Medicine qbank

Question 1

Serotonin Syndrome is characterized by what signs?

Answer 1

Lethargy, restlessness, hypertonicity, rhabdomyolysis, renal failure, and possible death.

Question 2

What are the characteristics of nephrotic syndrome?

Answer 2

1. Proteinuria (>3-3.5 g/day, most important manifestation)
2. Hypoalbuminenia
3. Edema
4. Hyperlipedemia & lipiduria

Question 3

What are the causes of nephrotic syndrome?

Answer 3

1. Minimal change disease (children) 2. Membranous glomerulopathy (adults) 3. Mesangial proliferative glomerulonephritis 4.membranoproliferative glomerulonephritis 5. Focal segmental glomerulosclerosis

Question 4

Pathophysiology of hypercoagulation in nephrotic syndrome?

Answer 4

Urinary loss of antithrombin III, altered protein C & S levels, increased platelet aggregation, increased liver fibrin production, and impaired fibrinolysis. Renal vein thrombosis is the most common. But PE and arterial thrombosis can occur

Question 5

Rupture of a brain or abdominal aortic aneurysm are likely to be seen in what kidney disease?

Answer 5

Polycyclic kidney disease

Question 6

Complications of nephrotic syndrome?

Answer 6

Protein malnutrition, iron resistant microcytic hypochromic anemia, increased susceptibility to infections, and Vit D deficiency

Question 7

Herpes zoster opthalmicus?

Answer 7

VZ virus lives in trigeminal ganglion, travels via opthalmic branch to forehead and eye during immunosuppression. Fever, malaise, burning/itching sensation in periorbital region. Conjunctivitis and dendriform corneal ulcers characterize the eye involvement. High dose acyclovir shortens course. Immunocompromised and old people

Question 8

Characteristics of herpes simplex keratitis?

Answer 8

Pain, photophobia, and decreased vision. Dendritic ulcer is the most common presentation. May be minute clear vesicles in the corneal epithelium.

Question 9

What is dacrocystitis?

Answer 9

Infection of the lacrimal sac due to obstruction of the nasal-lacrimal duct. Characterized by pain, swelling, redness, or tenderness in the tear sac area. Can be mucous or pus.

Question 10

What is bacterial keratitis?

Answer 10

It is common in contact lens wearers and follows corneal trauma. Cornea appears hazy with a central ulcer and an adjacent stromal abscess. Hypopyon may be present.

Question 11

What is shock liver?

Answer 11

Ischemic hepatic injury often following septic shock (or other hypovolemic shock). The hallmark of ischemic liver injury is a rapid and massive increase in transaminases with modest elevations in tBili and all phos. In patients who survive the septic shock event, liver enzymes return to normal within a week or two.

Question 12

Presentation of acute Hep A or Hep B?

Answer 12

Large AST & ALT elevations, typically accompanied by hyperbilirubinemia, nausea, and vomiting.

Question 13

Liver enzymes in alcoholic liver disease?

Answer 13

AST:ALT ratio is usually 1.5 or greater. AST itself is usually no greater than 300units/L

Question 14

Liver enzymes in autoimmune hepatitis?

Answer 14

Can see large increases in AST/ALT. High serum bilirubin seen too. Commonly presents in young women.

Question 15

How do you distinguish rotator cuff tendinitis from other rotator cuff pathology.

Answer 15

Lidocaine injection injection relieves pain and improves range of motion of rotator cuff tendinitis. Rotator cuff tendinitis is always associated with some form of impingement (tendons).

Question 16

Workup for fatigue?

Answer 16

A complete metabolic panel screens for electrolyte, renal, and hepatic problems
A TSH can detect hypothyroidism
A CBC will show anemia and vitamin deficiencies

Question 17

Clinical presentation of amyloidosis?

Answer 17

Asymptomatic protein urea or nephrotic syndrome. Restrictive cardiomyopathy, hepatomegaly, organomegaly (macroglossia), peripheral neuropathy/autonomic neuropathy. Waxy, thinning/ easy bruising skin. Diagnosed by tissue biopsy.

Question 18

What is the epidemiology and pathophys for amyloidosis?

Answer 18

Extra cellular deposits of polymeric protein fibers in tissues & organs. Can be primary (AL type) or secondary (AA type) to chronic inflammatory conditions like:
Inflammatory arthritis, chronic infections, IBD, malignancy, vasculitis.

Question 19

Characteristics of alcohol related heart disease?

Answer 19

Usually dilated cardiomyopathy with LV cavity dilation and impaired systolic function. Increased LV wall thickness and normal cavity diameter on echo.

Question 20

Chemo-therapy induced peripheral neuropathy (CIPN)

Answer 20

Causative agents include vincristine, platinum based meds (cisplatin), and taxanes (paclitaxel). Starts after weeks of treatment and presents as bilateral paresthesias in a stocking-glove distribution. Early loss of ankle jerk reflexes and pain and temp sensation.

Question 21

Treatments of osteoporosis. And side effects?

Answer 21

Bisphosphonates. Reduce osteoclasts activity and result in apoptosis. Can result in upbeat stomach and GI inflammation. Can have Osteonecrosis of jaw and femur.

Recombinant PTH (teriparitide).

Anti-osteoclast antibodies.

Hormone replacement therapy is only indicated in women who have hormone replacement symptoms.

Question 22

Treatment of acute gout?

Answer 22

Rest and NSAIDs. If NSAIDs are contraindicated, then colchicine or infra-articular steroids may be indicated. Allopurinol and other hypouricaemic drugs should not be used during an acute attack - can perpetuate attack.

Question 23

Carcinoid syndrome symptoms.

Answer 23

Episodic flushing (85% of patients). Secretory diarrhea, abdominal cramping. Cutaneous telangectasias, bronchspasm, tricuspid regurg.

Question 24

Carcinoid syndrome. Pathophys and diagnosis?

Answer 24

From well differentiated neuro endocrine tumors (near cecum, lungs most often with a strong propensity to metastasize to liver). These tumors can secrete histamine, serotonin, and vasoactive intestinal peptide that are broken down in the liver. Livers mets secrete these straight into systemic circulation leading to carcinoid syndrome. Diagnosed/confirmed by elevated 24 hr urinary 5-hydroxyindoleacetic acid.

Question 25

How does RA present?

Answer 25

RA presents with progressive and symmetric involvement of peripheral joints. MCP and PIP, metatarsophalangeal joints and the wrist are common sights. RA also commonly affects the cervical spine and can cause spinal cord compression or subluxation. Rheumatoid nodules appear in 30-40% of patients on pressure points.

Question 26

What organism/infection is a common trigger for guttate psoriasis?

Answer 26

Strep pharyngitis or perianal strep (more in kids). Can be at the same time or after (usually a couple weeks) time of infection

Question 27

3 different causes for posterior scalp pruritus in healthy child?

Answer 27

Exema, lice (itching, papules, lymphadenopathy), tinea capitis

Question 28

Tinea Cruris?

Answer 28

Jock itch. Fungal infection of the groin area. Treated with oral or topical antifungals (allylamine or azoles). Nail fungal infections always need oral.

Question 29

Treatment of lyme disease?

Answer 29

Doxycycline. Amoxicillin in kids <8.

Question 30

Ramsey Hunt syndrome?

Answer 30

Herpes zoster of cranial nerve VII. Vesicles within ear. Treat early. Treat with valcyclovir.

Question 31

Scabies

Answer 31

Super itchy, scaly red papules on the genitals. Abrupt onset. Also check hands for lesions. Always assume scabies if abrupt onset, really itchy genitals. Symptomatic relief for treatment.

Question 32

Indications for thrombolytic therapy (MI)?

Answer 32

Thrombolytic therapy is indicated if all of these are met:

1. Clinical presentation consistent with ischemic chest pain
2. ST-segment elevation more than 1 mm in at least 2 anatomically contiguous leads
3. No contraindications to thrombolytic therapy
4. Patient is younger than 75 (hemorrhage risk high in >75)

Maximal benefit is seen when drug is given 1-3 hours after onset of chest pain.

Question 33

Persistent ST segment elevation weeks after a cardiac event?

Answer 33

Suspect ventricular aneurysm

Question 34

Dressler syndrome

Answer 34

A late complication a couple weeks after an acute MI. An immune phenomenon characterized by pericarditis, pleuritis, and fever. It may remit and relapse. Treat with NSAIDs and sometimes prednisone.

Question 35

Most common pathology of analgesic nephropathy?

Answer 35

Papillary necrosis and chronic tubulointerstitial nephritis. Patients with analgesic abuse also experience premature aging, atherosclerotic vascular disease, and urinary tract cancer. Typically seen in women in their 50s with combined analgesic use (aspirin and naproxen for example)

Question 36

Clinical characterization of crystal induced acute kidney injury?

Answer 36

Acyclovir, sulfonamides, methotrexate, ethylene glycol, protease inhibitors. Drugs crystalize out and cause obstruction and AKI. Often a asymptomatic clinical presentation. Elevated creatinine 1-7 days after starting drug. Can have hematuria, pyuria, and crystals in the urine. Discontinue drug and give volume (can help protect against additional damage).

Question 37

What is pre-renal azotemia?

Answer 37

Often due to volume depletion and hypoperfusion of the kidneys.

Question 38

25 yo M w HIV comes in for recent onset fever and left sided weakness. L sided decreased power and hypereflexia. Multiple ring enhancing lesions found on CT. Next step?

Answer 38

The most common cause of central mass lesions inAIDS patients is toxoplasmosis. Ring enhancing lesions are found. Bacterium is prophylactic treatment while sulfasalazine + pyrimethamine are treatment for active infection.

Question 39

3 major treatment options for Grave’s disease?

Answer 39

1. Radioactive iodine ablation (preferred in US)
2. Anti thyroid drug therapy, propylthiouracil (PTU) or methimazole (MMI). PTU has high liver toxicity and is not preferred except during the first trimester of pregnancy because of teratogenic effects of MMI. Agranulocytosis is an uncommon but serious side effect (.3%) that patients must be warned about - watch out for sore throat and fever. 40% of patients are cured after a year of therapy.
3. Thyroidectomy (hypocalcemia and recurrent laryngeal nerve injury are common complications).

Question 40

Clinical features of Cushing’s syndrome? How is it diagnosed?

Answer 40

Progressive central obesity, skin atrophy and wide purplish striae, proximal muscle weakness, hypertension, glucose intolerance, skin hyper pigmentation (due to excess ACTH).

Diagnosis is made by 24 hour urinary cortisol collection, late evening salivary cortisol, or low-dose dexamethasone suppression test.

Question 41

Common locations and characteristics of ectopic ACTH production?

Answer 41

Ectopic ACTH production is associated with lung cancer (small cell lung cancer) and carcinoid (bronchial, pancreatic, and thymus). The ectopic ACTH is not suppressed by cortisol feedback.

Magnitude of clinical presentation is determined by rate of production. Malignant tumors with high ACTH production cause hypertension, hypokalemia, met alkalosis, and hyperpigmentation without other, more insidious, features of Cushing’s (moon facies, fat pads, striae, dorsal hump, and central obesity - these are seen is slow producing tumors).

Question 42

How does excess ACTH cause hypertension and hypokalemia?

Answer 42

Cortisol is converted into inactive cortisone by 11 beta HSD. When 11 beta HSD gets saturated, excess cortisol can bind to mineralocorticoid receptors (acts like aldosterone)

Question 43

Extra-colonic manifestations of UC?

Answer 43

Skin findings (erythema nodosum, pyoderma gangrenosum), episcleritis, arthritis (similar presentation to ankylosing spondylitis), and cholangitis. P-ANCA is often elevated in UC.

Question 44

Clinical characteristics of lymphedema? Causes?

Answer 44

Lymphedema is generally painless, but patients may experience a chronic dull, heavy sensation in the leg. In the early stages of lymphedema, the edema is soft and pits easily with pressure. In the chronic stages, the limb has a woody texture and the tissues become indurated and fibrotic. Lymphedema initially involves the foot and gradually progresses up the leg so that the entire limb becomes edematous.

Causes include primary (inherited) or secondary to trauma to the lymph vessels (lymph node dissection, surgery and/or radiation therapy-notably breast cancer).

Question 45

Clinical characteristics of cellulitis?

Answer 45

Acute swelling, warmth, erythema, +/- fever. Cellulitis is an acute inflammatory condition of the skin characterized by localized pain erythema, swelling, and heat. Small breaks of skin are associated with streptococcal infection, whereas staphylococcal cellulitis is commonly associated with larger wounds, ulcers, or abscesses. Diabetics are more susceptible to infections like cellulitis. Diabetic neuropathy causes an unawareness of abnormal pressure distribution, ill-fitting shoes, and cuts or punctures which then develop ulcers. Vascular disease with diminished blood supply contributes to the development of the lesion, and infection is common.

Question 46

Treatment of cellulitis?

Answer 46

Elevation of the affected area and treating the underlying condition.

Antibiotic therapy:

Purulent cellulitis - empiric therapy for MRSA
(Clindamycin, Trimethoprim-sulfamethoxazole, Tetracycline [doxycycline or minocycline] Linezolid)

Non-purulent cellulitis - empiric therapy for infection due to beta-hemolytic streptococci and MSSA
(Clindamycin, Amoxicillin combined with trimethoprim-sulfamethoxazole, Amoxicillin combined with a tetracycline [doxycycline or minocycline], Linezolid)

Usually 5-10 days if the symptoms resolves.

Question 47

Characteristics and clinical presentation of DVTs?

Answer 47

Classic symptoms of DVT include swelling, pain, and discoloration in the affected extremity.Physical examination may reveal the palpable cord of a thrombosed vein, unilateral edema, warmth, and superficial venous dilation.
Classic signs of DVT, including Homan’s sign (pain on passive dorsiflexion of the foot), edema, tenderness, and warmth, are difficult to ignore, but they are of low predictive value and can occur in other conditions such as musculoskeletal injury, cellulitis, and venous insufficiency.
Presence of risk factors such as previous DVT, obesity, smoking, and diabetes - make this DVT likely diagnosis.

Chronic venous insufficiency may result from DVT and/or valvular incompetence. Following DVT, the valve leaflets become thickened and contracted so that they are incapable of preventing retrograde flow of blood; the vein becomes rigid and thick-walled. Although most veins recanalize after an episode of thrombosis, some may remain occluded. Secondary incompetence develops in distal valves because high pressures distend the vein and separate the leaflets. Patients with venous thrombosis often complain of a dull ache in the leg that worsens with prolonged standing and resolves with leg elevation. Examination reveals increased leg circumference, edema, and superficial varicose veins. The presence of a thrombus in a vein may be accompanied by an inflammatory response in the vessel which may be minimal or may be characterized by granulocyte infiltration, loss of endothelium, and edema. This inflammatory process may also result in a low grade fever.

Question 48

Clinical characteristics of PAD?

Answer 48

Peripheral arterial disease (PAD) is the presence of systemic atherosclerosis in arteries distal to the arch of the aorta. As a result of the atherosclerotic process, patients with PAD develop narrowing of these arteries.
Patients with PAD have a history of claudication, which manifests as cramp-like muscle pain occurring with exercise and subsiding rapidly with rest. In addition, later in the course of the disease, patients may present with night pain, nonhealing ulcers, and skin color changes.

Question 49

Risk factors and diagnosis of PAD?

Answer 49

An ankle-brachial index (ABI) can be done to determine the presence of PVD. An ABI of 30) increases risk for PAD as well. Recent trials have added chronic renal insufficiency, elevated C-reactive protein levels, and hyperhomocysteinemia to the list of risk factors.
The greatest modifiable risk factor for the development and progression of peripheral arterial disease (PAD) is cigarette smoking.

Arterial insufficiency is four times more prevalent in patients with diabetes than in those without diabetes. Nearly half of patients who’ve had diabetes for 20 years or more have peripheral arterial disease (PAD), usually below the knees.

Question 50

Wells criteria for the diagnosis of DVT?

Answer 50

Active cancer (treatment ongoing or within previous 6 months or palliative) 1

Paralysis, paresis, or recent plaster immobilization of the legs 1

Recently bedridden for more than 3 days or major surgery within 4 weeks 1

Localized tenderness along the distribution of the deep venous system 1

Entire leg swollen 1

Calf swelling by more than 3 cm compared with the asymptomatic leg (measured 10 cm below the tibial tuberosity) 1

Pitting edema (greater in the symptomatic leg) 1

Collateral superficial veins (non-varicose) 1

Alternative diagnosis as likely or wider than that of deep vein thrombosis -2

Low probability 0 or less, moderate probability 1-2, high probability 3 or more.

Question 51

Differences between LMWH and unfractionated heparin?

Answer 51

LMWH:
Longer biologic half-life so it can be administered subcutaneously once or twice daily
Laboratory monitoring is not required
Thrombocytopenia is less likely although periodic monitoring of platelets may be needed
Dosing is fixed

Hence, LMWH may be used in the outpatient setting. Whereas unfractionated heparin requires hospitalization as it is administered intravenously with the dosage based on body weight and titrated based on the activated partial thromboplastin time.

Question 52

Two long term anticoagulation options? Not heparin…

Answer 52

Warfarin:
Prothrombopenic drugs like warfarin are not suitable for initial therapy in thromboembolism because their onset of action is too slow. Their only role is in maintaining anticoagulant protection for prolonged periods.

Monitor warfarin dose by measuring the INR and titrate the warfarin dose every three to seven days to an INR of 2.0-3.0.

Factor Xa inhibitors:
This relatively new class of drugs has the advantage of not requiring weekly lab monitoring of INR and thus makes adherence an easier process. Fondaparinux is the parental form of the drug and could be used instead of LMWH. Rivaroxaban is an oral factor Xa inhibitor and might be used in place of warfarin. Although these drugs have been found to be generally as safe and effective as warfarin and LMWH, the negatives of this class of medications includes high cost and difficulty in reversing the anticoagulation in the face of a bleed.

Question 53

Classes of diabetes medications?

Answer 53

1. Insulin
2. Sensitizers
   a. biguanides (metformin)
   b. thiazolidinediones (TZDs)
3. Secretagogues (increase insulin output from pancreas)
   a. sulfonylureas (glipizide, glyburide)
   b. non-sulfonylureas secretagogues
4. Alpha-glucosidase inhibitors (slow starch absorption)
5. Peptide analogs (Incretins - insulin secretagogues)
   a. GLP1 agonists (Exenatide [byetta], Liraglutide [victoza])
6. Glycosurics
   a. SGLT-2 inhibitors - increase urine glucose output

Question 54

What happens at an INR of 11? 5-9?

Answer 54

An INR of 11 increases the risk of bleeding complications significantly. Warfarin should be held, and an oral dose of Vitamin K to reduce INR is appropriate.

At 5-9 you can consider withholding the next warfarin dose and rechecking INR in 24hrs.

Question 55

Warfarin to heparin bridge guidelines?

Answer 55

The ACP guidelines recommend that LMWH, UFH, or fondaparinux be continued for “at least 5 days and until the INR is ≥2.0 for at least 24 hours.”

Question 56

Treatment of scabies? Diagnosis?

Answer 56

Diagnosis is confirmed by skin scrapings from lesions revealing mites, ova, and feces.

Treat involves permethrin 5% cream applied overnight and oral ivermectin. Antihistamine and steroids can be added for treatment of dermatitis.

Question 57

Characteristics and epidemiology of CLL?

Answer 57

CLL is the most common leukemia in western countries (30% of leukemias). It is almost always seen in the elderly and often has an asymptomatic presentation and incidental diagnosis.

Lymphocytosis is the classic mark of the disease. Most cells have nuclear pigmentation and look over matured. Smudge cells are the characteristic cell. Lymphadenopathy and splenomegaly can be seen. As the disease progresses anemia and thrombocytopenia are seen.

Question 58

Lambert-Eaton myasthenic syndrome vs. myasthenia gravis?

Answer 58

Lambert-eaton myasthenic syndrome is auto antibodies against presynaptic voltage gated calcium channels. MG has antibodies against post synaptic nicotinic acetylcholine receptors.

An endrophonium (acetylcholinesterase inhib) test will increase strength in MG but less so in lambert-eaton. Specific serum antibodies can be tested. EMG will also show increased fatiguability. I’ve should improve muscle strength.

Question 59

Immune clearance phase (#2) of Hep B infection on bloodwork?

Answer 59

ALT will be elevated due to immune mediated liver inflammation due to destruction of infected cells. HBV DNA levels and HBeAg will be elevated until the body clears infection. HBeAg positivity indicates high level of viral replication.

Serial HBeAg and ALT measurements are needed every 3-6 months to document immune clearance.

Question 60

Causes of sinus bradycardia? Treatment of symptomatic bradycardia?

Answer 60

Causes of sinus bradycardia include good physical conditioning, exaggerated vagal activity, sick sinus syndrome, hypoglycemia, and meds (beta-blockers, digitalis, calcium chan blockers).

Atropine is the first appropriate step in management. It increases HR by decreasing vagal tone. If patient is hemodynamically unstable, use epinephrine to increase BP too.

Question 61

Rectangular, envelope shaped crystals in the urine. Metabolic acidosis with an increased anion gap and increased osmolar gap?

Answer 61

Ethylene glycol poisoning. Antifreeze crystals are calcium oxalate

Question 62

“Snowfield” visual changes and acute pancreatitis with metabolic acidosis + anion gap + osmolar gap?

Answer 62

Methyl alcohol poisoning

Question 63

Signs and symptoms of multiple myeloma?

Answer 63

CRAB for tetrad of presentation. C - calcium (hypercalcemia) R - renal impairment (from accumulation of IgG antibodies in glomeruli) A - anemia B - bones (bone pain, lytic lesions, fractures)

Multiple myeloma patients are also at increased risk for infections due to decreased functional antibodies and leukopenia due to bone marrow crowding.

Paraprotein gap is also characteristic. Paraproteins add to serum protein, but not to albumin. Results in a 3-4g/dL difference between serum protein and albumin.

Question 64

Mycobacterium avium complex prophylaxis in HIV patients? Indications?

Answer 64

Azithromycin. Recommended for CD4+ counts

Question 65

Major side effect of calcium channel blockers?

Answer 65

Peripheral edema is reported in 25% of people after 6 months of therapy. It’s due to preferential dilation of precapillary (arteriolar) vessels which leads to fluid extravasation into the interstitial. DHP CCBs (amlodipine, nifedipine) are more potent arteriolar dilators compared to non-DHP CCBs (diltiazem, verapamil).

Other side effects associated with DHP CCBs include headache, flushing, dizziness.

Question 66

Alcohol and abdominal pain?

Answer 66

Pancreatitis, hepatitis, gastritis.

Question 67

Side effects/contraindications of PPIs?

Answer 67

Osteoporosis (impairs calcium absorption), B12 deficiency, increased c dif. infection, increased risk of aspiration pneumonia.

Question 68

Types of IBS?

Answer 68

Constipation only, diarrhea only (don’t miss celiac - often confused!), mixed, neither.

Rifaximin improves bloating and pain for some (bacterial overgrowth syndrome)

Question 69

Celiac disease clinical presentation?

Answer 69

Chronic diarrhea, wt loss, fatigue, bloating, abdominal pain.

Iron deficiency anemia, dermatitis hepatformis, decreased bone mineral density, neuropathy.

1% western population

Tissue transglutaminase test is the best diagnostically. Also check IgA. Then need biopsy of duodenum.

Question 70

What is Hypokalemic periodic paralysis?

Answer 70

Hypokalemic periodic paralysis is a rare syndrome characterized by episodes of general or focal weakness.
Episodes usually begin in childhood or adolescence.
Paralysis most often occurs during the rest period following, and not during, vigorous physical activity.

Question 71

Atrial fibrillation and differential?

Answer 71

Onset of atrial fibrillation (AF) reduces cardiac output by 10-20%. AF may be related to acute or temporary causes including: alcohol intake (“holiday heart syndrome”); surgery; electrocution; myocardial infarction; pericarditis; myocarditis; pulmonary embolism or other pulmonary diseases; or hyperthyroidism and other metabolic disorders. If one of these causes is present, successful treatment of the underlying condition often eliminates AF. New onset AF occurring in the setting of acute myocardial ischemia is associated with worse outcomes than when ischemic events occur in patients with pre-existing AF or sinus rhythm. AF may be associated with atrial flutter, the Wolf Parkinson White (WPW) syndrome, or AV nodal reentrant tachycardia, and treatment of the primary arrhythmias reduces or eliminates the incidence of recurrent AF. AF is a common early postoperative complication of cardiac or thoracic surgery.

The differential diagnosis of atrial fibrillation includes atrial flutter, premature atrial contractions, and multifocal atrial tachycardia.

Question 72

Persistent vs. paroxysmal A fib?

Answer 72

The clinician should attempt to categorize the timing of a first-detected episode of AF, whether or not it is symptomatic or self-limited, recognizing that there may be uncertainty about the duration of the episode and about previous undetected episodes. When a patient has had two or more episodes, AF is considered recurrent. If the arrhythmia terminates spontaneously, recurrent AF is designated paroxysmal; when sustained beyond seven days, AF is designated persistent. Termination with pharmacological therapy or direct-current cardioversion does not change the designation. First-detected AF may be either paroxysmal or persistent AF. The category of persistent AF also includes cases of long-standing AF (e.g., greater than one year), usually leading to permanent AF, in which cardioversion has failed or has not been attempted.

These categories are not mutually exclusive in a particular patient, who may have several episodes of paroxysmal AF and occasional persistent AF, or the reverse. Regarding paroxysmal and persistent AF, it is practical to categorize a given patient by the most frequent presentation.

The definition of permanent AF is often arbitrary. The duration of AF refers both to individual episodes and to how long the patient has been affected by the arrhythmia. Thus, a patient with paroxysmal AF may have episodes that last seconds to hours, occurring repeatedly for years.

Question 73

Treatment of A fib with rapid ventricular response?

Answer 73

Rate control: Controlling the heart rate with intravenous diltiazem, beta-blockers, or verapamil improves blood flow and does not delay immediate need for emergency stroke treatment.

Rhythm control: Cardioversion either via electric shock to the heart with the patient under sedation or via medications given orally or intravenously. Both methods carry a risk of stroke which is greatest in patients who have had atrial fibrillation for more than 48 hours, or who have not been given three weeks of prior anticoagulant therapy.

Question 74

Treatment of A fib with rapid ventricular response?

Answer 74

Rate control: Controlling the heart rate with intravenous diltiazem, beta-blockers, or verapamil improves blood flow and does not delay immediate need for emergency stroke treatment.

Rhythm control: Cardioversion either via electric shock to the heart with the patient under sedation or via medications given orally or intravenously.

Both methods carry a risk of stroke which is greatest in patients who have had atrial fibrillation for more than 48 hours, or who have not been given three weeks of prior anticoagulant therapy.

Question 75

Prevention of new stroke guidelines?

Answer 75

Adjusted-dose warfarin (target INR, 2.0–3.0).
Recommended for all patients with nonvalvular AF deemed to be at high risk and many deemed to be at moderate risk for stroke who can receive it safely (Class I; Level of Evidence A).

Antiplatelet therapy with aspirin.
Recommended for low-risk and some moderate-risk patients with AF on the basis of patient preference, estimated bleeding risk if anticoagulated, and access to high-quality anti­coagulation monitoring (Class I; Level of Evidence A).

Dual-antiplatelet therapy with clopi­dogrel and aspirin.
Offers more protection against stroke than aspirin alone but with an increased risk of major bleeding and might be reasonable for high-risk patients with AF deemed unsuitable for anticoagulation (Class IIb; Level of Evidence B).

Question 76

Prevention of Stroke in Patients With a History of Stroke or TIA?

Answer 76

For patients with ischemic stroke or TIA with parox­ysmal (intermittent) or permanent AF
Anticoagulation with a vitamin K antagonist (target INR, 2.5; range, 2.0–3.0) is recommended (Class I; Level of Evidence A).

For patients unable to take oral anticoagulants
As­pirin alone (Class I; Level of Evidence A) is recom­mended. The combination of clopidogrel plus aspirin carries a risk of bleeding similar to that of warfarin and therefore is not recommended for patients with a hemorrhagic contraindication to warfarin (Class III; Level of Evidence B).

Question 77

Viral arthritis?

Answer 77

Most commonly caused by Parvovirus B19. Most often presents as acute onset polyarticular symmetric disease. Often MCP PIP and wrists.