NBME Misses Flashcards Preview

Step 1 > NBME Misses > Flashcards

Flashcards in NBME Misses Deck (48)
Loading flashcards...

Antibiotics that work by inhibiting the ribosomal 30S subunit

Tetracyclines and aminoglycosides


Signs and symptoms of vitamin E deficiency

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


Signs and symptoms of biotin deficiency

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


Why do fevers often occur after aspirin overdose?

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.


Genetic mutation involved in beta-thalassemia?

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


Major mechanisms of glucocorticoid immunosuppression

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


Gram-positive algorithm



Gram-negative algorithm



Cytokines involved in DIC

IL-1 and TNF


Cyclosporine mechanism of action

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


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.

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


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

Selective IgA deficiency.


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

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


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

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


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

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


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

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.


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.

Chronic mucocutaneous candidiasis, due to T-cell dysfunction.


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.

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


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

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


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

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


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

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


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

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


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

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


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

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


Phases of clinical trials

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


Gout vs. pseudo gout crystals

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


Cavernous sinus anatomy



Brain lesion location that produces hemiballismus

Sub thalamic nucleus


Brain lesion location that produces Parkinsonian symptoms

Caudate nucleus


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

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