DailyReview Flashcards

1
Q

HBsAg: negative anti-HBc: negative anti-HBs: negative

A

Susceptible

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2
Q

HBsAg negative anti-HBc positive anti-HBs positive

A

Immune due to natural infection

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3
Q

HBsAg negative anti-HBc negative anti-HBs positive

A

Immune due to hepatitis B vaccination

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4
Q

HBsAg positive anti-HBc positive IgM anti-HBc positive anti-HBs negative

A

Acutely infected

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5
Q

HBsAg positive anti-HBc positive IgM anti-HBc negative anti-HBs negative

A

Chronically infected

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6
Q

HBsAg negative anti-HBc positive anti-HBs negative

A

Interpretation unclear; four possibilities: 1. Resolved infection (most common) 2. False-positive anti-HBc, thus susceptible 3. “Low level” chronic infection 4. Resolving acute infection

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7
Q

The hallmark of ongoing Hepatitis B infection

A

persistence of surface antigen and absence of surface antibody.

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8
Q

Diagnosis of diabetes

A
  1. Fasting glucose > 126 mg per deciliter (7.0 mmol per liter)
  2. A1C > 6.5% or more
  3. Confirmation by the same or the other test.
  4. OGTT 2-hour > 200 mg per deciliter (11.1 mmol per l); loading dose of 75 g
  5. 100 < Fasting glucose <= 125 mg (5.6 to 6.9 mmol per liter) is prediabetes;
  6. A1C criteria for prediabetes, ADA: 5.7 to 6.4%.
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9
Q

Why is prandial insulin the right strategy for steroid driven hyperglycemia?

A

Glucocorticoids impair glucose transport into cells; decrease islet cell function.

Glucocorticoids drive up post-prandial blood sugars much more than fasting glucose. So glucorticoid induced hyperglycemia is best treated by adjusting prandial insulin

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10
Q

Herpes Zoster vaccine: age

A

> 60

All without contraindications

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11
Q

Epinephrine in anaphylaxis

A
  1. Not profoundly hypotensive: 0.01 mg/kg IM into mid outer thigh, max dose 0.5 mg
  2. Profoundly hypotensive: slow IV at 0.1 mcg/kg/minute, and increase it every two to three minutes by 0.05 mcg/kg/minute until blood pressure and perfusion improve

The epinephrine dilution for IM injection contains 1 mg/mL and ampules may also be labeled as 1:1000.

Epinephrine is commercially available in several dilutions. Great care must be taken to use the correct dilution in order to avoid overdosing the patient [35]. To prepare an epinephrine IV maintenance infusion, the commercially available epinephrine solution (eg, ampule, syringe) must be further diluted. To reduce the risk of making a medication error, we suggest that centers have a protocol available that includes steps on how to prepare and administer an epinephrine infusion.

  • A simple method for quickly preparing a solution of 1 mcg/mL for adults and adolescents is to add the entire 10 mL contents of a 0.1 mg/mL (1:10,000) prefilled “cardiac” epinephrine syringe (1 mg) to a 1000 mL (1 liter) bag of normal saline. The resultant solution of 1 mcg/mL delivers 1 mcg/minute of epinephrine for each 60 mL/hour of solution infused. Therefore, 120 mL/hour will deliver 2 mcg/minute and so forth (table 3).
  • For adolescent/adult patients who have already received large quantities of IV fluids (four or more liters), a more concentrated solution (4 mcg/mL) is preferable. Using a more concentrated solution allows titration of epinephrine infusion and administration of bolus crystalloid solution to be done independent of one another. To prepare a 4 mcg/mL solution, add the entire 10 mL contents of one 0.1 mg/mL (1:10,000) epinephrine syringe to a 250 mL bag of normal saline. The resultant solution delivers 1 mcg/minute of epinephrine for each 15 mL/hour of infusion. Therefore, 30 mL/hour delivers 2 mcg/minute, 45 mL/hour delivers 3 mcg/minute, and so forth (table 4).

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12
Q

Early ejection click + soft systolic murmur in 2 RICS

A

Bicuspid aorta

A functionally normal bicuspid aortic valve produces an ejection sound or click heard best at the left lower sternal border or apex, often accompanied by a brief ejection murmur. Diagnosis is by TEE.

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13
Q

Bicuspid aortic valve risks

A

AS, Infective endocarditis, aortic dilation, aortic dissection

significant aortic stenosis much more frequently than significant aortic regurgitation and are at risk for infective endocarditis. (See ‘Valve disease’ above.)

●Patients with bicuspid aortic valve are at risk for aortic dilation (most commonly involving the ascending aorta) and aortic dissection. These aortic complications are caused by an underlying aortopathy with cystic medial degeneration as well as hemodynamic factors and abnormal aortic wall shear stress. (See ‘Aortic dilation and aortic dissection’ above and ‘Pathophysiology of aortic disease’ above.)

●A bicuspid aortic valve is frequently associated with other congenital cardiovascular defects, including coarctation of the aorta, supravalvular aortic stenosis, subvalvular aortic stenosis, ventricular septal defect, and sinus of Valsalva aneurysm. The combination of bicuspid aortic valve and coarctation of the aorta is associated with high risk of aortic complications. (See

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14
Q

AS versus aortic sclerosis murmur

A

Sclerosis murmur: brief, not loud

Aortic sclerosis, in the absence of stenosis, may be associated with a midsystolic ejection murmur, which is usually best heard over the right second interspace. In general, the murmur is brief and not very loud. Importantly, many patients with aortic sclerosis have no murmur on physical examination.

A normal carotid pulse and normal S2 suggest the absence of aortic stenosis (figure 1). (See “Auscultation of cardiac murmurs in adults”.)

However, the physical examination is neither sensitive nor specific for excluding aortic valve obstruction. Thus, echocardiography should be performed to distinguish aortic sclerosis from aortic stenosis and other cardiac abnormalities that might account for the murmur when present.

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15
Q

HOCM murmur

A

Harsh ejection murmur increasing with Valsalva

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16
Q

Live vaccines should either be given together or at least _ weeks apart

A

4

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17
Q

T1 vs T2

A

CSF is dark on T1-weighted imaging and bright on T2-weighted imaging.

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18
Q

Anatomy.radiculopathies

Weakness biceps, brachioradialis; numbness medial half of hand; absent biceps reflex?

A

C6

bi6

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19
Q

Live vaccines

A
  1. MMR;
  2. varicella-zoster (chickenpox);
  3. Shingles, influenza (intranasal)
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20
Q

Vertigo without hearing loss

A

Vestibular neuronitis

Labyrinthitis is a similar syndrome to vestibular neuritis, but with the addition of hearing symptoms (sensory type hearing loss or tinnitus). The symptoms of bothvestibular neuritis and labyrinthitis typically include dizziness or vertigo, disequilibrium or imbalance, and nausea. Acutely, the dizziness is constant.

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21
Q

Bronchiectasis, recurrent sinopulmonary infections + infertility

A

cystic fibrosis

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22
Q

Forms of varicella zoster infection

A
  1. Chicken pox
  2. Shingles

Primary infection with VZV results in varicella (chickenpox), characterized by vesicular lesions in different stages of development on the face, trunk, and extremities.

Herpes zoster, also known as shingles, results from reactivation of VZV infection within the sensory ganglia.

Cx: painful, unilateral vesicular eruption in a dermatome

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23
Q

Warfarin and enoxaparin: minimum overlap period

A

5 days

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24
Q

Jugular cannon waves + variable S1

A

Ventricular tachycardia

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25
Q

Axonal vs demylinating neuropathy

A
  1. Demyelinating: slow conduction
  2. Axonal: reduced amplitude of evoked compound action potentials with relative preservation of the nerve conduction velocity.

Electrodiagnostic studies can determine if the disorder is due to a primary nerve (neuropathy) or muscle disorder (myopathy). These tests also can identify whether the patient’s symptoms are secondary to a polyneuropathy or another peripheral nerve disorder (eg, polyradiculopathy from lumbar stenosis); if it is a polyneuropathy, EMG/NCS will reveal whether it is axonal or demyelinating in character. The clinical examination alone generally cannot make the latter distinction.

Electrodiagnostic features of demyelinating disorders include:

●Slow nerve conduction velocity

●Dispersion of evoked compound action potentials

●Conduction block (decreased amplitude of muscle compound action potentials on proximal compared with distal nerve stimulation)

●Marked prolongation of distal latencies

In contrast, axonal neuropathies are characterized by a reduced amplitude of evoked compound action potentials with relative preservation of the nerve conduction velocity.

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26
Q

Vaccines: It is not necessary to restart an interrupted vaccine series (except _ _)

A

oral typhoid

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27
Q

Vaccines: implication of local reaction and fever

A

Not a CIxn

Meta: CIxn

Many vaccines cause a local reaction and fever that lasts 24 to 48 hours. This does not contraindicate using the vaccine again and should not be considered an allergic response.

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28
Q

Vaccines: Influenza: Efficacy

A

60% to 80% effective in preventing disease, but 95% effective in preventing complications

NNV: 71 - 40

In a 2014 meta-analysis of randomized trials and observational studies of healthy adults, the overall efficacy of inactivated vaccines in preventing laboratory-confirmed influenza was 60 percent (53 to 66 percent), corresponding to a number needed to vaccinate (NNV) of 71 [28]. The overall effectiveness of inactivated vaccine against influenza-like illness was 16 percent (95% CI 5 to 25 percent), corresponding to a NNV of 40

Because influenza vaccines produced in eggs take approximately six months to manufacture, they necessarily contain antigens from strains that circulated during the previous year. The protective efficacy of the vaccine is largely determined by the relationship (closeness of “fit” or “match”) between the strains in the vaccine and viruses that circulate in the outbreak. A study that compared the effectiveness of the inactivated influenza vaccine during influenza seasons with differing degrees of vaccine match illustrates the importance of the fit between circulating influenza virus strains and the vaccine [37]. During the 2004 to 2005 influenza season, the antigenic match was only 5 percent compared with 91 percent during the 2006 to 2007 season, which resulted in a vaccine effectiveness of 10 versus 52 percent, respectively. During the 2014 to 2015 influenza season in the United States, influenza A H3N2 viruses predominated and more than half of these viruses contained H3N2 antigen that was antigenically different (drifted) from that included in that season’s influenza vaccines [38]. The adjusted overall vaccine effectiveness for the 2014 to 2015 influenza season was 19 percent; for H3N2-associated illness, the vaccine effectiveness was only 6 percent [39]. A meta-analysis of observational studies showed that influenza vaccines are less effective against H3N2 influenza A than against H1N1 influenza A and influenza B [40].

Influenza vaccine effectiveness in preventing laboratory-confirmed influenza in the United States is available from the Centers for Disease Control and Prevention (CDC) for influenza seasons from 2004-2005 to 2015-2016 [41].

A repeated finding in various studies is that vaccination produces a greater reduction in serologically confirmed influenza than in clinical influenza. Universal influenza vaccination in Ontario, Canada, has also been shown to reduce the number of antibiotic prescriptions during periods of peak influenza activity [42].

The primary means of assessing serum antibody responses to influenza vaccination is the serum hemagglutination (HA)-inhibition assay; in addition to the HA antibody response, other immune mechanisms that contribute to protection against influenza include mucosal immunity, antibodies to neuraminidase (NA), virus-specific CD4 and CD8 T cells, and possibly antibodies to minor envelope protein 2 (M2) and the structural nucleoprotein [3].

Healthy adults — A number of studies have evaluated the efficacy or immunogenicity of various influenza vaccines in different populations.

Trivalent inactivated vaccines — Although many studies evaluating the efficacy of influenza vaccines in healthy adults have been published and efficacy is often estimated to be between 70 and 90 percent, a 2012 comprehensive review suggested that efficacy may be considerably lower [43]. In a 2012 meta-analysis (performed by the same group that did the comprehensive review) that included eight randomized trials of the inactivated influenza vaccines in adults aged 18 to 64 years over nine influenza seasons, vaccine efficacy for preventing laboratory-confirmed influenza was 59 percent (95% CI 51 to 67 percent) [44]. Of note, higher rates of efficacy and effectiveness have been reported in trials that used serologic endpoints; such trials were excluded from this meta-analysis because using serologic endpoints is likely to lead to an overestimation of benefit.

In a 2014 meta-analysis of randomized trials and observational studies of healthy adults, the overall efficacy of inactivated vaccines in preventing laboratory-confirmed influenza was 60 percent (53 to 66 percent), corresponding to a number needed to vaccinate (NNV) of 71 [28]. The overall effectiveness of inactivated vaccine against influenza-like illness was 16 percent (95% CI 5 to 25 percent), corresponding to a NNV of 40 [28]. The difference between these two results relates to the different incidence of these endpoints among the study populations; 2.4 percent of unvaccinated individuals versus 1.1 percent of vaccinated individuals developed laboratory-confirmed influenza, whereas 15.6 percent of unvaccinated individuals versus 9.9 percent of vaccinated individuals developed an influenza-like illness, respectively. The discrepancy between protection against laboratory-confirmed influenza and influenza-like illness is likely related to the well-known lack of protection offered by influenza vaccines against non-influenza respiratory viruses.

The match between the antigens included in the influenza vaccines and circulating influenza strains would be expected to have an important influence on the efficacy of the vaccines. In the 2014 meta-analysis described above, inactivated vaccines were 16 percent effective (95% CI 9 to 23 percent) in preventing influenza-like illness when strains contained in the vaccine antigenically matched circulating strains [28]. On the other hand, inactivated vaccines were not protective against influenza-like illness when the degree of matching between the vaccine and circulating influenza strains was absent or unknown. In contrast, the efficacy of inactivated vaccines for preventing laboratory-confirmed influenza was similar when the match was good and when the match was absent or unknown (62 versus 55 percent, respectively).

Several studies have shown that influenza vaccination is less effective in individuals who were vaccinated during the current and previous season(s) compared with individuals who were vaccinated during the current season only [45-50]. Other studies have not shown a decrease in vaccine efficacy when influenza vaccination is given to people who were vaccinated the previous year [51,52].

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29
Q

Vaccines: Influenza: schedule

A

annual

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30
Q

Vaccines: Tdap

A

Td booster every 10 years

+ one Tdap

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31
Q

Vaccines: Varicella

A

2 doses at any time

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32
Q

Vaccines: HPV

A

3 doses

Age: 19-26

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33
Q

Vaccines: Zoster

A

1 dose

60 > Age

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34
Q

Vaccines: MMR: Schedule

(in adults)

A

1 dose below age 50,

1 dose above age 50 if risk factor

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35
Q
A
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36
Q

Vaccine: Adult: Pneumococcal: schedule

A

Age > 65

or

risk factor

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37
Q

Vaccine: Meningococcal

A

1 or more dose if risk factor

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38
Q

Vaccination: Hep A and Hep B: schedule

A

Only if risk factors

Hep B: 3 dose sequence,Hep A: two doses

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39
Q

HPV: About 70% of cervical cancers are caused by:

A

HPV-16 and HPV-18

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40
Q

MMR: CIxn

A

Do not give to patients who are pregnant or trying to get pregnant or to severely immunocompromised patients

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41
Q

HZV and Chicken-pox vaccines

A

Chicken pox:

Indications

All adults without evidence of immunity (Box 73-1)

Evidence of Immunity to Varicella for Adults

  1. Documentation of two-dose vaccine series
  2. Laboratory evidence of immunity
  3. Birth in the United States before 1980*
  4. Verification of history of chickenpox by a health-care provider†
  5. Verification of a history of herpes zoster by a health-care provider

Herpes zoster (shingles) vaccine

  1. Live vaccine
  2. About 50% to 60% effective in preventing shingles; about 60% to 70% effective in preventing postherpetic neuralgia
  3. Single shot; no revaccination currently recommended
  4. All 60 years and older
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42
Q

USPTF: Grading

A

A, B: Good; C: maybe; D: bad, I: insufficient

  1. A: Service recommended. Net benefit is thought to be substantial
  2. B: Service recommended. Net benefit is thought to be moderate to substantial
  3. C: Not routinely recommended. There may be some individuals for which service is appropriate
  4. D: Not recommended. Data show no benefit or potential for harm
  5. I: Current evidence insufficient to make a recommendation for or against the service
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43
Q

Screening: types

A
  1. Primary prevention: Intervention designed to avert disease before it develops (e.g., nutritional counseling)
  2. Secondary prevention: Intervention aimed at early detection of disease (e.g., mammography)
  3. Tertiary prevention: Preventing complications of a symptomatic disease (e.g., hepatitis B vaccine in hepatitis C patients)
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44
Q

Screening: ideal test properties

A
  1. Screens for a disease that has high morbidity and mortality
  2. Is sensitive with a confirmatory test available, inexpensive, and noninvasive
  3. Screens for a disease that has a long premorbid phase during which intervention can affect outcome
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45
Q

Screening: PSA

USPSTF recommends against screening men older than age _ years since harms outweigh benefits

A

USPSTF recommends against screening men older than age 75 years since harms outweigh benefits

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46
Q

Screening: Pap smear: frequency

A
  1. all sexually active women older than 21 years with a cervix (or within 3 years of onset of sexual activity)
  2. If no risk factors every 3 years
  3. ACS agrees but recommends three annual negative Pap smears before doing 3-year intervals.
  4. If no risk factors, stop after age 65
  5. If distant history of last Pap smear, all ages
  6. No Pap smears if hysterectomy for benign disease (USPTF)
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47
Q

Screening: Chlamydia

A

All asymptomatic adolescent sexually active women (24 years or younger) and high-risk adult women.

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48
Q

Screening: Tuberculosis

Meta: OpenQuestion

if IFN-gamma tests the same thing as skin why prefer IFN-gamma tests in BCG vaccinated patients?

A

Two types of tests now available: PPD and interferon-γ release assay blood test

Criteria for positive PPD test are as follows:

  1. Low-risk patients: 15-mm diameter or greater
  2. High-risk patients (any of the previous indications for screening makes a patient at least high risk): 10-mm diameter or greater
  3. Very-high-risk patients (HIV infection, abnormal chest film, recent contact with known infected patients): 5-mm diameter or greater

Blood test is preferred for patients who have had the BCG vaccine

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49
Q

Screening: hypercholesterolemia

A

all men 35 years or older and men and women 20 years and older if they have another risk factor for coronary heart disease

USPSTF recommends screening all men 35 years or older and men and women 20 years and older if they have another risk factor for coronary heart disease

USPSTF makes no recommendation for screening women without risk factors

National Cholesterol Education Program (NCEP) recommends screening all adults over age 20 years with a lipid profile

Ideal frequency of screening has not been established, but NCEP recommends every 5 years if profile is normal

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50
Q

Screening: Abdominal aortic aneurysm (AAA)

A

men ages 65 to 75 years who have ever smoked

USPSTF recommends one-time screening for AAA by ultrasound in men ages 65 to 75 years who have ever smoked

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51
Q

Vaccines: Td

A 38-year-old recent immigrant from Vietnam comes into the emergency room after cutting his foot on a nail. He does not recall receiving any vaccines as a child. Which regimen does he need?

A

Three-shot dT vaccine series plus tetanus toxoid now, with first dT shot now

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52
Q

Chemoprevention: aspirin

A

if risk: benefit ration favorable then aspirin

Use of aspirin for men ages 45 to 79 years is recommended when the potential benefit due to a reduction in myocardial infarctions outweighs the potential harm due to an increase in gastrointestinal hemorrhage

Use of aspirin for women ages 55 to 79 years is recommended when the potential benefit of a reduction in ischemic strokes outweighs the potential harm of an increase in gastrointestinal hemorrhage

Ideal dose is unclear since beneficial effects are shown for doses ranging from 75 mg to 325 mg

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53
Q

Screening: USPTF diseases

A

USPSTF Screening Guidelines for Common Disorders

  1. Obesity
  2. DM2
  3. Osteoporosis: Screen women >65 yr with a DEXA scan. Start earlier if risk factors exist
  4. Alcohol abuse
  5. Smoking
  6. Depression
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54
Q

Vaccination:

For which one of the following diseases can passive immunization with an immunoglobulin infusion not be given simultaneously with the vaccine for the disease?

Varicella

Hepatitis A

Hepatitis B

Tetanus

A

Varicella

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55
Q

Vaccination:

A 45-year-old man presents to your office in July of this year for a routine physical. He is currently drinking two six-packs of beer per day, but has no other medical problems. He believes he received all of his routine childhood vaccinations, but doesn’t recall getting any other shots since then. Which vaccine combination makes the most sense for him?

Hepatitis A, hepatitis B

Pneumococcus, meningococcus, Haemophilus influenzae

Pneumococcus, tetanus

Tetanus, influenza

Hepatitis A, hepatitis B, tetanus

A

Pneumococcus, tetanus

(because of EtOH use)

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56
Q

. Patients with chronic liver disease should be immunized against

A

hepatitis A and B

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57
Q

BMT: Vaccinations?

A
  1. Primary series dead vaccines at 12 months
  2. Live vaccines: after 24 months

Bone marrow transplantation patients need to be revaccinated with the primary series of all standard childhood vaccines after 12 months post-transplantation, assuming no complication from the transplantation. Live, attenuated vaccines, however, need to wait until 24 months after transplantation.

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58
Q

A 68-year-old gentleman with a history of hypertension and rheumatoid arthritis presents for a general medical evaluation. He says that he last had a tetanus shot 6 years ago but has not had any other immunizations in the recent past. His current medications include lisinopril 10 mg/day, prednisone 20 mg/day, and azathioprine 100 mg/day. Which of the following vaccines should be recommended?

A

pneumococcal vaccine, influenza vaccine.

However, he is immunosuppressed and so he should not receive any live vaccines, so the zoster vaccine should not be given. He does not need a tetanus shot since he had it within the last 10 years.

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59
Q

Hypotension after intubation for severe COPD: commonest cause

A

Air trapping

Rx: disconnect

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60
Q

ICU: common situations when auto-PEEP develops

A
  1. high minute ventilation,
  2. expiratory flow limitation
  3. expiratory resistance.

Auto-PEEP increases intrathoracic pressure, which can decrease venous return, reduce cardiac output, and potentially cause hypotension. It can also cause alveolar overdistension, increasing the likelihood of pulmonary barotrauma and ventilator-associated lung injury. Finally, auto-PEEP increases the work required for a patient to trigger a ventilator breath if pressure-triggering is being used. (See ‘Potential sequelae’ above.)

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61
Q

Epidemiology: histoplasmosis, coccidiomycosis, paracocidiomycosis

A
  1. Coccidio: Southwest
  2. Histo: Ohio+Mississippi
  3. Paracoc: South+Central America
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62
Q

Histo: DDx

A

Sarcoid

The clinical and radiographic findings in pulmonary histoplasmosis and sarcoidosis may be similar [25]. A mistake in diagnosis can be disastrous if the patient is treated with corticosteroids or other immunosuppressive medications [3]. Although such patients may appear to improve transiently, they eventually experience progressive disseminated disease, which may result in increased morbidity and mortality if the true diagnosis is not identified. I

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63
Q

Mass at jaw; woody; sinus

A

Actinomyces israeli, penicillin

Cervicofacial actinomycosis is a chronic disease characterized by abscess formation, draining sinus tracts, fistulae, and tissue fibrosis. It can mimic a number of other conditions, particularly malignancy and granulomatous disease. (See ‘Introduction’ above.)

●Cervicofacial actinomycosis is caused by branching gram-positive bacteria with a variable cellular morphology, ranging from diphtheroidal to coccoid filaments (picture 1) belonging to the genus Actinomyces. (See ‘Microbiology’ above.)

●Actinomyces are noted for forming characteristic sulfur granules in infected tissue but not in vitro (figure 1). (See ‘Sulfur granules’ above.)

●A hallmark of cervicofacial actinomycosis is the tendency to spread without regard for anatomical barriers, including fascial planes or lymphatic drainage, and the development of multiple sinus tracts. Actinomyces species capitalize on tissue injury or mucosal breach to invade adjacent structures; dental infections and oromaxillofacial trauma are common antecedent events. (See ‘Pathogenesis’ above.)

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64
Q

Leprosy: DxMethod

A

Skin biopsy

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65
Q

Pyelonephritis: not improving: CT or US?

A

CT

CT is much more sensitive, detects smaller lesions

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66
Q

Candidemia: Rx

A

Capsofungin

For nonneutropenic and neutropenic patients with candidemia, we recommend an echinocandin rather than fluconazole or amphotericin B (table 1) (Grade 1B).

ndergo an ophthalmologic examination by

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67
Q

can improve yield of fastidious organisms (eg, Brucella spp and fungi) [54,55]. This culture system contains components that lyse leukocytes and erythrocytes, as well as inactivate plasma complement and certain antibiotics.

A

Lysis centrifugation

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68
Q

Endocarditis: commonest complication

A

Cerebral complications are the most frequent and most severe extracardiac complications. Vegetations that are large, mobile, or in the mitral position and infective endocarditis due to Staphylococcus aureus are associated with an increased risk of

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69
Q

Infective focus: finding

A
  1. Echo
  2. CT abdomen/pelvis
  3. MRI spine
  4. Tagged WBC
  5. Special cultures: lysis centrifugation, for example.
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70
Q

Interferon-gamma release assays and tuberculin skin tests: role in the diagnosis of active disease.

A

None

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71
Q

Pleural TB: BestTest

A

Pleural biopsy + culture

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72
Q

Blood culture: large Gram+ with pseudohyphae

A

Candida

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73
Q

Enterococcus endocarditis: non-resistant org

A

Ampicillin + gentamicin

https://www.ncbi.nlm.nih.gov/pubmed/26373316?ssource=kplus

Enterococci are relatively resistant to the killing effects of cell wall–active agents (penicillin, ampicillin, and vancomycin) and are impermeable to aminoglycosides. Antibiotic regimens and doses for susceptible strains are outlined in the Table (table 1). (See ‘Approach to susceptible strains’ above.)

Treatment of bacteremia due to susceptible enterococci (in the absence of suspected endocarditis) consists of ampicillin. Bacteremia due to ampicillin- and vancomycin-resistant E. faecium bacteremia (in the absence of suspected endocarditis) may be treated with daptomycin (8 to 10 mg/kg/day). (See ‘Bacteremia’ above.)

●For treatment of enterococcal bacteremia with suspected endocarditis or critical illness, we recommend combination antimicrobial therapy over monotherapy (Grade 1B). Of the combination antimicrobial regimens, we suggest ampicillin plus ceftriaxone since it avoids the toxicity of aminoglycosides (Grade 2B); use of a cell wall–active agent in combination with a synergistically active aminoglycoside is also acceptable.

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74
Q

Viral pneumonia + conjunctivitis + military recruit: organism

A

Adenovirus

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75
Q

Plugged central line: needed for vasopressors

A

Remove line; insert new central

not femoral, not exchange

76
A

Seborrheic dermatitis, HIV testing

is a chronic, relapsing, and usually mild form of dermatitis of unknown origin occurring in areas rich in sebaceous glands (scalp, face, upper trunk, intertriginous areas); indirect evidence supports a pathogenetic role for the Malassezia yeast. (See ‘Pathogenesis’ above.)

Seborrheic dermatitis tends to be more extensive and severe in HIV/AIDS patients. It sometimes involves unusual sites, such as the extremities, and may be difficult to control [3,15]. Seborrheic dermatitis is frequently observed in patients with CD4 counts <400 cells/microL, and is more diffuse and severe in patients with CD4 counts <200 cells/microL [16,17]. It may regress with antiretroviral therapy (ART). However, seborrheic dermatitis also may be a cutaneous manifestation of the immune reconstitution inflammatory syndrome in patients on ART

77
Q

Indirect bilirubinemia: mild: HIV+: which drug?

A

Atazanavir

Indirect == unconjugated

advantage of better gastrointestinal tolerance than most other PIs, once-daily dosing, and good potency. Atazanavir is not associated with the development of insulin resistance when compared with some other PIs such as lopinavir-ritonavir. Lipid profiles show mild increases in cholesterol and triglycerides that are mainly related to ritonavir [125].

Adverse reactions include an increase in the indirect serum bilirubin concentration, which is benign but may cause jaundice. In antiretroviral-naïve persons with low cardiovascular risk, the hyperbilirubinemia associated with initiating atazanavir plus ritonavir may be responsible for slower progression of carotid artery intima-media thickening than observed in those who received darunavir boosted with ritonavir [126]. Atazanavir has also been associated with the development of renal stones and kidney injury (eg, proximal tubular dysfunction, interstitial nephritis, and acute kidney injury) [16,127-132]. (See “Overview of kidney disease in HIV-positive patients”, section on ‘Medication nephrotoxicity’.)

78
Q

Cellulitis: prophylaxis

A

penicillin

79
Q

Rabies exposure

A

Infiltrate wound with Ig; post-exposure vaccination

80
Q

CMV colitis: Post-transplant: Rx

A

Valgancilovir or ganciclovir

81
Q

When can a dialysis catheter be retained if there is bacteremia?

A

Uncomplicated CNS bacteremia

82
Q

HIV: post-exposure prophylaxis: non-occupational, high risk

A

28-day multidrug

83
Q

Gas gangrene: why not imaging work up if we suspect it?

A

Plain film, CT and MRI are insensitive!

Plan film may not pick up gas; CT/MRI OK for deep tissue stranding but not gas. Finally: delay

84
Q

Ritonavir inhibits

A

Cytochrome P450: prolongs fluticasone but not beclamethasone

85
Q

HIV: occupational exposure from high risk patient: Rx

A

3-drug prophylaxis

86
Q

HIV: which statins are to be avoided?

A

Simvastatin, lovastatin

87
Q

Meningitis: nosocomial: Rx

A

vancomycin + ceftazidime

meningitis develops after neurosurgery or for patients who are hospitalized for a prolonged period after penetrating head trauma or basilar skull fracture should consist of vancomycin in combination with cefepime, ceftazidime, or meropenem26; the choice of the second agent should be based on the antimicrobialsusceptibility profiles of the local gram-negative bacilli. Meropenem is the agent of choice if one of the carbapenems is used, given the lower risk of seizure with meropenem than with imipenem, and given the clinical studies that have shown its usefulness in the treatment of bacterial meningitis.26 Empirical therapy after basilar skull fracture or early after otorhinologic surgery should consist of vancomycin plus a third-generation cephalosporin (either cefotaxime or ceftriaxone).11,13

88
Q

PID: mild to moderate: Rx: ouptatient

A

ceftriaxone + metronidazole + doxycycline

89
Q

Syphilis: pregnant: serious penicillin allergy: Rx

A

Pencillin with desensitization

Penicillin is the DrugOfChoice for all stages of syphilis

90
Q

Hepatitis B: history of depression: Active: Rx indications and choice

A

Tenofovir or entecavir

Pegylated interferon alfa, lamivudine, adefovir, entecavir, tenofovir, and telbivudine are all FDA approved for treatment of chronic hepatitis B. Entecavir and tenofovir are associated with the most impressive reduction in viral load and lack of resistance.

Interferon alfa may provide a more durable response but is quite expensive and is associated with more side effects than the others (e.g., flu-like symptoms, cytopenias, elevated liver tests, mood changes)

Treatment indicated in HBeAg-negative patients with HBV DNA greater than 2000 IU/mL, in HBeAg-postive patients with HBV DNA greater than 20,000 IU/mL, or liver enzymes greater than 5× the upper limit of normal, or active necroinflammatory disease on liver biopsy

91
Q

Hepatitis B: Treatment parameters

A

HBeAg Status, HBV DNA, ALT

92
Q

Hep B: Rx

The patient is a 25-year-old Asian man who is hepatitis B surface antigen (HBsAg) (+) and hepatitis B e antigen (HBeAg) (+) with serum hepatitis B virus (HBV) DNA of 140 million international units/mL. He has mild inflammation on biopsy. His serum alanine transaminase (ALT) is 100.

A

Entecavir or tenofovir

This patient should be considered for therapy with entecavir, tenofovir, or pegylated interferon alfa. The degree of elevation of the serum ALT is particularly important in influencing the decision to treat HBeAg-positive patients since it has proven to be one of the most important predictors of HBeAg seroconversion. In one study on lamivudine, for example, the rates of HBeAg seroconversion for patients with pretreatment ALT levels within normal, one to two times normal, two to five times normal, and more than five times normal were 2, 9, 21, and 47 percent, respectively [5]. (See “Hepatitis B virus: Overview of management”, section on ‘Indications for antiviral therapy’.)

93
Q

Hep B: Precore: Rx

20-year-old woman who is hepatitis B surface antigen (HBsAg) (+) and hepatitis B e antigen (HBeAg) (-). Her hepatitis B virus (HBV) DNA is 250,000 international units/mL. She has mild portal inflammation and no fibrosis. Her serum alanine transaminase (ALT) is 60 international units/L.

A

Observe

I would follow this patient without recommending treatment at this time. Although this patient has the characteristics of HBeAg-negative chronic hepatitis, it is uncommon for patients to be in this phase of chronic HBV infection at such a young age. Thus, she is likely to be infected with a precore variant. All approved treatments: interferon, lamivudine, telbivudine, adefovir, entecavir, and tenofovir have a low rate of sustained response in such patients. Because she is young and has only mild histologic changes on liver biopsy, I think it is reasonable to observe her for the time being. I would repeat liver chemistries every three to six months, and I would start treatment if the ALT is persistently elevated and the HBV DNA remains high after one year of observation.

94
Q

Hep B: Rx

22-year-old man who is hepatitis B surface antigen (HBsAg) (+), hepatitis B e antigen (HBeAg) (+), and anti-HBe (-). His hepatitis B virus (HBV) DNA is 14 million international units/mL and serum alanine transaminase (ALT) is persistently in the range of 20 to 30 international units/L.

A

Observe

I would not treat this patient at this time although his HBV DNA level is high. He is very young, and has a serum ALT that is normal (which predicts low probability of HBeAg seroconversion to both peginterferon and nucleos[t]ide analogs).

Although antiviral therapy can decrease serum HBV DNA level in this patient, there is no evidence that treating this patient at seroconversion only occurred in three patients (5 percent) [6]. this stage will improve the clinical outcome. Given the low rate of HBeAg seroconversion, this patient will need to receive treatment for many years and even decades to derive a clinical benefit. As an example, in a study of 126 HBeAg-positive individuals receiving tenofovir alone, or in combination with emtricitabine, HBeAg

95
Q

Paromycin

A

Intra-luminal aminoglycoside, helpful in Enatameba as a second line agent

96
Q

GBS: Rx

A

IVIG +/- plasmapheresis

Intravenous immune globulin or plasma exchange should be administered in patients who are not able to walk unaided. In patients whose status deteriorates after initial improvement or stabilization, retreatment with either form of immunotherapy can be considered. However, plasma exchange should not be performed in patients already treated with immune globulin because it would wash out the immune globulin still present in the blood. Also, immune globulin should not be used in patients already treated with plasma exchange because this sequence of treatments is not significantly better than plasma exchange alone.6

97
Q

Tryptase and C1-esterase inhibitor

A
  1. High tryptase: anaphylaxis, mastocytosis
  2. Low C1-esterase inhibitor, C4 persistently down, C2 down during attacks: hereditary angioedema
98
Q

Fixed split S2

A

ASD

99
Q

Harsh systolic murmur lower sternal border

A

VSD

100
Q

Loud, continous murmur upper LSB

A

PDA

101
Q

is a congenital malformation characterized by variably malformed and displaced tricuspid valve leaflets that are partly attached to the tricuspid valve annulus and partly attached to the right ventricular endocardium. These features cause tricuspid valve regurgitation and right heart enlargement. (See ‘Morphology’ above.)

A

Ebstein anomaly

holosystolic murmur of TR

102
Q

Young woman: hypertension, low K, slightly high Cr; high renin

A

FMD

Fibromuscular dysplasia (FMD) is a noninflammatory, nonatherosclerotic disorder that leads to arterial stenosis, occlusion, aneurysm, and dissection. It has been observed in nearly every arterial bed. The most frequently involved arteries are the renal (75 to 80 percent of patients), internal carotid, and vertebral arteries (about 75 percent of patients have carotid and/or vertebral involvement), followed by visceral and external iliac arteries. Among adults, FMD is more common among females (approximately 90 percent of cases are in women). There does not appear to be a female predominance among children with FMD

103
Q

GPIIbIIIa inhibitor use: use in ACS

A

Only AFTER PCI, NEVER during ACS

104
Q

Clopidogrel: when to use in NSTEMI

A

Always

Load with 300 or 600

(unless CABG is being planned in 5 days)

105
Q

Chest pain worsened by nitro and exertion

A

Myocardial bridging

e major coronary arteries occasionally have a segmental intramyocardial course. During systole, this segment of the vessel is compressed, a condition referred to as milking or systolic “myocardial bridging.”

On angiography, bridging is recognized as compression of a segment of a coronary artery during systole, resulting in narrowing that reverses during diastole. This occurs most often in the left anterior descending coronary artery or its septal perforator branches. (See ‘Introduction’ above.)

106
Q

WPW Pattern + asymptomatic: FirstTest

A

Exercise stress test

107
Q

20% of Ebstein anomaly patients have which EKG anomaly?

A

WPW

http://www.nejm.org/doi/pdf/10.1056/NEJMicm031104?ssource=kplus

44-year-old woman presented with increasing dyspnea. the patient had Ebstein’s anomaly, which had first been diagnosed when she was in her early 20s. She had declined heart transplantation three years before her admission to our hospital. The findings on physical examination included atrial fibrillation, a diffuse anterior chest heave and friction rub, and severe right heart failure. The electrocardiogram showed atrial fibrillation and right bundle-branch block. Her chest x-ray films (Panels A and B) showed a cardiothoracic ratio of 1, splaying of the carina, and cardiac enlargement posterior to the vertebral bodies. On transthoracic echocardiography (Panel C and Video Clip), a small left ventricle was seen next to massively dilated right heart chambers. In addition, malposition of the anterior and septal tricuspidvalve leaflets with “atrialization” of the right ventricle and severe tricuspid regurgitation were found. Initially, the patient had a response to fluid restriction and intravenous furosemide and dobutamine. On the fifth day after her admission, she had a cardiac arrest and died four days later in the intensive care unit. Ebstein’s anomaly is an abnormality in the embryonic development of the tricuspid valve, with apical displacement and attachment of the septal, posterior, or (rarely) anterior leaflet to the right ventricle wall.

108
Q

Tendinous xanthoma

A

Familial hypercholesterolemia

109
Q

PAD: Drug Rx

A

Cilastozol

110
Q

AAA Repair: when?

A

> 5.5 cm

111
Q

Aortic dissection for surgical repair

A

Proximal to L subclavian, Type A

Type B: distal; uncomplicated: medical mx

Type B complicated by shock or rupture or endorgan damage: surgery or endovascular

112
Q

Stones + hypercalciuria: Rx

A

Chlorthalidone

Interesting: furosemide for hypercalcemia (to promote Ca excretion) but thiazide to decrease Ca excretion

113
Q

Monoclonal gammopathy+heart failure+renal failure+periorbital purpura

A

Amyloid light chain

Not Myeloma; not MGUS because these are not infiltrating disorders. AL amyloid is infection or lymphoma or RA associated.

114
Q

UACS Rx

A

oral antihistamine + decongestant

115
Q

Chronic tension headache+scalp muscle tenderness: rx

A

Amitryptiline

116
Q

Mild hypercal, anemia out of proportion to CKD

A

SPEP

117
Q

Parkinsons: Elderly patient with worsening symptoms + hallucinations on ropinorole: Rx

A

Replace ropinorole with carbidopa-levodopa

118
Q

Monitoring UFH Rx in patient with baseline abnormal PTT

A

anti-Factor Xa assay

119
Q

Pneumothorax: two commonest causes

A

COPD and PJP

120
Q

agranulocytosis

A

clozapine, methimazole

121
Q

ESLD, active bleeding, low fibrinogen: Rx

A

Cryoprecipitate

122
Q

Palmar xanthoma

A

Dysbetaliproteinemia

123
Q

Primary biliary cholangitis: antibody

A

mitochondrial

124
Q

PCOS: fertility desired: Rx

A

Clomiphene

not metformin

125
Q

Neurosyphilis: Rx

A

IV penicillin

not IM benzathine

126
Q

Asthma: BestTest

A

FEV1 before after bronchodilator

Improvement of 12% , 200 ml

127
Q

Primary sclerosing cholangitis: BestTest

A

MRCP

128
Q

Premature ovarian failure: OnDx: Screen for

A

hypothyroidism

129
Q

Tree pollen, Grass pollen, weed pollen

A

Tree: spring, Grass:late spring/summer, Weed: late summer, fall

130
Q

Annular, scaly rash on the arm, present since week after getting new cat

Raised, advancing erythematous margin and scale that is clear toward the center

A

Tinea

ris usually responds well to topical antifungal drugs, such as azoles, allylamines, butenafine, ciclopirox, and tolnaftate (table 1) [4,15].

Pooled data from randomized trials supports the efficacy of two allylamines, terbinafine and naftifine, for tinea corporis and tinea cruris [4]. There are also data that suggest similar efficacy of topical allylamines and topical azoles [4]. Topical nystatin is not effective for dermatophyte infections.

131
Q

Nystatin: good for candida or tinea?

A

Candida

Not effective for tinea which is a dermatophyte

132
Q

Dermatophytes

A

Tinea of various types

Dermatophytes are filamentous fungi in the genera Trichophyton, Microsporum, and Epidermophyton. Dermatophytes metabolize and subsist upon keratin in the skin, hair, and nails.

The major clinical subtypes of dermatophyte infections are:

●Tinea corporis – Infection of body surfaces other than the feet, groin, face, scalp hair, or beard hair

●Tinea pedis – Infection of the foot

●Tinea cruris – Infection of the groin

●Tinea capitis – Infection of scalp hair

●Tinea unguium (dermatophyte onychomycosis) – Infection of the nail

133
Q

Candida vs Tinea

A
  1. Tinea: dermatophyte – tinea cruris, pedis etc. Ringworm.
  2. Candida: mucocutaneous and invasive infection.
  3. Tinea: terbinafine etc.
  4. Candida: nystatin local or fluconazole systemic of capsofungin systemic.
134
Q

Intermittent mild pain and burning on the tongue

Variable, raised, yellow pattern on the tongue that changes position

A

Geographic tongue

Rx: reassurance

135
Q

Skin lesion on her forehead

History of extensive sun exposure as a child with repeated sunburns

Multiple rough, scaly patches on the forehead and dorsum of the hands

One of the scaly patches on the forehead is associated with a firm hyperkeratotic macule

A

multiple actinic keratoses (AK) and squamous cell carcinoma (SCC) in situ.

Rx:

136
Q

TENS vs SJS

A

> 30% of BSA is considered toxic epidermal necrolysis (TEN). SJS affects < 10% of the BSA. When 10–30% of the BSA is involved, it is considered SJS-TEN overlap

137
Q

Numerous scaly hypo- and hyperpigmented areas across the chest with a fine scale

No large isolated patch

No itching

KOH stain: “Spaghetti and meatball” elements

A

Diagnosis is tinea versicolor (TV). The associated microorganism is the fungus, Malassezia.

Rx:

Topical antifungals (selenium sulfide, ketoconazole shampoo) or oral antifungals (ketoconazole, itraconazole, and fluconazole).

138
Q

Scalp itching

Erythema at the base of the scalp

Mild, bilateral, posterior, auricular lymphadenopathy

Wood’s lamp: Small areas of pale blue fluorescence at base of multiple hair shafts

What is the diagnosis?

A

Diagnosis is pediculosis capitis (head lice).

Rx:

Diagnosis is pediculosis capitis (head lice).

139
Q

Rosacea: rx

A

Topical metronidazole or oral antibiotics for severe disease (tetracycline, doxycycline, or minocycline); laser therapy for telangiectasias. Topical corticosteroids worsen disease.

140
Q

Molluscum contagiosum: Rx

A

Liquid nitrogen

141
Q

Middle-aged Caucasian woman presents with:

Skin lesion on her thigh

History of extensive sun exposure as a child with repeated sunburns

Flat, asymmetric, pigmented lesion that lacks uniform color and is ~ 8 mm in size

Enlargement of the lesion over the past few months

What is the diagnosis?

Meta: looks benign, highly dangerous

A

elanoma.

Explanation

Remember the ABCDE features of melanoma: asymmetry, border irregularities, color variegation, diameter > 6 mm, enlargement or evolution of color change, shape, or symptoms. There are 4 types: Superficial spreading, lentigo maligna, acral lentiginous (palms, soles, nails, and mucosa), and nodular. Nodular is the only one of the 4 types that does not exhibit radial growth; instead, it grows deeply vertical, with an increased incidence of early metastasis.
Dx: Excisional skin biopsy.
Tx: Based on staging; surgical excision with wide margins ± sentinel lymph node biopsy. Regional mets treated with resection and adjuvant radiation (reduces local occurrence); adjuvant interferon alpha-2b x 1 year for stage 3 and higher disease. Distant mets (stage 4 disease) is incurable with survival average 6–15 months.

142
Q

Elderly, African American male patient presents with alopecia since getting his hair cut with an electric razor, in addition to:

Annular scaly patch of hair loss

Small black dots over the hair follicles

Palpable, small, posterior, cervical lymph nodes

What is the diagnosis?

A

tinea capitis. The fungal organisms that cause tinea infections are called “dermatophytes” (Epidermophyton, Trichophyton, and Microsporum species).
Dx: Clinical + KOH prep on hair to identify fungal spores on the shaft + fungal culture (Sabouraud medium); avoid empirically treating without doing a culture.
Tx: Oral antifungal (griseofulvin, terbinafine, itraconazole, fluconazole); topical treatments are ineffective for tinea capitis. Remember, nystatin does not treat dermatophyte infections, only Candida. Counsel close contacts not to share fomites (hairbrushes, hats). Corticosteroids are added when kerion (an intense inflammatory reaction resulting in a boggy and tender lesion) is present.

143
Q

Sexually active patient presents complaining of:

Multiple painless, cauliflower-like, verrucous lesions on the external genitalia

What is the diagnosis?

A

condylomata acuminata.

Explanation

These genital wart lesions of HPV are very easy to recognize. Occasionally they can be confused with condyloma lata of secondary syphilis. Condyloma lata are flat, wet lesions without any verrucous features. Some of the HPV subtypes that cause condylomata acuminata also can cause cervical cancer (especially 16, 18, and 31), but other subtypes (6 and 11) cause warts only. The appearance of condylomata acuminata can vary slightly from smooth to verrucous flesh-colored or pink lesions.
Dx: Clinical with biopsy of suspicious lesions.
Tx: Large lesions usually require surgical excision (if > 1 cm at the base). Cryotherapy with liquid nitrogen or CO2 laser is another option. Small warts can be treated topically with trichloroacetic acid or podophyllin in a practitioner’s office. However, podophyllin is teratogenic, so do not give to pregnant patients. Self-treatment with podofilox or imiquimod can be done at home in affected areas after initial treatment.

144
Q

Sexually active adult presents with:

Pain in the genital region

Rash on the forearm

Multiple small, painful blisters on the external genitalia with surrounding erythema

Several small, target-shaped lesions on forearm without scale or itch

No mucosal lesions

What is the name of the rash on the forearm?

A

erythema multiforme (EM).

Explanation

EM major includes mucosal involvement, where EM minor involves the skin only. This case presents erythema multiforme in the context of a herpes simplex infection (most common cause). EM lesions could show up in a clinical scenario of Mycoplasma pneumonia or secondary to certain drugs. The target lesions with or without mucosal involvement are classic.
Dx: Clinical with biopsy of suspicious cases.
Tx: Supportive; treatment may involve antimicrobial therapy if a causative organism is found (e.g., symptomatic Mycoplasma infection), or removal of an offending medication. Herpes-associated EM is often recurrent, and patients may benefit from suppressive antiviral therapy. Systemic steroids are often prescribed, but robust data regarding their effectiveness is lacking.

145
Q

Itching, worse at night, x ~ 1 month

Multiple excoriations in both axilla and groin, on the wrists, and between the fingers

What is the diagnosis?

A

Scabies

ermethrin 5% cream from neck to soles, even under finger and toenails, then wash off 8–14 hours later; antihistamines prn itching. A 2nd dose of permethrin in 7 days is recommended. Use oral ivermectin for severe or recalcitrant cases with a repeat dose in 2 weeks. Permethrin can be used in pregnancy. Treat all family members at the same time.

146
Q

Patient is prescribed doxycycline for empiric treatment of community-acquired pneumonia, and after 3 days develops:

A large erythematous, burning, annular plaque in the genital region (that may develop a central blister)

Same rash occurred in the same location when given doxycycline as an adolescent for acne

Lesion resolves upon discontinuation of the antibiotic

What is the diagnosi

A

fixed drug eruption (FDE).

Explanation

The clue to this case is the appearance of the same rash in the identical location each time the patient is given a particular drug. FDEs often occur in the genital region. The lesions can be multiple, especially with repeated exposure to the offending drug.
Dx: Clinical.
Tx: Stop the offending drug; reassurance.

147
Q

Elderly patient presents with an itchy recurrent skin rash:

Pruritic papulosquamous lesions in the right axilla and antecubital fossa → vesicles and bullae mostly intact

Lesions are not symmetric and do not always occur in the same place

Normal mucosal surfaces

Improvement with potent topical corticosteroid

What is the diagnosis?

A

ullous pemphigoid (BP).

Onset in older persons and intensely pruritic bullae that improve with topical corticosteroids. Dermatitis herpetiformis could look similar, except that it is not typically restricted to flexural areas (biopsy is needed for definitive exclusion) and is often presented in the context of celiac disease. It’s reasonable to remember the biopsy findings in the event they are included in a clinical scenario.
Dx: Skin biopsies for light microscopy (subepidermal blister with inflammatory cells in superficial infiltrate) and direct immunofluorescence shows linear deposition at the basement membrane. BP antibodies (BP180 and BP230) can be measured with ELISA with good sensitivity and specificity, but test is rarely available.

Tx: Systemic corticosteroids are 1st line treatment, although topical steroids can be used in mild disease. Immunosuppressants are often used as steroid sparing agents.

148
Q

Female patient with h/o recurrent axillary nodules for years presents with:

Pain in both axillary regions x ~ 2 months—began as small “bumps” but getting larger

Significant pain and erythema around the bumps x 24 hours

Deep, nodular lesions in both axillae without any central area of necrosis

Few comedones in the axillae

What is the diagnosis?

A

hidradenitis suppurativa (HS).

Tx: Weight loss and smoking cessation, if applicable; breathable clothing; avoid washcloths, depilatory creams/lotions, and shaving of the region; use gentle soaps; antiperspirants are okay as long as does not irritate; antibiotics, if cellulitis present; surgical incision and drainage, when necessary; immunomodulators or systemic retinoids are used in very severe disease (corticosteroids, infliximab or adalimumab, cyclosporin, isotretinoin).

149
Q

Dermatology: language

A

Macule - flat lesion less than 1 cm, without elevation or depression

Patch - flat lesion greater than 1 cm, without elevation or depression

Plaque - flat, elevated lesion, usually greater than 1 cm

Papule - elevated, solid lesion less than 1 cm

Nodule - elevated, solid lesion greater than 1 cm

Vesicle - elevated, fluid-filled lesion, usually less than 1 cm

Pustule - elevated, pus-filled lesion, usually less than 1 cm

Bulla - elevated, fluid-filled lesion, usually greater than 1 cm

150
Q

Chronic rhinorrhea and nasal congestion in spring and fall

Bilateralconjunctival injection, dark circles around both eyes, and Dennie-Morgan lines

Pale blue nasal mucosa with edematous turbinates

A

Allergic rhinitis

,” “Dennie-Morgan lines” (which are accentuations of lines under the eyes)

151
Q

Young adult with:

Recurrent sinus infections requiring extended antibiotic courses to clear

4 episodes of pneumonia in the past year

Chronic diarrhea

A

CVID

Dx: Decreased levels of serum IgG ± IgA and IgM; inability to mount appropriate response to vaccinations.
Tx: IVIG or SQIG. Monitor for signs of autoimmune complications and malignancy.

Dx: Decreased levels of serum IgG ± IgA and IgM; inability to mount appropriate response to vaccinations.
Tx: IVIG or SQIG. Monitor for signs of autoimmune complications and malignancy.

152
Q

Chronic nasal congestion, worse in the spring and fall

Swollen and “beefy red” nasal mucosa

A

rhinitis medicamentosa.

This contrasts with the “pale blue” or “boggy” nasal mucosa seen in patients with allergic rhinitis.

153
Q

Middle-aged woman presents with:

Chronic daily hives lasting > 24 hours

Hives described as painful and burning rather than pruritic

Joint pain and swelling

Malaise, fatigue, and weight loss

Associated purpura and ecchymosis

A

urticarial vasculitis.

Explanation

It is important to distinguish between urticarial vasculitis and chronic idiopathic urticaria. In urticarial vasculitis, patients report hives lasting ≥ 24 hours in a fixed location. In contrast, hives in chronic urticaria last only minutes to hours, or migrate to different locations. Often, patients describe the hives as burning and painful. Other red flags that distinguish urticarial vasculitis from chronic idiopathic urticaria include residual hyperpigmentation, purpura, ecchymosis, petechiae, arthralgia/arthritis, fatigue, malaise, and weight loss.
Dx: Skin biopsy. Occasionally, ↓ C4 and C3 levels.
Tx: Immunosuppressive agents (MTX, azathioprine, cyclosporine).

154
Q

Young adult on no meds presents with episodic, nonpitting, nonpruritic lip, facial, and extremity edema that:

Began in adolescence; +FH in parent

Symptoms triggered by visits to the dentist

Preceded by tingling in the lips with swelling over 24–72 hours

Occasionally progresses to laryngeal edema

Associated with intermittent abdominal colicky pain

Symptoms resolve after 1–2 days

Unresponsive to antihistamines

What is the diagnosis?

A

hereditary angioedema (HAE).

HAE is an autosomal dominant disorder caused by a decrease in C1 inhibitor (C1-INH) function. There are 2 types: Type I (85%) = decreased C1 inhibitor enzyme; Type II (15%) = nonfunctioning C1 inhibitor enzyme.

Patients have recurrent nonpitting edema, with each episode lasting 1–3 days. Unlike angioedema/urticaria caused by immediate hypersensitivity reactions, hereditary angioedema does not cause urticaria or itching.

Bradykinin is thought to be the key mediator in the angioedema attacks. Even minor trauma from dental procedures can precipitate attacks! Attacks may include laryngeal obstruction and very often affect the GI tract, causing severe abdominal pain.

Dx: ↓ C4 levels during attacks. C4 might be normal in between attacks. Low C1-INH function is diagnostic.

Type I: ↓ C1-INH level; decreased function. Type II: normal C1-INH level; decreased function.

Tx of acute attack: C1-INH protein infusion or icatibant (synthetic bradykinin receptor antagonist) or ecallantide (kallikrein inhibitor) or FFP (if others not available).

Do not use: Glucocorticoids, antihistamines, or epinephrine; they don’t work!
Prevention of attacks: Attenuated androgens (danazol) or C1-INH protein infusion.
Misc: The prescription of ACE inhibitors can worsen HAE because ACE breaks down bradykinin, so inhibition of ACE increases the level. Narcotics also can precipitate attacks.

155
Q

healthy patient develops:

Itchy hives on the thighs and chest after exercise and hot showers

No wheezing or breathlessness

What is the diagnosis?

A

cholinergic urticaria.

Explanation

Cholinergic urticaria is precipitated by heat (e.g., hot shower, hot day, exercise). It usually presents as punctate lesions that are very pruritic. Note that exercise-induced urticaria is a separate entity where the patient gets hives only with exercise. With cholinergic urticaria, the hives occur with any increase in body temperature such as heat, exercise, or warm blankets.
Dx: Heat provocation.
Tx: May treat symptoms with 1st generation antihistamines such as hydroxyzine or 2nd generation antihistamines such as cetirizine.

156
Q

NSVT: nonischemic cardiomyopathy on correct therapy: Asytmptomatic patient: Mx

A

Observation

157
Q

Tendinous xanthoma

A

xanthoma: familial hypercholesterolemia

Lipoprotein lipase defn: high triglycs

158
Q

Which platelet inhibitor is contraindicated in patients with a history of stroke?

A

pasugrel

159
Q

Should we bridge anti-coagulation for new onset atrial fibrillation?

A

No according to NEJM.

Should bridge for DVT/PE or thrombophilia

160
Q

Angina: Mx

A

beta blocker, nitrate, calcium

Ranolazine last of all

161
Q

Pagets disease: FirstTest

A

Bone scintigraphy

162
Q

Vesicular rash in patient who work with water

A

Dishydrotic eczema

triamcinolone cream

163
Q

Highly emetic chemo: Mx

A

Ondansetron, dexamethasone + aprepitant

164
Q

Severe hypoxemia, diffuse opacities: BestTest

A

BAL

ARDS: AEP, diffuse pulmonary hemorrhage

165
Q

Pneumothorax, ICU, stable: Mx

A

Small bore chest tube

Unstable: needle decompression

166
Q

Frail elderly, multiple co-morbidities, CKD: dialysis?

A

No

167
Q

Monofilament testing locations:

A

1st, 3rd, 5th heads of MTP and plantar hallux + heel

168
Q

Suspecting anaphylaxis: when to give epi

A

Right away: don’t wait for urticaria or wheezing to appear

1: 1000 == 1 mg/1 ml

give 0.3 to 0.5 ml (same as 0..3 to 0..5 mg)

169
Q

Pancytopenia, bone marrow dysplasia, abnormal karyotype

A

MDS

170
Q

Bakers cyst in the setting of osteoarthritis:

A

Aspirate + inject steroid

patients with painful symptomatic cysts, despite usual management of their joint disease, or those in whom temporary relief of symptoms would be of benefit prior to a more definite procedure (eg, in patients with a meniscal tear), we suggest treatment with a glucocorticoid injection of the knee joint (Grade 2C). (See ‘Management’ above and ‘Initial therapy’ above.)

●In patients with calf symptoms, we perform imaging, usually ultrasonography, to exclude DVT. We do not treat incidentally noted asymptomatic popliteal cysts, and children with primary cysts generally do not require treatment. We evaluate patients with symptomatic cysts resistant to these interventions for the accuracy of the diagnosis or the presence of persistent articular pathology or a noncommunicating cyst prior to direct cyst injection or referral for surgical excision. (See ‘Management’ above and ‘Initial therapy’ above and ‘Surgery’ above.)

171
Q

Trapeziometacarpal osteoarthritis: Rx

A

Splint

172
Q

SVC syndrome: stable, small cell lung cancer, lymphoma, germ cell tumor: Mx

A

Start with chemo

If unstable: radiation

173
Q

HIT: Anticoagulation to use

A

DTI like agatroban

174
Q

Primary hyperaldosteronism due to bilateral adrena hyperplasia: Mx

A

Spironolactone

175
Q

Lymphocytic, exudative pleural effusion: Cause

A

Malignancy

176
Q

RMSF: Rx

A

Doxy

ost cases of RMSF occur in the spring and early summer, when outdoor activity is most frequent. (See ‘Seasonal variation’ above.)

●RMSF is usually transmitted via a tick bite, although up to one-third of patients with proven RMSF do not recall a recent tick bite or recent tick contact. (See ‘Transmission’ above.)

●In the early phases of illness, most patients have nonspecific signs and symptoms such as fever, headache, malaise, myalgias, arthralgias, and nausea with or without vomiting. Children may also have prominent abdominal pain that may be mistaken for other intra-abdominal processes, like appendicitis. Most patients with RMSF develop a rash between the third and fifth days of illness. (See ‘Clinical manifestations’ above.)

●The diagnosis of RMSF can rarely be confirmed or disproved in its early phase. Thus, most patients will require empiric therapy for RMSF based upon clinical judgment and the epidemiologic setting. (See ‘Empiric diagnosis and early initiation of therapy’ above.)

177
Q

beta thal intermedia + subacute hypoxia

A

pulmonary hypertension

178
Q

High grade tubular adenoma < 10 mm; repeat colonoscopy after

A

3 years

179
Q

tumor lysis syndrome: Rx

A

IV hydration

low risk: allopurinol

high risk: rubricase

180
Q

Undercooked poultry + diarrhea: organism

A

Campylobacter

181
Q

Looks like mono; Monospot negative: NextTest

A

EBV IgM/IgG

182
Q

Diarrhea after Crohn’s resection: Rx

A

Cholestyramine

Stops EHC of bile salts

183
Q

Aortic dissection: unstable patient: BestTest

A

TEE

184
Q

LCIS: Post-excision +ve margin: Rx

A

Tamoxifen if pre-menopausal

Raloxifene, tamoxifen etc if post-menopausal

mastectomy/oophorectomy if high risk

185
Q

Parkinson’s vs LBD

A

Dementing sx in Parkinson’s appear years after motor sx

186
Q

Amiodarone for good PVC indxn: develops toxicity: Mx

A

Stop amio, start prednisone, start another anti-arrhythmic

187
Q

Amiodarone induced thyroid toxicity: Mx

A

Prednisone

Stopping amiodarone won’t help because of its long half-life