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
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)
3
Q
Hepatic Artery
Liver
A
supplies O2 rich blood from heart to liver
-20-30% of blood supply to liver
4
Q
Portal Vein
Liver
A
supplies nutrient rich blood from digestive tract
-70-80% of blood supply to liver
5
Q
Lobes of the Liver
A
-right lobe (largest)
-left lobe
-quadrate lobe
-caudate lobe
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
7
Q
Regenerative Tissue of Liver
A
regrowth after transplant grows to original shape/size
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
9
Q
Hepatic Vein
Liver
A
carries blood away from the liver
10
Q
Gallbladder
A
muscular bag for storage, concentration, acidification + delivery of bile to small intestine
- +Murphy’s sign = cholecystitis
11
Q
Liver moves with the diaphragm due to…
A
ligament attachment
-rises during exhalation
-lowers during inhalation
12
Q
Venous Ligament
Liver
A
remnant of ductus venosus extending from remnant of intra-abd portion of umbilical vein + IVC
13
Q
Right Fissure
Liver
A
impression of gallbladder + IVC
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
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
16
Q
Space of Disse
Liver Sinusoid
A
contains extracellular matrix components + hepatic stellate cells
-between liver plate + sinusoids
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
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)
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
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
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
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
23
Q
GB Before a Meal
A
may be full of bile
24
Q
GB After a Meal
A
gallbladder is empty + flat
25
Cholecystitis
## Footnote
GB
**RUQ pain after eating -> pain wraps around the back**
- + Murphy's sign
26
Cholelithiasis
| (gallstones)
**crystallization of bile in GB forming gallstones**
-common usually harmless
-pain, nausea, inflammation
27
Cholecystitis
**infection of GB often due to gallstones**
-severe pain/fever
-can require surgery if infection continues
28
GB Cancer
**rare/difficult to diagnose + found at late stages when symptoms appear**
-symptoms resemble gallstones
29
Gallstone Pancreatitis
**impacted gallstone blocks the ducts that drain the pancreas**
-results in inflammation of pancreas
-pancreas may begin to attack itself
30
Abdominal Ultrasound
## Footnote
GB Tests
**noninvasive test in which probe on skin bounces high frequency sound waves off of structures on the belly**
-checks for gallstones + GB wall
31
HIDA Scan
## Footnote
GB Tests
**radioactive dyeinjected intravenously + is secreted into bile**
-cholecystitis will show bile not making route from liver to GB
| cholescintigraphy
32
Endoscopic Retrograde Cholangiopancreatography
| (ERCP)
## Footnote
GB Tests
**using flexible tube inserted through mouth, through stomach into small intestine; inject dye into bile ducts**
-use surgical tools to treat gallstone conditions
33
Magnetic Resonance Cholangiopancreatography
| (MRCP)
## Footnote
GB Tests
**MRI scanner provides high resolution images of bile ducts, pancreas + GB**
-guides further tests/treatments
34
Endoscopic Ultrasound
## Footnote
GB Tests
**tiny ultrasound probe on the end of a flexible tube inserted through mouth to intestines**
-detect cholelithiasis + gallstone pancreatitis
35
Abdominal X Ray
## Footnote
GB Tests
cannot diagnose GB disease but may detect gallstones
36
Bile Contents
-HCO3- (bicarbonate)
-bile salts
-bile pigment
-cholesterol
37
Bile
## Footnote
GB
**concentrated/acidified in GB**
-discharged into small intestine via bile duct
38
Synthesis of Plasma Proteins
**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)
39
Transferrin
## Footnote
Plasma Proteins
transports iron
40
Macroglobulin
## Footnote
Plasma Proteins
inhibitor of serum endoproteases
41
Haptoglobin
## Footnote
Plasma Proteins
binding/trasnport of cell free hemoglobin
42
Synthesis of Cholesterol
-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
43
Catabolic Steroids
## Footnote
Cholesterol
**break down**
-ex. asthma
44
Anabolic Steroids
## Footnote
Cholesterol
**illegal/not specific to muscle type**
-increased hypertrophy of heart + brain
-prevents effectiveness of other steroids
45
Cirrhosis
| (nonfunctional)
## Footnote
Liver
**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
46
Common Causes of Cirrhosis
## Footnote
Liver
-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)
47
Ascites
## Footnote
Cirrhosis Complications
**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
Hepatic Encephalopathy
## Footnote
Complications of Cirrhosis
**(confusion + coma) in long standing alcoholics**
-sinusoid breakdown -> HTN, backup of waste destroys brain cells)
49
Fetor Hepaticus
## Footnote
Liver Dysfunction
musty breath odor resulting from increased dimethyl sulfide
50
Jaundice
## Footnote
Liver Dysfunction
**due to increased bilirubin **
-yellow discoloration of skin and mucous membranes (eye is very noticeable)
-urine may appear dark
51
Muehrcke's Lines
## Footnote
Cirrhosis Physical Exam
**paired horizontal bands separated by nromal color resulting from hypoalbuminemia**
-not specific to Cirrhosis
52
Terry's Nails
## Footnote
Cirrhosis Physical Exam
**proximal 2/3 of nail plate appears white w/ distal 1/3 red**
-also due to hypoalbuminemia
53
Clubbing
## Footnote
Cirrhosis Physical Exam
**angle between nail plate + proximal nailfold >180 degrees**
-not specific for Cirrhosis, also in pulmonary disorders
54
Hypertrophic Osteoarthropathy
## Footnote
Cirrhosis Physical Exam
**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
Dupuytren's Contracture
## Footnote
Cirrhosis Physical Exam
**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
Spider Angioma
## Footnote
Consequence of Nonfunctional Liver Cells
**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
Palmar Erythema
## Footnote
Consequence of Nonfunctional Liver Cells
**reddening of the palms at thenar and hypothenar eminences**
-result of increased estrogen
58
Gynecomastia
## Footnote
Consequence of Nonfunctional Liver Cells
**increase in breast gland size in men**
-not cancerous
-result of increased estradiol
-2/3 patients
59
Hypogonadism
## Footnote
Consequence of Nonfunctional Liver Cells
**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
Effects of Portal HTN
## Footnote
Liver
**blood cannot drain in HTN = backup + dysfunction of structure**
-liver cirrhosis increases resistance -> portal HTN
61
Splenomegaly
## Footnote
Effects of Portal HTN
**increased size of spleen = rupture of splenic sac**
-35-50% of pts
62
Esophageal Varices
## Footnote
Effects of Portal HTN
**result from collateral blood flow through vessels in the stomach and esophagus (portacaval anastomosis)**
-enlarged vessles = varices
-likely to burst
63
Caput Medusae
## Footnote
Effects of Portal HTN
**dilated periumbilical collateral veins due to portal HTN**
-blood from portal venous system shunted through periumbilical veins to abdominal wall veins
64
Cruveilhier-Baumgarten Murmur
## Footnote
Effects of Portal HTN
**venous hum heard in epigastric region due to collateral connections between portal system + periumbilical veins**
-result of portal HTN
65
Collateral Circulation
forming new arteries/veins in the event of obstruction in main artery
66
Celiac Trunk
major artery of abdomenarising from abdominal aorta, supplying many gastrointestinal viscerae
67
Left Gastric Artery
## Footnote
Main Branches of Celiac Trunk
**smallest branch ascending across diaphragm giving rise to esophageal branches**
-continues anteriorly along lesser curvature of stomach (anastomose w/ gastric artery)
68
Splenic Artery
## Footnote
Main Branches of Celiac Trunk
**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
Common Hepatic Artery
## Footnote
Main Branches of Celiac Trunk
**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
Pancreatitis
**blockage of junction of bile duct, pancreatic duct and duodenum**
-backup to the pancreas
-pancreas will eat itself
-creates major issues
71
Pancreatic Enzymes
-amylase
-lipase
-DNA-ase
-RNA-ase
-zymogens (trypsinogen, chmotrypsinogem, procarboxypeptidase A + B)
72
Agenesis
## Footnote
Congenital Pancreatic Diseases
partial or total loss of the body or tail of pancreas
| very rare
73
Pancreas Divisum
## Footnote
Congenital Pancreatic Diseases
**failure of 2 ducts to fuse **
-no pancreatic duct
-causes recurrent pancreatitis
| common
74
Annular Pancreas
## Footnote
Congenital Pancreatic Diseases
pancreas encircles duodenum
| rare
75
Ectopic Pancreas
## Footnote
Congenital Pancreatic Diseases
**pancreatic tissue appearing in the wrong place**
-such as outside the abdominal cavity
| common
76
Acute Pancreatitis
-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
Chronic Pancreatitis
-decreased tissue = scar tissue = calcifications
-causes:
1. **pseudocyst**
2. **duct obstruction**
3. **malabsorption, steatorrhea**
4. **secondary diabetes**
78
Appendicitis Incidence + Complications
-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
Anatomic Aspects of Appendix
-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
Classic Presentation of Appendicitis
**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
Physical Exam Findings of Appendicitis
-tenderness at McBurney's point
-cutaneous hyperesthesia in T10-T12 dermatomes
-Rovsing's sign
-Psoas sign
-Obturator sign
82
Rovsing's Sign
## Footnote
PE Appendicitis
**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
Psoas Sign
## Footnote
PE Appendicitis
**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
Obturator Sign
## Footnote
PE Appendicitis
**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
MANTRELS Score
## Footnote
Appendicitis
**M**igration of pain
**A**norexia
**N**ausea/vomiting
**T**enderness RLQ
**R**ebound
**E**levated temp
**L**eukocytosis
**S**hift to left (pain)
-<5 = high suspicion
-5-6 = possible
-5-8 = probable
-9-10 = very probable
86
Spleen
**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
Functions of the Spleen
-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
Major activation of white pulp
## Footnote
Spleen
lymphocytes
89
Major activation of red pulp
## Footnote
Spleen
RBCs
90
White Pulp
## Footnote
Spleen
**made of lymphocytes (function similar to lymph node)**
-circular, surrounded by red pulp
91
Red Pulp
## Footnote
Spleen
**made of RBCs and macrophages**
-surrounds white pulp
-function is to phagocytize old RBCs
92
Spleen Functions
-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
Idiopathic Throbocytopenia
| (ITTP)
**decreased platelets, increased bleeding**
-danger for clotting
94
Diagnosis of Splenic Trauma
**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
Treatment of Ruptured Spleen
-splenic preservation observations
-partial splenectomy
-capsular repair
-non-operative treatment
96
Delayed Rupture of the Spleen
**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
GERD
lower esophageal sphincter not functioning properly causing reflux of acid and food from stomach upwards into esophagus
98
Pyloric Stenosis
**pyloric valve/sphincter is narrowed + not functioning properly**
-children vomiting upon birth
99
Blood Supply of Stomach
-**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
Gastric Innervation
-**parasympathetic innervation**: from medulla via Vagus nerves
-**sympathetic innervation**: from celiac ganglia arising from T5-T9
101
Lymphatic Drainage of the Stomach
**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
Mucous Neck Cell
| (secrete mucus + bicarbonate)
## Footnote
Gastric Cells
-**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
Parietal Cells
| (secrete gastric acid [HCl] + intrinsic factor)
## Footnote
Gastric Cells
-**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
Enterochromaffin-like Cell
| (secretes histamine)
## Footnote
Gastric Cells
-**substance secreted**: histamine
-**stimulus for release**: ACh, gastrin
-**function**: stimulates gastric acid secretion
105
Chief Cells
| (secrete pepsinogen + gastric lipase)
## Footnote
Gastric Cells
-**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
D Cells
| (secretes somatostatin)
## Footnote
Gastric Cells
-**substance secreted**: somatostatin
-**stimulus for release**: acid in the stomach
-**function**: inhibits gastric acid secretion
107
G Cells
| (secrete gastrin)
## Footnote
Gastric Cells
-**substance secreted**: gastrin
-**stimulus for release**: ACh, peptides, aminon acids
-**function**: stimulates gastric acid secretion
108
Cardia
## Footnote
Gastric Mucosa
mainly mucus secreting cells
109
Fundus (Body)
## Footnote
Gastric Mucosa
aicd producing parietal cells, pepsin producing chief cells
110
Pylorus
## Footnote
Gastric Mucosa
hormone (gastrin) production
111
Neuroendocrine Cells
## Footnote
Gastric Cells
**part of diffused neuroendocrine system**
-secrete serotonin and other hormones
112
Acute Gastritis
**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
Causes of Acute Gastritis
-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
Adenocarcinoma
**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
Function of Stomach
**mixing food w/ acid and pepsin**
-unqie acidic environmentrequires functional gastric surface mucus (next cells) barrier, bicarbonate buffering + epithelial injury
116
Anything that destroys epithelial injury =
increased risk of gastritis + adenocarcinoma
