Liver

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-Diaphragmatic surface: the anterosuperior surface of the liver.
The posterior aspect of the diaphragmatic surface is not covered by
visceral peritoneum and is in direct contact with the diaphragm itself
(known as the ‘bare area’ of the liver). The left side of the liver has cardiac
impression.
-Falciform ligament: The falciform
ligament divides the liver into two lobes (2)
Its free edge contains the ligamentum
teres, a remnant of the umbilical vein.

-Caudate lobe – located on the

upper aspect of the visceral surface.
-Quadrate lobe – located on the lower aspect of the visceral surface. It lies
between the gallbladder and a fossa produced by the ligamentum teres.
-The portal vein is formed by the superior mesenteric vein and the splenic
vein anterior to the inferior vena cava, at the level of the first lumbar
vertebra (L1).

-The common bile duct runs within the lesser omentum. Gallbladder is
located at the 9th intercostal space
along the midclavicular line.

-Remak’s plates consist of two radial

rows of hepatocytes directed toward
the lobule, with a bile canaliculus
located between the two rows.
-The common hepatic duct has a diameter of 4-5 cm, and the common bile
duct has a diameter of 5-6 cm.

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-All three carbohydrate metabolic pathways can occur in the liver, but only
the uronic acid pathway is exclusive to the liver.
-Dietary fiber stimulates the greatest production of bile.
-Enterohepatic circulation: 95% of bile salts are reabsorbed and return to
the liver via the portal vein.
-Bile pigment refers to conjugated bilirubin.

Causes of cirrhosis/fatty liver:

-Parasitic infections such as malaria, liver flukes; E. coli infection;
tuberculosis; syphilis
-Malnutrition, gastrectomy
-Autoimmune disorders
-Right-sided heart failure, congestive heart failure, constrictive pericarditis
(pulmonary disease/inferior vena cava obstruction)
-Deficiency of G-6-phosphatase prevents G-6-phosphate from being
converted to glucose, leading to hepatic glycogen accumulation (Von
Gierke disease)
-Lack of lipotropic factors and hepatic steatosis in Wilson’s disease
(impaired copper excretion)
-Hyperthyroidism
-Hypophysectomy causing fatty liver
-Banti’s disease: cirrhosis secondary to splenomegaly

Fatty liver: fat accounts for 10–40% of liver weight:

-Deficiency of lipotropic factors (choline, methionine)
-Prolonged hypoxia: heart failure, anemia
-Chronic toxic exposure: alcohol, chloropropane, phosphorus

Fatty liver is a direct cause of cirrhosis.

Necrosis with regeneration (collapse of tissue causes bridging of vascular

structures toward the central vein, allowing blood to bypass sinusoids)
→ architectural distortion → local hepatic ischemia → necrosis.

“Nutmeg liver”: chronic hypoxia leads to necrosis of hepatocytes around the

central vein of the hepatic lobule.

Pain during acute hepatic congestion results from overstretching of

Glisson’s capsule. Gradual liver enlargement usually causes no pain
because the capsule has time to adapt and stretch.

Portal hypertension: congested blood returns to systemic circulation

through three pathways:
-Via gastric veins to esophageal veins → superior vena cava, causing
esophageal varices (60–70% of cirrhotic patients).
-Via umbilical and abdominal wall veins (prominent abdominal wall veins).
-Via rectal veins to the inferior vena cava, causing hemorrhoidal varices.

Fatty liver: plasma lipids decrease; cholesterol may be normal or

decreased, but esterified cholesterol decreases markedly due to reduced
hepatic esterification.
Obstructive jaundice: both lipids and cholesterol in the blood increase.

Liver failure: water-retaining hormones are not degraded → ADH ↑ (water

retention in kidneys), aldosterone ↑ (Na⁺ retention → water retention),
estrogen ↑ (interstitial water retention) → edema and effusion worsen.
In urine: Na/Cl decreases, Na/K decreases, K/Cl increases
→ indicates renal K⁺ excretion to retain Na⁺, but retained Na⁺ mainly
enters cells or deposits in bone, so serum Na⁺ does not appear elevated.

Unconjugated bilirubin is water-insoluble.

Hemolysis → increased bilirubin production → elevated conjugated bilirubin

in bile → precipitation with Ca²⁺ → formation of black pigment stones.

Hepatic encephalopathy occurs when severe liver failure prevents

detoxification and metabolic regulation:
-Ammonia (NH₃) increases: liver failure → NH₃ enters blood → crosses into
brain → forms glutamine → cerebral edema → altered consciousness.
-Intestinal toxins are not detoxified → enter systemic circulation.
-Hypoglycemia: impaired glycogen synthesis and glucose regulation →
brain energy deficiency → confusion, seizures.
-Water–electrolyte imbalance → cerebral edema.
-Increased false neurotransmitters: impaired degradation of phenylalanine
and tyrosine → production of octopamine, phenylethanolamine, etc.
In the brain: false neurotransmitters replace dopamine → flapping tremor,
confusion.
In the periphery: they replace noradrenaline → reduced vascular tone →
peripheral shunting → decreased renal perfusion → hepatorenal syndrome.

-Liver synthesizes Heparin, chondroitin sulfate.

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ALT (GPT) <40 IU/L; AST (GOT) <40 IU/L.
ALT is located mainly in the cytosol.
AST is present in both the cytosol and the mitochondria.
Approximately 80% of hepatic AST activity is mitochondrial.
In chronic or prolonged injury, mitochondrial destruction increases → AST
rises further over time.

ALT and AST have no tissue-specific isoenzymes; isoenzyme analysis

cannot be used to diagnose liver disease.
Mitochondrial AST increases markedly in acute myocardial infarction and in
chronic alcoholic liver disease (due to deep cellular injury and extensive
necrosis).

Alkaline phosphatase (ALP <290 U/L): elevated in both bone and

hepatobiliary diseases.
If ALP ↑ + GGT ↑ or 5’-nucleotidase ↑ → hepatobiliary origin.
If ALP ↑ but GGT and 5’-nucleotidase are normal → bone origin (or
physiologic causes such as late pregnancy).

Very low ALP levels occur in fulminant Wilson disease with hemolysis,
hypothyroidism, hemolytic anemia, zinc deficiency, and congenital
hypophosphatasia.

Elevated ALP from bone (non-hepatic ALP): indicates high bone turnover,
seen in healing fractures, osteomalacia, hyperparathyroidism,
hyperthyroidism, Paget’s disease, osteosarcoma, and heterotopic
ossification.

ALP increases mildly in hepatocellular dysfunction, markedly in biliary

obstruction, and is consistently elevated in metastatic liver disease.

5’-Nucleotidase is specific for hepatobiliary pathology → if ALP ↑ and 5’-NT

↑, ALP elevation is likely from liver or bile ducts (e.g., obstruction,
cholestatic disease).

If ALP ↑ but 5’-NT is normal → hepatobiliary disease cannot be completely

ruled out, as 5’-NT may remain normal in mild or early liver injury.

GGT elevation is not entirely specific for hepatobiliary disease. It also

increases with:
– Drug use (barbiturates, phenytoin)
– Heavy alcohol consumption (even when other enzymes and bilirubin
remain normal)

In cholestasis, GGT and ALP rise due to increased synthesis by biliary

epithelial cells.
Amylase <90 U/L.
Amylase rises 2–12 hours after onset, peaks at 12–22 hours, and returns to
normal within 3–4 days.

Pancreas
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-The pancreas lies posterior to the

stomach, and the tail of the pancreas
can move freely.

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Paraclinical findings in acute
pancreatitis:
-Serum amylase rises rapidly within
one hour after the onset of pain, then
gradually decreases.
-Urinary amylase increases after 12 to 24 hours.
-Electrolyte disturbances, most notably decreased serum calcium.
-Metabolic acidosis.
-Hyperglycemia.
-X-ray: gas-filled bowel loops, particularly in the colon.
Digestive tube
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-The muscles of the tongue are supplied by the hypoglossal nerve (CN XII).
-General sensation of the anterior two-thirds of the tongue is provided by
the trigeminal nerve (CN V).
-Sensation of the posterior one-third of the tongue is provided by the
glossopharyngeal nerve (CN IX).

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-When food stretches the stomach wall, the vagus nerve triggers increased
pyloric motility; protein-rich food stimulates G cells to secrete gastrin, which
further enhances motility.
-The vomiting center in the medulla receives impulses from the
gastrointestinal, urinary, and reproductive systems, as well as from
increased intracranial pressure.

-Gastrin, cholecystokinin, motilin, and insulin increase gastrointestinal

motility, whereas secretin and glucagon decrease intestinal motility.

-Intestinal obstruction compresses blood vessels, causing ischemia of the

intestinal muscle; stimulation of the visceral nerves leads to sweating,
hypotension, and vomiting, which may result in metabolic alkalosis and
dehydration.

-The parotid gland primarily secretes enzyme-rich and electrolyte-rich fluid,

whereas the submandibular and sublingual glands secrete predominantly
mucous components.

-When gastric acid enters the duodenum, S cells secrete prosecretin, which
is activated by acid into secretin; secretin travels via the bloodstream to the
pancreas and stimulates bicarbonate secretion.

-Bile salts are reabsorbed at the terminal ileum at a rate of about 95% and
return to the liver via the portal circulation.

-Secretin stimulates water and ion secretion in bile; the vagus nerve and
CCK mainly cause gallbladder contraction and relaxation of the sphincter of
Oddi.

-Cholera toxin stimulates the formation of intracellular cyclic AMP in

epithelial cells, opening chloride channels. The efflux of Cl⁻ pulls Na⁺ and
water along, resulting in severe dehydrating diarrhea.

-Digestive enzymes of the small intestine are not secreted into the lumen;
they are located on the brush border membrane of the epithelial cells.

-Sodium absorption and potassium secretion in the large intestine are

regulated by aldosterone.
-The colonic mucosa secretes bicarbonate in exchange for chloride
absorption; bicarbonate helps neutralize acids produced by bacterial
metabolism.

-The duodenum and jejunum absorb most nutrients and vitamins. Fat
absorption requires bile salts and therefore occurs mainly in the terminal
ileum (vitamin B12 is also absorbed in the ileum).

-Secretin: stimulates secretion of water and bicarbonate with minimal

enzyme release (in the liver and pancreas), enhances bile production.
-CCK: stimulates enzyme secretion, contracts the gallbladder, increases
intestinal motility, and slows gastric emptying by increasing pyloric tone.
-I cells: secrete CCK in response to amino acids, fatty acids, and peptides.
-S cells: secrete secretin when pH drops below 4.5.
-Hartnup disease causes a deficiency of amino acid transporters at the
basolateral membrane.
-Disorders of amino acid transport such as lysine, arginine, and cystine can
lead to cystine kidney stones.

Endocrine cells (argentaffin cells):

In the fundic glands, they secrete serotonin, somatostatin, and histamine.
In the pyloric glands, they secrete somatostatin and gastrin.

Gastric pits in the fundic region: The pits are short, accounting for about
one-quarter of the gland height. The underlying glands are long and contain
numerous parietal cells, chief cells, and histamine-secreting
enteroendocrine cells.
Gastric pits in the pyloric region: The pits are longer, sometimes occupying
up to one-half of the gland depth. The underlying glands are short,
tortuous, and have a wider lumen. They are composed mainly of mucous
cells and endocrine cells.
-Neck mucus, produced by mucous neck cells, is less viscous than the
mucus found on the surface epithelial cells.

-The fundic glands are branched tubular glands.

-Argentaffin cells in the fundic glands secrete serotonin, which enhances

the motility of the muscular layer.

-The muscularis mucosae in the esophagus, stomach, and duodenum is

not continuous.