Comprehensive Osteopathic Medical Licensing Examination (COMLEX-USA) Foundational Biomedical Sciences Flashcards

24 sample cards from the Foundational Biomedical Sciences deck

Sampled from the end of the deck, so these are different cards from the ones shown on the syllabus page.

1. Distinguish autosomal dominant, autosomal recessive, and X-linked recessive inheritance patterns.

   AD: affected in every generation, 50% offspring risk, both sexes (e.g., Marfan). AR: skips generations, carriers, 25% risk from two carriers (e.g., cystic fibrosis). X-linked recessive: males affected, no male-to-male transmission, carrier mothers (e.g., hemophilia).

2. What are the modes of inheritance and key examples of mitochondrial and trinucleotide repeat disorders?

   Mitochondrial: maternal inheritance, all offspring of affected mother at risk, heteroplasmy (e.g., MELAS, Leber optic neuropathy). Trinucleotide repeat: anticipation, e.g., Huntington (CAG), Fragile X (CGG), myotonic dystrophy (CTG).

3. Match these fat-soluble vitamins to their deficiency: A, D, E, K.

   Vitamin A deficiency: night blindness, xerophthalmia. Vitamin D: rickets/osteomalacia. Vitamin E: hemolytic anemia, neuropathy. Vitamin K: bleeding (impaired clotting factors II, VII, IX, X).

4. Which water-soluble vitamin deficiencies cause beriberi, pellagra, and megaloblastic anemia?

   Thiamine (B1) deficiency: beriberi and Wernicke-Korsakoff. Niacin (B3) deficiency: pellagra (diarrhea, dermatitis, dementia). Folate (B9) or B12 deficiency: megaloblastic anemia (B12 also causes neurologic deficits).

5. What are the structural and Gram-stain differences between Gram-positive and Gram-negative bacteria?

   Gram-positive: thick peptidoglycan, retains crystal violet (purple), no outer membrane, has teichoic acid. Gram-negative: thin peptidoglycan, outer membrane with LPS (endotoxin), stains red/pink with safranin counterstain.

6. Compare exotoxins and endotoxins.

   Exotoxins: secreted proteins from Gram-positive and Gram-negative bacteria, often highly toxic, antigenic (induce antibodies/toxoids), specific effects. Endotoxin: LPS lipid A of Gram-negative outer membrane, released on lysis, causes fever/shock/DIC, poorly antigenic, heat stable.

7. What are the main mechanisms of bacterial antibiotic resistance?

   Enzymatic inactivation (e.g., beta-lactamases), target modification (e.g., altered PBPs in MRSA, ribosomal methylation), decreased uptake/increased efflux, and bypass pathways. Genes spread via plasmids, transposons, and transformation/conjugation.

8. Classify viruses by genome: give examples of a dsDNA, ssRNA positive-sense, and ssRNA negative-sense virus.

   dsDNA: herpesviruses, adenovirus. ssRNA (+): picornavirus, coronavirus, flavivirus (directly translated). ssRNA (-): influenza, rabies, paramyxovirus (require RNA-dependent RNA polymerase carried in virion).

9. Differentiate the malaria species Plasmodium falciparum and P. vivax/ovale clinically.

   P. falciparum: most severe, irregular fever, cerebral malaria, high parasitemia, no dormant stage. P. vivax/ovale: tertian fever, form dormant hypnozoites in liver (cause relapse), require primaquine for radical cure.

10. What are the major dimorphic fungi and their characteristic feature?

    Dimorphic fungi are mold at ambient temperature (25C) and yeast at body temperature (37C): Histoplasma, Blastomyces, Coccidioides (spherule form), Paracoccidioides, Sporothrix. Mnemonic: mold in the cold, yeast in the heat.

11. Compare the four hypersensitivity reaction types with a prototype example of each.

    Type I: IgE-mediated immediate (anaphylaxis, allergy). Type II: antibody-mediated cytotoxic (autoimmune hemolytic anemia). Type III: immune complex (serum sickness, SLE). Type IV: delayed T-cell mediated (TB skin test, contact dermatitis).

12. Distinguish MHC class I and class II in terms of structure, cells, and T-cell interaction.

    MHC I: on all nucleated cells, presents endogenous (cytosolic) peptides to CD8+ T cells. MHC II: on antigen-presenting cells (dendritic, macrophages, B cells), presents exogenous peptides to CD4+ T cells.

13. What are the functions of the five immunoglobulin classes (IgG, IgA, IgM, IgE, IgD)?

    IgG: most abundant, crosses placenta, opsonization/secondary response. IgA: mucosal/secretory, in breast milk. IgM: first produced, pentamer, best complement activator. IgE: allergy and antiparasitic (mast cells). IgD: B-cell receptor, unclear function.

14. Compare live attenuated, inactivated, and toxoid vaccines including the type of immunity.

    Live attenuated: weakened organism, strong cellular + humoral immunity, lifelong, risk in immunocompromised (e.g., MMR). Inactivated/killed: humoral only, needs boosters, safer (e.g., rabies, polio Salk). Toxoid: inactivated toxin, antibody to toxin (e.g., tetanus, diphtheria).

15. What is the difference between bactericidal and bacteriostatic antibiotics, and name examples.

    Bactericidal kill bacteria (beta-lactams, vancomycin, aminoglycosides, fluoroquinolones, metronidazole). Bacteriostatic inhibit growth, relying on the immune system (tetracyclines, macrolides, clindamycin, sulfonamides, chloramphenicol).

16. What are the cardinal signs of acute inflammation and the principal cell type and mediators?

    Rubor (redness), calor (heat), tumor (swelling), dolor (pain), functio laesa (loss of function). Neutrophils are the predominant cells; mediators include histamine, prostaglandins, leukotrienes, bradykinin, and cytokines (TNF, IL-1).

17. Differentiate hypertrophy, hyperplasia, metaplasia, dysplasia, and anaplasia.

    Hypertrophy: increased cell size. Hyperplasia: increased cell number. Metaplasia: reversible change of one mature cell type to another. Dysplasia: disordered, atypical growth (premalignant). Anaplasia: loss of differentiation, hallmark of malignancy.

18. Compare the four types of tissue necrosis: coagulative, liquefactive, caseous, and fat.

    Coagulative: ischemic infarcts of most organs, architecture preserved. Liquefactive: brain infarcts and abscesses, enzymatic digestion. Caseous: TB and fungal, cheese-like granulomas. Fat necrosis: pancreatitis/trauma, saponification with calcium.

19. What is the difference between transudate and exudate effusions?

    Transudate: low protein, low specific gravity, from increased hydrostatic or decreased oncotic pressure (e.g., heart failure, cirrhosis). Exudate: high protein, high specific gravity, cloudy, from increased vascular permeability (inflammation, infection, malignancy).

20. Define zero-order versus first-order pharmacokinetic elimination with examples.

    Zero-order: constant amount eliminated per unit time, independent of concentration, saturable enzymes (e.g., ethanol, phenytoin, aspirin at high doses). First-order: constant fraction eliminated per unit time, rate proportional to concentration (most drugs).

21. What is the loading dose formula and the maintenance dose formula in pharmacokinetics?

    Loading dose = (Cp x Vd)/F. Maintenance dose = (Cp x CL x tau)/F, where Cp = target plasma concentration, Vd = volume of distribution, CL = clearance, F = bioavailability, tau = dosing interval.

22. Define therapeutic index, efficacy, and potency.

    Therapeutic index = TD50/ED50 (or LD50/ED50); higher = safer. Efficacy = maximal effect a drug can produce (Emax). Potency = amount of drug needed for a given effect (related to EC50); a more potent drug needs less dose.

23. Compare the mechanisms and key adverse effects of beta-blockers and ACE inhibitors.

    Beta-blockers: block beta-adrenergic receptors, decrease heart rate/contractility/renin; adverse: bradycardia, bronchospasm, masking hypoglycemia. ACE inhibitors: block angiotensin II formation, lower aldosterone/BP; adverse: dry cough (bradykinin), hyperkalemia, angioedema, teratogenic.

24. What is the mechanism of action of beta-lactam antibiotics, aminoglycosides, and fluoroquinolones?

    Beta-lactams (penicillins, cephalosporins): inhibit cell wall synthesis by binding penicillin-binding proteins (transpeptidases). Aminoglycosides: bind 30S ribosomal subunit, blocking protein synthesis (bactericidal). Fluoroquinolones: inhibit DNA gyrase (topoisomerase II) and topoisomerase IV.

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