Read GI Pathoma before starting.
Oral Cavity
Cleft lip/Palate: Full thickness defect of lip/palate due to failure of facial prominences to fuse. Occur
together and are multifactorial.
Aphthous ulcer: painful, superficial ulcerations of oral mucosa. Arises due to stress and resolves
randomly. Grayish base surrounded by erythema.
Bechet syndrome: Recurrent man of aphtohous ulcer (Stress caused, disappear spontaneously), uveitis
and genitcal ulcers. Due to Immune complex vasculitis.
Oral herpes: HSV-1 causes vesicles involving oral mucosa, rupturing results in shallow, painful red ulcers.
Occurs in childhood but remains dormant in ganglia of trigeminal nerve.
Squamous cell carcinoma: Malignant neoplasm of Oral mucosa. Tobacco/alcohol are major risk factors.
Floor of mouth most common location.
Oral leukoplakia and erythroplakia are precursor lesions.
1.
Leuokoplakia : white plaque which is NON scrapable and presents as squamous cell dysplasia
2.
Leukoplakia is distinct from oral candiasis (thrush) and hairy leukoplakia.
1.
Oral candiasis is white thrush on tongue and SCRAPPABLE.
2.
Hairy leukoplakia is white, rough (“HAIRY”) on LATERAL TONGUE, Immunocompromised
individuals. (AIDS)
3.
Erythroplakia (red plaque) represents VASCULORIZED LEUKOPLAKIAsquamous cell dysplasia.
4.
Erythroplkia and leukoplakia should be biopsied to rule out carcinoma.
Mumps: viral infection causing bilateral inflamed parotid glands.
Presentation: Orchitis, pancreatitis, aseptic meningitis. Risk of sterility in teenagers
Lab: serum amylase increased due to salivary/pancreatic gland involvement
Sialadenitis: Inflammation of salivary gland. Most common cause is (sialolthiasis) leading to S, Aureus
infection, usually unilateral
Plemorphic adenoma: benign tumor of stromal (cartilage) and epithelial tissue, most common tumor of
salivary gland
Presentation: occurs in parotid, mobile, painless mass at angle of jaw. High rate of reoccurrence.
May transform into carcinoma, which presents with signs of facial nerve damage (facial nerve runs
through parotid gland)
Warthin tumor: Benign cystic tumor with GERMINAL CENTERS (lymph node like stroma) and abundant
lymphocytes. Always occurs in parotid
Muceoepidermoid carcinoma: Malignant tumor of mucinious and squamous cells, most common
malignant tumor of salivary gland. Arises in parotid gland and involves facial nerve.
1.
False mucosal teeth: a false diverticulum is an outpouching of mucosa and submucosa only
(compare to true diverticulum which is out pouching of mucosa, submucosa and muscularis
propria and adventitia)
2.
Zanky Zenkers hoodie: Zenker diverticulm is a false diverticulum, in the posterior upper
esophagus
3.
Kids go for enjoyment: Zenker diverticulum is due to weakness of the cricopharyngeus muscle in
the killian triangle(area in the hypopharynx)
4.
Eating burning pizza: zenkers diverticulum may present with odynophagia (painful swallowing)
5.
Stinky cheese: zenkers diverticulum may present with halitosis (Bad breath)
6.
Regurigitating food: zenker’s diverticulum may present with regurigation
7.
Protruding “hit A mouse” game: in a Hiatial hernia, the stomach herniates into the thorax
through the esophageal hiatus
8.
Sliding mouse-spring junction: in a sliding hernia, the gastroesophageal junction herniates
through the esophageal hiatus (a type of hiatal hernia)
9.
2 protruding mice: in a paraesophageal hernia, gastic cardia herniates through the esophageal
hiatues (sneaks up besides a normally placed esophagus) (a type of hiatal hernia)
10.
Refleuxing acid: refluxing acid: hiatal hernias present with gastroesophageal influx (GERD)
11.
Marshmallow pit: Mallory -weiss tears (mucosal tears in proximal stomach and distal
esophagus)
12.
Linear scratches on distal slide: Mallory-Weiss tears consists of linear longitudinal lacerations in
the mucosa of the distal esophagus and proximal stomach
13.
Drinking at marshmallow pit: Mallory-weiss tears are often due to alcohol abuse (increases intra
gastric pressure from committing)
14.
Wrenching at marshallow pit: Mallory-weiss tears and Boerhaave syndrome are caused by
increased intragastric pressure during retching and vomiting
15.
Coughing up red drink: Mallory-weiss tears present with mild to moderate hematemesis
16.
Spilling red drink: Mallory-Weis tears can present with moderate hematemesis
17.
Kick to stomach: Mallory-Weiss tears can cause epigastric pain
18.
Ruptured bounce house: Boerhaave syndrome, there is transmural rupture of esophagus
19.
Wrenching at marshallow pit: Mallory-weiss tears and Boerhaave syndrome are caused by
increased intragastric pressure during retching and vomiting
20.
PeriSCOPE: Boerhaave syndrome can be caused by esophageal endoscopy
21.
Weakened bounce house: Conditions that weaken esophageal (infection, inflammation,
structural defects) are risk factor for Boerhaave syndrome
22.
Spilling red juice: Boerhaave syndrome causes severe hematemesis
23.
Air puffed induced chest injury: Boerhaave syndrome causes severe sharp chest pain
24.
Crunchy chip: Boerhaave syndrome can cause subcutaneous emphysema (pulpation of chest
causes crunchy sound)
25.
Wet pleural shirt: Boerhaave syndrome can cause pleural effusions (due to gastric contetns in
pleural space)
26.
Septic manhole cover and flame banada: Boeerhaave syndrome can cause fever, sepsis, and
septic shock
27.
Gargling: GERD is an imbalance between LES tone and intragastric pressure which causes reflux
of gastric acid into esophagus
28.
Loose drawstring: LES tone can cause GERD
29.
Smoker: smoking can cause GERD (decrased LES tone)
30.
Alcoholic: alcohol can cause GERD (decreases LES tone)
31.
Coffee: caffeine can cause GERD (decreases LES tone)
32.
Pregnant woman: pregnancy can cause GERD (decreased LES tone and increased intragastric
pressure)
33.
Obese guy: Obesity can cause GERD (increased intragastric pressure)
34.
Punching chest: Gerd can present with non cardiac chest pain like heartburn
35.
Coughing in bed: GERD can present with nocturnal cough
36.
Inhaler: Gerd can present with nocturnal asthma
37.
Choking throat: GERD can present with dysphagia (difficulty swallong)
38.
Burning hole: GERD can progress to erosive esophagitis or esophageal ulcers
39.
Clutching throat: erosive esophagitis due to GERD can present with odyophagia
40.
Mucosal cake with pink and blue sprinkles: GERD causes esophagitis (histology shows
eosinophils and lymphocytes infiltrating the mucosa)
41.
Tall lower cake layer with thick frosting: servere GERD causes elongation of papillae of the
lamina propria and hypertrophy of the basal cells of the mucosa
42.
Barretts bear: GERD can lead to barretts esophagus (intesntinal metaplasia of the distral
esophagus)
43.
Squamous tiles: esophageal is normally lined with stratified squamous epithelium
44.
Columnar stage: intestinal metaplasia of Baretts esophagus consist of columnar epitheilium
45.
Scatted mucus cups: Intestinal metaplasia of barretts esophagus contains goblet cell hyperplasia
46.
Metal intestines: intestinal metaplasia (baretts esophagus)
47.
Ascending red velvety curtains: Baretts esophagus columnar epithelium extend upward from
the gastroesophageal junction
48.
Dirty dysplastic floor: dysplasia is a precancerous condition (compared to metaplasia), which is
benign transformation of one cell type into another)
49.
Cancer crab: Barrett’s esophagus (Metaplasia) can progress to Dysplasia and eventually cancer
(esophageal adenocarcinoma)
50.
Parasol: Gerd is treated with proton pump inhibitors (PPIS, suffix is “prasol” or H2 blockers (both
reduce acid production in stomach)
51.
Eosinophilic bilobed sling shot: eosinophilic esophagitis presents similar to GERD (dysphagia,
chest/upper abdominal pain) after eating
52.
Slingshot kid: eosinophilic esophagitis often occurs in childhood (unlike GERD, which occurs in
adults)
53.
Pink eosinophilic granules: Eosinophilic esophagitis involves epithelial infiltration of eosinophils
through out the esophagus
54.
Itchy nose and hives: eosinophilic esophagitis may present along with other atopic symptoms
(eczema, allergic rhinitis, asthma, peripheral eosinophilia)
55.
Breaking through parasol: Eosinophilic esophagitis may be resistant to PPIS
Esophageal varices: Dilation of submucosal veins in lower esophagus caused by secondary portal
hypertension. Rupture can present with painless hematemesis. From diagram, you can see as blood is
backed up in the liver, it looks for other ways to escape. Esophagus veins
1.
Hooked at throat: Esophageal cancer and motility disorders all present with Dysphagia (difficulty
swallowing
2.
Cancers crab in bear den: esophageal adenocacrcinoma (most common esophageal malignancy
in the us)
3.
Glandular fluff : Esophageal adenocarcinoma has gland-like features on histology similar to
other adenocarcinomas
4.
Barretts bears: barretts esophagus can cause esophageal adenocarcinoma (via progregression to
dysplasia and then cancer)
5.
Metal instestines: Barretts esophagus from normal statfied squamous epithelium to intestinal
columnar epithelium
6.
Smoker: smoking increases risk of esophageal adenocarcinoma (especially if pre-existing
barretts esophagus)
7.
Distal velvety curtains: esophageal adenocarcinoma primarily affects the distal third of the
esophagus (including GE junction which is same area as GERD and barretts esophagus)
8.
Stuck Solid guy with liquid passing by: esophageal adenocarcinoma presents with dysphagia
(initiallty for solids, then also liquids)
9.
Thin bear: esophageal adenocarcinoma presents with weight loss
10.
Swalloing burning hot pizza: esophageal adenocarcinoma presents with odynophagia (painful
swallowing)
11.
Cancer crab on squamous table cloth : Esophageal squamous cell carcinoma is most common
type of esophageal cancer world wide
12.
Cured foods: foods with N-nitroso compounds (pickled egetables, meats) are all risk factor
13.
Hot tea: hot beverages are a risk factor for esophageal sqyamous cell carcinoma
14.
Chewable nut: betel nuts are a risk factor for esophageal squamous cell carcinoma
15.
Alcoholic : alcohol is a risk factor
16.
Smoker: tobacco smoke is a risk factor
17.
Mid-body tutu: esophageal cell carcinoma occurs in middle third of the esophagus
18.
Stuck solid guy with liquid passing by: Esophageal cell carcinoma presents with dysphagia
(initallity for solids then progresses to liquids)
19.
CLuthing throat: esophageal squamous cell carcinoma causes odynophagia (painful swallowing)
20.
Thin actress: esophageal squamous cell carcinoma causes weight loss
21.
Raised flat area: esophageal squamous cell carcinoma appears as raied plaques with ulceration
22.
Pearl necklace: histology will show kertain pearls and intracellular briding (similar to all forms of
squamous cell carcinoma)
23.
Plumber-vinson: Plummer-vinson syndrome is atriad of dysphagia, iron deficenecy anemia and
esophageal webs
24.
Falling iron tools: plummer vinson syndrome is caused by chronic iron deficiency
25.
Cobwebs: plummer-vinsion syndrome cause esophageal webs
26.
Mucosal protursions: esophageal webs in plummer vinson syndrome are thin protursions of
esophageal mucosa in the upper third of the esophagus->dysphagia for solids only
27.
Stuck solid guy: Plummer vinsion syndrome presents with dysphagia for solids
28.
Pale plubmbers overalls: plummer vinsion syndrome presents with iron defeicny anemia
29.
Irritated qumpous tiles: plummer-vinson syndrome increases the risk of esophageal squamous
cell carcinoma (due to irritant effect)
30.
Squeezing lower esophageal harness: Achalasia is esophageal dysmotility caused by impaired
relaxation of the LES->functional esophageal obstruction
31.
Loss of safety plexus: achalasia is caused by impaired relaxation of the LES due to loss of the
myenteric (Auerbach) plexus
32.
Rusty nitric oxide exhaust and falling VIP pass: in achalasia, loss of myenteric (Auerbach) plexus
causes decreased NO production and VIP which causes impaired relaxation of the LES smooth
muscle
33.
Idiot: Achalasia is usually idiopathic
34.
Che’sGas: acquired achalasia is caused by Chagas disease (trypanosoma cruzi destroys myentric
plexus)
35.
Bird beak: in achalasia , increased LES tone leads to constriction of the LES and dilation of the
esophagus more proximally (appears as bird beak on barium swallow)
36.
Regurgitation food: achalasia presents with regurgitation of undigested food
37.
Clutching chest: Achalasia presents with chest pain
38.
Difficulty funneling liquid: achalasia presents with dysphagia for liquids (in aiddtion to solids)
39.
Uncoordinated spasming ropeo: Diffuse esophageal spasm is a dysmotility disorder (in which
impaired inhibitory neurotransmission) within the myenterix plexus which results in
uncoordinated contractions
40.
Corkscrew rope: Diffuse esophageal spasm appears as a corckscrew on barium swallow
41.
Regurgitating: Diffuse esophageal spasm causes regurgitation
42.
Diffuse esophageal spasm causes dysphagia for liquids (in addition to slids)
43.
Sand bag crushing chest: diffuse esophageal spasm causes retrosternal chest pain
44.
Anginal anvil: in diffuse esophageal spasm, chest pain is similar to angina (and also relieved by
nitrates)
45.
Dragon talon crest: Crest syndrome (calcinosis, Raynaud syndrome, Esophageal dysmotility,
Sclerodactyly, Telangiectasias) is a variant of systemic sclerosis (autoimmune disease targeting
vascular endothelium, cause tissue fibrous)
46.
Fibrous vines in lower stage: Crest syndrome, esophageal dysmotility is due to fibrous
replacement of the muscularis in lower esophagus
47.
Dripping water: CREST syndrome presents with dysphagia for liquids and solids
48.
Refluxed acid: Crest syndrome, decreased esophageal tone can lead to GERD (increasing risk of
barrettes esophagus)
Squamous cell carcinoma spread
1. Upper 1/3-cervical nodes
2. Middle 1/3-mediastinal tracheobronchial nodes
3. Lower 1/3-celiac and gastric nodes
1.
Damaged peptic concrete: acute gastropathy (damaged gastric mucosa due to deficient mucus
lining or direct toxic effect)
2.
Fire extinguisher: NSAIDS can cause acute gastropathy (direct toxic effect; and inhibition of
COX1 which decreases prostaglandin synthesis and decreases mucus production)
3.
Smoking and drinking: both alcohol and tobacco have direct toxic effects on the gastric
epithelium, which can lead to acute gastropathy
4.
Flaming peptic concrete: acute gastropathy can lead to acute gastritis (vascular congestion,
edema, and neutrophilic infiltration on histology)
5.
Leaking shallow hole: severe damage may lead to an erosion which extends through the gastric
epithelium into the lamina propria (may cause acute hemorrhagic erosive gastropathy)
6.
Leaking deep hole through rebar layer: gastric ulcers are erosions that have extended through
the muscalris mucosa into the submucosa (risk for bleeding). Acid damage results in superficial
inflammation (damage to epithelium), Erosion (loss of epithelium), ulcer (Loss of mucosal layer)
7.
Curling ulcers can develop with severe burns
8.
Dumping bucket on burn: curling ulcers develop due to hypovolemia and creased gastric
mucosal perfusion (decreased blood flow)
9.
Burning curly drill bit: Cushing ulcers develop with high intracranial pressure
10.
Vegas sign: increased intracranial pressure causes massive vagal output->(ach will bind to
parietal cells) increases gastric acid producing causing Cushing ulcers
11.
Stomach on fire: acute gastritis can cause vague epigastric pain (dyspepsia)
12.
Nauseated: acute gastritis can cause nausea, vomiting, anorexia
13.
Chronic grandfather clock: chronic gastritis (H.Pylori, infection, Autoimmune gastritis)
14.
Helicopter: h.pylori infection is most common cause of chronic gastritis (T CELL, TYPE IV HSV)
15.
Helicopter sinking through mucus: H.pylori invades the stomach mucus layer to reside on the
gastric epithelium
16.
Pink commas: H.pylori is a comma-shaped gram-bacilli
17.
Helicopter adjacent to distal stomach: h.pylori usually infects the antrum first
18.
Fire under helicopter: initial infection wth H.pylori can cause acute gastritis
19.
Spotlight pointing across the stomach: H.pylori infection spreads from antrum to the body of the
stomach
20.
Chronic shack roof on fire: chronic h.pylori infection causes inflammation of gastric mucosa.
21.
First responders: chronic inflammation due to H.purlo infection displays a prominent neutrophil
infiltrate
22.
Thinning fabric: chronic inflammation from H.Pylori leads to chronic atrophic gastritis (mucosal
atrophy and loss of acid and hormone secreting glands which causes decreased gastrin and acid
secretion
23.
White mucus knots in columnar fence: chronic inflammation from H.pyrloi leads to intestinal
metaplasia ( normal gastric columnar epithelium develops goblet cell hyplerplasia)
24.
Intestinal metal pipes: Chronic inflammation from H.Pylori leads to intestinal metaplasia
25.
Cancer crab: intestinal metaplasia (due to chronic inflammation from H.pylori) can progress to
dysplasia and cancer
26.
Pile of lymphoid tissues: chronic H.pylori infection can lead to Mucosa-Association Lymphoid
(MALT). Chronic antigenic prescence of H.pylori causes accumulation of lymphocytes, which
organie into lymphoid tissue with germinal centers
27.
Blue tissues: histology will show MALT appear blue due to presence of lymphocytes
28.
Crab on helicopter: MALT (caued by H.pylori) can transform into gastric lymphoma
29.
Biopsy grabber: H.pylori infection can be diagnosed with gastric biopsy (antrum and body)
30.
Ammonia spray bottle: Urease testing of gastric biopsy specimen increases sensitivity of testing
for H.Pylori
31.
Gas from ammonia bottle: H.pylori can be diagnosed with a urea breath test (drinks
radiolabeled urea and urease in H.pylori metabolizes it into radiolabeled CO2 which is detected
on breath).
32.
Antibody forklift: autoimmune metaplastic atrophic gastritis, auto antibodies cause destruction
of parietal cells and intrinsic factor
33.
Targeting parietal protests: parietal cells location in body of stomach/fundus, are targeted in
autoimmune metaplastic atrophic gastritis
34.
Dropping lemons: autoimmune metaplastic atrophic gastritis, destruction of parietal cells causes
decreased secretion of gastric acid. Achloryhdria (no acid), which will cause G cells to undergo
hyperplasia
35.
Obserized “GAS” can: AMAG, gastin levels are increased (destruction of parietal cells, decreased
HCL secretion, hyplerplasia of gastin producing G cells in antrum causes hypergastinemia)
36.
“NO intrinsic right”: in autoimmune metaplastic atrophic gastritis, Intrinsic factor is decreased
(normally binds to vitamin B12 to facilitate its absorption). B12+Intrinsic factor complex is
absorbed in terminal ielum
37.
Mushroom cloud “blast”: AMAG, decreased B12 absorption causes pernicious anemia
(megalablastic anemia which has a large fragile erythrocytes). Non-infectious causes of chronic
gastritis (Chronic granulomatosis, sarcoidosis, Celiac, Radiation induced gastritis)
38.
Jackhammer eroding through rebar layer: Peptic ulcer disease penetrate through the muscularis
into the submucosa
39.
PUD helicopter: PUD develops over time with chronic gastritis (example H.pylori)
40.
Lesser curvate hole: Gastric ulcer most commonly occur in lesser curvature of stomach
41.
Distal duodenal ulcer: Duodenal ulcer (more common than gastric ulcer), NOT malignant
42.
Knocked-Over STOP sign: H.pylori-mediated chronic gastritis leads to destruction of antra delta
cells which causes decreased somatostain release. Triple therapy treatment will resolve
(Gastriti, ulcer and metaplasia)
43.
GAS tanks: in chronic gastritis, (H.pylori), loss of somatostatin leads to uninhibited gastrin
production, hypertrophy of brunners gland
44.
Activaated protester throwing lemons at gas guy: increased gastrin causes acid secretion by
parietal cells
45.
Lemon juice in duodenal hole: in chronic gastritis , increased acid delivery to the dueodenum
leads to dueondeal erosion and ulcers
46.
Fire extinguisher: NSAID use is a risk factor for peptic ulcer disease in the stomach (works with
H.pylori)
47.
Smoker: smoking is a risk factor for peptic ulcer disease (gastric and duodenal)
48.
Eating lunch with active jacke hammer: Gastric peptic ulcer disease, epigastric pain is worse with
meals (due to increased gastrin mediated acid secretion)
49.
Eating lunch with inactive jackhammer: duodenal peptic ulcer disease, epigastric pain is
improved with meals due to decreased passage of acid into duodenum after food intake, and
release of bicarbonate from pancreas. BLEEDING FROM GASTRODUODENAL ARTERY
50.
Hole leaking blood: peptic ulcer disease can cause upper GI bleeding (melena or hematemesis if
severe)
51.
Black tar: peptic ulcer disease can cause melena (“black tarry stools” due to oxidation of iron
from hemoglobin breakdown) a complication of upper GI bleeds (proximal to suspensory
ligament of the duodenum)
52.
Big gastric blood pipe: gastric ulcers may bleed heavily due to erosion into left gastric artery
53.
“Path obstructe0p d” Gastric outlet obstruction is a complication of peptic ulcer disease (due to
inflammation causing swelling of pylorus), presents with nonbilious emesis
54.
Big duodenal air pipe: duodenal ulcers can lead to perforation (most common in anterior
duodenum)
55.
Small gastric air pipe: gastric ulcers can lead to perforation (less common than in duodenal
ulcers)
56.
Suspender strap popping: ulcer perforation causes shoulder pain (acute peritonitis->irritation of
diaphragm and phrenic nerve->pain in C3-C5 dermatomes)
57.
Black belt: Ulcer perforations causes radiolucency, between right hemididaphragm and liver on
upright abdominal X-ray (due to free air in abdominal cavity)
58.
Grabbing crab: Peptic ulcers and surrounding areas are biopsied to rule out malignancy
How do you know if ulcer is benign or malignant?
->benign ulcer : SMALL, PUNCHED OUT
->malignant ulcer : LARGE, IREEGURAL, Heaped up margins
1.
Broken gastric rickshaw: gastroparesis (delayed gastric emptying WITHOUT mechanical
obstruction)
2.
Nauseated: gastroparesis presents with nausea and vomiting
3.
Holding abdomen: gastroparesis presents with abdominal pain
4.
Broken VEGAS sign: gastroparesis is caued by dysfunction of the vagus nerve (PNS) which
impairs peristalsis of food through stomach
5.
Severed wire: iatrogenic effects (example, surgical injury to vagus nerve)
6.
“idiot”: idiopathic cause
7.
Elevated candy: diabetes can cause gastroparesis
8.
Mortar/Pestle: CCBs and TCA can cause it
9.
“raMEN Try it”: Menetriers disease (hypertrophy of stomach rugal folds due to hyperplasia of
mucus-secreting cells)
10.
Thick ramen noodles: Menetries disease, hypertrophy of rugal folds inhibits peristalsis of food
through the stomach
11.
Excessive mucus: in menetriers disease, hyperplasia of mucus-secreting cells results in
decreased number of acid-secreting gastric glands which caused decreased protein digestion
12.
Nauseated: Menetriers disease presents with nausea and vomiting
13.
Holding abdomen Menetriers disease presents with abdominal pain and early satiety
14.
Tarry black borth: Menetriers disease can cause melena and hematemesis (symptoms of upper
GI bleeding)
15.
Losing meat chunks: menetriers disease is a “protein-losing enteropathy” due to increased
permeability of stomach mucosal cells
16.
Thin girl: Menetriers disease presents with weight loss, muscle wasting, hypoalbuminemia,
peripheral edema
17.
Cancer crab: Menetriers disease is a risk factor for gastric adenocarcinoma
18.
Giant cancer crab: Gastric adenocarcinoma (most common malignancy of stomach, more
common in East Asian countries)
19.
Hanging intestines: intestinal type gastric adenocarcinoma (large irregular, ulcer with heaped
up margins)
20.
Grandfather clock: Chronic atrophic metaplastic gastritis the biggest risk factor for intestinal
type gastric adenocarcinoma
21.
Helicopter fan: H.Pylori mediated chronic gastritis is a risk factor for ITGA
22.
Antibody on gastric pot: autoimmune gastritis is a risk factor for ITGA. Blood type A Risk factor
as well.
23.
Hanging meats: consumption of salt , salt preserved foods and nitrosamine preserved foods are
risk factor for gastric adenocarcinoma
24.
Smoking and drinking: smoking and drinking also causes gastric adenocarcinoma
25.
Epstein’s bar : EBV is a risk factor for gastric adenocarcinoma
26.
Cauliflower: intestinal type-gastric adenocarcinoma (forms a bulky exophytic mass) occurs in
lesser curvature of the antrum and pylorus
27.
Oozing red sauce: intestinal type gastric adenocarcinoma may cause bleeding and ulcerations
28.
Mucinous rice: histology, intestinal type gastric adenocarcinoma shows glandular structures
filled with mucin
29.
“claw adhering”: rubber band E cadherin (an intracellular adhesion molecule)
30.
Losing claw adhering band: in diffuse-type gastric adenocarcinoma, loss of normal E-cadherin
proteins results in decreased intracellular connections causing disorganized cell growth
31.
Crabs infiltrating along wall: diffuse type gastric adenocarcinoma, disorganized cells growth
leads to diffuse invasion through out stomach (“infiltrative growth pattern”)
32.
Leather stomach purse: diffuse type gastric adenocarcinoma causes a fibrosing desmoplastic
reaction->linits plastica (“leathre bottle” stomach)
33.
Ring jewlerry: hitology shows “signet rings” (mucin taining vacuoles displace nucleus to cell
membrane
34.
Rings on liver purse, lapels and pockets: gastric adenocarcinoma (intestinal and diffuse types),
most commonly go to liver, lungs and ovaries
35.
Chess board with white T knights and B antibody archers: Primary gastric lymphomas (B or T
type)
36.
Helicopter-like fan: H pylori mediated chronic gastritis is a risk factor for gastic lymphoma
37.
Grandfather clock: chronic atrophic metaplastic gastritis is a risk factor for gastric lymphoma
38.
Pile of blue lymphoid tissue: H.Pylori mediated chronic gastritis induces MALT (mucosa
associated lymphoid tissue), which can progress to gastric lymphoma
39.
Epstein stake Bar: EBV infection can cause gastric lymphoma
40.
Marginalized B archers and large B archers: gastric lymphomas are
most commonly marginal zone B cell or diffuse B cell lymphoma.
Chronic inflammation.
41.
GIST arcade hall: GI stromal tumor (GIST-mesenchymal tumor
derived from interstital cells of CAJAL)
42.
Rhythm game: GIST is derived from the interstial cells of Cajal (GI “pace maker” cells ,
responsible for Peristalsis
43.
Tool kit: GIST is caused by gain of mutation functions in C-KIT oncogene
44.
Tire swing game: C-kit is a tyrosine kinase
45.
Under mucosal door: GISTs form well-circumscribed fleshy, submucosal masses
46.
Mushroom family: familial adenomatous polyposis (FAP) causes colon polys, but NOT gastric
polys, and is a risk factor for adenocarcinoma
Metastatis via node/liver. Virchow node (involves left supraclavicular node-), Krukenberg tumor
(bilateral metastases to ovaries with signet ringsDIFFUSE TYPE), Sister Mary Joseph nodule
(subcutaneous periumbilical metastasisINTESTINAL TYPE).
1.
Small bowel obstruction
2.
Latching on to shirt: adhesions are most common cause of small bowel obstruction (due to
mechanical constriction of bowel)
3.
Scalpel graffiti: prior abdominal cause of abdominal adhesions (well-demarcated zones)
4.
Cancer crab skateboard: small bowel tumors can cause obstruction
5.
Green face: small bowel obstruction presents with nausea/vomiting
6.
Collie” small bowel obstruction presents with colicky abdominal pain
7.
Plunger: small bowel obstruction presents with constipation (inability to pass flatus or stool)
8.
Large belly: small bowel obstruction presents with distended abdomen (due to back up of gas in
intestines)
9.
Drun: small bowl obstruction presents with tympanic abdomen (due to backup of gas in
intestines)
10.
“tink, tink”: small bowel obstruction presents with high-pitched “tinkling” bowel sounds on
abdominal auscultation (due to abnormal peristalsis)
11.
Black cloud graffiti: X-ray shows small bowel obstruction displays bowel distension (dilated loops
of bowel) and air fluid levels (horizontal contrast line)
12.
Wide to narrow half-pipe: Xray of small bowel obstruction shows a “transition” point location of
obstruction, point where dilated proximal bowel meets normal distal bowel)
13.
Broken skateboard: Ileus is caused by hypomotility (similar to symptoms of small bowel)
14.
Dilated colon pants: Ileus, bowel is uniformly dilated (including colon and rectum)
15.
Broken boombox: Ileus presents with diminished or absent bowel sounds (due to decreased
peristalsis)
16.
Scalpel graffti: Surgery can cause ileus
17.
Drug bottles: drugs can cause ileus
18.
SEPTIC cover: sepsis can cause ileus
19.
Elevated candy jar: Diabetes can cause ileus (due to dysfunctional parasympathic nervous
system)
20.
Arterial rail: Superior mesenteric artery
21.
Red ramp: Aorta
22.
Crushed kid: Superior mesenteric artery syndrome, the third position of duodenum is
compressed between the aorta and SMA (can cause small bowel obstruction)
23.
Losing padding: SMA is caused by severe rapid weight loss (shrinking mesenteric fat
paddecreased cushioning around duodenumduodenal compression)
24.
Painful burrito: SMA presents with recurrent post prandial abdominal pain
25.
Telescoping camera lengs: Intussusception (occurs when segment of proximal bowel telescopes
beneath more distal bowel)
26.
Skull shirt: Intussception can cause bowel ischemia and necrosis (due to impaired venous return)
27.
Pile of lymphoid tissues: Hyperplastic lymphoid tissue (post viral infection, ROTA VIRUS) can
serve as a lead point to initiate intussception (usually in toddlers)
28.
Mecklers hecklers: Meckels diverticulum can serve as a lead point to initiate intussusception
29.
Mushroom hats: polys and tumors serve as a lead point to initiate intussception
30.
Small ramp meets large landing zone: Ileocecal junction is most common site for intussception
31.
Gooey red jelly: Intussusception presents with “currant jelly” stools (blood and mucus)
32.
Handle bat at RLQ: intussception presents with RLQ mass (location at illoceal junction)
33.
Target cushion: abdominal ultrasound, intusscepation has a target appearance due to
telescoped bowel
34.
“berry-yum”: barium enema can diagnose and treat intussception (moves telescoped bowel)
35.
Weakness in chain link fence: hernias can occur as a result of weakning of biromuscular tissue >intrabdominal contents protrude through defect
36.
Running: strenuous exercise is a risk factor for hernias
37.
Tight abdominal belt: chronic elevated intra-abdominal pressure (heavy lifting, chronic cought,
constipation, pregnancy) are all risk factors for hernia
38.
Older male: hernias are more common in older age (decreased tissue strength) and in men
39.
Hand cuffs: Incarcerated hernia (abdominal contetns[omentum, small bowel, colon] unable to
escape hernia
40.
Consticted blue and red strings: incarcerated hernias can cause constriction of veins within
bowel->decreased venous and lymphatic drainage->swelling->compromised arterial blood flow
41.
Skull tattoos: bowel strangulation can lead to necrosis
42.
Torn pants: bowel strangulation can lead to perforation
43.
Septic cover: bowel strangulation can lead to sepsis
44.
Hesselbachs construction: Hesselbachs triangle (bound by inguinal ligmanet, rectus abdominus,
inferior epigastric vessels)
45.
Tube: inguinal canal
46.
Tarp under skater tunnel: inguinal ligament (base of inguinal canal) forms inferior border of
hasselbachs triangle)
47.
Striated wooden wall: rectus abdominus muscle (medial border of hesselbachs triangle)
48.
Arterial and venous tubes: inferior epigastric vessels (lateral border of hesselbachs triangle)
49.
Directly pressing on fence: Direct inguinal hernias pass through hesselbachs triangle (medial to
inferior epigastric vessels)
50.
Sneaking though tube: Indirect inguinal hernias pass though canal (lateral to inferior epigastric
vessels)
51.
Sneaking from undertrap: Femoral hernias: pass through femoral canal (located inferior -postior
to inguinal ligament
52.
Shirt and hoodie: Indirect inguinal hernias are covered by all 3 layers of spermatic fascia
(external, oblique aponeurosis, cremastric fascia, transversalis fascia)
53.
Direct inguinal hernias are covered by external spermatic fasica
54.
Weakened fence: Direct inguinal hernias are a result of weakness in the floor of the inguinal
canal
55.
Virginia Co Patent: Indirect inguinal hernias are a result of persistent Patent processes vaginalis
56.
Woman with skull tattoo: femoral hernias occur mostly in females
1.
Ooze canister: carcinoid tumor (most common primary small bowel malignancy)
2.
Neural transformer: carcinoid tumors derived from neuroendocrine cells
3.
Ooze in distal intestinal pipes: ileum is most common site for carcinoid tumors
4.
Slime in gastric tunnel :Carcinoid tumors can occur in stomach
5.
Slime in haustra tunnel: carcinoid tumors can occur in the colon
6.
Ooze in appendiceal pipe: carcinoid tumors are the most common primary malignancy of
appendix
7.
Chest zone: carcinoid tumors can occur in the lungs
8.
Child in the ooze: Bronchial carcinoid tumors are most common primary lung cancer in children
9.
Coughing blood: bronchial carcinoids presents with coughing and hemoptysis
10.
Yellow ooze: carcinoid tumors appear yellow on gross pathology
11.
Purple spots on pink: histology shows islands of small round purple cells within pink connective
tissue (CHROMOGRANIN +)
12.
Granular granite: electron microscopy shows tumor cells display cytoplasmic granules (contain
secretory products and hormones)
13.
Path obstructed: small bowel carcinoid tumors may cause intestinal obstruction
14.
Inflamed appendiceal pipe: carcinoid tumors of the appendix may cause appendicitis (due to
obstruction of the appendiceal lumen)
15.
Climbing into liver base: GI carcinoid tumors may metastasizes to the liver
16.
Liver armor: because of first pass metabolism in liver, substances secreted by carcinoid tumors
in the GI tract do not cause systemic symptoms
17.
Consuming histamine bee: carcinoid tumors secrete histamine, which is metabolized by the liver
18.
Consuming smiley serotonin pizza: carcinoid tumors secrete serotonin, which is metabolized by
liver
19.
Bunch of pizza and bees: vasoactive substances (serotonin, histamine) cause symptoms
(“carcinoid syndrome”), if tumor metastasizes to the liver or beyond GI tract (by passes the first
pass metabolism)
20.
Red face: carcinoid syndrome causes episodic flushing (face, neck, chest) due to excessive
histamine secretion
21.
Red face mask: carcinoid syndrome causes vascular teleangictasias on nose and cheeks (due to
vasodilation from vasoactive factors)
22.
Brown waterfall: carcinoid syndrome cause secretary diarrhea (too much serotonin cause
increased intestinal motility)
23.
Wheezy party blower: carcinoid syndrome may cause episodic bronchospasm and wheezing
24.
Carcinoid syndrome can cause valvular disease (plaque like vegetations) in the right heart (for
example tricuspid and pulmonic valves)
25.
Smiley graffiti: carcinoid valvular disease is due to too much serotonin which causes increased
fibroblast growth
26.
Leaking wheel: carcinoid valvular disease can cause regurgitation (may later progress to
stenosis)
27.
Consuming serotonin smiley pizza: lung metabolize serotonin
28.
Catching histamine bee: lungs metabolize histamine
29.
Lung chest armour: lungs metabolize vasoactive substances secreted by carcinoid tumors
(including serotonin, there fore no serotonin reaches left heart, NO LEFT HEART VALVULAR
DISEASE)
30.
“HI-AA”: carcinoid syndrome is diagnosed with urine 5-HIAA (5-hydoxyindoeleactic acid) a
breakdown of serotonin
31.
Stop sign: somatostatin analogues are used to treat carcinoid syndrome (bind to somatostatin
receptors and inhibit release of serotonin)
32.
8 sides sign: OCTreodite is a somatstain analogue
33.
Super pincher crab: small bowel adenocarcinoma
34.
Glandy bubbles: histology shows glandular structures
35.
Proximal duodenal pipe: duodenum is the most common site for small bowel adenocarcniomas
36.
Mutated shroom family: Familial adenomatous polyposis (FAP), causes polys in duodenum and
colon and is a risk factor
37.
Lynch worm: Lynch syndrome is a risk factor for small bowel adenocarcinoma
38.
Peutz pop: Peutz-jeghers syndrome
39.
Hammers: Peutz-jeghers syndrome causes multiple non-neoplastic hamartomatous polys
through out GI system (mostly small bowel)
40.
Domino: Autosomal dominant
41.
Creeping crab: Peutz jegurs syndrome is a risk factor for small bowel adenocarcniomas (as well
as colorectal and non GI cancers)
42.
Peutz-jeghers syndrome causes mucocutaneous hyperpigmentation (mouth, lips, palms,
genitalia)
43.
Skipping cobble stones: Crohns disease is a risk factor for small bowel adenocarcinoma
44.
Distal pipe: Crohn disease (and resulting small bowel adenocarcinoma) commonly affects the
ileum
1.
Day of the dead: intestinal ischemia and necrosis occurs because of low perfusion to bowel
2.
Tall tombstone projections with vascular ivy: villi of small and large bowel (contain small
capillaries and venulues)
3.
Crypt: crypts of small and large bowel contains secretory and stem cells
4.
Small vascular ivy near surface: arteries become smaller and more susceptible to ischemia as
they move toward luminal surface of villi
5.
Cracking dead vascular ivy: bowel ischemia and necrosis start at the luminal surface of villi>leads to sloughing of villi
6.
Proliferating crypt flowers: in the bowel, crypts are initially spared from ischemia and become
hyperplastic (although later affected as ischemia progresses)
7.
First responders: ischemia leads to a neutrophilic infiltrate
8.
Patches of red marigolds: bowel ischemia leads to patchy areas of mucosal hemorrhage
9.
High pressure water: ischemia and inflammation lead to bowel wall edema->increased pressure
obstructs venous drainage->further decrease in perfusion
10.
Top arterial bowsprit: super mesenteric artery (SMA) supplied small intestines and proximal
large bowel
11.
Low arterial bowspirit: Inferior mesenteric artery supplies distal large bowel
12.
Black intestinal design: acute intestinal occlusion (most likely to occur in the SMA leads to acute
mesenteric ischemia)
13.
Poop emboli from thrombotic nest: occlusion of the SMA by an embolus causes acute
mesenteric ischemia
14.
Irregulary ireegular TV signal: acute mesenteric ischemia via embolus formation
15.
Thrombotic straw dress: thrombus formation in the SMA (due to rupture of atherosclerotic
plaques) causes acute mesenteric ischemia
16.
Abdominal pain perplexing doctor: acute mesenteric ischemia causes severe abdominal pain
(out of proportion to physical exam)
17.
Green face: acute mesenteric ischemia (causes nausea/vomiting)
18.
Broken speaker: acute mesenteric ischemia causes loss of bowel sounds (due to ileus)
19.
Dressed in all black with ripped sleeve: acute mesenteric ischemia can lead to bowel infarction
and perforation
20.
Septic: acute mesenteric ischemia can lead to sepsis
21.
Open door: non occlusive acute intestinal ischemia
22.
Hypotensive fainting: non occlusive acute intestinal ischemia is caused by hypoperfusion of
intestinal vessels
23.
Water shed: the colon has watershed areas (areas most susceptible to hypoperfusion)
24.
Arterial trees barley reaching each other: arteries in the colon connect with each other via small
shared vessels (anastomoses)
25.
Losing water: hypovolemia can cause acute colonic ischemia (because of poor perfusion)
26.
Septic: septic shock can cause acute colonic ischemia (because of poor perfusion)
27.
Heart shirt: cardiogenic shock can cause acute colonic ischemia
28.
Acute colonic ischemia: most commonly occurs in the elderly
29.
Corner tree attachment: watershed area between SMA and IMA (located at the splenic flexure),
where the transverse colon meets the descending colon
30.
Distal tree attachment: watershed area between IMA and rectal arteries (located at the distal
end of sigmoid colon)
31.
Catching left abdomen: acute colonic ischemia causes crampy left abdominal pain and
tenderness (Watershed areas are on the left side)
32.
Red blood puddle: acute colonic ischemia can cause bloody stools (due to necrosis and
hemorrhage)
33.
Broken speaker: acute colonic ischemia can cause loos of bowel sounds (due to ileus)
34.
Septic: acute colonic ischemia can cause sepsis
35.
Anvil: Chronic mesenteric ischemia causes intestinal angina
36.
Grandfather clock: chronic
37.
Greasy pipe: chronic mesenteric ischemia occurs secondary to atherosclerosis of mesenteric
vessels
38.
Obese grandma: chronic mesenteric ischemia is most common in obese older females
39.
Greasy spatula: other atherosclerosclerotic disease (coronary heart disease, cerebrovascular
disease, peripheral vascular disease) is a risk factor for chronic mesenteric ischemia
40.
Clutching belly: chronic mesenteric ischemia presents with postprandial abdominal pain (due to
increased oxygen demand during digestion)
41.
Aversion to burrito: Chronic mesenteric ischemia presents with aversion to eating (due to post
prandial abdominal pain()
42.
Thin skeleton: chronic mesenteric ischemia presents with weight loss
43.
Tangled red strings: Angiodysplasia of GI tracts (caused by malformed blood vessels which are
thin-walled, dilated, torturous, composed only of endothelium
44.
Colonic dress: angiodysplasia most often occurs in colon , especially cecum
45.
Pool of blood: angiodysplasia presents with recurrent, painless hematochezia
46.
Stenotic arched hat: bleeding of angiodysplasia is associated with aortic arch stenosis
Hereditary Hemorrhagic Telangiectasia: AD disorder, resulting in thin-walled vessels in GI and
nasopharync which rupture and bleed.
1.
Pinched stomach bottle: pyloric stenosis
2.
#1 bay boy: pyloric stenosis is far more common in males (especially in first-born males)
3.
Vomiting white milk: pyloric stenosis presents with non-bilious (because proximal to duodenum)
projectile vomiting immediately after feeding
4.
One month calendar: pyloric stenosis presents around 1 month
5.
Muscular baby sitter: pyloric stenosis is caused by hypertrophy of the pyloric sphincter (takes ~1
month to develop)
6.
Round bottle nipple: pyloric stenosis may present with a palpable “olive-shaped” mass at the
pylorus (periumbilical region)
7.
Schisis string next to umbilicus : gastroschisis (paraumbilical herniated of the abdominal
contents through the ventral abdominal wall)
8.
Uncovered string: in gastrochisis, herniated organs are NOT COVERED by peritoneum
9.
Elephant seal: omphalocele (failure of GI contents to return to the abdominal cavity during
embryologic development)
10.
Elephant seal collar: omphalocele is a true umbilical hernia (through umbilical ring)
11.
Hand covered by puppet: in omphalocele, herniated abdominal organs are COVERED by
peritoneum
12.
Trisomy triplets with chromosome waistbands: omphaloceles are associated with trisomies
(trisomy 18/13) and other defects like cardiac and neural tube
13.
Intestines springing out of box: congenital diaphragmatic hernia (CDH), abnormal organs
herniate through the left hemidiaphragm and into the thorax
14.
Scrunched up lung shirt: congenital diaphragmatic hernia can cause pulmonary hypoplasia and
pulmonary hypertension (due to compression of lungs by abdominal organs)
15.
Skull and X bones: chest X ray can be used to diagnose congenital diaphragmatic hernia (bowel
gas and abdominal organs above the diaphragm)
16.
Broken tracheal and esophageal slide: Tracheosphageal fistula
17.
September: the fistulas are a result of failure of SEPTAION of the trachoesophageal tube
18.
4th and 5th: tracheesophageal septation normally occurs at 4-5 weeks
19.
Tube-slide connection: TE fistula (trachea and esophagus and connected by a bridge)
20.
Stuck in tube: esophageal atresia (normal trachea)
21.
Distal tube connection: type C-TE fistula (most common ), proximal esophagus ends as blind
pouch, distal esophagus connects to trachea)
22.
Vomiting while stuck on esophageal ring: type-C TE fitisula causes non bilious emesis (proximal
esophagus ends in blind pouchfood never reaches intestines)
23.
Distended belly stuck in tube: Type C-TE fistula causes abdominal diestenion (due to flow of air
from trachea into stomach)
24.
Refluxing onto lung shirt: type-CTE fistula causes recurrent pneumonitis and aspiration
pneumonia (due to reflex of acidic stomach contents into lungs)
25.
Wet baby doll: type C-TE fistula causes polyhydramnios in utero (due to fetus unable to swallow
amniotic fluid)
26.
Abnormal doll: TE fistula can be associated with other congenital anomalies (including vacteral
association*vertebral defects, anal atresia, cardiac defects, tracheo-esophageal fistula,
renal anomalies, and limb abnormalities)
27.
C curved tube: duodenum
28.
Duodenal atresia occurs when second portion of duodenum fails to recanalize
29.
Green vomit: Duodenal atresia presents with BILIOUS emesis (due to obstruction distal to
ampulla of vater). ASSOCIATED WITH DOWN SYNDROME
30.
Two fun domes with skull and X bones: X ray shows double bubble sign (one bubble of air in
stomach and one in proximal duodenum)
31.
Obstructing end of tube: distal intestinal atresia (jejunum or ileum)
32.
Compressing red vascular hair: distal interstinal atresia is caused by in utero vascular accident
(decreased blood flow to intestine->decreased delivery of oxygen+nutrients->impaired intestinal
growth
33.
Green vomit: distal intestinal atresia presents with bilious vomiting (due to obstruction distal to
ampulla)
34.
Distal intestinal atresia presents with abdominal distension (due to accumulation of air proximal
to obstruction)
35.
Violinist: Vitellineduct (omphalomesentric duct, connects ileum to yolk sac during fetal life or
vitelline duct connects V(M)idgut to V(y)olk sac
36.
Meckler hecklers: Meckle divertcilulum (true diverticulum in the ileum), forms if vitelline duct
fails to obliterate
37.
Gastric violin : Meckel diverticula can contain gastric mucosa (most common)and other ectopic
issue, (pancreatic, endometrial etc)
38.
Tarry black paint: Meckel diverticula can present with painless melena (functional ectopicgastric
tissueulceration and bleeding
39.
2 signs: Meckel diverticulum occurs in 2% of population, exists 2 feet proximal to ileocecal valve,
2 inches in length, presents ~2 years of age, 2male:1female ratio
40.
Technique book: Mecker diverticulum can be diagnosed with a technetium-99m pertechenate
scan (gastric mucosa takes up technetium-99m)
41.
Horse-spring ride: Hirschsprungs disease RECTAL SUCTION BIOPSY+Removal of non ganglion
cells area
42.
Migrating crest border: Hirschsprung develops due to failed neural crest cell migration (normally
migrate from embryonic ectoderm into organs)
43.
Disconnected plug: In Hirschsprung’s disease, the impaired migration of neural crest cells leads
to absent innervation (absent neural ganglia) of distal colon (most likely includes rectum).
44.
Tightly wound rectum spring: in absence of innervation, the rectal muscles remain contracted
45.
Dilating “s” slinky: colon proximal to the constriction (sigmoid colon), fills with stool and dilated
forming a MEGAcolon
46.
Blackened stool stuck in spring: hirschsprungs disease presents with failure to pass meconium
within 48 hrs of birth
47.
Yo-yo not rotating: Intestinal malrotation (failure to undergo normal 270 degree counter
clockwise rotation during fetal development
48.
Yo-yo in RUQ pocket: intestinal malrotation, cecum is located in RUQ
49.
String compressed belly: can cause duodenal obstruction (due to fibrouds bands called LADDS
BANDS). Which connected abnormally located cecum to retroperitoneum
50.
Distended belly and green face: intestinal malrotation, duodenal obstruction can leadto
abdominal distension and vomiting
51.
Knot in waist sweater: intestinal malrotation, twisting around Ladds bands can cause midgut
volvulus (surgical emergency due to risk of bowel necrosis)
52.
Death metal baby: Necrotizing enterocolitis
53.
Small emancipated baby: necrotizing enterocolitis develops in premature and underweight
infants
54.
Baby bottle: necrotizing enterocolitis begins when some infant starts feeding (bacteria
introducts into gut overpowers the immature gastrointestinal immune system)
55.
Inner layer of bacterial wallpaper: necrotizing enterocolitis, bacteria invade the bowel wall
56.
Necrotizing enterocolitis: presents with abdominal distension and bloody stools
57.
Black outlines: Entercolitis causes pneumatosis intestinalis (pockets of gas in intestinal wall,
causes black outlines of bowel lumen on X-ray)
58.
Necrotizing enterocolitis can cause extensive bowel necrosis and death
1.
Saddle bags: Diverticulosis
2.
False mcusy teeth: colonic diverticula are false diverticular (herniated of mucosa and submucosa
only) vs (herniation of mucosa, submucosa and muscularis in true diverticula)
3.
Border: most colonic diverticula form on the mesenteric border
4.
S snake: diverticula are most commonly found in the sigmoid colon
5.
Red vines penetrating fence: vasa recta arteries penetrate the muscularis at the mesenteric
border (creates weakening that facilitates diverticulum formation)
6.
Plunger: chronic constipation is a risk factor for divertulosis (straining generates high pressure
within the colon)
7.
Dumping red: divertuclosis causes painless, hematochezia (vasa recta injury causes rupture)
8.
Fire next to saddle bag: diverticulitis is a complication of divertuclosis
9.
Leaking saddle bag: Diverticulitis is caused by perforation of a diverticulum (increased
intraluminar pressure or congealed food particles->erosion of diverticular wall->perforation)
10.
Flame bandan: divertulitis presents with fever
11.
Diverticulitis presents with nausea/vomiting
12.
Left lower abdominal fire: divertuclitis presents with LLQ pain (location of sigmoid colon)
13.
Red inflamed pouch: divericulitis can cause abscess formation (can cause partial colonic
obstruction)
14.
Leaking poopy water: diverticulitis can cause fistulas (most commonly colovesical fistula>pneumatruai->pyuria, fecaluria)
15.
Murkey pool: appendicitis
16.
Obstructing rock: adults, appendicitis is most commonly due to obstruction from an inspissated
fecalith (also fibrosis, malignancy or carcinoid tumor)
17.
Soggy tissues: children, appendicitis is most commonly due to obstruction from lymphoid tissue,
hyperplasia (follows infection)
18.
Applying pressure: appendicitis leads to increased intraluminal pressure (obstruction>accumulation of mucus->distension->pressure on appendiceal wall)
19.
Squeezing vascular sleeve: appendicitis, vessels and lymphatics in the wall of the appendix are
compressed (due to increased intraluminal pressure)
20.
Appendicitis can cause ischemia and necrosis (due to compression of vessels in appendiceal
wall)
21.
Fire next to murky pool: appendicitis causes inflammation
22.
First responders: appendicitis, histology shows neutrophil infiltration
23.
Appendicitis, bacterial overgrowth leads to bacterial invasion into the wall
24.
Inflamed red pouch: appendicitis can lead to abscess formation
25.
Perforating pouch: appendices can lead to perforation
26.
Clutching mid abdomen: appendicitis initially presents with vague periumbilical pain
(inflammation of visceral peritoneum is innervated by autonomic nervous system afferent fibers
(T10 spinal root T10 dermatome)
27.
Right -sides appendicitis presents with sharp localized RLQ pain (due to inflammation of parietal
peritoneum (somatic afferent fibers)
28.
Mcburnies lookout point: late appendices presents with localized RLQ pain at mcburnys point
(1/3 between umbilicus and right anterior superior iliac spine)
29.
Green face: appendicitis presents with nausea/vomiting
30.
Flame bandana: appendicitis presents with fever (usually later )
31.
Relieving defecation: Irritable bowel syndrome (IBS), presents with vague abdominal pain
relieved bydefecation
32.
Water and clumpy dirt: IBS may present with diarrhea and/or constipation (varying consistency)
33.
Radio frequency: IBS presents with varying bowel movement frequency
34.
Twisted leash: large bowel volvulus (twisting of a portion of bowel around its mesentry)
35.
Cactus roots: in volvulus, bowel twists at its mesenteric rotos
36.
Dead cactus: volvulus can cause strangulation (leads to ischemia and necrosis)
37.
Right gun pouch: children, volvulus occur in cecum
38.
S snake: adults, volvulus occurs in sigmoid
39.
Plunger: Chronic constipation most common risk factor for large bowel volvulus
40.
Obstructed canyon: large bowel obstruction
41.
Cancer crabs: malignancy is most common cause of large bowel obstruction
42.
Large painful belly: large bowel obstruction presents with abdominal pain and distension
43.
Green face dripping brown water: large bowel obstruction presents with nausea/vomiting
including feculent vomiting
44.
Collie: large bowel obstruction presents with colicky abdominal pain
45.
Tink: large bowel obstruction presents with high pitched tinkling bowel sounds
46.
Drumming: large bowel obstruction causes hyperresonance to percussion (due to gas filled
bowel)
47.
Dark clouds with horizontal base: X-ray, large bowel obstruction displays dilated loops of bowel
(appears as dark pockets of gas) and air fluid levels (appear as horizontal contrast lines)
1.
Fiery intestines: Inflammatory bowel disease (Ulcerative colitis and Crohn disease)
2.
Young white guy: IBD is common in Caucasian and jewish people
3.
Fiey hat: IBD presents with fever
4.
IBD presents with weight loss: IBD
5.
Clutching abdomen: IBD presents with abdominal pain
6.
Brown puddle: IBD presents with diarrhea
7.
Union canon: Ulcerative colitis (mucosal and submucosal) Ulcer means damage to mucosa and
submucosa
8.
Rusty rectal stool: Ulcerative colitis ALWAYS affects rectum
9.
Rust travelling proximally: ulcerative colitis spreads proximally from rectum in a continuous
pattern
10.
Smooth end of canon: ulcerative colitis, colon has a “lead pipe” appearance on contrast enema
(due to loss of normal haustral projections)
11.
First respodners with perinuclear battle plan: pANCA (perinuclear anti neutrophil cytoplasmic
antibibodies) are elevated in ulcerative colitis
12.
Eroding through 2 layers: Ulcerative colitis, inflammation affects only the mucosa and
submucosa
13.
Dirt islands in hole: Ulcerative colitis, colon contains “Pseudopolys” (islands of normal mucosa
within ulcerate tissue), loss of haustra
14.
Inflamed cannonball within wall: histology shows abscesses with colonic crypts
15.
Shrapnel striking left side: ulcerative colitis presents with left sided abdominal pain (due to
location in rectum and distal colon)
16.
Bloody puddle: Ulcerative colitis presents with blood diarrhea (frequent and small volume due
to rectal inflammation)
17.
Mega cannon: UC causes toxic mega colon (inflammation extends to colonic smooth muscle>smooth muscle paralysis->severe colonic dilation)
18.
Exploding canon: UC, toxic mega colon can lead to perforation
19.
Cancer crab belt: UC, increases risk of colon cancer (more then Crohn disease),Extent of disease
spread and time length determine outcome to cancer. SMOKING IS PROTECTIVE AGAINST
ULCERATICE COLITIS.
20.
Scaly snake in billary tree: UC, increases primary sclerosing cholangitis (PSC) (autoimmune
disorder of intra and extrahepatic bile ducts)
21.
Cobble stones patches: Crohn disease (full thickness damage)occurs as multiple separate areas
of disease (“skip lesions”)
22.
Cobblestone path from mouth to anus arch: Crohn disease can affect any portion of the GI tract
from mouth to anus
23.
Antibody sac: Anti-saccharomyces cerevisiae are present
24.
Hit on right waist: crohn disease presents with RLQ abdominal pain (due to location in ileum and
cecum)
25.
Debris-littered brown puddle: crohn disease presents with malabsorption of fats and fat-soluble
vitamins (inflammation of distal ileum->poor reabsorption of bile acids->impaired absorption of
fat)
26.
MacroCages: crohn disease causes formation of non caseating granulomas (containing
aggregations of macrophages)
27.
Broken through all wall layers: Crohn disease causes transmural bowel inflammation
28.
Tight abdominal gauze: Crohn disease can cause fibrotic strictures (transmural inflammation>bowel wall thickening->narrowed lumen)
29.
Pulling strings: Crohn disease, X-ray shows “string sign” due to strictures
30.
Obstructing rocks: Crohn disease, strictures can cause bowel obstruction
31.
Fistulizing trench: Crohn disease can lead to fistulas (transmural inflammation leads to
epithelization across bowel wall->connections between bowel and bladder, skin vagina or other
bowel segments)
32.
Pale erosions on mouth arch: Crohn disease causes aphthous ulcers in mouth and esophagus
33.
Inflammatory bowel disease can cause arthritis (migratory polyarthritis, sacroiliitis, ankylosing
spondylitis) (HLA-B27)
34.
Red spots on shin columns: inflammatory bowel disease can cause erythema nodosum (painful
erythematous nodular rash on shins) due to inflammation of fat cells
35.
Skin wounds: inflammatory bowel disease can cause pyoderma gangrenosum (skin ulcers due to
neutrophil dysfunction) not infectious or gangrenous
36.
Shrapnel on kidney tray: inflammatory bowel disease can cause renal calculi (due to increased
absorption of oxalate…calcium oxlate nephrolithiasis)
37.
Red-rimmed goggles:inflammatory bowel disease can cause eye disease (anterior uveitis, iritis,
episcleritits), (presents with eye pain and redness)
38.
5 pointed star: inflammatory bowel disease is treated with 5-ASA (sulfasalazine, mesalamine)
1.
Mushroom caps: polys are outgrowths of mucosa most commonly found in colon (pedunculated
or sessile or neoplastic vs non-neoplastic)
2.
Hamartomatous hammer: hamartomatous polys (non neoplastic)
3.
Hamartomatous polys are disorganized growths of mature cells
4.
Happy old guy: hamartomatous polys are mature and benign
5.
Peutz-pop: Pretuz-jeghers syndrome presents with hamartomatous polys in GI (commonly in
duodenum)
6.
Domino: Peutz-jeghers and juvenile polyposis syndromes (familial cause of hamartomatous)
polys ) are autosomal dominant
7.
Peutz-jeghers syndrome: presents with pigmented macules around mouth, lips, palms, gentalia
8.
Infant with hammer: Juvenille polyposis syndrome common in children <5 and presents with
hamartomatous polyps
9.
Mushroom emerging from the behind: Juvenille polys are most common in rectum and may
prolapse through anal sphincter
10.
Bleeding mushroom: juvenile polyps present with lower GI bleeding (hematochezia)
11.
Little mushroom spots: Juvenile polys display small cytic glands (filled with mucin and debris)
12.
Creeping carb beetle: Juvenile polyposis syndrome is associated with increased risk of colon
cancer (despite polys being benign)
13.
Big hyperplastic mushroom: hyperplastic poly (non-neoplastic epithelial proliferation)
14.
Happy lilpolyps: Hyperplastic polys are benign
15.
Mucous-y goblet shrooms: Hyperplastic polys are epithelial proliferations that contain abundant
goblet cells
16.
Sawing near the surface: hyperplastic polys have serrated architecture only at the surface
(crypts remain smooth shape)
17.
Sawing on stalk-less mushroom Sessile serrated polyp ( premalignant flat lesion of the colon)
18.
Sawing all the way through: Sessile serrated polyps have serrated architecture throughout (cryps
included)
19.
Creeping crab beetle: serrated polyps and adenomas have the potential to transform
20.
Adding shingles to mushroom house: adenomatous polys (adenomas) are the most common
type of poly
21.
Creeping crab beetle: Serrated polyps and adenomas have potential to transform into cancer
22.
Oversized mushroom next to crab beetle: larger adenomas are more likely to transform into
cancer
23.
1 horn: adenomas >1cm are more likely to transform into cancer
24.
increasingly disorganized purple weeds next to crab beetle: Adenomas with a greater degree of
dysplasia (more hyperchromatic, elongated and stratified epithelium) are more likely to
transform into cancer
25.
Tubular horn: Tubular adenomas (small pedunculated polys composed of dysplastic mucosal cell
that form tube-shaped glands)
26.
Tubular perforations: tubular adenomas display round tubular gland across sections on histology
27.
Finger-like stalk-less fungus: Villous adenomas (sessile, larger than tubular adenomas, long
glands with villi-like projections). Progress to carcinoma if >2m, VILLOUS, SESSILE GROWTH
28.
Villus fungus next to crab beetle: Villous adenomas are more likely to transform into cancer as
compared to tubular adenomas
29.
Polyp family: Family adenomatous poplyposis (FAP), inherited syndrome that causes thousand
of adenomatous polyps early in life
30.
Domino: FAP is AD
31.
A pulled carrot: germline mutation in the APC gene causes FAP
32.
Cancer fighting ribbon: APC is a tumor suppressor gene
33.
A single pulled carrot stalk: in FAP, only one APC allele has a germline mutation (second
mutation occurs during persons life time, referred to as a second hit
34.
Abundant mushrooms: FAP presents with thousands of poyls
35.
family crab beetle: FAP progresses to colon cancer in nearly 100% of cases (treated is
prophylactic colectomy)
36.
gardner with mushroom field: Gardner syndrome (FAP variant), presents with adenomatous
polys and SOFT TISSUE TUMORS
37.
Bone garden fence: Gardner syndrome presents with osetomas (benign bone tumor)
38.
Ski nrash: Gardner syndrome presents with cutanoues lesions
39.
Overgrowth sunglasses on gardner: gardner syndrome presents with hypertrophy of retinal
pigment epithelium
40.
Tooth gardening stool: Gardner syndrome presents with dental abnormalities (impacted and
supernumary teeth)
41.
Elder lillipolyp wearing tuban: Turcot syndrome (FAP variant), presents with colon adenomas
and brain tumors (medulloblastomas)
42.
Crab beetle attacking lilipolp: Colorectal cancer (most common adenocarcinoma-3rd most
common cancer and 2nd most common cause of cancer death). S.Bovis will cause COLORECTAL
CANCER. Second pathway is microsatellite sequences (unstable)
43.
Old man lilipoly riding crab: peak incidence of colorectal cancer is 60-70 years of age, with men
affected slightly more than women
44.
Family photo: family history of colorectal cancer is risk factor
45.
Smoker: smoking is a risk factor for colorectal caner
46.
Alcohol bottle: alcohol use is a risk factor for colorectal cancer
47.
Round lilipoly: obesity is a risk factor
48.
Fiery intestines: inflammatory bowel disease is a risk factor
49.
A pulled carrot: Mutations in APC gene can lead to adenomas or adenomatous polyps
50.
Carrots: APC gene product controls concentration of beta-catenin and interacts with E-cadherin
51.
Cancer-fighting ribbon: APC is a tumor suppressor gene
52.
Cancerous rat: mutations in the L-RAS protooncogene leads to unstoppable cell divions. KRAS
codes for a protein that regulates the cell cycle.
53.
Mushrooms increase in size: adenomas increase in size as a result of mutations in K-RAS
54.
Broken city wall: basement membrane invasion marks malignant transformation of an adenoma
into an adenocarcinoma
55.
Broken checkpoint: mutations in p53 gene contribute to malignant transformation ( a tumor
suppressor) normally prevents G1 to S phase transition.
56.
Broken “Don’t CCross”: deletetions in DCC (deleted colon cancer) contribute to malignancy
which normally activates apoptosis pathway
57.
Cauliflower on the right: Right sides colon cancer (proximal ascending colon) presents as an
EXOPHYTIC mass (usually non-obstructive despite extension into the lumen)
58.
Occult watchman dropping iron tools: Right sided colon cancer often presents with iron deficeny
anemia (from occult GI bleeding)
59.
“Path obstructed” on left: Left sided colon cancer (descending colon) may present with colonic
bstruction (due to luminal narrowing from infiltrative ulcerative lesions), leading to change in
bowel habits
60.
Apple core on left: Left sided colon cancer can present with an “apple core” lesion on imaging
due to luminal narrowing
61.
Sitting in red puddle: Left sided colon cancer presentswith hematochezia
62.
Periscope: Colonscopy is the gold standard for screening and diagnosis of colon cancer
63.
Fibrous hat: a higher fiber diet decreases the risk of colon cancer
64.
Aspirin umpire guard: regular aspirin use decrease the risk of colon cancer
65.
“CEA”: carcinoembryonic antigen can be used to monitor progression or recurrence of colon
cancer
66.
Lynch worm: Lynch syndrome (hereditary non-polyposis colorectal cancer) most common
familiar cause of colocrectal cancer (NO ADENOMATOUS POYLPS)
67.
Dominos: Lynch syndrome is autosomal dominant
68.
Mismatched colors; Lynch syndrome is caused by germline mutations in mismatch repair genes
(MSH2 and MLH1)
69.
Cancer fighting ribbon: mismatch repair genes (MSH2 MLH1) are tumor suppressor genes
70.
One falling antennae: Lynch syndrome is caused by inheritance of one germline mutation
(second mutation is acquired during persons lifetime)
71.
Crab belt buckle: Lynch syndrome is also associated with increased risk of other (endometrial,
ovarian, colorectal)
*p53 with COX (ASPIRIN PROTECTS AGAINST COX PRODUCTION)
APC (CHROMSOME 5) creates risk for development of polyp. Tumor suppressor gene (both copies must
be knocked out)
T: Depth of invasion
N: Spread to regional lymph nodes
M-Meteastatis : distance spread, most common site is liver
Lactulose intolerance: Decreased function of the lactase enzyme found in the brush border of
enterocytes. Lactase normally breaks down lactose into glucose and galactose.
Presentation: abdominal distension and diarrhea upon consumption of milk products;
undigested lactose is osmotically active.
Cause: Deficiency may be congenital (rare autosomal recessive disorder) or acquired (often
develops in late childhood); temporary deficiency is seen after small bowel infection (lactase is highly
susceptible to injury).
Celiac disease: Auto-immune-mediated damage of small bowel villi due to gluten exposure; associated
with HLA-DQ2 and DQS.
Presenttation: Diarrhea, bloating, abdominal pain. Dermatitis herpetiformis (herpes-like vesicles
on skin). IgA deposits on Tip of dermal papillae.
Pathophysiology: Gluten in in wheat and grains; contains GLIADIN. Once absorbed, gliadin is
deamidated by tissue transglutaminase (tTG).Deamidated gliadin is presented by antigen
presenting cells via MHC class II. 3. Helper T cells mediate tissue damage
Labs: IgA antibodies against endomysium, tTG, or gliadin; IgG antibodies are also present and
are useful for diagnosis in individuals with IgA deficiency (increased incidence of lgA deficiency is
seen in celiac disease). Duodenal biopsy reveals flattening of villi, hyperplasia of crypts, and
increased intra-epitheliallymphocytes . Damage is most prominent in the duodenum; jejunum
and ileum are less involved.
Solution: gluten-free diet.
Late complications: Small bowel carcinoma and T-cell lymphoma.
Tropical Sprue: Damage to small bowel villi due to an unknown organism resulting in malabsorption.
Presentation: Similar to celiac disease except, Ocurs in tropical regions (e.g., Caribbean) and
occurs after infectious diarrhea and responds to antibiotics .
Complications: Damage is most prominent in jejunum and ileum (secondary vitamin B12 or
folate deficiency may ensue); duodenum is less commonly involved.
Whipple disease: Systemic tissue damage characterized by macrophages loaded with Tropheryma
whippelii organisms; partially destroyed organisms are present in macrophage lysosomes (+Pas).
Foamy Whipped Cream in a CAN.
foamy macrophages, Cardiac symptoms, Arthralgias, Neurologic symptons
Location: small bowel lamina propria
Pathophysiology: Macrophages compress lacteals and chylomicrons cannot be transferred from
enterocytes to lymphatics. Results in fat malabsorption and steatorrhea
Abetalipoproteinemia: Autosomal recessive deficiency of apolipoprotein B-48 and B-100 B.
Presentation: Malabsorption-due to defective chylomicron formation (requires B-48)
Labs: Absent plasma VLDL and LDL (require B-100)
Hereditary hemorrhagic telangiectasia: Autosomal dominant disorder resulting in thin-walled blood
vessels, especially in the mouth and GI tract, rupture and might bleed.
Pancreatic insufficiency: Chronic pancreatitis, Cystic fibrosis, or obstructive cancer. Causes
malabsorption of fat soluble vitamin ADEK and B12.
1.
Canal entrance: rectum
2.
Cannal exit: anus
3.
Tooth bridge: rectum and anus converge at denate pectinate line
4.
Columnar bricks: Superior to the dentate line, tissue derived from the dnoderm (mucosa is
COLUMNAR)
5.
Squamous title: Inferior to the dentate line, tissue derived from ectoderm (mucosa is
SQUAMOUS)
6.
Rope plexus under stomach tower: Superior to dentate line, innervation is via the inferior
hypogastric plexus
7.
Automatic sensor: Superior to the dentate line, innervation is by autonomic nerves (inferior
hypogastric plexus) which detects STRECH only, NOT Pain.
8.
Pedaling: Inferior to the dentate line, innervation via the inferior rectal nerve
9.
Pedaler in pain: Any pathology below the dentate line can cause PAIN (innvervation via somatic
ncerves)
10.
Schooners PORThole: Above dentate line, venous blood drains into PORTAL circulation
11.
“Intentional Marine Vessel”: Superior to dentate line, venous blood travels via the superior
rectal vein->inferior mesenteric vein->portal vein
12.
Pudendal paddle boat: Below the dentate line, venous blood drains into Systemic circulation
(infefrior rectal vein->internal pudendal vein->internal iliac vein)
13.
Dilated arterio venous pipes: hemorrhoids are dilated vascular structures in the submucosa of
the anal canal
14.
Dilated upper pipes: Internal hemorrhoids occur above the dentate line
15.
Bleeding dilated pipes: Internal hemorrhoids cause bleeding (blood coating stool or dripping
after pooping)
16.
Happy canal worker: Internal hemorrhoids are painless (due to autonomic innvervation)
17.
Dilated lower pipes: External hemorrohids occur inferior to the dentate line
18.
Thrombotic driftwood: thrombosis of external hemorrhoids can cause acute pain
19.
Older man using plunger: hemorrhoids are associated with older adults and chronic constipation
(opiods, straining and pooping)
20.
Pregnant woman: hemorrhoids occur in pregnancy (increased intra-abdominal pressure and IVC
compression->venous pooling and engorgement)
21.
Connected pipes: Upper anus/lower rectum is a portcaval junction
(portal venous system communicates with the systemic venous
system)
22.
Steaming PORThole: high pressure in portal venous system (portal
hypertension) can cause hemorrhoids (pressure transmitted to
systemic venous system)
23.
Barge pushing through anal gate: rectal prolapse, rectum pushed through a weak pelvic floor>prolapse through the anus
24.
Telescoping; rectal prolapse, the layers of mucosa fold on each other
25.
Plungers: Chronic constipating can cause rectal prolapse
26.
Old woman holding baby: Rectal prolapse occurs in elderly women with a weak pelvic floor
(history of multiple pregnancies)
27.
Kid coughing: whooping cough can cause rectal prolapse (coughing -> increased intraabdominal
pressure)
28.
Thick tree sap: cystic fibrosis can cause rectal prolapse (coughing and strained defecation)
29.
Top of tree cleft: Pilonidal (between but cheeks) abscesses form at the natal cleft
(located at top of gluteal cleft)
30.
Hairy tree bulge: breakdown of hair follicles in natal clef->pit collecting debris
and flora->infection->pilonidal abscess
31.
Machete draining pus: a pilonidal abscess is a painful pustulent sacroccygeal mass
32.
Inner tube dragged over puddle with sharp rocks: anal fissures are initiated by trauma to the
anal sphincter (hard stool, severe diahrea, vaginal delivery)
33.
Shaky lines: in anal fissures, stretching and tearing of anal sphincter->spastic response>worsening stretching and tearing
34.
Posterior inner tube rider: majority of anal fissures are posterior near the midline
35.
Hat flaps: many fissures have an anal tag
36.
Anterior cobble stones with skip lesions: anterior anal fissures are associated with Crohns
disease, infection
37.
Pipe draining to ocean: ano-rectal fistulas run from anus or rectum to skin surface
38.
Epithelial pipe: fistuals are tunnels that eventually become epithelialized
39.
Radiation sign: pelvic radiation can cause anorectal fistuals
40.
Skipped cobble stones: crohn disease can cause anorectal fistuals (transmural inflammation of
bowel->sinus tracts->fistulas)
41.
Hermit crab shell: squamous crab shell: squamous cell carcinoma is the most common anal
cancer and displays keratinization (cross bridges, kertain pealrs)
42.
Un-shelled crab: basaloid carcinoma (non keratinized squamouscell) of the anus arises near the
dentate line
43.
Crab with glandular sponde: rectal adenocarcinoma arises above the dentate line and behaves
like colon adenocarcinoma
44.
Pill-bugs: infection with high risk HPV (16, 18) is a risk factor for squamous cell carcinoma of the
anus
45.
White wizard hat: HIV infection is a risk factor for squamous cell carcinoma of anus
46.
Crutches: immunocompromised states are a risk factor for squamous cell carcinoma of the anus
47.
Smoker: smoking risk factor for squamous cell carcinoma of the anus
48.
Kissing men: men who have sex with men have higher risk for squamous cell carcinoma of the
anus
49.
Pooling blood: anorectal cancer often presents with bleeding
Pancreas/Gall bladder/ Liver
Annular pancreas: congenital malformation due to pancreas forming a ring around duodenum.
Acute pancreatitis: inflammation and hemorrhage of pancreas due to autodigestion of pancreatic
parenchyma by pancreatic enzymes. Pancreas release enzymes which are inactivated to prevent autodigestion. If activated enzymes are released (trypsin) then it will cause auto immune damage.
Liquefactive necrosis, fat necrosis (sponififcation,pancreas is surrounded by fat).
Cause: Alcohol (contracts sphincter of Audi, back flow of enzymes), gall stones (clogs ampulla
and will clog the pancreatic duct). I GET SMASHED (Idiopathic, Ethanol, Trauma, Steroids,
Mumps, Autoimmune disease, Scorpion sting, Hypercalcemia (Ca2+ activates enzymes)
/Hypertryglyceridemia.
Clinical: Epigastric abdominal pain which radiates to back, Nausea, vomiting
Lab: Serum lipase (more specific) and amylase (both secreted from pancreas), Hypocalcaemia
(saponification will use up ca2+)
Complications: Shock (loss of blood), Pancreatic Pseudocyst (fibrous tissue will surround the
liquefactive necrosis). Pancreatic abscess (infected E.coli), DIC and ARDS (amylase can go into
blood and eat coagulation factors and activate them, enzymes chewing on alveolar surfaces can
cause acute respiratory distress syndrome)
Chronic Pancreatitis: recurrent acute pancreatitis which cause fibrosis of pancreatic parenchyma
Cause: alcohol, cystic fibrosis
Clinical: Epigastric abdominal pain radiating to back, Pancreatic insufficiency (not producing any
enzymes and cause fat soluble vitamin deficiency’s (ADEK) and seborrhea. Dystrophic
calcification of pancreas (heavily calcified), present with secondary diabetes mellitus (due to
damage of islets of Langerhans).
Complications: Increased risk of pancreatic adenocarcinoma.
Pancreatic Carcinoma: adenocarcinoma of pancreatic ducts in elderly.
Risk factors: Smoking and chronic pancreatitis
Clinical pain: epigastric abdominal pain and weight loss, Obstructive jaundice with pale stools
and palpable gall bladder (if at head of pancreas), secondary diabetes mellitus (body or tail).
(head of pancreas cancer, palpable gall bladder, blockage causes back up pressure
into gall bladder and makes it palpable)
(head of pancreas cancer, bile flow is obstructed and will leak into the blood
instead, conjugated bilirubin, will leak into blood causing jaundice. Since bile does not leak into
duodenum, you will not get mixing of bile and stool will be pale (stool color is caused by bilirubin)
**Thin, elderly patient, think of pancreatic cancer, especially if presenting with DIABETES
Clinical features: Pancreatitis, Migratory thrombophlebitis (swelling and tenderness in
extremities), Serum tumor marker is CA 19-9
Surgery: Whipple procedure, remove head/neck of pancreas. VERY POOR SURIVAL (<1 year)
Gall bladder/Billary Artesia
Billary Atresia: Failure to form or destruction of extrahepatic biliary tree. One or
more of the hepatic ducts exiting the liver are not formed.
Presentation: jaundice (conjugated bilirubin as it leaks into blood and does
not mix with pancreas) and progression to cirrhosis (back up of pressure
destroys the liver).
Cholelithiasis (gall bladder): cholesterol stones or bilirubin stones in the bile. Caused by supersaturation
(cholesterol/ca2+), decreased phospholipids or bile acids, Stasis. Cholestyramine decreases bile acids
and will cause gall stones. FFFF (female, fertile, Fat, fourty)
CholestrUl stones: most common in west and radioULscent.
.
Risk factors:
Age
Estrogen (increase HM-Coreductase which makes more cholesterol, and increase Lipo
protein receptors to on hepatocytes to increase cholesterol uptake.
Clofibrate (increases HMG-CoA reductase and decreases bile acids),
Native American
Crohn Disease (terminal ileum damage decreases reuptake bile acids/salts),
cirrhosis (decreased production of bile salts)
BillirubOn stones: radiOpaque
Risk factors: Extravascular hemolysis by Biliary tract infection (E.Coli, Ascaris lumbricoides and
Clonorchis sinesis). (reticulo-endothelial system)Splenic macrophages break down hemoglobin
into heme (iron +protoporhyn), protporhyn converted into UCB. Liver conjugates it (CB) and
throws it into bile, increasing risk of bilirubin gallstones.
Gallstones Complications
Bilary Colic: Gallstones lodged in cystic duct. As it contracts, causes PAIN (waxing and weaning),
symptoms relieved if it passes down the common bile duct but may obstruct common bile duct (increase
the risk of acute pancreatitis or obstructive jaundice.
Acute cholecystitis: Gallstone blocks the cystic duct, causes back up of pressure in gallbladder which
causes decreased perfusion and leading to inflammation.
Presentation: RUQ pain and RADIATES TO RIGHT SCAPULA, fever, HIGH WBC, Nausea and
vomiting, Increased ALP (epithelium contains ALP, which is released when the wall dies), rupture
risk
Chronic Cholecystitis: Chronic inflammation of gallbladder due to chemical irritation, histology shows
ROTIKANSKY-ASCHOFF sinus formation
Presentation: RUQ pain AFTER EATING, Porcelain gallbladder (dystrophic calcification) is late
complication
Ascending cholangitis: Bacterial infection of Bile ducts due to ascending infection of gram – bacteria.
Presentation: sepsis, jaundice, abdominal pain. Increased incidence with choledocholithiasis
(choledochlithiasis: obstruction makes it easy for bacteria to ascend and infecdt the bile duct
as the stone blocks flow, REMEMBER, ANYTIME YOU HAVE BLOCKAGE, THERE IS INFECTION IN ANY
SYSTEM)
Gallstone Ileus: Gallstone enters and obstructs small bowel because of cholecystitis causing fistula
between gallbladder and small bowel. Air in Biliary Tree (pneumobilia)
6
Gallbladder carcinoma: adenocarcinoma rising from glandular epithelstooium that lines the gallbladder
wall and gall stones with porcelain gallbladder is a major risk factor.
Presentation: cholecystitis in elderly woman and poor prognosis . VERY OLD WOMAN WITH
NEW ONSET CHOLESCYSTITIS, THINK ABOUT GALLBLADDER CARCINOMA.
Liver
Jaundice: yellow discoloration of skin, (especially scleral icterus) due to increased serum bilirubin
Bilirubin Metabolism: RBC break down hemoglobin into Heme + globin. Heme becomes iron
and unconjugated bilirubin which conjugates it and stores in gall bladder. Released from gall bladder
into duodenum and intestinal flora takes CB and convert it into Urobilinogen, which makes urine yellow.
Disease
Etiology
Lab findings
Extravascular
hemolysis/Ineffective
erythropoiesis
High levels of UCB which ↑UCB
overwhelm the livers
ability to conjugate.
Clinical features
Dark urine due to
↑urine urobilinogen.
Remember that UCB is
NOT water soluble and
absent in urine. Urine is
yellow color because of
CB.
↑Risk of bilirubin
gallstones
Physiologic jaundice of
the newborn
Newborn liver has low
UGT activity (enzyme
responsible for
conjugation)
↑ UCB
UCB is FAT SOLUBLE.
Deposit in basal
ganglia, neurologic
symptoms and death
(kerinictus).
Treatment:
Phototherapy makes
UCB urine soluble.
GilbARt syndrome
Low activity of UGT and
AR
Gilbert-Najjar syndrome NO UGT
↑UCB
Jaundice during stress
(infections) otherwise
healthy
↑UCB
Kerinicterus, fatal
DubAR-Johnson syndrome No bilirubin transport
↑CB
protein so it cannot be
transpoted into the
calculi. As concentrations
build up inside, CB leaks
into blood instead
Dark Liver,
Biliary tract obstruction
Dark urine
Gall stones, pancreatic
↑CB, ↑Alkaline
Rotor syndrome:
Exactly same , except
NO BLACK liver.
Viral Hepatitis
carcinoma,
cholangiocarcinoma,
parasites or liver fluke
phosphatse, ↓UCB
Inflammation disrupts
hepatocytes and small
bile ducts
↑ CB and ↑ UCB
Dark urine because of
when you destroy
↑Urine bilirubin.
hepatocytes, increase UCB
because they cannot be
conjugated. When you
destroy renal ducts, CB
leaks into blood
Whats in bile? CB, ALP,
Cholestrol. Obstruction
will cause leakage into
blood
(bilirubinuria) and pale
stool, pyruritis (due to
increased plasma bile
acids),
hypercholesteremia
with xanthomas.
Setorrhea with
malabsorption of
soluble vitamins.
Viral hepatitis: inflammation of liver parenchyma due to EBV, CMV and hepatitis
Acute hepatitis: Jaundice (Mixed CB and UCB) and <6 months
Lab: ALT>AST
Chronic hepatitis: 6> months.
Virus
Transmission
Comments
Hep A/E
Fecal-Oral
Hep A: travellers
Hep E: undercooked food/water
Acute hepatitis
IgM=ACTIVE INFECTION
IgG=Immunized or resolved
infection
*HEP E with pregnancy causes
fulminant hepatitis (liver necrosis)
Hep B
Acute hepatitis
(*Look at table below)
Parenternal transmission (child
birth, unprotected sex, IV drug
use)
Hep C
Parnertal , IV
Acute to chronic
*Look FOR HCV-RNA to CONFIRM
IFNECTION. Persistence of RNA
indicates chronic disease
Hep D
Preexisting Hep B, then get Hep D,
called superinfection (MORE
DEADLY)
Hep B + D at same time is
coinfection).
Stage
HBsAG
HBeAG
HBcAB
(surface antigen) (envelope)
(core)
Means that virus
can be transferred
to another person
HBsAB
(surface antibody)
Acute
+ (first marker)
+
IgM (*Acute
marker)
-
Window
-
-
IgM
-
Resolved
- (because IgM has - (resolved
destroyed surface because IgM has
antigen)
destroyed
envelope)
IgG (Appearance IgG (protective)
means that IgM
was successful and
acute infection has
resolved). IgG is
then activated to
be protective.
Chronic
+ ( >6 months
then IgM failed,
your in chronic
hepatitis now)
+/-
IgG
1.
Inflammation
-
-
-
IgG
Cirrhosis: End stage liver damage via bands of fibrosis and regenerative nodules
Pathophysiology: Fibrosis is mediated by TGF-B from Stellate cells
Complications
Portal HTN: Splenomegaly/ hypersplenism, portosystemic shunts (esophageal varices, Catpud
medusa, hemorrhoids) , hepatorenal syndrome (renal failure)
Decreased detoxification: Mental status changes, coma jaundice gynecomastia, spider
angiomata, palmar erythema
*Liver removes estrogen (gyno, spider angiomata, erythema), mental changes due to
increased ammonia (cannot remove if liver crossed)
Decreased protein synthesis: hypoalbuminemia (decrease oncotic pressure and cause edema),
coagulopathy (cannot make coagulation factors or Vit K via epoxide reductase)
Alcohol-Related liver disease (AST>ALT)
Fatty liver accumulation of fat in hepatocytes and reversible.
Alcoholic Hepatitis: binge drinking and damage mediated by acetaldehyde . swelling and
ballooning with Mallory body (damaged intermediate filaments) (bottom right).
Cirrhosis: Same as above cirrhosis
NON-Alcohol-Related liver disease (ALT>AST)
Hemochromatosis: Excess Iron deposits in organs, damaged caused by damage of free radicals (fenton
reaction)
Primary (defective HFE gene (C282Y) allows more Iron to enter blood, see image above) vs
Secondary hemochromatosis (Blood transfusions, every bag of blood is bag of Iron)
Presentation: Iron deposits in all organs ->Cirrhosis, secondary diabetes, bronze skin, cardiac
arrythmia, gonadal dysfunction
Lab: ↑Ferritin, ↓TIB , ↑Serum iron, ↑% saturation
Biopsy: Brown pigment in hepatocytes. Brown pigment can be IRON or LIPOFUSCIN (wear and
tear pigment). Differentiate between them, use Prussian blue stain, turns Iron BLUE
Treatment: Phlebetomty (remove RBC), may cause hepatoceullular carcinoma
WERlson disease: defects in (ATP7B gene), in ATP-mediated hepatocyte copper transport. Lack
of transport of copper into bile and put into ceruplasmin (molecule which carried Cu2+ in blood)
Pathogenesis: builds up in hepatocytes and leaks in serum, Cu+ mediated production of hydroxyl
free radicals lead to tissue damage. Presents in child hood.
Complications: Neurologic (present similar to other neuro degenerative diseases) , KAYSERFLEISHER RINGS in cornea,
Labs: Increased Urinary copper, Decreased serum ceruplasmin, Increased copper in liver biopsy
(copper cannot be put into bile)
Treatment: D-penicillamine
Primary Biliary Cirrhosis: (direct damage to bile ducts) granulomatous destruction of
intrahepatic bile ducts, autoimmune (women)
Etiology: ANTIBMITCONDRIAL ANTIBODY
Clinical: Obstructive jaundice
Primary Sclerosing Cholangitis: Inflammation and fibrosis of intrahepatic and extrahepatic bile
ducts
Histology: onion skin appearance or string of pearl appearance.
Labs: P-ANCA + and Associated with ULCERATIVE COLITIS
Clinical: Cirrhosis and cholangiocarcinoma
Reye syndrome: Complete liver failure due t viral infection worsened with ASPIRIN USE IN KIDS.
Pathogenesis: mitochondrial damage of hepatocytes
Labs: hypoglycemia, elevated liver enzymes, death
Liver tumors
Hepatic Adenoma: benign tumor of hepatocytes associated with use of ORAL CONTRACEPTIVES
Complications: Rupture and intraperitoneal hemorrhage, especially in pregnancy
Liver tumor Risk factors: Chronic Hepatitis, Cirrhosis, ALFATOXINS (induce P53) DERIVED FROM
ASPERGILLUS.
Budd-Chiari syndrome:
Central lobular congestion and fibrosis
Another example of budd chiari would be constructive pericariditis which increases venonus pressure on
liver.
Hepatocellular carcinoma , poor prognosis. TUMOR MARKER IS AFP.
Metastasis to liver: colon, lung, pancreas, breast. Multiple nodules in liver
UWORLD
Stress related mucosal disease: Shock trauma>hypovolemia/hypotension->local ischemia->Decreased
mucosal protectonUlcer formation OR Intrascranial
disase->vagal stimulation->Increased H+ secretion->Ulcer
formation
Comon tumor markers
Maker
Tumor
Alpha-fetoprotein
Germline/Hepatocellular
carcinoma
CA19-9
Pancreatic cancer
Ca125
Ovarian (Endometrial)
CEA
Gastrointestinal (colorectal)
HcG
Choriocarcinoma/Germ cell
Prostate specific Antigen
prostate
Hepatocellular Carcinoma by HEPTATITUS: virus
generates local cytokines (pro inflammatory) and cause
hepatocyte damage and fibrosis. Hepatic fibrosis will
show malignancy cells (pleomorphic, prominent nucleoli,
high nuclear to cytoplasmic ratio).
Common
hereditary
Cancer
syndromes
Syndrome Gene
Associated cancers AUTOSOMAL
DOMINANT
caused by
inactivating
tumor
suppressor
gene. Deletion
of remaining
allele (Second)
causes loss of
heterozygosity
and malignant
transformation
potential.
Lynch
MHSC1 Colorectal cancer,
syndrome MHSC 2 ovarian cancer,
Endometrial cancer
FAP
APC
Colorectal cancer,
Desmoids and
ostemoas , Brain
tumors
Von hippel VHL
lindau
sayndrome
Hemangioblastomas,
Clear cell renal
carcinoma,
Pheocytochroma
Li-fraumeni TP53
syndrome
Sarcomas, Breast
cancer, brain
tumors,
Adrenocoritcol
carcinoma ,
leukoemia,
MEN 1
MEN1
Parathyorid
adenomas, pituairty
adenomas,
pancreatic
adenomas
MEN 2 A
RET
Pheocytochroma
MEN 2B
Activating
Medullary thyroid (gain of
function) in
carcinoma
proto onco
Pheochromycytoma,
gene with
Mucosal neurons + continuous cell
RET and marfanoid division
habitus (Tall thin
long limbs)
How would you differentiate between ZES and
hypergastrienmia(acute gastritis?). Secretin test normally
decreases gastrin but WILL NOT DECREASE gastrin in ZES.
Rule this to rule out other tests. Also ulcers found
beyond duodenal bulb will suggest ZES.
Bile sludge: Bile sludge is caused by gastric hypomotility
and is seen with more precipitates.
Black or brown: Brown = infections. Black from
hemolytic anemias or increased enterohepatic recycling
of bilirubin (crohn disease)
Cystinuria: AR condition and defect in amino acid
transporter gene causing elevated urine cysteine levels.
Cystine kidney stones present in childhood.
Uric acid kidney stones: Turnor lysis syndrome (more
uric acid producted) of thiazides ( causing less uric acid
excretion) cause hyperuricemia and stones.
Cystic fibrosis: thick, dehydrated and viscous mucus in
organs with absence of vas deferens. Lungs (Thick
secretions), GI (malabsorption, biliary disease), sweat
glands (salty tasting). CFTR responsible for bringing in
water and CL into cell.
Cystic fibrosis clinical
features (Chromosome 7)
Respiratory
Obstructive lung disease
(bronchiectasis),
recurrent pneumonia,
chronic rhinosinusitis
Gastrointestinal
Obstruction->meconium
ileus (NEWBORNS) or distal
obstruction
Pancreatic disease
Billary Cirrhosis
Reproductive
Infertility (no vas deferens
but normal sperm)
Muscuoloskeletal
Osteopenia->fractures
Kypholiscyosis (SPINE
deformity)
Digital clubbing:
Bronchopulmonary sequestration: Congenital
malformation where lung is not connected to airway.
Common variable immunodeficiency: Defect in B cell
differentiation (low plasma and immunoglobins). High
risk for auto immune, lung infections, Lymphoid). Save
for IMMUNO.
Bacterial peritonitis: dull appearing peritoneal surface
with viscous white yellow-surface
Familial hypercholestremia: AD, ldl receptor mutation in
liver (cannot uptake cholesterol).
IBD can cause Colorectal cancer. Ulcerative colitis>pancolitis->colorectal cancer. Clitis-associated colorectal
cancer occurs in chronic inflammation and risk is
proportionate to duration and severity of inflammation.
Another way you can get colorectal cancer is sporadic
(Radnomly) but effect elderly and present later on witih
p53 gene mutation but early APC.
colitis associated
vs sporadic
colorectal cancer
Colitis-associated Sporadic
Age
Younger (40-55)
Older >60
Origin of dysplasia Flat lesions (non Polypoid (lesions)
polypoid) lesions
Location
Proximal >distal
particulary with
CD
Distal>proximal
Tumros
Multifocal
Singular
Histology
Mucionuss/signet Rarely mucinious
ring cells
Mutations:
Early P53 mutation Early APC gene
Late APC gene
mutation
mutation
Late p53 mutation
Anatomy of Colon blood supply: Question ID 413
Seborrheic dermatitis: scaly, greasy skin on scalp, face ,
ears, eyebrowns/eye lids in Parkison disease and HIV
Causs of Cholestasis
Intrahepatic
Drug (erythromycin,
contraceptives)
Primary biliary cholangitis
Cholestasis/Pregnancy
Extrahepatic
Choledoclithliasis
Malignany (gall bladder,
pancreatic cancer)
Cyptococcus neoformans: yeast with a polysaccharide
capsule that can be detected with india ink stain and can
infect ANY organ.
Pancreatic serous cystadenoma: benign tumor of
pancreas, associated with VHL disease. Histology shows
glycogen rich cuboidal epithelium.
Intrapapillary mucinous neoplasm: atypical cells forming
papillary projections and are benign tumors with
malignancy potential.
Pathogenesis of granulomas with Th1 and Th2 usmle ID
406
C.Difficle
Risk factors
Recent antibiotics,
Hospitalization, PPI
Pathogenesis
Disruption of intestinal flora
Exotoxins cause mucosal
injury
Pseudomembrane
formation
Clinical presentation
Diarrhea, fulfilment colitis
(common)
Diagonisis
EIA (enzyme immune essay)
for bacterial toxin or
glutamate dehydrogenase
Treatment
Oral vancomycin or
fidaxomicin
MICRO question->USMLE id 1396
Question ID 1143->Micro question again
ID 431: Biochem last 2 options->go over, xanthine
oxidase and also go over Glutamate dehydrogenase
Fibroid necrosis : deposition of protenious material in
blood vesels due to HTN
Intragluteal pilonidal disease: acquired skin infection of
natal cleft of buttocks. May present with draining sinus
tracts, abd tenderness but NOT diarrhea.
Entamoeba histolytica : amoebic dysentery which is
hematochezia, abdominal pain, FLAST SHAPED ULCERS.
PHARM
(Vomitting)
Pharmacology
ok
1.
2.
3.
4.
5.
Solitary track runner: the nucleus tractus solitaries (NTS, or vomiting center)
located in the medulla, receives inputs from the GI tract, vestibular system,
and area postremia
Vomiting on track: the NTS projects neurons to other medullary nuclei to
coordinate the vomiting response
Stomach hammer throw area: The GI tract blood barrier (bb) communicates
directly with the NTS (via CN X)
Vegas sign at the stomach area: vagal afferents from the GI tract
communicate with the NTS
Smiley hammer at the stomach area: GI irritation (due to infection,
chemotherapy, distension) causes mucosal serotonin release.
6.
17.
(diphenhydramine, Meclizine) treat vestibular nausea (motion sickness)
18.
19.
9.
10.
M1 motorcycle parking: the vestibular system contains M1 muscarinic
receptors
20.
Telescope: scopolamine (muscarinic agonist) treats vestibular nausea
(motion sickness)
21.
Seasick Sailor outfits: motion sickness (vestibular nausea) is treated with
1st generation H1 antagonists (diphenhydramine) and scopolamine
22.
7.
8.
Bee swatters: 1st generation H1 receptor blockers
“1-2-3” Hammer Throw!”: serotonin activates 5HT-3 receptors on the vagal
afferents
Semicircular canal: the vestibular system communicates directly with the NTS
(via CN III)
23.
Vests at the semicircular canal: the vestibulocochlear nerve (CN
24.
III) from the vestibular system communicates with the NTS
Seasick at the canal: the vestibular system is responsible or vertigo and
11. motion sickness (vestibular nausea)
Tickler blocking the D-rings: metoclopramide antagonizes D2 receptors
in the area postrema (treats chemotherapy induced vomiting)
25.
26.
27.
Extreme postures on the pommelhorse next to the track: the area postrema
12. (chemoreceptor trigger zone) is located adjacent to the NTS (outside the BBB
th
13. in the 4 ventricle) and responds to
emetogenic substances (chemotherapeutic agents)
16. (treats chemo-induced or post-op vomiting)
Hammer tightening gut: ondansetron can cause constipation
Hammer hitting head: Ondansetron can cause headache and dizziness
Twisted torsade’s streamer: ondansetron can prolong the QT interval and
induce torsade’s
Pile of smiley faces: Ondansetron can cause serotonin syndrome
(symptoms include rigidity, tremor, hyperthermia, confusion) Allergy
inducing, Q shaped dandelions: the vestibular system contains H1 histamine
receptors (coupled to Gq)
Contracted stomach: metoclopramide has upper GI prokinetic effects
(increased esophageal peristalsis, decreased lower esophagus sphincter
pressure, and enhanced gastric emptying) (useful for treatment of
delayed gastric emptying due to postsurgical disorders and diabetic
gastroparesis)
28.
“Do not obstruct”: metoclopramide (D2 Antagonist) is
29.
14.
Ribbon dancer blocking the hammer throw: Ondan”setron” antagonizes
5-HT3 receptor on vagal afferents in the GI tract (decreases vagal
15. stimulation)
Extreme posture 2 D-Ring ropes: the area postrema contains D2 receptor
30.
contraindicated in small bowel obstruction
Adverse effects
Mud puddle: metoclopramide can cause diarrhea (prokinetic effects)
Sleeping judge: Metoclopramide can cause drowsiness, especially in the
elderly
Crying coach: metoclopramide can cause depression (central D2
blockade)
EXTRA pyramidal newspaper hat: metoclopramide can cause
extrapyramidal effects due to central D2 blockade (dystonia, akathisia,
parkinsonian features)
Sticking out tongue: metoclopramide can cause tardive dyskinesia with
chronic use (central D2 blockade), especially in the elderly
1.
Now More Spicy chicken: metoclopramide (D2 antagonist
gonist) can cause neuroleptic malignant syndrome
(symptoms include fever, rigidity, mental status changes,
autonomic instability, rhabdomyolysis)
2.
Elevated milk release: metoclopramide can cause elevated
prolactin levels (central D2 blockade), leading to
gynecomastia, amenorrhea, and decreased sexual drive
3.
Twisted torsade’s streamer: metoclopramide can cause QT
prolongation and induce torsade’s
4.
plaNK1 pommel horse: the area postrema contains neurokinin
1 (NK1) receptors (activated by substance P)
5.
Substance Pee check: substance P binds to the NK1 receptors
in the area postrema
6.
“participants”: aprepitant antagonizes the NK1 receptors in
the area postrema (treats chemotherapy induced vomiting),
the “a preppy aunt” is a better mnemonic
1.
2.
3.
4.
5.
6.
“pour it all”: parietal cells in the gastric mucosa are responsible
for acid secretion
Battery powered puree pump: H+/K+ ATPase (proton pump) on
the luminal membrane pumps H+ into the lumen
Banana into the pump, lemons out: the H+/K+ ATPase
exchanges one K+ for one H+ at the luminal membrane
Sidewalk: lumen of the stomach
Three P batters: ATPase driven process
7.
8.
Bees swarming honey pot: histamine (released by the ECL cell)
activates H2 receptors on the parietal cell
Honey pot with 2 “S” handles: H2 histamine receptors
9. (coupled to Gs to increase cAMP) on the basolateral
membrane Honey pot kid knocking over acid pitcher:
10.
activation of H2 receptors upregulates the H+/K+ ATPase 
11. increased acid secretion
12.
13.
Enter CarefuLly: enterochromaffin –like (ECL) cells
Bees released from ECL tree: the ECL cell releases histamine
(activates the parietal cells)
14. Gas Powered blower releasing bees from ECL tree: gastrin
20. Tie dye t shirt: “-tidine” suffix of H2 receptor antagonists
(ranitidine, cimetidine, famotidine, nizatidine) @ antagonists
reduce the acid secretion that is mediated by histamine, this
comes from the enterocrhomaffin like cell, this cell is initially by
gastrin by the G cell, which is brought on by vagal stimulation.
So H2 blockers work with Histamine, gastrin, and Vagal
stimulation. But Vagal stimulation will also stimulate the parietal
cell directly to secrete acid. H2 blockers are used at night to
prevent nocturnal secretion of acid that is largely dependent on
histamine, but only a modest effect on meal stimulation
because vagus nerve will stimulate Parietal cells directly
21. Gargling: H2 blockers (ranitidine, cimetidine) treat GERD (PPI’s
are first line)
22.
23.
Ulcerated sidewalk: H2 blockers (ranitidine, cimetidine) treat
duodenal ulcers (PPI’s are first line)
Tie dye kid on the cement: cimetidine (H2 blocker with
24. antiandrogenic side effects)
25.
Dented chrome bumper: Cimetidine inhibits cytochrome P-450
26. Pot lids on chest: cimetidine can cause gynecomastia when used
27. long term or in high doses
28.
Droopy honey wand: cimetidine can cause impotence
Milk shooting from nose: cimetidine can cause elevated serum
prolactin levels
29.
Girl scout blocking puree pump: Proton Pump Inhibitors (PPI’s)
15. (released by G cells) stimulates the ECL Cell to release histamine
30. irreversibly inhibit the H+/K+ ATPase (the final common
Gas truck releasing gas tanks: G cells release gastrin (Which
pathway for H+ secretion)
stimulates ECL and parietal cells)
16.
Gas powered acid pump: gastrin (released by G cells) stimulates 31.
PRIZE: “-prazole” suffix of PPI’s (omeprazole, lansoprazole,
the parietal cell to secrete H+ (minor effect) gastrin’s major
17.
rabeprazole)
effect is release of Histamine from ECL cells
32.
18.
Motorcycle attached to stand in M3: M3 acetylcholine receptors
are located on the parietal cell
19. Vegas sticker: vagal stimulation stimulates the parietal by the
vagus nerve (M3 receptor)
Vegas Sticker: vagal stimulation stimulates the G cell to release
gastrin (VIA GRP)
Gate release pull: gastrin releasing peptide (GRP) from the vagus
nerve activates G Cells
Gargling: H2 blockerrs (ranitidine, cimetidine) treat GERD but
PPI’s are the first line
Ulcerated sidewalk: PPI’s provide faster symptom relief for
gastric and duodenal ulcers
Jumbo gas tank on mower with crab logo: gastrinoma causing
hypersecretion of gastric acid (Zollinger-Ellison syndrome – treat
with PPI’s)
1.
Swarm of bees over lawn
mower: extra gastrin will
stimulate parietal cell directly
with increasing Histamine, PPI’s
are the best medical treatment
2.
Helicopter hat: PPI’s treat
H.Pylori infection, with
clarithromycin or
amoxicillin/metronidazole 36.
Adverse effects
1.
Chocolate fondue fountain: PPI’s increase the risk for
C.Diff infection
2.
Dirty lung spots: PPI’s increase the risk for
respiratory infections (pneumonia)
3.
Medals bound to wagon: PPI’s decrease the
absorption of Ca2+, Mg2+, and Fe2+ (requires acidic
environment)
4.
Fractured Axel: PPI’s increase the risk of
osteoporotic hip fractures (due to decreased Ca2+
2 bee swatters: H2 histamine receptor antagonists
(rani”tidine”, cimetidine) inhibit acid secretion by parietal cells
absorption)
10.
5.
Porous wood: PPI’s may worsen osteoporosis (due to
decreased Ca2+ absorption)
6.
Falling magnets on girl scout: PPI’s can cause
hypomagnesia
7.
Stop sign: Somatostatin (octeoride ) inhibits release
of histamine by ECL cells
8.
Stop sign: Somatostatin (SST) inhibits the release of
gastrin by G cells (and SST receptor positive
gastrinomas)
9.
Octagon shape of stop sign: octreotide (a long
acting SST analog) inhibits ECL production
Octagon: octreotide (a long acting SST analog) inhibits G cells
(useful in the treatment of gastrinoma/Zollinger Ellison
syndrome
1.
Spa water: osmotic laxatives (magnesium compounds,
lactulose, polyethylene glycol) are non-absorbable substances
that draw water into the intestinal lumen and cause distension
and peristalsis
2.
3.
4.
16.
Magnets magnesium compounds (magnesium hydroxide (milk
of magnesia), magnesium citrate) are osmotic laxatives
PEG drain cover: polyethylene glycol (PEG) is an osmotic
laxative (non absorbable sugar), commonly is iso electrolytic so
not to draw electrolytes into the lumen (used for complete GI
emptying before colonscopy)
5.
6.
Relaxulose: lactulose is an osmotic laxative (non absorbable
sugar) sever flatus and cramps may be AE’s
Relaxulose into the liver and brain coral tank: lactulose is useful
7.
14. Stimulating suntan lotion: senna is a stimulant laxative a.k.a
cathartic (stimulation of enteric nervous system and colonic
secretions)
15. Brown gut: chronic use of senna causes melanosis coli (brown
pigmentation of the colon)
in the treatment of hepatic encephalopathy
17.
Muddy slippers left outside: antidiarrheal agents (featured in
massage room)
Utopia: Opiate agonists (diphenoxylate, loperamide) treat
18. diarrhea
MUssage: opioids treat diarrhea by activating u-opioid receptors
19. in the GI tract
Lop-eared rabbit: Loperamide treats diarrhea (u-opioid agonist
that does not cross the BBB (no analgesia or potential for
20. addiction)
Loop eared rabbit hopping back and forth: opioid agonists
(loperamide) increase colonic phasic segmenting activity which
21. increased colonic transit time 0
Dolphins: Diphenoxylate treats diarrhea (u-opioid agonist with
some ability to cross the BBB (combines with atropine to prevent
22. abuse)
Red stool and inflammatory candles outside door: antidiarrheal
Cirrhotic liver and brain coral: hepatic encephalopathy (a
23. agents are contraindicated in patients with bloody diarrhea or
neurologic complication of cirrhosis due to the buildup of
24. fever (treat the underlying cause) Clogged: opioids can cause
constipation
9. ammonia ( NH3+) and other toxins) as ammonia gets shunted
past the liver and ends up in the brain, leads to the rhythmic
25. VIP CUSTOMERS only crab: VIPoma and carcinoid tumor cause
flapping of hands (asterixs)
secretory diarrhea, pancreatic endocrine tumor secreting VIP
Fish eating lactulose: intestinal bacteria metabolize lactulose
10.
STOP sign: Octreotide treats the symptoms of VIPoma and
into acidic metabolites
carcinoid syndrome (secretory diarrhea)
Acidic pH meter: acidic metabolites decrease the pH of the
intestinal lumen
11.
12. Worker on the NH4+ release valve carrying the ammonia bottle:
ammonia (NH3) is trapped as ammonium (NH4+) in the acidic
lumen and excreted
Fisherman removing fish: rifaximin (a poorly absorbed
antibiotic) eradicates ammonia producing intestinal bacteria
13.
(treats hepatic encephalopathy)
8.
Spoiling mud bath: laxatives can cause diarrhea and dehydration
Bulky seaweed outside of the shop: psyllium is a bulk forming
laxative (indigestible hydrophilic colloid causes water
absorption, distension and peristalsis.
Water penetrating a canoe at the DOCK: docusate is a stool
softener (surfactant agent that facilitates penetration pf stool
by water and lipids)