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Clinical Anatomy > Liver etc. > Flashcards

Liver etc. Flashcards

1
Q

Liver location

A
  1. Upper right quadrant, beneath the diaphragm. Largest internal organ
    Weighs ~ 1500 grams
  2. The liver is the largest gland in the body. It extends from the right to the left hypochondriac region (¾ of the liver is in the right superior quadrant).
  3. Immediately adjacent to the inferior surface of the diaphragm → location is breath-dependent (rises during exhalation, lowers during inhalation)

Superior limit height of the 5th intercostal space during exhalation

Inferior limit curve of the right costal arch during inhalation

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2
Q

Liver basic and major functions

A

Basic -
Metabolic
Secretory
Vascular

Major -
Excretion of waste products from bloodstream by excretion into bile

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3
Q

Four specific functions of the liver

A
  1. processing of dietary amino acids, carbohydrates, lipids and vitamins
  2. removal of microbes and toxins in splanchnic blood
  3. synthesis of plasma proteins
  4. detoxification and excretion into bile of endogenous waste products & pollutant xenobiotics
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4
Q

Hepatic artery

A
  1. Supplies O2 rich blood from heart to liver
  2. Provides 20-30% of blood supply to liver
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5
Q

Portal Vein

A
  1. Supplies nutrient rich blood from the digestive tract
  2. Provides 70-80% of blood to liver
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6
Q

Lobes of the Liver

A
  1. RIght
  2. Left
  3. Caudate
  4. Quadrate
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7
Q

Ligaments of the liver

A
  1. Falciform Ligament
  2. Teres Ligament
  3. Coronary Ligament
  4. Right Triangular Ligament
  5. Left Triangular Ligament

Ligaments of the liver are double layers of visceral peritoneum that fix the position of the liver by attaching it to the surrounding structures

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8
Q

Unique organ feature of the liver

A

The liver is the only human organ that has the remarkable property of self-regeneration. If a part of the liver is removed, the remaining parts can grow back to its original size and shape.

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9
Q

Coronary Ligament

A

Peritoneal reflection from the diaphragm to the liverDemarcates the bare area (surface of the liver with no peritoneal covering)

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10
Q

Falciform Ligament

A

Peritoneal reflection from the umbilicus to the liverRemnant of the embryonic ventral mesentery Its free edge contains the round ligament of the liver.

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11
Q

Hepatoduodenal ligament

A

Portion of the lesser omentum Extends from the porta hepatis to the superior part of the duodenum contents: hepatic artery proper, portal vein, common hepatic duct

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12
Q

Hepatogastric ligament

A

Extends from the liver to the lesser curvature of the stomach contents: gastric arteries

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13
Q

Round ligament (also known as ligamentum teres)

A

Remnant of the intra-abdominal portion of the umbilical vein Extends from the umbilicus to the liver on the free edge of the falciform ligament

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14
Q

Triangular Ligaments

A

Formed by the fusion of the anterior and posterior folds of the coronary ligament1 left and 1 right; both extend from the liver to the diaphragm

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15
Q

Venous Ligament

A

Remnant of the ductus venosus Extends from the remnant of the intra-abdominal portion of the umbilical vein to the inferior vena cava

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16
Q

Left and Right Fissures

A

Left Fissure
Impression of the round and venous ligaments

Right Fissure
Impression of the Gallbladder and Inferior Caval Vein

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17
Q

Liver Sinusoid

A

Hepatocytes are aligned radially to form the liver plate along with the sinusoids. The portal veins and hepatic artery branches terminate in the sinusoids, draining blood into the sinusoids and through the acinus to the central vein. The sinusoids are lined by fenestrated liver sinusoidal endothelial cells with Kupffer cells interspersed onto the endothelium. Between the liver plate and the sinusoids is the space of Disse, containing extracellular matrix components and hepatic stellate cells

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18
Q

Kuppfer Cells

A

Resident liver macrophages and play a critical role in maintaining liver functions. Under physiological conditions, they are the first innate immune cells and protect the liver from bacterial infections

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19
Q

Liver blood flow direction

A
  1. Deoxygenated blood from stomach or small intestine
  2. Hepatic
    3.Portal Vein - venules
  3. sinusoids
  4. central vein
  5. hepatic vein
  6. vena cava
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20
Q

Bile flow

A
  1. Bile produced in hepatocytes
  2. secreted into canaliculi
  3. bile ductules
  4. common duct
  5. gall bladder
  6. bile duct
  7. small intestine
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21
Q

Liver functions

A

The liver has more than 200 functions, including:

  1. Storage of Nutrients
  2. Breakdown of erythrocytes
  3. Bile Secretion
  4. Synthesis of plasma Proteins
  5. Synthesis of cholesterol
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22
Q

nutrients the liver stores

A

Hepatocytes absorb and store excess nutrients in the blood

  1. Glucose (glycogen)
  2. Iron
  3. Retinol (Vitamin A)
  4. Calciferol (Vitamin D)

Nutrients released when levels are too low

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23
Q

Breakdown of erythrocytes

A

RBC’s weaken and rupturee, releasing hemoglobin into the blood plasma.
Hemoglobin is absorbed by phagocytosis by Kuppfer cells in the liver.

Hemoglobin is split into
Heme groups
Iron is removed from heme leaving a substance called bilirubin (bile pigment).

Iron is carried to bone marrow where it is used to new hemoglobin for RBC’s
Bilirubin becomes a component of bile

Globins
Hydrolysed to amino acids and returned to the blood

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24
Q

Gallbladder Tests

A
  1. Abdominal ultrasound
  2. HIDA scan (cholescintigraphy)
    In this nuclear medicine test, radioactive dye is injected intravenously and is secreted into the bile. Cholecystitis is likely if the scan shows bile doesn’t make it from the liver into the gallbladder.
  3. Endoscopic retrograde cholangiopancreatography (ERCP): Using a flexible tube inserted through the mouth, through the stomach, and into the small intestine, a doctor can see through the tube and inject dye into the bile system ducts. Tiny surgical tools can be used to treat some gallstone conditions during ERCP.
  4. Magnetic resonance cholangiopancreatography (MRCP): An MRI scanner provides high-resolution images of the bile ducts, pancreas, and gallbladder. MRCP images help guide further tests and treatments.
  5. Endoscopic ultrasound: A tiny ultrasound probe on the end of a flexible tube is inserted through the mouth to the intestines. Endoscopic ultrasound can help detect choledocholithiasis and gallstone pancreatitis.
  6. Abdominal X-ray: Although they may be used to look for other problems in the abdomen, X-rays generally cannot diagnose gallbladder disease. However, X-rays may be able to detect gallstones.
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25
Q

Bile Content

A

HCO3- (Bicarbonate)
Bile salts
Bile pigment
Cholesterol

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26
Q

Synthesis of plasma proteins

A

Produced by RER of Hepatocytes -
3 main types
Albumin
Globulin
Fibrinogen

27
Q

Synthesis of Cholesterol

A
  1. Produced by hepatocytes
    Some used for bile production
    Some trasnsported for use in the rest of the body.
  2. Synthesis and repair of cell membranes or stored in the liver.
    Precursor by testis, ovaries or the adrenal gland to make steroid hormones.

progestins
glucocortoids
androgens
estrogens
mineralocortoids

  1. It is also a precursor to vitamin D.
28
Q

cirrhosis

A
  1. Cirrhosis is a result of advanced liver disease. It is characterized by replacement of liver tissue by fibrosis (scar tissue) and regenerative nodules (lumps that occur due to attempted repair of damaged tissue).
  2. These changes lead to loss of liver function. Cirrhosis is most commonly caused by alcoholism, hepatitis B and hepatitis C, and fatty liver disease, but has many other possible causes. Some cases are idiopathic (of unknown cause).
29
Q

Manifestations of Cirrhosis

A

1.Ascites (fluid retention in the abdominal cavity) is the most common complication of cirrhosis. It is associated with a poor quality of life, increased risk of infection, and a poor long-term outcome.

  1. Other potentially life-threatening complications are hepatic encephalopathy (confusion and coma) and bleeding from esophageal varices.
  2. Cirrhosis is irreversible, and treatment usually focuses on preventing progression and complications. Advanced stages of cirrhosis the only option is a liver transplant.
30
Q

Cirrhosis causes

A

Alcoholism
Hepatitis
Biliary
Hemochromatosis
Wilson’s disease
Alpha-1 antitrypsin deficiency

31
Q

Liver Dysfunction results

A
  1. Spider angioma or spider nevi are vascular lesions consisting of a central arteriole surrounded by many smaller vessels (hence the name “spider”), occur due to an increase in estradiol. One study found that spider angioma occur in about 1/3 of cases.
  2. Palmar erythema is a reddening of palms at the thenar and hypothenar eminences also as a result of increased estrogen.
  3. Gynecomastia, or increase in breast gland size in men that is not cancerous, is caused by increased estradiol and can occur in up to 2/3 of patients. This is different from increase in breast fat in overweight patients.
  4. Hypogonadism, a decrease in sex hormones manifest as impotence, infertility, loss of sexual drive, and testicular atrophy, can result from primary gonadal injury or suppression of hypothalamic/pituitary function. Hypogonadism is associated with cirrhosis due to alcoholism and hemochromatosis.
32
Q

Portal Hypertension

A
  1. Splenomegaly (increase in size of the spleen) is found in 35% to 50% of patients.
  2. Esophageal varices result from collateral portal blood flow through vessels in the stomach and esophagus (a process called Portacaval anastomosis). When these blood vessels become enlarged, they are called varices and are more likely to burst.[10]

3 .Caput medusa are dilated periumbilical collateral veins due to portal hypertension. Blood from the portal venous system may be shunted through the periumbilical veins and ultimately to the abdominal wall veins, manifesting as a pattern that may resemble the head of Medusa.[10]

  1. Cruveilhier-Baumgarten murmur is a venous hum heard in the epigastric region (on examination by stethoscope) due to collateral connections forming between portal system and the periumbilical veins as a result of portal hypertension
33
Q

Celiac Trunk

A
  1. The celiac trunk is a major artery of the abdomen. It arises from the abdominal aorta, and supplies many of the gastrointestinal viscera.
  2. After emerging from the aorta, the celiac trunk extends approximately 1cm before dividing into three major branches –left gastric, splenic and common hepatic arteries.
34
Q

Left gastric artery

A

The smallest of the three branches of the celiac trunk. It ascends across the diaphragm, giving rise to esophageal branches,before continuing anteriorly along the lesser curvature of the stomach. Here, it anastomoses with the right gastric artery.

35
Q

Splenic artery

A

I. The splenic artery arises from the celiac trunk just inferior to the left gastric artery. It then travels left towards the spleen, running posterior to the stomach and along the superior margin of the pancreas.

II. During its course, it is contained within the splenorenal ligament. It terminates into five branches whichsupply the segments of the spleen.

In addition to supplying the spleen, the splenic artery also gives rise to several important vessels:

  1. Left gastroepiploic: supplies the greater curvature of the stomach. Anastomoses with the right gastroepiploic artery.
  2. Short gastrics: 5-7 small branches supplying the fundus of the stomach.
    Pancreatic branches: supply the body and tail of the pancreas.
  3. The splenic artery has a tortuous appearance (similar to the facial branch of the external carotid artery) and thus is easily identifiable from other nearby vessels.
36
Q

Common Hepatic Artery

A
  1. The common hepatic artery is the sole arterial supply to the liver and the only branch of the celiac artery to pass to the right.
  2. As it travels past the superior aspect of the duodenum, it divides into its two terminal branches – theproper hepatic and gastroduodenal arteries. Each of these arteries has multiple branches and variation in the arrangement of these branches is common.
37
Q

Pancreatic Enzymes

A
  1. Amylase
  2. Lipase
  3. DNA-ase
  4. RNA-ase
  5. Zymogens: Trypsinogen
    6.Chymotrypsinogen
    7.Procarboxypeptidase A, B
38
Q

PANCREAS DISEASES

A

Congenital
Inflammatory
Acute
Chronic
Cysts
Neoplasms

39
Q

Congenital Pancreatic diseases

A

Agenesis (very rare)
Pancreas Divisum (failure of 2 ducts to fuse) (common)
Annular Pancreas (pancreas encircles duodenum) (rare)
Ectopic Pancreas (very common)

40
Q

Acute Pancreatitis consequences

A
  1. Systemic Organ Failure
  2. Shock
  3. ARDS
  4. Acute Renal Failure
  5. Disseminated intravascular coagulation
  6. Pancreatic abscess
  7. Pancreatic Pseudocyst
  8. Duodenal Obstruction
41
Q

Chronic Pancreatitis

A
  1. Pseudocyst
  2. Duct Obstruction
  3. Malabsorption
  4. Steatorrhea
  5. Secondary Diabetes
42
Q

Appendicitis incidence and complication

A

6 % lifetime incidence
69 % are ages 10 to 30
Up to 30 % misdiagnosed initially
20 to 30 % ruptured at surgery
Mortality : 0.1 to 0.2 % unruptured, 3 to 5 % ruptured
Significant morbidity

43
Q

Appendix anatomic aspects

A

Blind pouch off of cecum
Contains lymphoid tissue which peaks in adolescence, atrophies with age
Function still unclear
Appendix can be anywhere within peritoneal cavity
One study showed 65 % retrocecal, 31 % pelvic
Review of 70,000 cases showed 4 % in RUQ, 0.06 % LUQ, 0.04 % LLQ

44
Q

Appendicitis classic presentation

A

Seen in 60 %
Anorexia
Periumbilical pain, nausea, vomiting
RLQ pain developing over 24 hrs.
Anorexia and pain are most frequent
Usually nausea, sometimes vomiting
Diarrhea, esp. with pelvic location
Usually tender to palpation
Rebound is a later finding

45
Q

appendix Physical Exam

A

Tenderness at McBurney’s point
Cutaneous hyperesthesia in T 10 to 12 dermatomes
Rovsing’s sign
Psoas sign
Obturator sign

46
Q

ROVSING’S SIGN

A

If palpation of the left lower quadrant of a person’s abdomen increases the pain felt in the right lower quadrant, the patient is said to have a positive Rovsing’s sign and may have appendicitis.

In acute appendicitis, palpation in the left iliac fossa may produce pain in the right iliac fossa.

47
Q

PSOAS SIGN

A

The psoas sign is a medical sign that indicates irritation to the iliopsoas group of hip flexors in the abdomen, and consequently indicates that the inflamed appendix is retrocaecal in orientation (as the iliopsoas muscle is retroperitoneal).

It is elicited by performing the psoas test by passively extending the thigh of a patient lying on his side with knees extended, or asking the patient to actively flex his thigh at the hip. If abdominal pain results, it is a “positive psoas sign.

48
Q

Obturator Sign

A

The obturator sign is an indicator of irritation to the obturator internus muscle.

The technique for detecting the obturator sign, called the obturator test, is carried out on each leg in succession. The patient lies on her/his back with the hip and knee both flexed at ninety degrees. The examiner holds the patient’s ankle with one hand and knee with the other hand. The examiner rotates the hip by moving the patient’s ankle away from the patient’s body while allowing the knee to move only inward. This is flexion and internal rotation of the hip.

In the clinical context, it is performed when acute appendicitis is suspected. In this condition, the appendix becomes inflamed and enlarged. The appendix may come into physical contact with the obturator internus muscle, which will be stretched when this maneuver is performed on the right leg. This causes pain and is an evidence in support of an inflamed appendix.

49
Q

MANTRELS Score

A

Migration of pain
Anorexia
Nausea / vomiting
Tenderness RLQ
Rebound
Elevated temp.
Leukocytosis
Shift to left

SCORING

<5 High Suspicions

5-6 Possible

7-8 Probable

9-10 Very Probable

50
Q

Spleen general overview

A

Largest lymphoid tissue of the body
Serves two main functions
Filters blood to remove damaged/old RBC- red pulp
Serves as secondary lymphoid tissue by removing infectious agents and using them to activate lymphocytes- white pulp
A significant reservoir for T lymphocytes
Plays an active role in the production of IgM antibodies and complement
Has significant role in the functional maturation of antibodies

51
Q

Splenic white and red pulp functions

A
  1. The white pulp is circular in
    structure and is made up mainly
    of lymphocytes. It functions in a
    manner similar to the nodules of the
    lymph node.
  2. The red pulp surrounds the white
    pulp and contains mainly red blood
    cells and macrophages. The main
    function of the red pulp is to
    phagocytize old red blood cells.
52
Q

Spleen general function

A

The spleen is a sophisticated filter that monitors and manages blood cells and immune functions

During fetal development the spleen produces red and white blood cells

By the fifth month of gestation the spleen no longer has hematopoietic function but retains the capacity throughout life

Red cells that pass through the spleen undergo a “cleaning” or repair
Abnormal and old cells are destroyed

53
Q

Other spleen specific blood and immune function

A

Reticulocytes loose their nuclear remnants and excess membrane before entering the circulation
RBC’s coated with IgG and IgM are removed and destroyed

The spleen is the site of destruction in autoimmune disease states (ITTP and hemolytic anemia)

Parasites such as malaria can be removed as well
The spleen is involved in specific and nonspecific immune responses (promotes phagocytosis and destruction of bacteria

54
Q

Splenic trauma

A

Injury should be suspected in blunt upper abdominal injuries ( MVA and Bike)
Injuries are often associated with fractured ribs of the left chest
Splenic injuries can cause extensive and continued hemorrhage, others can cause subcapsular hematomas that are subject to rupture at any time
If splenic injury is suspected, admission to the hospital for monitoring is mandatory
The signs and symptoms of splenic trauma are those of hemoperitoneum (generalized LUQ pain)

55
Q

Delayed rupture of the spleen

A

Injury to the pulp sometimes cannot be contained indefinitely by the splenic capsule
The usual interval between injury and hemorrhage is within two weeks (longer intervals have been reported)
The incidence is between 15-30%
It is hoped that as imaging techniques improve the incidence will decrease

56
Q

Gastric Innervation

A

Receives Parasympathetic innervations from medulla via vagus nerves

Receives Sympathetic innervations from celiac ganglia arising from T5 – T9

57
Q

Gastric Lymphatic Drainage

A

Mainly to the gastric lymph nodes, pancreaticosplenic lymph nodes, pyloric lymph nodes and pancreatic-oduodenal lymph nodes

then drainage accompany the large arteries to the celiac lymph nodes

58
Q

The normal gastric mucosa

A
  1. Cardia – mainly mucus-secreting cells
  2. Fundus (body) – acid producing parietal cells, pepsin producing chief cells
  3. Pylorus – hormone (gastrin) production
59
Q

Structure of Glands of the stomach

A
  1. Surface/Neck mucous cells- secrete protective bicarbonate ions
  2. ParietalCells- most numerous in the isthmusof the glands, secrete gastric acid (HCL) as well asintrinsic factor.
  3. Chief,pepticorzymogenic cells- located towards the bases of the gastric glands. Secrete gastric lipase and pepsinogen.
  4. Neuroendocrine cells- part of the diffuse neuroendocrine system, secrete serotonin and other hormones
  5. Stem cells- divide continuously to replace all other types of cell in the glands. Not easily but become very prominent with plentiful mitotic figures after damage to the mucosa has occurred, e.g. after an episode of gastritis.
    ie. important histopathology feature
60
Q

Acute Gastritis

A

a transient mucosal inflammatory process that may be asymptomatic or cause variable degrees of epigastric pain, nausea, and vomiting. In more severe cases there may be mucosal erosion, ulceration, hemorrhage, hematemesis, melena, or, rarely, massive blood loss.

Pathophysiology: The gastric lumen is strongly acidic with pH close to 1. This harsh environment contributes to digestion but also has the potential to damage the gastric mucosa, if any of the protective mechanisms that have evolved are disrupted.

61
Q

More acute gastritis consequences

A
  1. Reduced mucin synthesis in the elderly
  2. NSAIDs prevents synthesis of prostaglandins, which enhance bicarbonate secretion, inhibit acid secretion, promote mucin synthesis, and increase vascular perfusion
  3. urease-secreting H. pylori inhibitions gastric bicarbonate transporters by ammonium ions.
  4. Direct cellular injury due to excessive alcohol consumption, NSAIDs, radiation therapy, and chemotherapy.
62
Q

Adenocarcinoma

A

Adenocarcinoma is the most common malignancy of the stomach, comprising over 90% of all gastric cancers.
Unfortunately early symptoms resemble those of chronic gastritis.

Although specific sequences of events have not been defined, it is clear that chronic inflammation promotes neoplastic progression.

63
Q

Gastric genetic mutations related to cancer

A

BRCA2 mutations are at increased risk of developing diffuse gastric cancer.

several genes including TGFβRII, BAX, IGFRII, and p16/INK4a have also been described in sporadic intestinal-type gastric cancer.

Clinical Anatomy (7 decks)

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