1
Q
Retroperitoneal structures:
A
“SAD PUCKER”
- Suprarenal (adrenal) gland
- Aorta and IVC
- Duodenum (2nd, 3rd, and 4th parts)
- Pancreas (except tail)
- Ureters
- Colon (descending and ascending)
- Kidneys
- Esophagus (lower 2/3)
- Rectum (upper 2/3)
2
Q
GI ligament that is a derivative of the fetal umbilical vein? what structure does it contain? what does it connect?
A
Falciform ligament
- contains the ligamentum teres
- derivative of the fetal umbilical vein
- connects liver to anterior abdominal wall
3
Q
GI ligament that contains the portal triad (hepatic artery, portal vein, common bile duct)?
A
Hepatoduodenal ligament
4
Q
Which GI ligament may be compressed to control bleeding by placing fingers in the omental foramen?
A
Hepatoduodenal ligamentf
5
Q
Frequency of waves/peristalsis in stomach? duodenum? ileum?
A
stomach–> 3 waves/min
duodenum–> 12 waves/min
ileum–> 8-9 waves/min
6
Q
Meissner’s plexus:
- where’s it located?
- other name?
- what’s its function?
A
- located in Submucosa
- “submucosal plexus”
- controls secretory activity; secretes mucus (so is near the lumen…)
7
Q
Auerbach’s plexus:
- where’s it located?
- other name?
- what’s its function?
A
- located in Musculara externa (really, between muscularis externa inner circular and outer longitudinal layers)
- “Myenteric plexus”
- controls muscle contractions; coordinates motility along entire gut wall
8
Q
Roles of the mucosa of the GI tract?
A
mucosa = innermost layer of gut wall
- has 3 parts, each with a role:
- epithelium–> absorption
- lamina propria–> support
- muscularis mucosa–> motility
9
Q
cell type in esophagus?
A
stratified squamous epithelium
10
Q
cell type in stomach?
A
gastric glands
11
Q
where in GIT are Brunner’s glands?
A
Duodenum
–>submucosal glands that produce alkaline-rich/bicarb secretion
12
Q
Where in GIT are Crypts of Lieberkuhn?
A
Duodenum, Jejunum, Ileum, and Colon
13
Q
Where in GIT are villi and microvilli?
A
Small intestine; not Colon (makes sense, b/c villi are there to increase absorptive surface)
14
Q
Where in GIT are goblet cells?
A
Ileum–> has most goblet cells in the small intestine; but, also found in other parts of small intestine: as go along the small intestine, # of goblet cells increases
15
Q
Where in GIT are Peyer’s patches?
A
only in Ileum
16
Q
Where does celiac trunk come off the abdominal aorta?
A
T12
17
Q
Where does the SMA come off the abdominal aorta?
A
L1
18
Q
Where do the renal arteries come off the abdominal aorta?
A
L1
19
Q
Where does the inferior mesenteric artery come off the abdominal aorta?
A
L3
20
Q
What level is the bifurcation of the abdominal aorta?
A
L4
21
Q
Muscle types composing the Esophagus:
A
- upper 3rd–> striated muscle (voluntary)
- middle 3rd–> striated + smooth muscle
- lower 3rd–> smooth muscle (involuntary)
22
Q
Artery that supplies the Foregut? Innervation of the foregut?
A
- Celiac artery
- Vagus nerve
23
Q
Artery and Nerve that supply the Midgut?
A
- SMA
- Vagus nerve
24
Q
Artery and Nerve that supply the hindgut?
A
- IMA
- Pelvic nerve
25
Watershed area of the GIT?
=> splenic flexure
| -supplied by the terminal branches of the IMA and SMA, so most sensitive to hypoxia
26
What structures make up the foregut? midgut? hindgut?
* foregut: stomach to proximal duodenum; also: liver, gallbladder, pancreas, spleen
* midgut: Distal duodenum to proximal 2/3 of transverse colon
* hindgut: distal 1/3 or transverse colon to upper part of rectum; inludes splenic flexure (watershed area)
27
Portal triad:
- Hepatic artery
- Portal vein
- Common bile duct
28
Branches of celiac trunk?
* celiac trunk comes off abdominal aorta at T12
* branches:
- common hepatic artery
- splenic artery
- left gastric artery
--> these branches make up the main blood supply of the stomach!
29
Which arteries supply the lesser curvature of the stomach? greater curvature?
* lesser curvature --> L and R gastric arteries (L gastric comes off the Celiac trunk; the two gastrics anastamose)
* Greater curvature: L and R gastro-omental arteries (also anastomose with each other)
30
3 Portosystemic shunts (alleviate portal hypertension)
1) Esophageal varices --> anastomosis at the esophagus
2) Caput medusae --> anastomosis at the umbilicus
3) Internal hemorrhoids --> anastomosis at the rectum
31
type of hemorrhoids and cancers seen above and below the pectinate line:
* above pectinate line:
- internal hemorrhoids (not painful)
- adenocarcinoma
* below pectinate line:
- external hemorrhoids (painful)
- squamous cell carcinoma (main risk factor for squamous cell carcinoma here = HPV 16,18,31)
32
Pathway of bile: from production to secretion into duodenum:
Bile made in liver --> R and L hepatic ducts --> Common hepatic duct --> some into common bile duct, some into cystic duct --> from cystic duct, stored in gallbladder, then released back into cystic duct when needed, into common bile duct --> common bile duct meets pancreatic duct at Ampulla of Vater --> bile released via Sphincter of Oddi into Ampulla of Vater in duodenum!
33
Lodging of a gallstone where may lead to obstruction of both bile and pancreatic ducts?
if gallstone is lodged in Ampulla of Vater
34
What sort of tumor may obstruct the common bile duct?
Tumors of head of pancreas --> can compress ampulla, like a gallstone, thus obstructing common bile duct
35
Lateral to Medial organization of the Femoral Region:
Lateral: "NAVeL" :Medial
- Nerve
- Artery
- Vein
- Lymphatics
36
Femoral triangle:
- formed by?
- contains?
* formed by:
- inguinal ligament
- sartorius muscle
- adductor longus muscle
* contains:
- femoral nerve, artery, vein (lateral-->medial)
37
What does the femoral sheath contain?
-Contains femoral vein, artery, and lymphatics, but NOT femoral nerve
38
Sliding vs Paraesophageal Hiatal Hernias:
* Both are types of diaphragmatic hernias, which occur at the gastro-esophageal jxn; stomach herniates upward through the esophageal hiatus of the diaphragm.
- sliding hiatal hernia: GE jxn is displaced; have an "hourglass stomach"
- paraesophageal hernia: GE jxn is normal; cardia of stomach moves into the thorax
39
"hourglass stomach"
sliding hiatal hernia
40
What kind of inguinal hernia occurs in infants?
INdirect inguinal hernia in INfants
-->goes through the INternal/deep inguinal ring, external/superficial inguinal ring, and into the scrotum (Basically, follows the path of the testes)
-->occurs in infants d/t failure of processus vaginalis to close
--> Covered by all 3 layers of spermatic fascia
41
What type of inguinal hernia passes through the inguinal/Hesselbach's triangle?
Direct inguinal hernia
- -> only covered by external spermatic fascia (unlike indirect, which is covered by all 3 layers)
- ->usually in older men
42
Hernia that's most common in women?
Femoral hernia
43
Hernia that's a leading cause of bowel incarceration/obstruction?
Femoral Hernia
44
Hesselbach's triangle:
- borders?
- what type of hernia goes through it?
* Borders:
- inguinal ligament
- inferior epigastric artery
- lateral border of rectus abdominis
*Direct inguinal hernias (older men) go through Hesselbach's triangle
45
G cells (antrum of stomach) secrete?
Gastrin ("pro-gastric")
46
I cells (duodenum, jejunum) secrete?
CCK ("pro-duodenum", "anti-gastric"--> CCK stimulates pancreatic secretions)
47
S cells (duodenum) secrete?
Secretin ("pro-HCO3", "nature's antacid")
48
D cells (pancreatic islets, GI mucosa) secrete?
Somatostatin (inhibits everything!)
49
Which hormone is increased in Zollinger-Ellison syndrome?
Gastrin
| ="gastrinoma"
50
Which GI hormone is stimulated by Phenylalanine and Tryptophan?
Gastrin
51
What AAs may stimulate gastrin release?
Phenylalanine and Tryptophan
52
What does CCK cause?
Stimulates pancreatic secretion, gallbladder contraction, and gastric emptying
53
What does Secretin do?
Stimulates pancreatic HCO3- secretion, decreased gastric acid secretion, increased bile secretion
--> it's "nature's antacid" --> neutralizes gastric acid in duodenum to allow pancreatic enzymes to function
54
Somatostatin:
- where is it secreted from?
- what does it do?
- secreted from D cells in pancreas (islets) and GI mucosa
- inhibits:
- ->decreased gastric acid and pepsinogen secretion
- ->decreased pancreatic and intestinal secretions
- ->decreased gallbladder contraction (so, if lots of somatostatin, may get biliary stones)
- ->decreases insulin and glucagon release
***so overall inhibits digestion and absorption of substances needed for growth...
55
What is used more rapidly: oral glucose load or equivalent given by IV?
oral glucose is used more rapidly, d/t GIP = Gastric Inhibitory Peptide = Glucose-dependent insulinotropic peptide
56
VIP = Vasoactive Intestinal Peptide:
- secreted from?
- actions?
*source: Parasympathetic ganglia in sphincters, gallbladder, small intestine
* actions:
- increases intestinal water and electrolytes secretion
- increases relaxation of intestinal smooth muscle and sphincters
57
VIPoma:
- origin
- symptoms?
non-alpha, non-beta pancreatic islet cell tumor
- may be associated with MEN I
- secretes VIP
- symptoms:
- ->tons of watery diarrhea (b/c VIP stimulates intestinal water and electrolyte secretion) --> so, as a result also have: dehydration, hypokalemia, etc...
58
Endocrine tumor that leads to lots of watery diarrhea?
VIPoma (pancreatic tumor, secretes tons of VIP)
59
Action = binds vitamin B12 to allow uptake of B12 in terminal ileum?
Intrinsic Factor
60
Which substances are secreted by Parietal Cells of stomach?
- Intrinsic Factor
| - Gastric Acid
61
Gastrinoma
gastrin-secreting tumor; get constant high levels of acid secretions and ulcers
-->=zollinger-ellison syndrome
62
Secreted by chief cells of stomach
Pepsin
63
Action of pepsin?
protein digestion
64
what activates pepsinogen-->pepsin?
Acid (H+)
65
Which cells secrete HCO3-?
- mucosal cells (in stomach, duodenum, salivary glands, pancreas)
- Brunner's glands (in submucosa of duodenum)
66
How do NSAIDs lead to acidic damage in stomach?
- Prostaglandins generate mucus that covers that covers the gastric epithelium
- ->NSAIDs-->decrease PGs--> decrease mucus --> decrease HCO3- --> increased susceptibility to acidic damage in stomach
67
Which glands secrete saliva? What stimulates saliva secretion (PSNS, SNS?)? When is saliva hypotonic/isotonic?
- secreted from parotid, submandibular, sublingual glands
- stimulated by Sympathetic AND Parasympathetic activity
- Normally is hypotonic, but is more isotonic with higher flow rates, b/c less time for absorption
* **Sympathetic stimulation--> thicker secretions
* **Parasympathetic stimulation--> watery secretions
68
How does Gastrin stimulate acid secretion in stomach?
G cells in antrum of stomach are stimulated by vagus nerve (via GRP transmitter)--> release Gastrin into circulation --> Gastrin stimulates ECL (EnteroChromaffin-Like) cells to release Histamine --> Histamine induces Parietal cells to secrete HCl
69
Affects of atropine on GI secretions?
Atropine = anti-cholinergic
- -> blocks vagal stimulation of parietal cells (use ACh as transmitter)
- -> BUT, no effect on G cell stimulation by vagal cells, because G cells use a different transmitter, GRP (not ACh) --> so, Gastrin can still stimulate parietal cells to secrete Intrinsic Facor and (via enterochromaffin-like cells and histamine) to secrete HCl
70
How do prostaglandins protect the stomach?
- decrease acid secretion (Gi-->decreased cAMP-->decreased proton pumping)
- increase mucus and HCO3- production
71
3 factors that stimulate G-cells to make Gastrin?
- Hypercalcemia
- Phenylalanine
- Tryptophan
72
What may cause hypertrophy of Brunner's glands?
Peptic ulcer disease (b/c lots of acid to deal with)
-->Brunner's glands are located in duodenal submucosa; function = secrete alkaline mucus to neutralize acid contents entering duodenum from stomach
73
Trypsinogen:
- secreted by?
- converted to trypsin by?
- action?
- secreted by pancreas
- enterokinase/enteropeptidase converts trypsinogen-->trypsin
- converts other proenzymes/zymogens and more trypsinogen to active form
- trypsin (and other zymogens)--> involved in protein digestion
74
alpha-amylase
secreted by pancreas
- digests starch
* **also have amylase in saliva, which digests starch in saliva
75
Lipase
secreted by pancreas
| -digests fat
76
salivary amylase vs pancreatic amylase:
* both digest starch
- salivary: hydrolyzes alpha-1,4-linkages to form disaccharides
- pancreatic: hydrolyzes starch to oligosaccharides and disaccharides
77
D-Xylose absorption test
Test to distinguish GI mucosal damage from other causes of malabsorption
-->D-xylose is normally easily absorbed by intestines; if problem with intestinal absorption, get low levels of D-xylose in urine and blood
78
SGTL1 = Sodium-Glucose-Co-Transporter:
Na-dependent transporter; absorbs Glucose and Galactose in enterocytes
79
GLUT-5
absorbs Fructose (by facilitated diffusion) into enterocytes
80
GLUT-2
Transports all monosaccharides (Glucose, Galactose, Lactose) from intestines into blood
81
Where in GIT is Iron absorbed?
Duodenum
82
Where in GIT is folate absorbed?
Jejunum
83
Where in GIT is Vitamin B12 absorbed?
Terminal ileum, along with bile acids; requires intrinsic factor (from parietal cells)!
84
Peyer's patches:
- where?
- function?
- located in ileum
- Peyer's patches = lymphoid tissue in lamina propria and submucosa of small intestine
- function:
- ->contain M-cells that take up antigen
- ->B-cells stimulated in germinal centers of Peyer's patches differentiate into IgA-secreting plasma cells. IgA ultimately resides in lamina propria. IgA protects gut from pathogens!
85
Lymphoid tissue of the GIT?
Peyer's patches
- located in ileum
- B-cells in germinal centers of Peyer's patches differentiate into IgA-secreting plasma cells --> IgA lives in lamina propria and protects gut from pathogens!
86
specialized M-cells that take up antigen in GIT?
-in Peyer's patches --> the lymphoid tissue of GIT!
87
IgA in GIT comes from?
Peyer's patches: have B-cells in germinal centers of Peyer's patches (lymphoid tissue) that differentiate into IgA-secreting plasma cells
-->IgA protects the gut from pathogens!
88
Only way body can excrete cholesterol?
Bile
89
How is copper excreted from the body?
Bile; can't excrete it in Wilson's disease though...
90
3 functions of Bile:
1) Digest and absorb lipids and fat-soluble vitamins
2) Excrete cholesterol
3) Anti-microbial activity (by disrupting membranes)
91
Pale/Clay-colored stools?
-problem processing bilirubin
92
Cholestyramine
- Bile Acid Resin --> a lipid-lowering agent
- ->interferes with ability to reabsorb Urobilinogen--> so, more is excreted in stool or kidney; the liver then must use cholesterol to make more...
93
Colestipol
Bile-acid resin (like Cholestyramine; lipid-lowering agent)
94
Colesevelam
-Bile-acid resin (like cholestyramine; lipid-lowering agent)
95
Urobilin
breakdown product of bilirubin, excreted in urine; gives urine it's color
96
Stercobilin
breakdown product of bilirubin, excreted in feces; gives color of stool (without it, have pale/clay-colored stool)
97
Urobilinogen
- breakdown product of conjugated/direct bilirubin, after gut bacteria alter it in the gut; has 3 possible fates:
1) excreted in feces as Stercobilin (about 80% of it)
2) excreted in urine as Urobilin (very little of it --> about 2%)
3) reabsorbed by liver via enterohepatic circulation (about 18% of it)
98
Biggest risk factor for a malignant salivary gland tumor?
Smoking
99
most common location of benign salivary gland tumor?
Parotid gland
100
Pleomorphic salivary gland adenoma:
- most common salivary gland tumor
| - painless, movable mass, benign, recurs
101
Warthin's tumor
-benign salivary gland tumor; trapped in a lymph node, surrounded by lymph tissue
102
Mucooepidermoid carcinoma
-most common malignant salivary gland tumor
103
loss of Myenteric/Auerbach's plexus?
Achalasia
- ->can't relax Lower Esophageal Sphincter
- ->get esophageal aperistalsis
- ->progressive dysphagia of solids and liquids (vs obstruction, which is dysphagia to solids only)
- ->increased risk of esophageal carcinoma
104
Bird's beak on barium swallow
Achalasia (esophageal aperistalsis; can't relax LES d/t loss of Myenteric/Auerbach's plexus)
105
2 conditions that may lead to secondary achalasia?
- Chaga's disease (mega-esophagus)
| - CREST scleroderma (Esophageal dysmotility)
106
increased risk of what cancer with Achalasia?
--> esophageal carcinoma
107
progressive dysphagia of solids AND liquids, vs just solids vs progressive dysphagia first of solids THEN of liquids?
* solids + liquids--> Achalasia
* only solids--> obstruction
* solids, then liquids--> esophageal cancer
108
Painless bleeding in lower 1/3rd of esophagus?
Esophageal varices
| -->associated with portal HTN
109
Dysphagia + Glossitis (swollen, smooth tongue) + Iron-deficiency anemia
Plummer-Vinson syndrome
- ->Dysphagia is d/t esophageal webs = thin membrane-like protrusion into esophagus
- ->associated with increased risk of Squamous Cell Carcinoma of Esophagus
110
Boerhaave syndrome:
- TRANSMURAL esophageal rupture d/t violent vomiting
| - -> vs Mallory-Weiss which is just lacerations at the G-E jxn
111
Esophageal pathology associated with lye ingestion and acid reflux?
Esophageal strictures
112
Barrett's esophagus: what sort of metaplasia occurs? increased risk of what kind of cancer?
Glandular metaplasia: squamous epithelium of distal esophagus is replaced with columnar/intestinal epithelium
- d/t chronic GERD
- assoc w/increased risk of Adenocarcinoma of esophagus
- also associated with esophagitis and esophageal ulcers
113
What type of esophageal cancer is most common worlwide? in US?
- worlwide: Squamous cell > Adenocarcinoma
| - US: Adenocarcinoma > Squamous Cell
114
* What part of esophagus is affected in each of these cancers?
- What risk factors cause Squamous Cell Carcinoma?
- What risk factors associated with Adenocarcinoma?
* Squamous Cell: upper 2/3
- smoking
- alcohol
- achalasia
- esophageal webs (ie Plummer-Vinson syndrome)
* Adenocarcinoma: lower 1/3
- Barret's esophagus
- Esophagitis
- Diverticula (like Zenker's)
115
Whipple's disease:
- Tropheryma whippelii infection (gram +)
- PAS + foamy macrophages in intestinal lamina propria
- mostly older men
- CAN:
- ->cardiac symptoms
- ->Arthralgias
- ->Neurologic symptoms
* **Also, classic malabsorption symptoms: diarrhea, steatorrhea, weight loss, weakness
- treat with antibiotics!
116
Which part of intestine is affected in Celiac sprue?
-Proximal small bowel, mostly
117
What part of intestine is affected in lactase deficiency?
only tips of intestinal villi (b/c that's where lactase is located)
-->so, get normal look villi
118
fat accumulation in enterocytes + malabsorption in childhood + neurologic manifestations?
Abeta-lipoproteinemia
- ->have decreased synthesis of apo-B --> can't generate chylomicrons --> decreased secretion of cholesterol and VLDL into bloodstream --> so, fat accumulates in enterocytes
* **this is a malabsorption syndrome
- treat with vitamin E supplementation (helps body produce some apoproteins)
119
Causes of pancreatic insufficiency? What must be supplemented?
Causes:
- cystic fibrosis
- obstructing cancer
- chronic pancreatitis
* get malabsorption of fat and fat-soluble vitamins (A, D, E, K)
* get increased fat in stool
* treat by pancreatic enzyme replacement, limit fat intake, and supplement A, D, E, K.
120
List the Malabsorption syndromes:
"These Will Cause Devastating Absorption Problems"
- Tropical sprue
- Whipple's disease
- Celiac sprue
- Disaccharidase deficiency (like lactose intolerance)
- Abetalipoproteinemia
- Pancreatic insufficiency
121
Blunting of villi + Crypt hyperplasia in small intestines?
Celiac sprue
122
Curling's ulcer
Burning of the esophagus --> can lead to sloughing of gasric mucosa and Acute Erosive Gastritis
123
Cushing's ulcer
Brain injury that can lead to Acute Erosive Gastritis:
| brain injury--> increased vagal stimulation --> increased ACh --> increased H+ production --> Gastritis
124
Main causes of Acute Erosive Gastritis:
*Acute Erosive Gastritis = disrupton of mucosal barrier --> inflammation
* Main causes:
- Alcoholics
- Pts taking daily NSAIDs (ie Rheumatoid Arthritis pts)
- Curling's ulcer = burning esophagus
- Cushing's ulcer = brain injury resulting in increased vagal stimulation
- Stress
125
Autoimmune disorder with:
- autoantibodies to parietal cells
- pernicious anemia (b/c no parietal cells, so no IF, so no B12)
- Achlorydia (b/c no acid from parietal cells)
Chronic/Non-erosive gastritis of the Fundus/Body = Type A
126
Cause of chronic/non-erosive gastritis to the fundus/body of the stomach
Autoimmune disorder with:
- autoantibodies to parietal cells
- pernicious anemia
- achlorydia
127
Cause of chronic/non-erosive gastritis affecting the antrum of the stomach?
H. pylori
- this is the most common type of chronic gastritis
- increased risk of MALT lymphoma
128
What part of the stomach does H. pylori affect?
Antrum
129
Disease in which rugae of stomach look like brain gyrae?
Menetrier's disease
- ->gastric hypertrophy
- protein loss
- parietal cell atrophy
- increased mucous cells
- precancerous
- ->rugae are so hypertrophied that look like brain gyri!
130
Main type of stomach cancer?
Adenocarcinoma (almost always)
131
Acanthosis nigricans
seen in hyperinsulinemia and in visceral malignancies; often seen in gastric adenocarcinoma
132
Virchow's node:
metastasis from stomach to left supraclavicular node
133
Krukenberg's tumor:
bilateral metastasis from stomach to ovaries
| -->see lots of mucus and signet ring cells in ovaries
134
Sister Mary Joseph's nodule:
metastasis from stomach adenocarcinoma to subcutaneous periumbilical area
135
signet ring cells
cells seen in diffuse stomach cancer
- ->filled with mucin; nucleus is pushed to periphery
- ->see in stomach; also see if metastasis from stomach to ovaries (Krukenber's tumor)
136
Linitis Plastica
Stomach adenocarcinoma; stomach looks like a leather bottle --> thickened and leathery
137
Pain is increased with eating? decreased with eating?
* Increased with eating --> gastric peptic ulcer
| * Decreased with eating --> duodenal peptic ulcer (b/c have bicarb secretion, which soothes ulcer)
138
Role of H. pylori in gastric and duodenal peptic ulcers?
* gastric ulcers--> H. pylori in 70% of cases
| * duodenal ulcers--> H. pylori in about 100% of cases
139
Is there an increased risk of cancer with Peptic Ulcer disease?
Trick question:
* If gastric ulcer --> increased risk of carcinoma
* If duodenal ulcer --> NO increased risk of carcinoma
140
Recurrent ulcers despite treatment?
Check gastrin levels; may be Zollinger-Ellison syndrome
141
Part of Intestines affected in Crohn's?
Any part of GIT can be affected; but, usually involves terminal ileum and colon; have skip lesions
-->rectal sparing!
142
Part of intestines affected in ulcerative colitis?
- always the rectum
| - then, have continuous colonic lesions up from there
143
How much of intestinal wall is affected in Crohn's? in Ulcerative colitis?
Crohn's--> transmural
| Ulcerative Colitis--> only mucosal and submucosal
144
Creeping fat
Crohn's
145
Cobblestone mucosa
Crohn's
146
"string sign" on barium swallow
Crohn's
147
"lead pipe" appearance of intestines on imaging?
Ulcerative Colitis (d/t loss of haustra)
148
IBD with: Noncaseating granulomas and Th1 mediated lymphoid aggegates on microscopy:
Crohn's disease
| no granulomas in UC; also UC is Th2-mediated
149
IBD that has a higher association with colorectal cancer?
Ulcerative Colitis
| Crohn's also is associated with it; but higher risk with UC
150
Treatment for Crohn's?
- Corticosteroids
| - Infliximab
151
Treatment for Ulcerative Colitis?
- Aminosalicylic Acid preparations (like Sulfasalazine)
- 6-MP
- Infliximab
- Colectomy
152
STD that is commonly mistaken for IBD?
L1,L2, L3 subtypes of Chlamydia --> cause Lymphogranuloma venereum
153
Dx criteria for IBS?
Recurrent abdominal pain + at least 2 of:
- pain improves with defecation
- change in stool frequency
- change in appearance of stool
154
McBurney's point:
1/3 distance from ASIS to umbilicus (or 2/3 distance from umbilicus to ASIS!)
-->pain is localized here in appendicitis
155
Risk/Complication of appendicitis?
Perforation--> get peritonitis
156
"true" vs "false" diverticulum?
true: all 3 gut wall layers involved (ie Meckel's)
false: only mucosa and submucosa outpouch
157
Most common site of diverticula?
Sigmoid colon
158
Most common cause of severe left lower quadrant pain?
Diverticulitis (inflammation of diverticula)
159
Treatment for diverticulitis?
Antibiotics
160
left lower quadrant pain + bright red rectal bleeding?
Diverticulitis
161
stinky breath (halitosis) + dysphagia + esophageal obstruction?
Zenker's diverticulum = "false" diverticulum at junction of pharynx and esophagus
-->have stinky breath d/t trapped food!
162
Cause of Meckel's diverticulum?
Persistent vitelline duct or yolk sac
163
Most common congenital anomaly of GI tract?
Meckel's diverticulum
164
Pertechnetate study
Dx for Meckel's diverticulum
165
The five 2's of Meckel's diverticulum?
- 2 inches long
- 2 ft from ileocecal valve
- 2% of popl
- usually presents during first 2 years of life
- may have 2 types of epithelia (gastric/pancreatic)
166
currant jelly stools?
Intussusception
167
Where does intussusception commonly occur?
commonly at ileocecal junction
168
What age group does volvolus usually affect? Where does volvulus usually occur?
- usually in elderly
| - may occur at cecum and sigmoid colon (b/c have redundant mesentery)
169
Congenital megacolon d/t failure of neural crest migration?
Hirschsprung's disease
| -lack of ganglion cells/enteric nervous plexuses (Auerbach's and Messner's) in segment of intestines
170
What part of GIT is usually affected in Hirschsprung's?
Involves rectum
171
Failure to pass meconium?
- Hirschsprung's
| - Cystic Fibrosis
172
Increased risk of Hirschsprung in people with what other syndrome?
Down syndrome
173
4 GI conditions associated with Down syndrome:
- Hirschsprung
- Celiac
- Duodenal atresia
- Annular pancreas
174
Bilous vomiting in baby + "double bubble" (proximal stomach distention)
Duodenal atresia = blind duodenum
| -->associated with Down syndrome
175
Necrotizing enterocolitis: most common in what pt popl?
-preemie infants (b/c decreased immunity)
176
Pain after eating in elderly + weight loss (but, not a gastric ulcer...)
ischemic colitis
| -->usually occurs at splenic flexure (watershed area) and distal colon
177
Sawtooth appearance of masses in gut lumen?
Colonic polyps
178
Area often involved in colonic polyps?
-Rectosigmoid
179
90% of colonic polyps are not malignant; which types are most likely to be malignant?
-Adenomatous, villous polyps (more villous the polyp, more likely to be malignant)
180
multiple non-malignant hamartomas throughout GIT + hyperpigmented mouth, lips, hands, genitalia (so, hyperpigmented mucosal surfaces) + increased risk of Colorectal cancer?
Peutz-Jeghers syndrome
| -->autosomal dominant
181
autosomal dominant mutation of APC gene on chromosome 5q?
FAP = Familial Adenomatous Polyposis
| -->100% of pts progress to colorectal cancer
182
Lynch syndrome/HNPCC (Hereditary NonPolyposis Colorectal Cancer)
- ->autosomal dominant mutation of DNA mismatch repair genes
- -> 80% of pts progress to Colorectal Cancer
- -> always involves proximal colon
183
FAP + osseous and soft tissue tumors + retinal hypertrophy?
Gardner's syndrome
184
FAP + malignant CNS tumor?
Turcot's syndrome
185
"apple core" lesion on barium enema?
colorectal cancer
186
CEA tumor marker
colorectal cancer
187
Iron deficiency anemia in older males or post-menopausal females?
Suspect colorectal cancer
188
Most common sites of carcinoid tumors?
- appendix
- rectum
- ileum
189
Bronchospasm + Flushing + Diarrhea + Right-sided heart lesion
Serotonin Syndrome (carcinoid tumor that secretes serotonin)
190
Why is carcinoid syndrome only a "syndrome" once it metastasizes out of GI system?
- -> b/c just tumor alone = carcinoid tumor, not syndrome
- -> if tumor is in the GI, it may secrete serotonin, but don't see any of the symptoms, b/c the liver metabolizes serotonin
- ->once it metastasizes, usually to liver, then start seen symptoms associated with serotonin secretion; then it becomes "syndrome"
191
form of bilirubin in bloodstream?
unconjugated bilirubin-albumin complex = indirect (water-insoluble) bilirubin
192
form of bilirubin in liver?
conjugated/direct (water-soluble) bilirubin
193
form of bilirubin in stool?
stercobilin
194
form of bilirubin in urine?
urobilin
195
uridine glucuronyl transferase = UDP glucuronyl transferase
enzyme, converts indirect bilirubin to direct bilirubin in liver
196
Effects of Portal Hypertension
- Esophageal varices --> Hematemesis
- Melena
- Splenomegaly
- Caput medusae, ascites
- Hemorrhoids
- Portal hypertensive gastropathy
197
Effects of liver cell failure:
- Coma--> hepatic encephalopathy; from release of ammonia and other toxic metabolites from liver
- Scleral icterus
- musty smelling breath
- gynecomastia
- jaundice
- testicular atrophy
- asterixis (hand flap)
- bleeding tendency (from decreased prothrombin and clotting factors)
- anemia
- ankle edema
198
liver enzymes (AST, ALT) in alcoholic vs viral hepatitis?
alcoholic hepatitis: AST>ALT
| viral hepatitis: ALT>AST
199
Lactulose
- Osmotic laxative
- Also: Treatment for hepatic encephalopathy (in liver failure) --> b/c gut bacteria break it down, promoting nitrogen excretion as NH4+
200
GGT (gamma-glutamyl transpeptidase)
serum marker for liver disease; elevated with heavy alcohol consumption
201
decreased ceruloplasmin?
Wilson's disease
202
elevated amylase?
- acute pancreatitis
| - also elevated in MUMPS!
203
elevated lipase?
acute pancreatitis
204
elevated Alkaline Phosphatase?
* non-specific:
- obstructive liver disease (hepatocellular carcinoma)
- bone disease
- bile duct disease
*if elevated ALP, can then check GGT. If elevated GGT, then know it's d/t liver disease
205
What is Reye's syndrome? What are the signs/symptoms?
=Childhood Hepatoencephalopathy:
- ->mitochondrial abnormalities
- ->fatty liver (microvesicular fatty change)
- ->hypoglycemia
- ->vomiting
- ->hepatomegaly
- ->coma
Mechanism: aspirin metabolites decrease Beta-oxidation by reversible inhibition of mitochondrial enzymes
206
One disease when children should be treated with aspirin?
Kawasaki's (to prevent coronary artery thrombosis)
207
Best indicators of Liver function and progrnosis?
Prothrombin time and Serum albumin (albumin is made in liver, as are clotting factors)
*hypoalbuminemia + elevated PT = POOR prognosis.
208
3 stages of alcoholic liver injury:
| -Reversible?
1) Hepatic steatosis
- -> Macrovesicular steatosis/fatty change associated with moderate alcohol intake
- ->REVERSIBLE with alcohol cessation
2) Alcoholic hepatitis:
- ->from sustained, long-term alcohol intake
- ->swollen and necrotic hepatocytes; neutrophil infiltration
- ->Mallory bodies (intracytoplasmic eosinophilic inclusions)
3) Alcoholic cirrhosis:
- ->shrunken liver with "hobnail" appearance
- ->sclerosis around central vein
- ->looks like chronic liver disease: hypoalbuminemia, jaundice...
- ->IRREVERSIBLE
209
Hepatic steatosis:
- macrovesicular fatty change of liver; see hepatocytes filled with lipid droplets
- Reversible effect of moderate alcohol intake; can reverse by stopping to drink alcohol
* **can also get fatty liver from certain HIV drugs; metabolic syndrome; etc...
210
Mallory bodies
intracytoplasmic eosinophilic inclusions within hepatocytes; see in alcoholic hepatitis
211
7 diseases associated with increased risk of hepatocellular carcinoma:
- Hepatitis B
- Hepatitis C
- Hemochromatosis
- Carcinogens (specifically Alfatoxin from Aspergillus)
- Alcoholic cirrhosis
- alpha-1-antitrypsin deficiency
- Wilson's disease
212
cancer associatd with elevated alpha-fetoprotein?
Hepatocellular carcinoma
213
Common benign liver tumor in 30-50 year olds?
- Cavernous Hemangioma
| - ->DON'T biopsy it! b/c may lead to hemorrhage
214
Nutmeg liver
Backup of blood into liver; d/t right heart failure and Budd-Chiari syndrome
-->if it persists, may result in cardiac cirrhosis
215
Condition that looks similar to Right Heart Failure (Hepatomegaly, etc) BUT, absence of jugular venous distension:
Budd-Chiari syndrome
216
Budd-Chiari syndrome:
- Occlusion of IVC or hepatic veins --> leads to congestive liver disease (hepatomegaly, ascites, abdominal pain, eventually liver failure)
- ->may have varices and visible abdominal/back veins
- ->Looks kind of similar to Right heart failure, BUT absence of JVD
- ->Associated with:
- hepatocellular carcinoma
- pregnancy
- polycythemia vera
- hypercoagulable state
217
Liver cirrhosis + Panacinar Emphysema?
alpha-1-antitrypsin deficiency
| -->this is a CODOMINANT trait
218
PAS-positive globules in liver?
alpha-1-antitrypsin deficiency
219
Cause of physiologic jaundice in neonates? Treatment?
Immature UDP-glucuronyl transferase at birth (physiologic): can't convert unconjugated bilirubin to conjugated in liver --> get unconjugated/indirect hyperbilirubinemia --> Jaundice
*Treat with phototherapy: converts unconjugated bilirubin to a water-soluble form, so it can be renally excreted! COOL!
220
What is jaundice? What are the 3 causes/types of pathologic jaundice (not counting physiologic neonatal jaundice)?
Jaundice = yellowing of skin and/or sclerae d/t elevated bilirubin
* Causes:
- Hepatocellular injury
- Obstruction to bile flow
- Hemolysis
221
Jaundice, elevated bilirubin in response to fasting, stress, exercise?
- -> Gilbert's syndrome
- -> have mildly decreased UDP-glucuronyl transferase (so decreased conversion of indirect to direct bilirubin) or decreased bilirubin intake
- ->mild disease; quite common, but most pts don't even know they have it
- ->when flares: have indirect hyperbilirubinemia
222
pathologic jaundice early in life + kernicterus (bilirubin deposition in brain) + elevated unconjugated bilirubin
Crigler-Najjar Syndrome Type 1
-->absent UDP-glucuronyl transferase (so can't convert indirect to direct bilirubin) --> get elevated indirect/unconjugated bilirubin
223
Treatment for Crigler-Najjar syndrome type 1?
- phototherapy (makes Unconjugated bilirubin water-soluble, so can excrete in urine)
- Plasmapheresis (get rid of excess unconjugated bilirubin)
-->Crigler Najjar type 1 is fatal within a few years
224
Crigler-Najjar type 2:
- what is it?
- treatment?
milder form of Crigler-Najjar type 1; have decreased amount of UDP-glucuronyl transferase (not absent, as in type 1)
-->can treat with phenobarbital (increases synthesis of liver enzymes, including UDP glucuronyl transferase)
225
Phenobarbital
Treatment for Crigler-Najjar type 2 (and can be used for symptomatic Gilbert's)
-->increases synthesis of liver enzymes --> so, increases synthesis of UDP-glucuronyl transferase
226
Conjugated Hyperbilirubinemia + Black liver on gross examination
-->otherwise benign
=Dubin-Johnson syndrome
| -->defective liver excretion of bilirubin; so get elevated conjugated bilirubin in blood
227
Rotor's syndrome:
mild disorder, similar to Dubin-Johnson syndrome (but less severe); have defective liver excretion of bilirubin, so mildly elevated conjugated bilirubin in blood; unlike Dubin-Johnson syndrome, does not cause black liver
228
Disease d/t problem with bilirubin uptake into liver?
- Gilbert's
| - ->elevated unconjugated bilirubinemia
229
Diseases d/t problem with bilirubin conjugation
- Gilbert's
- Crigler-Najjar types 1 and 2
- physiologic neonatal jaundice
-->elevated unconjugated bilirubinemia
230
Diseases d/t problem with bilirubin excretion from liver?
- Dubin-Johnson
- Rotor's
-->elevated direct/conjugated bilirubinemia
231
Penicillamine
Treatment for Wilson's disease
232
Kayser-Fleischer ring
yellow-green-golden brown corneal ring seen in Wilson's disease
233
decreased levels of ceruloplasmin?
seen in Wilson's disease
| -->ceruloplasmin=major copper-carrying protein in blood
234
Signs/symptoms of Wilson's disease: "CCCCCopper is Hella BADDD"
- decreased Ceruloplasmin
- Corneal deposits = Kayser-Fleischer rings
- Cirrhosis
- Copper accumulation (in liver, brain, cornea, kidneys, joints, etc)
- hepatocellular Carcinoma (increased risk)
- Hemolytic anemia
- Basal ganglia degeneration (specifically, degeneration of PUTAMEN); get parkinsonian symptoms
- Asterixis
- Dementia
- Dyskinesia
- Dysarthria
***Treat with Penicillamine
235
What part of brain is degenerated in Wilson's disease?
Basal ganglia, specifically Putamen, degeneration
| -->get Parkinsonian symptoms
236
micronodular Cirrhosis + Diabetes + skin pigmentation?
Hemochromatosis = "Bronze" diabetes
237
Deferoxamine
Treatment for hereditary Hemochromatosis
| -->also do repeated phlebotomy
238
Causes of hemochromatosis?
- herditary (autosomal recessive)
| - secondary to repeated blood transfusions (ie in Beta-thalassemia major)
239
lab findings in Hemochromatosis: ferritin, iron, TIBC, transferring?
- elevated ferritin (stores iron within cells)
- elevated iron
- decreased TIBC (indirect measure of transferrin, which transports iron in blood)
- elevated transferritin saturation (serum Fe/TIBC)
240
Which HLA is associated with hemochromatosis?
HLA-A3
241
Complications/Results of Hemochromatosis:
- CHF
- Testicular atrophy in males
- increased risk of hepatocellular carcinoma
242
Cause of primary biliary cirrhosis?
- ->Autoimmune reaction: get lymphocytic infiltrate and granulomas
- ->mostly seen in middle-aged women
- ->anti-mitochondrial antibodies
243
Elevated anti-mitochondrial antibodies?
Primary biliary cirrhosis
244
Causes and pathophysiology of Secondary Biliary Cirrhosis?
-->Extrahepatic biliary obstruction (like a gallstone, biliary stricture, carcinoma of head of pancreas, chronic pancreatitis) --> so, get increased pressure in intrahepatic ducts --> injury and fibrosis --> bile stasis
245
"onion skin" bile duct fibrosis?
Primary Sclerosing Cholangitis (a biliary tract disease)
246
Presentation and Labs in Biliary Tract Diseases (Primary and Secondary Biliary Cirrhosis, Primary Sclerosing Cholangitis):
Presentation:
- Pruritis
- Jaundice
- Dark urine (b/c elevated urobilinogen in urine)
- Pale stools (b/c bile not making it into stools)
- Hepatosplenomegaly
Labs:
- Conjugated/Direct Hyperbilirubinemia
- elevated cholesterol
- elevated ALP
247
Pruritus in a middle-aged woman + elevated conjugated bilirubinemia?
- ->Consider primary biliary cirrhosis
| - ->may also consider primary sclerosing cholangitis
248
Complication of Secondary Biliary Cirrhosis?
Ascending cholangitis = infection of biliary tree (makes sense, b/c have an obstruction of bile flow; bile stasis; etc...)
249
What condition is Primary Sclerosing Cholangitis associated with?
Ulcerative Cholitis
| -primary sclerosing cholangitis can also lead to secondary biliary cirrhosis
250
Biliary tract disease with Hypergammaglobulinemia (IgM)?
-->Primary sclerosing cholangitis
251
5 main risk factors for gallstones/cholelithiasis:
5 F's:
- Female
- Forty
- Fat
- Fertile (multiparity)
- Feathers (Native Americans)
252
Charcot's triad of cholangitis (infection of biliary tree/common bile duct):
1) Jaundice
2) Fever
3) RUQ pain
253
Murphy's sign
- ->positive in cholecystitis; good way to dx pain in the RUQ
- ->positive: when deeply palpate, pt has inspiratory arrest b/c such deep pain
254
Pain on deep palpation, causing inspiratory arrest
Positive Murphy's sign
| --> positive in cholecystitis; way to dx RUQ pain
255
3 causes of gallstones:
- elevated cholesterol and/or bilirubin
- decreased bile salts
- gallbladder stasis
-->all of these can cause stones
256
Most common cause of cholecystitis (inflammation of gallbladder)?
Gallstones
| -->have positive Murphy's sign!
257
Ascending cholangitis =
inflammation of bile duct; usually d/t obstruction of duct by gallstones
258
What is acute pancreatitis?
=autoingestion of pancreas by pancreatic enzymes. ouch.
259
Causes of Acute Pancreatitis:
"GET SMASHED"
- ->Gallstones and Ethanol = Most common causese
- Gallstones
- Ethanol
- Trauma
- Steroids
- Mumps
- Autoimmune disease
- Scorpion sting
- Hypercalcemia/Hypertriglyceridemia
- ERCP (Endoscopic Retrograde Cholangiopancreatography = endoscopic technique to dx/treat problems of pancreatic or biliary ducts; but, main risk of it = acute pancreatitis)
- Drugs (ie sultas, HIV drugs...)
260
```
#1 cause of chronic pancreatitis?
-other main cause?
```
```
#1 = alcoholism
other main cause = smoking
```
261
labs in acute pancreatitis:
-elevated amylase and lipase (lipase = more specific)
262
steatorrhea, fat-soluble vitamin deficiency, diabetes
pancreatic insufficiency; may be a result of chronic pancreatitis (which is usually d/t alcoholism or smoking)
263
CA-19-9
specific tumor marker for Pancreatic adenocarcinoma
264
CEA
less specific tumor marker for pancreatic adenocarcinoma
265
painless jaundice in male >50 years old?
consider Pancreatic adenocarcinoma
266
```
#1 risk factor for Pancreatic Adenocarcinoma?
-other risk factors?
```
#1 = Smoking (but, not alcoholism)
* other risk factors:
- chronic pancreatitis (which is usually caused by alcoholism or smoking... kind of contradicts the not alcoholism thing...)
- Jewish and African American males
- >50 years old
- Diabetes
- Genetics
267
Courvoiseier's sign:
- obstructive jaundice with palpable gallbladder
- ->pruritus, dark urine, pale stools (all signs of obstructive jaundice...)
- ->see with pancreatic adenocarcinoma
268
Trousseau's syndrome:
- migratory thrombophlebitis--> redness and tenderness on palpation of extremities
- ->see with pancreatic adenocarcinoma
269
Presentation of pancreatic adenocarcinoma:
- abdominal pain that radiates to back
- weight loss
- redness and tenderness on palpation of extremities (migratory thromboephlebitis = Trousseau's sign)
- Obstructive jaundice and palpable gallbladder --> pruritus, dark urine, pale stools (=Courvoiseier's sign)
270
Asterixis:
See in:
- liver cell failure
- Wilson's disease
- Uremia (increased BUN and Creatinine, like in renal failure)
271
Drugs that end in "-dine"
H2 blockers: Cimetadine, Ranitidine, Famotidine, Nizatidine
| --> take H2 blockers before you "dine"
272
Ranitidine
H2 blocker
273
Cimetidine
H2 blocker
- ->inhibits cytochrome P450!
- ->also:
- gynecomastia, impotence, decreased libido in males (anti-androgen effects)
- can cross BBB (headaches, dizziness, confusion)
- can cross placenta
274
Famotidine
H2 blocker
275
Nizatidine
H2 blocker
276
Drugs that can cause gynecomastia? (random, not necessarily GI)
"Some Drugs Create Awesome Knockers"
- Spirinolactone
- Digitalis
- Cimetidine
- Alcohol
- Ketoconazole
277
Mechanism of H2 blockers?
- reversibly block Histamine (released from ECL cells, after stimulation by Gastrin) from binding to the H2 receptor on gastric parietal cells
- ->get decreased cAMP, meaning no stimulation of the ATP-ase --> decreased H+ secretion from parietal cells into gastric lumen
278
What are more potent drugs: H2 blockers or PPIs?
PPIs are more potent than H2 blockers; so, use H2 blockers for less severe cases; PPIs for more severe
*note: H2 blockers are reversible; PPIs are irreversible
279
drugs ending in "-prazole"
PPIs (proton pump inhibitors)
- Omeprazole
- Lansoprazole
- Pantroprazole
- Esomeprazole
280
Omeprazole
PPI
281
Lansoprazole
PPI
282
1st line treatment for Zollinger-Ellison syndrome?
Proton Pump Inhibitors
283
Mechanism of PPIs?
Irreversibly inhibit Proton Pump (H/K-ATPase) in parietal cells (so, can't excrete H+ into gastric lumen from parietal cells)
284
Bismuth
- treatment of ulcers and traveler's diarrhea
- mechanism: binds to ulcer base, providing physical protection; thus allowing HCO3- secretion to reestablish pH gradient in mucus layer
285
Sucralfate
Same mechanism as bismuth; treatment of ulcers and traveler's diarrhea
- ->bind to ulcers, providing physical protection; allows HCO3- secretion to reestablish pH gradient in mucus layer
- Requires an acidic environment to polymerize; WONT WORK IF TAKING ANTACIDS CONCURRENTLY!
286
Misoprostol:
- mechanism
- clinical uses
- side effect
- contraindications
* Prostaglandin analog
* Mechanism: binds receptor on parietal cell --> stimulates Gi --> decreased cAMP --> decreased stimulation of Proton Pump --> decreased acid production/secretion into gastric lumen
* Clinical uses:
- Prevent NSAID-induced peptic ulcers (b/c NSAIDs decrease prostaglandins)
- Treatment of PDA
- Induce labor
* Side effect:
- Diarrhea
* Conraindication:
- Pregnant women/women of child-bearing age (b/c induces labor)
287
Octreotide:
- mechanism
- clinical uses
Somatostatin analog
*Somatostatin/Octreotide --> Gi --> blocks/decrease cAMP --> blocks Proton Pump --> decreased acid secretion into gastric lumen
* Uses:
- secretory diarrhea
- acute variceal bleeds
- acromegaly (inhibits GH)
- VIPoma (pancreatic islet cell tumor that secretes lots of Vasoactive Intestinal Polypeptide, causing lots of diarrhea)
- Carcinoid tumors
288
Treatment of VIPoma?
Octreotide
289
Treatment of Carcinoid Syndrome?
Octreotide
290
Diphenoxylate
opiate-anti-diarrheal drug;
| -->binds to Mu opiate receptors in GI tract and slows motility
291
Side effects of Antacids?
- all can cause hypokalemia (b/c block H/K-ATPase)
| - Can chelate and decrease effectiveness of other drugs
292
Side effects of Aluminum Hydroxide (antacid) overuse?
- "aluMINIMUM of feces"= constipation
- hypokalemia and decrease efficacy of other drugs (all antacids)
- others
293
Side effects of Magnesium Hydroxide (antacid) overuse:
"Must Go to the bathroom" = diarrhea
- hypokalemia and decrease efficacy of other drugs (all antacids)
- others
294
Side effects of Calcium carbonate (antacid = TUMS!)
- Hypercalcemia
- may cause rebound increase in acid!
- hypokalemia and decrease efficacy of other drugs (all antacids)
295
Magnesium hydroxide
- osmotic laxative
| - also an antacid (with side effect of diarrhea!)
296
Magnesium citrate
-osmotic laxative
297
Polyethylene glycol
Osmotic laxative
298
Infliximab clinical uses?
- monoclonal anti-TNF antibody
* Uses:
- Crohn's disease
- Rheaumatoid arthritis
299
Sulfasalazine:
- mechanism?
- clinical uses?
=combo of Sulfapyridine (antibacterial) + 5-ASA (aminosalicylic acid = anti-inflammatory)
-->activated by colonic bacteria (so, only effective in distal ileum and colon)
* clinical uses:
- Ulcerative Colitis (always)
- Crohn's (but, only acts in distal ileum and colon; so, only if disease is localized to those areas, which it often is)
300
Odansetron:
- mechanism
- clinical uses
- side effects
=anti-serotonin and anti-emetic
* Clinical uses:
- pts undergoing chemo, to combat nausea/vominiting
- pregnant women with morning sickness
* side effects:
- headache (think opposite of triptans, which are serotonin-agonists; relieve headaches)
- constipation (think opposite serotonin/carcinoid syndrome, which causes diarrhea)
301
Metoclopramide:
- mechanism
- uses
- toxicity/side-effects
- contraindications
=D2-receptor antagonist (Dopamine-blocker)
* uses:
- diabetic and post-surgery gastroparesis (delayed gastric emptying)
* Toxicities/Side effects:
- may lower seizure threshold
- parkinsonian symptoms (b/c block dopamine)
- diarrhea, etc...
* Contraindications:
- Parkinson's disease (duh)
- small bowel obstruction (duh)
302
4 Drugs that may lower seizure threshold? (random, not specific to GI)
1) Metoclopramide (treats gastroparesis)
2) Buproprion (anti-depressant w/out sexual side effects; increased seizures, especially pts with bulemia or anorexia)
3) Tramadol (used to treat chronic pain; weak opiod-agonist; inhibits serotonin and NE reuptake, but not used to treat depression)
4) Enflurane (inhaled anesthetic)
FirstAID
flashcards
Decks in class (24)
# Cards
-
Rapid Review: Lab/Diagnostic Findings and Clinical Presentations; and MISC!596
-
Equations26
-
Drugs28
-
DIT notes36
-
pharm cards140
-
Behavioral Science94
-
Biochemistry293
-
Cardiovascular222
-
Musculoskeletal198
-
Neurology313
-
Immunlogy154
-
Endocrine158
-
Microbiology324
-
Embryology86
-
Hematology/Oncology109
-
Renal135
-
Pathology94
-
Gastrointestinal302
-
Everything1178
-
Micro and Neuro part 283
-
Respiratory176
-
Psychiatry167
-
Reproductive158
-
Pharmacology107
