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gastrointestinal Flashcards

1
Q
  1. GI embryology
  2. gastroschisis
  3. omphalocele
A
  1. foregut-pharynx to duodenum
  2. midgut-duodenum to transverse colon
  3. hindgut-distal transverse colon to rectum

-developmental defects of anterior abdominal wall due to failure of:
1.rostral fold closure: sternal defects
2.lateral fold closure: omphalocele, gastroschisis
3.caudal fold closure: bladder exstrophy
-omphalocele–persistence of herniation of abdominal contents into umbilical cord, covered by peritoneum
-gastroschisis–extrusion of abdominal contents through abdominal folds; not covered by peritoneum
-duodenal atresia–failure to recanalize (trisomy 21)
-jejunal, ileal, colonic atresia–due to vascular accident (apple peel atresia)
-midgut development:
6th week–midgut herniates through umbilical ring
10th week–returns to abdominal cavity + rotates around SMA
-pathology–malrotation of midgut, omphalocele, intestinal atresia or stenosis, volvulus

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2
Q

tracheoesophageal anomalies

A
  • esophageal atresia (EA) with distal tracheoesophageal fistula (TEF) is most common (85%)
  • results in drooling, choking, vomiting with first feeding
  • TEF allows air to enter stomach (visible on CXR)
  • cyanosis is 2’ to laryngospasm (to avoid reflux-related aspiration)
  • clinical test: failure to pass NG tube into stomach
  • in H-type it is a fistula alone
  • in pure atresia (isolated) EA the CXR shows gasless abdomen
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3
Q

congenital pyloric stenosis

A
  • hypertrophy of the pylorus causes obstruction
  • palpable “olive” mass in epigastric region and nonbilous projectile vomiting at ~2 wks of age.
  • tx is surgical incision
  • occurs in 1/600 live births, more often in first born males
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4
Q

pancreas & spleen embryology

A

pancreas–derived from foregut. ventral pancreatic buds contribute to the pancreatic head and main pancreatic duct. The uncinate process is formed by the ventral bud alone. The dorsal pancreatic bud becomes everything else (body, tail, isthmus, accessory pancreatic duct)

  • annular pancreas–ventral pancreatic bud normally encircles 2nd part of duodenum; forms a ring of pancreatic tissue that may cause duodenal narrowing
  • pancreas divisum–ventral and dorsal parts fail to fuse at 8 wks.
  • spleen– arises in mesentery of stomach (hence is mesodermal) but is supplied by foregut (celiac artery)
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5
Q

retroperitoneal structures

A
  • retroperitoneal structures include GI structures that lack a mesentery and non-GI structures
  • injuries to retroperitoneal structures can cause blood or gas accumulation in retroperitoneal space
SAD PUCKER:
Suprarenal (adrenal) gland
Aorta & IVC
Duodenum (2nd & 3rd parts)
Pancreas (except tail)
Ureters 
Colon (descending & ascending)
Kidneys
Esophagus (lower 2/3)
Rectum (lower 2/3)
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6
Q 
important GI ligaments:
connects-->structures contained-->notes
1.facioform
2.hepatoduodenal
3.gastrohepatic
4.gastrocolic
5.gastrosplenic
6.splenorenal
A
  1. liver to anterior abdominal wall–>ligamentum teres hepatis (derivative of fetal umbilical vein)–>derivative of ventral mesentery
  2. liver to duodenum–>portal triad: hepatic artery, portal vein, common bile duct–>pringle maneuver–ligament may be compressed btw thumb and index finger placed in omental foramen to control bleeding. Connects greater and lesser sacs
  3. liver to lesser curvature of stomach–>gastric arteries–>separates greater and lesser sacs on the right. May be cut during surgery to access lesser sac
  4. greater curvature and transverse colon–>gastroepiploic arteries–>part of greater omentum
  5. greater curvature and spleen–>short gastric, left gastroepiploic vessels–>separates greater and lesser sacs on the left
  6. spleen to posterior abdominal wall–>splenic artery and vein, tail of pancreas
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7
Q

digestive tract anatomy

A
  • layers of gut wall (inside to outside)–MMS):
    1. mucosa–epithelium (absorption), lamina propria (support), muscularis mucosa (motility)
    2. submucosa–includes Submucosal nerve plexus (Meissner’s)
    3. Muscularis externa–includes myenteric nerve plexus (Auerbach’s)
    4. Serosa (when intraperitoneal)/adventitia (when retroperitoneal)
  • ulcers can extend into submucosa, inner or outer muscular layer. Erosions are in the mucosa only
  • frquencies of basal electric rhythm (slow waves):
    1. stomach–3 waves/min
    2. duodenum–12 waves/min
    3. ilieum–8-9 waves/min
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8
Q

Digestive tract histology: organ based

  1. esophagus
  2. stomach
  3. duodenum
  4. jejunum
  5. ileum
  6. colon
A
  1. nonkeratinized stratified squamous epithelium
  2. gastric glands
  3. villi and microvilli inc absorptive surface. Brunner’s gladns (submucosa) and crypts of Lieberkuhn.
  4. Plicae circulares and crypts of Lieberkuhn
  5. Peyer’s patches (lamina propria, submucosa), plicae circulares (proximal ileum), and crypts of Lieberkuhn. largest number of goblet cells in the small intestine
  6. colon has crypts but no villi, numerous goblet cells
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9
Q

abdominal aorta and superior mesenteric artery syndrome

A
  • arteries supplying GI structures branch anteriorly. Arteries supplying non-GI structures branch laterally
  • superior mesenteric artery (SMA) syndrome occurs when the transverse portion (third segment) of the duodenum is entrapped between SMA and aorta, causing intestinal obstruction.
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10
Q

GI blood supply and innervation

  1. embryonic gut regions (3)
  2. artery
  3. parasympathetic innervation
  4. vertebral level
  5. structures supplied
A

Foregut

  1. artery–celiac
  2. parasympathetic innervation–vagus
  3. vertebral level–T12/L1
  4. structures supplied–>stomach to proximal duodenum; liver, gallbladder, pancreas, spleen (mesoderm)

Midgut

  1. artery–SMA
  2. parasympathetic innervation–vagus
  3. vertebral level–L1
  4. structures supplied–distal duodenum to proximal 2/3 of transverse colon

Hindgut

  1. artery–IMA
  2. parasympathetic innervation–pelvic
  3. vertebral level–L3
  4. structures supplied–distal 1/3 of transverse colon to upper portion of rectum; splenic flexure is a watershed region
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11
Q

celiac trunk

A
  • branches of celiac trunk: common hepatic, splenic, left gastric. These constitute the main blood supply of the stomach
  • short gastrics have poor anastomoses if splenic artery is blocked
  • strong anastomoses exist btw: L & R gastroepiploics, L&R gastrics
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12
Q

collateral circulation

A
  • if branches off the abd aorta are blocked, these arterial anastomosis (origin) compensate:
    1. superior epigastric (internal thoracic/mammary) inferior epigastric (external iliac)
    2. superior pancreaticoduodenal (celiac trunk) inferior pancreaticoduodenal (SMA)
    3. middle colic (SMA) left colic (IMA)
    4. superior rectal (IMA) middle and inferior rectal (internal iliac)
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13
Q

Portosystemic anastomases

  1. site of anastomosis (3)
  2. clinical sign
  3. portal systemic

what’s commonly seen with portal HTN?

What treatment relieves portal HTN and how?

A

Esophagus

  1. clinical sign
    - esophageal varices
  2. portal systemic
    - L gastric esophageal

Umbilical

  1. clinical sign
    - Caput medusae
  2. portal systemic
    - paraumbilical superificial and inferior epigastric below the umbilicus, superior epigastric & lateral thoracic above the umbilicus

Rectum

  1. clinical sign
    - internal hemorrhoids
  2. portal systemic
    - superior rectal middle and inferior rectal
  • varices of gut, butt, caput (medusae) are commonly seen with portal HTN
  • tx c a transjugular intrahepatic portosystemic shunt (TIPS) btw portal vein & hepatic vein percutaneously relieves portal HTN by shunting blood to systemic circulation
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14
Q

Pectinate (dentate) line

  1. where is it form?
  2. above pectinate line
  3. below pectinate line
A
  1. formed where endoderm (hindgut) meets ectoderm
  2. above pectinate line
    - internal hemorrhoids, adenocarcinoma. Arterial supply from superior rectal artery (branch of IMA). Venous drainage is to superior rectal vein–>inferior mesenteric vein–>portal system.
    - internal hemorrhoids receive visceral innervation and are therefore not painful
    - lymphatic drainage to deep nodes
  3. below pectinate line
    - external hemorrhoids, squamous cell carcinoma
    - arterial supply frm inferior rectal artery (branch of internal pudendal artery).
    - venous drainage to inferior rectal vein–>internal pudendal vein–>internal iliac vein–>IVC
    - external hemorrhoids receive somatic innervation (inferior rectal branch of pudendal nerve) and are therefore painful
    - lymphatic drainage to superficial inguinal nodes
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15
Q

liver anatomy

Zones I-III

A
  • apical surface of hepatocytes faces bile canaliculi
  • basolateral surface faces sinusoids
  • Zone I: periportal zone affected 1st by viral hepatitis
  • Zone II: intermediate zone
  • Zone III: pericentral vein (centrilobular) zone:
    1. affected 1st by ischemia
    2. contains P-450 system
    3. most sensitive to toxic injury
    4. site of alcoholic hepatitis
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16
Q

Biliary structures

A
  • gallstones that reach the common channel at ampulla of Vater can block both the bile and pancreatic ducts
  • tumors that arise in the head of the pancreas (near the duodenum) can cause obstruction of the common bile duct
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17
Q

Femoral region

  1. organization
  2. femoral triangle
  3. femoral sheath
A
  1. organization
    - lateral to medial: Nerve-Artery-Vein-Empty-space-Lymphatics
    - you go from lateral to medial to find your NAVEL
  2. femoral triangle
    - contains femoral vein, artery, nerve
    - venous near the penis
  3. femoral sheath
    - fascial tube 3-4cm below inguinal ligament
    - contains femoral vein, artery, and canal (deep inguinal lymph nodes) but not femoral nerve
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18
Q

Hernias:

Diaphragmatic hernia

A
  • a protrusion of peritoneum through an opening, usually a site of weakness
  • abdominal structures enter the thorax; may occur in infants as a result of defective development of pleuroperitoneal membrane
  • most commonly a hiatal hernia, in which stomach herniates upward through the esophageal hiatus of the diaphragm
  • sliding hiatal hernia is most common. GE junction is displaced incr; “hourglass stomach.”
  • paraesophageal hernia- GE junction is normal. Fundus protrudes into the thorax
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19
Q

Hernias:

Indirect inguinal hernia

A
  • goes through the internal (deep) inguinal ring, external (superfiical) inguinal ring, and into the scrotum.
  • enters internal inguinal ring lateral to inferior epigastric artery
  • occurs in infants owing to failure of processus vaginalis to close (can form hydrocele). much more common in males
  • an indirect inguinal hernia follows the path of descent of the testes. Covered by all 3 layers of spermatic fascia
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20
Q

Hernias:direct inguinal hernia

A

-protrudes through the inguinal (Hesselbach’s) triangle.
-bulges directly through abdominal wall medial to inferior epigastric artery
-goes through the external (superficial) inguinal ring only
-covered by external spermatic fascia
-usually in older men
**MDs don’t LIe:
medial to inferior epigastric artery=direct hernia
lateral to inferior epigastric artery=indirect hernia

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21
Q

Hernias: femoral hernia

Hesselbach’s

A

-protrudes below inguinal ligament through femoral canal below and lateral to pubic tubercle
-more common in XX
leading cause of bowel incarceration
-Hesselbach’s triangle:
1. inferior epigastric vessels
2. lateral border of rectus abdominis
3. inguinal ligament

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22
Q

GI hormone: gastric

  1. source
  2. action-
  3. regulation-
  4. notes-
A

GI hormone: gastric

  1. source- G cells (antrum of astomach)
  2. action-
    - inc gastric H+ secretion
    - inc growth of gastric mucosa
    - inc gastric motility
  3. regulation-
    - inc by stomach distention/alkalinization, amino acids, peptides, vagal stimulation
    - dec by stomach pH < 1.5
  4. notes-
    - much inc in Zollinger-Ellison syndrome
    - inc by hcronic PPI use
    - phenylalanine and tryptophan are potent stimulators
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23
Q

GI hormone: cholecystokinin

  1. source-
  2. action-
  3. regulation-
  4. notes-
A

GI hormone:cholecystokinin

  1. source- I cells (duodenum, jejunum)
  2. action-
    - inc pancreatic secretion
    - inc gallbladder contraction
    - decr gastric emptying
    - inc sphincter of Oddi relaxation
  3. regulation-incr by fatty acids, amino acids
  4. notes-CCK acts on neural muscarinic pathways to cause pancreatic secretion
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24
Q

GI hormone: secretin

  1. source
  2. action-
  3. regulation-
  4. notes-
A 
GI hormone:secretin
1.source- S cells (duodenum)
2. action- 
-incr pancreatic HCO3- secretion
-decr gastric acid secretion
-incr bile secretion
3. regulation-
incr by acid, fatty acids in lumen of duodenum
4. notes-
--incr HCO3- neutralizes gastric acid in duodenum, allowing pancreatic enzymes to function
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25
Q

GI hormone:somatostatin

  1. source
  2. action-
  3. regulation-
  4. notes-
A

GI hormone:somatostatin

  1. source- D cells (pancreatic islets, GI mucosa)
  2. action-
    - decr gastric acid and pepsinogen secretion
    - decr pancreatic and small intestine fluid secretion
    - decr gallbladder contraction
    - decr insulin and glucagon release
  3. regulation-
    - incr by acid
    - decr by vagal stimualtion
  4. notes-
    - inhibitory hormone
    - antigrowth hormone effects (inhibits digestion and absorption of substances needed for growth)
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26
Q

GI hormone: glucose-dependent insulinotropic peptide

  1. source-
  2. action-
  3. regulation-
  4. notes-
A

GI hormone: glucose-dependent insulinotropic peptide

  1. source- K cells (duodenum, jejunum)
  2. action-
    - exocrine: decr gasric H+ secretion
    - endocrine: incr insulin release
  3. regulation-
    - incr by fatty acids, amino acids, oral glucose
  4. notes-
    - also known as gastric inhibitory peptide (GIP)
    - an oral glucose load is used more rapidly than the equivalent given by IV due to GIP secretion
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27
Q

GI hormone: vasoactive intestinal polypeptide (VIP)

  1. source
  2. action-
  3. regulation-
  4. notes-
A

GI hormone:vasoactive intestinal polypeptide (VIP)

  1. source- parasympathetic ganglia in sphincters, gallbladder, small intestine
  2. action-
    - incr intestinal water and electrolyte secretion
    - incr relaxation of intestinal smooth muscle and sphincters
  3. regulation-
    - incr by distention and vagal stimulation
    - decr by adrenergic input
  4. notes-
    - VIPoma- non alpha, non-beta islet cell pancreatic tumor that secretes VIP.
    - copius Water Diarrhea Hypokalemia Achlorhydria (WDHA syndrome)
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28
Q

GI hormone: nitric oxide

  1. source
  2. action-
  3. regulation-
  4. notes-
A

GI hormone: nitric oxide

  1. source-
  2. action- incr smooth muscle relaxation, including lower esophageal sphincter
  3. regulation-
  4. notes-loss of NO secretion is implicated in incr lower esophageal tone of achalasia
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29
Q

GI hormone: motilin

  1. source
  2. action-
  3. regulation-
  4. notes-
A

GI hormone: motilin

  1. source- small intestin
  2. action- produces migrating motor complexes (MMCs)
  3. regulation- inc in fasting state
  4. notes- motilin receptor agonists (such as erythromycin) are used to stimulate intestinal peristalsis
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30
Q

GI secretory products: intrinsic factor

  1. source-
  2. action-
  3. regulation-
  4. notes-
A

GI secretory products: intrinsic factor

  1. source- parietal cells (stomach)
  2. action- vitamin B12 binding protein (required for B12 uptake in terminal ileum)
  3. regulation-
  4. notes- autoimmune destruction of parietal cells–>chronic gastritis and pernicious anemia
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31
Q

GI secretory products: gastric acid

  1. source-
  2. action-
  3. regulation-
  4. notes-
A

GI secretory products: gastric acid

  1. source-parietal cells (stomach)
  2. action-decr stomach pH
  3. regulation-incr by histamine, ACh, gastrin; decr by somatostatin, GIP, prostaglandin, secretin
  4. notes- Gastrinoma–gastrin-secreting tumor that causes continuouos high levels of acid secretion and ulcers
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32
Q

GI secretory products: pepsin

  1. source-
  2. action-
  3. regulation-
  4. notes-
A

GI secretory products: pepsin

  1. source- chief cells (stomach)
  2. action- protein digestion
  3. regulation- incr by vagal stimulation, local acid
  4. notes- inactive pepsinogen–>pepsin by H+
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33
Q

GI secretory products: HCO3-

  1. source-
  2. action-
  3. regulation-
  4. notes-
A

GI secretory products: HCO3-

  1. source- mucosal cells (stomach, duodenum, salivary glands, pancreas) and Brunner’s glands (duodenum)
  2. action- neutralizes acid
  3. regulation- incr by pancreatic and biliary secretion with secretin
  4. notes- HCO3- is trapped in mucus that covers the gastric epithelium
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34
Q

Saliva

A
  • secretion from parotid, submandibular, sublingual glands
  • stimulated by sympathetic and parasympathetic activity
  • amylase digests starch, HCO3- neutralizes bacterial acids, mucins lubricate food
  • normally hypotonic because of absorption but more isotonic with higher flow rates (less time for absorption)
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35
Q

Brunner’s gland location

A

in duodenal submucosa

  • secrete alkaline mucus
  • hypertrophy seen in peptic ulcer disease
36
Q

Pancreatic secrtions

-list 6 enzymes

A
  1. alpha amylase
  2. lipase
  3. phospholipase A
  4. colipase
  5. proteases
  6. trypsinogen
37
Q

alpha amylase

  1. what organ secrets it
  2. role
  3. notes
A
  1. pancreatic secretion
  2. starch digestions
  3. secreted in active form
38
Q

lipase, phospholipase A, colipase

  1. what organ secrets it
  2. role
  3. notes
A
  1. pancreatic secretion
  2. fat digestion
  3. none
39
Q

proteases

  1. what organ secrets it
  2. role
  3. notes
A
  1. pancreatic
  2. protein digestion
  3. includes trypsin, chymotrypsin elastase, carboxypeptidases. secreted as proenzymes also known as zymogens
40
Q

Trypsinogen

  1. what organ secrets it
  2. role
  3. notes
A
  1. pancreatic
  2. converted to active enzyme trypsin–>activation of other proenzymes and cleaving of other trypsinogen molecules into active trypsin (positive feedback loop)
  3. converted to trypsin by enterokinase/enteropeptidase, an enzyme secreted from duodenal mucosa
41
Q

3 enzymes that digest carbohydrate

A
  1. salivary amylase
  2. pancreatic amylase
  3. oligosaccharide hydrolases
42
Q

salivary amylase

  1. function
  2. description
A
  1. carbohydrate digestion

2. starts digestion, hydrolyzes alpha-1,4 linkages to yield disaccharides (maltose and alpha-limit dextrins)

43
Q

pancreatic amylase

  1. function
  2. description
A
  1. carb digestion

2. highest concentration in duodenal lumen, hydrolyzes starch to oligosaccharides and disaccharides

44
Q

oligosaccharide hydrolases

  1. function
  2. description
A
  1. carb digestion
  2. at brush border of intestine, the rate-limiting step in carb digestion, produce monosaccharides from oligo- and disaccharides
45
Q

Vitamin/mineral absorption

  1. iron
  2. folate
  3. B12
A
  1. absorbed as Fe2+ in duodenum
  2. absorbed in jejunum
  3. absorbed in terminal ileum along with bile acids, requires intrinsic factor
46
Q

Peyer’s patches

A
  • unencapsulated lymphoid tissue found in lamina propria and submucosa of ileum
  • contain specialized M cells that take up antigen
  • B cells stimulated in germinal centers of Peyer’s patches differentiate into IgA-secreting plasma cells, which ultimately reside in lamina propria
  • IgA receives protective secretory component and is then transported across the epithelium to the gut to deal with intraluminal antigen
  • ** Think of IgAm the Intra-gut-antigbody. And always say secretory IgA
47
Q

BIle

A
  • composed of bile salts (bile acids conjugated to glycine or taurine, making them water soluble), phospholipids, cholesterol, bilirubin, water, and ions.
  • cholesterol 7alpha-hydroxylase catalyzes rate-limiting step
  • functions:
    1. digestion absoprtion of lipids and fat-soluble vitamins
    2. cholesterol excretion (body’s only means of eliminating cholesterol)
    3. antimicrobial activity (via membrane disruption)
48
Q

Bilirubin

A
  • product of heme metabolism
  • bilirubin is removed from blood by liver, conjugated with glucoronate, excreted in bile
  • direct bilirubin–conjugated with glucuronic acid; water soluble
  • indirect bilirubin–unconjugated; water insoluble
49
Q

salivary gland tumors

  • 3 types
  • where do they occur?
  • benign or malignant?
A
  • generally benign and occur in parotid gland:
    1. pleomorphic adenoma
    2. warthin’s tumor
    3. mucoepidermoid carcinoma
50
Q

Pleomorphic adenoma

  1. type of tumor
  2. description
A
  1. salivary gland tumor in parotid
  2. benign mixed tumor; is most common salivary gland tumor. presents as a painless, mobile mass. It is composed of cartilage and epithelium and recurs frquently
51
Q

Warthin’s tumor

  1. type of tumor
  2. description
A
  1. salivary gland in parotid

2. papillary cystadenoma lymphomatosum; benign cystic tumor with germinal centers

52
Q

Mucoepidermoid carcinoma

  1. type of tumor
  2. description
A
  1. salivary gland in parotid
  2. most common malignant tumor and has mucinous nad squamous components. Presents as painful mass bcuz of common involvement of the facial nerve
53
Q

Achalasia

A
  • failure of relaxation of lower esophageal sphincter (LES) due to loss of myenteric (Auerbach’s) plexus. High LES opening pressure and uncoordinate peristalsis–>progressive dysphagia to solids and liquids (vs. obstruction–solid only).
  • barium swallow shows dilated esophagus with an area of distal stenosis.
  • associated with an incr risk of esophageal squamous cell carcinoma
  • A-chalasia: absence of relaxation
  • :bird’s beak” on barium swallow
  • 2’ achalasia may arise from Chaga’s disease
  • scleroderma (CREST syndrome) is associated with esophageal dysmotility involving low pressure proximal to LES
54
Q

Esophageal pathologies:

gastroesophageal reflux disease (GERD)

A
  • commonly presents as heartburn and regurgitation upon lying down
  • may also present with nocturnal cough and dyspnea, adult onset asthma
  • decrease in LES tone
55
Q

Esophageal pathologies:

esophageal varices

A

-painless bleeding of dilated submucosal veins in lower 1/3 of esophagus secondary to portal hypertension

55
Q

Esophageal pathologies:

esophageal varices

A

-painless bleeding of dilated submucosal veins in lower 1/3 of esophagus secondary to portal hypertension

56
Q

Esophageal pathologies:

esophagitis

A

-associated with reflux, infection (candida: white pseudomembrane; HSV-1: punched out ulcers; CMV: linear ulcers), or chemical ingestion

56
Q

Esophageal pathologies:

esophagitis

A

-associated with reflux, infection (candida: white pseudomembrane; HSV-1: punched out ulcers; CMV: linear ulcers), or chemical ingestion

57
Q

Esophageal pathologies:

Mallory-Weiss syndrome

A
  • mucosal lacerations at the gastroesophageal junction due to severe vomiting
  • leads to hematemesis
  • usually found in alcoholics and bulimics
57
Q

Esophageal pathologies:

Mallory-Weiss syndrome

A
  • mucosal lacerations at the gastroesophageal junction due to severe vomiting
  • leads to hematemesis
  • usually found in alcoholics and bulimics
58
Q

Esophageal pathologies:

BoerHaave Syndrome

A
  • transmural esophageal rupture due to violent retching

- “Been-Heaving Syndrome”

58
Q

Esophageal pathologies:

BoerHaave Syndrome

A
  • transmural esophageal rupture due to violent retching

- “Been-Heaving Syndrome”

59
Q

Esophageal pathologies:

esophageal strictures

A

-associated with lye ingestion and acid reflux

59
Q

Esophageal pathologies:

esophageal strictures

A

-associated with lye ingestion and acid reflux

60
Q

Esophageal pathologies:

Plummer-vinson syndrome

A
  • triad of:
    1. dysphagia (due to esophageal webs)
    2. glossitis
    3. iron deficiency anemia
60
Q

Esophageal pathologies:

Plummer-vinson syndrome

A
  • triad of:
    1. dysphagia (due to esophageal webs)
    2. glossitis
    3. iron deficiency anemia
61
Q

Barrett’s esophagus

A
  • glandular metaplasia–replacement of nonkeratinized (stratified) squamous epithelium with intestinal (nonciliated columnar) epithelium in the distal esophagus.
  • due to chronic acid reflux (GERD).
  • associated with esophagitis, esophageal ulcers, increased risk of esophageal adenocarcinoma
62
Q

Esophageal cancer

A

can be squamous cell carcinoma or adenocarcinoma

  • typically presents with progressive dysphagia (firs solids, then liquids) and weight loss; poor prognosis.
  • Risk factors include:
    1. Achalasia
    2. Alcohol-squamous
    3. Barrett’s esophagus–adeno
    4. Cigarettes–both
    5. Diverticula (eg. Zenker’s)–squamous
    6. Esophageal web–squamous
    7. Familial
    8. Fat (obesity)–adeno
    9. GERD–adeno
    10. Hot liquids–squamous
  • *AABCDEFFGH
  • world wide, squamous cell is more common
  • US, adenocarcinoma is more common
  • squamous cell–upper 2/3
  • adenocarcinoma–lower 1/3
63
Q

Malabsorption syndromes:

pancreatic insufficiency

A
  • due to cystic fibrosis, obstructing cancer, nad chronic pancreatitis
  • causes malabsorption of fat and fat-soluble vitamins (ADEK)
  • incr neutral fat in stool
64
Q

Malabsorption syndromes:

trpical sprue

A
  • unknown cause, but responds to antibiotics

- similar to celiac sprue, can affect entire small bowel

65
Q

Malabsorption syndromes:

whipple’s disease

A
  • infection with Tropheryma whipplei (gram positive); PAS-positive foamy macrophages in intestinal lamina propria, mesenteric nodes
  • Cadiac symptoms, Arthralgia, and Neurologic symptoms are common. Most often occurs in older men
  • Foamy Whipped cream in a CAN
66
Q

Malabsorption syndromes:

celiac sprue

A
  • autoantibodies to gluten (gliadin) in wheat and other grains
  • primarily affects distal duodenum or proximal jejunum
  • histology shows loss of villi
67
Q

Malabsorption syndromes:

dissacharidase deficiency

A
  • most common is lactase deficiency–>milk intolerance
  • normal appearing villi
  • osmotic diarrhea
  • since lactase is located at tip of intestinal villi, self-liited lactase deficiency can occur following injury (eg. viral diarrhea)
  • lactose tolerance test: positive for lactase deficiency if:
    1. administration of lactose produces symptoms,
    2. glucose rises <20mg/dL
68
Q

Malabsorption syndromes:

abetalipoproteinemia

A
  • decrease synthesis of apolipoprotein B–>inability to generate chylomicrons–>decr secretion of cholesterol, VLDL into bloodstream–>fat accumulation in enterocytes
  • presents in early childhood with malabsorption and neurologic manifestations
69
Q

Malabsorption syndromes:

pancreatic insufficiency

A
  • due to cystic fibrosis, obstructing cancer, nad chronic pancreatitis
  • causes malabsorption of fat and fat-soluble vitamins (ADEK)
  • incr neutral fat in stool
70
Q

celiac sprue

A
  • autoimmune-mediated intolerance of gliadin (wheat) leading to steatorrhea
  • associated with HLA-DQ2, HLA-DQ8, and people of northern European descent.
  • findings: anti-gliadin antibodies, anti-tissue transglutaminase, anti-endomysial; blunting of villi; and lymphocytes in the lamina propria
  • decr mucosal absorption that primarily affects jejunum
  • serum levels of tissue transglutaminase antibodies are used for screening.
  • associated with dermatitis herpetiformis
  • moderately incr risk of malignancy (eg. T-cell lymphoma)
71
Q

Acute gastritis (erosive)

A
  • disruption of mucosal barrier–>inflammation
  • can be caused by stress, NSAIDs (decr PGE1–> decr gastric mucosa protection), alcohol, uremia, burns (Curling’s ulcer- decr plasma volume–> sloughing of gastric mucosa), and brain injury (Cushing’s ulcer-inc vagal stimulation–>incr ACh–>inc H+ production)
  • burned by the Curling iron
  • always Cushion the brain
  • especially common among alcoholics and patients taking daily NSAIDs (eg pts with rheumatoid arthritis)
72
Q

inflammation bowel disease:

a) Crohn’s vs. b) Ulcerative colitis
1. possible etiology
2. location

A

inflammation bowel disease:

a) Crohn’s vs. b) Ulcerative colitis
1. possible etiology
a) disordered response to intestinal bacteria
b) autoimmune
2. location
a) any portion of the GI tract, usually the terminal ileum and colon. Skip lesions, rectal sparing
b) colitis= colon inflammation. continuous colonic lesions, always with rectal involvement

73
Q

Menetrier’s disease

A
  • gastric hypertrophy with protein loss, parietal cell atrophy, and incr mucous cells
  • precancerous
  • rugae of stomach are so hypertrophied that they look like brain gyri
74
Q

stomach cancer

  • intestinal
  • diffuse
A

almost always adenocarcinoma

  • early aggressive local spread and node/liver metastases
  • often presents with acanthosis nigricans
    1. intestinal–associated with H pylori infection, dietary nitrosamines (smoked foods), achlorhydria, chronic gastritis, type A blood. Commonly on lesser curvature; looks like ulcer with raised margins
    2. Diffuse–not associated with H pylori; signet ring cells; stomach wall grossly thickened and leathery (linitis plastica)
75
Q

stomach cancer:

  1. virchow’s node
  2. Krukenberg’s tumor
  3. sister Mary Joseph’s nodule
A
  1. involvement of left supraclavicular node by metastasis from stomach
  2. bilateral metastases to ovaries. Abundant mucus, signet ring cells
  3. subcutaneous periumbilical metastasis
76
Q

Peptic ulcer disease: a)gastric vs. b) duodenal ulcer

  1. pain
  2. H. pylori infection
  3. cause
  4. risk of carcinoma
  5. other
A
  1. pain
    a) can be greater with meals–wt loss
    b) decrease with meals–wt gain
  2. H. pylori infection
    a) 70%
    b) almost 100%
  3. cause
    a) decr mucosal protection against gastric acid; NSAID use also implicated
    b) decr mucosal protection or incr gastric acid secretion (eg. Zollinger-Ellison syndrome)
  4. risk of carcinoma
    a) increased
    b) generally benign
  5. other
    a) often occurs in older pts
    b) hypertrophy of Brunner’s glands
77
Q

Ulcer complications

  1. hemorrhage
  2. perforation
A
  1. gastric, duodenal (posterior>anterior)
    - ruptured gastric ulcer on the lesser curvature of the stomach–>bleeding from left gastric artery
    - an ulcer on the posterior wall of the duodenum–>bleeding from gastroduodenal artery
  2. duodenal (anterior>posterior)
78
Q

inflammation bowel disease:

a) Crohn’s vs. b) Ulcerative colitis

A
  1. possible etiology
79
Q

inflammation bowel disease:

a) Crohn’s vs. b) Ulcerative colitis
3. gross morphology
4. microscopic morphology

A

inflammation bowel disease:

a) Crohn’s vs. b) Ulcerative colitis
3. gross morphology
a) transmural inflammation. Cobblestone mucosa, creeping fat, bowel wall thickening (string sign on barium swallow x-ray), linear ulcers, fissures, fistulas
b) mucosal and submucosal inflammation only. Friable mucosal pseudopolyps with freely hanging mesentery. Loss of haustra–>lead pipe appearance on imaging
4. microscopic morphology
a) noncaseating granulomas and lymphoid aggregates (Th1 mediated)
b) crypt abscesses and ulcers, bleeding, no granulomas (Th2 mediated)

80
Q

inflammation bowel disease:

a) Crohn’s vs. b) Ulcerative colitis
5. intestinal manifestation
6. extraintestinal manifestations

A

inflammation bowel disease:

a) Crohn’s vs. b) Ulcerative colitis
5. intestinal manifestation
a) diarrhea that may or may not be bloody
b) bloody diarrhea
6. extraintestinal manifestations
a) migratory polyarthritis, erythema nodosum, ankylosing spondylitis, uveitis, kidney stones
b) pyoderma gangrenosum, 1’ sclerosing cholangitis, ankylosing spondylitis, uveitis

81
Q

inflammation bowel disease:

a) Crohn’s vs. b) Ulcerative colitis
7. complications
8. treatment

A

inflammation bowel disease:

a) Crohn’s vs. b) Ulcerative colitis
7. complications
a) strictures, fistulas, perianal dx, malabsorption, nutritional depletion, colorectal cancer
b) malnutrition, sclerosing cholangitis, toxic megacolon, colorectal carcinoma (worse with right sided colitis or pancolitis)
8. treatment
a) corticosteroids, azathioprine, methotrexate, infliximab, adalimumab
b) ASA preparation (sulfasalazine), 6-mercaptopurine, infliximab, colectomy

**for crohn’s think of fat granny and old crone skipping down a cobblestone road away from the wreck (rectal sparing)

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