NBME Misses

Question 1

Antibiotics that work by inhibiting the ribosomal 30S subunit

Answer 1

Tetracyclines and aminoglycosides

Question 2

Signs and symptoms of vitamin E deficiency

Answer 2

Similar to B12 deficiency with posterior column deficits, but no megaloblasts. Also associated with hemolytic anemia because it stabilizes the RBC membrane.

Question 3

Signs and symptoms of biotin deficiency

Answer 3

Rare and associated with eating excess egg whites and taking antibiotics. Symptoms include dermatitis, alopecia and enteritis.

Question 4

Why do fevers often occur after aspirin overdose?

Answer 4

It increases the permeability of the inner mitochondrial membrane. This decreases the proton gradient and increases O2 consumption. Although ATP synthesis stops, electron transport continues and produces heat.

Question 5

Genetic mutation involved in beta-thalassemia?

Answer 5

Point mutation that obliterates the boundary between exons and introns, including part of an intron into the mature mRNA.

Question 6

Major mechanisms of glucocorticoid immunosuppression

Answer 6

NF-kB suppression leads to decreased cytokine production that reduces B and T cell activation.

Question 7

Gram-positive algorithm

Answer 7

*

Question 8

Gram-negative algorithm

Answer 8

*

Question 9

Cytokines involved in DIC

Answer 9

IL-1 and TNF

Question 10

Cyclosporine mechanism of action

Answer 10

Binds cyclophilin, inhibits calcineurin and prevents T-cell activation by preventing transcription of IL-2.

Question 11

Immunodeficiency seen in boys after 6 months of age with no B-cells in peripheral blood, decreased Ig in all classes and absent lymph nodes and tonsils.

Answer 11

X-linked (Bruton) agammaglobulinemia. This causes a defect in Bruton’s tyrosine kinase gene that prevents B-cell maturation.

Question 12

Immunodeficiency that is typically asymptomatic, but can present with decreased IgA and normal IgG and IgM levels. This is also the most common immunodeficiency.

Answer 12

Selective IgA deficiency.

Question 13

Immunodeficiency that can be acquired in the 20-30s, presents similar to cystic fibrosis and presents with decreased plasma cells and Ig.

Answer 13

Common variable immunodeficiency due to a defect in B-cell differentiation.

Question 14

Patients present with low T-cells, low PTH, low calcium, truncal cardiac defects and an absent thymic shadow on CXR.

Answer 14

DiGeorge syndrome. 22q11 deletion results in failure of 3rd and 4th pharyngeal pouches to develop, causing T-cell deficiency.

Question 15

Patients present with disseminated mycobacterial and fungal infections, sometimes even after receiving BCG vaccine.

Answer 15

IL-12 receptor deficiency. This results in decreased interferon-gamma.

Question 16

Patients present with coarse facies, non-inflamed staph abscesses, retained primary teeth, elevated IgE and eczema.

Answer 16

AD hyper-IgE syndrome (Job syndrome). This is due to a STAT3 mutation causing a deficiency in Th17 cells and poor PMN recruitment to infection sites.

Question 17

Patients present with noninvasive candida infection of skin and mucus membranes. In the lab they have no T-cell proliferation in response to Candida antigens.

Answer 17

Chronic mucocutaneous candidiasis, due to T-cell dysfunction.

Question 18

Patients present with failure to thrive, recurrent infections, absent thymic shadow, no germinal centers on lymph node biopsy and no T-cells on flow cytometry.

Answer 18

SCID due to defective IL-2 receptor and adenosine deaminase deficiency.

Question 19

Patients present with the triad of ataxia, angiomas (spider) and IgA deficiency. Labs show increased AFP, decrease IgG/IgA/IgE and cerebellar atrophy.

Answer 19

Ataxia-telangiectasia due to defects in ATM gene resulting in failure to repair double stranded DNA and causing cell cycle arrest.

Question 20

Patients present with sever pyogenic infections early in life, opportunistic infections, elevated IgM and depressed IgG, IgA and IgA.

Answer 20

Hyper IgM syndrome due to defective CD40L on Th cells resulting in inability to switch classes.

Question 21

Patients present with thrombocytopenia purpura, eczema and recurrent infections. They carry an increased risk for malignancy, have decreased IgG/IgM and increased IgE/IgA.

Answer 21

Wiskott-Aldrich syndrome due to mutation the WAS and T-cells are unable to recognize actin cytoskeleton.

Question 22

Patients present with = recurrent bacterial skin infections without pus, impaired wound healing and delayed separation of the umbilical cord

Answer 22

LAD type I due to defect in LFA-1 (CD18) on phagocytes that prevent them from migrating and chemotaxis.

Question 23

Patients present with recurrent pyogenic infections, partial albinism, peripheral neuropathy and infiltrative lymphhistiocytosis. Labs will show giant granules in granulocytes and platelets with pancytopenia.

Answer 23

Chédiak-Higashi syndrome due to defect in lysosomal trafficking regulator gene. This results in microtubule dysfunction in the phagolysosome.

Question 24

Patients present with increased susceptibility to catalase positive organisms and negative nitroblue tetrazolium dye reduction test.

Answer 24

Chronic granulomatous disease due to defect of NADPH oxidase leading to decreased ROS production and limited oxidative burst.

Question 25

Phases of clinical trials

Answer 25

I) First in humans, find safe dose, identify safe route and identify side effects. II) Assess treatment efficacy against disease in a smaller group III) Large trial with treatment vs. placebo

Question 26

Gout vs. pseudo gout crystals

Answer 26

Gout = negative birefringence, crystals. Pseudo gout = positive birefringence, boxcars.

Question 27

Cavernous sinus anatomy

Answer 27

*

Question 28

Brain lesion location that produces hemiballismus

Answer 28

Sub thalamic nucleus

Question 29

Brain lesion location that produces Parkinsonian symptoms

Answer 29

Caudate nucleus

Question 30

Autosomal recessive familial disease that causes elevated chylomicrons, triglycerides and cholesterol. Patients may present with pancreatitis, HSM and eruptive/pruritic xanthomas.

Answer 30

Hyperchylomicronemia due to lipoprotein lipase deficiency or altered apolipoprotein C-II.

Question 31

Autosomal dominant familial disease resulting in increased LDL around 300, accelerated atherosclerosis, corneal Marcus and tendon xanthomas.

Answer 31

Familial hypercholesterolemia due to absent or defective LDL receptors on hepatocytes.

Question 32

Autosomal dominant familial disease resulting in increased VLDL and triglycerides with pancreatitis if TGs > 1000.

Answer 32

Hypertriglyceridemia due to hepatic overproduction of VLDL.

Question 33

Organ other than the liver than can release glucose if the body is in desperate need.

Answer 33

Kidney

Question 34

Mechanism of cholera toxin

Answer 34

B subunit allows entry to enterocyte, then A subunit causes Gas activation -> adenylate cyclase activation -> increased cAMP -> CFTR activation -> efflux of ions and water into intestinal lumen

Question 35

Cyclophosphamide mechanism of action

Answer 35

Guanine alkylating agent

Question 36

Bethanechol mechanism of action

Answer 36

Stimulates muscarinic receptors only, is not degraded by AChE and has a long duration of action, used for post-op urinary retention and dry mouth.

Question 37

What embryologic structure do the thymus and inferior parathyroid glands originate from?

Answer 37

Pharyngeal POUCH

Question 38

Lesions that can cause homonymous hemianopia

Answer 38

Optic tract lesion or occipital lobe lesion (however this will be macular sparing)

Question 39

Slipped-strand mispairing

Answer 39

During replication, one strand slips off and binds to a different complementary sequence on the other strand, forming a loop. The loop is excised; however, an additional nucleotide may be added, resulting in a frameshift mutation.

Question 40

Imatinib mechanism of action

Answer 40

Philadelphia chromosome tyrosine kinase inhibitor used in CML treatment

Question 41

Km = ?

Answer 41

1/2 Vmax. A low Km means the enzyme binds the substrate with high affinity and you do not need a ton of substrate to get the enzyme at 50% its maximum operating rate (1/2 Vmax).

Question 42

Only pharyngeal constrictor muscle not innervated by CN X?

Answer 42

Stylopharyngeus (CN IX)

Question 43

How does glycine function as a neurotransmitter?

Answer 43

Inhibitory

Question 44

Protease inhibitor mechanism of action?

Answer 44

Inhibit cleavage of polypeptides and viral maturation.

Question 45

Big lifestyle change for people with PUD

Answer 45

Stop smoking, it inhibits the body’s ability to heal the ulcer.

Question 46

What happens to endogenous insulin in a DM II when you start supplementing their insulin

Answer 46

It drops precipitously

Question 47

Type of seizure between simple partial where the patient remains conscious and generalized tonic clonic where the patient completely loses consciousness?

Answer 47

Complex partial

Question 48

Lesion location in a patient with left homonymous hemianopia

Answer 48

Contralateral optic tract (right)