Internal Medicine

Every organ system, diagnosis, classification, medication, risk score, and management strategy — cardiovascular through rheumatology — in one place.

01 Systems-Based Approach

Internal medicine is the parent specialty of adult non-surgical care — its scope spans every organ system, and its intellectual core is the integration of multi-system pathology in a single patient. The internist's daily work is diagnosis under uncertainty, multi-drug optimization, and the longitudinal management of chronic disease superimposed on acute illness. Unlike organ-based subspecialties, general internal medicine owns the whole patient, which means the differential diagnosis list is always broad before it is narrow.

The Organ-System Framework

SystemCore Diagnoses Managed by IMKey Diagnostic Anchors
CardiovascularHTN, HF, CAD, AFib, VTE, valvular diseaseECG, troponin, BNP, echo
PulmonaryCOPD, asthma, pneumonia, PE, ILD, pleural effusionPFTs, CXR, CT chest, ABG
GI / HepatologyGERD, PUD, IBD, cirrhosis, pancreatitis, GI bleedLFTs, lipase, endoscopy, imaging
NephrologyAKI, CKD, electrolyte disorders, glomerulonephritisCr, BUN, UA, electrolytes, biopsy
EndocrinologyDM (types 1/2), thyroid, adrenal, calcium/boneA1C, TSH, cortisol, calcium/PTH
HematologyAnemia, coagulopathy, thrombocytopenia, VTECBC, smear, iron studies, coags
Infectious DiseaseSepsis, pneumonia, UTI, endocarditis, HIV, C. diffCultures, procalcitonin, imaging
RheumatologyRA, SLE, gout, vasculitis, sarcoidosisANA, RF, CCP, uric acid, ESR/CRP
Diagram of the major organs of the human body including heart, lungs, liver, kidneys, and GI tract
Figure 1 — Major Organ Systems. Internal medicine integrates pathology across all organ systems shown. The internist must understand how disease in one system propagates to others (e.g., CKD driving anemia, hyperkalemia, and secondary hyperparathyroidism simultaneously). Source: Wikimedia Commons. Public domain.
The hallmark of internal medicine reasoning is Occam's razor vs Hickam's dictum. A medical student looks for one diagnosis to explain everything (Occam's). An internist knows that a 72-year-old with DM, CKD, CHF, and COPD who presents with dyspnea may have all four contributing simultaneously (Hickam's). The skill is determining relative contribution, not forcing a single answer.

02 The Internal Medicine Physical Exam

The IM exam is the most comprehensive in medicine — a full head-to-toe assessment on admission, then focused daily exams targeting active problems. Key elements that change management daily: volume status, cardiopulmonary findings, abdominal exam, and mental status.

Volume Status Assessment

FindingHypovolemiaEuvolemiaHypervolemia
JVPFlat, < 6 cm H₂O6–8 cm H₂OElevated > 8 cm, hepatojugular reflux +
Mucous membranesDry, tackyMoistMoist
Skin turgorTenting (less reliable in elderly)NormalTaut, shiny
EdemaAbsentAbsentPitting (grade 1–4+)
OrthostaticsSBP drop ≥ 20 or HR rise ≥ 20 on standingNormalUsually normal
Urine output< 0.5 mL/kg/hr0.5–1.0 mL/kg/hrVariable

Cardiac Auscultation — Murmur Grading (Levine Scale)

GradeDescription
I/VIBarely audible, heard only in a quiet room with concentration
II/VISoft but readily audible
III/VIModerately loud, no thrill
IV/VILoud with palpable thrill
V/VIVery loud, thrill present, audible with stethoscope partially off chest
VI/VIAudible without stethoscope
Anterior view of the human heart showing the four chambers, coronary arteries, and great vessels
Figure 2 — Anterior Heart Anatomy. The four chambers, coronary arteries, and great vessels. Understanding surface anatomy guides auscultation: aortic valve (right 2nd ICS), pulmonic (left 2nd ICS), tricuspid (left lower sternal border), mitral (apex, 5th ICS MCL). Source: Wikimedia Commons, by Patrick J. Lynch. Licensed under CC BY 2.5.

Lung Auscultation Findings

SoundCharacterImplies
Crackles (rales)Discontinuous, inspiratory, fine or coarseFine = fibrosis, early CHF; Coarse = pneumonia, pulmonary edema
WheezesHigh-pitched, musical, expiratoryBronchospasm (asthma, COPD), CHF ("cardiac asthma")
RhonchiLow-pitched, rumbling, clears with coughSecretions in large airways
StridorHigh-pitched, inspiratory, monophonicUpper airway obstruction — emergency
Diminished/absentReduced air entryEffusion, pneumothorax, severe COPD, obesity
Egophony ("E to A")Spoken "E" sounds like "A"Consolidation (pneumonia) above effusion

03 Key Terminology

TermDefinition / Clinical Relevance
PreloadVolume/pressure stretching the ventricle at end-diastole (approximated by LVEDP, CVP). Elevated in volume overload; reduced in hemorrhage/dehydration.
AfterloadResistance the ventricle must overcome to eject blood (approximated by SVR, MAP). Elevated in HTN, aortic stenosis. Vasodilators reduce afterload.
Anion gapNa − (Cl + HCO₃). Normal 8–12. Elevated = unmeasured acid accumulation (MUDPILES: Methanol, Uremia, DKA, Propylene glycol, INH/Iron, Lactic acidosis, Ethylene glycol, Salicylates).
GFRVolume of plasma filtered by the glomeruli per minute. Gold standard for kidney function. Normal ~120 mL/min/1.73 m². Estimated by CKD-EPI equation (preferred over MDRD).
A-a gradientPAO₂ − PaO₂. Normal = 2.5 + (0.21 × age). Elevated in V/Q mismatch, shunt, diffusion impairment. Normal in hypoventilation.
Sensitivity / SpecificitySensitivity = true positives / (TP + FN) — rules OUT when negative (SnNOut). Specificity = TN / (TN + FP) — rules IN when positive (SpPIn).
NNT / NNHNumber needed to treat (benefit one patient) and number needed to harm. NNT = 1/ARR. Lower NNT = more effective intervention.

04 Hypertension Cardiovascular

Hypertension affects ~47% of US adults under the 2017 ACC/AHA guideline thresholds. It is the single largest modifiable risk factor for stroke, MI, HF, CKD, and aortic dissection. Most cases (90–95%) are primary (essential) — no identifiable cause. Secondary causes must be considered in resistant HTN, onset < 30 years, or abrupt worsening.

Classification (ACC/AHA 2017)

CategorySBP (mmHg)DBP (mmHg)Action
Normal< 120< 80Reassess annually
Elevated120–129< 80Lifestyle modification
Stage 1 HTN130–13980–89Lifestyle + meds if ASCVD risk ≥ 10%
Stage 2 HTN≥ 140≥ 90Lifestyle + medication (usually 2 agents)
Hypertensive crisis> 180> 120Urgency (no organ damage) vs emergency (end-organ damage — treat IV)

Secondary Causes of HTN

CauseClueWorkup
Renal artery stenosisRefractory HTN, flash pulmonary edema, renal bruit, Cr rise with ACEIRenal duplex, CTA/MRA
Primary aldosteronismHypokalemia, resistant HTN, adrenal incidentalomaAldosterone/renin ratio (> 30 with aldo > 15)
PheochromocytomaParoxysmal HTN, headache, palpitations, diaphoresis (triad)24-hr urine metanephrines or plasma free metanephrines
Cushing syndromeCentral obesity, striae, moon facies, hyperglycemia24-hr urine cortisol, overnight dexamethasone suppression, late-night salivary cortisol
Coarctation of aortaYoung patient, upper > lower extremity BP, rib notching on CXREcho, CT/MRA
OSASnoring, daytime somnolence, obesity, resistant HTNPolysomnography (AHI ≥ 5)
Illustration comparing normal blood pressure vessel to a hypertensive vessel with increased pressure on arterial walls
Figure 3 — Hypertension Pathophysiology. Chronic elevated pressure damages the arterial endothelium, promoting atherosclerosis, LV hypertrophy, and end-organ injury (kidneys, brain, retina, heart). Source: Wikimedia Commons, by BruceBlaus. Licensed under CC BY 3.0.

First-Line Agents

ClassExamplesPreferred IndicationKey Pearl
ACE inhibitorsLisinopril 10–40 mg, enalapril 5–20 mg BIDDM with proteinuria, HFrEF, post-MI, CKDMonitor K+ and Cr; cough in ~10% (switch to ARB)
ARBsLosartan 50–100 mg, valsartan 80–320 mgSame as ACEI (ACEI-intolerant)Do NOT combine with ACEI (hyperkalemia, no benefit)
CCBs (dihydropyridine)Amlodipine 5–10 mg, nifedipine ERElderly, black patients, isolated systolic HTNPeripheral edema is dose-dependent, not allergic
Thiazide diureticsChlorthalidone 12.5–25 mg, HCTZ 25 mgElderly, black patients, osteoporosisChlorthalidone preferred (longer half-life, better outcomes data); hypoK+, hypoNa+
Hypertensive Emergency Management

Target: reduce MAP by no more than 25% in the first hour, then to 160/100 over the next 2–6 hours. Avoid precipitous drops (risk of watershed stroke). IV agents: nicardipine (5–15 mg/hr, titratable), labetalol (20 mg IV bolus then drip), nitroprusside (0.25–10 mcg/kg/min — cyanide toxicity risk with prolonged use). Exception: aortic dissection — target HR < 60 and SBP < 120 rapidly with IV esmolol or labetalol before vasodilators.

05 Heart Failure Cardiovascular

Heart failure is a clinical syndrome of dyspnea, fatigue, and volume overload resulting from structural or functional cardiac impairment. Prevalence: ~6.7 million US adults. Five-year mortality: ~50%. HF is the #1 cause of hospitalization in adults > 65.

Classification by Ejection Fraction

CategoryEFKey FeatureEvidence-Based Therapies
HFrEF (reduced)≤ 40%Systolic dysfunction, dilated LVGDMT: ACEI/ARB/ARNI + BB + MRA + SGLT2i (the "four pillars")
HFmrEF (mildly reduced)41–49%Intermediate — may respond to HFrEF therapiesSGLT2i, consider ARNI/BB/MRA
HFpEF (preserved)≥ 50%Diastolic dysfunction, stiff LV, normal sizeSGLT2i (EMPEROR-Preserved, DELIVER), diuretics, BP/rate control

NYHA Functional Classification

ClassSymptoms
INo limitation of physical activity; ordinary activity does not cause symptoms
IISlight limitation; comfortable at rest, ordinary activity causes fatigue/dyspnea/palpitations
IIIMarked limitation; comfortable at rest, less-than-ordinary activity causes symptoms
IVUnable to carry on any physical activity without symptoms; symptoms at rest

ACC/AHA Stages

StageDescriptionManagement
AAt risk (HTN, DM, CAD) but no structural disease or symptomsRisk factor control, ACEI if appropriate
BStructural heart disease (LVH, prior MI, low EF) but no symptomsAll Stage A + ACEI/ARB + beta-blocker
CStructural disease with current or prior HF symptomsFull GDMT, devices (ICD, CRT), diuretics
DRefractory HF requiring advanced therapiesLVAD, transplant, inotropes, palliative care

The Four Pillars of HFrEF (2022 AHA/ACC/HFSA Guideline)

All four should be initiated and uptitrated as tolerated — each independently reduces mortality (Heidenreich et al., 2022):

PillarDrugTarget DoseMortality Reduction
ARNI (or ACEI/ARB)Sacubitril/valsartan (Entresto)97/103 mg BID~20% (PARADIGM-HF)
Beta-blockerCarvedilol, metoprolol succinate, bisoprololCarvedilol 25 mg BID (50 if >85 kg)~34% (MERIT-HF, COPERNICUS)
MRASpironolactone 25–50 mg or eplerenone 50 mgSpironolactone 50 mg daily~30% (RALES)
SGLT2 inhibitorDapagliflozin 10 mg or empagliflozin 10 mg10 mg daily (no titration)~17% (DAPA-HF, EMPEROR-Reduced)
Start all four pillars early — do not wait to uptitrate one before starting the next. The largest mortality benefit comes from getting all four on board quickly, even at low doses, rather than maximizing one agent sequentially.
Illustration comparing a normal heart with a heart in failure showing dilated chambers and reduced contractility
Figure 4 — Heart Failure. Comparison of normal cardiac output with reduced output in systolic heart failure (dilated, weakened LV) and diastolic heart failure (thickened, stiff LV). Source: Wikimedia Commons, by BruceBlaus. Licensed under CC BY 3.0.
Acute Decompensated HF (ADHF) — Emergency

Presentation: Acute dyspnea, orthopnea, PND, crackles, S3 gallop, elevated JVP, peripheral edema, weight gain. BNP > 400 pg/mL (or NT-proBNP > 900 age-adjusted) strongly supports diagnosis. Management: IV furosemide (double home dose or 40 mg if diuretic-naive, target UOP 100–150 mL/hr), upright positioning, supplemental O₂/NIPPV if SpO₂ < 90%, hold beta-blocker if hypotensive or in cardiogenic shock. Vasodilators (IV nitroglycerin) if SBP > 100. Daily weights and strict I&O. Transition to oral diuretics when euvolemic.

06 Coronary Artery Disease Cardiovascular

CAD is atherosclerotic narrowing of the coronary arteries — the #1 cause of death worldwide. Manifests as stable angina (supply-demand mismatch with exertion), unstable angina (rest pain, new-onset, crescendo), NSTEMI (troponin elevation without ST elevation), or STEMI (transmural ischemia with ST elevation — door-to-balloon < 90 minutes).

Acute Coronary Syndrome Spectrum

EntityTroponinECGPathologyManagement
Stable anginaNormalST depression with exerciseFixed stenosis ≥ 70%Anti-anginals, risk factor modification, stress test
Unstable anginaNormalST depression, T-wave inversion, or normalPlaque rupture, non-occlusive thrombusAntiplatelet, anticoagulant, invasive strategy
NSTEMIElevatedST depression, T-wave inversionPartial occlusion with myocyte necrosisSame as UA + urgent cath (< 24 hr if high risk)
STEMIElevated≥ 1 mm ST elevation in 2+ contiguous leadsComplete occlusion (transmural infarct)Emergent PCI (door-to-balloon < 90 min)

Post-MI GDMT

All patients without contraindication: DAPT (ASA 81 mg + ticagrelor 90 mg BID or clopidogrel 75 mg daily × 12 months), high-intensity statin (atorvastatin 80 mg), beta-blocker (metoprolol succinate, carvedilol), ACEI/ARB (especially if EF ≤ 40%, anterior MI, or DM). Cardiac rehab referral is a Class I recommendation (Virani et al., 2021).

Cross-section of a coronary artery showing progressive plaque buildup narrowing the lumen
Figure 5 — Coronary Artery Plaque. Progressive atherosclerotic narrowing of a coronary artery. Plaque rupture exposes the lipid-rich core to circulating blood, triggering platelet aggregation and thrombus formation — the mechanism of acute coronary syndrome. Source: Wikimedia Commons, by BruceBlaus. Licensed under CC BY 3.0.

07 Atrial Fibrillation Cardiovascular

AFib is the most common sustained arrhythmia — irregular, chaotic atrial activity replacing organized P waves, producing an "irregularly irregular" ventricular response. Prevalence: ~5 million US adults, rising with age (10% of those > 80). Key risks: 5× stroke risk, 2× mortality, HF progression.

Classification

TypeDurationTerminates Spontaneously?
Paroxysmal≤ 7 days (usually < 48 hr)Yes
Persistent> 7 daysNo — requires cardioversion
Long-standing persistent> 12 monthsNo, but rhythm control still considered
PermanentIndefinite (accepted by patient/clinician)Rate control strategy only
ValvularAssociated with moderate–severe mitral stenosis or mechanical heart valveRequires warfarin (DOACs not approved)

CHA₂DS₂-VASc Score (Stroke Risk)

FactorPoints
CHF (or LVEF ≤ 40%)1
Hypertension1
Age ≥ 752
Diabetes1
Stroke/TIA/VTE history2
Vascular disease (MI, PAD, aortic plaque)1
Age 65–741
Sex category (female)1

Score ≥ 2 in men or ≥ 3 in women: anticoagulate. Score 1 in men / 2 in women: consider anticoagulation. Score 0 in men / 1 in women: no anticoagulation needed.

Rate vs Rhythm Control

Rate control: Target resting HR < 110 bpm (lenient) or < 80 bpm (strict — no proven benefit over lenient per RACE II). Agents: beta-blockers (metoprolol, carvedilol), non-DHP CCBs (diltiazem, verapamil — avoid in HFrEF), digoxin (adjunct, narrow therapeutic window 0.5–0.9 ng/mL). Rhythm control: Favored in symptomatic patients, early AFib, younger patients — EAST-AFNET 4 showed early rhythm control reduces CV outcomes (Kirchhof et al., 2020). Agents: flecainide (no structural heart disease), amiodarone (any substrate, but toxicity profile), sotalol, dofetilide (requires inpatient initiation with QTc monitoring). Catheter ablation (pulmonary vein isolation) for symptomatic drug-refractory AFib.

08 Venous Thromboembolism (DVT/PE) Cardiovascular

VTE encompasses DVT and PE — a single disease continuum. DVT: most commonly in the deep veins of the lower extremities (iliac, femoral, popliteal). PE: thrombus embolizes to pulmonary vasculature — can be fatal. Virchow's triad: stasis, endothelial injury, hypercoagulability.

Wells Score — DVT

CriterionPoints
Active cancer (treatment within 6 months)1
Paralysis/paresis/recent immobilization of lower extremity1
Bedridden > 3 days or major surgery within 12 weeks1
Localized tenderness along deep venous system1
Entire leg swollen1
Calf swelling > 3 cm vs asymptomatic side1
Pitting edema confined to symptomatic leg1
Collateral superficial veins (non-varicose)1
Alternative diagnosis as likely or more likely−2

≥ 2 points = DVT likely → ultrasound. < 2 points = DVT unlikely → D-dimer first (if negative, DVT excluded).

PE Severity & Management

CategoryHemodynamicsRV DysfunctionTroponinTreatment
Low-riskStableNoNormalAnticoagulation alone (DOAC preferred)
SubmassiveStableYes (echo/CT)Often elevatedAnticoagulation ± catheter-directed therapy; monitor in ICU
MassiveHypotensive (SBP < 90)YesElevatedSystemic thrombolysis (tPA 100 mg over 2 hr), surgical/catheter embolectomy

Anticoagulation for VTE

First-line: DOACs — apixaban (10 mg BID × 7 days, then 5 mg BID) or rivaroxaban (15 mg BID × 21 days, then 20 mg daily). Alternative: LMWH bridge to warfarin (target INR 2–3). Duration: provoked VTE = 3 months; unprovoked = at least 3 months then reassess (consider extended if low bleeding risk); cancer-associated = LMWH or DOAC long-term.

09 COPD Pulmonary

COPD is a chronic, progressive airflow limitation that is not fully reversible — caused by significant exposure to noxious particles (cigarette smoke in > 80% of cases). It encompasses chronic bronchitis (productive cough ≥ 3 months/year for 2 consecutive years) and emphysema (destruction of alveolar walls, loss of elastic recoil, air trapping). Third leading cause of death worldwide.

Diagnosis

Spirometry is required: post-bronchodilator FEV₁/FVC < 0.70 confirms airflow obstruction. Severity is graded by FEV₁:

GOLD StageFEV₁ (% predicted)Severity
1≥ 80%Mild
250–79%Moderate
330–49%Severe
4< 30%Very severe

GOLD ABE Assessment (2023 Update)

GroupExacerbation HistorySymptoms (mMRC/CAT)Initial Therapy
A0–1 moderate (no hospitalization)Low (mMRC 0–1, CAT < 10)Bronchodilator (SABA or LABA or LAMA)
B0–1 moderate (no hospitalization)High (mMRC ≥ 2, CAT ≥ 10)LABA + LAMA
E≥ 2 moderate OR ≥ 1 hospitalizationAnyLABA + LAMA (add ICS if eos ≥ 300)
Acute COPD Exacerbation

Triggered by viral/bacterial infection, pollution, or non-adherence. Treatment: SABA (albuterol nebulizer q4–6h), systemic corticosteroids (prednisone 40 mg daily × 5 days — REDUCE trial showed 5 days = 14 days), antibiotics (if purulent sputum or severe exacerbation — azithromycin 500 mg then 250 mg × 4 days, or doxycycline, or amoxicillin-clavulanate). NIPPV (BiPAP) reduces intubation and mortality in acute hypercapnic respiratory failure (pH < 7.35, PaCO₂ > 45). Supplemental O₂ target: SpO₂ 88–92% — avoid hyperoxia (suppresses hypoxic drive, worsens CO₂ retention).

Comparison of normal lung alveoli with emphysematous destroyed alveoli showing loss of surface area
Figure 6 — Normal vs. Emphysematous Lung. In emphysema, destruction of alveolar walls reduces gas exchange surface area and creates hyperinflated air spaces with air trapping. Source: Wikimedia Commons, by BruceBlaus. Licensed under CC BY 3.0.

10 Asthma Pulmonary

Asthma is reversible airflow obstruction due to airway hyperresponsiveness, chronic inflammation, and mucus hypersecretion. Unlike COPD, spirometry shows improvement post-bronchodilator (≥ 12% and ≥ 200 mL increase in FEV₁). Peak incidence in childhood but can present at any age. Type 2 (eosinophilic) inflammation drives most cases — IL-4, IL-5, IL-13 pathway.

Stepwise Therapy (GINA 2023)

StepPreferred ControllerReliever
1Low-dose ICS-formoterol PRNICS-formoterol PRN
2Low-dose ICS daily (or ICS-formoterol PRN)ICS-formoterol PRN
3Low-dose ICS-LABA (budesonide/formoterol)ICS-formoterol PRN
4Medium-dose ICS-LABAICS-formoterol PRN
5High-dose ICS-LABA + add-on (tiotropium, anti-IL5, anti-IgE, anti-IL4R)ICS-formoterol PRN
GINA 2023 no longer recommends SABA-only treatment at any step. All patients should receive ICS at every step (even Step 1 as PRN ICS-formoterol). SABA monotherapy increases exacerbation risk and death.
Status Asthmaticus

Life-threatening asthma not responding to standard bronchodilators. Management: continuous albuterol nebulization, ipratropium bromide 0.5 mg q20min × 3, IV methylprednisolone 125 mg, IV magnesium sulfate 2 g over 20 min (smooth muscle relaxation). If impending respiratory failure (silent chest, declining mental status, PaCO₂ rising): intubation with ketamine (bronchodilatory) for induction, low tidal volume/low rate ventilation (permissive hypercapnia — avoid dynamic hyperinflation).

11 Pneumonia Pulmonary

Pneumonia is infection of the lung parenchyma causing consolidation. Leading infectious cause of death globally. Classification determines empiric antibiotic choice:

TypeCommon OrganismsEmpiric Treatment
Community-acquired (CAP) — outpatient, no comorbiditiesS. pneumoniae, M. pneumoniae, H. influenzae, respiratory virusesAmoxicillin 1 g TID or doxycycline 100 mg BID
CAP — outpatient with comorbiditiesSame + S. aureus, gram-negativesAmoxicillin-clavulanate + macrolide, or respiratory fluoroquinolone (levofloxacin 750 mg)
CAP — inpatient (non-ICU)Same spectrumBeta-lactam (ceftriaxone 2 g IV, or ampicillin-sulbactam) + macrolide (azithromycin), or respiratory FQ alone
CAP — ICUAdd Legionella, S. aureusBeta-lactam + macrolide (both required); add vancomycin if MRSA risk
Hospital-acquired (HAP) / VAPPseudomonas, MRSA, Acinetobacter, ESBL gram-negativesAnti-pseudomonal beta-lactam (piperacillin-tazobactam, cefepime, or meropenem) ± vancomycin/linezolid if MRSA risk

Severity Assessment — CURB-65

CriterionPoints
Confusion (new)1
Urea > 7 mmol/L (BUN > 19)1
Respiratory rate ≥ 301
Blood pressure (SBP < 90 or DBP ≤ 60)1
Age ≥ 651

0–1: outpatient. 2: consider short inpatient stay. 3–5: inpatient, 4–5 consider ICU.

12 Interstitial Lung Disease & Pleural Disease Pulmonary

ILD is a group of disorders causing progressive fibrosis or inflammation of the lung interstitium. PFTs show a restrictive pattern: reduced FVC and TLC with preserved or elevated FEV₁/FVC ratio. DLCO is characteristically reduced (impaired gas diffusion across thickened alveolar membrane). HRCT is the key diagnostic imaging modality.

Major ILD Categories

CategoryExamplesKey Features
Idiopathic pulmonary fibrosis (IPF)UIP pattern on HRCT (basal-predominant honeycombing, traction bronchiectasis). Median survival 3–5 yr. Antifibrotics: pirfenidone (Esbriet), nintedanib (Ofev)
Connective tissue disease-ILDRA-ILD, SSc-ILD, myositis-ILDScreen all CTD patients with PFTs + HRCT. Treatment: immunosuppression + antifibrotics
Hypersensitivity pneumonitisBird fancier's, farmer's lungAntigen exposure history critical. Remove exposure. Acute: corticosteroids. Chronic: may progress to fibrosis
Sarcoidosis-relatedNon-caseating granulomas. Bilateral hilar lymphadenopathy. See Section 36
Drug-inducedMethotrexate, amiodarone, bleomycin, nitrofurantoinTemporal relation to drug initiation. Withdraw offending agent

Pleural Effusion — Light's Criteria

Thoracentesis fluid is exudative if any one criterion is met (sensitivity 98%, specificity 83%):

CriterionExudative Threshold
Pleural protein / serum protein> 0.5
Pleural LDH / serum LDH> 0.6
Pleural LDH> 2/3 upper limit of normal serum LDH

Common transudates: CHF (most common overall), cirrhosis (hepatic hydrothorax), nephrotic syndrome. Common exudates: pneumonia (parapneumonic), malignancy, PE, TB, autoimmune.

13 GERD & Peptic Ulcer Disease GI

GERD: reflux of gastric acid into the esophagus causing heartburn, regurgitation, and risk of erosive esophagitis, stricture, Barrett's esophagus (intestinal metaplasia — premalignant, requires surveillance EGD). Diagnosis: clinical for typical symptoms; pH monitoring or impedance testing for refractory cases. Treatment: lifestyle (elevate HOB, avoid eating 3 hr before bed, weight loss) + PPI (omeprazole 20 mg, pantoprazole 40 mg daily). Step down to H2RA if controlled. Long-term PPI risks (generally low but real): C. diff, hypomagnesemia, osteoporosis, B12 deficiency, AIN.

PUD: mucosal ulceration of the stomach or duodenum. Two dominant causes: H. pylori infection (~60% duodenal, ~40% gastric) and NSAIDs. Diagnosis: EGD (gold standard) — biopsy gastric ulcers to rule out malignancy. H. pylori testing: stool antigen (preferred), urea breath test, or biopsy-based testing. Treatment: PPI BID + triple therapy (clarithromycin 500 mg BID + amoxicillin 1 g BID × 14 days) or bismuth quadruple therapy if clarithromycin resistance is suspected (> 15% local rate).

Anatomical illustration of the abdominal organs including stomach, liver, intestines, and pancreas
Figure 7 — Abdominal Organ Anatomy. The major GI organs relevant to internal medicine: stomach (PUD, GERD), liver (cirrhosis, hepatitis), pancreas (pancreatitis), small and large intestine (IBD, celiac, malabsorption). Source: Wikimedia Commons, by BruceBlaus. Licensed under CC BY 3.0.

14 Inflammatory Bowel Disease GI

IBD comprises two chronic idiopathic inflammatory disorders of the GI tract. Bimodal age onset: 15–30 and 50–70.

FeatureCrohn's DiseaseUlcerative Colitis
LocationMouth to anus (terminal ileum most common)Rectum → proximal colon (continuous)
DepthTransmural (full-thickness)Mucosa/submucosa only
PatternSkip lesions, cobblestoningContinuous, no skip lesions
HistologyNon-caseating granulomas (pathognomonic)Crypt abscesses, pseudopolyps
ComplicationsFistulae, strictures, abscesses, B12 deficiency (ileal disease)Toxic megacolon, colorectal cancer risk
SurgeryNot curative (recurrence at anastomosis)Total proctocolectomy is curative
SmokingWorsens diseaseProtective (paradoxically)

Treatment Ladder

Mild: 5-ASA (mesalamine — UC only, not effective in Crohn's), budesonide (ileal/right-sided Crohn's). Moderate-severe: corticosteroids for induction only (prednisone 40–60 mg taper over 8–12 weeks — never maintenance), immunomodulators (azathioprine/6-MP, methotrexate for Crohn's). Moderate-severe or steroid-refractory: biologics — anti-TNF (infliximab, adalimumab), anti-integrin (vedolizumab — gut-selective), anti-IL-12/23 (ustekinumab), JAK inhibitors (tofacitinib — UC only). Screen for TB and hepatitis B before starting biologics.

15 Liver Disease & Cirrhosis GI

Cirrhosis is the end stage of chronic liver injury — replacement of functional hepatocytes with fibrosis and regenerative nodules. Common causes: alcohol (60–70%), NAFLD/NASH (rising rapidly, now called MASLD/MASH), hepatitis C, hepatitis B, autoimmune hepatitis, hemochromatosis, Wilson disease, alpha-1 antitrypsin deficiency, PBC, PSC.

Child-Pugh Score

Parameter1 Point2 Points3 Points
Bilirubin (mg/dL)< 22–3> 3
Albumin (g/dL)> 3.52.8–3.5< 2.8
INR< 1.71.7–2.3> 2.3
AscitesNoneSlight (controlled)Moderate-severe (refractory)
EncephalopathyNoneGrade I–IIGrade III–IV

Class A (5–6): well-compensated, 1-year survival ~100%. Class B (7–9): significant functional compromise, 1-year survival ~80%. Class C (10–15): decompensated, 1-year survival ~45%.

MELD-Na Score

Used for organ allocation in liver transplantation. Variables: bilirubin, INR, creatinine, sodium. Range 6–40. MELD ≥ 15 = consider transplant listing. MELD ≥ 30 = high 3-month mortality (> 50%).

Complications of Cirrhosis

ComplicationPathophysiologyManagement
AscitesPortal HTN + low albumin + splanchnic vasodilationNa restriction (< 2 g/day), spironolactone 100 mg + furosemide 40 mg (100:40 ratio), paracentesis, TIPS for refractory
SBPTranslocation of gut bacteria into ascitic fluidDiagnostic paracentesis (PMN ≥ 250 = SBP). Treat: cefotaxime 2 g IV q8h. Prophylaxis: ciprofloxacin or TMP-SMX if prior SBP or GI bleed
Variceal bleedingPortal HTN → portosystemic collaterals → esophageal/gastric varicesPrimary prophylaxis: NSBB (propranolol, carvedilol) or EBL. Acute bleed: octreotide + ceftriaxone + emergent EGD with banding. TIPS if refractory
Hepatic encephalopathyAmmonia (and other toxins) bypass hepatic clearanceLactulose (titrate to 3–4 BMs/day) + rifaximin 550 mg BID. Identify precipitant (infection, GI bleed, constipation, meds, electrolytes)
Hepatorenal syndromeSplanchnic vasodilation → renal vasoconstrictionType 1 (rapid, Cr doubles in < 2 weeks): IV albumin + vasopressors (terlipressin preferred, or norepinephrine/midodrine-octreotide). Definitive: liver transplant
HCC screeningCirrhosis of any cause = HCC riskUltrasound ± AFP every 6 months
Photograph of a cirrhotic liver showing nodular surface and fibrotic changes
Figure 8 — Cirrhotic Liver. Gross specimen showing the nodular, fibrotic surface characteristic of end-stage cirrhosis. The regenerative nodules separated by fibrous septa distort the hepatic architecture and obstruct portal venous flow, driving portal hypertension. Source: Wikimedia Commons. Public domain.

16 Pancreatitis GI

Acute pancreatitis: inflammatory injury to the pancreas. Diagnosis requires 2 of 3: (1) characteristic abdominal pain (epigastric, radiating to back), (2) lipase ≥ 3× ULN, (3) characteristic imaging findings on CT. Causes: gallstones (~40%) and alcohol (~30%) account for ~70%. Others: hypertriglyceridemia (> 1000 mg/dL), post-ERCP, drugs (azathioprine, valproic acid, didanosine), autoimmune (IgG4-related), trauma.

Severity — Revised Atlanta Classification

SeverityOrgan FailureLocal ComplicationsMortality
MildNoneNone< 1%
Moderately severeTransient (< 48 hr) or local complications alonePeripancreatic collections, necrosis~5%
SeverePersistent (> 48 hr)Usually present20–40%

Management: Aggressive IV fluid resuscitation (LR preferred, goal-directed — target UOP ≥ 0.5 mL/kg/hr), pain control (IV opioids, multimodal), early oral feeding as tolerated (within 24 hr if mild — no need for NPO until "pain-free"). Antibiotics only if infected necrosis is suspected or confirmed (not for prophylaxis in sterile necrosis). Cholecystectomy before discharge for gallstone pancreatitis (index admission if mild). Necrotizing pancreatitis with infection: step-up approach — percutaneous drainage first, surgical necrosectomy if drainage fails (van Santvoort et al., 2010 — PANTER trial).

17 Celiac Disease & Malabsorption GI

Celiac disease: autoimmune enteropathy triggered by dietary gluten (wheat, barley, rye) in genetically susceptible individuals (HLA-DQ2 in ~95%, DQ8 in ~5%). Prevalence ~1%. Presents with chronic diarrhea, steatorrhea, weight loss, iron deficiency anemia (refractory to oral iron), and dermatitis herpetiformis (pruritic vesicular rash on extensor surfaces). Can be silent — screen high-risk groups (T1DM, Down syndrome, autoimmune thyroid, first-degree relatives).

Diagnosis: Serology — tissue transglutaminase IgA (tTG-IgA) is the preferred screening test (sensitivity/specificity > 95%). Check total IgA simultaneously (IgA deficiency in ~3% of celiacs causes false-negative). Confirm with duodenal biopsy: villous atrophy, crypt hyperplasia, intraepithelial lymphocytosis (Marsh classification). Patient must be on gluten-containing diet during workup. Treatment: strict lifelong gluten-free diet — clinical improvement in weeks, mucosal healing in months.

Malabsorption — Differential by Nutrient

DeficiencyAbsorption SiteCauses
IronDuodenumCeliac, Crohn's (proximal), gastrectomy, chronic blood loss
B12Terminal ileumCrohn's (ileal), pernicious anemia, ileal resection, bacterial overgrowth, metformin
FolateProximal jejunumCeliac, tropical sprue, alcohol, phenytoin, methotrexate
Fat-soluble vitamins (A, D, E, K)Proximal small bowel (bile-dependent)Cholestatic liver disease, pancreatic insufficiency, short bowel, bile salt malabsorption
CalciumDuodenum/proximal jejunumVitamin D deficiency, celiac, post-bariatric surgery

18 Acute Kidney Injury Nephrology

AKI is defined by KDIGO as any of: Cr rise ≥ 0.3 mg/dL within 48 hr, Cr rise ≥ 1.5× baseline within 7 days, or UOP < 0.5 mL/kg/hr for 6 hours. Incidence: 10–15% of hospitalized patients, up to 50% in ICU.

KDIGO Staging

StageSerum CreatinineUrine Output
11.5–1.9× baseline OR ≥ 0.3 mg/dL increase< 0.5 mL/kg/hr for 6–12 hr
22.0–2.9× baseline< 0.5 mL/kg/hr for ≥ 12 hr
3≥ 3.0× baseline OR Cr ≥ 4.0 OR initiation of RRT< 0.3 mL/kg/hr for ≥ 24 hr OR anuria ≥ 12 hr

Etiology — Pre-Renal vs Intrinsic vs Post-Renal

CategoryMechanismFENaBUN/Cr RatioUrine FindingsCommon Causes
Pre-renal (~60%)Decreased perfusion< 1%> 20:1Bland, concentratedDehydration, hemorrhage, HF, sepsis (early), hepatorenal
Intrinsic (~35%)Tubular, glomerular, or interstitial injury> 2%~10–15:1Muddy brown granular casts (ATN), RBC casts (GN), WBC casts/eosinophils (AIN)ATN (ischemic/toxic), GN, AIN (drugs), TTP/HUS
Post-renal (~5%)ObstructionVariableVariableVariableBPH, kidney stones, tumor, retroperitoneal fibrosis
FENa is unreliable on diuretics — use FEUrea instead (< 35% = pre-renal). Every AKI workup should include: renal US (rule out obstruction), UA with microscopy (casts!), and FENa or FEUrea. Avoid nephrotoxins (NSAIDs, contrast, aminoglycosides) and dose-adjust renally cleared medications.

19 Chronic Kidney Disease Nephrology

CKD is defined as kidney damage or GFR < 60 mL/min/1.73 m² for ≥ 3 months. Most common causes: diabetes (40%), hypertension (28%), glomerulonephritis (10%). CKD is a cardiovascular risk multiplier — patients are more likely to die of CV disease than progress to ESRD.

CKD Staging (KDIGO)

StageGFR (mL/min/1.73 m²)DescriptionAction
G1≥ 90Normal/high GFR with kidney damage (proteinuria, hematuria)Identify cause, ACEI/ARB if proteinuria, CVD risk reduction
G260–89Mildly decreasedEstimate progression rate
G3a45–59Mild-moderately decreasedMonitor complications (anemia, bone disease, acidosis)
G3b30–44Moderate-severely decreasedRefer to nephrology, adjust medications
G415–29Severely decreasedPrepare for RRT (access planning, transplant evaluation)
G5< 15Kidney failureRRT (dialysis or transplant) if symptomatic

CKD Complications & Management

ComplicationMechanismTreatment
AnemiaDecreased EPO productionIron repletion first (ferritin > 100, TSAT > 20%), then ESA (epoetin, darbepoetin) targeting Hgb 10–11.5
Metabolic bone disease (CKD-MBD)Decreased 1,25-vit D → hypocalcemia → secondary hyperPTH → bone resorptionPhosphate binders (calcium acetate, sevelamer, lanthanum), calcitriol, calcimimetics (cinacalcet)
Metabolic acidosisDecreased acid excretionOral sodium bicarbonate (target HCO₃ ≥ 22)
HyperkalemiaDecreased K excretionDietary K restriction, avoid K-sparing diuretics, patiromer or SZC for chronic management
Volume overloadDecreased Na/water excretionLoop diuretics (dose escalation as GFR falls), Na restriction

SGLT2 inhibitors (dapagliflozin, empagliflozin) reduce CKD progression and cardiovascular events in CKD patients with or without diabetes — now a pillar of CKD management (DAPA-CKD trial, Heerspink et al., 2020).

Cross-section of the kidney showing cortex, medulla, renal pelvis, and major vessels
Figure 9 — Kidney Cross-Section. The cortex (glomeruli, proximal/distal tubules), medulla (loops of Henle, collecting ducts), and renal pelvis. Glomerular filtration occurs in the cortex; concentration gradients in the medulla drive water reabsorption. Source: Wikimedia Commons. Public domain.

20 Electrolyte Disorders Nephrology

Sodium Disorders

DisorderDefinitionKey CausesTreatment Principles
Hyponatremia (< 135)Most common electrolyte disorder in hospitalized patientsHypovolemic: diuretics, vomiting. Euvolemic: SIADH (most common), hypothyroidism, adrenal insufficiency. Hypervolemic: CHF, cirrhosis, nephrotic syndromeCorrect no faster than 8 mEq/L per 24 hr (risk of osmotic demyelination syndrome). Severe/symptomatic: 3% hypertonic saline 100 mL bolus
Hypernatremia (> 145)Always indicates water deficitInadequate water intake (elderly, intubated), diabetes insipidus (central vs nephrogenic), osmotic diuresisFree water replacement. Correct no faster than 10 mEq/L per 24 hr (risk of cerebral edema). D5W or free water via NGT

Potassium Disorders

DisorderECG ChangesCausesTreatment
Hypokalemia (< 3.5)Flattened T waves, U waves, ST depression, prolonged QTDiuretics, vomiting/NG suction (alkalosis shifts K intracellular), diarrhea, renal tubular acidosis, hypomagnesemiaOral/IV KCl (10 mEq raises serum K by ~0.1). Always replete Mg concurrently (refractory hypoK if Mg low). Max IV rate 10 mEq/hr peripheral, 20 mEq/hr central
Hyperkalemia (> 5.0)Peaked T waves → flattened P → widened QRS → sine wave → VFib/asystoleCKD, ACEI/ARB, K-sparing diuretics, acidosis, rhabdomyolysis, tumor lysis, hemolysis (pseudo)K > 6.5 or ECG changes: calcium gluconate 1 g IV (cardioprotection, onset 1–3 min), insulin 10 units + D50 (shifts K intracellular), albuterol neb, kayexalate/patiromer (K removal), HD if refractory
Always check Mg in a patient with refractory hypokalemia. Magnesium is required for the Na-K-ATPase pump to retain potassium — you cannot correct K without correcting Mg.

21 Acid-Base Disorders & Glomerulonephritis Nephrology

Acid-Base — Systematic Approach

Step 1: pH < 7.35 = acidemia, > 7.45 = alkalemia. Step 2: Primary disorder — same direction as pH? (low HCO₃ = metabolic acidosis, high PaCO₂ = respiratory acidosis). Step 3: Calculate expected compensation (Winter's formula for metabolic acidosis: expected PaCO₂ = 1.5 × HCO₃ + 8 ± 2). Step 4: Calculate anion gap = Na − (Cl + HCO₃). Step 5: If AG elevated, calculate delta-delta = (AG − 12) / (24 − HCO₃). Delta-delta > 2 = concurrent metabolic alkalosis; < 1 = concurrent non-AG metabolic acidosis.

Common Acid-Base Patterns

DisorderpHPrimary ChangeCompensationCommon Causes
AG metabolic acidosis↓ HCO₃↓ PaCO₂MUDPILES: Methanol, Uremia, DKA, Propylene glycol, INH/Iron, Lactic acidosis, Ethylene glycol, Salicylates
Non-AG metabolic acidosis↓ HCO₃↓ PaCO₂Diarrhea, RTA (types 1, 2, 4), normal saline infusion, acetazolamide
Metabolic alkalosis↑ HCO₃↑ PaCO₂Vomiting/NG suction (saline-responsive), diuretics, Cushing, Conn (saline-resistant)
Respiratory acidosis↑ PaCO₂↑ HCO₃COPD, obesity hypoventilation, neuromuscular disease, opioid overdose
Respiratory alkalosis↓ PaCO₂↓ HCO₃Anxiety, pain, PE, early sepsis, high altitude, pregnancy, salicylate toxicity (early)

Glomerulonephritis — Nephritic vs Nephrotic

FeatureNephritic SyndromeNephrotic Syndrome
ProteinuriaSubnephrotic (< 3.5 g/day)≥ 3.5 g/day
HematuriaPresent (RBC casts = pathognomonic)Usually absent
EdemaMild (periorbital)Severe (anasarca, periorbital, peripheral)
HypertensionCommonVariable
AlbuminNormal or mildly lowLow (hypoalbuminemia)
Key diseasesIgA nephropathy (most common worldwide), post-infectious GN, anti-GBM, ANCA vasculitis, lupus nephritisMinimal change (children), FSGS (adults, most common cause of nephrotic in Black adults), membranous nephropathy, diabetic nephropathy, amyloidosis

22 Diabetes Mellitus Endocrinology

Diabetes affects ~37 million Americans (~11%). Type 2 accounts for 90–95% of cases. Diagnosis: fasting glucose ≥ 126 mg/dL, random glucose ≥ 200 with symptoms, OGTT 2-hr ≥ 200, or A1C ≥ 6.5% (confirmed on repeat testing unless unequivocal hyperglycemia). Prediabetes: A1C 5.7–6.4%, FG 100–125, OGTT 140–199.

Type 1 vs Type 2

FeatureType 1Type 2
MechanismAutoimmune beta-cell destruction (anti-GAD, anti-IA2, anti-insulin Ab)Insulin resistance + progressive beta-cell failure
OnsetUsually childhood/young adult; can occur at any age (LADA)Usually adult; increasingly in adolescents
Body habitusOften leanOften obese (80%)
C-peptideLow/absentNormal/high (early), low (late)
Ketosis-proneYes (DKA is presenting feature in ~30%)Less common (but can occur under stress)
TreatmentInsulin always (basal-bolus or pump)Stepwise: lifestyle → metformin → add agents → insulin

Type 2 DM — Pharmacotherapy (ADA Standards of Care 2023)

ClassExampleMechanismA1C ReductionKey Pearl
BiguanideMetformin 500–2000 mgDecreases hepatic glucose output, improves insulin sensitivity1.0–1.5%First-line for all T2DM. Hold if eGFR < 30. GI side effects common, use XR formulation
SGLT2 inhibitorEmpagliflozin 10–25 mg, dapagliflozin 10 mgBlocks glucose reabsorption in proximal tubule (glycosuria)0.5–0.9%CV and renal benefits independent of A1C. Risk: euglycemic DKA, genital mycotic infections, Fournier gangrene (rare)
GLP-1 receptor agonistSemaglutide (Ozempic) 0.5–2 mg/wk, liraglutide (Victoza)Incretin mimetic — glucose-dependent insulin secretion, slows gastric emptying, reduces appetite1.0–1.8%CV benefit (SUSTAIN-6, LEADER). Weight loss 5–15%. GI side effects (nausea). Avoid in MEN2/medullary thyroid cancer (animal data)
DPP-4 inhibitorSitagliptin (Januvia) 100 mgPrevents incretin degradation0.5–0.8%Weight-neutral, well-tolerated, but weaker A1C lowering. Do not combine with GLP-1 RA
SulfonylureaGlipizide 5–20 mg, glimepirideStimulates insulin secretion (K-ATP channel)1.0–1.5%Cheap, effective, but hypoglycemia risk and weight gain. Avoid glyburide (highest hypo risk)
ThiazolidinedionePioglitazone 15–45 mgPPAR-gamma agonist, improves insulin sensitivity0.5–1.4%Fluid retention, CHF exacerbation, weight gain, bladder cancer risk (debated), fractures
InsulinBasal: glargine (Lantus), detemir; Bolus: lispro (Humalog), aspartExogenous insulin replacementNo ceilingAlways needed in T1DM. In T2DM: start basal 10 units or 0.2 units/kg, titrate by 2–4 units q3 days to fasting goal
DKA vs HHS
FeatureDKAHHS
Typical patientT1DM (or T2DM under stress)T2DM, elderly
Glucose> 250 mg/dL (can be lower — "euglycemic DKA")> 600 mg/dL
pH< 7.30> 7.30
Bicarbonate< 18> 18
KetonesPositive (serum beta-hydroxybutyrate > 3)Absent or trace
OsmolalityVariable> 320 mOsm/kg
Mental statusAlert to obtundedOften obtunded/comatose
Mortality1–5%10–20%
TreatmentIVF (NS then switch to D5 1/2 NS when glucose < 200), insulin drip 0.1 units/kg/hr, K+ replacement (add K when < 5.3, hold insulin if K < 3.3), monitor AG closureAggressive IVF (often 6–9 L deficit), insulin drip (lower dose), gradual glucose correction
Illustration comparing normal insulin and glucose physiology with Type 1 and Type 2 diabetes mechanisms
Figure 10 — Diabetes Mellitus Pathophysiology. In Type 1, autoimmune destruction of beta cells eliminates insulin production. In Type 2, peripheral insulin resistance and progressive beta-cell dysfunction produce hyperglycemia. Source: Wikimedia Commons, by BruceBlaus. Licensed under CC BY 3.0.

23 Thyroid Disorders Endocrinology

Approach: TSH Is the Screening Test

TSHFree T4InterpretationCommon Cause
HighLowPrimary hypothyroidismHashimoto's (anti-TPO+), post-ablation, iodine deficiency
HighNormalSubclinical hypothyroidismTreat if TSH > 10 or symptomatic
LowHighHyperthyroidismGraves' (TRAb+), toxic multinodular goiter, toxic adenoma
LowNormalSubclinical hyperthyroidismObserve vs treat based on age, AFib risk, bone density
LowLowCentral hypothyroidismPituitary disease (tumor, surgery, Sheehan's)

Hypothyroidism treatment: levothyroxine (Synthroid) 1.6 mcg/kg/day, taken on empty stomach 30–60 min before food. Recheck TSH in 6–8 weeks. In elderly/cardiac patients, start low (25–50 mcg) and titrate slowly.

Hyperthyroidism treatment: Graves' — three options: (1) antithyroid drugs (methimazole preferred, start 10–30 mg daily — monitor for agranulocytosis, check WBC if sore throat/fever; PTU only in first trimester pregnancy or thyroid storm), (2) radioactive iodine ablation (I-131 — results in permanent hypothyroidism), (3) thyroidectomy. Thyroid storm: life-threatening decompensation — tachycardia, hyperthermia, AMS, HF. Treatment: PTU loading dose (500–1000 mg) + iodine (SSKI) 1 hr after PTU + beta-blocker (propranolol) + hydrocortisone 100 mg IV q8h + cooling.

Illustration of thyroid gland with goiter showing enlarged thyroid in the anterior neck
Figure 11 — Thyroid Gland and Goiter. The thyroid sits anterior to the trachea, just below the cricoid cartilage. Diffuse enlargement (goiter) can occur in both hypo- and hyperthyroidism. Source: Wikimedia Commons, by BruceBlaus. Licensed under CC BY 3.0.

24 Adrenal Disorders Endocrinology

Adrenal Insufficiency

Primary (Addison's): destruction of the adrenal cortex (autoimmune in developed countries, TB worldwide). Cortisol AND aldosterone deficient. Presentation: fatigue, weight loss, hypotension, hyperpigmentation (ACTH excess drives MSH), hyponatremia, hyperkalemia. Secondary: pituitary ACTH deficiency (most common cause = chronic exogenous steroid use then abrupt withdrawal). No hyperpigmentation, no hyperkalemia (aldosterone intact via RAAS). Diagnosis: morning cortisol < 3 = diagnostic, > 18 = excludes AI. 3–18 = cosyntropin stimulation test (cortisol should rise to ≥ 18 at 30 or 60 min). Treatment: hydrocortisone 15–25 mg/day in divided doses (2/3 AM, 1/3 PM) + fludrocortisone 0.05–0.2 mg daily (primary only). Adrenal crisis: IV hydrocortisone 100 mg bolus + aggressive IVF — do not wait for lab confirmation in shock.

Cushing Syndrome

Excess cortisol. Most common cause overall: exogenous steroids. Most common endogenous cause: pituitary adenoma (Cushing's disease, ~70%). Features: central obesity, moon facies, dorsocervical fat pad, abdominal striae (purple, wide), proximal myopathy, hyperglycemia, hypertension, osteoporosis, easy bruising. Screening: 24-hr urine free cortisol, late-night salivary cortisol, 1 mg overnight dexamethasone suppression test (cortisol > 1.8 = positive). If confirmed, check ACTH: suppressed = adrenal source (CT adrenals); elevated = pituitary vs ectopic (high-dose dex suppression + pituitary MRI + IPSS if needed).

25 Calcium & Bone Disorders Endocrinology

Calcium Homeostasis

Always correct for albumin: corrected Ca = measured Ca + 0.8 × (4.0 − albumin). Or check ionized calcium directly. Two key hormones: PTH (raises Ca: bone resorption, renal reabsorption, activates vitamin D) and calcitonin (lowers Ca — clinically minor).

DisorderCalciumPTHKey CausesTreatment
Primary hyperPTHHighHigh (inappropriate)Parathyroid adenoma (85%), hyperplasia (15%)Surgery if symptomatic, Ca > 1 above normal, GFR < 60, T-score < −2.5, or age < 50
Hypercalcemia of malignancyHighLow (suppressed)PTHrP (squamous cell, renal), bone mets (breast, lung), 1,25-vit D (lymphoma)IVF (aggressive), calcitonin (rapid, transient), zoledronic acid (onset 2–4 days), denosumab
Vitamin D deficiencyLow-normalHigh (secondary)Inadequate sun/intake, malabsorption, CKDErgocalciferol 50,000 IU weekly × 8 weeks then 1000–2000 IU daily maintenance
HypoparathyroidismLowLowPost-thyroidectomy (#1 cause), autoimmune, DiGeorgeCalcium + calcitriol supplementation
Severe Hypercalcemia (> 14 mg/dL) — Emergency

Symptoms: "stones, bones, groans, psychiatric overtones" — kidney stones, bone pain, abdominal pain/constipation, confusion/lethargy. ECG: shortened QT. Treatment: IV NS 200–300 mL/hr (volume repletion first), calcitonin 4 IU/kg q12h (onset 4–6 hr, tachyphylaxis after 48 hr), zoledronic acid 4 mg IV over 15 min (onset 2–4 days, lasts weeks). Loop diuretics only after volume resuscitation (forcing calciuresis). Dialysis for refractory cases.

26 Anemia Hematology

Anemia is defined as Hgb < 13.5 g/dL (men) or < 12.0 g/dL (women). The MCV-based approach is the diagnostic backbone:

MCV CategoryMCV (fL)Key DiagnosesDiagnostic Tests
Microcytic (< 80)< 80Iron deficiency (#1 worldwide), thalassemia, anemia of chronic disease, sideroblastic, lead poisoningIron studies: ferritin (< 30 = IDA), TIBC (high in IDA), Fe (low), TSAT (< 20%). Hgb electrophoresis for thalassemia
Normocytic (80–100)80–100Anemia of chronic disease/inflammation, CKD (EPO deficiency), acute blood loss, hemolytic anemia, bone marrow failureReticulocyte count (high = destruction/loss, low = underproduction). Hemolysis labs: LDH ↑, haptoglobin ↓, indirect bili ↑, smear (schistocytes = MAHA)
Macrocytic (> 100)> 100B12 deficiency, folate deficiency, MDS, liver disease, hypothyroidism, reticulocytosis, drugs (MTX, hydroxyurea, AZT)B12 and folate levels. If B12 borderline: methylmalonic acid (elevated in B12 def only) + homocysteine (elevated in both)
Iron deficiency anemia in a post-menopausal woman or any man is GI malignancy until proven otherwise — requires colonoscopy and upper endoscopy. Do not simply prescribe iron and stop.
Microscopic comparison of normal red blood cells with sickle-shaped cells in sickle cell disease
Figure 12 — Normal vs. Sickle Red Blood Cells. Sickle cell disease (HbSS) produces rigid, sickle-shaped RBCs that cause vaso-occlusion and hemolysis. Hydroxyurea increases fetal hemoglobin (HbF) and reduces crises. Source: Wikimedia Commons. Public domain.

27 Coagulation Disorders Hematology

Coagulation Cascade — Key Lab Correlations

TestPathwayMeasuresProlonged In
PT / INRExtrinsic + commonFactors VII, X, V, II, fibrinogenWarfarin, liver disease, vitamin K deficiency, DIC
aPTTIntrinsic + commonFactors XII, XI, IX, VIII, X, V, II, fibrinogenHeparin (UFH), hemophilia A (VIII) / B (IX), lupus anticoagulant, DIC
Thrombin timeCommon (final)Fibrinogen → fibrin conversionDabigatran, heparin contamination, low fibrinogen, FDPs
Mixing studyCorrects = factor deficiency; Doesn't correct = inhibitorFactor inhibitors, lupus anticoagulant

DIC (Disseminated Intravascular Coagulation)

Pathologic activation of coagulation with simultaneous consumption of clotting factors and platelets — producing both thrombosis and hemorrhage. Causes: sepsis (#1), trauma, malignancy (especially AML M3/APL), obstetric complications (abruption, amniotic fluid embolism). Labs: platelets ↓, PT/aPTT ↑, fibrinogen ↓, D-dimer ↑↑, schistocytes on smear. Treatment: treat the underlying cause. Supportive: platelets if < 10 (or < 50 with active bleeding), cryoprecipitate if fibrinogen < 100, FFP if bleeding with prolonged PT/aPTT.

HIT (Heparin-Induced Thrombocytopenia)

Type II HIT: immune-mediated (IgG against PF4-heparin complex). Platelet drop ≥ 50% typically 5–10 days after heparin exposure (or sooner if prior exposure). Paradoxically pro-thrombotic — venous and arterial thrombosis in 30–50%. Use 4T score to estimate probability. If HIT suspected: stop ALL heparin (including flushes), start alternative anticoagulant (argatroban, bivalirudin, fondaparinux). Do NOT give warfarin until platelets recover (causes skin necrosis/venous limb gangrene via protein C depletion). Confirm with anti-PF4 ELISA then serotonin release assay (gold standard).

28 Transfusion Medicine Hematology

ProductContentsIndication / ThresholdVolume / Details
Packed RBCsRed cells in additive solutionHgb < 7 (restrictive, most patients). Hgb < 8 (cardiac disease, symptomatic). Active hemorrhage~300 mL/unit. Expected rise: 1 g/dL per unit. Type and screen before transfusion
PlateletsConcentrated platelets< 10K (prophylactic). < 50K (active bleeding or pre-procedure). < 100K (neurosurgery/ocular surgery)1 apheresis unit raises count ~30–50K. Irradiated if immunocompromised
FFPAll clotting factorsINR > 1.5–2.0 with active bleeding. Warfarin reversal (if PCC unavailable). DIC. TTP (plasma exchange)10–15 mL/kg. Takes ~30 min to thaw. Contains ~250 mL/unit
CryoprecipitateFibrinogen, vWF, Factor VIII, XIIIFibrinogen < 100–150 (DIC, massive transfusion). Hemophilia A (if factor concentrate unavailable)1 pool (10 units) raises fibrinogen ~60–100 mg/dL
PCC (4-factor)Factors II, VII, IX, X, protein C & SWarfarin reversal (urgent/emergent — preferred over FFP), factor deficiency25–50 units/kg IV. Onset 10–15 min. Much smaller volume than FFP

Transfusion Reactions

ReactionTimingFeaturesManagement
Febrile non-hemolyticDuring or within 4 hrFever, chills, rigors (no hemolysis)Stop transfusion, acetaminophen. Resume if no hemolysis suspected. Leukoreduced products prevent recurrence
Allergic (mild)DuringUrticaria, pruritusDiphenhydramine. May resume if symptoms resolve
Acute hemolyticWithin minutesFever, flank pain, dark urine, hypotension, DICStop immediately. IVF, send direct Coombs, free Hgb, repeat type & screen. ABO mismatch is clerical error
TRALIWithin 6 hrAcute bilateral pulmonary edema, hypoxia, normal cardiac pressuresSupportive (O₂, possible intubation). No diuretics (not volume overload)
TACOWithin 6 hrVolume overload — dyspnea, HTN, elevated BNP, elevated JVPSlow rate, diuretics, sit upright

29 Sepsis & SIRS Infectious Disease

Sepsis (Sepsis-3, 2016): life-threatening organ dysfunction caused by a dysregulated host response to infection, operationally defined as suspected/documented infection + acute increase in SOFA score ≥ 2. Septic shock: sepsis + vasopressor requirement to maintain MAP ≥ 65 + lactate > 2 mmol/L despite adequate fluid resuscitation. Hospital mortality: sepsis ~10%, septic shock ~40% (Singer et al., 2016).

Surviving Sepsis Campaign — Hour-1 Bundle

ActionDetails
Measure lactateRemeasure within 2–4 hr if initial > 2 mmol/L
Obtain blood culturesBefore antibiotics (2 sets from 2 sites). Do not delay antibiotics > 45 min for cultures
Administer broad-spectrum antibioticsWithin 1 hour of recognition. Common: vancomycin + piperacillin-tazobactam (or cefepime or meropenem)
Administer 30 mL/kg crystalloidFor hypotension or lactate ≥ 4. Balanced crystalloid (LR) preferred over NS
Start vasopressorsIf MAP < 65 despite fluids. Norepinephrine first-line. Vasopressin (0.03 units/min) as second agent
Lactate is a marker of tissue hypoperfusion and anaerobic metabolism — lactate clearance (≥ 10% per 2 hours) is a prognostic marker and resuscitation target. A lactate > 4 mmol/L carries > 25% mortality. Serial lactate trends are more useful than single values.

30 UTI & Pyelonephritis Infectious Disease

EntityPresentationDiagnosisTreatment
Uncomplicated cystitis (women)Dysuria, frequency, urgency, suprapubic pain. No feverUA (pyuria, nitrites, LE positive). Culture optional in uncomplicatedNitrofurantoin 100 mg BID × 5 days (first-line), TMP-SMX DS BID × 3 days (if local resistance < 20%), fosfomycin 3 g single dose
Complicated UTIUTI with structural abnormality, catheter, male sex, pregnancy, immunocompromisedUA + culture + sensitivitiesFluoroquinolone or beta-lactam; duration 7–14 days. Remove/replace catheter if present
PyelonephritisFever, flank pain, CVA tenderness ± lower urinary symptoms, nausea/vomitingUA + culture. Consider CT if no improvement in 48–72 hr (rule out abscess, obstruction)Outpatient: ciprofloxacin 500 mg BID × 7 days or TMP-SMX × 14 days. Inpatient: ceftriaxone 1 g IV daily or fluoroquinolone IV. Blood cultures if systemic
Asymptomatic bacteriuria: treat ONLY in pregnancy and before urologic procedures. Do not treat ASB in elderly, catheterized, or diabetic patients — it does not improve outcomes and promotes resistance.

31 Infective Endocarditis Infectious Disease

Infection of the endocardial surface, usually a heart valve. Most common organisms: S. aureus (#1 overall and in acute IE/IVDU), viridans group streptococci (subacute, native valve), Enterococcus (elderly, GU source), HACEK organisms (subacute, culture-negative for days), coagulase-negative staph (prosthetic valves).

Modified Duke Criteria

Definite IE: 2 major, or 1 major + 3 minor, or 5 minor criteria.

Major CriteriaMinor Criteria
Positive blood cultures (typical organisms from 2 separate cultures, or persistently positive)Predisposing condition (IVDU, prosthetic valve, congenital heart disease)
Endocardial involvement on echo (vegetation, abscess, new dehiscence of prosthetic valve, new valvular regurgitation)Fever ≥ 38°C
Vascular phenomena (Janeway lesions, arterial emboli, mycotic aneurysm, conjunctival hemorrhage)
Immunologic phenomena (Osler nodes, Roth spots, glomerulonephritis, positive RF)
Positive blood culture not meeting major criteria

Treatment: Prolonged IV antibiotics (4–6 weeks). Native valve S. aureus: nafcillin/oxacillin (or vancomycin if MRSA) × 6 weeks. Viridans strep: penicillin G or ceftriaxone × 4 weeks (± gentamicin × 2 weeks for synergy). Prosthetic valve S. aureus: vancomycin + rifampin × ≥ 6 weeks + gentamicin × 2 weeks. Surgical indications: HF from valvular dysfunction, uncontrolled infection, large/mobile vegetations (> 10 mm with embolic event), abscess.

Illustration of infective endocarditis showing vegetation on mitral valve leaflet
Figure 13 — Infective Endocarditis. Vegetation (infected platelet-fibrin mass) on the mitral valve. Vegetations can embolize to the brain (stroke), kidneys (infarction), skin (Janeway lesions), and other organs. Source: Wikimedia Commons, by BruceBlaus. Licensed under CC BY 3.0.

32 HIV & C. difficile Infectious Disease

HIV

Diagnosis: 4th-gen HIV Ag/Ab combo test (detects p24 antigen + HIV-1/2 antibodies). If positive, confirm with HIV-1/HIV-2 differentiation assay. Acute HIV: mononucleosis-like illness 2–4 weeks post-exposure (fever, pharyngitis, rash, lymphadenopathy) — high viral load, may be antibody-negative (Ag/Ab detects p24). Start antiretroviral therapy (ART) immediately upon diagnosis regardless of CD4 count (INSIGHT START trial, 2015). Preferred initial regimens: integrase inhibitor-based (bictegravir/emtricitabine/TAF = Biktarvy, or dolutegravir + emtricitabine/TAF).

Opportunistic infections by CD4 count: < 200: Pneumocystis jirovecii pneumonia (PJP — prophylaxis: TMP-SMX DS daily), oral candidiasis. < 100: Toxoplasma encephalitis, Cryptococcus meningitis. < 50: Mycobacterium avium complex (MAC), CMV retinitis.

Clostridioides difficile Infection

Toxin-producing anaerobic gram-positive bacillus — #1 cause of healthcare-associated infectious diarrhea. Risk factors: antibiotics (fluoroquinolones, clindamycin, cephalosporins), age > 65, hospitalization, PPI use. Diagnosis: stool PCR (toxin gene) — highly sensitive but may detect colonization; IDSA recommends testing only formed stools (never test formed stool).

SeverityCriteriaTreatment (IDSA/SHEA 2021)
Non-severeWBC ≤ 15K, Cr < 1.5Fidaxomicin 200 mg BID × 10 days (preferred) or vancomycin 125 mg PO QID × 10 days
SevereWBC > 15K or Cr ≥ 1.5Vancomycin 125 mg PO QID × 10 days (or fidaxomicin)
FulminantHypotension, ileus, megacolon, or organ failureVancomycin 500 mg PO/NGT QID + vancomycin rectal enema + IV metronidazole 500 mg q8h. Surgical consult for colectomy
Recurrence (1st)Symptoms recur within 2–8 weeksFidaxomicin (pulsed-taper if prior vanco), or bezlotoxumab (anti-toxin B monoclonal) adjunct, or FMT for ≥ 2 recurrences

33 Rheumatoid Arthritis & SLE Rheumatology

Rheumatoid Arthritis

Chronic systemic autoimmune disease causing symmetric inflammatory polyarthritis, predominantly affecting the small joints of the hands (MCP, PIP — spares DIP) and feet. Morning stiffness > 1 hour (improves with activity, unlike OA which worsens). Seropositive: RF (70–80%) and anti-CCP (more specific, ~95%). Extra-articular manifestations: rheumatoid nodules (subcutaneous, extensor surfaces), interstitial lung disease, pericarditis, Felty syndrome (RA + splenomegaly + neutropenia), secondary amyloidosis (AA type).

Treatment: Early aggressive DMARD therapy — methotrexate 15–25 mg/week (cornerstone, start within 3 months of diagnosis) + folic acid 1 mg daily. If inadequate response: add biologic — anti-TNF (adalimumab, etanercept, infliximab), IL-6 inhibitor (tocilizumab), B-cell depletion (rituximab), T-cell co-stimulation blocker (abatacept), or JAK inhibitor (tofacitinib, baricitinib). Treat-to-target: DAS28 remission or low disease activity.

Systemic Lupus Erythematosus

Systemic autoimmune disease with multi-organ involvement. Classic: young women (F:M = 9:1), photosensitive malar (butterfly) rash, arthritis, serositis, cytopenias, nephritis. Hallmark: ANA (positive in > 95% — sensitive but not specific). Specific antibodies: anti-dsDNA (lupus nephritis, disease activity), anti-Smith (most specific for SLE), anti-Ro/La (neonatal lupus, Sjogren overlap), antiphospholipid antibodies (thrombosis, pregnancy loss).

Lupus nephritis (occurs in ~50%): classified ISN/RPS Class I–VI. Class III (focal) and IV (diffuse) require aggressive immunosuppression — induction: mycophenolate mofetil (MMF) or cyclophosphamide + corticosteroids. Maintenance: MMF or azathioprine. Belimumab (anti-BLyS) added for active lupus. Voclosporin added for nephritis (AURORA trial, 2021). Hydroxychloroquine for ALL lupus patients (reduces flares, improves survival, renal protection) — annual eye exam for retinal toxicity.

34 Gout & Pseudogout Rheumatology

FeatureGoutPseudogout (CPPD)
CrystalMonosodium urate (MSU)Calcium pyrophosphate dihydrate (CPPD)
Polarized microscopyNeedle-shaped, negatively birefringent (yellow parallel)Rhomboid-shaped, positively birefringent (blue parallel)
Classic joint1st MTP (podagra, 50% of first attacks)Knee (most common), wrist
X-rayErosions with overhanging edges ("rat bite"), tophiChondrocalcinosis (linear calcification of cartilage)
Risk factorsHyperuricemia, alcohol (beer > liquor), purine-rich diet, CKD, diureticsElderly, hemochromatosis, hyperPTH, hypomagnesemia, hypothyroidism
Acute treatmentNSAIDs (indomethacin 50 mg TID), colchicine (1.2 mg then 0.6 mg in 1 hr), corticosteroids (if NSAID/colchicine CI)Same acute management as gout
Chronic (urate-lowering)Allopurinol (start 100 mg, titrate to urate < 6), febuxostat, pegloticase (refractory). Start with colchicine 0.6 mg daily prophylaxisNo urate-lowering therapy. Low-dose colchicine for prophylaxis if recurrent
Never start or change urate-lowering therapy during an acute gout flare — it can prolong or worsen the attack. Start prophylactic colchicine or NSAID when initiating allopurinol and continue for 3–6 months.

35 Vasculitis Rheumatology

Vasculitis = inflammation of blood vessel walls. Classified by vessel size (Chapel Hill Consensus):

Vessel SizeDiseaseKey FeaturesDiagnosis / Treatment
LargeGiant Cell Arteritis (GCA)Age > 50, new headache, jaw claudication, visual loss (ophthalmic artery — emergency), ESR/CRP markedly elevated, PMR overlapTemporal artery biopsy (skip lesions — sample ≥ 2 cm). Start high-dose prednisone 60 mg immediately (do not wait for biopsy). Tocilizumab for steroid-sparing
Takayasu ArteritisYoung women (< 40), aortic arch/branch stenosis, "pulseless disease," limb claudication, BP discrepancy between armsCTA/MRA showing wall thickening/stenosis. Steroids + methotrexate. Tocilizumab for refractory
MediumPolyarteritis Nodosa (PAN)Hep B association. Skin (livedo, nodules), renal (microaneurysms, NOT glomerulonephritis), neuropathy (mononeuritis multiplex), GI (mesenteric ischemia). ANCA negativeAngiography (microaneurysms). Steroids + cyclophosphamide. Treat Hep B if associated
Kawasaki DiseaseChildren < 5, fever ≥ 5 days + 4 of 5: bilateral conjunctival injection, oral changes, rash, extremity changes, cervical LADIVIG + high-dose ASA. Risk of coronary artery aneurysms
Small (ANCA-associated)GPA (Wegener's)Upper airway (sinusitis, saddle-nose deformity), lungs (cavitary lesions), kidneys (RPGN). c-ANCA / anti-PR3Steroids + rituximab (preferred over cyclophosphamide per RAVE trial). Maintenance: rituximab or azathioprine
MPA (Microscopic Polyangiitis)Kidneys (RPGN, most common finding), lungs (alveolar hemorrhage). p-ANCA / anti-MPOSame as GPA
EGPA (Churg-Strauss)Asthma, eosinophilia (> 1500), neuropathy, cardiac involvement. p-ANCA in ~40%Steroids + mepolizumab (anti-IL5). Cyclophosphamide if organ-threatening
Small (immune complex)IgA Vasculitis (HSP)Children. Palpable purpura (buttocks/legs), abdominal pain, arthritis, IgA nephropathyUsually self-limited. NSAIDs for arthritis, steroids if renal or severe GI involvement
Clinical photograph showing palpable purpura on the lower extremities characteristic of small vessel vasculitis
Figure 14 — Palpable Purpura in Small-Vessel Vasculitis. Non-blanching, raised purpuric lesions on the lower extremities — classic for leukocytoclastic vasculitis. Biopsy shows neutrophilic infiltration and fibrinoid necrosis of small vessel walls. Source: Wikimedia Commons. Licensed under CC BY-SA 3.0.

36 Sarcoidosis Special

Systemic granulomatous disease of unknown etiology characterized by non-caseating granulomas in affected organs. Peak incidence: 25–35 years; 3× more common and more severe in Black Americans. Most common presentation: bilateral hilar lymphadenopathy (BHL) on CXR, often discovered incidentally.

Organ Involvement

OrganFrequencyManifestations
Lungs> 90%BHL, parenchymal infiltrates, restrictive PFTs. Staging: I (BHL alone), II (BHL + parenchymal), III (parenchymal alone), IV (pulmonary fibrosis)
Skin25–35%Erythema nodosum (NOT granulomatous — good prognosis), lupus pernio (violaceous facial plaques — poor prognosis), papules, plaques
Eyes25–50%Anterior uveitis (most common ocular finding), lacrimal gland enlargement. All sarcoid patients need ophthalmologic exam
Liver60–80% (biopsy)Granulomatous hepatitis, elevated ALP. Usually subclinical
Heart5–25%Conduction defects (AV block), cardiomyopathy, sudden death. Screen with ECG; cardiac MRI if suspected
Neuro5–10%CN VII palsy (most common), meningitis, hypothalamic/pituitary dysfunction, seizures
Calcium/endocrine10–20%Hypercalcemia (granulomas produce 1,25-vit D via 1-alpha-hydroxylase), hypercalciuria, nephrolithiasis

Diagnosis: Clinical + radiographic + histologic (non-caseating granulomas on biopsy of accessible tissue — skin, lymph node, lung via bronchoscopy with EBUS-TBNA). Elevated ACE level is supportive but neither sensitive nor specific. Must exclude TB and fungal infection (both cause granulomas). Treatment: Many cases resolve spontaneously (especially Lofgren syndrome: BHL + erythema nodosum + fever + polyarthralgia). Treat when symptomatic or organ-threatening: prednisone 20–40 mg/day, taper over 6–12 months. Steroid-sparing: methotrexate, azathioprine, mycophenolate. Refractory: infliximab.

37 Amyloidosis Special

Amyloidosis is the deposition of misfolded protein fibrils (amyloid) in tissues, disrupting organ function. Congo red stain shows apple-green birefringence under polarized light — pathognomonic.

TypePrecursor ProteinAssociationsKey Organ InvolvementTreatment
AL (primary)Immunoglobulin light chain (lambda > kappa)Plasma cell dyscrasia (myeloma, MGUS)Heart (restrictive CMP — "thick walls, low voltage on ECG"), kidney (nephrotic syndrome), liver, neuropathy, macroglossia, periorbital purpuraChemo targeting plasma cells: daratumumab + bortezomib/CyDex. Stem cell transplant if eligible
AA (secondary)Serum amyloid AChronic inflammation (RA, IBD, FMF, chronic infections)Kidneys (proteinuria, nephrotic syndrome)Treat underlying inflammatory disease
ATTR (transthyretin)Transthyretin (wild-type or mutant)Wild-type: elderly men ("senile cardiac amyloidosis"). Hereditary: Val122Ile (cardiac, Black Americans), Val30Met (neuropathic)Heart (HFpEF phenotype, often CTS), neuropathyTafamidis (Vyndamax) — TTR stabilizer, reduces mortality in ATTR-CM. Patisiran/inotersen for neuropathic
Suspect cardiac amyloidosis in any patient with HFpEF + LVH + low-voltage ECG (discordance between wall thickness and voltage) + diastolic dysfunction. Technetium pyrophosphate scan (PYP) is a non-invasive diagnostic test for ATTR cardiac amyloidosis (Grade 2–3 uptake = positive).

38 Autoimmune Hepatitis Special

Chronic liver inflammation caused by autoimmune attack on hepatocytes. Bimodal: young women (Type 1, most common) and children (Type 2). Presents with fatigue, jaundice, elevated transaminases (often ALT > AST, sometimes dramatically elevated — can mimic acute viral hepatitis), hypergammaglobulinemia (elevated IgG), and autoantibodies. Can progress to cirrhosis if untreated.

Classification

TypeAutoantibodiesDemographics
Type 1ANA, anti-smooth muscle antibody (ASMA)Any age, most common in North America/Europe
Type 2Anti-LKM-1, anti-LC1Children and young adults, more severe

Diagnosis: Simplified AIH scoring (IAIHG): autoantibodies + IgG elevation + liver histology (interface hepatitis, lymphoplasmacytic infiltrate, hepatocyte rosettes) + exclusion of viral hepatitis. Treatment: Induction: prednisone 30–60 mg/day tapered over weeks, plus azathioprine 50 mg then 1–2 mg/kg/day as steroid-sparing agent. Maintenance: azathioprine alone or low-dose prednisone + azathioprine. Remission goal: normal transaminases + IgG. Check TPMT before starting azathioprine (toxicity risk if deficient). Second-line: mycophenolate mofetil. Liver transplant for decompensated cirrhosis or fulminant presentation (can recur post-transplant in 20–30%).

39 Imaging & Diagnostics

ModalityPrimary Use in IMKey Interpretation Points
Chest X-rayPneumonia, CHF, pleural effusion, pneumothorax, massesCHF: cephalization, Kerley B lines, peribronchial cuffing, bilateral pleural effusions. Pneumonia: lobar consolidation (air bronchograms) vs interstitial pattern
ECG (12-lead)Arrhythmia, ACS, PE, electrolyte abnormalitiesSTEMI criteria, AFib (absent P waves, irregular RR), PE (S1Q3T3, RV strain), hyperK (peaked T), hypoK (U waves)
Echocardiography (TTE)EF, valvular disease, wall motion, pericardial effusion, diastolic functionHFrEF ≤ 40%, severe AS (AVA < 1.0 cm², mean gradient > 40 mmHg), vegetation in IE
CT chest (with contrast)PE (CTPA), ILD (HRCT), aortic dissection, lung massPE: filling defect in pulmonary artery. UIP pattern (IPF): basal honeycombing. Dissection: intimal flap
CT abdomen/pelvisPancreatitis complications, abscess, obstruction, renal stonesPancreatitis: peripancreatic fat stranding, necrosis (non-enhancing areas), fluid collections
Abdominal ultrasoundGallstones, liver/renal morphology, ascites, hydronephrosisCirrhosis: nodular liver, splenomegaly, ascites. Hydronephrosis in obstructive AKI
Renal ultrasoundAKI workup (obstruction), CKD (kidney size)Normal kidney 9–12 cm. Small kidneys = CKD (chronic). Large kidneys: DM nephropathy, amyloid, HIV, polycystic
PFTs (spirometry, lung volumes, DLCO)Obstructive vs restrictive, severity, response to bronchodilatorObstructive: FEV₁/FVC < 0.70 (COPD, asthma). Restrictive: FVC ↓, TLC ↓, FEV₁/FVC normal/↑. DLCO ↓ = ILD, emphysema, PAH
Paracentesis fluid analysisSBP vs secondary peritonitis, portal HTN assessmentSAAG ≥ 1.1 = portal hypertension. PMN ≥ 250 = SBP. Total protein, glucose, LDH, culture
Bone marrow biopsyUnexplained cytopenias, MDS, leukemia, myelofibrosis, amyloidosisCellularity, blast percentage, iron stores, flow cytometry, cytogenetics
Standard 12-lead ECG showing normal sinus rhythm with labeled leads
Figure 15 — Standard 12-Lead ECG. The 12-lead ECG is the single most important bedside diagnostic tool in internal medicine — interpretable within seconds for STEMI, arrhythmias, conduction disease, electrolyte disturbances, and drug toxicity. Source: Wikimedia Commons. Public domain.

40 Classification Systems (All)

SystemUsed ForKey Features
ACC/AHA HTN (2017)Blood pressure classificationNormal/Elevated/Stage 1/Stage 2/Crisis. Stage 1 starts at 130/80 (lowered from 140/90)
NYHA (I–IV)Heart failure functional statusI = no limitation, IV = symptoms at rest. Guides device therapy (ICD if EF ≤ 35% + NYHA II–III)
ACC/AHA HF Stages (A–D)Heart failure progressionA = at risk, D = refractory (LVAD/transplant). Unlike NYHA, stages only advance (never regress)
CHA₂DS₂-VAScStroke risk in AFibScore 0–9. ≥ 2 men / ≥ 3 women: anticoagulate
HAS-BLEDBleeding risk on anticoagulationScore 0–9. ≥ 3 = high risk — does NOT contraindicate anticoagulation, but mandates closer monitoring
Wells (DVT / PE)Pre-test probabilityDVT: ≥ 2 = likely. PE: > 4 = likely. Low probability + negative D-dimer = excludes VTE
GOLD (COPD)Airflow obstruction severityStages 1–4 by FEV₁. ABE groups guide therapy
GINA Steps (1–5)Asthma controller therapyStep up if uncontrolled, step down after 3 months of control
CURB-65CAP severity0–1 outpatient, 2 short stay, 3–5 inpatient/ICU
Light's CriteriaPleural effusion (exudate vs transudate)Any 1 of 3 criteria met = exudate. Sensitivity 98%
Child-Pugh (A/B/C)Cirrhosis severity5 parameters, each 1–3 points. A = compensated, C = decompensated
MELD-NaLiver transplant allocationBilirubin, INR, Cr, Na. Range 6–40. ≥ 15 = consider listing
Revised AtlantaAcute pancreatitis severityMild/Moderate/Severe by organ failure + local complications
KDIGO (AKI & CKD)Kidney disease stagingAKI: stages 1–3 by Cr/UOP. CKD: G1–G5 by GFR + A1–A3 by albuminuria
Marsh (I–IIIc)Celiac disease histologyI = intraepithelial lymphocytosis, IIIc = total villous atrophy
ISN/RPS (I–VI)Lupus nephritisIII (focal) and IV (diffuse) = aggressive immunosuppression
Modified Duke CriteriaInfective endocarditis diagnosisMajor (blood cultures, echo) + minor criteria. 2 major = definite IE
Sepsis-3 / SOFASepsis definition & organ dysfunctionSuspected infection + SOFA ≥ 2. qSOFA (bedside): RR ≥ 22, AMS, SBP ≤ 100
Schofield/Sarcoid Staging (0–IV)Pulmonary sarcoidosis0 = normal CXR, I = BHL, II = BHL + parenchymal, III = parenchymal alone, IV = fibrosis
Chapel Hill ConsensusVasculitis classificationBy vessel size: large, medium, small. Guides workup and treatment

41 Medications Master Table

Cardiovascular

Generic (Brand)ClassMechanismTypical DoseIndicationCritical Pearl
Lisinopril (Zestril)ACEIBlocks ACE → decreases angiotensin II → vasodilation + decreased aldosterone10–40 mg dailyHTN, HFrEF, DM nephropathy, post-MIMonitor K+/Cr. Cough 10%. Angioedema rare but life-threatening. CI in pregnancy
Sacubitril/valsartan (Entresto)ARNINeprilysin inhibitor + ARB97/103 mg BID (target)HFrEF (replaces ACEI/ARB)36-hr washout from ACEI before starting (angioedema risk). Do not use with ACEI
Metoprolol succinate (Toprol-XL)Beta-blocker (selective)Beta-1 blockade → decreased HR, contractility, renin25–200 mg dailyHFrEF, HTN, rate control AFib, post-MISuccinate (XR) for HF, not tartrate (IR). Do not stop abruptly (rebound tachycardia)
Amlodipine (Norvasc)DHP-CCBBlocks L-type Ca channels → arterial vasodilation5–10 mg dailyHTN, anginaPeripheral edema is dose-related, not allergic. Safe in HFrEF (unlike verapamil/diltiazem)
Spironolactone (Aldactone)MRAAldosterone antagonist → K-sparing diuresis25–50 mg dailyHFrEF, resistant HTN, ascites, primary aldosteronismGynecomastia (switch to eplerenone). Hyperkalemia risk with ACEI/ARB + CKD
Furosemide (Lasix)Loop diureticBlocks NKCC2 in thick ascending limb20–80 mg IV/PO (up to 600 mg/day in CKD)CHF, edema, CKD fluid overloadIV:PO ratio is 1:2. Causes hypoK, hypoNa, hypoMg, hypoCa, ototoxicity (high dose)
Apixaban (Eliquis)DOAC (Xa inhibitor)Direct factor Xa inhibition5 mg BID (VTE, AFib). 2.5 mg BID if ≥ 2 of: age ≥ 80, weight ≤ 60 kg, Cr ≥ 1.5AFib stroke prevention, VTE treatmentNo routine monitoring. Reversal: andexanet alfa. Avoid if CrCl < 25 (or < 15). Fewest GI bleeds among DOACs

Pulmonary

Generic (Brand)ClassDoseUsePearl
Albuterol (ProAir, Ventolin)SABA2 puffs q4–6h PRN or nebulizer 2.5 mgAcute bronchospasm (COPD, asthma)Tachycardia, tremor, hypokalemia at high doses
Tiotropium (Spiriva)LAMA18 mcg inhaled daily (HandiHaler) or 2.5 mcg (Respimat)Maintenance COPD, step-up asthmaDry mouth common. Do not use with short-acting antimuscarinics
Budesonide/formoterol (Symbicort)ICS/LABA160/4.5 mcg 2 puffs BID + PRN (SMART therapy)Asthma (Steps 3–5), COPD with eos ≥ 300Rinse mouth after ICS to prevent oral candidiasis. LABA monotherapy in asthma = increased death

Endocrine & GI

Generic (Brand)ClassDoseUsePearl
Metformin (Glucophage)Biguanide500–2000 mg daily (XR preferred)T2DM first-lineHold if eGFR < 30 or before iodinated contrast (risk of lactic acidosis). GI side effects common — start low, go slow
Semaglutide (Ozempic)GLP-1 RA0.25 mg → 0.5 mg → 1 mg → 2 mg SQ weeklyT2DM, obesity (Wegovy formulation)Nausea common initially. CV benefit. Weight loss 10–15%. Pancreatitis risk (debated)
Empagliflozin (Jardiance)SGLT2i10–25 mg dailyT2DM, HFrEF, HFpEF, CKDGenital mycotic infections. Euglycemic DKA (rare). Hold before surgery
Levothyroxine (Synthroid)Thyroid hormone1.6 mcg/kg/dayHypothyroidismEmpty stomach, 30–60 min before food. Ca, Fe, PPIs reduce absorption (separate by 4 hr)
Omeprazole (Prilosec)PPI20–40 mg dailyGERD, PUD, H. pylori (with abx)Long-term risks: C. diff, hypoMg, B12 def, osteoporosis, AIN. Step down to H2RA when possible
LactuloseOsmotic laxative15–45 mL PO q1–2h initially, then titrate to 3–4 BMs/dayHepatic encephalopathyWorks by converting NH₃ to NH₄⁺ (non-absorbable) in the colon. Diarrhea and electrolyte depletion if over-dosed

Infectious Disease & Rheumatology

Generic (Brand)ClassDoseUsePearl
Vancomycin (Vancocin)Glycopeptide15–20 mg/kg IV q8–12h (AUC/MIC target 400–600)MRSA (bacteremia, endocarditis, pneumonia)Nephrotoxicity, red man syndrome (infuse over ≥ 1 hr). Oral form for C. diff only (not absorbed)
Piperacillin-tazobactam (Zosyn)Beta-lactam/BLI4.5 g IV q6h (extended infusion over 4 hr preferred)Broad-spectrum empiric (HAP, intra-abdominal, febrile neutropenia)Pseudomonal coverage. Increased AKI risk when combined with vancomycin (use cefepime instead)
MethotrexateDMARD (antimetabolite)15–25 mg PO/SQ weeklyRA (cornerstone), psoriasis, SLE, sarcoidosisAlways give folic acid 1 mg daily. Hepatotoxicity, myelosuppression, ILD. CI in pregnancy (teratogen). Hold for surgery/infection
Hydroxychloroquine (Plaquenil)Antimalarial/immunomodulator200–400 mg dailySLE (all patients), RARetinal toxicity with long-term use — annual eye exam after 5 years. QTc prolongation at high doses
Allopurinol (Zyloprim)Xanthine oxidase inhibitor100 mg → titrate to urate < 6 mg/dL (max 800 mg)Chronic gout, tumor lysis prophylaxisStart low, go slow. HLA-B*5801 testing in SE Asian/Black patients (DRESS/SJS risk). Never start during acute flare

42 Abbreviations Master List

General & Cardiovascular

AbbreviationMeaning
ACEI / ARBAngiotensin-converting enzyme inhibitor / angiotensin receptor blocker
AFibAtrial fibrillation
ACSAcute coronary syndrome
BNP / NT-proBNPB-type natriuretic peptide / N-terminal pro-BNP
CADCoronary artery disease
CCBCalcium channel blocker
CHA₂DS₂-VAScCHF, HTN, Age, DM, Stroke, Vascular, Age, Sex category
DAPTDual antiplatelet therapy
DOACDirect oral anticoagulant
EF / LVEFEjection fraction / left ventricular EF
GDMTGuideline-directed medical therapy
HFrEF / HFpEFHeart failure with reduced / preserved ejection fraction
HTNHypertension
INRInternational normalized ratio
MAPMean arterial pressure
MI / NSTEMI / STEMIMyocardial infarction / non-ST-elevation MI / ST-elevation MI
MRAMineralocorticoid receptor antagonist
NYHANew York Heart Association
PCIPercutaneous coronary intervention
VTE / DVT / PEVenous thromboembolism / deep vein thrombosis / pulmonary embolism

Pulmonary & GI

AbbreviationMeaning
ABGArterial blood gas
ARDSAcute respiratory distress syndrome
BiPAP / NIPPVBilevel positive airway pressure / non-invasive positive pressure ventilation
CAP / HAP / VAPCommunity-acquired / hospital-acquired / ventilator-associated pneumonia
COPDChronic obstructive pulmonary disease
DLCODiffusing capacity of the lungs for carbon monoxide
FEV₁ / FVCForced expiratory volume in 1 second / forced vital capacity
GERDGastroesophageal reflux disease
GIGastrointestinal
IBD / UC / CDInflammatory bowel disease / ulcerative colitis / Crohn's disease
ICS / LABA / LAMAInhaled corticosteroid / long-acting beta-agonist / long-acting muscarinic antagonist
ILDInterstitial lung disease
LFTsLiver function tests (AST, ALT, ALP, bilirubin, albumin)
MELDModel for End-Stage Liver Disease
PFTsPulmonary function tests
PPIProton pump inhibitor
PUDPeptic ulcer disease
SBPSpontaneous bacterial peritonitis (or systolic blood pressure, context-dependent)
TIPSTransjugular intrahepatic portosystemic shunt

Nephrology, Endocrine, Heme, Rheum, ID

AbbreviationMeaning
AKIAcute kidney injury
ANAAntinuclear antibody
ANCAAnti-neutrophil cytoplasmic antibody (c-ANCA = PR3, p-ANCA = MPO)
ATNAcute tubular necrosis
BUN / CrBlood urea nitrogen / creatinine
CBCComplete blood count
CKDChronic kidney disease
DICDisseminated intravascular coagulation
DKA / HHSDiabetic ketoacidosis / hyperosmolar hyperglycemic state
DMARDDisease-modifying antirheumatic drug
EPO / ESAErythropoietin / erythropoiesis-stimulating agent
FENaFractional excretion of sodium
GFR / eGFRGlomerular filtration rate / estimated GFR
GN / RPGNGlomerulonephritis / rapidly progressive GN
A1C / HbA1cGlycosylated hemoglobin
HITHeparin-induced thrombocytopenia
MAHAMicroangiopathic hemolytic anemia
MCVMean corpuscular volume
MRSAMethicillin-resistant Staphylococcus aureus
PF4Platelet factor 4
PTHParathyroid hormone
RA / SLERheumatoid arthritis / systemic lupus erythematosus
RRTRenal replacement therapy (dialysis)
SGLT2iSodium-glucose cotransporter 2 inhibitor
SIRSSystemic inflammatory response syndrome
SOFA / qSOFASequential Organ Failure Assessment / quick SOFA
TSHThyroid-stimulating hormone
TTP / HUSThrombotic thrombocytopenic purpura / hemolytic uremic syndrome
UAUrinalysis

43 Risk Scores & Preventive Guidelines

Key Risk Scores

ScorePurposeComponentsAction Threshold
ASCVD Pooled Cohort Equation10-year CV risk (primary prevention)Age, sex, race, total/HDL cholesterol, SBP, BP treatment, DM, smoking≥ 7.5%: moderate-intensity statin. ≥ 20%: high-intensity statin + ASA discussion
HEART ScoreChest pain risk stratification in EDHistory, ECG, Age, Risk factors, Troponin (each 0–2)0–3: low risk (discharge). 4–6: intermediate. 7–10: high (admit, early cath)
RCRI (Revised Cardiac Risk Index)Perioperative cardiac riskHigh-risk surgery, CAD, HF, CVA/TIA, DM on insulin, Cr > 2.00 = 3.9% MACE, 1 = 6%, 2 = 10%, ≥ 3 = 15%
MELD-NaLiver disease mortality / transplant priorityBilirubin, INR, Cr, Na≥ 15: transplant evaluation. ≥ 30: high 3-month mortality
qSOFABedside sepsis screeningRR ≥ 22, AMS, SBP ≤ 100 (each 1 point)≥ 2: high risk, further evaluation
4T ScoreHIT probabilityThrombocytopenia, Timing, Thrombosis, oTher causes (each 0–2)0–3: low. 4–5: intermediate. 6–8: high probability
STOPBANGOSA screeningSnoring, Tired, Observed apnea, Pressure (HTN), BMI > 35, Age > 50, Neck > 40 cm, Gender male≥ 3: high risk for OSA, refer for polysomnography

USPSTF Screening Guidelines (High-Yield)

ConditionScreenPopulationInterval
Colorectal cancerColonoscopy, FIT, or stool DNAAge 45–75Colonoscopy q10yr, FIT annually, Cologuard q3yr
Breast cancerMammographyWomen 40–74Every 2 years (biennial)
Cervical cancerPap smear ± HPV co-testingWomen 21–65Pap q3yr (21–29), Pap + HPV q5yr (30–65)
Lung cancerLow-dose CT chestAge 50–80, ≥ 20 pack-year smoking hx (current or quit < 15 yr)Annually
AAAAbdominal USMen 65–75 who have ever smokedOnce
OsteoporosisDEXAWomen ≥ 65 (or younger with risk factors)Baseline, repeat based on T-score
DiabetesFasting glucose, A1C, or OGTTAge 35–70 with BMI ≥ 25 (overweight/obese)Every 3 years if normal
Hepatitis CAnti-HCV antibodyAll adults 18–79 (one-time)Once
HIVHIV Ag/Ab comboAll adults 15–65Once (more frequent if high-risk)
LipidsLipid panelMen ≥ 35, women ≥ 45 (earlier if risk factors)Every 5 years
Conceptual illustration of preventive healthcare screening measures including blood pressure monitoring, blood tests, and imaging
Figure 16 — Preventive Medicine Screening. Guideline-based screening is a pillar of internal medicine practice. Age-appropriate screening for cancer, metabolic disease, and cardiovascular risk reduces morbidity and mortality across populations. Source: Wikimedia Commons. Public domain.