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Semiology > Liver > Flashcards

Liver Flashcards

1
Q

• mental status- portal encephalopathy

A
  • Type A: Hepatic encephalopathy associated with acute liver failure
  • Type B: Hepatic encephalopathy associated with portal-systemic bypass with no intrinsic hepatocellular disease –
  • Type C: Hepatic encephalopathy associated with cirrhosis and portal hypertension or portal-systemic shunts.
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2
Q

Portosystemic encephalopathy Grades

A
  • Subclinical portosystemic encephalopathy (minimal): patients perform poorly on psychometric testing (tasks that require rapid reaction times) Judgment also may be mildly affected.
  • Grade 1 portosystemic encephalopathy: difficulty with memory, mild confusion, agitation, irritability; restlessness or sleeping during the day and insomnia at night; tremor, incoordination
  • Grade 2: a slowing of mentation and speech, with the appearance of lethargy; difficulty with orientation to time, and loss of inhibition; asterixis (flapping tremor), dysarthria, ataxia, hypoactive deep- tendon reflexes
  • Grade 3: Patients are drowsy but can be woken up; they remain markedly confused, aggressive behavior; asterixis persists, but the deep-tendon reflexes become hyperactive as they are disinhibited, a process that culminates in the development of the decerebration, Babinski sign
  • Grade 4: hepatic coma
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3
Q

Skin and mucosa changes

A

– Jaundice SCLERA !!! • Pre-hepatic jaundice • Hepatic jaundice – Pallor (hypersplenism, sec.to hemorrhage) – Liver palms – Spider nevi- upper part of the body – Purpura – Scratch marks- sec.to pruritus

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4
Q

Subcutaneous tissue

A

– Edema lower limbs, ascites; anasarca

– Collateral circulation

– Clubbing- cirrhosis

– Gynecomastia (hormonal changes, spironolactone)

– Terry’s nails= leuconychia- due to hypoalbuminaemia

– Dupuytrene contracture

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5
Q

Involuntary movements

A

Flapping tremor

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6
Q

Face

A

Kaiser fliescher ring Xanthelasma

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7
Q

Respiratory

A

Pleural syndrome

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8
Q

Cardiac

A

Diastolic dysfunction Pericarditis

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9
Q

Liver Palpation Description of hepatomegaly

A

– Size (cm/fingers below the last rib) – Consistence- firm/normal-soft – Surface- regular, irregular – Pain while palpating – The edge: sharp/ rounded – The hepato-jugular reflux

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10
Q

Inspection

A

– Foetor hepaticus- a specific smell due to methylmercaptans (severe liver disease)

– Distension of the abdomen- ascites

– Hernia

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11
Q

Causes of hepatomegaly

A

• chronic parenchymal liver disease
– Alcoholic liver disease
– Autoimmune hepatitis
– Viral hepatitis – Primary biliary cirrhosis
• Malignancy
– Primary hepatocellular cancer
– Secondary metastatic cancer
• Right heart failure

– Lymphoma
– Leukaemia
– yelofibrosis
– Polycythaemia
• Rarities
– Amyloidosis
– Budd-Chiari syndrome
– Glycogen storage disorders

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12
Q

Peculiar aspect

A

– Sharp edge, irregular surface, firm- cirrhosis

• In cirrohis: normal, increased or decreased size of the liver!

– Presence of reflux- hepatomegaly due to cardiac failure

– Asymmetrical hepatomegaly: hydatid cyst, tumor, abscess

– Painful: abscess, possible- acute hepatitis

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13
Q

Askultation of the liver

A

– Friction rub – Venous hum- portal hypertension

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14
Q

Gallbladder Palpation

A

– murphy sign: abrupt interruption of inspiration while palpating due to severe pain= cholecystitis

– Hydrops :

• with jaundice
1 Carcinoma of the head of pancreas= ourvoisier gallbladder
2 Carcinoma of the ampulla of Vater
3 In-situ gallstone formation in the common bile duct

• without jaundice
1 empyema of the gallbladder.
2 Carcinoma of the gallbladder (stone hard, irregular swelling)
3 Acute cholecystitis

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15
Q

Hydrops Def causes

A

an overdistended gallbladder filled with mucoid or clear and watery content
• Causes:
– Impacted stone in the gallbladder neck or cystic duct
– Tumors
– Extrinsic compression of the neck or cystic duct by lymph nodes, fibrosis, by adjacent malignancies in the liver, duodenum, or colon
– Prolonged total parenteral nutrition or ceftriaxone therapy
– Congenital narrowing of the cystic duct
– Parasites, such as ascaris

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16
Q

Inspection gallbladder

A

possible mass in the right hypocondrium: hydrops

17
Q

Manifestation of hydrops

A

– Pain: severe
• persistence of pain and tenderness on RQ longer than 6 hours indicates possible acute cholecystitis

– Nausea, vomiting

– Fever, chills- empyema

18
Q

• bilirubinuria

A

reflects the presence of conjugated bilirubin in urine

– acute viral hepatitis or other hepatobiliary disorders, even before jaundice appears.

19
Q

PT and INR

A

– Are a valuable measure of the liver’s ability to synthesize fibrinogen and vitamin K
– dependent clotting factors: factors II (prothrombin), V, VII, and X
. – Abnormalities indicate severe hepatocellular dysfunction, in acute liver disorders.

• In chronic liver disorders, an increasing PT or INR indicates progression to liver failure.

– The PT or INR does not increase in mild hepatocellular dysfunction and is often normal in cirrhosis.

20
Q

Causes for abnorma pt inr

A

–Fat malabsorption, cholestasis, can cause vitamin K deficiency.
–In chronic cholestasis, marked hepatocellular dysfunction can be ruled out if vitamin K replacement corrects PT (by ≥ 30% within 24 h).

21
Q

Serum albumin

A

Commonly decreased sin chronic liver disorders

22
Q

Portal hypertension

A

Portal hypertension = portal pressure gradient of 12 mm Hg or greater
• pathoph.:
– Increase in vascular resistance to the portal flow
– Increase in portal blood flow

23
Q

Preheating causes for portal hypertension

A

– Portal vein thrombosis
– Splenic vein thrombosis
– Congenital atresia or stenosis of portal vein
– Extrinsic compression (tumors)
– Splanchnic arteriovenous fistula

24
Q

Intrane hepatic causes for portal hypertension

A

– Hepatic cirrhosis – Acute alcoholic hepatitis – Schistosomiasis – Primary biliary cirrhosis (advanced stage) – Idiopathic portal hypertension (advanced stage) – Acute and fulminant hepatitis – Congenital hepatic fibrosis – Vitamin A toxicity- pericellular fibrosis – Budd-Chiari syndrome

25
Q

Post hepatic causes for portal hypertension

A

– Inferior vena cava (IVC) obstruction – Right heart failure – Constrictive pericarditis – Tricuspid regurgitation – Budd-Chiari syndrome – Arterial-portal venous fistula – Increased portal blood flow – Increased splenic flow

26
Q

Manifestations consequences of portal hypertension

A

– the development of new vessels that directly connect the portal blood vessels to the general circulation, bypassing the liver: at the lower end of the esophagus and at the upper part of the stomach- varices
– These engorged vessels are prone to bleeding
– Other collateral vessels may develop on the abdominal wall and at the rectum- hemorrhoids
- Leads to splenomegaly
- Ascites

  • Hemorrhage- varices
27
Q

Ascitis most common causes

A
  • cirrhosis
  • heart failure
  • cardiac cirrhosis
  • a manifestation of anasarca (nephrotic sdr)
28
Q

Ascitis Transudate

A

cirrhosis, heart failure

– Increased pressure in portal vein

29
Q

Ascitis Exudate:

A

peritoneal carcinomatosis

  • Due to inflam., malignancy
  • high win protein, high in lactate dehydrogenase, low pH, low glucose level
  • a difference of less than 1 g/dl (10 g/L) between ascitic and seric albumin levels
30
Q

Ascitis Complication

A

spontaneous bacterial peritonitis
– acute bacterial infection of ascitic fluid
– Especially in cirrhosis
– Fever, abd pain, ascites without resp at therapy, encephalopathy, diarrhea, ileus; 30%: asymptomatic

31
Q

Clinical Ascitis

A

– Bulging of the flanks

– Shifting dulness – Thrill (wave) sign

– Signs dep. upon the etiology

32
Q

Ascitis grading

A
  • Grade 1: mild, only visible on ultrasound
  • Grade 2: detectable with flank bulging and shifting dullness
  • Grade 3: directly visible, confirmed with fluid thrill
33
Q

General symptoms

A

Tiredness Pain due to glissonitis (correlated with effort due to relight cardiac failure)

34
Q

Markedly high values of ALT

A

>500UI/L
•Acute viral hepatitis
•Toxin- or drug-induced hepatitis
•Ischemic hepatitis or hepatic infarction
•Acute exacerbation of autoimmune hepatitis
•Reactivation of chronic hepatitis B
•Acute fatty liver of pregnancy

35
Q

ALT LEVELS

A

–Moderate elevations (300 to 500 IU/L):
•chronic liver disorders (chronic hepatitis, alcoholic hepatitis)
•biliary obstruction, except where passage of a common duct stone can transiently result in markedly high levels
–Mild increases (
•Cirrhosis secondary to viral hepatitis
•Nonalcoholic fatty liver disease (NAFLD)
•Cholestatic liver disorders
•Hepatocellular cancer
–Aminotransferases can be normal in certain liver disorders:
•Hemochromatosis
•Methotrexate - induced liver injury
•Chronic hepatitis C
•NAFLD

Semiology (13 decks)

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