Gi Fa Mnemonics & Facts

Front 1

Important GI ligaments--
Falciform
Hepatoduodenal
Gastrohepatic
Gastrosplenic
Splenorenal

Back 1

F: liver to anterior abdominal wall; ligamentum teres

H: liver to duodenum; carries portal triad (hepatic a., portal v., common bile duct)

GH: liver to lesser curvature of stomach; contains gastric arteries

GS: greater curvature of stomach to spleen; contains short gastric aa.

S: spleen to posterior abdominal wall; contains splenic a. & v.

Front 2

Layers of gut wall

Basal electric rhythm: stomach, duodenum, ileum

Back 2

"MSMS"
Mucosa
Submucosa--includes submucosal nerves (Meissner); control secretions
Muscularis externa--includes myenteric nerves (Auerbach); controls motility
Serosa

Stomach--3 waves/min
Duodenum 12 waves/min
Ileum 8 waves/min

Front 3

GI histology--
Esophagus
Stomach
Duodenum
Jejunum
Ileum
Colon

Back 3

E: nonkeratinized stratified squamous epithelium
S: gastric glands
D: villi, brunner glands (submucosal, secrete bicarb)
J: plicae circulares
I: peyer patches (lymphoid aggregates); largest portion of goblet cells in small intestine
C: no villi, numerous goblet cells

Front 4

Common abdominal aorta branches
Celiac trunk
Bifurcation of abdominal aorta
Renal arteries

Back 4

C: T12
B: bi"four"cation--L4
R: L1--"only need one" kidney

Front 5

Anal fissure

Back 5

"Pain while Pooping"--tear in anal mucosa below pectinate line; commonly in posterior area as this area is poorly perfused

Front 6

Liver anatomy--
Zone 1
Zone 3

Back 6

**Z1: periportal--**first affected by viral hepatitis

**Z3: pericentral vein (centrilobular)--affected first by ischemia, contains P-450 system (sensitive to toxins; **site of acetaminophen toxicity), **site of alcoholic hepatitis

Front 7

Indirect versus Direct hernias

Back 7

"MDs don't LIe"--medial~direct; lateral~indirect

I: IN the scrotum, INternal inguinal ring, INfants; due to failure of processus vaginalis to close (can form hydrocele); covered by all 3 layers of spermatic fascia
Lateral to inferior epigastric aa.

D: typically older men, only passes thru external inguinal ring-->only have external spermatic fascia
Medial to inferior epigastric aa.

Front 8

GI regulatory substances--
CCK
Gastrin
Motilin

Back 8

CCK: duodenum/jejunum; inc gallbladder contraction, sphincter of Oddi relaxation, and potentiates pancreatic secretion; regulated by FA's and AA's

G: antrum of stomach; inc gastric H+ secretion and growth of gastric mucosa; regulated by stomach distention, alkalinization, AA's, peptides, vagal stimulation

M: small intestine; produces migrating motor complexes (MMCs), inc in fasting state; **erythromycin is motilin receptor agonist**

Front 9

GI regulatory substances--
Secretin
Somatostatin
Vasoactive intestinal peptide (VIP)

Back 9

Se: duodenum; increase pancreatic HCO3- secretion; regulated by acid and FAs in lumen of duodenum

So: pancreatic islets & GI mucosa; inhibitory hormone; shuts down GI tract

V: inc intestinal water and electrolyte excretion, relaxes sphincters
*VIPoma: islet cell pancreatic tumor-->watery diarrhea, hypokalemia, achlorhydria

Front 10

Gastric parietal cell--
Vagal stimulation
Gastrin
Histamine

Back 10

V: stimulates both parietal and G cells to potentiate acid secretion

G: stimulated by vagus n. (GRP not ACh-->atropine does not block gastrin stimulation); directly stimulates parietal cell and also stimulates ECL cell (most important mechanism)

H: ECL cells secrete histamine to directly stimulate acid secretion via H+/K+ ATPase

Front 11

Vitamin absorption
Bile acids
Folate
Iron
Vitamin B12

Back 11

"Iron Fist, Bro"

Iron: duodenum
Folate: jejunum
B12: ileum, along w/bile; requires intrinsic factor from parietal cells

Front 12

Bilirubin

Back 12

Product of heme metabolism (M0's); removed from blood by liver, conjugated w/glucuronate, excreted in bile

Direct--conjugated w/glucuronic acid-->water soluble
Indirect--unconjugated; water insoluble

Front 13

Salivary gland tumors--
Pleomorphic adenoma
Warthin tumor
Mucoepidermoid carcinoma

Back 13

Pleomorphic: benign, painless, mobile mass; biphasic--cartilage (chondromyxoid stroma) and epithelium; **high rate of recurrence

WARthin: lymphocytes and germinal centers; need these components for war

Mucoepidermoid: malignant; mucinous & squamous cells

Front 14

Esophageal cancer--
Adenocarcinoma
Squamous cell

Back 14

Present w/progressive dysphagia (first solids, then liquids); Worldwide squamous more common, in US adenocarcinoma is.

A: lower 1/3 of esophagus;
Risk factors: achalasia, barret, cigarettes, obesity, GERD

S: upper 2/3;
Risk factors: hot liquids, alcohol, tobacco, smoked foods (nitrosamines), diverticula

Front 15

Acute gastritis (erosive)

Back 15

AKA acute stress ulcers; disruption of mucosal barrier leading to inflammation

Due to stress, NSAIDs, alcohol as well as:

burns (curling ulcer--dec plasma volume->sloughing of gastric mucosa)
brain injury (cushing ulcer--inc vagal stimulation->H+ production)

**"Burned by curling iron" or "Cushioned by brain"

**Erosions do not fully extend thru the muscularis mucosa

Front 16

Chronic gastritis (nonerosive)--
Type A
Type B

Back 16

A: Autoimmune; autoabs to parietal cells-->dec H+ and dec intrinsic factor (pernicious anemia); typically seen in "first" part of stomach

B: due to H. pylori Bacteria; commonly seen in antrum; inc risk of gastric adenocarcinoma & MALT lymphoma

Front 17

Stomach cancer--
Intestinal
Diffuse

*3 most common mets of gastric Ca*

Back 17

Almost always adenocarcinoma, aggressive, **acanthosis nigricans**

I: associated w/ H. pylori, nitrosamines, tobacco; commonly on lesser curvature of stomach

D: NOT associated w/H. pylori; "signet ring cells"--nucleus pushed off to side due to mucin

Common mets:
Virchow node--left supraclavicular node
Krukenberg--bilateral mets to ovaries; signet ring cells
Sister Mary Joseph--subcutaneous periumbilical nodule

Front 18

Peptic ulcer disease
Gastric
Duodenal

Back 18

G: pain greater w/meals; inc risk of carcinoma; possibly due to NSAIDs

D: pain decreases w/meals; 100% association w/H. pylori infxn; may be due to zollinger-ellison syndrome (tx-remove tumor); can see hypertrophy of brunner glands; no association w/risk of carcinoma

Best long-term tx is to eradicate H. pylori infxn
*antrum (prepylorus) most commonly colonized area*
H. pylori decreases somatostatin secreting cells-->increased acid secretion-->ulcers

Front 19

Abetalipoproteinemia

Back 19

Dec synthesis of apolipoprotein B-->inability to generate chylomicrons

Presents early in childhood w/failure to thrive, steatorrhea, night blindness (dec fat-soluble vitamin absorption)

Front 20

Crohn disease

Back 20

"A fat granny in a sting bikini and an old crone skipping down a cobblestone path away from the train wreck"

Creeping fat
Granulomas--TH1
String sign
Skip lesions
Cobblestone mucosa
Transmural inflammation-->fistulas
Rectal sparing

***Ileum always involved-->impaired bile acid absorption->fat malabsorption->lipids binds Ca-->increased oxalate and oxalate kidney stones

Front 21

Ulcerative colitis

Back 21

ULLCCCERS

Ulcers
Large intestine, Lead pipe appearance
Continuous, CRC, Crypt abscesses
Extends proximally
Red diarrhea
Sclerosing cholangitis

Front 22

False versus True diverticuli

Back 22

F: only mucosa and submucosa outpouch; occurs where vasa recta perforate muscularis externa, commonly in sigmoid colon; due to inc intraluminal pressure and dec dietary fiber
i.e. Zenker--dysphagia, halitosis

*may cause colovesical fistula--pneumaturia*

T: all 3 gut wall layers outpouch; i.e. meckel--persistence of vitelline duct; may see ectopic gastric mucosa/pancreatic tissue
T

Front 23

Colonic polyps--
Adenomatous
Juvenile
Hamartomatous

Back 23

A: inc size, inc epithelial dysplasia, villous histology-->inc malignancy risk; may cause lower GI bleed or secretory diarrhea; precancerous

J: <5yo; if single->no malignant potential; juvenile polyposis syndrome--multiple juvenile polyps-->inc risk of adenocarcinoma

H: Peutz-Jeghers--AD, multiple nonmalignant hamartomas thru out GI tract, hyperpigmented (freckled) mouth/lips/hands

Front 24

CRC Genetics--
Familial adenomatous polyposis
Gardner syndrome
Turcot syndrome
Hereditary nonpolyposis CRC

Back 24

FAP: AD, mutation of APC; 100% progress to CRC-->prophylactic colon resection; rectum always involved

G: FAP + osseous and soft tissue tumors

T: FAP + malignant CNS tumor; turcot=turban

HNPCC/lynch: AD, mutation of DNA mismatch repair genes; proximal colon always involved

Front 25

CRC--
Presentation
Dx
Pathogenesis (2 methods)

Back 25

P: most often in rectosigmoid, association w/S. bovis
Right side: iron deficiency anemia, bleeding, exophytic mass
Left side: obstruction (napkin-ring lesion), colicky pain

D: Iron deficiency anemia in males >50 and postmenopausal females raises suspicion

Pa: 1-microsatellite instability~DNA mismatch repair gene mutations
2-APC/b-catenin (small polyp)-->k-RAS (polyp grows)-->p53, DCC mutations
"AK-53"

Front 26

Cirrhosis and Portal HTN
Sx's due to liver cell failure
-inc NH3
-inc estrogen
-dec protein synthesis (albumin)

Back 26

C: diffuse fibrosis and nodular regeneration

inc NH3: hepatic encephalopathy, fetor hepaticus
inc estrogen: spider nevi, gynecomastia, testicular atrophy
dec protein: ankle edema, bleeding tendency

Front 27

Serum markers of liver/pancrease--
Alkaline phosphatase (ALP)
Aminotransferases (AST, ALT)
Amylase
Ceruloplasmin
g-glutamyl transpeptidase (GGT)
Lipase

Back 27

ALP: obstructive hepatobiliary disease, HCC, bone disease
ALT>AST--viral hepatitis
AST>ALT--alcoholic hepatitis-"make a toAST w/alcohol"
Amylase: acute pancreatitis
Cerulo: dec in wilson
GGT: more specific than ALP for biliary/liver disease
Lipase: acute pancreatitis

Front 28

Alcoholic liver disease--
Hepatic steatosis
Alcoholic hepatitis
Alcoholic cirrhosis

Back 28

HS: reversible change of macrovesicular fatty deposits; reversed w/alcohol cessation
Alcohol-->inc NADH-->dec b-oxidation of FFA & dec gluconeogenesis

AH: affect centrilobular region first; swollen, necrotic hepatocytes; mallory bodies (eosinophilic inclusions)
**acetaldehyde mediates damage**
AST>ALT

AC: irreversible, shrunken

Front 29

Non-alcoholic fatty liver disease

Back 29

NAFLD (NASH): ALT>AST; insulin resistance common
Fatty infiltration of hepatocytes-->cellular ballooning and eventual necrosis
May cause cirrhosis and HCC

Independent of alcohol use

Front 30

Hepatic encephalopathy
Define
Triggers

Back 30

cirrhosis-->decreased NH3 metabolism-->neuropsych dysfxn

T:
Inc NH3--dietary protein, GI bleed, constipation
Dec NH3--renal failure, diuretics, post-TIPS

T: lactulose (acidifies GI to generation NH4+)

Front 31

HCC--
Risk factors
Findings
Presentation

Back 31

RF: HBV, HCV, wilson, hemochromatosis, a1-antitrypsin deficiency, alcoholic cirrhosis, carcinogens (aflatoxin->p53 mutation)

Spread hematogenously; elevated AFP

P: jaundice, tender hepatomegaly, ascites, anorexia

*Most common hepatic malignancy is mets from another site, not HCC*-->multiple nodules

Front 32

Other liver tumors--
Cavernous hemangioma
Hepatic adenoma
Angiosarcoma

Back 32

CH: most common, benign; biopsy contraindicated due to risk of hemorrhage

HA: benign, related to oral contraceptive or anabolic steroid use

A: malignant tumor; due to exposure to arsenic and vinyl chloride

Front 33

Hereditary hyperbilirubinemias--
Gilbert syndrome
Crigler-Najjar syndrome
Dubin-Johnson syndrome
Rotor syndrome

Back 33

UGT--conjugation enzyme (UDP-glucuronosyltransferase)
GS: low UGT; jaundice during stress, otherwise a-sx

CN (sounds evil): absent UGT; kernicterus, fatal

DJ: deficiency of CB canalicular transport (ATP-dependent process); black liver, benign

R: milder DJ, no black liver

Front 34

Wilson disease--
Cause
Findings
Tx

Back 34

Inadequate hepatic copper excretion (bile)-->copper accumulation-->produces free radicals->tissue damage

F: dec ceruloplasmin, corneal deposits (kayser-fleischer rings), **basal ganglia degeneration (parkinsonian Sx's), dementia, dyskinesia

Tx: penicillamine or trientine; AR inheritence

Front 35

Hemochromatosis
Findings
Etiology: primary, secondary
Tx

Back 35

Cirrhosis, "Bronze diabetes"

Primary: AR mutation of protein on basolateral surface of intestinal cells that regulates tranferrin/iron complex-->excessive uptake due to lack of regulation
Secondary: chronic transfusion

Tx: phlebotomy

*menstruation slows progression as iron is lost during bleeding

Front 36

Biliary tract diseases--
Primary biliary cirrhosis
Primary sclerosing cholangitis

Back 36

PBS: autoimmune rxn-->lymphocytic infiltrate + granulomas-->destruction of intralobular bile ducts; serum mitochondrial abs (IgM) and other autoimmune conditions
pts present: pruritis, jaundice, dark urine; may see xanthelasma formation (inc cholesterol)
labs: inc CB, inc ALP

PSC: concentric "onion skin" bile duct fibrosis-->alternating strictures and dilation w/beading on ERCP;
Same pt presentation, and same labs
**Associated w/ulcerative colitis; +p-anca**

Front 37

Gallstones--
Risk factors
Types

Back 37

RFs (4 F's): Fertile, Fat, Forty, Female
Inc cholesterol, dec bile salt or biliary stasis==> inc risk of gallstone

Cholesterol stones: estrogen tx (stimulates HMG-CoA reductase activity-->**inc cholesterol synthesis), rapid weight loss, fibrate & bile resin tx

**Pigment stones**
Black--radiopaque, chronic hemolysis
Brown--radiolucent, infxn
Associated w/biliary infxns of E. coli or flukes
Infxn-->release of b-glucuronidase by injured hepatocytes & bacteria-->inc UCB in bile

**opioid analgesics and alcohol can cause contraction of sphincter of oddi-->biliary colic

Front 38

Pancreatitis--
Acute
pseudocyst
Chronic

Back 38

A: often due to alcohol, gallstones, trauma
Elevated amylase & lipase (higher specificity)
Can lead to DIC, ARDS, hypocalcemia

P: persistently elevated amylase; lined by granulation tissue, not epithelium; filled with fluid rich w/enzymes and debris

C: alcohol abuse most common cause, CF in kids; often calcifications present (chains of lakes)
Can lead to pancreatic insufficiency->steatorrhea, fat-soluble vitamin deficiencies; increased risk for pancreatic adenocarcinoma

Front 39

Pancreatic adenocarcinoma--
Origin
Marker
Risk factors
Co-presentation
Tx

Back 39

O: arises from pancreatic ducts (glandular)
M: CA-19-9
RF: *smoking*, chronic pancreatitis, age >50
Co:
Obstructive jaundice w/palpable nontender gallbladder (courvoisier sign--tumor in head of pancreas)
Migratory thrombophlebitis--redness & tenderness on palpation of extremities; essentially superficial venous thrombosis (trousseau syndrome)
Secondary DM if tumor in body or tail

Tx: whipple procedure--remove head/neck of pancreas, proximal duodenum, & gall bladder

Front 40

H2 blockers--
Mechanism
Toxicity

Back 40

CimetiDINE, ranitiDINE, ~dine
M: reversible block of H2 receptors-->decreased H+ secretion by parietal cells

T: Cimetidine is potent P450 inhibitor, also causes gynecomastia/impotence

Front 41

PPI's--
Mechanism
Toxicity

Back 41

Omeprazole, ~"prazole"
M: irreversibly inhibit H+/K+ ATPase in stomach parietal cells

T: increased risk of C. diff; may see hypergastrinemia; decreased Mg2+ with long-term use

Front 42

Bismuth, Sucralfate
Mechanism; Use

Misoprostol
Mechanism; Use

Octreotide
Use

Back 42

B,S: bind to ulcer base, providing physical protection-->allows HCO3 to establish mucous layer

M: PGE analog; inc production of mucous barrier
Prevents NSAID-induced ulcers; also ripens cervix

O: acute variceal bleeds, acromegaly, VIPoma, carcinoid tumor

Front 43

Antacid use--
Aluminum hydroxide
Magnesium hydroxide

Back 43

AlOH: Alu"minimum" amount of feces--constipation
also hypophosphatemia, proximal weakness

Mg: "Must Go to the bathroom"--diarrhea
also cardiac arrest (prolong QT), htn

Front 44

Osmotic laxatives--
Magnesium hydroxide, magnesium citrate, polyethylene glycol, lactulose
Mechanism
Use

Back 44

M: provide osmotic load to draw water out

U: constipation
Lactulose used in hepatic encephalopathy to excrete NH4+

Front 45

Infliximab

Sulfasalazine

Back 45

I: anti-TNF; crohn disease, ulcerative colitis, RA, ankylosing spondylitis, psoriasis

S: combination of sulfa (abx) & aspirin (ASA); activated by colonic bacteria
may cause sulfonamide toxicity

Front 46

Odansetron, Alosetron

Metoclopramide

Back 46

O: 5-HT3 antagonist, also decreases vagal stimulation
controls vomiting postop & after CTX
may cause HA

M: D2 receptor antagonist (prokinetic); increases motility and LES tone
**used in gastroparesis and antiemetic**
*can cause parkinsonian effects**