancy, but corrective surgery was unavailable. They cannot recall the details of his diagnosis. He takes a daily multivitamin and no medications. Pulse oximetry of the right hand shows 99% on room air. Physical examination reveals no murmurs. There is bilateral cyanosis and clubbing of the toes. The fingers are normal. All extremity pulses are full and equal. Which of the following is the most likely diagnosis? A. Atrial septal defect B. Patent ductus arteriosus C. Tetraology of Fallot D. Transposition of the great arteries E. Ventricular septal defect

This patient with cyanosis and clubbing of the feet but normal peripheral pulses most likely has a large patent ductus arteriosus (PDA). A PDA initially results in a left-to-right shunt with increased pulmonary blood flow. Over time, this can lead to increased pulmonary vascular resistance (PVR) due to progressive vascular remodeling. If the shunt is not corrected, PVR can eventually exceed systemic resistance and cause reversal of the shunt to right-to-left blood flow (ie, Eisenmenger syndrome), resulting in arterial hypoxemia, cyanosis, and eventually clubbing. Differential clubbing and cyanosis in the lower extremities occurs when there is a significant decrease in postductal oxygen saturation (the arteries perfusing the head and upper extremities arise proximal to the ductus). In patients with a PDA and Eisenmenger syndrome, the upper extremities are supplied by oxygenated blood from the left ventricle, but deoxygenated blood flows right-to-left across the PDA and supplies the descending aorta, resulting in lower body hypoxemia and cyanosis of the toes.

This patient with decompensated heart failure (eg, progressive dyspnea, weight gain, peripheral edema) has copious pink, amorphous material (hyaline) on cardiac biopsy, which is characteristic of ?

This patient with decompensated heart failure (eg, progressive dyspnea, weight gain, peripheral edema) has copious pink, amorphous material (hyaline) on cardiac biopsy, which is characteristic of amyloid cardiomyopathy

A 46-year-old woman is admitted to the hospital with dehydration secondary to excess output from an ileostomy. Five years ago, the patient had a total colectomy with a diverting ileostomy for colon cancer. For the last 6 months, she has had increased output from the ileostomy and has been admitted to the hospital twice with similar episodes of dehydration. On the second day of admission, she reports right flank pain. X-ray of the abdomen reveals a nonspecific bowel gas pattern with no evidence of renal calculi. Ultrasound of the abdomen shows a 4-mm stone in the distal right ureter. The patient is treated with analgesics and the stone passes spontaneously. Microscopic analysis of the stone reveals a pure uric acid stone. Which of the following is the most likely underlying mechanism leading to stone formation in this patient? A. Bile salt malabsorption in the ileum B. Concentrated acidic urine C. Increased uric acid production D. Infection with urea-splitting bacteria E. Overproduction of parathyroid hormone

This patient with recurrent episodes of dehydration due to fluid loss from her ileostomy developed a uric acid stone. Pure uric acid stones are radiolucent and cannot be visualized on x-ray but appear as yellow/brown agglomerations of rhomboid-shaped crystals on gross/microscopic examination. Biochemical risk factors include low urine pH, low urine volume (eg, dehydration), and hyperuricemia. Patients with chronic diarrhea or those who have had a colectomy have reduced bicarbonate reabsorption from the gut, leading to a state of chronic metabolic acidosis. The kidneys compensate by increasing the excretion of hydrogen ions (H+) and reabsorption of bicarbonate in the collecting ducts. This lowers urine pH (acidic urine), increasing the conversion of soluble urate ion into insoluble uric acid. Conversely, alkalinization of the urine with potassium citrate favors formation of urate and can prevent, and in some cases dissolve, uric acid stones. Other commonly associated conditions include gout, high cell turnover states (eg, lymphoproliferative disorders), and metabolic syndrome.

A 25-year-old man/ chest heaviness and palpitations for the last 3 hours/Had a similiar episode, resolved with deep breathing, but not this time/no chronic medical conditions/regular heart/no meds/ takes no stimulants/pulse 160/min/no thyroid problems/ lungs clear/ ECG QRS complex tachycardia with regular rhythm/nonvisible P waves.

This patient's ECG reveals a narrow QRS complex tachycardia with a regular rhythm and nonvisible P waves. These findings are consistent with paroxysmal supraventricular tachycardia (PSVT), an episodic cardiac arrhythmia that originates at or above the atrioventricular (AV) node. The most common type of PSVT is AV nodal reentrant tachycardia (AVNRT), which usually affects young patients (eg, age <40) with an otherwise normal heart.

aortic regurgitation describe it and where can you hear it pressure graph, what changes would you see?

This patient's cardiac catheterization shows a hemodynamic profile consistent with aortic regurgitation (AR); the characteristic decrescendo diastolic murmur is best heard with the patient leaning forward. The peak intensity of the murmur occurs just after aortic valve closure when the pressure gradient between the aorta and the left ventricle is maximal (point C). This pressure gradient falls progressively during diastole as blood regurgitates into the left ventricle, accounting for the decrescendo nature of the murmur. Notable changes to the pressure tracings that occur in AR include: Loss of the aortic dicrotic notch: On the normal aortic pressure tracing the dicrotic notch is created by a small and abrupt increase in aortic pressure as blood is secured in the aorta by closure of the aortic valve. However, with an incompetent aortic valve there is immediate backflow of blood into the left ventricle, resulting in loss of pressure in the aorta and disappearance of the dicrotic notch. Steep diastolic decline of aortic pressure: Aortic diastolic pressure declines more rapidly than normal as blood regurgitates into the left ventricle and nadirs at a lower than normal level. High-peaking left ventricular and aortic systolic pressures: The left ventricle attempts to compensate for regurgitant backflow by increasing stroke volume, resulting in higher systolic blood pressures, which combined with low aortic diastolic pressure leads to a wide pulse pressure.

A 53-year-old man comes to the emergency department with shortness of breath and chest tightness. The patient was playing in a poker tournament when his symptoms first began. He has a history of hypertension and is not compliant with his medications. His last medical follow-up was a year ago. Blood pressure is 195/115 mm Hg and pulse is 90/min and regular. Lung examination reveals bibasilar crackles. Nitroglycerin infusion is started and results in significant symptomatic improvement. Repeat blood pressure is 165/90 mm Hg. Which of the following intracellular events is most likely responsible for the beneficial effects of this patient's treatment? A. Actin phosphyorylation B. Calcium release from sarcoplasmic reticulum C. Enhanced cyclic mononucleotide degradation D. Inositol triphosphate accumulation E. Myosin dephosyphoylation F. Tyronsine kinase activat

This patient's clinical presentation is consistent with acute pulmonary edema due to severely elevated blood pressure (hypertensive emergency). In such cases, intravenous vasodilators (nitroglycerine, sodium nitroprusside) are often used to improve the acute heart failure by reducing preload and afterload. Nitrates are metabolized within vascular smooth muscle cells to nitric oxide, which activates guanylate cyclase and promotes the conversion of guanosine triphosphate (GTP) to cyclic guanosine monophosphate (cGMP). Increased levels of cGMP lead to decreased intracellular calcium (reduces the activity of myosin light-chain kinase) and activation of myosin light chain phosphatase. This promotes myosin light-chain dephosphorylation and vascular smooth muscle relaxation. (Choice A) Actin phosphorylation has no role in smooth or skeletal muscle relaxation. In smooth muscle, a stimulus to contract leads to increased intracellular calcium, which leads to myosin phosphorylation. Once myosin is phosphorylated, it is able to bind directly to actin and cause muscle contraction. (Choice B) Calcium release from sarcoplasmic reticulum would lead to increased contraction of the cardiac myocytes. It is not involved in the mechanism of action of nitrates on vascular smooth muscle cells. (Choice C) Nitrates do not cause an increase in cyclic mononucleotide degradation. On the contrary, they activate guanylate cyclase and promote conversion of GTP to cGMP, which ultimately leads to smooth muscle relaxation. (Choice D) Inositol triphosphate binds to its receptor on the endoplasmic reticulum and leads to the release of Ca2+ into the cytoplasm. In vascular smooth muscle cells, this increased concentration of cytoplasmic Ca2+ results in increased smooth muscle contraction. (Choice F) Tyrosine kinases play a role in a wide variety of intracellular processes and pathways. The effects of insulin and insulin-like growth factor occur via activation of receptor tyrosine kinases, which in turn cause phosphorylation of tyrosine residues on intracellular proteins important for signal transduction. Educational objective:Nitrates (via conversion to nitric oxide) activate guanylate cyclase and increase intracellular levels of cyclic guanosine monophosphate (cGMP). Increased levels of cGMP lead to myosin light-chain dephosphorylation, resulting in vascular smooth muscle relaxation.

68 yr old/ several weeks of progressive exertional dyspnea and lower extremity edema/med hx non-hodgkin lymphoma (in remission after chem)/ bibasilar lung crackles and 1+ bilateral lower extremity edema. Eco shows biventricular dilation and LVEF of 35%/ is inicative of?

This patient's clinical presentation is consistent with decompensated systolic heart failure (HF) due to nonischemic cardiomyopathy, likely as a result of chemotherapy for non-Hodgkin lymphoma. After initial stabilization, long-term use of beta blockers (eg, carvedilol, metoprolol) has been shown to improve survival in patients with HF due to left ventricular systolic dysfunction.

Jervell and Lange-Nielsen syndrome describe it?

This patient's clinical presentation is suggestive of Jervell and Lange-Nielsen syndrome, an autosomal recessive disorder characterized by profound bilateral sensorineural hearing loss and congenital long QT syndrome, which predisposes individuals to syncope and sudden cardiac death. This syndrome occurs secondary to mutations in genes (eg, KCNQ1, KCNE1) that encode the alpha and beta subunits of voltage-gated potassium channels. These subunits contribute to the slow-acting component of the outward-rectifying potassium current, which is responsible for ventricular repolarization during phase 3 of the cardiac action potential. Mutations in the potassium channel lead to a decrease in potassium current with prolongation of action potential duration and the QT interval. QT interval prolongation predisposes to the development of life-threatening ventricular arrhythmias, such as torsades de pointes and ventricular fibrillation.

This patient's constipation and new-onset second-degree atrioventricular (AV) block (causing syncope) could be due to?

This patient's constipation and new-onset second-degree atrioventricular (AV) block (causing syncope) are likely adverse effects of therapy with a nondihydropyridine calcium channel blocker (CCB) (eg, diltiazem, verapamil). These drugs are frequently used to treat hypertension, angina pectoris, and supraventricular arrhythmias, including atrial fibrillation (as in this patient).

This patient's holosystolic murmur along the lower left sternal border and a palpable thrill are consistent with ?

This patient's holosystolic murmur along the lower left sternal border and a palpable thrill are consistent with a ventricular septal defect (VSD), an abnormal communication between the right ventricle (RV) and the left ventricle (LV).

What is PNH due to?

This patient's presentation is consistent with paroxysmal nocturnal hemoglobinuria (PNH), a disorder due to complement-mediated hemolysis. PNH is usually due to a mutated phosphatidylinositol glycan class A (PIGA) gene, which helps synthesize the glycosylphosphatidylinositol (GPI) anchor protein. This protein helps attach several cell surface proteins (eg, CD55 decay accelerating factor, CD59 MAC inhibitory protein) that inactivate complement. Absence of these proteins leads to uncontrolled complement-mediated hemolysis.

Fibrous thickening and fusion of the valve leaflets in which disease?

This patient's presentation suggests mitral stenosis (MS) due to rheumatic heart disease. Fibrous thickening and fusion of the valve leaflets in chronic rheumatic heart disease following acute rheumatic fever is the most common cause of MS, accounting for up to 99% of cases. There is often a latency period of 10-20 years between the initial episode of rheumatic fever and symptomatic MS, with most patients manifesting during the fourth or fifth decade of life. Mitral stenosis can cause atrial enlargement, which may lead to atrial fibrillation and/or atrial mural thromboses. Thrombi dislodged from the wall of the left atrium may later cause an embolic stroke, which likely occurred in this patient. Cardiac auscultation in mitral stenosis often reveals a loud first heart sound (S1), an early diastolic sound (opening snap), followed by a mid-diastolic murmur from turbulent flow across the mitral valve.

What is the strongest risk factor for aortic dissection.

Medical therapy for aortic dissection is aimed at reducing aortic wall shear stress to limit extension of the dissection- what can be used?

This patient's severe chest pain radiating to the back and a widened mediastinum on chest x-ray are consistent with acute aortic dissection. Uncontrolled hypertension, suggested by the patient's nonadherence with medical therapy and ECG evidence of left ventricular (LV) hypertrophy, is the strongest risk factor for aortic dissection. With each LV contraction, the ejected stroke volume rapidly increases aortic pressure and generates shear stress on the aortic wall. Medical therapy for aortic dissection is aimed at reducing aortic wall shear stress to limit extension of the dissection. This is accomplished via anti-impulse therapy to decrease the rate of change in aortic blood pressure per time (ie, reduce dP/dt).

Describe clonidine, how it works and how it can cause orthostatis?

This patient's syncopal episodes are due to bradycardia and decreased peripheral vascular resistance caused by clonidine. Clonidine is used in the treatment of severe or refractory hypertension. It exerts its effects on both heart rate and blood pressure by stimulating presynaptic alpha-2 adrenergic receptors in the rostral ventrolateral medulla (area responsible for basal and reflex control of sympathetic activity). This effect results in a subsequent decrease in presynaptic release of norepinephrine and decreased sympathetic outflow causing both bradycardia and a decrease in peripheral vascular resistance.

What sound would you expect to hear for mitral regurgitaion?

This point corresponds to the start of left ventricular contraction, just after mitral valve closure and just prior to the opening of the aortic valve; it would mark the onset of the holosystolic murmur of mitral regurgitation.

Describe wolff-parkinson-white sydrome?

This young patient's repeated episodes of palpitations are suggestive of paroxysmal supraventricular tachycardia, and the physician suspects Wolff-Parkinson-White (WPW) syndrome. WPW syndrome is caused by an accessory conduction pathway (bundle of Kent) that allows electrical conduction impulses to bypass the atrioventricular node and cause preexcitation of the ventricles. This preexcitation leads to characteristic findings on baseline ECG, including a shortened PR interval (often <0.12 seconds), early upslope of the QRS complex (delta wave), and a widened QRS complex.

How does thrombotic microangiopathies cause problems for the kidney, would you see any type of crystals?

Thrombotic microangiopathies (eg, hemolytic uremic syndrome) cause endothelial injury characterized by microthrombi in the glomerular capillaries and fibrinoid necrosis of the arterioles; schistocytes are commonly seen on microscopy. Proximal tubules are typically unaffected, and oxalate crystals would not be seen.

Transcatheter aortic valve implantation (TAVI) what is it, how can be shown on intraoperative readings, and what are complications?

Transcatheter aortic valve implantation (TAVI) allows for minimally invasive management of severe aortic stenosis in elderly patients who are unable to tolerate open surgical valve replacement. Paravalvular aortic regurgitation is a common complication of TAVI, resulting from improper sealing of the prosthetic valve to the native aortic valve annulus. This patient's intraoperative pressure readings of decreased diastolic blood pressure and increased LVEDP (left ventricular end-diastolic pressure) are consistent with aortic regurgitation, a common complication of TAVI that results from improper sealing of the prosthetic valve to the native valve annulus, leading to paravalvular leak (blood leakage around the valve). Inappropriate valve size or improper valve positioning is often responsible.

Where do you see transmural inflammation of the arterial wall with fibrinoid necrosis?

Transmural inflammation of the arterial wall with fibrinoid necrosis can be seen in several types of systemic vasculitis, including polyarteritis nodosa (PAN). PAN affects small and medium-sized arteries and can involve numerous organs (eg, kidney, gastrointestinal system, skin). Patients commonly present with fever, hypertension, abdominal pain, and/or cutaneous lesions (eg, nodules, livedo reticularis).

What risk does trastuzumab have on the heart?

Trastuzumab is a monoclonal antibody used in the treatment of breast cancer caused by tumor cells that overexpress human epidermal growth factor receptor-2 (HER2). By binding to HER2, trastuzumab blocks downstream signaling that promotes cellular proliferation and thereby encourages malignant cell apoptosis. The major adverse effect of trastuzumab is a risk of cardiotoxicity, likely because HER2 signaling plays a role in minimizing oxidative stress on cardiomyocytes and preserving cardiomyocyte function. Cardiotoxicity typically manifests as a decrease in myocardial contractility (myocardial stunning) without cardiomyocyte destruction or myocardial fibrosis. Patients usually experience an asymptomatic decline in left ventricular ejection fraction; however, overt heart failure can also occur. Unlike the cardiotoxicity that occurs with anthracyclines (eg, doxorubicin), trastuzumab-induced cardiotoxicity is not related to the cumulative chemotherapy dose and is often reversible with discontinuation of therapy.

What is tropical sprue? What is the presentation?

Tropical sprue can occur with extended travel to the tropics and presents with chronic diarrhea, abdominal pain, and flatulence along with similar histologic findings to celiac disease (eg, villous atrophy). The etiology is likely infectious, and the disease is treated with antibiotics. However, this patient has no history of travel.

What is the preferred initial imaging for diagnosis of acute cholecystitis and if it doesn't work what do you use?

Ultrasonography is the preferred initial imaging test for the diagnosis of acute cholecystitis; however, nuclear medicine hepatobiliary scanning (ie, cholescintigraphy) can be an alternate means when ultrasonography is inconclusive. During a hepatobiliary scan, a radiotracer is administered intravenously and is preferentially taken up by hepatocytes and excreted into bile. Images of the tracer as it moves through the hepatobiliary system and intestine are then obtained for up to several hours after injection.

What is the more specific investigation findings for cholecystitis? What do you do if ultrasound is unclear?

Ultrasound findings more specific for acute cholecystitis include gallbladder wall thickening, pericholecystic fluid, and a positive sonographic Murphy sign. When ultrasound is inconclusive, nuclear medicine hepatobiliary scanning (ie, cholescintigraphy) can be used to assess cystic duct patency and make the diagnosis.

How do astrocytes prevent excessive neural excitation?

Under normal conditions, astrocytes regulate neurotransmission by taking up glutamate present in the synapse, preventing excessive neuronal excitation. Through the action of glutamine synthetase, glutamate undergoes a condensation reaction with ammonia to form glutamine (a non-neuroactive compound). Glutamine is then released by the astrocytes and taken up by neurons, where it is converted back to glutamate for use as a neurotransmitter (glutamate-glutamine cycle).

What are upper airway manifestations?

Upper airway: otitis media, nasal crusting/ulcers, rhinorrhea

With ethylene glycol poisoning, what do you expect to see on lab and urine analysis

Urinalysis shows tubular casts and oxalate crystals. Other common laboratory findings include a markedly elevated anion gap metabolic acidosis (due to acid metabolite formation) and an elevated osmolar gap (due to the uncharged parent alcohol).

Valsartan is what type of drug, used for? What is the common adverse effects?

Valsartan is an angiotensin II receptor blocker used in the management of hypertension and heart failure with reduced ejection fraction. Common adverse effects include hypotension and hyperkalemia.

Viral hepatitis induces a robust _________ response against infected hepatocytes, which typically leads to elevations in _________. Although viral hepatitis may cause acute liver failure, it would be associated with________.

Viral hepatitis induces a robust CD8+ T-cell response against infected hepatocytes, which typically leads to elevations in aminotransferases. Although viral hepatitis may cause acute liver failure, it would be associated with increased bilirubin and jaundice (especially with marked AST/ALT elevation).

What is the purpose of vitamin E? What happens when you have a vitamin E deficiency? Which cells are most susceptible when you have a vitamin E deficiency?

Vitamin E primarily serves to protect fatty acids from oxidation; vitamin E deficiency predisposes cell membranes to oxidative injury. The cells that are most susceptible include neurons with long axons (due to large membrane surface area) and erythrocytes (due to high oxygen exposure).

When there is excess ammonia, what happens to astrocytes?

When excess ammonia is present in the blood, it crosses the blood-brain barrier and is taken up by astrocytes, increasing glutamine production. The presence of excess glutamine within astrocytes leads to increased intracellular osmolarity, causing astrocyte swelling and impaired glutamine release. Hyperammonemia consequently decreases the amount of glutamine available for conversion to glutamate in neurons, resulting in disruption of excitatory neurotransmission.

Describe the triggers to autoregulate?

When myocardial perfusion pressure decreases, there is decreased oxygen delivery to the myocardium and less ATP is regenerated via oxidative metabolism, resulting in increased levels of adenosine. Myocardial hypoxia also triggers increased synthesis of nitric oxide. Increased levels of both adenosine and nitric oxide act on vascular smooth muscle to stimulate vasodilation, allowing for a relative increase in coronary blood flow at the new, lower perfusion pressure (ie, coronary blood flow is maintained). A similar process occurs when coronary perfusion pressure increases; decreased levels of adenosine and nitric oxide increase vascular resistance, causing coronary blood flow to remain relatively unchanged at the new, higher perfusion pressure. The myocardium has the highest resting oxygen requirement of any tissue in the body, extracting >70% of available oxygen from the blood at baseline (compared to ~30% in most other tissues). As such, a significant increase in myocardial oxygen demand can only be met through a corresponding increase in coronary blood flow.

What's the smaller vs larger VSDs oxygen shunt?

With smaller VSDs, blood is shunted mainly from left to right due to the high pressure differential between the ventricles. As a result, right ventricular SpO2 increases but left ventricular SpO2 remains relatively normal. Larger VSDs allow equalization of chamber pressures, which results in more bidirectional mixing and decreased left ventricular SpO2. Right atrial SpO2 remains normal with VSDs of any size, unless tricuspid regurgitation is also present.

When autoregulation falls in the region of 60-140 mmHg describe what drives the changes?

Within the region of autoregulation (eg, 60-140 mm Hg), changes in coronary blood flow are driven primarily by myocardial oxygen demand.

Coronary autoregulation is

a process that maintains myocardial blood flow in settings of decreased coronary perfusion pressure (eg, hemorrhage, sepsis).

This patient with fatigue, dyspnea on exertion, orthopnea, cough, and lower extremity swelling is in what can they have?

acute decompensated heart failure

Echinococcus is what and how is it diagnosed?

an animal tapeworm (eg, dogs, sheep) that can cause large liver cysts and pulmonary symptoms in humans. It is usually diagnosed with a combination of imaging (eg, hydatid cysts are visualized on liver ultrasound) and serologic tests.

patient/2 week hx of progressive fatigue and exertional dyspnea/evidence of not being able to breath while walking/no chest pain or palpitations/no stimulant problems/cardiac ausculation reveals murmur that is heard when the patient sits up and leans forward.

aortic regurgitation

head bobbing is a sign of and what other physical examination findings would you see?

aortic regurgitation. Forceful pulsations in the intracranial arteries can cause head bobbing with each heart beat (de Musset sign), and patients may experience palpitations due to forceful left ventricular contraction. In addition, physical examination can show abrupt distension and collapse of the carotid arteries (Corrigan sign) and peripheral arteries ("water-hammer" pulse), and reveal "pistol-shot" femoral pulses (Traube sign) on auscultation.

Postprandial alkaline tide is defined

as an increase in plasma HCO3‾ and decrease in plasma Cl‾ secondary to the surge of acid within the gastric lumen. It is not an important factor in the down-regulation of postprandial gastric secretion. Educational

Arterial narrowing can manifest as?

audible bruits

This patient with elevated blood pressure, tachycardia, palpitations, and anginal pain following recent discontinuation of metoprolol is most likely experiencing ?

beta blocker withdrawal syndrome. With changes in environmental stimulus, the feedback mechanisms in cells adjust the density of cell surface membrane receptors to regulate sensitivity to the stimulus. Prolonged beta-adrenergic blockade, for example, stimulates an increase in surface membrane expression of beta-adrenergic receptors, a process called upregulation. When beta-adrenergic blockade is abruptly withdrawn, the increased density of beta-adrenergic receptors creates an amplified response to circulating catecholamines (ie, increased sensitivity). Because metoprolol is cardioselective and primarily blocks beta-1 receptors, abrupt cessation stimulates beta-1 receptor-mediated increased heart rate and cardiac contractility. There is also increased blood pressure due to increased cardiac output. These changes create increased oxygen demand that may cause ischemia (evidenced by ST depression on ECG) and trigger angina in patients with underlying coronary artery disease.

Nondihydropyridine calcium channel blockers (eg, diltiazem, verapamil) works by?

block calcium channels in the atrioventricular node and ventricular myocardium, resulting in slowed cardiac conduction (ie, heart rate) and decreased contractility, which can contribute to orthostatic syncope. Amlodipine, a dihydropyridine calcium channel blocker, has minimal effect on the heart and functions primarily as a direct vasodilator.

impaired bilirubin conjugation also occurs in Crigler-Najjar syndrome but what's the difference between that and Gilbert Disease?

but patients typically have severe, chronic hyperbilirubinemia that begins in the neonatal period and can be associated with bilirubin-induced neurologic dysfunction.

What is C-myc overexpressed in?

c-MYC is a protooncogene overexpressed in Burkitt lymphoma, which usually presents with a facial mass (eg, endemic African form) or with ascites and multi-organ involvement (eg, sporadic form).

Chronic gastroesophageal reflux disease and esophagitis? And risk of?

can lead to Barrett metaplasia and can increase the risk for esophageal adenocarcinoma.

A 14-month-old girl is brought to the office due to a 2-month history of diarrhea. Her parents report that she has 3-5 loose, nonbloody bowel movements daily with occasional episodes of vomiting. She was breastfed exclusively until age 9 months and has since had a well-varied diet including whole milk, fruits, vegetables, bread, and meats. However, the girl has been less interested in food over the past several weeks. There is no history of travel or contacts with similar symptoms. On physical examination, the patient appears well but has lost 1.1 kg (2.5 lb) in the last 2 months. After laboratory evaluation, duodenal biopsy findings are shown in the exhibit. Which of the following would most likely improve this patient's symptoms?

celiac disease less gluten

Glutathione peroxidase actually reduces what activity?

cellular injury by catalyzing free radical breakdown. The presence of this enzyme is not responsible for the release of creatine kinase.

Decreased presynaptic release of acetylcholine occurs with?

certain toxins (eg, botulinum) and some medications (eg, aminoglycoside antibiotics). This effect leads to muscle weakness and does not contribute to syncope.

Cellular swelling arises secondary to and considered a hallmark of?

changes in ion concentration and the influx of water. This state is considered a hallmark of reversible injury

Common bile duct obstructions increase what and lead to what?

conjugated bilirubin in the bloodstream, leading to jaundice and dark-colored urine; they also prevent bilirubin from entering the digestive tract, which results in clay-colored (acholic) stools. The vast majority (>85%) of obstructing pancreatic masses are due to pancreatic ductal adenocarcinoma.

The combination of recurrent respiratory infections and diarrhea in a child or young adult is strongly suggestive of

cystic fibrosis with secondary exocrine pancreatic insufficiency. Because pancreatic enzymes are necessary for the proper absorption of nutrients in the gut, fat malabsorption with deficiencies of the fat-soluble vitamins A, D, E, and K frequently occurs in patients with cystic fibrosis.

Progressive dyspnea, weight gain, peripheral edema is indicative of?

decompensated heart failure

Cabergoline is what type of drug?

dopamine agonist used in growth hormone-secreting pituitary tumors or prolactinoma.

What are manifestations of superficial thrombophlebitis?

erythema, tenderness along veins

Beta blockers are commonly used for and the adverse effects?

heart rate control in patients with atrial fibrillation and can cause or worsen AV block. However, propranolol is a nonselective beta blocker that impairs bronchodilation and is typically avoided in patients with severe chronic obstructive pulmonary disease. In addition, constipation is not a significant adverse effect of beta blockers.

What are hemosiderin laden macrophages from?

his patient's autopsy demonstrates an abundance of alveolar macrophages filled with brown pigment in the lung parenchyma. Hemosiderin-laden macrophages located in the lungs are usually the result of chronic passive lung congestion in the setting of heart failure (eg, left ventricular systolic dysfunction). Elevated pulmonary venous pressure leads to transudation of fluid across the alveolar-capillary membrane (pulmonary edema) and can cause breaks in the endothelium with extravasation of red blood cells into the alveoli and lung parenchyma. As alveolar macrophages engulf and degrade the extravasated red blood cells, the released iron accumulates as intracellular hemosiderin.

What influences down regulation of gastric acid secretions?

intestinal influences are effective in down-regulating gastric acid secretion after a meal. The ileum and colon release peptide YY, which binds to receptors on the endocrine, histamine-containing cells described as enterochromaffin-like (ECLs). Such binding counteracts the cephalic and gastric phases of acid secretion by inhibiting gastrin-stimulated histamine release from ECLs. Other factors that inhibit acid secretion include somatostatin and prostaglandins.

Coarctation of the aorta is associated with and puts you at risk for?

is a congenital cardiac defect associated with secondary hypertension and is a risk factor for cerebral aneurysm development

What are the lab findings indicative of glomerulonephritis>

laboratory findings of glomerulonephritis (hematuria, increased creatinine). (eg, microscopic hematuria, red cell casts, negative nitrate/bacteriuria)

What is indicative of an infant having a large VSD?

large VSDs often present in early infancy with signs of heart failure (eg, poor feeding, sweating/tachypnea with feeds) and failure to thrive due to left-sided volume overload with inability to maintain adequate cardiac output.

Most gastric ulcers arise along the?

lesser curvature of the stomach, usually at the transitional zone between the gastric corpus (body) and antrum. Glands in the corpus contain parietal cells that produce hydrochloric acid and intrinsic factor; mucosal glands in the antrum contain G cells that secrete gastrin. This transitional zone provides the optimal microenvironment (eg, pH, host immune factors) for H pylori proliferation.

How do Direct arteriolar vasodilators?

lower blood pressure but trigger reflex sympathetic activation and stimulate the renin-angiotensin-aldosterone axis. This results in tachycardia and edema. To counteract such compensatory effects, these agents are often given in combination with sympatholytics and diuretics. Although selective arteriolar vasodilators trigger reflex sympathetic activation, this does not raise blood pressure above baseline unless they are discontinued abruptly.

Waht is coarctation of the aorta?

narrowing of the aortic arch near the ligamentum arteriosum (remnant of ductus arteriosus) with localized medial and intimal hyperplasia.

Normal villi function is for?

normal intestinal villi allow for increased small intestinal surface area to begin the process of digestion and nutrient absorption.

An isolated pancreatic mass with common bile duct obstruction is far more likely to be?

pancreatic adenocarcinoma.

What can be given and how does it help?

patient has decompensated heart failure with ongoing volume retention despite high doses of oral furosemide (ie, loop diuretic) therapy. Thiazide diuretics, especially metolazone, potentiate the diuretic effect of loop diuretics and can be helpful in treating refractory volume overload. Sodium is the major determinant of volume status. Loop diuretics function by inhibiting the Na-K-2Cl cotransporter in the ascending limb of the loop of Henle to block sodium absorption and encourage the excretion of sodium and water in the urine. However, the sodium excretion caused by loop diuretics is limited by the reabsorption of sodium in the distal convoluted tubule; the Na-Cl cotransporter in the distal tubule counteracts some of the effect of loop diuretics by absorbing much of the sodium that is not absorbed in the loop of Henle. Inhibition of the Na-Cl cotransporter with metolazone prevents reabsorption of the increased sodium delivered to the distal tubule, significantly increasing total sodium excretion.

This patient with fever, dysuria, flank pain, and right costovertebral angle tenderness likely has

pyelonephritis. In addition, her hypotension in the setting of infection suggests septic shock. Septic shock is the most common type of distributive shock; other types include anaphylactic shock and neurogenic shock.

Thiazide diuretics have what metabolic complications?

s (eg, chlorthalidone, hydrochlorothiazide) treatment of hypertension. However, thiazides, especially in higher doses, can cause a variety of metabolic complications, including hypercalcemia, hyperglycemia, hyperlipidemia, hyponatremia, and hypokalemia.

Hydrochlorothiazide is what type of drug and then what is the adverse effect?

thiazide diuretic used for the treatment of hypertension. It has no role in the management of atrial fibrillation. Adverse effects include hypokalemia and hyponatremia.

Describe persisten

this patient has an extracardiac right-to-left shunt across a patent ductus arteriosus (PDA), a condition typically associated with persistent pulmonary hypertension of the newborn (PPHN) or congenital heart diseases with left-sided outflow tract obstruction (eg, severe aortic coarctation).

This patient with dyspnea and dry cough has pulmonary infiltrates and hilar adenopathy with multiple, noncaseating granulomas is suggestive of?

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