NFNP 5230 Final Exam – Health Promotion & Disease Prevention (Management 2) | Complete Study & Review Guide | SUNY Downstate | 2025–2026
Final Exam Study Guide – December 11th, 2025
Week One: Health Promotion and Disease Prevention
Levels of Prevention
Level What It Does Example
Primary Prevent the disease before it occurs Immunizations, lifestyle counseling
Secondar
y
Detect early disease (screening) BP screening, cancer screening
Tertiary Limit disability/progression of known disease PT/OT, chronic disease management
Health Promotion Counseling
Behavior Key PDF Points
Smoking Ask about current use; advise quitting; assist with plan
Alcohol Ask about frequency + quantity
Nutrition Encourage balanced diet + limit saturated fat
Exercise Increase activity (no specific time listed in file)
Sexual Health Education on safe sex practices
Decision-Making Capacity needs all 5
1. Understand relevant info
2. Appreciate consequences
3. Express consistent choice
4. Communicate decision
5. Explain Reasoning (most important)
If a patient cannot explain WHY, they lack capacity.
VACCINATIONS (Adult)
From your file: Do NOT give live vaccines to pregnant or immunocompromised.
Vaccine Who Gets It Interval / Notes
Tdap/Td All adults Tdap once, then Td/Tdap every 10 yrs
Influenza All adults Yearly
HPV Up to age 45
Pneumococca
l
Adults ≥65 receive
once
Shingrix Age ≥50, 2-dose series
USPSTF SCREENINGS
Screening Who Grade PDF Notes
AAA Ultrasound Men 65–75 who ever smoked Grade B One-time screening
Cervical Cancer Women 21–65 Grade A Pap per age guidelines
Colorectal Cancer Adults 50–75 Grade A Your file starts at 50 (not 45)
Lung Cancer (LDCT) 55–80 w/ 30 pack-year & smoked in past
15 yrs
Grade B Stop if 15 yrs quit
Breast Cancer (Mammogram) Women 50–74 Grade B Q2 yrs
BP Screening All adults Grade A Routine
Obesity All adults BMI Grade B Counseling recommended
HIV Screening 15–65 yrs, sexually active Grade A Offer testing
Hepatitis C Screening Born 1945–1965 Grade B One-time
USPSTF PearlsGrade A = Strongly recommended; high certainty of net benefit.
Grade B = Recommend; moderate benefit.
HIGH-YIELD EXAM CLUES
Clue Answer
Only give live vaccines to? Do NOT give to pregnant or immunocompromised
Single AAA screen Men 65–75 who ever smoked
Capacity MOST important criterion Explains reasoning behind choice
Shingles vaccine Shingrix at age ≥50, 2 doses
Mammograms Women 50–74 Q2 yrsWeek Two: Endocrine (DM, Adrenal Disorders)
Type 1 vs Type 2 vs LADA
Feature Type 1 DM Type 2 DM LADA (Latent Autoimmune Diabetes in Adults)
Cause Autoimmune β-cell
destruction
Insulin resistance + β-cell dysfunction Autoimmune like Type 1, but slow onset in adults
Age Onset Children/young Adults, obese Adults (often misdx as T2DM)
Body Size Thin or normal Overweight/obese Normal or overweight
Treatment
Needs
Insulin required Lifestyle + oral meds → maybe insulin Initially responds to oral agents, but eventually
needs insulin
Key Clue DKA risk Metabolic syndrome Initially looks like T2DM but fails oral therapy
quickly
Insulin Management Basal vs Bolus
Type Action
Basal
insulin
Controls glucose between meals and
overnight
Bolus
insulin
Controls glucose after meals
How to Start InsulinSituation What to Do
Marked hyperglycemia at
diagnosis
Start insulin immediately
Type 1 & LADA requiring
insulin
Long-term → follow
endocrinology
Somogyi vs Dawn Phenomenon
Feature Somogyi Effect Dawn Phenomenon
Cause Nighttime hypoglycemia → rebound morning
hyperglycemia
Early-morning rise in hormones (cortisol, GH) →
hyperglycemia
Clue Check 3 AM glucose is LOW Check 3 AM glucose is HIGH/normal
Treatment Decrease evening insulin Increase evening insulin
Hypoglycemia
Level Blood
Glucose
Symptoms
Mild 70 mg/dL Shaky, sweating, hungry
Moderat
e
54 mg/dL Confusion, slurred speech,
weakness
Severe Requires
help
Seizure, coma
Treatment of HypoglycemiaStep What to Do
Conscious patient 15 g fast carbs → recheck in 15 min
Severe/unconscious Glucagon IM or IV dextrose
If on insulin Adjust regimen to prevent
recurrence
ADDISON’S vs. CUSHING’S
Feature Addison’s Disease (Adrenal Insufficiency) Cushing’s Syndrome (Cortisol Excess)
Key Problem ↓ Cortisol ± ↓ Aldosterone ↑ Cortisol
Symptoms Weight loss, fatigue, hyperpigmentation, hypotension,
N/V, abdominal pain
Weight gain (central obesity), moon face, buffalo hump,
purple striae, HTN, hyperglycemia
Crisis Risk Adrenal crisis = emergency —
Emergency
Tx
IV fluids + high-dose steroids —
Diagnosis ACTH stimulation test 24-hr urine free cortisol or dexamethasone suppression
Adrenal Crisis Clinical Clue
Hypotension + weakness + abdominal pain + history of steroid withdrawal → Immediate IV steroids + fluids
Exam Quick Facts
Clue Answer
Normal adult who “looks Type 2” but fails oral meds fast LADA
Morning high blood sugar + low 3 AM glucose Somogyi effect
Morning high blood sugar + high 3 AM glucose Dawn phenomenon
Hyperpigmentation + weight loss Addison’s
Purple striae + moon face Cushing’s
Suspected adrenal crisis Immediate IV steroidsWeek Three HEENT
EYE DISORDERS
Disorder Key Findings Red Flags / Risks Management
Cataracts Progressive cloudy/blurred vision,
glare, halos
Painless vision loss Refer for surgery when affecting
ADLs
Glaucoma(Chronic/Primary
Open Angle)
↑ IOP → damage to optic nerve Can lead to blindness
if untreated
Lower intraocular
pressure (specific meds not listed →
managed by ophthalmology)
Macular Degeneration (AMD) Loss of central vision; difficulty
reading or recognizing faces
Wet type more severe Refer; nutritional counseling
discussed in notes (general)
Diabetic Retinopathy Leading cause of blindness in 20–
74 yrs
Retinal damage from
chronic hyperglycemia
Yearly eye exam recommended
Retinal Detachment Sudden flashes, floaters, curtain
over vision
EMERGENCY to
prevent blindness
Immediate referral / Emergency
care
HIGH-YIELD EXAM CLUES
Clue in Stem Diagnosis
“Painless progressive blurry vision + glare” Cataracts
“Gradual vision loss, optic nerve damage, ↑ pressure” Glaucoma
“Central vision loss → can’t read or recognize faces” Macular Degeneration
“Floaters + flashing lights + curtain over vision” Retinal Detachment
(Emergency)
“Leading cause of blindness age 20–74” Diabetic Retinopathy
When to Refer Immediately
Situation Action
Sudden vision changes, flashes, curtain Emergency Retinal Referral
Visual loss interfering with ADLs (e.g.,
cataract)
Refer for surgery
Suspicion of glaucoma or AMD Refer for management
Diabetic patient → routine Yearly screeningONE-LINE MEMORY TRICK
Cataract = cloudy.
Glaucoma = pressure.
AMD = central loss.
Retinal detachment = curtain emergency.
EAR DISORDERS
Disorder Key Symptoms Special Clues Management
Otitis Media (OM)
(Middle Ear Infection)
Ear pain, fever, hearing changes Often follows URI Antibiotics if persistent,
otherwise supportive
Meniere’s Disease Recurrent episodes of vertigo,
nausea/vomiting, hearing loss, tinnitus
Symptoms occur in
attacks
Dietary changes (low
salt) + symptom control
Vestibular Neuritis Sudden vertigo without hearing loss Often post-viral Steroids + symptomatic care
Labyrinthitis Vertigo + hearing loss Distinguishes it
from neuritis
Steroids (in notes with others)
Otosclerosis Gradual conductive hearing loss Bony overgrowth in
ear
Refer for possible surgical
treatment
HIGH-YIELD EXAM CLUES
Clue Condition
Vertigo + hearing loss + tinnitus Meniere’s Disease
Sudden vertigo after viral
infection
Vestibular Neuritis
Vertigo + hearing loss (not neuritis) Labyrinthitis
Gradual hearing loss, no vertigo Otosclerosis
Ear pain + recent URI Otitis Media
WHICH NEEDS REFERRAL?
Disorder Referral?
Otosclerosis Yes → possible surgery
Sudden hearing loss Yes (under OM/Meniere’s caution)
Persistent OM symptoms Yes if non-responsive
Severe vertigo + neurologic symptoms Urgent eval (general warning
implied)
ONE-LINE MEMORY TRICKHearing loss + tinnitus + vertigo = Meniere’s
Hearing loss + vertigo after virus = Labyrinthitis
Vertigo only = Vestibular Neuritis
Conductive hearing loss = Otosclerosis
Week Four: Respiratory (Chronic Cough and Lung Cancer)
CHRONIC COUGH Causes & Workup
Key Points (From Notes)
GERD may cause cough → try PPI trial
Treat the underlying cause
Remove triggers: smoking, ACE inhibitors, allergens
Patients often expect antibiotics, but many coughs are viral and may last 4–8 weeks
Educate about avoiding unnecessary antibiotics
When to Refer or Hospitalize (Pulmonary Red Flags)
Referral to Specialist When Hospitalization When
Chronic cough does not resolve with treatment Wheezing + hypoxia
Cough related to cardiac disease, carcinoma, foreign body, or other pathology Oxygen instability
Refer to Pulmonology, ENT depending on presentation —
LUNG CANCER (Bronchogenic Carcinoma)
Epidemiology & Risk
Key Stats
• Leading cause of cancer death in US (men & women)
• Median diagnosis age: 70 years
• Cigarette smoking accounts for 85–95% of cases
• Other risks: secondhand smoke, pollution, asbestos, radon, chemicals
• ↑ Risk with pulmonary fibrosis, COPD, sarcoidosis
Types of Lung CancerType Key Fact
NSCLC (85%) Most common
Adenocarcinoma (40%) Most common in non-smokers
Squamous Cell (25–
30%)
Smoking association
SCLC (10–15%) Small “blue” cells, aggressive, smokers
Clinical Presentation
Symptoms That Should Alarm You
• Cough, weight loss, chest pain, dyspnea, hemoptysis
• Persistent cough in a smoker or ex-smoker
• Change in chronic cough or new cough
• Recurrent pneumonia in the same lobe
Metastatic Disease Indicators
Diagnostics
Tests Purpose
Chest X-ray, CT chest/abdomen/pelvis Imaging
PET scan Staging
Sputum cytology Diagnosis
CBC, CMP, LFTs, creatinine Workup
Biopsy = Gold Standard Diagnosis
Refer to Pulmonology for bronchoscopy and biopsy Specialist care
STAGING & TREATMENT (NSCLC)
Stage Treatment
Stage I & II Surgical therapy (curative)
Stage I may not need
chemo
—
Stage II Chemo recommended
If not surgical candidate Radiation (SBRT)
Stage III Curative intent + non-consensus therapy
Stage IV Palliative chemo/immunotherapy
SCLC Treatment (Aggressive)
Type Treatment
Limited stage Chemo + radiation
Extensive stage NOT curable → chemo
When Lung Cancer Requires Emergency Action
Site Symptoms
Bones Focal skeletal pain
Liver Hepatomegaly
Brain Headache, extremity weakness, neuro deficits
Weight loss 10 lbs Red flag
DVT due to hypercoagulable
state
Also seenRed Flag Emergencies
• Severe back pain + neuro deficits
• Plethora + dilated neck veins (SVC syndrome)
• Severe respiratory compromise
• Seizures
• Unilateral leg edema
• Tumor-related fever, pneumonitis, colitis
HIGH-YIELD QUESTIONS
Clue Diagnosis
“Persistent cough in a smoker” Lung cancer
“Recurrent pneumonia in the same location” Lung tumor
“Weight loss + bone pain + cough” Metastatic lung cancer
“Horner syndrome (ptosis, miosis,
anhidrosis)”
Lung tumor compression
Week Five: Infectious Diseases
Cellulitis (including Purulent vs Non-purulent)
Aspect Details
Definition Infection of skin + soft tissue underneath; involves deeper dermis + subcutaneous fat; spreads rapidly and can
extend deep; can progress to severe infection/osteomyelitis or life-threatening disease.
Portal of entry Non-intact skin: traumatic lacerations, diabetic/vascular ulcers, chronic dermatoses w/ skin breakdown (eczema,
macerated tinea pedis), surgical wounds, insect bites.
Risk factors Venous/lymphatic compromise from prior cellulitis, peripheral edema, prior radiation, lymph node resection,
lymphedema, obesity.
Common organisms Group A β-hemolytic strep (most common in adults); non-group A strep (lymphedema); Staph aureus (purulent);
CA-MRSA; others w/ animal bites, water exposure, immunocompromise.
Clinical presentation Local erythema, swelling, warmth, tenderness, pain; often pus, induration; systemic: fevers, chills, malaise; possible
bullae, abscess, erosions, necrosis, hemorrhage; most common on lower extremities.
Purulent vs Non-purulent + Severity
Type Key Points Typical Bugs Work-up/Treatment
Purulent
cellulitis /
Abscess
Pus collection in dermis or deeper
tissue; painful, raised, fluctuant, red or
nodular lesion, often w/ central pustule
+ erythematous margins.
Includes furuncles (at hair follicles)
+ carbuncles (coalesced furuncles).
Management Exam 2 Study Guide 2
Polymicrobial from
skin/mucosal flora.
I&D is key; small furuncles may drain w/ moist
heat; larger furuncles/carbuncles/abscesses
require surgical I&D + debridement; NSAIDs for
pain.
Non-purulent Diagnosis is mostly clinical; may not Usually Streptococcus; If no obvious source: start empiric antibiotics;cellulitis have a drainable source.
Management Exam 2 Study Guide 2
sometimes Staph. obtain cultures from vesicle/pus/ulcer if present.
Blood cultures only if extensive involvement,
immunocompromised/comorbid, water/animal
bite exposure, or recurrent/refractory disease.
Severity Levels & Antibiotics
Severity Definition Treatment
Mild Hemodynamically stable; outpatient; may only need I&D
± oral antibiotics.
Target Strep + Staph; 5–7 days (extend to 14 if slow). Options:
penicillin, amoxicillin, amoxicillin-clavulanate, dicloxacillin,
cephalexin, or clindamycin. Adjust dose in renal/hepatic
impairment.
Moderate Purulent drainage with systemic involvement. Needs systemic antibiotics; often oral or IV depending on status.
Severe Refractory to PO or I&D; hemodynamic changes (T
100.4, HR90, RR24, WBC12K or 400);
immunocompromised → hospital.
IV antibiotics + possible admission; broader coverage and
surgical consult if necrosis.
MRSA vs MSSA Empiric (Moderate/Severe Purulent)
Bug Target Oral Options
MRSA TMP-SMX or Doxycycline PLUS Amoxicillin (for Strep coverage).
MSSA Penicillinase-resistant penicillin (Dicloxacillin).
Key Pearls Always reassess in 48–72 hrs; extend therapy up to 14 days if slow; diabetics/immunocompromised need broader coverage
± IV. Elevate limb, consider compression if vascular status OK.
Herpes Simplex Virus (HSV-1/2)
Aspect Details
Types HSV-1: usually oral; HSV-2: usually genital. Both are DNA viruses; no animal vectors/seasonality;
asymptomatic shedding common.
Transmission & Patho Direct contact with infected lesions/secretions; enters via skin breaks or mucosa, replicates in epithelial cells
→ vesicles; then spreads via sensory/autonomic nerves to ganglia → latent; reactivation travels back along
axon to same dermatome.
Phases of HSV
Phase Key Features
Primary Most severe; incubation 2–14 days (up to 26). Multiple painful vesicles that ulcerate + crust; burning/tingling
prodrome; tender LAD; may have fever, dysuria, discharge, malaise. Heals in 2–3 wks in immunocompetent.
Latent Virus dormant in ganglion of nerve serving dermatome.
Recurrent Reactivation in same dermatome; triggered by immunosuppression, stress, local trauma, poor sleep, etc. Episodes
shorter + milder with fewer lesions.
Diagnosis & Treatment
Category Details
Dx Clinical (history + exam). Lab confirms recommended for new diagnoses. Gold standard: viral culture of
lesion. PCR highly sensitive; HSV type-specific serology detects IgG.
Topical/oral
management
Oral herpes often self-limiting. OTC: Docosanol (Abreva). Rx topicals: Penciclovir cream (q2h while awake × 4
days), Xerese (acyclovir/hydrocortisone) 5×/day × 5 days. Avoid salicylic-acid products. Use OTCanalgesics/anesthetics & skin protectants.
Key pearl Start antivirals within 48–72 hours of symptom onset; consider suppressive therapy for frequent recurrences;
immunocompromised or pregnant patients need specialist management.
Herpes Zoster (Shingles)
Aspect Details
Etiology Reactivation of latent varicella-zoster virus in dorsal root or cranial nerve ganglion after primary chickenpox. Incidence ↑
with age & immunosuppression; younger pts milder, older ↑ complications.
Clinical Papular/vesicular rash on erythematous base in dermatomal distribution; painful, burning, itching. Prodrome:
pain/tingling/dysesthesia days before rash. Contagious from rash onset until all lesions crusted. Dx usually clinical; confirm
with PCR (best), culture, or scraping if needed.
Treatment
Component Details
Antivirals (start ≤48–72 hrs) Valacyclovir 1000 mg TID ×7 days (preferred) OR Famciclovir 500 mg TID ×7 days OR Acyclovir 800
mg 5×/day ×7–10 days. Continue until all lesions crusted; 7 days if immunocompetent, 7–14 days if
immunocompromised.
Pain control (acute) NSAIDs or Tylenol; sometimes gabapentin, pregabalin, amitriptyline, or opioids as last resort.
Post-herpetic neuralgia
(PHN)
Pain 4 months after rash; symptomatic only. Options: topical lidocaine/capsaicin (after healing), oral
analgesics, gabapentin/pregabalin, TCAs, nerve blocks/epidural.
Prevention & Referral
Topic Details
Vaccine Shingrix (recombinant): ≥50 yrs, 2 doses 2–6 months apart; give regardless of prior shingles or Zostavax.
Contact precautions Immunocompetent w/ localized disease: completely cover lesions + standard precautions until crusted.
Immediate ophthalmology
referral
Lesions on tip of nose, forehead, around eyes (ophthalmic branch of trigeminal nerve) → risk keratitis,
scarring, vision loss. Immunocompromised may need IV acyclovir + hospitalization.
PARASITIC: SCABIES
Aspect Details
Cause Infestation with mite Sarcoptes scabiei (not visible to naked eye).
Transmission Direct, prolonged skin-to-skin contact; sexual contact; sharing a bed; more common in hot, humid, overcrowded,
low-SES settings.
Symptoms Intense pruritus, especially at night (hypersensitivity reaction). Signs 2–4 weeks after first infection. Burrows in
web spaces of fingers, flexor wrists/arms, genitals, feet, buttocks, axillae. Small papules on erythematous base;
serpiginous intra-epidermal burrows. Head/palms/soles usually spared in adults.
Dx Scabies prep: mineral oil on burrow, scraped + microscopic ID of mites/eggs/feces. Adhesive tape test is another
option.
Treatment First-line: Permethrin 5% cream – apply to body, leave 8–12 hrs then wash off; repeat in 7–14 days. Oral
ivermectin 200 mcg/kg single dose, repeat in 1–2 weeks; benzyl benzoate lotion as alternative.
Important Treat all household contacts; wash clothing/bedding in hot water + hot dry; bag non-washables for 1 week or dryinstructions clean; vacuum furniture; symptoms can persist up to 2 weeks after treatment. Have pt list contacts from past 30
days.
HIV / AIDS
Aspect Details
Definition / AIDS HIV destroys CD4 T-lymphocytes (normal 500–1500).
AIDS: CD4 200 or any AIDS-defining condition (e.g., oral candidiasis, Kaposi’s, Pneumocystis).
Median 10 yrs from infection to AIDS.
Acute HIV Very infectious (viral load 100,000). 50–90% symptomatic 2–4 weeks after infection: fever, HA, sore
throat, lymphadenopathy, rash, arthralgia, myalgia – mimics mono.
During acute phase, antibodies may be negative; PCR detects 7–28 days post-exposure.
Testing (4th gen
algorithm)
Step 1: HIV-1/2 Ab + p24 Ag combo immunoassay.
If +, Step 2: HIV-1/2 Ab differentiation.
If indeterminate → HIV RNA NAT.
Older method: ELISA + confirm Western blot.
HIV RNA PCR also used for infants of HIV+ moms and indeterminate cases.
Viral load # HIV RNA copies/mL; higher → faster CD4 drop, more progression.
Best marker of success = undetectable VL (50 copies/mL).
CD4 counts Used to stage disease & monitor ART response; test same time of day and same lab.
Opportunistic Infections
Infection CD4 Features 1st-line Tx
Toxoplasma gondii
(CNS)
10
0
HA, fever, blurred vision,
confusion, imbalance; brain
abscesses.
Sulfadiazine + pyrimethamine or TMP-SMX. Test for IgG
after HIV dx.
Pneumocystis
jirovecii PNA (PCP)
20
0
Opportunistic pneumonia. TMP-SMX; if sulfa allergy → Dapsone + trimethoprim.
Check G6PD before Dapsone (risk hemolytic anemia).
Vaccines (HIV)
• Use inactivated vaccines only: Hep A, Hep B, annual inactivated flu, pneumococcal, Td/Tdap q10 yrs, HPV if eligible.
• Best if CD4 200. Usually given by HIV/ID specialist—coordinate care.
PEP vs PrEP (high yield)
PEP (Post-Exposure) PrEP (Pre-Exposure)
For emergency exposures (occupational, sexual assault, needle sharing).
Start ASAP, within 72 hrs, don’t wait for labs if delayed. Use ≥3 ART
drugs for 28 days. Baseline labs: HIV rapid & Ab/Ag, HCV RNA,
For ongoing high-risk HIV-negative individuals
(partner w/ HIV, high-risk sexual behavior). Daily oral
regimen; check HIV before start, then q3 months.HBsAg. Reduces transmission 90%.
Week 6: Infections and Inflammations
Feature Coronavirus (SARS) MERS (Middle East Respiratory Syndrome)
Type Coronavirus in humans & animals; cause
of emerging infectious disease
Previously unknown coronavirus now called MERSCoV
Origin Emerged in 2002, Guangdong Province, China Linked to Arabian Peninsula (Saudi Arabia, Qatar,
Jordan, UAE)
Symptoms - Severe, often fatal pneumonia
- Fever, influenza-like illness
- Fever, cough, shortness of breath
- GI symptoms: diarrhea, nausea, vomiting- Diarrhea, leukopenia,
thrombocytopenia, lymphopenia
Incubation 4–7 days 2–14 days
Complications About 25% develop severe pneumonia → ARDS Most patients also progress to ARDS with multiorgan failure
Mortality Up to 50% in older patients & those with
comorbidities
Mortality approx. 55%
Counseling /
Prevention
Screen travel history; consult infectious disease if
needed
For travelers → strict handwashing, avoid contact,
avoid sharing utensils, disinfect doorknobs
• Emerging diseases + COVID intro
• SARS symptoms, mortality, ARDS
• MERS origin, symptoms, mortality, prevention
High-Yield Clues
Clue Answer
Severe pneumonia + diarrhea + lymphopenia SARS
Came from Arabian Peninsula + GI symptoms MERS
Both may progress to ARDS with multiorgan
failure
TRUE
Mortality higher in MERS ~55
%
One-Sentence Memory Trick
SARS kills lungs + low WBC; MERS comes from Middle East + causes GI symptoms + higher mortality.
GI & SYSTEMIC INFECTIOUS DISEASES (Overview)
Infectious & Traveler’s Diarrhea
• Non-inflammatory: Enterotoxin/virus in proximal small bowel; large-volume watery stools (e.g., cholera, viral
gastroenteritis).
• Inflammatory: Bloody, small-volume stools + fever, severe abd pain, tenesmus; colon involvement (dysentery).
• Penetrating: Invasion into wall w/ systemic manifestations (enteric fever, Salmonella typhi).Traveler’s Diarrhea
• Usually non-inflammatory, short, fecal-oral (food/water). Common: EAEC/ETEC E. coli; also Campylobacter, Shigella,
Salmonella.
• Prevention: Avoid untreated water/ice, unpasteurized milk, raw fruits/veg, undercooked meat; drink only sealed/carbonated
beverages.
• Tx: Oral fluids; Loperamide 4 mg, then 2 mg after each stool (max 16 mg/day). Bismuth subsalicylate 2 tabs q30–60 min
(avoid in gout, ASA allergy, renal insufficiency). If needed: Cipro 500 mg BID ×3–5 days or Azithro 500 mg daily ×3 days.
Antibiotics not usually for prophylaxis.
Vibrio Cholera
• Massive watery diarrhea → dehydration, electrolyte imbalance, renal failure, metabolic acidosis.
• Think in severe watery diarrhea with rapid volume depletion, esp. if from endemic areas.
• Main Tx: Rapid rehydration + electrolyte replacement (IV for severe/hypovolemic shock). Oral fluids as adjunct. Antibiotics
as adjunct after rehydration to shorten disease.
Clostridioides difficile
• Follows broad-spectrum antibiotic use → alters flora → C. diff overgrowth; can cause pseudomembranous colitis. High-risk
drugs: fluoroquinolones, clindamycin.
• First-line for initial, non-severe:
o Fidaxomicin 200 mg BID ×10 days (targets C. diff, less recurrence)
o OR Vancomycin 125 mg QID ×10 days
o Alternative: Metronidazole 500 mg TID ×10–14 days
• Severe/complicated: may need IV Flagyl + rectal vanco, fecal microbiota transplant, or colectomy in toxic
megacolon/perforation.
• Prevention: Antibiotic stewardship; soap and water (hand sanitizer doesn’t kill spores).
Norovirus & General Diarrhea Management
• Norovirus = most common cause of self-limited noninflammatory gastroenteritis: diarrhea, N/V, stomach pain, fever, resolves
in 2–3 days.
• Antibiotics NOT indicated for typical norovirus.
• Red flags for bacterial/inflammatory diarrhea: fever, severe abd pain, tenesmus, 6 stools/day, blood/mucus, frail/elderly,
immunocompromised → consider stool testing & empiric abx.
• Always assess dehydration, chronic illness, HIV status; consider noninfectious causes (hyperthyroid, malignancy, fecal
impaction, gynecologic, etc.).
UTI’s
Overview
Key Points Source
Most common outpatient infectious disease in adults Management Exam 2 Study Guide 2
40% of women experience at least one UTI in their lifetime Management Exam 2 Study Guide 2
Common pathogens: E.
coli, Proteus, Klebsiella, Enterococcus
Management Exam 2 Study Guide 2Community-acquired UTIs usually treatable outpatient Management Exam 2 Study Guide 2
UTI TYPE BREAKDOWN
Type Definition Symptoms Notes
Cystitis (lower UTI) Bladder infection Dysuria, frequency, urgency, suprapubic
pain, foul odor, hematuria
Most common
Pyelonephritis (upper
UTI)
Kidney infection Flank pain, fever/chills, N/V, CVA
tenderness, systemic symptoms
Requires urgent
treatment
Complicated UTI Infection with structural, functional,
or comorbid issues
May be severe or atypical Examples below
Complicated UTI — Who is High Risk?
Risk Factors Examples
Structural abnormalities Stones, stents, obstruction
Functional changes Neurogenic bladder, reflux
Comorbidities Diabetes, CKD, immunocompromised
Males, pregnancy,
children
All need special evaluation
Diagnostic Evaluation
Test Purpose High Yield
Urinalysis (UA) Initial screen Leukocyte esterase, nitrites
Urine culture Not always needed for simple cystitis; must for pyelo, recurrent,
complicated, pregnancy
ID organism & resistance
Additional tests STI workup if needed Dysuria + discharge may indicate
STI
TREATMENT
1) Uncomplicated Cystitis
First-line agents Notes (from PDF)
Nitrofurantoin Common outpatient drug
Trimethoprim–sulfamethoxazole (TMP–
SMX)
Avoid if sulfa allergy
Cephalexin or other oral cephalosporins Good if allergy/alternative needed
Duration commonly short (3–7 days).
2) Pyelonephritis
Action Medication
MUST obtain urine culture –
Often treat outpatient if stable Fluoroquinolones (e.g., Ciprofloxacin) per PDF
If severe/systemic →
ED/hospital
IV antibiotics
3) Complicated UTI
Recommendation Notes
Broader antibiotics based on culture Delay culture? Start empiric
Address pathology (stones,
obstruction)
May require imaging
Refer or hospitalize if moderate/severe Decision varies by case
Pregnancy and UTIs
Key Points Source
Always treat bacteriuria in pregnancy Prevent pyelonephritisMust obtain urine culture Required
Avoid fluoroquinolones & TMP-SMX late
trimester
Safety consideration
(Pregnancy management implied in high-risk category & typical outpatient practice from PDF.)
HIGH-YIELD “DON’T MISS” PEARLS
Pearl Meaning
Dysuria + discharge? Evaluate for STI, not only UTI
CVA tenderness + fever Think pyelonephritis, NOT cystitis
Recurrent UTIs → get culture Needed due to resistance
Immunocompromised? Diabetic?
Male?
Treat as complicated
Hospitalize if toxic, vomiting, septic For IV therapy
Prevention & Education
Counseling Points Source
Hydration & hygiene Management Exam 2 Study Guide 2
Avoid unnecessary antidiarrheals & misuse of meds GI overlap in patient teaching
Food safety in immunocompromised patients Applicable to UTI risk
Exam Tip Summary (Rapid Fire)
• Most UTIs = E. coli
• Nitrofurantoin, TMP-SMX, or Cephalexin = common outpatient cystitis treatment
• Get a urine culture in: pyelo, recurrent, pregnant, complicated, immunocompromised
• CVA tenderness + fever = Pyelonephritis
• Pregnancy UTIs always treat
• Males = complicated until proven otherwiseDIVERTICULOSIS vs DIVERTICULITIS MASTER CHART
Feature Diverticulosis Diverticulitis
Definition Presence of diverticula (outpouchings) in colon Inflammation or infection of diverticula
Symptoms Often asymptomatic; may have mild LLQ
discomfort, changes in bowel habits
LLQ abdominal pain, fever, N/V, constipation or
diarrhea
Complications Risk of bleeding; most people never progress Abscess, perforation, peritonitis, obstruction, fistula
Diagnosis Typically found incidentally (screening
colonoscopy, imaging)
Clinical diagnosis with LLQ pain + systemic
symptoms; CT abdomen if severe/complicated
Location Most common in sigmoid/descending colon Same area most affected
Treatment High-fiber diet, lifestyle management Antibiotics for moderate/severe; bowel rest; fluids
Who is at higher
risk?
Age, low fiber diet Same risks + infection/inflammation present
MANAGEMENT PEARLS
Topic Key Points
Diet High fiber diet recommended for diverticulosis; limit red meat; increase physical activity.
Fluids & Motility Poor bowel motility + constipation = higher risk. Encourage hydration & exercise.
Complications Diverticulitis can lead to perforation, abscess, or bleeding; can become surgical emergency.
Clinical Presentation Diverticulitis symptoms: LLQ abdominal pain, nausea, fever, constipation/diarrhea. Pain increases after
meals, decreases after defecation.
Diagnosis
Consideration
Most mild cases diagnosed clinically based on symptoms + risk factors; CT used for severe cases or
complications.
When to Refer Complicated cases & recurrent episodes may need surgical consultation.
TREATMENT SUMMARY
Severity Treatment
Mild diverticulitis (uncomplicated) Outpatient: bowel rest, diet adjustment, hydration, oral
antibiotics
Moderate/severe or complicated (fever, persistent pain,
comorbid, elderly)
Hospital referral → IV fluids + IV antibiotics + CT scan
Recurrent or chronic disease Refer to GI or surgery for further evaluation
Diverticulosis (no infection) NO antibiotics; lifestyle & diet only
RED FLAG SYMPTOMS
If present → Hospital evaluation + CT imaging
• High fever
• Severe abdominal pain
• Peritonitis signs (rigidity, guarding, rebound)
• Inability to tolerate PO
• Immunocompromised or elderly
• Suspected abscess or perforation
HIGH-YIELD EXAM CLUES
Clue Diagnosis
LLQ pain + fever + constipation/diarrhea Diverticulitis
LLQ pain that improves after bowel movement Diverticulosis (or mild diverticular disease)
Found incidentally during screening
colonoscopy
Diverticulosis
Needs antibiotics Diverticulitis ONLYDiet change only Diverticulosis
Diverticulosis = pouches, no infection, no antibiotics.
Diverticulitis = infected pouches, LLQ pain + antibiotics.
Week Seven/ Week Eight Cardiology Part 1/ Part 2
CARDIAC ARRHYTHMIAS
Rhythm Key Features (PDF) Symptoms Treatment (PDF) Special HighYield
Atrial Fibrillation
(A-Fib)
Disorganized atrial activity
→ irregularly irregular rhythm;
atria quiver, blood pools, clot risk
Palpitations, fatigue,
dizziness, SOB; may
be asymptomatic
Rate or rhythm control +
anticoagulation based on
stroke risk
Cardiovert
within 48 hours
if unstable or
new onset
Atrial Flutter Atrial impulses fire rapidly in
a circuit → sawtooth pattern
Similar to A-fib;
may feel less
symptomatic
Managed similar to A-fib;
control HR, consider
cardioversion,
anticoagulate if risk
Regular rhythm
but fast atrial rate
Sick Sinus
Syndrome (SSS)
SA node dysfunction →
alternating tachycardia +
bradycardia, long pauses
Dizziness, syncope,
palpitations, fatigue
Pacemaker for
symptomatic SSS
Calcium channel
blockers may
worsen symptoms
Sinus Tachycardia HR 100 bpm originating in SA
node
Anxiety, pain, fever,
hyperthyroid
Treat underlying cause Normal
physiologic
response
PVCs (Premature
Ventricular
Contractions)
Early beat from ventricle; may be
unifocal or multifocal
“Skipped beats,”
palpitations
Address electrolyte
imbalance, avoid
stimulants
Can indicate
myocardial
irritability
A-FIB & FLUTTER: MANAGEMENT & PEARLS
RATE vs. RHYTHM CONTROL
Strategy When Used Drugs Mentioned in PDF
Rate Control Stable patients; chronic management Beta-blockers, calcium channel blockers
Rhythm Control New onset, symptomatic, persistent despite rate control Cardioversion (timing important)
Cardioversion Rule
If onset 48 hours, may cardiovert directly. If 48 hrs or unknown → anticoagulation first.
ANTICOAGULATION PEARLS
PDF Notes
• Anticoagulation is based on stroke risk.
• Not every A-fib pt gets anticoagulated.
• NOACs are contraindicated in pregnancy. (high yield)
SPECIAL ARRHYTHMIA PEARLS
Arrhythmia Don’t Forget
A-Fib “Irregularly irregular”; can cardiovert 48 hrs if unstable or new
A-Flutter “Sawtooth” pattern
SSS (Sick Sinus
Syndrome)
Pacemaker if symptomatic
PVCs May be early sign of myocardial irritability
NOACs Do NOT use in pregnancy
Rate control meds caution In SSS, calcium channel blockers can worsen symptomsWHEN TO SEND TO ED
Send to ED if:
• Hemodynamic instability (hypotension, altered mental status)
• New onset A-fib with symptoms + unable to cardiovert in office
• Severe symptoms (syncope, chest pain, severe SOB)
• Suspected severe electrolyte imbalance or acute ischemia
RHYTHM IDENTIFIERS (Rapid Recognition)
Clue Arrhythmia
“Irregularly irregular” A-Fib
Sawtooth pattern Atrial Flutter
Tachy-brady syndrome Sick Sinus Syndrome
Early wide beat w/ pause PVC
HR 100 due to underlying issue Sinus Tachycardia (not primary arrhythmia)
ONE-LINE MEMORY TRICKS
A-Fib = chaotic atria → clot risk → anticoagulate by stroke risk.
Flutter = sawtooth circuit → treat like A-Fib.
SSS = broken SA node → pacemaker only if symptomatic.
PVCs = ventricular irritability → check electrolytes & triggers.
HEART FAILURE (HFrEF vs HFpEF) MASTER CHART
Feature HFrEF HFpEF
Name Heart Failure with reduced EF Heart Failure with preserved EF
EF Value 40% 40%
Former Name Systolic HF Diastolic HF
Primary Problem Ventricles cannot pump/eject enough
blood
Ventricles are stiff and cannot fill
Mechanism Weak LV muscle → ↓ contractility Stiff LV wall → ↓ filling capacity
Common Cause CAD, MI, dilated cardiomyopathy Long-standing HTN leading to LV hypertrophy
Stroke Volume Decreased Normal/near-normal, but poor ventricular filling
HFrEF = pump problem. HFpEF = filling problem.
LEFT vs. RIGHT HEART FAILURE
Side of Heart Key Symptoms
Left HF Dyspnea on exertion, orthopnea, PND (night SOB), dry cough, crackles, fatigue
Right HF Ascites, JVD, hepatosplenomegaly, N/V, weight gain, LE edema, tachycardia
DIAGNOSTICS
Test Purpose
EKG Assess rhythm complications (A-Fib)
Echocardiograph
y
Determines EF & structure
Chest X-Ray Fluid overload
BNP Confirms HF severity
Labs CBC, CMP, TSH, cardiac enzymesWeight checks Track fluid status
HEART FAILURE TREATMENT HFrEF (Systolic 40% EF)
Drug Class Medications in PDF
ACE Inhibitors For systolic HF
ARNI
(Preferred)
Sacubitril/Valsartan (Entresto)
Beta Blockers Metoprolol, Carvedilol, Bisoprolol
Diuretics Loop diuretics; Spironolactone
Digoxin For symptomatic control
Lifestyle ↓ Na intake, exercise, no alcohol/tobacco, flu & pneumonia vaccines
Contraindications/Barriers to Entresto
Do NOT start if:
• SBP 100 mmHg
• Serum K+ 5 mmol/L
• eGFR 30 mL/min/1.73m2
• History of angioedema
When to Send to ED
Red Flags
• Hemodynamic instability (decompensated HF)
• Worsening symptoms needing IV therapy
• Severe dyspnea, pulmonary edema
• New arrhythmia with instability
HIGH-YIELD HF EXAM PEARLS
Clue Diagnosis
EF 40% + pump issue HFrEF
EF 40% + stiff ventricles HFpEF
No ACE/ARNI if SBP 100, K+ 5,
angioedema
Entresto Barrier
A-Fib causes ↓ cardiac output HF contributor
Weight gain 2–4 lbs/week → adjust diuretics Fluid overload
Flu & Pneumonia vaccines HF management
Quick Memory Trick
HFrEF = Reduced = weak pump. Treat with ACE/ARNI + Beta Blockers + Diuretics.
HFpEF = Preserved = stiff ventricle. Manage symptoms + causes (HTN, CAD).Week Nine: Genitourinary and Gastrointestinal
Hepatitis Quick Charts
Viral Hepatitis Comparison
Feature HAV HBV HCV HDV HEV
Genetic
material
RNA DNA RNA RNA RNA
Chronic
infection
No Yes Yes Yes (only w/ HBV) No
Transmission Fecaloral
Parenteral,
sexual, vertical
Parenteral Must have HBV Fecal-oral
Prevention Vaccine Vaccine No vaccine No vaccine Vaccine outside US
Notes Acute
only
Risk cirrhosis &
HCC
Screen age 18–79; leading
cause cirrhosis & transplant
Coinfection causes
fulminant hepatitis
Occurs in poor
sanitation areas
Serology Interpretation (HBV)
Status HBsAg AntiHBc
Anti-HBs IgM anti-HBc
Susceptible
Immune (vaccine)
Immune (prior infection)
Acute infection
Chronic infection
HBeAg indicates active viral replication and infectivity.
Key Diagnostic Tests
Virus Screening Test What Positive Means Next Step
HAV IgM anti-HAV Acute infection & contagion None, supportive care
HBV HBsAg Active infection Interpret full panel
HCV Anti-HCV Ab Exposure (not immune) Order HCV RNA PCR
Treatment Summary
Condition Treatment
Acute HAV Supportive care, avoid hepatotoxins, hospitalize severe cases
Acute HBV Supportive, monitor LFTs q2 weeks
Chronic HBV Interferon alfa-2b, nucleoside analogs (Entecavir, Tenofovir)
Hepatitis C (HCV) Direct acting antivirals (Mavyret, Harvoni, Epclusa)
Drug-induced
hepatitis
Stop agent; may use N-acetylcysteine for acetaminophen
Alcoholic hepatitis Alcohol abstinence, vitamin replacement (parenteral B vitamins)
NASH/NAFLD Weight loss, Vit E 400–800 IU, treat hyperlipidemia
Autoimmune hepatitis Corticosteroids, Azathioprine (may need transplant)Clinical Presentation Summary
Type Notable Findings
General/acute viral hepatitis Fever, anorexia, myalgia, nausea, RUQ pain, jaundice
Alcoholic Hepatitis Fever, jaundice, leukocytosis, tender hepatomegaly, spider telangiectasia, ascites, encephalopathy
Autoimmune Hepatitis Fatigue, malnourished, RUQ pain, arthralgia, diarrhea; often cirrhosis at diagnosis
Drug-Induced Hepatitis Fever, rash, eosinophilia (drug hypersensitivity)
Common Hepatotoxic Drugs
May cause drug-induced liver injury
• Antibiotics: Augmentin (most common), Bactrim, Ciprofloxacin, INH
• NSAIDs
• Green tea extract, anabolic steroids, multi-ingredient supplements
• Statins, Amiodarone
• Valproate, Phenytoin
• Methotrexate
MASTER RENAL FAILURE CHART (AKI vs CKD vs ESRD)
Feature AKI CKD ESRD
Definition Abrupt loss of kidney function within ≤7
days
Progressive decline in kidney
function
End stage; requires
renal replacement
Key Criteria ↑ Creatinine 0.3 mg/dL in 48 hrs OR 1.5×
baseline in 7 days
GFR 60 mL/min/1.73m² ≥ 3
months
GFR very low, usually
no urine output
Urine Output 0.5 mL/kg/hr for 6–12 hrs (oliguria) May be normal until late stage Anuria (100
mL/day)
Etiologies Volume depletion, hypotension,
nephrotoxins, hospitalization
DM, HTN, nephrotoxins,
autoimmune/inflammatory
Final progression of
CKD
Risk Factors Advanced age, liver disease, diabetes,
vascular disease, hospitalization
HTN, DM, nephrotoxic
medications, recurrent kidney
damage
Same as CKD; longterm uncontrolled
factors
Clinical Presentation Sudden confusion, anorexia, N/V, edema,
weight gain
Few symptoms early; ↓ GFR, ↑
Cr, albuminuria
Anuria, uremic
symptoms, needs
transplant or dialysis
Urgent Signs Oliguria or anuria + ↑ creatinine Persistent albuminuria &
decreasing GFR
Severe
metabolic/electrolyte
derangement
Diagnostics ↑ Creatinine, ↓ urine output, AlbuminCreatinine Ratio, UA, CMP, CBC, renal
US
Same + ACR preferred method
for albuminuria screening (30
mg/g, repeat on morning sample)
Labs to monitor
electrolytes, anemia,
etc.
Screening Monitor patients on nephrotoxins or
hospitalized
ACR (preferred) + eGFR Dialysis monitoring
Differential Etiologies Pre-renal: volume
loss; Medications:NSAIDs/antibiotics; To
xic chemicals, radiation, contrast dye
Same + inflammatory &
autoimmune
Final stage of prior
causes
Management Remove offending agents/nephrotoxins,
correct electrolytes
BP control (ACE), HbA1c 7%,
protein reduction, smoking
cessation
Dialysis, transplant
When to Refer to
Nephrology
AKI with oliguria/anuria + ↑ Cr GFR 30 (stage 4–5),
albuminuria 300 mg/g,
refractory HTN, persistent K+
imbalance, urine RBC 20/hpf,
CKD progression
ESRD: continue care,
dialysis, transplantHospitalization AKI with oliguria/anuria + ↑ Cr;
hypotensive crisis; systemic inflammation
or sepsis
Pulmonary edema, HF
exacerbation, acute fluid
derangement
Required for many
cases
Complications Volume overload, electrolyte imbalance CV disease, HF, anemia,
metabolic issues
LV hypertrophy (70%
on dialysis have LVH),
infection risk,
metabolic
derangements
Immunization/Prevention Avoid nephrotoxins Smoking cessation, early
referral, BP & DM control
Vaccines: Flu,
Pneumonia, Hep B
Nutrition — ↓ Protein diet Varies by dialysis type
Anemia Management — Consider if chronic RBC transfusion,
ESAs
HIGH-YIELD TEST PEARLS
Topic High-Yield Clue
Best screening for albuminuria Albumin/Creatinine Ratio (ACR) — random sample first, repeat in morning if 30
mg/g
Most common cause of AKI Hospitalization with reduced perfusion + nephrotoxin exposure
Most common AKI causes: medications NSAIDs, antibiotics, antineoplastics, HIV drugs, illicit drugs
Dialysis fistula Takes 4–6 weeks to mature
Dialysis complications LVH, pulmonary edema, infection, electrolyte imbalances
When to hospitalize AKI with oliguria/anuria and electrolyte crisis, sepsis, pulmonary edema, acute HF
Parkinson’s Disease + Trigeminal Neuralgia MASTER CHART
Feature Parkinson’s Disease Trigeminal Neuralgia
Definition Slowly progressive neurodegenerative disease; loss of
dopamine receptors in substantia nigra
Nerve pain disorder affecting the trigeminal
nerve (5th cranial nerve)
Cause / Pathology Dopamine depletion in the basal ganglia; loss of
smooth purposeful movement
Compression of trigeminal nerve root (most
common), blood vessel pressure; can be
secondary or idiopathic
Risk Factors Age 50; men women; genetics; pesticides/cleaning
chemicals; heavy metals; concussions; obesity; anemia
Aging, aneurysm, AV malformation, tumors,
multiple sclerosis, stroke, facial trauma, surgical
injury; genetic abnormal blood vessel formation
Key Symptoms 3 classic symptoms: tremor (pill rolling, worse at
rest), muscular rigidity, bradykinesia; shuffling gait,
postural instability; hypophonia, masked facies;
cognitive decline, depression, hallucinations
Sudden, severe, unilateral electric shock-like
facial pain episodes; triggered by chewing,
talking, brushing teeth, cold air, smiling; pain
lasts seconds–minutes; may have burning/aching
Later / Additional
Symptoms
Difficulty initiating voluntary movement (freezing),
festination, decreased arm swing, sleep disturbance
Facial muscle spasms; pain-free periods between
attacks; progressive worsening
Physical Exam
Findings
Cogwheeling rigidity when flexing/rotating arm;
reduced arm swing; flexed posture; pull test for
postural reflexes
No specific physical test confirms diagnosis;
symptoms and history most important
Diagnostics Clinical diagnosis (2 of 3: tremor, bradykinesia,
rigidity); response to levodopa supports Dx; no
standard labs; neuroimaging only to rule out other
disorders
Clinical diagnosis; MRI may be used to identify
vascular compression, MS, tumor
First-Line
Treatment
Carbidopa-Levodopa (Sinemet) for motor symptoms
(tremor, rigidity)
Carbamazepine (Tegretol), Oxcarbazepine
(Trileptal)Other Medications Dopamine agonists (Requip, Mirapex) — risk impulse
disorders & hypotension; MAO-B inhibitors
(Selegiline, Rasagiline); COMT inhibitors
(Entacapone); Anticholinergics (Cogentin) for younger
pts
Adjuncts: Gabapentin, Lamotrigine, Baclofen;
taper meds if pain-free 6–8 weeks
Surgical Options Deep brain stimulation Rhizotomy, nerve blocks, or surgery for
refractory cases
Contraindications /
Cautions
Don’t stop dopamine agonists abruptly (withdrawal
syndrome); anticholinergics avoid in older adults;
interaction with SSRIs, MAOIs, TCAs
None specified beyond med usage in file
Disease Progression Progressive; may develop dementia, psychosis; falling
risk
May worsen; periods of remission possible
Patient Education Fall risk; medication side effects; support groups;
speech & physical therapy
Avoid triggers; medication adherence; consider
taper when symptoms improve
Medication Key Pearls
Medication Type Key Notes
Carbidopa-Levodopa Most effective; don’t stop abruptly; treats tremor + rigidity; dyskinesia risk
Dopamine Agonists (Requip, Mirapex) Start low; risk for hallucinations, impulse disorders; can cause orthostatic hypotension
MAO-B Inhibitors Avoid with SSRIs, TCAs; side effects: insomnia, confusion in older adults
Anticholinergics (Artane, Cogentin) Avoid in elderly; useful for tremors in young patients
Carbamazepine/Oxcarbazepine (TN) First-line; slowly taper after sustained improvement
Gabapentin/Baclofen (TN) Adjunct options; used when first-line insufficient
Hallmark Exam Clues
Disease Must Remember
Parkinson’s Resting tremor that improves with movement; masked facies; cogwheel rigidity
Trigeminal
Neuralgia
Sudden shock-like unilateral facial pain triggered by touch, chewing, cold
HEADACHE MASTER CHART
Feature Migraine Tension-Type Headache Cluster Headache Medication Overuse
Headache (Rebound)
Type Primary Primary Primary Secondary (due to overuse)
Key
Description
Moderate–severe
throbbing/pounding
headache
Tight “band-like” pressure Severe, unilateral,
retro-orbital “ice
pick”
Headache from frequent
analgesic use
Duration 4–72 hours Minutes to hours 15 min–3 hours
(often ~90 min)
Persistent headaches
Pain Location Ipsilateral; often temporal Bilateral Unilateral behind
eye
Diffuse
Triggers /
Aggravating
Exercise, stress, foods,
light, sound
Stress; not worsened by
physical activity
Often wakes patient
up at night, same
time daily
Frequent
NSAIDs/opioids/caffeine
combos
Associated
Symptoms
Nausea/vomiting,
photophobia, phonophobia;
aura may precede
Muscle tightness, trapezius
spasm; no N/V
Ipsilateral tearing,
conjunctival
injection, rhinorrhea,
ptosis, miosis,
lacrimation
Headache increases when
meds wear off
Aura Visual scotomas, flashing
lights
NONE NONE NONE
Onset Variable; women men Any age; very common Men 30–40 yrs Chronic headache sufferersAge/Sex
Diagnostics Clinical; rule out CVA if
severe
Clinical MRI recommended
initially
Clinical history
First-Line
Treatment
Acute: Triptans + NSAIDs
(Sumatriptan + Naproxen);
antiemetics if vomiting
NSAIDs/Acetaminophen;
can use Excedrin (caffeine
combo)
Oxygen 100% (≥12
L/min NRB) + SubQ
or intranasal triptan
Stop overused medication;
limit acute meds
Preventive
Treatment
Beta-blockers, TCAs
(Amitriptyline), SNRIs
(Effexor), CGRP
(Aimovig), Topiramate,
Valproate
Lifestyle + NSAIDs PRN;
avoid triggers
Verapamil,
Prednisone;
alternatives:
Topiramate,
Valproate, nerve
blocks
Preventive therapy for
underlying headache
Emergent
Treatment
Needs
Severe complicated
migraine w/
nausea/vomiting → IV
antiemetic + nonoral meds
Rarely emergent Urgent MRI first
diagnosis
Consider withdrawal +
prevention
Avoid Triptans in ischemia,
uncontrolled HTN, stroke
Opioids Mixing triptans +
ergots
Using 10 days/month
analgesics
RED FLAGS: “SNOOP” + Physical Exam Danger Signs
Red Flag Category Examples (from file)
S – Systemic Fever, chills, weight loss, HIV, cancer
N – Neurological Mental status change, seizure, asymmetric reflexes
O – Onset Sudden, worst “thunderclap” headache
O – Older age New headache ≥ 50 years
P – Previous hx First or different headache, worsening pattern
Physical Exam Red Flags
• Papilledema
• Painful temporal arteries
• Personality change
• “Worst headache ever”
• Asymmetry of pupils or reflexes
Medication Pearls (by disorder)
Medication Used For Notes
Sumatriptan + Naproxen (Treximet) Migraine abortion Most effective combo
CGRP Antagonists (Nurtec,
Ubrelvy)
Acute + preventive migraine For triptan contraindications
Lasmiditan (Reyvow) Migraine No vasoconstriction — safer for cardiac risks
Ergotamine/Caffeine (Cafergot) Migraine DO NOT MIX WITH TRIPTANS
Topiramate/Valproate Migraine prevention; Cluster alt Antiseizure meds
Verapamil Cluster prevention First-line prophylaxis
Prednisone Cluster prevention Used acutely early
Oxygen ≥12 L/min Cluster acute First-line!
Excedrin / Fioricet Tension But risk MOH warning: limit usage
High-Yield Exam Clues
Clue Diagnosis
“Ice-pick pain” + tearing, rhinorrhea, ptosis Cluster
Pulsating + N/V + photophobia Migraine
Headache with stress, no N/V, “tight band” Tension
Headache worsens when meds wear off Medication OveruseNew headache age 50 + jaw pain + visual
changes
Think Temporal Arteritis workup (from PMR section)
AUTOIMMUNE MASTER CHART
Feature SLE (Systemic Lupus) Rheumatoid Arthritis
(RA)
Polymyalgia
Rheumatica
(PMR)
Temporal
Arteritis /
Giant Cell
Arteritis
(GCA)
Fibromyalgia
(FMS)
Type Multisystem autoimmune
disease
Systemic autoimmune
inflammatory arthritis
Chronic
systemic
inflammatory
condition
Vasculitis of
large &
medium
vessels
Chronic pain
syndrome (not
inflammatory)
Key Patho Autoantibodies form immune
complexes → tissue
inflammation (skin, kidneys,
heart, vessels)
Synovial inflammation
→ pannus → joint
destruction
Inflammatory
arthritis, nonerosive;
associated w/
GCA
Vessel
inflammation
→ stenosis,
aneurysm,
ischemia
CNS dysfunction
→ amplified pain
signals
Common
Population
Women (childbearing age); ↑ in
African American & Hispanic
women
Women; ↑ with age Age ≥50 (peak
70–79); women
men
Average age
~70
More common in
females
Major
Symptoms
Fatigue, fever, weight loss,
anemia, lymphadenopathy;
malar rash; discoid rash
Bilateral & symmetric
joint swelling, warmth,
stiffness ≥1 hour;
systemic fatigue
Severe morning
stiffness;
aching
in shoulders &
hips; difficulty
dressing/getting
up
Severe
unilateral
headache,
scalp
tenderness, ja
w
claudication,
visual changes
Widespread
musculoskeletal
pain, fatigue, nonrestorative sleep,
headaches, IBS
Specific
Signs
Photosensitive “butterfly” rash;
discoid lesions
Swan neck, boutonniere
deformity; rheumatoid
nodules
“Gel
phenomenon”
(severe
stiffness after
rest)
Tender, cordlike temporal
artery; risk of
blindness
≥6 pain sites;
extreme fatigue;
normal labs
ExtraRenal/Orgs
Nephritis (proteinuria, RBC
casts)
Pericarditis, uveitis,
scleritis, vasculitis
Systemic
symptoms
possible
Vision loss,
stroke risk
Mood issues,
memory issues
Key Labs +ANA; anti–dsDNA + antiSmith specific; CBC
abnormalities; ↑ESR/CRP;
urinalysis protein/casts
↑ESR/CRP;
+RF, +Anti-CCP (very
specific); anemia
↑ESR & CRP;
normal RF,
ANA, anti-CCP
↑ESR & CRP;
biopsy gold
standard
Normal labs
(CBC, ESR/CRP,
thyroid).
Diagnosis based
on symptoms
Special
Labs
Antiphospholipid antibodies
(risk thrombosis, fetal loss)
Check CV risk; check
for TB before biologics
— Liver enzymes
may be ↑
Do NOT order
ANA/RF unless
symptoms of
SLE/RA
Treatment NSAIDs, Early rheumatology Steroids High-dose Amitriptyline,steroids, Hydroxychloroquine,
Methotrexate, anticoagulants,
biologics
referral; DMARDs
(MTX, HCQ);
NSAIDs;
steroids; Anti-TNF
biologics
(rapid
improvement)
steroids
immediately!;
+/- MTX or
Tocilizumab
for steroidsparing
SSRIs/SNRIs,
Cyclobenzaprine,
Pregabalin,
Gabapentin
Must
Avoid /
Caution
Methotrexate contraindicated
in pregnancy
Avoid biologics in
infection; screen TB
first
Risk for GCA
(educate
patients on
symptoms)
Delay →
bilateral
blindness
Avoid opioids,
NSAIDs not
effective
Referral Rheumatology; nephrology for
renal
Ophthalmology for
uveitis; surgery for
deformities
Rheumatology
if unclear
Rheumatology
+
Ophthalmolog
y or ED
urgently
Psych, Rheum,
Pain Mgmt if
needed
Unique
Pearl
Antiphospholipid syndrome →
clots + miscarriages
Rheumatoid nodules;
hand deformities
Very high risk
for GCA
development
Temporal
artery biopsy
gold standard
Pain without
inflammation;
labs normal
Medication Pearls ONLY from Your File
Medication Used For Key Notes
Hydroxychloroquine (Plaquenil) SLE & RA May require eye exams (risk retinal damage)
Methotrexate (MTX) SLE, RA, PMR (steroid-sparing),
GCA (steroid-sparing)
Do NOT use in pregnancy; give folic acid 1
mg daily
Biologics / anti-TNF (Humira, Enbrel,
Remicade)
RA Check TB before starting; ↑ risk infection,
squamous cell cancer, lymphoma
Tocilizumab (TCZ) GCA steroid-sparing Used for high-risk or adverse steroid effects
Steroids (High Dose) PMR, GCA, severe SLE Must start IMMEDIATELY in suspected GCA
Anticoagulation Lupus w/ antiphospholipid syndrome Prevent thrombosis
Amitriptyline, Duloxetine, Pregabalin,
Cyclobenzaprine
Fibromyalgia Helps pain, mood, and sleep
HIGH-YIELD EXAM CLUES
Clue Disorder
“Butterfly rash + proteinuria + anemia” SLE
“Morning stiffness 1 hour + symmetric swollen joints” RA
“Older patient can’t lift arms to dress + high ESR” PMR
“Unilateral headache + jaw claudication + risk
blindness”
Temporal Arteritis (GCA)
“Pain everywhere but labs normal, sleep problems, IBS” Fibromyalgia
DERMATOLOGY MASTER CHART
Condition Key Features Population Notes Diagnosis Treatment (from file) Pearls
Acne
Vulgaris
Comedones, papules,
pustules, nodules;
scarring with squeezing
Pomade acne common in
African Americans (hair
products)
Clinical;
evaluate
type,
severity
Normalize
keratinization, ↓
sebum, ↓ P. acnes;
varies by severity
Post-inflammatory
hyperpigmentation
common in darker
skin
Seborrheic
Dermatitis
Greasy, scaling plaques;
erythematous or
hypo/hyperpigmented in
dark skin
Common in
immunocompromised;
cradle cap infants
KOH prep
to rule
fungus
Adjust to hairgrooming practices;
topical agents
Color differences
make it subtle in
darker skin
Psoriasis Well-demarcated Young adulthood; linked Clinical Topical steroids (higher In dark skin →plaques w/ silvery scale;
may affect scalp, knees,
elbows
to arthritis & CV disease potency on extender
surfaces), retinoids,
UVB, emollients,
biologics for severe
violet plaques, gray
scale; risk
dyspigmentation
Atopic
Dermatitis
(Eczema)
Chronic pruritic rash;
flexural folds;
lichenification;
hyperpigmentation in
dark skin
Associated w/ asthma,
allergic rhinitis
Clinical Topical steroids +
emollients;
antihistamines if severe
itch
Appears “bumpy” in
dark skin;
dyspigmentation
risk
Contact
Dermatitis
Bright red pruritic rash
after irritant/allergen
exposure
Under-recognized in
darker skin
History +
exam
Identify & remove
irritant; topical steroids
1–2 weeks;
antihistamines;
oatmeal/calamine
Systemic steroids if
severe (gradual
taper)
Tinea
(Fungal)
Tan/white or
brown/black lesions in
skin of color
Tinea versicolor: nonpruritic hypopigmented
macules on trunk
KOH prep;
fungal
culture
Antifungals (not
specified beyond test in
file)
May lack redness in
dark skin
Rosacea Flushing,
papules/pustules,
telangiectasia; can
mimic acne but no
comedones
Harder to see erythema
in darker skin
Clinical Metronidazole
gel/cream, azelaic acid,
sulfacetamide cleanser,
OCPs/beta
blockers/clonidine (off
label), oral
tetracyclines;
isotretinoin per derm
Eye involvement
→ refer
ophthalmology
immediately
Alopecia Hair loss; scarring vs.
non-scarring; pattern
varies
Central Centrifugal
Cicatricial Alopecia
common in African
American women;
traction alopecia
Scalp
exam +
“hair pull”
Minoxidil; Finasteride
(Pregnancy X); treat
underlying cause
Traction alopecia
requires hair
practice education
SKIN CANCER MASTER MINI-CHART
Type Key Features Risk Factors Treatment Notes
Melanoma Dark, changing, irregular lesions;
ABCDE
Fair skin, dysplastic nevi, 50
nevi; men 50
Biopsy; check non–sun-exposed
areas in skin of color (palms, soles,
nails)
Basal Cell
Carcinoma
Pearly/waxy; ulcerated center;
bleeds easily; may be dark in skin of
color
Severe sunburns Biopsy; often translucent or glossy
black in Asian/dark skin
Squamous Cell
Carcinoma
Rough, scaly, non-healing lesion;
may mimic psoriasis/eczema in dark
skin
Most common skin cancer in
Blacks and Indians (non–sunexposed sites)
Biopsy; attention to lower
extremities, genital area, scalp
Actinic
Keratosis
Dry, scaly, red lesions; sun-exposed;
precancerous for SCC
Fair-skinned, older Cryotherapy, curettage, chemical
peel
Seborrheic
Keratosis
“Stuck-on” wart-like papules;
painless; middle age
Common in dark skin
(Dermatosis Papulosa Nigra)
Cryotherapy, curettage,
electrosurgery
Vehicle Selection Cheat Sheet
Vehicle Best Use Notes
Ointment Thick plaques (psoriasis) Most potent; avoid hairy areas
Cream Mild inflammatory lesions Less potent
Lotion Moist, pruritic, large areas “Cooling effect”
Gel Hairy areas Transparent; good absorptionHIGH-YIELD DERM EXAM CLUES
Clue Likely Condition
Hypopigmented trunk macules, non-pruritic Tinea versicolor
Violet plaques w/ gray scale Psoriasis in dark skin
Flushing + papules but no comedones Rosacea
Papules worsen with hair products Pomade Acne
“Stuck on” papules, dark, small on face Seborrheic Keratosis (DPN variant)
Scaly non-healing lesion that bleeds SCC
Pearly ulcerated lesion BCC