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CHRONIC LIVER DISEASE – CLINICAL APPROACH

Overview
1. Cirrhosis
2. Portal Hypertension
3. Hepatic encephalopathy
4. Etiology CLD
5. Reason for hospitalisation in CLD

Cirrhosis
End stage liver disease characterised by diffuse damage to hepatic parenchymal cells, fibrosis and disturbance of normal architecture. Assoc w failure of hepatic cell function and interference w liver blood flow. Frequently results in jaundice, portal HT, ascites and ultimately biochem and functional signs of hepatic failure.

Signs of Chronic Liver Disease
1. Ascites
2. Hands
a. Clubbing
b. Dupytrens contractures
c. Palmar erythema (also in pregnancy)
d. Leukonychia (hypoalbuminemia nailbed)
3. Jaundice
4. Bruising (both decreased clotting factors and qualitative/quantitative defect of platelets)
5. Hormonal (reduced E2 b/down by liver)
a. Gynocomastia
b. Testicular atrophy
c. Trend toward female hair distribution (eg loss of axillary hair in males)

Signs of Portal Hypertension
1. Ascites
2. Dilated veins abdo (occur long before caput medusae – extremely rare)
3. Maleana/Hemoptysis (esophageal varices)
4. Hemorrhoids
5. Splenomegaly (enlarged spleen causing pan cytopenia)

Signs of Hepatic Encephalopathy
1. Mental changes (confusion, drowsy, delirious, agitation, memory decline, disorientated, seizures, coma)
2. Hepatic flap (asterixis)
3. Fetor hepaticus (sweet smell breath)
4. Constructional apraxia (draw star or house – effectively assess disease progression also)
5. Other non-specific signs (variable – eg hyper-reflexia, upward plantar reflex)
Hepatic encephalopathy often triggered by a specific event – eg GI bleed, obstructive constipation.

So, if a patients presents with signs of chronic liver disease, look for signs of portal hypertension and signs of hepatic encephalopathy.

If patient presents with these signs – look for a cause.

Etiology CLD
1. Chronic alcoholism (signs -)
a. Heavyset – dilated capillaries, ruddy, suffused face, congested, fat face, bloaty, shiny (pseucocushings – cortisol levels affected)
b. Thin malnourished – multiple vitamin deficiencies
c. Peripheral neuropathies
d. Hyperaesthesia (esp feet) – due to toxic effect or 2ndry to vitamin deficiencies)
e. Parotid gland enlargement (subacute parotiditis)
f. Alcoholic tremor
2. Hepatitis
a. Hep C – IV drug users (look for needle marks)
b. Hep B – homosexuals, tattoed, racial (esp mainlaind china, SE Africa)
3. Hemachromatosis – excessive absorption ingested iron, IBP sat, deposition hemosiderin in tis (esp liver, pancreases, skin) – cirrhosis, diabetes, bronze pigmentation skin, heart failulre.
4. Autoimmune liver dis (younger females)
5. Primary biliary cirrhosis – typically middle-aged women, obstructive jaundice + hyperlipidemia + pruritis + hyperpigmentation, liver shows cirrhosis w marked portal infiltration by lymphocytes/plasma cells.
6. Primary sclerosing cholangitis – recurrent or persistent obstructive jaundice, freq w ulcerative colitis, due to extensive oblitertive fibrosis of extra and intrahepatic bile ducts, generally progresses to cirrhosis, portal HT, liver failure, typically young men.
7. Drugs (eg methotrexate, amioadarone)

Reason for CLD Hospitalisation
Decompensated Cirrhosis
1. GI bleed – eg esophageal varices
2. Hepatic encephalopathies
3. Portal HT, ascites, edematous legs
4. Complications of cirrhosis (eg ?spontaneous bacterial peritonitis)
5. Electrolyte imbalance
6. Hepatoma (LT complication cirrhosis)
7. Other unrelated condition

Ixs
Range of results depending what etiology is.
LFT, FBC, INR etc.

Tx – depends on what patient presents with.

COPD – CLINICAL APPROACH

COPD
Progressive d/o of airway obstruction (FEV1 <80% predicted, FEV1/FVC <0.7) + No or little reversibility
Dx – COPD v Asthma (COPD favoured if age onset >35 yrs, smoking, chr dyspnea, sputum prodn, no marked day-to-day FEV1 variation
COPD includes chronic bronchitis and emphysema (in reality, most pts have features of both)

1. Chronic Bronchitis (blue bloater)

Clin dx Cough + excessive mucus production (>5ml) >3 months in at least 2 consecutive years + not due to any other dis/condition
Path a. Enlargement mucus glands → hypersecretion
b. Irritation → Inflammation + Edema → Bronchospasm, Fibrosis + Narrowing
c. Superadded infection
Progression → mucobronchitis → mucopurulent bronchitis → Chronic wheezy bronchitis (obstruction)
Pres Few signs → Blue Bloater - Cyanosis (blue) + loss of hypercapnic drive + cor pulmonale → edema/congestion (bloating)
Dyspnea
Cyanosis (↓ Hb sat)
Productive cough (sputum)
Wheeze
Plethoric face (polycythemia 2ndry to chr hypoxia)
Frequent respiratory infections that worsen sxs
Fatigue
Asterixis (severe CO2 retention)
Ixs ABG - ↓ PaO2, ↑ PaCO2
Pulmonary function tests, CXR, Pulse oximetry, FBC, Exercise testing, Chest CT
Complics Early cor pulmonale, Acute bronchitis, Pneumonia, Emphysema, Respiratory failure, Cardiac arrhythmia

2. Emphysema (pink puffer)

Histol dx Enlarged air spaces distal to terminal bronchioles with destruction of alveolar wall
Path Destruction of alveolar walls (↑ elastase activity) → Enlargement of air spaces
a. ↓ surface area → ↓ O2 transfer
b. ↓ elasticity → Dyspnea
Small airways collapse during exhalation → airflow obstructive
Pres Pink Puffer – Excess work of breathing, More responsive to hypercapnic drive (hyperventilation allows them to maintain almost normal ABGs)
Tachypneic
Thin (↑ rate of work)
Anxious
Pursed lip breathing (chest cant expand, pt uses chest wall to collapse the airway (functional obstruction) → ↑ pres forces air out)
SCM + accessory respiratory muscle hypertrophy
Tracheal tug
Hyperinflated chest (AP diameter)
Intercostal and subcostal indrawing
↓ Chest expansion
Loss of cardiac and liver dullness
↓ breath sounds
Ixs ABG - ↓ PaO2, ↓ PaCO2 (CO2 is 200x more diffusible so it is more readily excreted)
Spirometry - ↑ TLC, ↓ FEV1
Complics Late cor pulmonale

3. Cor Pulmonale

Def R Heart failure caused by chr pulmonary HT
Causes Chr lung dis, pulm vascular d/os, neuromuscular and skeletal diseases (In COPD – extra work is reqd by the heart to get blood flow through to the lungs)
Signs a. ↑ JVP (v wave) – coming from ventricles (pulm HT → dilated RA/RV → T.Regurg
b. Pulsatile liver
c. Edema
d. Murmur – Pan-systolic over parasternal border, heard better on inspiration
e. RV gallop (lub-da-dub)
Ixs FBC – Hb + hemotocrit ↑ (2ndry polycythemia)
ABG – hypoxia w or w/o hypercapnia
CXR – enlarged RA and RV, prominent pulmonary arteries
ECG – R axis deviation, RV hypertrophy

4. Respiratory Failure (aka Respiratory acidosis)

Type 1 ↓ O2 (<6 – 10-13 normal)
Type 2 ↑↑ CO2
Both chr bronchitis and emphysema → respiratory failure (CO2 retention occurs in emphysemic patients who have chest inf etc)
Signs of Respiratory Failure
↑ CO2
Anxiety
Confusion
Delirious
Agitation
Lethargy
Coma
Asterixis
Warm peripheries (CO2 = vasodilator)
Muscle twitching
Brisk reflexes, Babinski
Hypoxia Dyspnea, restlessness, agitation, confusion, central cyanosis (chr → polycythemia, pulmonary HT, cor pulmonale)
Hypercap Headache, peripheral vasodilation, tachycardia, bounding pulse, asterixis, papilloedema, confusion, drowsiness, coma

5. Why hospital now?

a. INFECTION – viral (influenza), bacterial (Strep.pneumoniae, H.influenzae, M.catarrahalis)
b. Cor pulmonale
c. Respiratory failure
d. Arrhythmia (AF) – in 1/3 of patients eventually
e. Pneumothorax
f. Ca lung (smoking major cause of COPD)
g, PE
h. Natural hx of dis (progression)
i. Poor compliance with meds
j. Unrelated to lung

6. Management - COPD

Treat the cause – Antibiotics!!!
Non-phar Smoking cessation, exercise encouragement, obesity tx, influenza, pneumococcal vaccination, pulm rehab
Pharm Mild Antimuscarinic (M3) eg Ipratropuim OR B2 agonist inhaled PRN
Mod a. Regular ipratropum OR long acting inhaled B2 agonist (eg salmeterol)
b. +/- Inhaled steroid (eg fluticasone)
Seretide = salmeterol + fluticasone
Symbicort = budesonide + formoterol
c. Oral theophylline
Severe Combination therapy – regular short acting B2 agonist + anti-cholinergic, steroids, home nebulisers
Treat associated problems (eg diuretics for cor pulmonale, rate control meds for arrhythmias etc)

COPDX Plan Confirm dx and assess severity, Optimise function, Prevent deterioration, Develop support network and self-mgt plan, manage exacerbations

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