UW Step 2 mostly cardiovascular

Treatment of supraventricular and ventricular tachyarrhythmias.

Amiodarone- not used in cases of bradycardia because it slows the SA and AV nodes.

Treatment of hypertrophic cardiomyopathy

15-25% of patients report syncope as a symptom. Many others will have presyncope and chest pain with exertion as this pt has had previously. The disease has an autosomal dominant inheritance pattern and can often lead to sudden death so the sudden death of his uncle is a strong clue. Finding of a systolic murmur at eh left sternal border points to hypertrophic cardiomyopathy as opposed to aortic stenosis, which typically creates a murmur at the RIGHT upper sternal border. The murmur classically worsens with maneuvers that decrease preload since the smaller ventricular volume then leads to a higher degree of obstruction. Hypertrophied myocardium leads to primarily diastolic heart failure. Therefore, beta blockers are one of the treatments of choice since they slow the heart and prolong diastole, leading to more time for the heart to fill and therefore less outflow obstruction. Beta blockers have an anti-anginal effect as well. A calcium channel blocker like diltiazem is also a good option if patients are unable to tolerate beta blockers. Disopyramide is an antiarrhythmic drug with negative inotropic properties as well, and is an option for treating patients with hypertrophic cardiomyopathy. It is very effective in reducing the pressure gradient across the obstructing hypertrophied myocardium, however it is not considered first line therapy in part to its potential to be pro-arrhythmogenic.

36 year old man presents to your office for a routine pre-employment physical. No complaints except occasional mornign headaches. Father died suddenly at age 54. Patient's blood pressure is 175/103 mm Hg in the right arm and 180/105 in teh left arm. HR 82. Lungs clear bilaterally and his heart sounds are normal. Bilateral, non-tender, upper abdominal masses are palpated on exam. His Hemoglobin level is 15.2 g/dl and creatinine concentration is 0.8 mg/dl. What is needed to diagnose pt?

Abdominal ultrasound Pt most likely has PKD and should undergo abdominal ultrasonography, PKD is an autosomal dominant condition characterized by bilateral cystic dilation of the renal tubules. Hypertension is one of the earliest manifestations of the disease. Hematuria is often the presenting symptom. Other signs and symptoms icnlude flank or abdominal masses, pain, secondary erythrocytosis due to increased erythropoietin production, and renal failure. PKD is associated with cerebral aneurysms and patients with PKD may have a family hx of stroke or sudden death. Easily diagnosed by abdominal ultrasound.

Sarcoidosis

African-American woman in the 3rd or 4th decades of life- half of cases are diagnosed based on incidental findings on chest x-rays. Cough, dyspnea, fever and weight loss. While lungs are the most frequently involved organ system, the skin (erythema nodosum), eyes (anterior uveitis), joints (arthritis), and many other organ systems may be affected. Classic findings on chest x ray include bilateral hilar adenopathy and reticular opacities, both of which are present in this patient. Descriptoin of red eye with leukocytes in the anterior chamber is consistent with anterior uveitis.

Which clotting factors does the liver synthesize?

All EXCEPT VIII. Chief among these are Vitamin K dependent factors like Factor II, VII, IX and X. Fresh frozen plasma is the therapeutic agent of choice for the coagulopathy in patients with liver failure.

Acute renal failure, associated with arthralgia, rash, WBC casts made of mostly eosinophils

Allergic interstitial nephritis: cephalosporins, penicillins, sulfonamides, NSAIDS, rifampin, phenytoin, and allopurinol. Patients present with arthralgias, raqsh, renal failure and the urinalysis will show eosinophiluria.

55 year old male with a hx of rheumatoid arthritis and rheumatoid lung disease is admitted with palpitations. Restrictive lung disease is moderate severity, req use of 2 L o2 by nasal cannula at all times. No known hx of CAD, HTN or DM. On PE, BP is 110/70, hr is 120 and irregular. EKG shows atrial fibrillation with rapid vent rate. avoid what medication?

Amiodarone- can cause pulmonary toxicity adn should be avoided in pts with perexisting lung disease. Can cause chronic interstitial pneumonitis, organizing pneumonia, and even ARDS. Lung toxicity is related to the cumulative total dose administered.

Treatment for stable chronic angina

Anti anginal: Beta blocker- 1st line therapy for anginal symptoms, improves exercise tolerance. Relieves angina by decreasing myocardial contractility and HR. Improves survival in those with MI. Calcium channel blocker can combine with beta if angina persists or as alternate therapy. improves by causing peripheral and coronary vasodilation Nitrates- short acting form is used in the acute setting. Long acting form is an add-on therapy for persistent angina. Preventative -aspirin -statin -smoking cessation -regular exercise and weight loss -control of blood pressure and diabetes

65 year old bedridden woman- weight loss, weakness, malaise. COPD and HTN. Quit smoking 2 years ago but previous smoked 3 packs daily since she was 20. Severe weakness in her proximal muslces, loss of DTR. CXR shows right upper lung mass with mediastinal lymphadenopathy. CPK is normal. Cause of weakness?

Antibodies to voltage gated calcium channels. Small cell carcinoma of the lung is associated with Lambert Eaton or Myasthenia gravis. Tx: plasmapheresis/immunosuppresive drug therapy. In myasthenia gravis, DTR are usually preserved.

Syncope with exertion or during exercise

Aortic stenosis, hypertrophic cardiomyopathy, anomalous coronary arteries

Which arrhythima is most specific for digitalis toxicity?

Atrial tachycardia with AV block- dig can increase ectopy in teh atria or ventricles, which can lead to atrial tachycardia. A tach is distinguished from atrial flutter by its somewhat slower atrial rate (150-250 bpm as opposed to 250-350 bpm). P-waves are present, but may appear different from teh p-waves normally seen when conduction originates in the SA node. in atrial tachycardia, the closer the ectopic focus is to the SA node, the closer the resemblance of its p-waves to normal p-waves originating from the SA node. In addition to causing ectopic rhythms, digitalis can also increase vagal tone and decrease conduction through the AV node, potentially causing AV block. Since it is rare for both ectopy and av block to occur at the same time, when they do, the combination is fairly specific for digitalis toxicity.

Secondary causes of hypertension, clinical clues/features: Elevated serum creatinine and abnormal urinalysis (proteinuria, RBC casts)

renal prenchymal disease

Causes of A-fib

Cardiac causes- hypertension, acute ischemia, heart failure, myopericardial inflammation, valve disease, surgery Pulmonary causes- acute lung disease (eg pneumonia), pulmonary emboli, and hypoxia Metabolic conditions- catecholamine surges or hyperthyroidism also. Drugs- alcohol, cocaine, amphetamines and theophylline.

Most patients present with hypertension and are asymptomatic. Headaches, epistaxis, blurred vision, or heart failure due to severe hypertension 29 year old male, ED visit for epistaxis requiring anterior nasal packing. BP was 170/110. Occasional headaches and fatigue but no chest pain, palpitations or syncope. PMH unremarkable and doesn't use tobacco, alcohol or illicit drugs. Current BP is 180/112 and pulse 78 and regular. Cardiac ausc in supine position shows no murmurs or additional sounds. No periumbilical bruits. ECG shows normal sinus rhythm, high voltage QRS complexes, downsloping ST segment depression adn t wave inversion in leads V5 and V6. Hb 14.2, Platelets 230,000, creatinine 1.0 Best next step?

Bilateral arm and leg blood pressure measurements PE: brachial-femoral delay differential bp in the upper and lower extremities well dev'p upper body compared to lower body continuous cardiac murmur from flow through large collateral vessels ECG- left ventricular hypertrophy CXR- notching of the 3rd-8th ribs due ot eroson by enlarged intercostal arteries Classic " 3 " sign caused by indentation of the aorta at the site of coarctation with pre and post stenotic dilatation. Echocardiography, CT or MRI will diagnose. Associated with: bicuspid aortic valve, patent ductus arteriosus, ventricular septal defect, Turner syndrome

vomiting/retching and chest/upper abdominal pain with rapid progression to odynophagia, fever, dyspnea, and septic shock.

Boerhaave syndrome. Often shows fever, tachycardia, tachypnea, cyanosis, and subcutaneous emphysema. Chest xray may reveal pneumomediastinum or unilateral pleural effusions (usually left) with or without pneumothorax. Computed tomography or contrast esophagography with gastrografin confirms the diagnosis. Constrast esophagography with gastrografin will show contrast extravasation from the esophagus into surrounding areas. Pleural fluid analysis is typically exudative with low pH and very high amylase (>2500 IU due to saliva in the esophageal contents) and may contain food particles.

Site of hemorrhage: Cerebellum

Neck stiffness Facial weakness Usually NO hemiparesis Stupor or coma from brainstem herniation

Pericardial tamponade and pressures

Causes increased right atrial and ventricular pressures in addition to characteristic equalization of right atrial, right ventricular end diastolic, and PCW pressures. A decrease in cardiac output would also cause low mixed venous oxygen saturation.

Site of hemorrhage: Cerebral lobe

Can be associated with seizures Contralateral homonymous hemianopsia (occipital lobe) Contralateral plegia/paresis (frontal lobe) Contralateral hemiparesis (parietal lobe) Eyes are deviated away from the hemiparesis The most common (30%) site of hypertensive hemorrhages is the putamen. The internal capsule that lies adjacent to theputament is almost always involved, leading to contralateral dense hemiparesis.

Diagnosis of renal artery stenosis- technique

Captopril renal scan- RAS typically presents with refractory hypertension but few other symptoms. Does not cause bilateral kidney enlargement.

CHADS2 score

Choice of anticoagulation depends on the patient's CHADS2 score: Age > or = 75 1pt HTN 1 pt DM 1 pt CHF 1 pt Prior stroke 2 pts CHADS2 score of 0= low risk and can be treated with aspirin. CHADS2 score > 2 higher risk and should get anticoagulation with eithre warfarin or dabigatran (new direct thrombine inhibitor), patients with chads2 score of 1 or 2 are considered intermediate risk and may receive either aspirin or anticoagulation depending on the clinical circumstances and patient preference. This patient has a CHADS2 score greater than 3 and would benefit most from anticoagulation to prevent embolic stroke, a long-term complication of atrial fibrillation

Etiology of acute pancreatitis

Chronic alcohol use, gallstones HLD types I, IV, and V Drugs: eg didanosine, azathioprine, valproic acid Infections eg cytomegalovirus, legionella, aspergillus Trauma iatrogenic (post-ercp)

Secondary causes of hypertension, clinical clues/features: Differential hypertension with brachial-femoral pulse delay

Coarctation of the aorta

Syncope: Family history of sudden death, prolonged QT inteval on ECG, syncope with triggers (exercise, swimming, sudden noise, during sleep)

Congenital long QT syndrome

Clinical manifestations of hereditary hemochromatosis

Constitutional- lethargy, fatigue, malaise and weakness integumentary- skin pigmentation or discoloration (bronze diabetes) musculoskeletal- arthralgia, arthropathy and chondrocalcinosis gastrointestinal- elevated heaptic enzymes with hepatomegaly (early), fibrosis and cirrhosis (later) and increased risk of heaptocellular carcinoma Endocrine- diabetes mellitus, hypogonadotropic hypogonadism (impotence, decrease in libido, premature amenorrhea), and hypothyroidism Cardiac- restrictive or dilated cardiomyopathy and conduction abnormalities Infections- increased susceptibility to infections with listeria, vibrio vulnificus and yersinia enterocolitica

Secondary causes of hypertension, clinical clues/features: Central obesity, facial plethora, proximal muscle weakness, abdominal striae, ecchymosis, amenorrhea/erectile dysfunction, hypertension with adrenal incidentaloma

Cushing's syndrome

Systolic heart failure Cardiac index TPR LVEDV

Systolic heart failure- CI is decreased, LVEDV- increased, TPR- increased due to neurohumoral activation that includes sympathetic hyperactivity and activation of the renin-angiotensin-aldosterone system.

Side effect of niacin- pathophysiology

Cutaneous flushing and intensive generalized pruritus are well-known side effects of high dose niacin therapy (high dosage is required to treat lipid abnormalities). These effects are explained by niacin-induced peripheral vasodilation, not vasoconstriction. MOA- drug-induced release of histamine and prostaglandins, not a true hypersensitivity rxn. The role of prostaglandins is confirmed by the fact that low-dose aspirin can greatly reduce or prevent cutaneous flushing and pruritus if taken 30 minutes before niacin. Therefore, niacin is frequently prescribed with aspirin. Flushing and pruritus usually improve after 2-4 weeks of thearpy.

Patient presents with abdominal pain and suprapubic fullness several days after starting amitryptyline for chronic pain

amitriptyline induced urinary retention. Amitriptyline is a tricyclic antidepressant with anticholinergic properties. Because both the detrusor muscle and urethral sphincter are under muscarinic control, anticholinergic agents will reduce detrusor contraction adn prevent urethral sphincter relaxation>urinary retention. Urinary catherization- 1. document a postvoid residual bladder volume of greater than 50 ml = urinary retention 2. symptomatic relief as it drains urine from the bladder. Discontinue TCA.

Site of hemorrhage: Pons`

Deep coma and total paralysis within minutes after hemorrhage Pinpoint reactive pupils

Common acute life-threatening reactions associated with HIV therapy include:

Didanosine-induced pancreatitis Abacavir-related hypersensitivity syndrome lactic acidosis secondary to the use of any of the NRTIs Stevens-Johnson syndrome secondary to the use of any of the NNRTIs nevirapine-associated liver failure Indinavir induced crystal induced nephropathy (needle shaped crystals)

32 year old F, fatigue, progressively worsening shortness of breath and swelling of the feet for several days. Denies chest pain. No other medical problems except for a recent cold 2 weeks ago. Takes no medication. Temperature 98. BP 110/65, pulse 90/min, respirations 20/min. PE reveals bilateral basal crackles, elevated jugular venous pressure and 2+ bilateral pitting edema extending above the ankles. CBC shows no abnormalities. Which of the following will most likely be shown on an echocardiogram?

Dilated ventricles with diffuse hypokinesia Hx of a recent upper respiratory tract infection followed by sudden onset cardiac failure in an otherwise healthy patient is suggestive of dilated cardiomyopathy, most likely secondary to acute viral myocarditis. Dilated cardiomyopathy is the end result of myocardial damage produced by a variety of toxic, metabolic, or infectious agents. Viral or idiopathic myocarditis is most commonly seen following Coxsackievirus B infection and occurs in about 3.5-5% of infected patients. Other viruses commonly implicated include parvo B19, human herpesvirus 6, adenovirus and enterovirus. Viral myocarditis can cause dilated cardiomyopathy via direct viral damage and as a result of humoral or cellular immune responses to persistent viral infections. The dx of dilated cardiomyopathy is made by echocardiogram, which typically shows dilated ventricles with diffuse hypokinesia resulting in a low ejection fraction. Treatment is largely supportive, involving mainly the management of CHF symptoms.

Coronary steal

Dipyridamole can be used during myocardial perfusion scanning to reveal the areas of restricted myocardial perfusion. The redistribution of the coronary blood flow to "non diseased" segments induced by this drug is called coronary steal phenomenon.

One or more symptoms of epigastric pain, postprandial fullness or early satiety and can often coexist with abdominal burning, nausea and/or bloating.

Dyspepsia Heartburn is associated with GERD, not dyspepsia. Patients aged 55+ with new onset symptoms of dyspepsia and those of any age who have alarm symptoms (weight loss, dysphagia, or persistent vomiting) should be evaluated with upper endoscopy. Other patients should have Helicobacter pylori serology testing or empiric treatment with PPI.

Renovascular hypertension should be suspected and evaluated in the following situations:

Elevation in serum creatinine >30% from baseline after starting angiotensin-converting enzyme inhibitor or angiotensin-receptor blocker Severe hypertension in patients with recurrent flash pulmonary edema Severe hypertension in patients with diffuse atherosclerosis Onset of severe hypertension after age 55 Hypertension in a patient with asymmetric kidney size or a small atrophic unilateral kidney presence of abdominal bruit

Characteristics of GI mural injury- boerhaave syndrome

Etiology- esophageal transmural tear, cuased by foreceful retching (increased pressure) esophageal air/fluid leakage into nearby areas (eg pleura) Clinical presentation- vomiting, retching, chest and upper abdominal pain, odynophagia, fever, dyspnea and septic shock can ensue. Subcutaneous emphysema may be seen. Laboratory/imaging: CT or contrast esophageography with Gastrografin confirms diagnosis chest x-ray- pneumomediastinum and pleural effusions pleural fluid analysis: exudative, low pH, very high amylase (>2500 IU) Tx: Surg- for thoracic perforations, conservative measures (eg antibiotics): for cervical perforations

characteristics of Gi mural injury- mallory weiss tear

Etiology: Upper GI mucosal tear caused by forceful retching increased pressure, submucosal arterial or venule plexus bleeding. Clinical presentation- vomiting, retching, hematemesis, epigastric pain Laboratory/imaging- EGD confirms diagnosis Treatment- Most tears heal spontaneously, endoscopic therapy for continual bleed

A 65 year old male presents to the emergency dept with substernal chest pain, severe shortness of breath, and diaphoresis that began suddenly 40 minutes ago. Since the pain started, the pt has vomited twice. The pain radiates to his left arm and does not remit with sublingual nitroglycerine. EKG shows 2mm ST elevations in teh anterior leads. On physical exam ination the sat is 90% on 4L oxygen by nasal canula. Cardiac exam reveals a muffled S1 and S2 and the presence of an S43. Lung exam reveals basilar crackles that extend halfway up the lung fields bilaterally. Which of the following is the best next step in managing this patient?

Furosemide Pt has acute heart failure causing pulmonary edema or "flash pulmonary edema," secondary to an acute anterior wall MI. A diuretic such as furosemide is the drug of choice in this setting. Furosemide rapidly relieves pulmonary edema by decreasing the cardiac preload, thereby decreasing pulmonary capillary pressure. Furosemide also causes venodilation, which futher decreases the preload. Other appropriate treatments in this situation include morphine (Beneficial to both anxiolytic and preload-reducing effects), nitrates, and oxygen. This patient also needs emergent PTCA or thrombolysis since he has ST elevations on EKG; in teh meantime, anticoagulation with heparin is warranted. Beta blocksers are a standard therapy in MI but should be avoided in this scenario as they can worsen acute heart failure.

27 year old man, 2 week hx of hemoptysis, breathing difficulty, ankle edema and dark urine. PMH insignificant. Not taking any meds. Doesn't use tobacco, alcohol or drugs. Labs: Hb 10.5g/dL Serum Na 135 mEq/L Serum K 4.8 mEq/L BUN 36 mg/dL Serum creatinine 2.8mg/dL UA shows numerous dysmorphic red blood cells/HPF, moderate proteinuria, and red cell casts. Chest x-ray reveals bilateral alveolar infiltrates. Dx that requires emergency plasmapheresis?

Goodpasture's syndrome- requires emergency plasmapheresis Granulomatosis with polyangiitis (wegener's) is treated with a combination of cyclophosphamide and steroids.

Site of hemorrhage: Thalamus

Hemiparesis, hemi-sensory loss upgaze palsy nonreactive miotic pupils eyes deviate towards hemiparesis

Site of hemorrhage: Basal ganglia

Hemiplegia, hemi-sensory loss Homonymous hemianopsia, gaze palsy Stupor and coma

Thiazide diuretic side effects

Hyperglycemia, increased LDL cholesterol and plasma triglycerides. Electrolyte abnormalities: hyponatremia, hypokalemia and hypercalcemia.

Heart murmur at the left lower sternal border that decreased with an increase in preload

Hypertrophic cardiomyopathy. Increased preload distends the myocardium and decreases the outflow obstruction from the hypertrophied myocardium. Contrast with most murmurs- typically more severe with increased preload. Young age, lack of coronary disease risk factors points to hypertrophic cardiomyopathy. More common in african americans as well. variety of different genes for myocardial contractile proteins have been implicated in hypertrophic cardiomyopathy. all are transmitted in autosomal dominant fashion.

Secondary causes of hypertension, clinical clues/features: Fatigue, dry skin, cold intolerance, constipation, weight gain, bradycardia

Hypothyroidism

hypovolemic shock and pressures

Hypovolemic shock has reduced preload (PCWP) and reduced cardiac output. SVR increases in an attempt to maintain adequate perfusion to the vital organs. MvO2 is low due to reduced tissue perfusion and increased oxygen extraction by hypoperfused tissue.

Treatment for supraventricular tachycardia

IV adenosine- causes temporary AV block- identifies adn in some cases terminates supraventricular tachycardia.

Symptomatic sinus bradycardia- treatment

IV atropine, followed by transcutaneous pacing definition of sinus bardycardia = HR < 60 with regular rhythm and constant PR interval. Associated with excellent physical conditioning, exaggerated vagal activity, sick sinus syndrome, hypoglycemia and certain meds- digitalis, beta blockers, calcium channel blockers. Most individuals with sinus brady are asymptomatic but some develop dizziness, light-headedness, syncope, fatigue, and worsened angina. In hemodynamically unstable patients with sinus bradycardia, use epinephrine.

Etiology of community acquired pneumonia, most likely from aspiration

Impaired swallowing and epiglottic reflex are frequent abnormalities in patients with advanced dementia and other neurologic disorders. They are then predisposed to aspiration of oropharyngeal secretions. Anaerobic bacteria in combination with some aerobic oral flora are the usual etiologic factors of aspiration pneumonia. The infection may be necrotic and quickly progress to an abscess

Histopathologically, what is required to differentiate follicular cancers from follicular adenomas

Invasion of the capsule and blood vessels

Potassium and magnesium due to: furosemide spironolactone

Loops: hypokalemia and hypomagnesemia- can cause ventricular tachycardia and potentiate the side effects of digoxin spironolactone- potassium sparing

Paroxysmal supraventricular tachycardia

Most common paroxysmal tachycardia in people without structural heart disease. Attacks begin abruptly and are characterized by heart rates between 160 and 220 bpm. Most common mechanism underlying PSVT is re-entry into the AV node. Mechanical and medical therapies for PSVT decrease AV node conductivity. Vagal maneuvers such as Valsalva, carotid sinus massage and immersion in cold water increase vagal tone adn decrease conduction through the AV node. This slows the heart rate and can often break teh rhythm. Adenosine is a very short acting AV nodal blocker that is often used as well.

MEN syndromes

Multiple endocrine neoplasia Type 1- parathyroid adenoma, pituitary tumors, enteropancreatic tumors Type 2A- medullary thyroid cancer, pheochromocytoma, parathyroid hyperplasia Type 2B- medullary thyroid cancer, pheochromocytoma, other- mucosal and intestinal neuromas, marfanoid habitus, kyphoscoliosis, lordosis Men 2 is an AD disorder caused by germline mutations involving the RET protooncogene located on Ch 10. MEN 2A predisposes to medullary thyroid cancer (100%), pheochromocytoma (60%), and parathyroid tumors (25%). Both MTC and pheochromo occur in MEN 2B, but primary hyperparathyroidism isn't seen. MTC in MEN 2B is more aggressive then in MEN 2A.

Fever, muscle rigidity, autonomic instability, mental status change. Often an elevated serum CK.

Neuroleptic malignant syndrome. Typical antipsychotics like haldol are implicated in NMS. Dantrolene, a muscle relaxant is the most common drug used to reverse the condition, followed by bromocriptine (a dopamine agonist) and amantadine (an antiviral drug with dopaminergic properties). Stop the causative agent and give supportive care.

56 yo man > ED with dyspnea. Waking up during te night with difficulty breathing and chest pain that keeps him from falling back asleep. Long-standing HTN and non-compliance with antiHTN therapy. 30 pack ears. BP 170/100, HR 120/min and regular. Lung auscultation - bibasilar rales and scattered wheezes. What do u use to relieve pts dyspnea?

Nitroglycerin- Pt presents with paroxysmal nocturnal dyspnea in setting of long-standing HTN and pulmonary exam concerning Cardiogenic pulmonary edema. Likely developed diastolic dysfxn (impaired ventricular relaxation) from his long-standing tn and is now in left ventricular failure. NTG either IV< subL or topical relieves the dyspnea adn tachy asso with cardiogenic pulmonary edema by rapidly reducing preload. Several studies have suggested it works quicker than morphine or loops. NTG is not part of the long-term management of patients with HF but can be beneficial in acutely alleviating symptoms. Should be used cautiouly in pts with hypotension. Beyond NTG, loops are themainstay of therapy for decompensated HF and principally work by reducing total bodyvolume.

Patients with RA are at greater risk of developing what bone disorders?

Osteopenia Osteoporosis

Patient presents with fatigue and irregularly irregular heart rhythm consistent with likely new onset atrial fibrillation, which is a common arrhythmia in men and older individuals.

The main complication of AF is embolic stroke (up to 5 events per 100 patient-life years) due to stasis of blood in the atria leading to thrombi. The risk is higher in older patients and those with previous stroke, heart failure, valvular disease, diabetes or hypertension.

Secondary causes of hypertension, clinical clues/features: severe hypertension (>180 mm Hg systolic and/or 120 mm Hg diastolic) after age 55, possible recurrent flash pulmonary edema or resistant heart failure, unexplained rise in serum cretainine. Abdominal bruit

renovascular disease

Secondary causes of hypertension, clinical clues/features: Paroxysmal elevated blood pressure with tachycardia, pounding headaches, palpitations, diaphoresis, hypertension with adrenal incidentaloma

Pheochromocytoma

sore throat/skin infection followed by generalized edema, dark urine adn hypertension.

Post-strep glomerulonephritis

Secondary causes of hypertension, clinical clues/features: easily provoked hypokalemia, slight hypernatremia, hypertension with adrenal incidentaloma

Primary aldosteronism

Secondary causes of hypertension, clinical clues/features: Hypercalcemia (polyuria, polydipsia), kidney stones, neuropsychiatric (confusion, depression, psychosis)

Primary hyperparathyroidism

Nitroglycerin effects on vessels/cardiovascular system

Primary: dilation of capacitance vessels/veins, decreases ventricular preload and O2 demand of the heart. Also dilates arterial system- so decreases ventricular afterload, but this effect has less significance in relieving anginal pain.

Pleuritic chest pain in the setting of prolonged immobility, hempotysis, dyspnea, tachycardia, and OCP use

Pulmonary embolism... One common cause of pleuritic chest pain is a pulmonary embolism with subsequent minor or massive pulmonary infarction. Other common causes include pneumonia, pneumothorax, collagen vascular disease, viral pleuritis, and radiation pneumonitis. Diagnostic test of choice = Helical CT of the chest with IV contrast.

Syncope def

an abrupt and transient loss of consciuosness with loss of postural tone, followed by a spontaneous and ocmplete recovery. It is usually benign and self-limiting, but it can be the initial presenting symptom of a life-threatening disease process. The cuase of syncope can be often determined by careful hx, PE, simple labs and ECG.

Cardiogenic pulmonary edema results from and is characterized by:

Results from Left herat failure nad is characterized by crackles on pulmonary exam. NTG is the most rapidly acting medication to relieve the symptoms of pulmonary edema.

Clinical features of aortic dissection

Risk factors/associations- hypertension (most common) Marfan syndrome, cocaine use Clinical features- severe, sharp, tearing chest or back pain, >20mm Hg variation in systolic blood pressure between arms Complications (involved structure)- stroke (carotid arteries), acute aortic regurg (aortic valves), horner's syndrome (superior cervical sympathetic ganglion), aute myocardial ischemia/infarction (coronary artery) pericardial effusion,/cardiac tamponade (pericardial cavity), hemothorax (pleural cavity), lower-extremity weakness or ischemia (spinal or common iliac arteries), abdominal pain (mesenteric artery) Dx can be confirmed with contrast chest computed tomography or transesophageal echocardiogram.

A 53 year old woman is admitted to the intensive care unit with hypotension. She is receiving no vasoactive agents and is breathing room air. Blood pressure measured by an intra-arterial line is 72/46 mm Hg. Her pulse is 120/min and regular. Invasive hemodynamic monitoring is established and initial readings are as follows: Pulmonary capillary wedge pressure: 6 mm Hg (N:6-12 mm Hg) Mixed venous oxygen saturation 78% (N: 65%-75%) Most likely cause of this patient's condition

Septic shock This patient's presentation with low pulmonary capillary wedge pressure (PCWP) and high mixed venous oxygen saturation (MvO2) is most consistent with septic shock. Septic shock is a form of distributive shock due to an underlying systemic infection involving the circulatory system. The systemic inflammatory response causes peripheral vasodilation and decreased systemic vascular resistance (SVR). The decreased blood flow returning to the heart also lowers PCWP. Cardiac output is often increased to compensate and maintain adequate tissue perfusion. MvO2 is high due to hyperdynamic circulation, imporper distribution of cardiac output, and inability of the tissues to adequatesly extract oxygen. Hypotension, warm (early)/cool (late) extremities, adn elevated lactate levels are common clinical findings.

hypertensive emergency

Severe hypertension with acute, life threatening, end organ complications. Malignant hypertension: severe hypertension with retinal hemorrhages, exudates or papilledema Hypertensive encephalopathy: severe hypertension with cerebral edema and non-localizing neurologic symptoms and signs.

Syncope: sinus pauses on monitor, prolonged PR interval or QRS duration- can be intermittent

Sick sinus syndrome, bradyarrhythmias, atrioventricular block AV block can be intermittent, normal heart rate does not exclude bradyarrhythmia due to the intermittent nature of te block in many patients. Should be referred for additional electrophysiologic testing and evaluation for a pacemaker implantation.

Side effect of statins

Statins inhibit intracellular HMG-CoA reductase enzyme, prevent conversion of HMG CoA to mevalonic acid, and increase the number of cell membrane LDL receptors. Statins also decrease coenzyme Q10 synthesis, which is involved in muscle energy production and possibly contributes to statin-induced myopathy Statin induced myalgias can occur in 2-10% of pts, but significant with myositis with elevated creatine kinase is uncommon. Myalgias tend to present as symmetrical proximal muscle weakness or tenderness.

Factors associated with poor outcome after witnessed out-of-hospital sudden cardiac arrest

Time elapsed prior to effective resuscitation (delayed bystander cpr, delayed defibrillation) initial rhythm of pulseless electrical activity or asystole Prolonged CPR (>5minutes) absence of vital signs advanced age prior history of cardiac disease >2 chronic illnesses persistent coma after CPR need for intubation or vasopressors Pneumonia or renal failure after CPR Sepsis, cerebrovascular accident or class III or IV heart failure

Syncope: Hypokalemia, hypomagnesemia, medications causing prolonged QT interval

Torsades de pointes (acquired long QT syndrome)

Syncope: Triggers- prolonged standing or emotional distress, painful stimuli Prodromal symptoms: nausea, warmth, diaphoresis

Vasovagal or neurally mediated syncope

Syncope: Prior history of coronary artery disease, myocardial infarction , cardiomyopathy or reduced ejection fraction.

Ventricular arrhythmias

WPW summary and treatment

WPW- an accessory pathway conducts depolarization directly from teh atria to the ventricles without transversing the AV node. In general, patients with atrial fibrillation and a rapid ventricular rate are treated with AV nodal blockers like beta blockers, calcium channel blockers, digoxin, and adenosine. However, in WPW, drugs that increase refractoriness of the AV node only serve to increase conduction across the accessory pathway, which can lead to degeneration into ventricular fibrillation. Thus, the best tx for a patient with WPW and atrial fib is conversion back to sinus rhythm, either through electrical cardioversion or with antiarrhythmic medications like procainamide.

Treatment of hypertension: Modification, recommende dplan and approximate decreased systolic BP mm HG

Wt loss, reduce bmi to <25 kg/m2, decreased in systolic = 5-10 per 10kg weight loss DASH diet- diet high in fruits and vegetables, and low in sat and total fat. 8-14 drop in systolic Exercise- 30 min/day for 5-6 days/week. drop of 4-9 systolic Dietary sodium <3g/day, 3-8 drop in systolic Alcohol intake- 2 drinks/day in men, 1 drink/day in women, 2-4 drop of systolic Lifestyle modification should be the first-line intervention for newly diagnosed stage I htn. The most effective lifestyle intervention for reducing bp is weight loss in obese pts. All pts should be encouraged to follow thte DASH diet (rich in fruits, veges adn low-fat dairy products), restrict dietary salt intake, engage in regular aerobic exercise to maintain normal body weight and limit alcohol intake

Control of Atrial fibrillation

a-fib is a common arrhythmia in older adults that is characterized by an irregularly irregular heart rhythm often with a rapid rate. Rate control plus anticoagulation is preferred over rhythm control plus anticoagulation in most patients to decrease the risk of embolic stroke. Warfarin or dabigatran can be used for anticoagulation.

Diagnostic criteria for ARDS

acute onset PaO2/FiO2<200 Presence of bilaterla infiltrates on chest x-ray adn a swan ganz pressure <18 mm Hg. ARDS is a form of non-cardiogenic pulmonary edema, should be distinguished from cardiogenic pulmonary edema as happens in CHF. A low swan ganz pressure and the absence of JVD and cardiomegaly aid in distinguishing ARDS from CHF.

two most common causes of acute pancreatitis

alcohol and gallstones. ARDS can result from endothelial injury and the leakage of fluid from capillaries. The fluid then fills the interstitial spaces adn alveoli. ARDS results in intrapulmonary shunting and therefore the hypoxia suffered by patients is typically refractory to o2 administration. Alveoli are so full of fluid that they are unable to participate in gas exchange.

Alanine aminotransferase >150 U/L with elevated alkaline phosphatase

biliary pancreatitis

Decreased upper-to-lower body ratio, yhypermobile joints, scoliosis

marfanoid habitus

Eccentric hypertophy of the heart develops following

chronic volume overload as seen in valvular regurgitation. Eccentric hypertrophy is not seen in cases of acute heart failure, as it develops slowly over time in response to ventricular volume overload.

hard thyroid nodule, elevated calcinonin, malignant cells

medullary thyroid cancer

2 main approaches to decreasing stroke risk in AF patients

rhythm control (via chemical or electrical cardioversion to restore sinus rhythm) plus anticoagulation/rate control (av nodal blocking agents) plus anticoagulation. The preferred rate-controlling drugs include diltiazem, verapamil, metoprolol and digoxin

Which drugs cause peripheral edema?

dihydropyridine calcium channel antagonists- like amlodipine. Due to the dilation of peripheral blood vessels (not an allergic reaction)

Concentric hypertrophy of the heart is seen

following chronic pressure overload, as with valvular aortic stenosis or untreated hypertension. Concentric hypertrophy develops only in chronic conditions and does not present as acute heart failure.

systolic-diastolic abdominal bruit in a patient with htn and atherosclerosis

renal artery stenosis

Hypogonadism, arthropathy, diabetes and hepatomegaly

hereditary hemochromatosis- autosomal recessive disorder due to HFE gene mutation causing increased intestinal iron absorption. The iron (in the form of hemosiderin) deposits in teh body organs to cause multisystem end-organ damage. However the degree of iron deposition varies greatly in each patient. Most HH pts are asymptomatic and diagnosed early in the disease by elevated liver enzymes on routine lab studies. Disease progression with further iron deposition can cause hepatic fibrosis and cirrhosis, diabetes mellitus, arthropathy (associated with pseudogout), skin pigmentation adn erectile dysfunction in men. Only a small percentage present with the classic triad of cirrhosis, dm and skin pigmentation seen in the later stages of the disease. Iron deposition within the cardiac myocardium can cause dilated or restrictive cardiomyopathy. Conduction defects (eg sick sinus syndrome) can also occur due to iron deposition interfering with teh cardiac electrical conduction pathways. Cardica magnetic resonance imaging is often used to detect the myocardial iron overload.

Asymmetric septal hypertrophy is present in

hypertrophic cardiomyopathy which is usually seen in younger patients and less likely to present with acute heart failure. Hypertrophic cardiomyopathy often manifests as sudden cardiac death.

Heterophile antibody test

infectious mono due to EBV can be detected- both sensitive and specific. Heterophile antibodies arise within one week of sx and persist for up to a year. Testing for anti-EBV antibodies is another way to diagnose EBV infection. Primary HIV infection casues a febrile illness that can closely resemble infectious mononucleosis. The key distinctions between the two are that rash (unless antibiotics have been administered) and diarrhea are LESS common in infectious mononucleosis and the finding of a tonsillar exudate is uncommon in primary HIV.

A-fib on ekg

irregularly, irregular, narrow QRS complex tachycardia that lacks P waves. Causes are numerous and include cardiac, pulmonary, metabolic and drug-related etiologies.

Cardiogenic shock and pressures

is usually due to significant left ventricular dysfunction and reduced pump function. There is often low cardiac output, elevated PCWP, and increased SVR. The decreased cardiac output decreases tissue perfusion, which signals tissues to extract more oxygen from teh blood and decrease MvO2.

Restrictive cardiomyopathy

less common than dilated or hypertrophic cardiomyopathy.l May be caused by infiltrative diseases (sarcoidosis, amyloidosis), storage diseases (hemochromatosis), endomyocardial fibrosis, or it may be idiopathic. Pts present with primary diastolic dfxn which explains teh patients prominent PE findings of heart failure with only mild systolic dysfunction on echocardiography. LV volume is normal in restrictive cardiomyopathy adn the wall thickness may be normal or symmetrically thickened. Symmetric thickening of teh ventricle helps to differentiate restrictive from hypertrophic cardiomyopathy in which the interventricular septum is thickest. Signs of right sided heart failure often predominate in restrictive cardiomyopathy as evidenced by this pts prominent jugular venous distension, bilat ankle edema and tender hepatomegaly. REstrictive cardiomyopathy can cause signs and sx of left sided heart failure as well, such as the pts bibasilar rales and pleural effusion.

Crescendo-decrescendo murmur at the left loewr sternal border in a young individual

most likely due to hypertrophic cardiomyopathy- disease is more common in african americans. murmur classically increases during valsalva maneuver due to decreased preload and decreased filling of the left ventricle. This is in contrast to most other cardiac murmurs which decrease in intensity with decreased preload. The outflow obstruction in hypertrophic cardiomyopathy is due to both a hypertrophied interventricular septum and an abnormality in the motion of the mitral valve leaflets referred to as systolic anterior motion (SAM). SAM results in increased outflow obstruction, and in some patients may be of greater clinical consequence than septal hypertrophy . Outflow obstruction in hypertrophic cardiomyopathy results from both septal hypertrophy and systolic anterior motion (SAM of the mitral valve)

Clinical presentation of acute pancreatitis

needs to include 2 of the following: acute epigastric ab pain often radiating to the back increased amylase/lipase > 3 times normal limit Ab imaging showing focal or diffuse pancreatic enlargement with heterogenous enhancement with intravenous contrast (CT) or diffusely enlarged and hypoechoic. Complications: pleural effusion Ileus Pancreatic pseudocyst/abscess/necrosis ARDS

norepinephrine effect on vasculature

norepinephrine has alpha-1 agonist properties which cause vasoconstriction; this property is useful when trying to increase the bp of hypotensive patients. In some patients with decreased blood flow, vasoconstriction can result in ischemia and necrosis of the distal fingers and toes. A similar phenomenon can occur in the intestines (resulting in mesenteric ischemia) or kidney (causes renal failure). Pressors such as norepinephrine can cause ischemia of the distal fingers and toes secondary to vasospasm. The diagnosis is suggested by symmetric duskiness and coolness of all fingertips.

Bilateral pitting edema, varicose veins, venous ulcer

peripheral edema due to venous insufficiency. Normal jvp <3cm above teh sternal angle suggests normal central venous pressure and makes right and left heart failure less likely. Chrnoic lower extremity venous disease refers to functional or anatomic venous abnormalities that lead to venous reflux or dilated lower-extremity veins. Pts present with leg discomfort, pain, or swelling that typically worsens with prolonged standing and improves after walking or limb elevation. Initial treatment of chronic venous disease includes leg elevation, exercise adn compression stockings. Pts not responding to these may require venous duplex ultrasound to identy venous reflux or innsufficiency. Pts with persistent symptoms and documented reflux shoudl be referred for endovenous ablation.

increased urinary metanephrine adn norepinephrine levels

pheochromocytoma

Hypertensive urgency

severe hypertension (usually > 180/120 mm hg) with no symptoms or acute end organ damage

Gradually developing tinnitus and hearing loss

suggestive of an acoustic neuroma- best diagnosed using MRI with gadolinium enhancement. Presence of multiple cafe-au-lait spots and relatively young age in pateitns suggests neurofibromatosis type II as the cause of the problem. Acoustic neuromas are frequently bilateral in patients with NF type II. Sporadic unilateral acoustic neuroma usually presents after 40 years of age and has no associated findings.

Vascular and immunologic manifestations of infective endocarditis

vASCULAR PHENOMENA -SYSTEMIC ARTERIAL EMBOLI (FOCAL NEUROLOGIC DEFICITS, RENAL OR SPLENIC INFARCTS) -septic pulmonary infarcts -mycotic aneurysm -conjunctival hemorrhages -janeway lesions- macular, erythematous, nontender lesions on the palms and soles Immunologic phenomena -osler's nodes- painful, violaceous nodules seen on the fingertips and toes -Roth spots, edematous and hemorrhagic lesions of the retina -glomerulonephritis -arthritis or positive rheumatoid factor