---

Alcoholic Liver Disease (ALD) - Complete MBBS Guide

Your Patient's Presentation - Decoded First

---

1. SPECTRUM OF ALCOHOLIC LIVER DISEASE

Alcohol use
     ↓
1. Alcoholic Fatty Liver (Steatosis)  ← reversible with abstinence
     ↓
2. Alcoholic Hepatitis (Steatohepatitis) ← partially reversible
     ↓
3. Alcoholic Cirrhosis ← IRREVERSIBLE (but progression can be halted)

• Cirrhosis develops in only 10-20% of heavy drinkers - requiring typically 10-15 years of chronic drinking
• Alcoholism is the most common cause of cirrhosis in the United States (~48% of all cirrhotic deaths)
• (Rosen's Emergency Medicine, p.2885)

---

2. PATHOLOGY (Histological Stages)

Stage 1 - Fatty Liver (Steatosis)

• Earliest and most common change
• Fat accumulates as large lipid droplets in hepatocytes (macrovesicular steatosis)
• Mechanism: Alcohol is metabolized → NADH excess → impaired fatty acid beta-oxidation → fat accumulation
• Completely reversible with abstinence

Stage 2 - Alcoholic Hepatitis (Steatohepatitis)

• Mallory-Denk bodies (Mallory's hyaline) - eosinophilic intracytoplasmic aggregates of cytokeratin intermediate filaments - pathognomonic
• Hepatocyte ballooning and necrosis
• Neutrophilic infiltrate (important - it's neutrophils, NOT lymphocytes)
• Centrilobular inflammation

Stage 3 - Cirrhosis

• Micronodular cirrhosis early (nodules <3mm) → may become macronodular
• Disruption of normal hepatic architecture by fibrosis and regenerating nodules
• Irreversible - but progression halts with abstinence

---

3. PATHOGENESIS

Ethanol
   ↓ (alcohol dehydrogenase + MEOS/CYP2E1)
Acetaldehyde  ←  main toxic metabolite
   ↓
• Lipid peroxidation (oxidative stress via ROS)
• Mitochondrial dysfunction
• Impaired protein secretion
• Adduct formation with proteins → immune response → Mallory bodies
• Activates Kupffer cells → TNF-α, IL-1, IL-6 release → hepatocyte death
• Gut microbiome changes → increased LPS → more Kupffer cell activation

---

4. CLINICAL FEATURES

Symptoms

• Anorexia, nausea, vomiting, weight loss
• Right upper quadrant pain
• Fever (temperatures up to 104°F, mediated by IL-1, TNF - can persist for weeks)
• Dark urine, pale stools

Signs - Frequency in Hospitalized ALD Patients (Sleisenger & Fordtran)

Full Set of Physical Signs to Know:

• Jaundice (scleral icterus first)
• Parotid enlargement (bilateral, painless)
• Dupuytren's contracture (palmar fibrosis - ring and little finger)
• Palmar erythema
• Leukonychia (white nails) / Muehrcke's lines
• Clubbing (hepatopulmonary syndrome)
• Asterixis (liver flap - encephalopathy)

• Spider angiomata (>5 are significant - in SVC drainage territory)
• Gynecomastia (estrogen excess - reduced hepatic clearance)
• Testicular atrophy
• Loss of axillary/pubic hair
• Caput medusae (dilated periumbilical veins - portal HTN)
• Muscle wasting

• Hepatomegaly (tender in acute hepatitis; hard and nodular in cirrhosis)
• Audible hepatic bruit (in alcoholic hepatitis - AV shunts)
• Splenomegaly
• Ascites (shifting dullness, fluid thrill)

• Loud S1 - from hyperdynamic circulation (high cardiac output, increased blood flow)
• Tachycardia
• Raised JVP - from hyperdynamic/high output state OR cirrhotic cardiomyopathy

---

5. YOUR PATIENT'S FINDINGS - MECHANISM

Jaundice

• Hepatocytes cannot conjugate bilirubin (damaged glucuronyl transferase)
• In severe disease, bilirubin >5 mg/dL = "moderate" disease by definition
• Bilirubin >25 mg/dL = poor prognostic sign

Hepatomegaly

• Most common finding in ALD (87% overall)
• Due to fat infiltration + edema + inflammation
• In cirrhosis, liver can eventually become small and hard (nodular)
• Tender in acute alcoholic hepatitis

Splenomegaly

• Portal hypertension → increased portal venous pressure → back-pressure on spleen → congestive splenomegaly
• Leads to hypersplenism → thrombocytopenia (splenic sequestration)
• Thrombocytopenia is often the first lab clue to portal hypertension

Raised JVP + Loud S1 - The Hyperdynamic Circulation

"A hyperdynamic circulation characterized by a high cardiac output, low arterial blood pressure, and low systemic vascular resistance is the hallmark of end-stage liver disease." (Miller's Anesthesia)

1. Portal hypertension → portosystemic shunting
2. Liver fails to clear vasodilatory mediators - natriuretic peptides, cytokines, nitric oxide - from portal blood
3. Nitric oxide = potent vasodilator → splanchnic vasodilation
4. Effective arterial underfilling → baroreceptor activation → sympathetic activation, RAAS activation → sodium/water retention → increased total blood volume
5. High CO + high blood volume → increased flow across cardiac valves → loud S1 (mitral valve closes with more force)
6. Increased venous return → raised JVP

• Defined since 2005 as a spectrum of cardiac changes in cirrhosis
• Diastolic dysfunction in >50% of patients with liver disease
• QTc prolongation - most recognized ECG change
• Systolic dysfunction (blunted response to stress, decreased LVEF <55%)
• Correlates with severity of liver disease

---

6. LABORATORY INVESTIGATIONS

---

7. SEVERITY SCORING - MUST KNOW FOR MBBS

Maddrey's Discriminant Function (DF) - Most Tested

DF = 4.6 × (PT patient - PT control) + Serum Bilirubin (mg/dL)

MELD Score

MELD = (0.957 × log[creatinine] + 0.378 × log[bilirubin] + 1.12 × log[INR] + 0.643) × 10

• MELD ≥29 = 30% 3-month mortality; MELD ≥38 = 80% 3-month mortality

ABIC Score

ABIC = (Age × 0.1) + (Bilirubin × 0.08) + (Creatinine × 0.3) + (INR × 0.8)

• Score ≥9.0 = 75% 90-day mortality

Glasgow Alcoholic Hepatitis Score (GAHS)

• Uses: Age, WBC, BUN, Bilirubin, INR
• Score ≥9 = poor prognosis

---

8. DIAGNOSIS

• History of significant alcohol use (men >30 units/week, women >20 units/week for >5 years)
• Clinical + biochemical features as above
• AST:ALT >2 (if >3, highly suggestive of ALD)
• Exclusion of other liver disease (viral hepatitis, autoimmune, etc.)

---

9. COMPLICATIONS (from portal hypertension + hepatic failure)

• Esophageal/gastric varices → variceal bleeding (life-threatening)
• Ascites → spontaneous bacterial peritonitis (SBP)
• Splenomegaly → hypersplenism → pancytopenia
• Hepatic encephalopathy (ammonia toxicity)
• Caput medusae, hemorrhoids (anorectal varices)

• Coagulopathy
• Hypoalbuminemia → edema
• Hepatorenal syndrome
• Hepatopulmonary syndrome (shunts → hypoxia)
• Hepatocellular carcinoma (10-15x increased risk)

• Wernicke's encephalopathy / Korsakoff's (thiamine deficiency) - give thiamine BEFORE glucose
• Peripheral neuropathy (B12, thiamine)
• Pellagra (niacin deficiency)

---

10. MANAGEMENT

General

• Abstinence - single most important intervention; can halt cirrhosis progression
• Nutritional support - 35-40 kcal/kg/day, 1.2-1.5 g protein/kg/day
• Thiamine (B1) - always first, before glucose to prevent Wernicke's
• Folate supplementation
• Avoid hepatotoxic drugs (NSAIDs, paracetamol excess)

Specific - Acute Alcoholic Hepatitis

• If DF ≥32 (severe disease):
  • Prednisolone 40 mg/day × 28 days (if no contraindications - infection, GI bleed, renal failure)
  • Use Lille score at Day 7 to assess response; if score >0.45 = no response → stop steroids
  • Pentoxifylline - was used (TNF-alpha inhibitor), but evidence shows inferior to prednisolone; no longer first-line
  • N-acetylcysteine may be added to prednisolone

Complications Management

• Ascites: Salt restriction + spironolactone ± furosemide; large-volume paracentesis with albumin replacement
• Variceal bleeding: Octreotide + endoscopic band ligation + propranolol (prophylaxis)
• SBP: Cefotaxime; primary prophylaxis with norfloxacin in high-risk patients
• Hepatic encephalopathy: Lactulose (reduces ammonia) + rifaximin
• Hepatorenal syndrome: Terlipressin + albumin

Definitive Treatment

• Liver transplantation - for end-stage disease (MELD ≥15)
• Most centers require 6 months of abstinence before listing
• 5-year survival post-LT is 70-80%

---

11. PROGNOSIS - KEY NUMBERS

• Fatty liver: Excellent if abstinence achieved
• Alcoholic hepatitis: 25-35% 1-month mortality in severe disease
• Cirrhosis: 5-year mortality 60-85%
• If decompensated cirrhosis + variceal bleed + ascites: 50% 1-year mortality
• Hepatic encephalopathy development: 65% 1-year mortality

---

12. QUICK MEMORY TRICKS

• Maddrey (DF ≥32 → steroids)
• ABIG (ABIC score)
• Glassgow score

---

---

Alcoholic Liver Disease - Deep Dive: Signs, Definitions & Why

---

PART 1: ALCOHOL DEFINITIONS - WHAT IS "STANDARD DRINK"?

Standard Drink (1 Unit)

Units = Volume (ml) × ABV% ÷ 1000

---

Risk Categories (NIAAA Definitions)

Why Women Have Lower Limits - The Science

1. Lower total body water - women have ~50% body weight as water vs ~60% in men → same alcohol in less water = higher blood alcohol concentration (BAC)
2. Less gastric alcohol dehydrogenase - the enzyme that metabolizes alcohol before it even reaches blood ("first-pass metabolism") is present in lower amounts in women
3. Hormonal effects - estrogen may enhance liver toxicity of alcohol
4. Result: Women develop cirrhosis at lower doses and shorter durations of drinking compared to men. For ALD to develop: men typically need >80g/day for 10+ years; women only need >20g/day

---

PART 2: PHYSICAL SIGNS - DEFINITION + HOW TO ELICIT + WHY IT OCCURS

---

🔶 JAUNDICE

• Look at the sclera first - most sensitive site (sclera has high elastin which binds bilirubin)
• Check under the tongue (sublingual jaundice)
• Look at palms, skin in good white light
• Grading: Scleral jaundice first → then skin → frank yellow skin = severe

• Hepatocytes are damaged → cannot conjugate bilirubin (glucuronyl transferase is impaired)
• Bilirubin backs up in blood → deposits in tissues
• In cirrhosis, intrahepatic bile duct compression also contributes (cholestatic component)
• Type: Predominantly HEPATOCELLULAR jaundice (both conjugated + unconjugated raised, but conjugated dominates; dark urine + pale stools present)

---

🔶 HEPATOMEGALY

1. Start palpation from right iliac fossa (so you don't miss a very enlarged liver)
2. Ask patient to breathe in - liver descends on inspiration, you feel its edge
3. Percuss upper border (normally 5th ICS, midclavicular line) and lower border
4. Normal liver span = 8-12 cm in midclavicular line
5. Describe: size (cm below costal margin), consistency (soft/firm/hard), surface (smooth/irregular/nodular), tenderness, pulsatility

---

🔶 SPLENOMEGALY

1. Start from right iliac fossa (enlarged spleen grows toward RIF)
2. Move diagonally toward left hypochondrium
3. Features that confirm it's spleen (not kidney): moves with respiration, cannot get above it, has a notch on medial border, dull to percussion (vs. kidney: resonant, ballottable, can get above it)
4. Normal spleen weighs ~150g; splenomegaly when >500g

Liver fibrosis + regenerative nodules
        ↓
Obstruction to portal blood flow (sinusoidal/post-sinusoidal)
        ↓
Portal venous pressure rises (normal: 5-10 mmHg → >12 mmHg = portal HTN)
        ↓
Back-pressure transmitted to splenic vein
        ↓
Spleen becomes congested with blood = CONGESTIVE SPLENOMEGALY
        ↓
Spleen enlarges + traps blood cells = HYPERSPLENISM
        ↓
Thrombocytopenia (low platelets) + mild anemia + leukopenia

---

🔶 RAISED JVP (Elevated Jugular Venous Pressure)

1. Position patient at 45° recline
2. Turn head slightly to left
3. Look for the internal jugular vein pulsation (between the two heads of SCM) - NOT the external jugular (less reliable)
4. Identify the highest point of visible pulsation
5. Measure vertical height above sternal angle
6. Characteristics: JVP has TWO waves (a and v) and TWO descents (x and y) - helps distinguish from carotid (which has one impulse, is palpable, not obliterable)

Alcohol → liver failure → nitric oxide NOT cleared by liver
        ↓
Splanchnic vasodilation
        ↓
Effective underfilling of arterial circulation
        ↓
RAAS + SNS activation → sodium + water retention
        ↓
Increased total blood volume
        ↓
Increased venous return to right heart
        ↓
RAISED JVP + tachycardia + loud S1

• Diastolic dysfunction (impaired LV relaxation) → increased filling pressures → raised JVP
• Seen in >50% of cirrhotic patients (Miller's Anesthesia)

---

🔶 LOUD S1 (First Heart Sound)

• Auscultate at apex (5th ICS, midclavicular line) with diaphragm
• S1 = "lubb" (coincides with apex beat, precedes carotid pulse)
• Loud S1 when it is clearly louder than normal or louder than S2 at apex

1. Position of mitral valve leaflets at START of systole (how far open they are before closing)
2. Speed/force of valve closure
3. Cardiac output and blood flow velocity

High cardiac output + high blood volume + increased blood flow velocity
        ↓
Mitral valve leaflets are wide apart at end of diastole (high flow filling)
        ↓
They must travel further and close with greater velocity
        ↓
LOUD S1

---

🔶 SPIDER ANGIOMA (Spider Naevi)

• Press the central red dot with a pen tip or glass slide
• Blanches when pressed (because blood is forced out of arterioles)
• Refills from center outward when pressure released (diagnostic)

• 5 spider naevi = significant; 1-5 can be normal in pregnancy/OCP use

• Liver fails to metabolize estrogen → hyperestrogenemia
• Estrogen causes arteriolar dilatation + angiogenesis
• The same mechanism causes palmar erythema, gynecomastia, and testicular atrophy

---

🔶 PALMAR ERYTHEMA

• Look at both palms
• Press - it blanches, then refills
• Compare with your own palm

---

🔶 DUPUYTREN'S CONTRACTURE

• Ask patient to lay hand flat on table - ring/little finger cannot be fully extended = positive tabletop test
• Feel for thickened fibrous cord in the palm

---

🔶 GYNECOMASTIA + TESTICULAR ATROPHY

• Gynecomastia = benign proliferation of glandular breast tissue in males
• Testicular atrophy = reduced testicular volume (<15 ml normal adult)

• Pinch tissue behind nipple with two fingers
• If glandular disc is felt (firm, mobile, rubbery behind nipple) = true gynecomastia
• If just fat = pseudogynecomastia (lipomastia)

Liver damage → reduced hepatic clearance of estrogen
        ↓
Elevated estrogen levels in males
        ↓
Estrogen stimulates breast glandular tissue → GYNECOMASTIA
        ↓
Estrogen suppresses LH → reduced testosterone production
        ↓
TESTICULAR ATROPHY + reduced libido + impotence

---

🔶 ASTERIXIS (Flapping Tremor / Liver Flap)

1. Ask patient to extend arms in front with wrists extended (dorsiflexed) and fingers spread - "like stopping traffic"
2. Keep eyes open initially, then close eyes
3. Positive = sudden rapid downward flap of the wrist followed by correction - irregular, non-rhythmic, bilateral
4. Can also be elicited at ankles and tongue

Liver fails to detoxify ammonia (NH3)
        ↓
NH3 crosses blood-brain barrier
        ↓
Converts to glutamine in astrocytes → astrocyte swelling (cerebral edema)
        ↓
Disrupts reticular activating system and motor pathway function
        ↓
Intermittent lapses in motor neuron firing = ASTERIXIS

---

🔶 CAPUT MEDUSAE

• Inspect the abdomen with patient lying flat
• Look for dilated veins around umbilicus
• Flow direction test: Place two fingers on the vein, compress it, lift one finger and see which direction fills - in caput medusae, flow is away from the umbilicus in all directions (distinguishes from IVC obstruction where all flow goes upward)

Portal hypertension → portal venous pressure rises
        ↓
Blood finds alternative routes to bypass the liver (portosystemic collaterals)
        ↓
Para-umbilical veins (embryological remnants in falciform ligament) reopen
        ↓
Veins dilate and become visible = CAPUT MEDUSAE
        ↓
Flow: FROM the portal system → through umbilicus → INTO systemic veins
∴ Away from umbilicus

---

🔶 ASCITES

• Shifting dullness (most reliable): Percuss from umbilicus laterally until dull → keep finger there → roll patient toward you → wait 30 seconds → percuss again → if now resonant = shifting dullness (fluid has shifted)
• Fluid thrill: One hand on one flank, flick the other flank, ask patient to place edge of hand along midline (stops fat wave) - feel the transmitted wave (only works in massive ascites)
• Puddle sign: Patient on hands and knees - percuss umbilicus area - dull = even small amounts of fluid (>120 ml)

1. Portal hypertension → increased hydrostatic pressure in portal capillaries → fluid transudes into peritoneum
2. Hypoalbuminemia (liver can't make albumin) → reduced oncotic pressure → fluid stays in interstitium
3. Activation of RAAS (due to underfilling) → sodium + water retention → more fluid
4. Lymphatic overflow from liver surface (hepatic sinusoidal HTN)

• SAAG = serum albumin - ascites albumin
• SAAG ≥1.1 g/dL = portal hypertension (includes ALD)
• SAAG <1.1 g/dL = exudative (malignancy, TB)

---

🔶 LEUKONYCHIA (WHITE NAILS) + MUEHRCKE'S LINES

• Definition: White discolouration of nails with loss of normal pink color; only 1-2mm of normal nail at the distal tip
• Why: Hypoalbuminemia alters nail bed vascularity
• Also in: renal failure, cardiac failure, malnutrition

• Definition: Paired, white, transverse bands parallel to the lunula (not in the nail itself but in the nail bed - they don't move with nail growth)
• Why: Hypoalbuminemia → edema of the nail bed → compresses the vascular bed → white lines
• When albumin normalizes → lines disappear

---

PART 3: PUTTING IT ALL TOGETHER FOR YOUR PATIENT

Alcohol (chronic heavy use)
          ↓
LIVER DAMAGE
    ├── Hepatocyte necrosis
    │       ↓ Jaundice (can't process bilirubin)
    │       ↓ Hepatomegaly (swollen, tender liver)
    │       ↓ ↑AST/ALT, ↑Bilirubin, ↓Albumin, ↑PT
    │
    ├── PORTAL HYPERTENSION
    │       ↓ Splenomegaly (back-pressure on spleen)
    │       ↓ Caput medusae (collateral veins)
    │       ↓ Ascites (fluid in peritoneum)
    │       ↓ Varices (esophageal - danger of bleeding)
    │
    ├── REDUCED SYNTHETIC FUNCTION
    │       ↓ Low albumin → edema, leukonychia, Muehrcke's lines
    │       ↓ Low clotting factors → coagulopathy
    │
    ├── HYPERESTROGENEMIA
    │       ↓ Spider naevi, Palmar erythema
    │       ↓ Gynecomastia, Testicular atrophy
    │
    ├── HYPERDYNAMIC CIRCULATION
    │       ↓ High CO, Low SVR
    │       ↓ LOUD S1 (high flow across mitral valve)
    │       ↓ RAISED JVP (increased venous return)
    │       ↓ Tachycardia, bounding pulse
    │
    └── HEPATIC ENCEPHALOPATHY (if severe)
            ↓ Asterixis, confusion, drowsiness, coma

---

PART 4: RISK DRINKING SUMMARY TABLE

1. Less body water (higher BAC per drink)
2. Less gastric ADH (more alcohol reaches liver)
3. Hormonal effects of estrogen on hepatotoxicity
4. Women develop cirrhosis faster and at lower doses

---

---

CAGE Questionnaire + Alcohol Risk in Grams - India Context

---

1. STANDARD DRINK IN INDIA

What Does 10g Look Like in Indian Drinks?

Grams of pure alcohol = Volume (ml) × ABV% × 0.789 (density of alcohol) ÷ 100

---

2. RISK CATEGORIES IN GRAMS - INDIA (NDDTC/AIIMS)

In Practical Indian Terms:

---

3. THE CAGE QUESTIONNAIRE

Origin & Purpose

• Developed by Ewing JA (1984)
• Takes <1 minute to administer
• Screens for alcohol use disorder (not just risky drinking)
• The word "ever" is used = detects lifetime alcohol problems
• Does NOT distinguish current from past problems (limitation)

The 4 Questions - Remember the Acronym

---

Scoring + Interpretation

---

Limitations of CAGE (Important for Exams)

1. Uses word "ever" - cannot identify current drinkers vs. reformed drinkers
2. Less sensitive for women (designed in male populations)
3. Misses early/hazardous drinking (catches established disorder, not risky drinking)
4. No questions about quantity or frequency
5. For early detection → AUDIT is better

---

4. AUDIT vs CAGE - COMPARISON

---

5. DSM-5 ALCOHOL USE DISORDER (replaces "abuse" and "dependence")

1. Taking more or for longer than intended
2. Persistent desire or failed attempts to cut down
3. Craving
4. Much time spent obtaining, using, recovering

---

6. PUTTING IT TOGETHER FOR YOUR PATIENT IN INDIA

• "What do you drink - whisky, beer, desi daru?"
• "How many pegs/bottles per day?" → convert to grams
• "How long have you been drinking this much?"

• Hooch/Country liquor: often adulterated with methanol → acute methanol poisoning → optic nerve damage, blindness, death (separate emergency!)
• Desi sharab: variable ABV - always estimate by asking volume + brand if possible
• Old Monk, Royal Stag, etc.: ~40-43% ABV - calculate by peg size

---

7. QUICK SUMMARY CARD

CAGE Scoring:
C - Cut down?
A - Annoyed by criticism?
G - Guilty feelings?
E - Eye-opener in morning?

Score ≥2 = Alcohol Use Disorder (sensitivity 43-94%)
Score ≥1 = Warrants further evaluation

India Safe Limits (10g = 1 standard drink):
Men:   ≤20g/day (≤2 pegs whisky)
Women: ≤10g/day (≤1 peg whisky)

Cirrhosis threshold:
Men:   >80g/day for 10-15 years
Women: >20-40g/day (lower and sooner)

---

---

Drinker/Smoker Classifications + Alcohol System-wise Effects

---

PART 1: CLASSIFICATION OF DRINKERS

---

Categories of Drinkers

---

Why "Reformed Drinker" is Tricky - The J-curve Paradox

• Never-drinkers: moderate mortality
• Moderate drinkers: LOWEST mortality (the controversial "protective effect")
• Heavy drinkers: HIGHEST mortality

• When did they stop?
• How much did they drink before?
• Why did they stop? (Did doctor advise them? Did they feel sick?)
• Liver damage from prior use may still be present even after years of abstinence

---

How to Document in India (for Case Records)

Alcohol history:
- Status: Current drinker / Former drinker / Never drinker
- Type: Whisky / Beer / Country liquor / Mixed
- Quantity: ___ pegs/bottles per day = ___ grams/day
- Frequency: Daily / Weekly / Binge
- Duration: ___ years
- Total pack-equivalent years: (if documenting)
- CAGE score: ___ / 4
- Last drink: (date/time - important for withdrawal timing)

---

PART 2: CLASSIFICATION OF SMOKERS

---

Categories of Smokers

---

Pack-Year Calculation - VERY IMPORTANT for MBBS

Pack-Years = (No. of cigarettes per day ÷ 20) × Years of smoking
            = Packs per day × Years smoked

• >10 pack-years: Spirometry screening for COPD
• >20 pack-years: Significant COPD / cancer risk
• >30 pack-years: High-risk group; Low-dose CT screening for lung cancer (USPSTF)
• >40 pack-years: Very high risk for COPD, lung cancer, CVD

• 1 bidi ≈ 0.2-0.5 cigarettes (lower tobacco, unfiltered, actually more toxic per gram)
• Bidi pack-year: same formula but note bidi packs = 25 bidis
• Hookah/Chillum: harder to quantify; equivalent to multiple cigarettes per session
• Smokeless tobacco (gutka, pan masala, khaini): oral cancer risk, different calculation

• Risk begins falling within 20 minutes (BP and pulse normalize)
• 1 year: MI risk halved
• 5 years: Stroke risk equals non-smoker
• 10 years: Lung cancer risk halved
• 15 years: CVD risk equals non-smoker

---

PART 3: ALCOHOL - SYSTEM-WISE EFFECTS

---

🫀 CARDIOVASCULAR SYSTEM

---

🧠 CENTRAL NERVOUS SYSTEM

Remember: Give thiamine BEFORE glucose - glucose infusion in B1-deficient state precipitates acute Wernicke's

---

🍺 GASTROINTESTINAL SYSTEM

---

🫁 RESPIRATORY SYSTEM

---

🩸 HAEMATOLOGICAL SYSTEM

---

🦴 MUSCULOSKELETAL SYSTEM

---

🫘 RENAL / ENDOCRINE SYSTEM

---

🎗 CANCER RISK (Alcohol)

• Oral cavity
• Pharynx
• Larynx
• Esophagus (squamous)
• Liver (HCC)
• Colon / Rectum
• Breast (even moderate drinking increases risk)

---

🤰 REPRODUCTIVE / PERINATAL

---

🧫 IMMUNE SYSTEM / INFECTIONS

---

⚠️ ALCOHOL WITHDRAWAL SYNDROME - Timeline

• Disorientation + agitation
• Fever (>38°C)
• Tachycardia, hypertension, diaphoresis
• Visual hallucinations (characteristically seeing small animals - "pink elephants")
• Tremors

• Benzodiazepines - drug of choice (long-acting: diazepam/chlordiazepoxide; short-acting: oxazepam/lorazepam if liver disease)
• Thiamine 250-500 mg IV/IM before glucose - ALWAYS
• Correct hypomagnesemia (required as cofactor for thiamine)
• CIWA-Ar score to guide dosing

---

QUICK SUMMARY TABLE

---