Physician Assistant National Certifying Examination (PANCE) Dermatology, EENT, and Hematology-Oncology Flashcards

24 sample cards from the Dermatology, EENT, and Hematology-Oncology deck

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

1. What are the symptoms of retinal detachment and the appropriate management?

   Sudden flashes of light (photopsia), increased floaters, and a 'curtain' or shadow over the visual field. Painless. It is an ophthalmologic emergency requiring urgent referral for surgical repair (laser, cryopexy, vitrectomy, or scleral buckle).

2. What is a hyphema and what causes orbital 'blowout' fractures?

   Hyphema = blood in the anterior chamber, usually from blunt trauma; keep head elevated and refer. Orbital blowout fracture (often inferior wall) from blunt force can cause diplopia, restricted upward gaze (inferior rectus entrapment), and infraorbital numbness.

3. How is orbital (postseptal) cellulitis distinguished from periorbital (preseptal) cellulitis?

   Periorbital is anterior to the orbital septum: eyelid swelling/erythema WITHOUT pain on eye movement, proptosis, or vision change. Orbital cellulitis involves pain with extraocular movements, proptosis, ophthalmoplegia, and vision changes—an emergency requiring IV antibiotics and CT.

4. What is the most common origin of orbital cellulitis and the imaging study of choice?

   Most commonly spreads from the ethmoid sinusitis. CT scan of the orbits/sinuses with contrast is the imaging study of choice. Treat with IV broad-spectrum antibiotics; surgical drainage if abscess.

5. What are the most common pathogens and the diagnostic criteria for acute otitis media?

   Most common: Streptococcus pneumoniae, Haemophilus influenzae, Moraxella catarrhalis. Diagnosis requires a bulging, erythematous tympanic membrane with decreased mobility on pneumatic otoscopy and middle ear effusion. First-line: amoxicillin (high-dose).

6. How does otitis externa ('swimmer's ear') present, and what is the most common pathogen?

   Pain with tragus manipulation/pinna traction, ear canal edema and discharge, often after water exposure. Most common pathogen is Pseudomonas aeruginosa (also S. aureus). Treat with topical antibiotic drops (e.g., ciprofloxacin/dexamethasone).

7. What is malignant (necrotizing) otitis externa and who is at risk?

   An invasive Pseudomonas infection spreading to the skull base/temporal bone, seen in elderly diabetics and immunocompromised patients. Presents with severe pain, granulation tissue in the canal, and possible cranial nerve palsies. Requires systemic antibiotics and imaging.

8. How do the Weber and Rinne tests distinguish conductive from sensorineural hearing loss?

   Conductive loss: Weber lateralizes to the AFFECTED ear; Rinne shows bone conduction > air conduction (abnormal) in the affected ear. Sensorineural loss: Weber lateralizes to the UNAFFECTED ear; Rinne shows air > bone (normal) bilaterally.

9. Compare benign paroxysmal positional vertigo (BPPV), Meniere disease, and vestibular neuritis.

   BPPV: brief (seconds) vertigo with position change, +Dix-Hallpike, no hearing loss. Meniere disease: episodic vertigo (minutes-hours) with tinnitus, fluctuating sensorineural hearing loss, ear fullness. Vestibular neuritis: acute, continuous vertigo lasting days after a viral illness, no hearing loss.

10. What maneuver treats BPPV, and what is the underlying pathophysiology?

    BPPV is caused by displaced otoliths (canaliths) in the semicircular canals. The Epley maneuver (canalith repositioning) is the treatment. Diagnosis is confirmed by the Dix-Hallpike maneuver eliciting nystagmus and vertigo.

11. How are allergic rhinitis and viral rhinitis distinguished, and what is first-line therapy for allergic rhinitis?

    Allergic rhinitis: itching, sneezing, clear rhinorrhea, pale/boggy nasal turbinates, allergic shiners, seasonal/perennial. Viral: associated with URI, often fever/malaise. First-line for allergic rhinitis is intranasal corticosteroids.

12. What criteria distinguish bacterial from viral acute sinusitis, and what is first-line treatment?

    Bacterial is suggested by symptoms $> 10$ days without improvement, severe symptoms (fever $\geq 39^\circ\text{C}$, purulent discharge) for 3-4 days, or 'double worsening' after initial improvement. First-line antibiotic is amoxicillin-clavulanate.

13. Apply the Centor criteria for streptococcal pharyngitis.

    Centor criteria (1 point each): tonsillar exudates, tender anterior cervical lymphadenopathy, fever $> 38^\circ\text{C}$, and ABSENCE of cough. Add a point for age 3-14, subtract for age $\geq 45$. Higher scores warrant rapid strep test/culture; treat GAS with penicillin/amoxicillin.

14. How does a peritonsillar abscess present, and what is the management?

    Severe unilateral sore throat, 'hot potato'/muffled voice, trismus, and a 'uvula deviated to the contralateral side' with a bulging peritonsillar area. Management: needle aspiration or incision and drainage plus antibiotics.

15. What is the most common site of anterior epistaxis and the initial management?

    Most anterior bleeds arise from Kiesselbach plexus (Little's area) on the anterior nasal septum. Initial management: lean forward and pinch the nares for 10-15 minutes; if persistent, use topical vasoconstrictors, cautery (silver nitrate), or nasal packing.

16. How do aphthous ulcers, oral leukoplakia, and oral hairy leukoplakia differ?

    Aphthous ulcers (canker sores): painful, shallow ulcers with a gray base, non-infectious, recurrent. Leukoplakia: painless white plaque that does NOT scrape off—potentially precancerous, biopsy. Oral hairy leukoplakia: EBV-associated, on lateral tongue, seen in HIV/immunosuppression.

17. Classify anemias by MCV (microcytic, normocytic, macrocytic) with examples.

    Microcytic ($\text{MCV} < 80\,\text{fL}$): iron deficiency, thalassemia, anemia of chronic disease, sideroblastic. Normocytic ($80\text{-}100\,\text{fL}$): acute blood loss, hemolysis, aplastic anemia. Macrocytic ($> 100\,\text{fL}$): $\ce{B12}$/folate deficiency, alcohol, hypothyroidism, myelodysplasia.

18. What are the characteristic iron-study findings in iron-deficiency anemia?

    Low ferritin (most specific), low serum iron, HIGH total iron-binding capacity (TIBC), and low transferrin saturation. Peripheral smear shows microcytic, hypochromic RBCs. Ferritin $< 15\,\text{ng/mL}$ is diagnostic.

19. How do vitamin $\ce{B12}$ and folate deficiency differ clinically and in labs?

    Both cause macrocytic megaloblastic anemia with hypersegmented neutrophils. $\ce{B12}$ deficiency adds neurologic deficits (subacute combined degeneration, paresthesias) and elevated methylmalonic acid. Folate deficiency has NO neuro symptoms and normal methylmalonic acid; both have elevated homocysteine.

20. What lab and smear findings characterize the major hemolytic anemia categories?

    Hemolysis shows elevated indirect bilirubin and LDH, low haptoglobin, and reticulocytosis. Smear clues: schistocytes (microangiopathic, e.g., TTP/DIC), spherocytes (hereditary spherocytosis, autoimmune), bite cells (G6PD deficiency), sickle cells (sickle cell disease).

21. Describe the genetic defect and complications of sickle cell disease.

    Autosomal recessive point mutation (glutamate→valine) in the beta-globin chain producing HbS, which polymerizes when deoxygenated. Complications: vaso-occlusive pain crises, acute chest syndrome, autosplenectomy (encapsulated organism infections), aplastic crisis (parvovirus B19). Hydroxyurea increases HbF.

22. How is beta-thalassemia distinguished from iron-deficiency anemia?

    Both are microcytic, but thalassemia has a NORMAL or elevated RBC count, normal/high iron and ferritin, target cells, and a low Mentzer index ($\frac{\text{MCV}}{\text{RBC}} < 13$). Hemoglobin electrophoresis shows elevated HbA2 and/or HbF in beta-thalassemia.

23. Differentiate the intrinsic (PTT) and extrinsic (PT/INR) coagulation pathways and what each measures.

    PT/INR measures the extrinsic and common pathways (factors VII, X, V, II, fibrinogen)—monitors warfarin. aPTT measures the intrinsic and common pathways (factors XII, XI, IX, VIII, X, V, II)—monitors unfractionated heparin.

24. Compare hemophilia A, von Willebrand disease, and immune thrombocytopenia (ITP) in lab findings.

    Hemophilia A: deficiency of factor VIII, prolonged PTT, normal PT/platelets, deep joint/muscle bleeds. von Willebrand disease (most common inherited bleeding disorder): mucocutaneous bleeding, prolonged PTT and bleeding time. ITP: isolated low platelets with normal PT/PTT and mucocutaneous bleeding/petechiae.

What this deck covers

Dermatology, EENT, and Hematology-Oncology flashcards FAQ