First Aid for the USMLE Step 1 2022, Thirty Second Edition 32nd Edition PDF
Preview First Aid for the USMLE Step 1 2022, Thirty Second Edition 32nd Edition
Contents Contributing Authors vii General Acknowledgments xiii Associate Authors viii How to Contribute xv Faculty Advisors ix How to Use This Book xvii Preface xi Selected USMLE Laboratory Values xviii Special Acknowledgments xii First Aid Checklist for the USMLE Step 1 xx ` SECTION I GUIDE TO EFFICIENT EXAM PREPARATION 1 Introduction 2 Test-Taking Strategies 19 USMLE Step 1—The Basics 2 Clinical Vignette Strategies 21 Learning Strategies 11 If You Think You Failed 22 Timeline for Study 14 Testing Agencies 22 Study Materials 18 References 23 ` SECTION I SUPPLEMENT SPECIAL SITUATIONS 25 ` SECTION II HIGH-YIELD GENERAL PRINCIPLES 27 How to Use the Database 28 Pathology 203 Biochemistry 31 Pharmacology 229 Immunology 93 Public Health Sciences 257 Microbiology 121 v FFAASS11__22002222__0000__FFrroonnttmmaatttteerr..iinndddd 55 1111//1100//2211 1100::5500 AAMM ` SECTION III HIGH-YIELD ORGAN SYSTEMS 281 Approaching the Organ Systems 282 Neurology and Special Senses 503 Cardiovascular 285 Psychiatry 575 Endocrine 331 Renal 601 Gastrointestinal 365 Reproductive 635 Hematology and Oncology 411 Respiratory 683 Musculoskeletal, Skin, and Connective Tissue 453 Rapid Review 713 ` SECTION IV TOP-RATED REVIEW RESOURCES 737 How to Use the Database 738 Biochemistry 742 Question Banks 740 Cell Biology and Histology 742 Web and Mobile Apps 740 Microbiology and Immunology 742 Comprehensive 741 Pathology 743 Anatomy, Embryology, and Neuroscience 741 Pharmacology 743 Behavioral Science 742 Physiology 744 ` Abbreviations and Symbols 745 Index 771 Image Acknowledgments 753 About the Editors 828 vi FFAASS11__22002222__0000__FFrroonnttmmaatttteerr..iinndddd 66 1111//1100//2211 1100::5500 AAMM 47 BIOCHEmISTRY ` BIOCHEMISTRY—CEllUlAR SECTION II Cilia structure Motile cilia consist of 9 doublet + 2 singlet arrangement of microtubules (axoneme) A. Basal body (base of cilium below cell membrane) consists of 9 microtubule triplets B with no central microtubules. Nonmotile (primary) cilia work as chemical signal sensors and have a role in signal transduction and cell growth control. Dysgenesis may lead to polycystic kidney disease, mitral valve prolapse, or retinal degeneration. Axonemal dynein—ATPase that links peripheral 9 doublets and causes bending of cilium by new differential sliding of doublets. image Gap junctions enable coordinated ciliary movement. for 2022 2nd pass A B art Dynein revised arm for 2022 3rd pass Microtubule A Microtubule B Nexin Doublets Triplets art moved for 2022 1st pass Primary ciliary Also called Kartagener syndrome. Autosomal recessive. Dynein arm defect immotile cilia dyskinesia dysfunctional ciliated epithelia. Developmental abnormalities due to impaired migration and orientation (eg, situs inversus A, hearing A loss due to dysfunctional eustachian tube cilia); recurrent infections (eg, sinusitis, ear infections, R L bronchiectasis due to impaired ciliary clearance of debris/pathogens); infertility ( risk of ectopic pregnancy due to dysfunctional fallopian tube cilia, immotile spermatozoa). Lab findings: nasal nitric oxide (used as screening test). Sodium-potassium Na+/K+-ATPase is located in the plasma 2 strikes? K, you’re still in. 3 strikes? Nah, you’re pump membrane with ATP site on cytosolic side. For out! each ATP consumed, 2 K+ go in to the cell Cardiac glycosides (digoxin and digitoxin) (pump dephosphorylated) and 3 Na+ go out of directly inhibit Na+/K+-ATPase indirect the cell (pump phosphorylated). inhibition of Na+/Ca2+ exchange [Ca2+] i cardiac contractility. Extracellular 3Na+ 2K+ space Plasma membrane P Cytosol 2K+ 3Na+ ATP ADP P © 2022 First Aid for the USMLE Step 1 82 SECTION II BIOCHEmISTRY ` BIOCHEMISTRY—METABOlISM Phenylketonuria Caused by phenylalanine hydroxylase (PAH). Autosomal recessive. Tyrosine becomes essential. phenylalanine Screening occurs 2–3 days after birth (normal at Fact phenyl ketones in urine. birth because of maternal enzyme during fetal revised Tetrahydrobiopterin (BH ) deficiency—BH life). for 2022 4 4 4th pass essential cofactor for PAH. BH deficiency Findings: intellectual disability, microcephaly, 4 phenylalanine. Varying degrees of clinical seizures, hypopigmented skin, eczema, musty severity. Untreated patients typically die in body odor. infancy. Treatment: phenylalanine and tyrosine in Phenylalanine embryopathy— phenylalanine diet (eg, soy products, chicken, fish, milk), levels in pregnant patients with untreated tetrahydrobiopterin supplementation. PKU can cause fetal growth restriction, Phenyl ketones—phenylacetate, phenyllactate, microcephaly, intellectual disability, and phenylpyruvate. congenital heart defects. Can be prevented Disorder of aromatic amino acid metabolism with dietary measures. musty body odor. Patients with PKU must avoid the artificial sweetener aspartame, which contains phenylalanine. Dietary protein Phenyl ketones PKU art Aspartame Phenylalanine Thyroxine revised hydroxylase for 2022 Phenylalanine Tyrosine Dopamine Norepinephrine/epinephrine 4th pass Melanin Endogenous TetrahydrobiopterinBH₄ BH₂ protein deficiency Dihydropteridine reductase NAD+ NADH + H+ Maple syrup urine Blocked degradation of branched amino acids Autosomal recessive. disease (Isoleucine, leucine, valine) due to branched- Presentation: vomiting, poor feeding, urine chain α-ketoacid dehydrogenase (B). Causes smells like maple syrup/burnt sugar. Causes 1 α-ketoacids in the blood, especially those of progressive neurological decline. leucine. I love Vermont maple syrup from maple trees Treatment: restriction of isoleucine, leucine, (with Branches). 1 valine in diet, and thiamine supplementation. Alkaptonuria Congenital deficiency of homogentisate oxidase in the degradative pathway of tyrosine to fumarate pigment-forming homogentisic acid builds up in tissue A. Autosomal recessive. Usually benign. A Findings: bluish-black connective tissue, ear cartilage, and sclerae (ochronosis); urine turns black on prolonged exposure to air. May have debilitating arthralgias (homogentisic acid toxic to cartilage). © 2022 First Aid for the USMLE Step 1 109 Immunology ` Immunology—Immune reSponSeS SECTIon II Vaccination Induces an active immune response (humoral and/or cellular) to specific pathogens. This page: VaccIne type deScrIptIon proS/conS eXampleS 5 new Live attenuated Microorganism rendered Pros: induces cellular and Adenovirus (nonattenuated, images for 2022 vaccine nonpathogenic but retains humoral responses. Induces given to military recruits), 3rd pass capacity for transient growth strong, often lifelong typhoid (Ty21a, oral), This page: within inoculated host. MMR immunity. polio (Sabin), varicella 5 images and varicella vaccines can be Cons: may revert to virulent (chickenpox), smallpox, removed given to people living with form. Contraindicated in BCG, yellow fever, influenza for 2022 4th pass HIV without evidence of pregnancy and patients with (intranasal), MMR, rotavirus. immunity if CD4+ cell count immunodeficiency. “Attention teachers! Please ≥ 200 cells/mm3. vaccinate small, Beautiful young infants with MMR regularly!” Killed or inactivated Pathogen is inactivated by heat Pros: safer than live vaccines. Hepatitis A, Typhoid vaccine or chemicals. Maintaining Cons: weaker cell-mediated (Vi polysaccharide, epitope structure on surface immune response; booster intramuscular), Rabies, antigens is important for shots usually needed. Influenza (intramuscular), immune response. Mainly Polio (SalK). induces a humoral response. A TRIP could Kill you. Subunit, recombinant, All use specific antigens that Pros: targets specific epitopes HBV (antigen = HBsAg), polysaccharide, and best stimulate the immune of antigen; lower chance of HPV, acellular pertussis conjugate system. adverse reactions. (aP), Neisseria meningitidis Cons: expensive; weaker (various strains), Streptococcus immune response. pneumoniae (PPSV23 polysaccharide primarily T-cell–independent response; PCV13 conjugated polysaccharide produces T-cell–dependent response), Haemophilus influenzae type b, herpes zoster. Toxoid Denatured bacterial toxin with Pros: protects against the Clostridium tetani, an intact receptor binding bacterial toxins. Corynebacterium diphtheriae. site. Stimulates immune Cons: antitoxin levels decrease system to make antibodies with time, thus booster shots without potential for causing may be needed. disease. mRNA A lipid nanoparticle delivers Pros: high efficacy, safe in SARS-CoV-2 mRNA, causing cells to pregnancy. synthesize foreign protein (eg, Cons: local and transient spike protein of SARS-CoV-2). systemic (fatigue, headache, Induces cellular and humoral myalgia) reactions are immunity. common. Rare myocarditis, pericarditis particularly in young males. © 2022 First Aid for the USMLE Step 1 128 SEcTioN ii Microbiology ` microbiology—basic bacteriology Bacterial genetics Transformation Competent bacteria can bind and import short Degraded uncombined Recipient DNA pieces of environmental naked bacterial DNA Donor DNA chromosomal DNA (from bacterial cell lysis). The transfer and expression of newly Naked DNA Recipient cell Transformed cell transferred genes is called transformation. A feature of many bacteria, especially S pneumoniae, H influenzae type b, and Neisseria (SHiN). Adding deoxyribonuclease degrades naked DNA, preventing transformation. Conjugation F+ × F– F+ plasmid contains genes required for sex pilus and conjugation. Bacteria without this plasmid F+ plasmid contains Single strand of genes for sex pilus and Sex pilus forming congugal plasmid DNA No transfer of are termed F–. Sex pilus on F+ bacterium conjugation bridge “mating bridge” transferred chromosomal DNA new contacts F− bacterium. A single strand F+ plasmid contains Single strand of image genes for sex pilus and Sex pilus forming congugal plasmid DNA No transfer of for 2022 of plasmid DNA is transferred across the conjugation bridge “mating bridge” transferred chromosomal DNA F+ cell F– cell F+ cell F– cell F+ cell F– cell F+ cell F+ cell 1st pass conjugal bridge (“mating bridge”). No transfer High-frequency recombination Leading portion of plasmid of chromosomal DNA. (Hfr) cell contains F+ plasmid transfers along with flanking F+ cinelclorpFo–r caetelld into baFc+t ceerilall DNF–A c.ell baFc+t ceerilall chFr–o cmelolsome F+ cell F+ cell new Hfr × F– F+ plasmid can become incorporated into image High-frequency recombination Leading portion of plasmid bacterial chromosomal DNA, termed high- Plasmid (Hfr) cell contains F+ plasmid transfers along with flanking for 2022 incorporated into bacterial DNA. bacterial chromosome 1st pass frequency recombination (Hfr) cell. Transfer F+ cell F– cell Hfr cell F– cell Hfr cell F– cell Hfr cell Recombinant Plasmid F– cell of leading part of plasmid and a few flanking chromosomal genes. High-frequency F+ cell F– cell Hfr cell F– cell bactFe–rH ciaferll Dl ceNlAl +F– ceblalctFe+r ciaell lDHNfrA ce+ll Rpelacsommidb icnoapnyt art F– cell revised recombination may integrate some of those for 2022 bacterial genes. Recipient cell remains F– but bactFe–r ciaell DlNA + bactFe+r ciaell lDNA + plasmid copy 3rd pass now may have new bacterial genes. art Transduction revised for 2022 Generalized A “packaging” error. Lytic phage infects Cleavage of Bacterial DNA packaged 4th pass Lytic Bacteria bacterial DNA in phage capsids bacterium, leading to cleavage of bacterial phage DNA. Parts of bacterial chromosomal DNA may become packaged in phage capsid. Phage infects another bacterium, transferring these genes. Release of new phage Infects other Genes transferred from lysed cell bacteria to new bacteria Specialized An “excision” event. Lysogenic phage infects Viral DNA Viral DNA Lysogenic incorporates in Phage particles bacterium; viral DNA incorporates into phage Bacteria bacterial DNA carry bacterial DNA bacterial chromosome. When phage DNA is excised, flanking bacterial genes may be excised with it. DNA is packaged into phage capsid and can infect another bacterium. Genes for the following 5 bacterial toxins are encoded in a lysogenic phage (ABCD’S): Group A strep erythrogenic toxin, Botulinum toxin, Release of new phage Infects other Genes different from Cholera toxin, Diphtheria toxin, Shiga toxin. from lysed cell bacteria donor and recipient © 2022 First Aid for the USMLE Step 1 150 SEcTioN ii Microbiology ` microbiology—mycology Opportunistic fungal infections Candida albicans alba = white. Dimorphic; forms pseudohyphae and budding yeasts at 20°C A, germ tubes at 37°C B. Systemic or superficial fungal infection. Causes oral C and esophageal thrush in immunocompromised (neonates, steroids, diabetes, AIDS), vulvovaginitis (diabetes, use of antibiotics), diaper rash, infective endocarditis (people who inject drugs), disseminated candidiasis (especially in neutropenic patients), chronic mucocutaneous candidiasis. Treatment: oral fluconazole/topical azoles for vaginal; nystatin, azoles, or, rarely, echinocandins for oral; fluconazole, echinocandins, or amphotericin B for esophageal or systemic disease. Aspergillus Septate hyphae that branch at 45° Acute Angle D. fumigatus Causes invasive aspergillosis in immunocompromised patients, especially those with neutrophil dysfunction (eg, chronic granulomatous disease) because Aspergillus is catalase ⊕. Can cause aspergillomas E in pre-existing lung cavities, especially after TB infection. Some species of Aspergillus produce Aflatoxins (associated with hepatocellular carcinoma). Treatment: voriconazole or echinocandins (2nd-line). Allergic bronchopulmonary aspergillosis (ABPA) F—hypersensitivity response to Aspergillus growing in lung mucus. Associated with asthma and cystic fibrosis; may cause bronchiectasis and eosinophilia. Cryptococcus 5–10 μm with narrow budding. Heavily encapsulated yeast. Not dimorphic. ⊕ PAS staining. neoformans Found in soil, pigeon droppings. Acquired through inhalation with hematogenous dissemination to meninges. Highlighted with India ink (clear halo G) and mucicarmine (red inner capsule H). Latex agglutination test detects polysaccharide capsular antigen and is more sensitive and specific. Causes cryptococcosis, which can manifest with meningitis, pneumonia, and/or encephalitis (“soap bubble” lesions in brain), primarily in immunocompromised. Treatment: amphotericin B + flucytosine followed by fluconazole for cryptococcal meningitis. Mucor and Rhizopus Irregular, broad, nonseptate hyphae branching at wide angles I . spp Causes mucormycosis, mostly in patients with DKA and/or neutropenia (eg, leukemia). Inhalation of spores fungi proliferate in blood vessel walls, penetrate cribriform plate, and enter brain. Rhinocerebral, frontal lobe abscess; cavernous sinus thrombosis. Headache, facial pain, black necrotic eschar on face J; may have cranial nerve involvement. Treatment: surgical debridement, amphotericin B or isavuconazole. new A B C D E images (D, E) for 2022 1st pass images E, F swapped for 2022 2nd pass F G H I J new image (B) for 2022 3rd pass © 2022 First Aid for the USMLE Step 1 169 Microbiology ` microbiology—Virology SEcTioN ii Rabies virus Bullet-shaped virus A. Negri bodies Infection more commonly from bat, raccoon, and (cytoplasmic inclusions B) commonly skunk bites than from dog bites in the United A found in Purkinje cells of cerebellum and States; aerosol transmission (eg, bat caves) also in hippocampal neurons. Rabies has long possible. incubation period (weeks to months) before symptom onset. Postexposure prophylaxis is wound cleaning plus immunization with killed vaccine and rabies immunoglobulin. Example of passive-active immunity. B Travels to the CNS by migrating in a retrograde fashion (via dynein motors) up nerve axons after binding to ACh receptors. Progression of disease: fever, malaise agitation, photophobia, hydrophobia, hypersalivation paralysis, coma death. Ebola virus A filovirus A. Following an incubation period Transmission requires direct contact with bodily of up to 21 days, presents with abrupt onset fluids, fomites (including dead bodies), infected A of flulike symptoms, diarrhea/vomiting, high bats or primates (apes/monkeys); high incidence fever, myalgia. Can progress to DIC, diffuse of healthcare-associated infection. hemorrhage, shock. Supportive care, no definitive treatment. Diagnosed with RT-PCR within 48 hr of Vaccination of contacts, strict isolation of infected symptom onset. High mortality rate. individuals, and barrier practices for healthcare workers are key to preventing transmission. Fact Severe acute SARS-CoV-2 is a novel ⊕ ssRNA coronavirus Spreads through respiratory droplets and revised respiratory syndrome and the cause of the COVID-19 pandemic. aerosols. Host cell entry occurs by attachment for 2022 2nd pass coronavirus 2 Clinical course varies; often asymptomatic. of viral spike protein to ACE2 receptor on cell Symptoms include membranes. Anti-spike protein antibodies Common: fever, dry cough, shortness of confer immunity. breath, fatigue. Vaccination induces humoral and cellular More specific: anosmia (loss of smell), immunity, which decreases risk of contracting dysgeusia (altered taste). or transmitting the virus and prevents more Complications include acute respiratory distress serious disease, hospitalization, and death. syndrome, hypercoagulability ( thrombotic Supplemental oxygen and supportive complications including cryptogenic and/or care remain the mainstay of therapy for art ischemic stroke), shock, organ failure, death. hospitalized patients. Dexamethasone, enlarged Risk factors for severe illness or death include remdesivir, and IL-6 pathway inhibitors may for 2022 3rd pass increasing age (strongest risk factor), obesity, benefit some severely ill patients. diabetes, hypertension, chronic kidney disease, Spike (S) Lipid bilayer severe cardiopulmonary illness. protein Diagnosed by NAAT (most commonly Membrane (M) protein RT-PCR). Tests detecting viral antigen are typically less sensitive than NAATs, but can be Envelope (E) Helical protein performed rapidly and may be more accessible. capsid with viral RNA © 2022 First Aid for the USMLE Step 1 227 Pathology ` PATHOLOGY—AGInG SECtIoN II ` PATHOLOGY—AGInG New content for 2022 Normal aging Time-dependent progressive decline in organ function resulting in susceptibility to disease. 1st Pass Associated with genetic (eg, telomere shortening), epigenetic (eg, DNA methylation), and metabolic (eg, mitochondrial dysfunction) alterations. Cardiovascular arterial compliance ( stiffness), aortic diameter, left ventricular cavity size and sigmoid- shaped interventricular septum (due to myocardial hypertrophy), left atrial cavity size, aortic and mitral valve calcification, maximum heart rate. Gastrointestinal LES tone, gastric mucosal protection, colonic motility. Hematopoietic bone marrow mass, bone marrow fat; less vigorous response to stressors (eg, blood loss). Immune Predominant effect on adaptive immunity: naive B cells and T cells, preserved memory B cells and T cells. Immunosenescence impairs response to new antigens (eg, pathogens, vaccines). Musculoskeletal skeletal muscle mass (sarcopenia), bone mass (osteopenia), joint cartilage thinning. Nervous brain volume (neuronal loss), cerebral blood flow; function is preserved despite mild cognitive decline. Special senses Impaired accommodation (presbyopia), hearing (presbycusis), smell and taste. Skin Atrophy with flattening of dermal-epidermal junction; dermal collagen and elastin (wrinkles, senile purpura), sweat glands (heat stroke), sebaceous glands (xerosis cutis). Intrinsic aging (chronological aging)— biosynthetic capacity of dermal fibroblasts. Extrinsic aging (photoaging)—degradation of dermal collagen and elastin from sun exposure (UVA); degradation products accumulate in dermis (solar elastosis). Renal GFR ( nephrons), RBF, hormonal function. Voiding dysfunction (eg, urinary incontinence). Reproductive Males—testicular atrophy ( spermatogenesis), prostate enlargement, slower erection/ejaculation, longer refractory period. Less pronounced in libido as compared to females. Females—vulvovaginal atrophy; vaginal shortening, thinning, dryness, pH. Respiratory lung compliance ( elastic recoil), chest wall compliance ( stiffness), respiratory muscle strength; FEV, FVC, RV (TLC is unchanged); A-a gradient, V/Q mismatch. 1 Ventilatory response to hypoxia/hypercapnia is blunted. Less vigorous cough, slower mucociliary clearance. © 2022 First Aid for the USMLE Step 1
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