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Anatomy 1 - MD > Week 5 - Liver, GB, Pancreas, Spleen, Stomach > Flashcards

Week 5 - Liver, GB, Pancreas, Spleen, Stomach Flashcards

1
Q

Liver

A

RUQ beneath diaphragm + behind lower ribs
-largest internal organ weighing 3 pounds
-vascular organ (rib fracture can puncture)
-incr. blood thinners = incr. rate of bleed
-Murphy’s Law = RUQ pain + cessation of breathing upon palpation

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2
Q

Functions of the Liver

A

Major function = excretion of waste products from bloodstream by excretion into bile
-processing of dietary amino acids, carbohydrates, lipids + vitamins
-removal of microbes + toxins in splanchic blood
-synthesis of plasma proteins + cholesterol
-detoxification + excretion into bile of endogenous waste products + pollutant xenobiotics
-storage of nutrients (glycogen, iron, retinol/Vitamin A, calciferol/Vitamin D)
-breakdown of RBCs (breakdown into hemoglobin + absorbed by Kupffer cells, carried to bone marrow)

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3
Q

Hepatic Artery

Liver

A

supplies O2 rich blood from heart to liver
-20-30% of blood supply to liver

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4
Q

Portal Vein

Liver

A

supplies nutrient rich blood from digestive tract
-70-80% of blood supply to liver

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5
Q

Lobes of the Liver

A

-right lobe (largest)
-left lobe
-quadrate lobe
-caudate lobe

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6
Q

5 Ligaments of the Liver

A

-Falciform ligament: from umbilicus to liver, free edge containing Teres ligament
-Teres ligament: umbilicus to liver on free edge of Falicform ligament
-Coronary ligament: from diaphragm to liver on bare area / surface of the liver
-Right Triangular ligament: extend from liver to diaphragm + fusion of Coronary ligament
-Left triangular ligament: extend from liver to diaphragm + fusion of Coronary ligament

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7
Q

Regenerative Tissue of Liver

A

regrowth after transplant grows to original shape/size

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8
Q

Location of Liver

A

R to L hypochondriac region
-3/4 of liver in superior quadrant
-adjacent to inferior surface of diaphragm
-location is breath dependent (rises during exhalation, lowers during inhalation)
-superior height (exhalation): 5th intercostal space
-inferior limit (inhalation): R costal arch

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9
Q

Hepatic Vein

Liver

A

carries blood away from the liver

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10
Q

Gallbladder

A

muscular bag for storage, concentration, acidification + delivery of bile to small intestine
- +Murphy’s sign = cholecystitis

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11
Q

Liver moves with the diaphragm due to…

A

ligament attachment
-rises during exhalation
-lowers during inhalation

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12
Q

Venous Ligament

Liver

A

remnant of ductus venosus extending from remnant of intra-abd portion of umbilical vein + IVC

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13
Q

Right Fissure

Liver

A

impression of gallbladder + IVC

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14
Q

Liver Sinusoid

A

endothelial cells that put blood in and out of the liver
-lined with fenestrated liver sinusoidal endothelial cells
-Kupffer cells interspersed on endothelium
-blood and bile flow in opposite directions

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15
Q

Hepatocytes

Liver Sinsusoid

A

drains blood into sinusoids + through acinus to central vein
-aligned radially to form liver plate along the sinusoids
-absorb + store excess nutirents in the blood

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16
Q

Space of Disse

Liver Sinusoid

A

contains extracellular matrix components + hepatic stellate cells
-between liver plate + sinusoids

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17
Q

Kupffer Cells

Liver Sinusoid

A

resident liver macrophages playing critical role in maintaining liver functions
-1st innate immune response under physiological conditions + protect liver from bacteral infections
-phagocytize hemoglobin for absorption

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18
Q

Fat Storing Cells

(adipose)

Liver Sinusoid

A

main storage site of Vitamin A derivatives (mainly retinyl plamitate + oleate)
-Vitamin A important for eyes
-phenotype alters during liver injury (cells lose fat droplets, proliferate + synthesize alrge amounts of connective tissue molecules)

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19
Q

Blood Flow through Sinusoid

Liver Sinusoid

A

deoxygenated blood from stomach or small intestine -> hepatic portal vein -> venules -> sinusoids -> central vein -> hepatic bvein -> vena cava

deoxy blood passes thru liver before IVC/heart to remove waste products

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20
Q

Bile Flow through Sinusoid

Liver Sinusoid

A

bile produced in hepatocytes -> secreted into calaliculi -> bile duct -> common duct -> GB -> bile duct -> small intestine

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21
Q

Liver obstruction destroys sinusoid

Liver Sinusoid

A

-incr. pressure
-incr. back up of “waste” blood
-portal HTN
-slow blood flow w/ poor drainage
-bulging varicose veins = esophageal varices
-rupture

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22
Q

Gallbladder

A

sits underneath the liver + stores bile (produced by liver)
-non-essential organ (removal -> diarrhea + fat malabsorption)
-squeezes stored biile into small intestine through ducts

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23
Q

GB Before a Meal

A

may be full of bile

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24
Q

GB After a Meal

A

gallbladder is empty + flat

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25
Q

Cholecystitis

GB

A

RUQ pain after eating -> pain wraps around the back
- + Murphy’s sign

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26
Q

Cholelithiasis

(gallstones)

A

crystallization of bile in GB forming gallstones
-common usually harmless
-pain, nausea, inflammation

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27
Q

Cholecystitis

A

infection of GB often due to gallstones
-severe pain/fever
-can require surgery if infection continues

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28
Q

GB Cancer

A

rare/difficult to diagnose + found at late stages when symptoms appear
-symptoms resemble gallstones

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29
Q

Gallstone Pancreatitis

A

impacted gallstone blocks the ducts that drain the pancreas
-results in inflammation of pancreas
-pancreas may begin to attack itself

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30
Q

Abdominal Ultrasound

GB Tests

A

noninvasive test in which probe on skin bounces high frequency sound waves off of structures on the belly
-checks for gallstones + GB wall

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31
Q

HIDA Scan

GB Tests

A

radioactive dyeinjected intravenously + is secreted into bile
-cholecystitis will show bile not making route from liver to GB

cholescintigraphy

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32
Q

Endoscopic Retrograde Cholangiopancreatography

(ERCP)

GB Tests

A

using flexible tube inserted through mouth, through stomach into small intestine; inject dye into bile ducts
-use surgical tools to treat gallstone conditions

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33
Q

Magnetic Resonance Cholangiopancreatography

(MRCP)

GB Tests

A

MRI scanner provides high resolution images of bile ducts, pancreas + GB
-guides further tests/treatments

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34
Q

Endoscopic Ultrasound

GB Tests

A

tiny ultrasound probe on the end of a flexible tube inserted through mouth to intestines
-detect cholelithiasis + gallstone pancreatitis

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35
Q

Abdominal X Ray

GB Tests

A

cannot diagnose GB disease but may detect gallstones

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36
Q

Bile Contents

A

-HCO3- (bicarbonate)
-bile salts
-bile pigment
-cholesterol

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37
Q

Bile

GB

A

concentrated/acidified in GB
-discharged into small intestine via bile duct

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38
Q

Synthesis of Plasma Proteins

A

produced by RER of hepatocytes
-decr. IgG + IgM = decreased immune response
-decreased albumin = dysfunctional osmotic pressure
-3 types:
1. albumin (most abundant/osmotic pressure regulation)
2. globulin (antibodies)
3. fibrinogen (clotting)

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39
Q

Transferrin

Plasma Proteins

A

transports iron

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40
Q

Macroglobulin

Plasma Proteins

A

inhibitor of serum endoproteases

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41
Q

Haptoglobin

Plasma Proteins

A

binding/trasnport of cell free hemoglobin

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42
Q

Synthesis of Cholesterol

A

-produced by hepatocytes
-some used ofr bile production
-some transported for use in the rest of the body
-synthesis + repair of cell membranes stored in liver
-precursor by testes, ovaries, adrenal gland to make steroid hormones (progestins, glucocorticoids, androgens, estrogens, mineralcorticoids)
-precursor to Vitamin D

cholesterol feeds your brain -> decr. cholesterol = doggy brain

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43
Q

Catabolic Steroids

Cholesterol

A

break down
-ex. asthma

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44
Q

Anabolic Steroids

Cholesterol

A

illegal/not specific to muscle type
-increased hypertrophy of heart + brain
-prevents effectiveness of other steroids

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45
Q

Cirrhosis

(nonfunctional)

Liver

A

result of advanced liver disease
-characterized by replacement of liver tissue by fibrosis (scar tissue) + regenerative nodules
-lumps occur due to attempted repair of tissue
-changes = loss of liver function
-irreversible
-advanced/end stage needs liver transplant
-liver can be shruken, enlarged or normal

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46
Q

Common Causes of Cirrhosis

Liver

A

-alcoholism
-hepatitis B + C
-fatty liver disease
-biliary stones
-hemochromatosis
-Wilson’s disease
Alpha 1 antitrypsin deficiency
-some cases are idiopathic (unknown cause)
-Hep C is most concerning for liver cancer (can lay dormant for years)

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47
Q

Ascites

Cirrhosis Complications

A

fluid retention in abdominal cavity (albumin decr. fluid moving extracellularly)
-common complication of Cirrhosis
-gives rise to flank dullness
-1500 mL minimum needed for visibility as increase w/ abdominal girth
-poor quality of life
-increased risk of infection
-poor long term outcome

48
Q

Hepatic Encephalopathy

Complications of Cirrhosis

A

(confusion + coma) in long standing alcoholics
-sinusoid breakdown -> HTN, backup of waste destroys brain cells)

49
Q

Fetor Hepaticus

Liver Dysfunction

A

musty breath odor resulting from increased dimethyl sulfide

50
Q

Jaundice

Liver Dysfunction

A

**due to increased bilirubin **
-yellow discoloration of skin and mucous membranes (eye is very noticeable)
-urine may appear dark

51
Q

Muehrcke’s Lines

Cirrhosis Physical Exam

A

paired horizontal bands separated by nromal color resulting from hypoalbuminemia
-not specific to Cirrhosis

52
Q

Terry’s Nails

Cirrhosis Physical Exam

A

proximal 2/3 of nail plate appears white w/ distal 1/3 red
-also due to hypoalbuminemia

53
Q

Clubbing

Cirrhosis Physical Exam

A

angle between nail plate + proximal nailfold >180 degrees
-not specific for Cirrhosis, also in pulmonary disorders

54
Q

Hypertrophic Osteoarthropathy

Cirrhosis Physical Exam

A

chronic proliferative periostitis of the long bones that can cause considerable pain
-problem w/ Vitamin D synthesis (decr. absorption of Ca2+)
-takes Vitamin D from other joints (knees, hips, etc)

55
Q

Dupuytren’s Contracture

Cirrhosis Physical Exam

A

thickening and shortening of palmar fascia that leads to flexion deformities of the fingers
-caused by fibroblastic proliferation (increased growth) + disorderly collagen deposition
-relatively common (33% of pts)

56
Q

Spider Angioma

Consequence of Nonfunctional Liver Cells

A

vascular lesions consisting of central arteriole surrounded by many smaller vessels
-1/3 cases
-occur due to increased estradiol
-venous swelling, abdomen

aka spider nevi

57
Q

Palmar Erythema

Consequence of Nonfunctional Liver Cells

A

reddening of the palms at thenar and hypothenar eminences
-result of increased estrogen

58
Q

Gynecomastia

Consequence of Nonfunctional Liver Cells

A

increase in breast gland size in men
-not cancerous
-result of increased estradiol
-2/3 patients

59
Q

Hypogonadism

Consequence of Nonfunctional Liver Cells

A

decrease in sex hormones manifesting as impotenence, infertility, loss of sexual drive and testicular atrophy
-result from primary gonadal injury or suppression of hypothalamic/pituitary function
-associated w/ Cirrhosis due to alcoholism + hemochromatosis

60
Q

Effects of Portal HTN

Liver

A

blood cannot drain in HTN = backup + dysfunction of structure
-liver cirrhosis increases resistance -> portal HTN

61
Q

Splenomegaly

Effects of Portal HTN

A

increased size of spleen = rupture of splenic sac
-35-50% of pts

62
Q

Esophageal Varices

Effects of Portal HTN

A

result from collateral blood flow through vessels in the stomach and esophagus (portacaval anastomosis)
-enlarged vessles = varices
-likely to burst

63
Q

Caput Medusae

Effects of Portal HTN

A

dilated periumbilical collateral veins due to portal HTN
-blood from portal venous system shunted through periumbilical veins to abdominal wall veins

64
Q

Cruveilhier-Baumgarten Murmur

Effects of Portal HTN

A

venous hum heard in epigastric region due to collateral connections between portal system + periumbilical veins
-result of portal HTN

65
Q

Collateral Circulation

A

forming new arteries/veins in the event of obstruction in main artery

66
Q

Celiac Trunk

A

major artery of abdomenarising from abdominal aorta, supplying many gastrointestinal viscerae

67
Q

Left Gastric Artery

Main Branches of Celiac Trunk

A

smallest branch ascending across diaphragm giving rise to esophageal branches
-continues anteriorly along lesser curvature of stomach (anastomose w/ gastric artery)

68
Q

Splenic Artery

Main Branches of Celiac Trunk

A

arises from celiac trunk (inferior to L gastric artery) travels toward spleen (running posterior to stomach + along superior argin of pancreas)
-contained w/in splenorenal ligament
-terminates into 5 branches
1. left gastroepiploic: supplies greater curvature of stomach; anastomoses w/ R gastroepiploic artery
2. short gastrics: 5-7 small branches supplying fundus of the stomach
3. pancreatic branches: supply the body + tail of the pancreas

69
Q

Common Hepatic Artery

Main Branches of Celiac Trunk

A

sole arterial supply to the liver and the only branch of celiac to pass to the right
-travels past superior aspect of duodenum
-divides into two terminal branches
1. proper hepatic artery
2. gastroduodenal artery

70
Q

Pancreatitis

A

blockage of junction of bile duct, pancreatic duct and duodenum
-backup to the pancreas
-pancreas will eat itself
-creates major issues

71
Q

Pancreatic Enzymes

A

-amylase
-lipase
-DNA-ase
-RNA-ase
-zymogens (trypsinogen, chmotrypsinogem, procarboxypeptidase A + B)

72
Q

Agenesis

Congenital Pancreatic Diseases

A

partial or total loss of the body or tail of pancreas

very rare

73
Q

Pancreas Divisum

Congenital Pancreatic Diseases

A

**failure of 2 ducts to fuse **
-no pancreatic duct
-causes recurrent pancreatitis

common

74
Q

Annular Pancreas

Congenital Pancreatic Diseases

A

pancreas encircles duodenum

rare

75
Q

Ectopic Pancreas

Congenital Pancreatic Diseases

A

pancreatic tissue appearing in the wrong place
-such as outside the abdominal cavity

common

76
Q

Acute Pancreatitis

A

-commonly Type 2 Diabetics
-discontinue medications at signs of pancreatitis
-causes:
1. systemic organ failure (shock, ARDS, acute renal failure)
2. disseminated intravascular coagulation/DIC (bleeding out from every orifice, no platelets - common in pregnancy)
3. pancreatic abscess (pus filled)
4. pancreatic pseudocysts
5. duodenal obstruction

inflammatory, very serious

77
Q

Chronic Pancreatitis

A

-decreased tissue = scar tissue = calcifications
-causes:
1. pseudocyst
2. duct obstruction
3. malabsorption, steatorrhea
4. secondary diabetes

78
Q

Appendicitis Incidence + Complications

A

-6% lifetime incidence
-69% are ages 10-30
-up to 30% are initally misdiagnosed
-20-30% ruptured at surgery
-mortality: 0.1-0.2 unruptured, 3-5% ruptured
-significant morbidity

79
Q

Anatomic Aspects of Appendix

A

-blind pouch of the cecum
-contains lymphoid tissue which peaks in adolescence, atrophies w/ age
-unclear function
-appendix can be anywhere w/in peritoneal cavity
-65% retroceal
-31% pelvic
-4% RUQ
-0.06% LUQ
-0.04% LLQ

80
Q

Classic Presentation of Appendicitis

A

seen in 60% anorexia, periumbilical pain, nausea, vomiting, RLQ pain developing over 24 hours
-anorexia and pain are more frequent
-diarrhea especially w/ pelvic location
-tender to palpation
-rebound tenderness = later finding

81
Q

Physical Exam Findings of Appendicitis

A

-tenderness at McBurney’s point
-cutaneous hyperesthesia in T10-T12 dermatomes
-Rovsing’s sign
-Psoas sign
-Obturator sign

82
Q

Rovsing’s Sign

PE Appendicitis

A

palpation LLQ of abdomen w/ increased pain felt in RLQ = positive Rovsing’s sign + possible appendicitis
-in acute appendicitis, palpation in left illiac fossa may produce pain in R iliac fossa

83
Q

Psoas Sign

PE Appendicitis

A

indicates irritation to iliopsoas group of hip flexors in the abdomen + indicates inflamed appendix (retrocecal in orientation)
-extending the thigh of the pt lying on their side w/ knees extended/flex thigh at hip resulting in abdominal pain = + psoas sign

84
Q

Obturator Sign

PE Appendicitis

A

indication of irritation to obturator internus muscle; suspects acute appendicitis
-carried out in each leg in succession
-pt lies on back w/ hip and knee flexed at 90 degrees
-examiner holds pt’s ankle w/ one hand and knee w/ other hand
-exmainer rotates hip by moving the pt’s ankle from the body while allowingthe knee to only move inward (flexion + internal rotation)

85
Q

MANTRELS Score

Appendicitis

A

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

-<5 = high suspicion
-5-6 = possible
-5-8 = probable
-9-10 = very probable

86
Q

Spleen

A

largest lymphoid tissue of the body (immune defense)
-important following trauma to LUQ
-site of destruction in autoimmune disease
-problem w/ splenic cuntion = problem w/ RBCs
-enalrged spleen = danger for mononucleosis

87
Q

Functions of the Spleen

A

-filters blood to remove damaged / old RBCs (red pulp)
-serves as secondary lymphoid tissue by removing infectious agents + using them to activate lymphocytes (white pulp)
-significant role of maturation of antibiotics
-spleen helps in prevention of Ab-Ag-C3 complex to prevent destruction
-activation of T-lymphocytes

88
Q

Major activation of white pulp

Spleen

A

lymphocytes

89
Q

Major activation of red pulp

Spleen

A

RBCs

90
Q

White Pulp

Spleen

A

made of lymphocytes (function similar to lymph node)
-circular, surrounded by red pulp

91
Q

Red Pulp

Spleen

A

made of RBCs and macrophages
-surrounds white pulp
-function is to phagocytize old RBCs

92
Q

Spleen Functions

A

-filter that monitors + manages blood cells + immune functions
-produced WBCs and RBCs during fetal development (loses hematopoietic function in 5th month of gestational age)
-RBCs undergo cleaning/repair
-reticulocytes lose nuclear remnants + excess membrane before entering circulation
-RBCs coasted w/ IgG + IgM are removed/destroyed
-specific + non-specific immunity (phagocytosis + destruction of bacteria)

93
Q

Idiopathic Throbocytopenia

(ITTP)

A

decreased platelets, increased bleeding
-danger for clotting

94
Q

Diagnosis of Splenic Trauma

A

diffused LUQ pain, bruising, rigidity, increased pain upon palpation to site
-splenic injury should be suspected in blunt upper abdominal injuries
-associated w/ L fractured ribs
-cause extensive hemorrhage + subscapular hematomas (can rupture at any time)

95
Q

Treatment of Ruptured Spleen

A

-splenic preservation observations
-partial splenectomy
-capsular repair
-non-operative treatment

96
Q

Delayed Rupture of the Spleen

A

injury to pulp sometimes cannot be contained indefinitely by splenic capsule
-interval between injury + hemorrhage in adults = 2 weeks
-interval between injury + hemorrhage in children = 20 minutes
-incidence = 15-30%
-see capsular expansion on MRI

97
Q

GERD

A

lower esophageal sphincter not functioning properly causing reflux of acid and food from stomach upwards into esophagus

98
Q

Pyloric Stenosis

A

pyloric valve/sphincter is narrowed + not functioning properly
-children vomiting upon birth

99
Q

Blood Supply of Stomach

A

-arterial supply = celiac trunk
-lesser curvature = R + L gastric arteries
-greater curvature = R + L gastroepiploic arteries
-fundus/upper body = short + posterior gastric arteries
-veins are parallel to arteries in position and course

100
Q

Gastric Innervation

A

-parasympathetic innervation: from medulla via Vagus nerves
-sympathetic innervation: from celiac ganglia arising from T5-T9

101
Q

Lymphatic Drainage of the Stomach

A

mainly to gastric lymph nodes, plus:
-pancreatosplenic lymph nodes
-pyloric lymph nodes
-pancreatic-oduodenal lymph nodes
-then, drainage accompanies large arteries to the celiac lymph nodes

102
Q

Mucous Neck Cell

(secrete mucus + bicarbonate)

Gastric Cells

A

-substance secreted: mucus
-stimulus for release: tonic secretion; increased irritation of mucosa
-function: physical barrier between epithelium and lumen

-substance secreted: bicarbonate
-stimulus for release: secreted w/ mucus
-function: buffers gastric acid to prevent damage to epithelium (none = ulcer formation)

bicarbonate is IMPORTANT

103
Q

Parietal Cells

(secrete gastric acid [HCl] + intrinsic factor)

Gastric Cells

A

-substance secreted: gastric acid (HCl)
-stimulus for release: ACh, gastrin, histamine
-function: activates pepsin; kills bacteria

-substance secreted: intrinsic factor
-stimulus for release: ACh, gastrin, histamine
-function: complexes w/ vitamin B12 to permit absorption (decreases B12)

gastric acid release controlled by somatostatin; most + in isthmus

104
Q

Enterochromaffin-like Cell

(secretes histamine)

Gastric Cells

A

-substance secreted: histamine
-stimulus for release: ACh, gastrin
-function: stimulates gastric acid secretion

105
Q

Chief Cells

(secrete pepsinogen + gastric lipase)

Gastric Cells

A

-substance secreted: pepsinogen
-stimulus for release: ACh, acid, secretin
-function: digests proteins

-substance secreted: gastric lipase
-stimulus for release: ACh, acid, secretin
-function: digests fats

major digestive cells in stomach located in bases of gastric glands

106
Q

D Cells

(secretes somatostatin)

Gastric Cells

A

-substance secreted: somatostatin
-stimulus for release: acid in the stomach
-function: inhibits gastric acid secretion

107
Q

G Cells

(secrete gastrin)

Gastric Cells

A

-substance secreted: gastrin
-stimulus for release: ACh, peptides, aminon acids
-function: stimulates gastric acid secretion

108
Q

Cardia

Gastric Mucosa

A

mainly mucus secreting cells

109
Q

Fundus (Body)

Gastric Mucosa

A

aicd producing parietal cells, pepsin producing chief cells

110
Q

Pylorus

Gastric Mucosa

A

hormone (gastrin) production

111
Q

Neuroendocrine Cells

Gastric Cells

A

part of diffused neuroendocrine system
-secrete serotonin and other hormones

112
Q

Acute Gastritis

A

transient mucosal inflammatory process that may be asymptomatic or cause variable degrees of epigastric pain, nausea + vomiting
-severe cases = mucosal erosion, ulceration, hemorrhage, hematemesis, melena, massive blood loss
-decreased buffer agents -> erosion -> decreased bicarbonate
-gastric lumen is strongly acidic (pH of 1) can damage gastric mucosa

113
Q

Causes of Acute Gastritis

A

-reduced mucin synthesis in elderly
-NSAIDS prevent synthesis of prostaglandins (incr. bicarb, decr, acid, incr, mucin, incr. vascular perfusion)
-H-pylori (urease secreting) inhibits gastric bicarb transporters by ammonium ions
-direct cell injury
-alcoholism
-radiation/chemotherapy
-increased adenocarcinoma incidence w/ increased gastritis incidence

114
Q

Adenocarcinoma

A

most common malignancy of the stomach (90% of all gastric cancers)
-early symptoms resemble chronic gastritis
-chronic inflammation increases neoplastic progression
-BRCA mutation
-other mutations: TGFBRII, BAX, IGFRII, p16/INK4a

115
Q

Function of Stomach

A

mixing food w/ acid and pepsin
-unqie acidic environmentrequires functional gastric surface mucus (next cells) barrier, bicarbonate buffering + epithelial injury

116
Q

Anything that destroys epithelial injury =

A

increased risk of gastritis + adenocarcinoma

Anatomy 1 - MD (6 decks)

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