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Physician Assistant National Certifying Examination (PANCE) Infectious Disease, Professional Practice, and Clinical Skills Syllabus

The Infectious Disease, Professional Practice, and Clinical Skills syllabus for Physician Assistant National Certifying Examination (PANCE) in full: 5 chapters, 21 topics and 6 sub-topics, every one listed below, plus 51 Infectious Disease, Professional Practice, and Clinical Skills flashcards with answers.

5Chapters
21Topics
6Sub-topics
51Flashcards

Infectious Disease, Professional Practice, and Clinical Skills syllabus: all 5 chapters

Expand any chapter to see its topics and sub-topics.

  1. Systemic and Multisystem Infections

    4 topics
    • Sepsis and septic shock
      • Sepsis recognition and early resuscitation bundles
    • HIV/AIDS
      • Diagnosis, antiretroviral therapy, opportunistic infections
    • Tick-borne and vector-borne illnesses
    • Fungal and parasitic infections
  2. Antimicrobial Therapy and Stewardship

    4 topics
    • Antibiotic classes and spectra
    • Antiviral, antifungal, and antiparasitic agents
    • Antimicrobial resistance and stewardship
    • Vaccination and immunization schedules
  3. Pharmacology and Therapeutics

    4 topics
    • Pharmacokinetics and pharmacodynamics
    • Drug interactions and adverse reactions
    • Toxicology and common overdoses
      • Acetaminophen, opioids, anticholinergics, antidotes
    • Pain management and controlled substance prescribing
  4. Professional Practice and Patient Safety

    4 topics
    • Medical ethics and informed consent
    • Health maintenance and preventive screening
    • Evidence-based medicine and biostatistics
      • Sensitivity, specificity, predictive values
      • Study design and interpretation
    • Patient safety, quality improvement, and risk management
  5. Emergency and Acute Care Skills

    5 topics
    • Basic and advanced cardiac life support
    • Shock recognition and management
    • Trauma assessment and primary survey
    • Environmental emergencies
      • Burns, hypothermia, heat illness, bites
    • Procedural skills and clinical interventions

Physician Assistant National Certifying Examination (PANCE) Infectious Disease, Professional Practice, and Clinical Skills flashcards — 51 questions with answers

  1. What are the SOFA-based criteria (Sepsis-3 definition) for sepsis and septic shock?

    Sepsis = life-threatening organ dysfunction caused by a dysregulated host response to infection, identified clinically by an increase in SOFA score of $\geq 2$ points. Septic shock = sepsis with persistent hypotension requiring vasopressors to maintain MAP $\geq 65$ mmHg AND serum lactate $> 2$ mmol/L despite adequate fluid resuscitation.

  2. What are the qSOFA criteria used to rapidly screen for poor outcomes in suspected sepsis?

    qSOFA ($\geq 2$ of 3 predicts higher mortality): respiratory rate $\geq 22$/min, altered mentation (GCS $< 15$), and systolic blood pressure $\leq 100$ mmHg.

  3. In the Surviving Sepsis 1-hour bundle, what are the core early interventions?

    Measure lactate (remeasure if $> 2$), obtain blood cultures before antibiotics, give broad-spectrum antibiotics, begin rapid crystalloid $30\ \text{mL/kg}$ for hypotension or lactate $\geq 4$ mmol/L, and start vasopressors if hypotensive during/after fluids to keep MAP $\geq 65$ mmHg.

  4. What is the first-line vasopressor in septic shock?

    Norepinephrine is first-line. Vasopressin or epinephrine may be added; dobutamine is added for persistent hypoperfusion with adequate filling (cardiac dysfunction).

  5. What CD4 count defines AIDS, and what are the AIDS-defining opportunistic infections at key thresholds?

    AIDS = CD4 $< 200\ \text{cells}/\mu\text{L}$ (or an AIDS-defining illness). Prophylaxis thresholds: CD4 $< 200$ → Pneumocystis (PCP) prophylaxis with TMP-SMX; CD4 $< 100$ → add Toxoplasma prophylaxis (TMP-SMX); CD4 $< 50$ → Mycobacterium avium complex prophylaxis (azithromycin).

  6. What is the recommended first-line ART regimen class backbone for treatment-naive HIV patients, and what is the treatment goal?

    An integrase strand transfer inhibitor (INSTI, e.g., bictegravir or dolutegravir) plus two NRTIs (e.g., tenofovir + emtricitabine). Goal is sustained virologic suppression: undetectable plasma HIV RNA (viral load $< 50$ copies/mL); U=U (undetectable = untransmittable).

  7. What is the classic clinical presentation and treatment of Lyme disease?

    Caused by Borrelia burgdorferi via Ixodes (deer) tick. Early localized: erythema migrans ("bull's-eye" rash). Disseminated: facial nerve palsy, AV block/carditis, migratory arthritis. Treatment: doxycycline (first-line); amoxicillin or cefuroxime as alternatives; IV ceftriaxone for carditis/CNS disease.

  8. Contrast the vectors and key features of Rocky Mountain spotted fever vs. ehrlichiosis vs. babesiosis.

    RMSF: Rickettsia rickettsii, Dermacentor tick, petechial rash spreading from wrists/ankles to trunk → treat doxycycline. Ehrlichiosis: Ehrlichia chaffeensis, Lone Star tick, morulae in monocytes → doxycycline. Babesiosis: Babesia microti, Ixodes tick, hemolytic anemia with intraerythrocytic "Maltese cross" → atovaquone + azithromycin.

  9. What is the treatment of choice for malaria caused by chloroquine-resistant Plasmodium falciparum?

    Artemisinin-based combination therapy (ACT) for uncomplicated disease; IV artesunate for severe malaria. For P. vivax/ovale add primaquine (after checking G6PD) to eradicate hypnozoites and prevent relapse.

  10. Name the first-line treatment for cryptococcal meningitis and how it differs from candidemia treatment.

    Cryptococcal meningitis: induction with liposomal amphotericin B + flucytosine, then fluconazole consolidation/maintenance. Candidemia: an echinocandin (e.g., caspofungin, micafungin) is first-line; step down to fluconazole if susceptible.

  11. Match these antibiotic classes to their mechanism: beta-lactams, aminoglycosides, fluoroquinolones, macrolides, glycopeptides.

    Beta-lactams (penicillins, cephalosporins, carbapenems): inhibit cell wall synthesis (bind PBPs). Aminoglycosides: bind 30S, inhibit protein synthesis (bactericidal). Fluoroquinolones: inhibit DNA gyrase/topoisomerase IV. Macrolides: bind 50S, inhibit protein synthesis (bacteriostatic). Glycopeptides (vancomycin): inhibit cell wall by binding D-Ala-D-Ala.

  12. Which antibiotics provide reliable anti-pseudomonal coverage?

    Piperacillin-tazobactam, cefepime, ceftazidime, carbapenems (except ertapenem), aztreonam, fluoroquinolones (ciprofloxacin, levofloxacin), aminoglycosides, and ceftolozane-tazobactam.

  13. What are the first-line antibiotic options for MRSA?

    Vancomycin (IV) or linezolid for serious/invasive MRSA; daptomycin (not for pneumonia—inactivated by surfactant); ceftaroline. For mild skin/soft tissue MRSA: TMP-SMX, doxycycline, or clindamycin.

  14. Which antibiotic classes are most associated with these toxicities: QT prolongation, nephrotoxicity/ototoxicity, tendon rupture, and red man syndrome?

    QT prolongation: macrolides and fluoroquinolones. Nephrotoxicity/ototoxicity: aminoglycosides (and vancomycin nephrotoxicity). Tendon rupture/tendinopathy: fluoroquinolones. Red man syndrome: rapid vancomycin infusion (histamine release).

  15. What is the mechanism and clinical use of oseltamivir, acyclovir, and ganciclovir?

    Oseltamivir: neuraminidase inhibitor for influenza A/B (best within 48 h). Acyclovir: guanosine analog activated by viral thymidine kinase, treats HSV/VZV. Ganciclovir: treats CMV (more myelosuppressive); valganciclovir is the oral prodrug.

  16. Compare the mechanisms of azole antifungals vs. echinocandins vs. amphotericin B.

    Azoles (fluconazole, voriconazole): inhibit ergosterol synthesis via lanosterol $14\alpha$-demethylase (CYP-dependent). Echinocandins (caspofungin): inhibit $\beta$-(1,3)-D-glucan synthase (cell wall). Amphotericin B: binds ergosterol, forms membrane pores (nephrotoxic, infusion reactions).

  17. What is the drug of choice for the common helminth and protozoal infections: pinworm, giardiasis, and toxoplasmosis?

    Pinworm (Enterobius): albendazole or pyrantel pamoate. Giardiasis: metronidazole (or tinidazole/nitazoxanide). Toxoplasmosis: pyrimethamine + sulfadiazine + leucovorin.

  18. Define the major mechanisms of antimicrobial resistance.

    1) Enzymatic inactivation (e.g., $\beta$-lactamases, ESBLs, carbapenemases). 2) Target site modification (e.g., altered PBP2a in MRSA, ribosomal methylation). 3) Decreased uptake / porin loss. 4) Efflux pumps. 5) Metabolic bypass (e.g., altered folate pathway).

  19. What are the core principles of antimicrobial stewardship?

    Right drug, dose, route, and duration; obtain cultures before antibiotics; use narrowest effective spectrum; de-escalate based on culture data; switch IV to oral when appropriate; set a defined duration/stop date; avoid antibiotics for viral or non-infectious illness.

  20. What are the routinely recommended childhood vaccines given at birth and the typical 2/4/6-month series?

    Birth: HepB. At 2, 4, 6 months: DTaP, Hib, IPV, PCV (pneumococcal conjugate), rotavirus, and HepB. Rotavirus is oral and live-attenuated; the series provides primary immunity against these pathogens.

Show the other 31 Infectious Disease, Professional Practice, and Clinical Skills flashcards
  1. At what age are MMR, varicella, and HPV vaccines typically given, and which are contraindicated in pregnancy/immunocompromise?

    MMR and varicella: first dose at 12–15 months (live vaccines, contraindicated in pregnancy and significant immunocompromise). HPV: routinely at age 11–12 (2-dose if started before 15; 3-dose if $\geq 15$ or immunocompromised).

  2. Which vaccines are recommended for adults age $\geq 65$?

    Annual influenza, pneumococcal (PCV20 alone or PCV15 followed by PPSV23), recombinant zoster (RZV/Shingrix, 2 doses), Tdap/Td boosters every 10 years, and COVID-19 per current guidance.

  3. Define the pharmacokinetic parameters: bioavailability, volume of distribution, clearance, and half-life, with their formulas.

    Bioavailability ($F$): fraction of dose reaching systemic circulation (IV $F=1$). Volume of distribution: $V_d = \frac{\text{amount of drug in body}}{C_p}$. Clearance: $CL = \frac{\text{rate of elimination}}{C_p}$. Half-life: $t_{1/2} = \frac{0.693 \times V_d}{CL}$.

  4. How long does it take to reach steady state, and what is the loading dose formula?

    Steady state is reached after approximately $4$–$5$ half-lives. Loading dose $= \frac{C_{target} \times V_d}{F}$. Maintenance dose rate $= C_{ss} \times CL$ (adjusted for $F$).

  5. Differentiate zero-order from first-order elimination kinetics.

    First-order: a constant fraction is eliminated per unit time; rate is proportional to concentration (most drugs). Zero-order: a constant amount is eliminated per unit time regardless of concentration (saturable); examples include ethanol, phenytoin (at high doses), and aspirin at high doses.

  6. Distinguish pharmacokinetics from pharmacodynamics, and define potency vs. efficacy.

    Pharmacokinetics = what the body does to the drug (absorption, distribution, metabolism, excretion). Pharmacodynamics = what the drug does to the body (receptor effects). Potency = dose required for an effect (lower $EC_{50}$ = more potent). Efficacy = maximal achievable effect ($E_{max}$).

  7. What is the therapeutic index, and why does a low value matter clinically?

    $TI = \frac{TD_{50}}{ED_{50}}$ (or $\frac{LD_{50}}{ED_{50}}$). A low/narrow therapeutic index (e.g., warfarin, digoxin, lithium, phenytoin, theophylline) means a small change in dose/level can cause toxicity, requiring monitoring.

  8. Which CYP450 enzyme handles most drug metabolism, and give a key inhibitor and inducer of CYP3A4.

    CYP3A4 metabolizes the largest share of drugs. Inhibitors (raise drug levels): macrolides, azole antifungals, grapefruit juice, ritonavir. Inducers (lower drug levels): rifampin, carbamazepine, phenytoin, St. John's wort.

  9. Classify hypersensitivity drug reactions (Gell and Coombs types I–IV) with an example each.

    Type I (IgE, immediate): anaphylaxis to penicillin. Type II (antibody-mediated cytotoxic): drug-induced hemolytic anemia. Type III (immune complex): serum sickness. Type IV (delayed, T-cell): contact dermatitis, Stevens-Johnson syndrome/DRESS.

  10. What is the antidote for: acetaminophen, opioid, benzodiazepine, and warfarin overdose?

    Acetaminophen: N-acetylcysteine. Opioid: naloxone. Benzodiazepine: flumazenil (use cautiously—seizure risk). Warfarin: vitamin K (plus 4-factor PCC or FFP for serious bleeding).

  11. What are the antidotes for: organophosphate poisoning, beta-blocker overdose, digoxin toxicity, and methanol/ethylene glycol?

    Organophosphates: atropine + pralidoxime. Beta-blocker: glucagon (plus high-dose insulin/euglycemia). Digoxin: digoxin-specific antibody fragments (Fab). Methanol/ethylene glycol: fomepizole (or ethanol) + dialysis.

  12. What does the toxidrome of anticholinergic poisoning look like, and how does it differ from cholinergic toxicity?

    Anticholinergic: "hot as a hare, dry as a bone, red as a beet, mad as a hatter, blind as a bat" — hyperthermia, dry skin, flushing, delirium, mydriasis, urinary retention. Cholinergic (SLUDGE/DUMBELS): salivation, lacrimation, urination, defecation, GI distress, emesis, miosis, bronchorrhea, bradycardia.

  13. What is the toxic alcohol osmolal gap, and what does it indicate?

    Osmolal gap = measured osmolality $-$ calculated osmolality, where calculated $= 2[\text{Na}^+] + \frac{\text{glucose}}{18} + \frac{\text{BUN}}{2.8}$. A gap $> 10$ suggests an unmeasured osmole such as methanol or ethylene glycol; these also cause a high anion-gap metabolic acidosis.

  14. What is the WHO analgesic ladder approach to pain management?

    Step 1 (mild): non-opioids — acetaminophen, NSAIDs $\pm$ adjuvants. Step 2 (moderate): weak opioids (codeine, tramadol) + non-opioids. Step 3 (severe): strong opioids (morphine, oxycodone, hydromorphone, fentanyl) + non-opioids/adjuvants. Reassess and titrate to effect.

  15. What are the DEA controlled substance schedules and an example of each?

    Schedule I: no accepted medical use, high abuse (heroin, LSD). Schedule II: high abuse, accepted use, no refills (morphine, oxycodone, fentanyl, amphetamines). Schedule III: moderate abuse (buprenorphine, ketamine, anabolic steroids). Schedule IV: low abuse (benzodiazepines, tramadol, zolpidem). Schedule V: lowest (pregabalin, low-dose codeine cough syrup).

  16. What are key safe-prescribing practices for opioids to reduce abuse and overdose?

    Check the prescription drug monitoring program (PDMP), use lowest effective dose/shortest duration, avoid concurrent benzodiazepines, calculate morphine milligram equivalents (caution at $\geq 50$ MME/day), co-prescribe naloxone for high-risk patients, and screen for opioid use disorder.

  17. What are the four core ethical principles of medical practice?

    Autonomy (respect patient's right to self-determination), beneficence (act in the patient's best interest), non-maleficence (do no harm), and justice (fair distribution of resources and equitable treatment).

  18. What are the required elements for valid informed consent?

    1) Decision-making capacity, 2) disclosure of the diagnosis, nature/purpose of treatment, risks, benefits, and alternatives (including no treatment), 3) patient understanding, and 4) voluntariness (free of coercion). Documentation should reflect these elements.

  19. How is decision-making capacity assessed, and how does it differ from competence?

    Capacity (clinical determination) requires the patient to: communicate a choice, understand relevant information, appreciate the situation/consequences, and reason about options. Competence is a legal determination made by a court. Capacity can be decision-specific and fluctuate.

  20. List the recommended screening ages for breast, cervical, and colorectal cancer (USPSTF).

    Breast: biennial mammography ages 40–74. Cervical: Pap every 3 years ages 21–29, then Pap + HPV co-test every 5 years (or HPV alone) ages 30–65. Colorectal: begin at age 45 (colonoscopy every 10 years or stool-based testing) through 75.

  21. What are the USPSTF recommendations for lung cancer and abdominal aortic aneurysm screening?

    Lung cancer: annual low-dose CT for adults age 50–80 with a $\geq 20$ pack-year smoking history who currently smoke or quit within 15 years. AAA: one-time ultrasound for men age 65–75 who have ever smoked.

  22. Define sensitivity, specificity, PPV, and NPV with their formulas.

    Sensitivity $= \frac{TP}{TP+FN}$ (rules OUT when negative, SnNout). Specificity $= \frac{TN}{TN+FP}$ (rules IN when positive, SpPin). PPV $= \frac{TP}{TP+FP}$. NPV $= \frac{TN}{TN+FN}$. PPV and NPV depend on disease prevalence; sensitivity and specificity do not.

  23. How are likelihood ratios calculated and interpreted?

    $LR+ = \frac{\text{sensitivity}}{1-\text{specificity}}$; $LR- = \frac{1-\text{sensitivity}}{\text{specificity}}$. $LR+ > 10$ or $LR- < 0.1$ strongly changes the post-test probability. They are independent of prevalence and combine with pre-test odds to give post-test odds.

  24. Define relative risk, absolute risk reduction, and number needed to treat.

    Relative risk $RR = \frac{\text{risk in exposed}}{\text{risk in unexposed}}$. Absolute risk reduction $ARR = |\text{risk}_{control} - \text{risk}_{treatment}|$. Number needed to treat $NNT = \frac{1}{ARR}$ (rounded up). NNT is the number of patients treated to prevent one additional bad outcome.

  25. Differentiate Type I error, Type II error, and statistical power.

    Type I error ($\alpha$): false positive — rejecting a true null hypothesis (typically set at $0.05$). Type II error ($\beta$): false negative — failing to reject a false null hypothesis. Power $= 1 - \beta$; increases with larger sample size and effect size.

  26. Rank the levels of evidence in the evidence-based medicine hierarchy from strongest to weakest.

    Strongest to weakest: systematic reviews/meta-analyses of RCTs → individual randomized controlled trials → cohort studies → case-control studies → case series/case reports → expert opinion. RCTs minimize bias via randomization and blinding.

  27. In the Swiss cheese model and root cause analysis of patient safety, what is the difference between an error and an adverse event, and active vs. latent failures?

    Error = failure of a planned action to be completed as intended; adverse event = injury caused by medical care rather than the underlying disease. Active failures are unsafe acts at the point of care; latent failures are hidden system/organizational weaknesses (the "holes" that align to allow harm).

  28. What does the Plan-Do-Study-Act (PDSA) cycle represent in quality improvement?

    An iterative method for testing change: Plan (objective and prediction), Do (carry out the test on a small scale), Study (analyze results vs. prediction), Act (adopt, adapt, or abandon). Repeated cycles drive continuous improvement; a Just Culture supports reporting near-misses without blame.

  29. What is the correct adult Basic Life Support sequence and high-quality CPR parameters?

    C-A-B: check responsiveness/pulse, activate emergency response, start Compressions. Rate $100$–$120$/min, depth $\geq 2$ inches ($5$ cm, up to $6$ cm), allow full recoil, minimize interruptions, compression-to-ventilation ratio $30{:}2$ (single rescuer), and defibrillate shockable rhythms promptly.

  30. In ACLS, which rhythms are shockable vs. non-shockable, and what is the first-line drug for cardiac arrest?

    Shockable: ventricular fibrillation and pulseless ventricular tachycardia (defibrillate + epinephrine + amiodarone/lidocaine). Non-shockable: pulseless electrical activity (PEA) and asystole (epinephrine, no shock; treat reversible causes). Epinephrine $1$ mg IV every $3$–$5$ minutes is first-line in all arrests.

  31. Classify the four major types of shock with their hemodynamic profiles (preload, cardiac output, SVR).

    Hypovolemic: $\downarrow$ preload, $\downarrow$ CO, $\uparrow$ SVR. Cardiogenic: $\uparrow$ preload, $\downarrow$ CO, $\uparrow$ SVR. Obstructive (PE, tamponade, tension pneumo): $\uparrow$ or variable preload, $\downarrow$ CO, $\uparrow$ SVR. Distributive (septic, anaphylactic, neurogenic): $\downarrow$/normal preload, $\uparrow$/normal CO, $\downarrow$ SVR (warm shock).

Physician Assistant National Certifying Examination (PANCE) Infectious Disease, Professional Practice, and Clinical Skills FAQ

What is in the Physician Assistant National Certifying Examination (PANCE) Infectious Disease, Professional Practice, and Clinical Skills syllabus?

Physician Assistant National Certifying Examination (PANCE) Infectious Disease, Professional Practice, and Clinical Skills is split into 5 chapters: Systemic and Multisystem Infections, Antimicrobial Therapy and Stewardship, Pharmacology and Therapeutics, Professional Practice and Patient Safety and Emergency and Acute Care Skills. Together they contain 21 topics and 6 sub-topics.

How many chapters are in Physician Assistant National Certifying Examination (PANCE) Infectious Disease, Professional Practice, and Clinical Skills?

5 chapters, containing 21 topics and 6 sub-topics. The largest chapter is Emergency and Acute Care Skills, with 5 topics.

Are there flashcards for Physician Assistant National Certifying Examination (PANCE) Infectious Disease, Professional Practice, and Clinical Skills?

Yes — a 51-card Infectious Disease, Professional Practice, and Clinical Skills deck, printed in full in the flashcards section of this page and available in the Examius app with spaced repetition. The free plan covers one exam of your choice, including its flashcards; Examius Pro, a one-time purchase, unlocks every other exam and deck.