Mix2

Question 1

What is the treatment for meningococcal meningitis?

Answer 1

Third gen cephalosporin (ceftriaxone) and vancomycin

Question 2

What’s the next step if you have suspected DVT in a patient based on clinical presentation?

Answer 2

Perform compression ultrasonography. This should be done prior to starting anticoagulation because anticoagulation itself has risks.

Question 3

If a patient presents with exertional dyspnea, pounding heart sensation worse in left lateral decubitus, and widened pulse pressure, then he is most likely to have this valvular deficiency:

Answer 3

Aortic regurg.

In aortic regurg, part of the LV output flows back into the left ventricle&raquo_space; ^ LV EDV&raquo_space; myocardial hypertrophy/chamber enlargement. Increase in LV size brings ventricular apex closer to chest wall&raquo_space; pounding heart sensation in L lateral decubitus. Generally due to aortic root dilation or congenital bicuspid aortic valve.

Question 4

Clinical presentation of diastolic decrescendo murmur, widened pulse pressure, collapsing/water hammer pulse, and signs of HF are characteristic of what valvular deficiency?

Answer 4

Aortic regurg.

Excessive LV stretching eventually leads to decreased stroke volume, decreased forward flow, systolic HF, and ^ LV end diastolic pressure&raquo_space; pulmonary congestion.

Question 5

How is neurocysticercosis typically transmitted?

Answer 5

Taenia solium = pork tapeworm. Typically transmitted from ingestion of undercooked/contaminated pork. Ingested eggs hatch in the small intestines and spread hematogenously (brain, muscle, liver). Most Pt are asymptomatic, but cysts can degenerate&raquo_space; inflammation, edema, clinical illness.

Question 6

Why are you more likely to develop acute hypocalcemia from high volume blood transfusions in Pt with liver damage?

Answer 6

High volume blood transfusions can cause symptomatic hypocalcemia (seizure, muscle cramp, chvostek + trousseau sign, hyperreflexia, and paresthesia) due to chelation of ionized calcium by citrate in transfused blood. Citrate is typically metabolized by the liver.

Question 7

What ECG changes would you see in a patient with right coronary artery STEMI?

Answer 7

1. ST depression in leads I and aVL (reciprocal changes)
2. Q wave and ST elevation in leads II, III, and aVF (inferior wall MI)
3. ST depression in leads V1 and V2 (posterior wall MI)

Question 8

What cardiac vessel is blocked in an anterior MI and what changes would you see on ECG?

Answer 8

Anterior MI = LAD

• See some or all V1-V6 leads affected.

Question 9

What cardiac vessel is blocked in an inferior MI and what changes would you see on ECG?

Answer 9

Inferior MI = RCA or LCX (left circumflex)

• See ST elevation in leads II, III, and aVF.

Question 10

What cardiac vessel is blocked in a posterior MI and what changes would you see on ECG?

Answer 10

Posterior MI = RCA or LCX

• ST depression in leads V1-V3.
• ST elevation in leads I and aVL (LCX)
• ST depression in leads I and aVL (RCA)

Question 11

What cardiac vessel is blocked in a lateral MI and what changes would you see on ECG?

Answer 11

Lateral MI = LCX or diagonal artery

• ST elevation in leads I, aVL, V5 and V6
• ST depression in leads II, III, and aVF.

Question 12

What is the standard initial treatment for osteomyelitis due to deep puncture wounds?

Answer 12

Blood cultures, bone biopsy with culture. Rx = IV antibiotics (Cipro, pip-tazo) and surgical debridement.

MCC = pseudomonas and S. aureus

Question 13

Why do you typically have high urine pH with proteus mirabilis infections?

Answer 13

Proteus is a urease producing bacteria. Urease splits urea into ammonia (NH3) and CO2. Ammonia (NH3) then converts to ammonium (NH4+) and alkalinizes the urine. High urine pH reduces PO4 solubility and increases risk of developing struvite stones (Mg NH3PO4)

Question 14

Why is there an increased risk of atherosclerotic disease with nephrotic syndrome?

Answer 14

Low plasma oncotic pressure from proteinuria and subsequent hypoalbuminemia&raquo_space; increased lipoprotein synthesis&raquo_space; increased serum cholesterol and triglyceride levels&raquo_space; increased risk of atherosclerotic disease.

** Pt with nephrotic syndrome are also hypercoagulable due to loss of antithrombin III in urine&raquo_space; increased risk of stroke/MI. Aggressive management with statins is indicated.

Question 15

How do serum Na+ levels differ in central vs nephrogenic diabetes insipidus?

Answer 15

Central DI = decreased ADH release from pituitary
Nephrogenic DI = ADH resistance in kidney.

High serum Na+ in central DI because there is loss of thirst mechanism. Normal serum Na+ in nephrogenic DI because thirst response compensates for loss of free water.

Question 16

In volume resuscitation due to HHS, when do you transition from normal saline to 1/2 normal saline?

Answer 16

Always start off volume repletion with normal saline (regardless of serum Na+ levels). Change to 1/2 NS if corrected Na+ is normal or high.

** Corrected Na+ = measured Na + (2 mEq/L Na+ for each 100 mg/dL that serum glucose is over 100mg/dL)

Question 17

How would you distinguish the difference between Grave’s disease and painless thyroiditis?

Answer 17

Painless thyroiditis = acute thyrotoxicosis + mild thyroid gland enlargement and suppressed TSH.

Pt with hyperthyroidism and suppressed TSH should have thyroid radioiodine scintigraphy to distinguish painless thyroiditis from Graves. In painless thyroiditis, radioactive iodine uptake is decreased (due to release of preformed thyroid hormone) whereas uptake is increased in Grave’s disease (due to increased synthesis of thyroid hormone).

Question 18

What’s the first step in treating diabetic nephropathy?

Answer 18

BP control. Done to slow the decline of GFR once azotemia develops. Most guidelines are target of 130/80. ACEi or ARB are used because they may be renoprotective by reducing intraglomerular pressure.

** BUT start low because ACEi and ARB can induce an acute decline in GFR and may cause hyperkalemia.

Question 19

What therapy should be offered first to a patient with suspected spinal cord compression?

Answer 19

IV glucocorticoids. Spinal cord compression can be due to metastasis, infection (epidural abscess), and spinal injury. IV glucocorticoids can decrease vasogenic edema caused by an obstructed epidural venous plexus. They can also help minimize pain and may restore neurologic function if given early enough.

You should also order an emergency MRI.

Question 20

Why does B12 deficiency occur with pernicious anemia (what’s the MOA)?

Answer 20

Pernicious anemia = autoimmune d/o where antibodies are made to intrinsic factor (IF).

Also, these pt develop chronic atrophic gastritis with decreased production of IF by gastric parietal cells (leads to ^ cancer risk).

Question 21

What is the treatment of choice for nocardia infection?

Answer 21

Nocardia is a filamentous, aerobic, gram pos branching rod that is partially acid fast staining. It can cause pulmonary or disseminated disease (esp to brain) in immunocompromised hosts. Treatment of choice is TMP-SMX (with carbapenems added for better coverage)

Question 22

What is the most likely diagnosis in a patient who recently returned from a trip to Caribbean islands with fever, malaise, rash, lymphadenopathy, and polyarthralgias?

Answer 22

Chikungunya. Mosquito borne viral illness with acute infection lasting 7-10 days. Rx is supportive. Clinical manifestations include high fever, severe polyarthralgias (almost always present), HA, peripheral edema, myalgia, conjunctivitis, and maculopapular rash along with lymphopenia/thrombocytopenia.

Question 23

Is deficiency in folate or B12 more commonly the cause of anemia in alcoholics?

Answer 23

Folate