Easy LIVER

Medicine
CLCF
"Chronic liver cell failure"
C/P Pathophysiology
● Definition: Progressive deterioration of liver function more than six mouth causing
o Toxemia
characteristic clinical syndrome Fatigue o Pyrogen
o Bacteremia:
● Causes: Fever − xx Kupffer - Shunts
3F o Pyrogens
C I T T O Fetor Hepaticus o Toxemia
o No detoxification (Mercapten)
‫تفاح معطب‬
(Fecal sweaty) o Shunt
Congenital Inflammatory Tumor Trauma Other 1- Jaundice: o Failure of all liver steps
Infection (Hepatitis) Liver cirrhosis (Yellow discoloration) (Uptake – Conjunction – Secretion)
Idiopathic is most 2- Encephalopathy: See later
Iatrogenic: - INH common cause
- Parastomal H A L O
o 2H:
− Hypoalbuminemia < 2.5 − 3 𝑔𝑚
● Clinical Picture/Pathophysiology:
▪ Production
− Hypertension portal
3F
3 Cell ▪ Hydrostatic → blood escapes in
General abdomen more than periphery →
Localizing factor only
(Blood escapes after
Fatigue Fever Fetor Ascites Encephalitis Jaundice 3 Hypoalbuminemia)
Hepaticus Cell o 2A:
3- Ascites: − Aldosterone
(Distended abdomen)
▪ Hypovolemia – Renin →
H E S − ADH
▪ Hypovolemia
▪ No distraction by liver
Hepatorenal Endeocrianl Skin o Lymphorrhea:
Edema
Hepatological − Post sinusoidal obstruction
Hepatopulmonary (Weeping liver)
Heart o Other condition:
− SBP
− Malignancy

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 Easy LIVER
Medicine
C/P Pathophysiology C/P Pathophysiology
H E S 1. Palmer erythema: o VDM
1. Hepatorenal: See later • Not specific
• Erythema with center pallor
2. Hepatopulmonary: o Opening of closed AV shunt (VDM)
o VDM
• Hypoxia o Porto pulmonary shunt 2. Paper money skin:
o Basel lung collapse • Small vessel on dorsum of hand
− Cyanosis
− Clubbing 3. Spider Nevi: o VDM
− Platypnea: dyspnea on standing • Dilated arterial with radiating
erect capillary

Skin
(On sleeping Ascites close open • > 5 → LCF
shunts) • Above nipple in distribution on
o RAAS system hyper function SCC
4H 3. Heart: o VDM (No) • DD (Campbell De Morgan)
o Micro:
− Varices (PHTN) Campbell
Spider Nevi
4. Hematological

− Peptic ulcer De Morgan

▪ PHTN - gastrin Dilated Beingn growth
o Normo: Blanching No blanching
• Anaemia 4. Leukonychia: o Hypoalbuminemia
− Hypersplenism (PHTN)
− Toxic BM depression • White nail
o Micro:
− Vit 𝐵12
− Folic acid
o Hypersplenism: platelets
• Bleeding tendency o Coagulation factor
(All synthesized by liver except …..!‫ ؟‬VIP )

1. Endocrinal: o Distribution of pituitary function

(Toxaemia)
E E o Metabolism of opposite hormone
• Gynecomastia • Brest atrophy White nail Ascitis Palmer erthyma
• Impotence • Amenorrhea
• Famine Hair
disruption ▼
2E
2. Edema: o Aldosterone: (2ry hyperaldosteronism)
Generalized
(Anasarca)
Start by Assists the whole body

Spider nevi
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 Easy LIVER
Medicine
Hepatic encephalopathy
● Clinical picture: History or sign of liver cell failure.
● Definition: Reversible neuropsychiatric complex.
● Types: Pre-coma Coma
Symptom Sign (neuro examination) ❖ Irritable
• Inverted sleep • Patient alert, conscious, ❖ DD with Hypoglycaemia &
• Childish attitude cooperative, oriented to hepatic coma
Acute Chronic time – place – person
Acute fulminant liver with average mood and
failure mentality
Chronic liver Chronic portal "Encephalopathy ‫"العكس‬
failure hypertension (shunt) • Flopping tremors
DD 1. Other faultier
● Pathogenesis :
2. metabolic
1) Protein → Colon→ Bacteria → Metabolites → Problem → systemic → BBB → • Foetor hepatitis
encephalopathy
• Problem: − xx Liver
− xx shunt Clinical test
• Metabolites: 1. Constructional apraxia:
Not able to draw a star
1. 𝐍𝐇𝟑 → xx Krebs cycle
2. Reitan number connection test:
2. Merceptens → inhibitory Unable to join numbers
3. Gamma-Aminobutyric acid (GABA) → inhibitory
4. Aromatic amino acid Tyrosine
Branched amino acid Valine ● Investigation – Clinical diagnosis
Normal: branched AA → Noradrenaline → NO effect on dopamine 1. 𝐒𝐞𝐫𝐮𝐦 𝐍𝐇𝟑 Level (not sure)
Aromatic → synthesis of Octopamine → inhibition of dopamine (false 2. EEG:
neurotransmitter) • Triphasic waves
2) Hypokalmia & Alkalosis caused by: • Delta activity (slow high amplitude)
(hypovolemia)
Due to result in
1. Aldosterone 1. Glucose for brain
2. Diuretics 2. Renal 𝐍𝐇𝟑
● Precipitating factor: VIP √√

Metabolites (ptn) 4 Hypovolemia 1 Both

3 ❖ Diuretics ❖ Git Bleeding from
❖ High protein diet
2 ❖ Constipation ❖ Paracentesis 1. varices 2. Peptic ulcer
❖ Peritonitis Hematemesis or Melena

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 Easy LIVER
Medicine
● Treatment:
Acute encephalopathy chronic encephalopathy Hepato-Renal Syndrome
1. Stabilization (TTT of precipitating 1. Avoid precepting factor
factor)
● Def: Functional Renal failure (non-approved prerenal, renal, post renal cause of
• Varices → See later 2. Diet ptn 1gm/Kg/d
to limit of tolerance failure by examination or investigation) in patient with liver cell failure.
• Hypovolemia → Fluid
2. Main triad of encephalopathy:
3. Lactulose 10-30ml/8hr ● Pathophysiology: unknown but ● Criteria:
• Enema / Ryle / 8hr
1. Under fill theory hepato renal failure
• Antibiotic → Bacteria 4. Liver transplantation (best choice) VD of splanchnic arteries by portal
− Metronizole: 500/8hr History Failure NO cause of RF
hypertension → Pooling of blood to
− Gastrobiotic (Rifaximin): 400/8hr splanchnic arteries → Under fill of
, signs , High 1.Prerenal:
• Lactulose: VIP √√ investigation creatinine ✓ No shock
systemic circulation → RAAS of LCF only ✓ Not improved
− 10-30ml/8hr activation → V.C of renal artery → Low GFR < by fluid
− Non absorbable disaccharide GFR → Renal failure 40 2.Renal:
− Osmotic diarrhea 2. Hypovolemia: 1. Albumin ✓ No drugs
− Acid production → 𝑯+ 2. Diuretic ✓ No US finding
𝐴𝑚𝑜𝑛𝑖𝑎 𝑁𝐻3 𝑁𝐻4+ 𝐴𝑚𝑜𝑛𝑖𝑎 3.Postrenal: No
𝑎𝑏𝑠𝑜𝑟𝑏𝑎𝑏𝑙𝑒 𝑛𝑜𝑛 − 𝑎𝑏𝑠𝑜𝑟𝑏𝑎𝑏𝑙𝑒 stone
3. Adjusted Diet: ● Types of heptrorenal
− ptn 0.6gm/Kg/d 1. Type 1: rapidly progressive (creatinine ˃2.5 within 2 weeks) , poor
− K: fruit prognosis
− CHO: ptn sparing → Ammonia 2. Type 2: slowly progressive (creatinine ˃1.5 more than 2 weeks) , Good
prognosis

● Precipitating factor: hypovolemia VIP √√

1. Paracentesis
• Recent trends: 2. Peritonitis
1. Flumazenil (Anti GABA) 3. Diuretics
2. L dopa → dopamine more than octopamine 4. Diarrhea
3. L- ornithine L- aspartate (LoLa) → 𝑁𝐻3 → urea
● Treatment:
1. Correction of Hypovolemia:
• IV fluid
• Albumin √√
2. Correction of under fill:
• VD of splanchnic artery: Octreotide (somatostatin √√)
• VD of renal arteries: Dopamine moderate dose
3. Liver transplantation (best choice)

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 Internal Medicine Jaundice Made easy

Hyperbilirubinemia [Jaundice]

0 1 2 2.5 3 4 5 6

Increase serum Clinical finding yellowish discoloration

Normal Hyperbilirubinemia
bilirubin above normal of sclera & skin and mucus membrane Lab only Jaundice
level >1 mg/dl. occur when bilirubin>2.5 mg/dl

biliverdin

Y,Z receptors

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 Internal Medicine Jaundice Made easy

Bilirubin total 0.2-1mg/dl Types

Indirect Direct
70% 30%
Gilbert
Hyperbilinemia >1 mg/dl Hemolysis Crigler-najgar
syndrome
C/P • Common • Common • Common
Indirect higher
Direct equal • Anemia • Second decade 1. Kernicterus Lead
(indirect to death
or higher (Pallor+ fatigue) • Male>female
hyperbilinemia) 2. Adulthood
• Dark urine • only with fasting
Hemolysis Defect in secretion (Hb urea)
(Hemolytic anemia) pre hepatic Dubin jonson $ & rotor $ Labs • Indirect • Indirect • Indirect
defect in uptake Hepato.cellular jundice • CBC anemia • No anemia • No anemia
(Gilbert syndrome) CITTO • investigation of • Bilirubin • Genetics
Defect in conjugation Obstructive jundice haemolysis never>6 1. AR
Crigler-najgar syndrome • normal liver 2. AD
• Bilirubin never >5
• genetics AD

TTT see later • Reassurance • Reassurance

• Phenobarbitol • phenobarbitol
• Liver
➢ Common pathophysiology & clinical picture transplantation

Indirect Lemon yellow jaundice

Stercobilin Dark Brown stool

Urobilin Normal colored urine (Colorless)

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 Internal Medicine Jaundice Made easy

Pure
Mixed (Biphasic)

↑↑ Direct olive green

jaundice ↑↑ Direct Orange
3- Obstructive ↑↑ Indirect yellow
↓↓ very pale clay jaundice
Stercobilin stool Causes Obstruction ↓↓ very pale
Intrahepatic Extrahepatic Stercobilin clay stool
↑↑ Direct Dark urine • 1ry Billary Outside
cirrhosis Wall ↑↑ Direct Dark urine
Luman
• Sclerosing
cholangitis • Lumen gallstone parasite
• Hepatitis • Wall structure Hepatocellular
1- Dubin Johnson 2- Rotor • Outside cancer pancrease CITTO

C/P Common C/P of pure direct C/P CP as before+ manifestation

C/P Common Common
C/P due to other elements: of liver cell failure
Genetics AD AD Bile salt Cholesterol Labs • ↑ direct + ↑ indirect
Biopsy yellow pigmented Non-pigmented • Abnormal liver function
In blood Not in git • Xanthelasma
hepatocytes hepatocytes • Vitamin k test = ↑ PT
• itching • ↓ Lipid absorption
• puriritis steatorrhea • Cause
• bradycardia • ↓ lipid soluble Vitamin TTT Cause
o K: bleeding tendency
• D: osteomalacia &
hepatic osteodystrophy
`
C/P of the cause
Labs 1. ↑↑ Direct bilirubin
2. Investigation of billary obstruction see later
3. Vitamin k test = ↓ PT
4. Cortisone = ↑ in intra ↓ in extra
5. Cause
TTT 1. Cause
2. Saline + manitol to prevent AKI
3. Cholestyramine & UDCA = ↓ Bilirubin by chelation

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Obstructive Hepatocellular Aproach

History Examination Investigation

Pathophysiology

Prehepatic Obstructive Hepatocellular

• Obstruction ↑ Direct • Failure of liver step (uptake, Diseases • Hemolytic crisis • Gall stones • Hepatitis
(uniphasic) conjugation) ↑ Indirect • Gilbert (willson)
• Secretion = ↑ direct Drug • Methyldopa • Anabolic • INH
(Biphasic) • Rifampcin steroids • Paracetamol
• Jaundice • Jaundice
o Olive green o orange yellow
o Dark urine o less dark urine
Clinical Picture

o Very pale stool o less pale stool

• Other bile salt • Liver cell failure
o Itching o Ascites
o Bradycardia o Encephalopathy
o Steatorrhea o Skin manifestation
o Bleeding tendency o Spider nevi
o Osteomalacia
o Hepatic osteodystrophy
1. ↑ Direct 1. ↑ Direct & indirect
2. ↓ Steroblinogin 2. ↓ Steroblinogin
Investigations

high clearance less decrease

3. ↓ Urobilinogen 3. ↑ Urobilinogen
4. Biliary obstruction pattern as enterohepatc is lost so
5. Cortisone test +ve stero pass in only 2 routes
6. Vitamin k test ↑ PT 4. ↓ Liver function test
5. Cortisone test Not present
6. Vitamin k remain high

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