Embryo/Anatomy/Physiology Flashcards

1
Q

What structures are derived from the foregut, midgut and hindgut?

A

Foregut- pharynx to duodenum
Midgut- duodenum to proximal 2/3 of transverse colon
Hindgut- distal 1/3 of transverse colon to anal canal above pectinate line

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2
Q

Defects of anterior abdominal wall

A

Rostral fold closure failure- sternal defects

Lateral fold closure failure- omphalocele, gastroschisis

Caudal fold closure failure- bladder exstrophy

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3
Q

Gastroschisis

A

extrusion of abdominal contents through abdominal folds; NOT covered by peritoneum

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4
Q

Omphalocele

A

persistant herniation of abdominal contents into umbilical cord, sealed by peritoneum

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5
Q

Duodenal atresia

A

congenital failure of duodenum to canalize; associated with Down syndrome

Clinical features:

  1. polyhydramnios
  2. distention of stomach and blind loop of duodenum -> ‘double bubble’ sign on imaging
  3. bilious vomiting
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6
Q

Midgut developement

A

6th wk: midgut herniates through umbilical ring

10th wk: returns to abdominal cavity and rotates 270deg (90deg counterclockwise) around SMA

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7
Q

Most common tracheoesophageal anomaly

A

Esophageal atresia with distal tracheoesophageal fistula (TEF)

Symptoms: drooling, choking and vomiting with feeding, polyhydramnios, cyanosis secondary to laryngospasm

TEF allows air to enter stomach (air bubble on CXR)

Diagnosis: failure to pass NG tube into stomach

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8
Q

Congenital pyloric stenosis

A

Hypertrophy of pyloris -> obstruction; more common in males

Clinical features: typically presents ~2weeks

  • nonbilious vomiting at 2-6weeks old
  • visible peristalsis
  • palpable olive mass in epigastric region
  • hypokalemic hypochloremic metabolic alkalosis (secondary to vomiting of gastric acid and volume contraction)

Treatment: pyloromyotomy

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9
Q

What is derived from the ventral and dorsal pancreatic buds?

A

Ventral pancreatic buds: uncinate process and main pancreatic duct

Dorsal pancreatic bud: body, tail, isthmus, accessory pancreatic duct

Both: pancreatic head

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10
Q

Annular pancreas

A

ventral pancreatic bud encircles 2nd part of duodenum, may cause duodenal narrowing

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11
Q

Pancreas divisum

A

ventral and dorsal parts fail to fuse at 8 wk

usually asymptomatic, may cause chronic abdominal pain and/or pancreatitis

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12
Q

What is the embryological derivation of the spleen?

A

Mesoderm: arises in mesentery of stomach

Supplied by foregut- celiac artery

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13
Q

Retroperitoneal structures

A
Suprarenal (adrenal) glands
Aorta and IVC
Duodenum (2nd -4th parts)
Pancreas (except tail)
ureters
colon (descending and ascending)
Kidneys
Esophagus (thoracic portion, lower 2/3)
Rectum (upper 2/3)
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14
Q

Falciform ligament

A

Connects: liver to anterior abdominal wall

Structures contained: ligamentum teres hepatis (derived from fetal umbilical vein)

Notes: Derivative of ventral mesentery

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15
Q

Heaptoduodenal ligament

A

Connects: liver to duodenum

Structures contained: portal triad: proper hepatic artery, portal vein, common bile duct

Notes: Pringle maneuver- compress ligament to control bleeding; borders omental foramen which connects greater and lesser omental sacs (part of lesser omentum)

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16
Q

Gastrohepatic ligament

A

Connects: liver to lesser curvature of stomach

Structures contained: gastric arteries

Notes: separates greater and lesser sacs on right; may be cut during surgery to access lesser sac (part of lesser omentum)

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17
Q

Gastrocolic ligament

A

Connects: greater curvature and transverse colon

Structures contained: gastroepiploic arteries

Notes: Part of greater omentum

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18
Q

Gastrosplenic ligament

A

Connects: greater curvature of stomach and spleen

Structures contained: short gastrics, left gastroepiploic vessels

Notes: separates greater and lesser omental sacs on left

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19
Q

Splenorenal ligament

A

Connects: spleen to posterior abdominal wall

Structures contained: splenic artery and vein, tail of pancreas

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20
Q

Layers of gut wall (inside to outside)

A

Mucosa- epithelium, lamina propria, muscularis mucosa

Submucosa- includes Submucosal (Meissner) nerve plexus -> controls GI secretions

Muscularis externa - Myenteric (Auerbach) nerve plexus: controls motility

Serosa (intraperitoneal), adventitia (retroperiotoneal)

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21
Q

Ulcers vs erosions

A

ulcers extend into submucosa, inner or outer musxular layer

erosions - mucosa only

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22
Q

Digestive tract histology- esophagus and stomach

A

esophagus- non-keratinized stratified squamous epithelium

Stomach- nonciliated columnar epithelium with goblet cells

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23
Q

Digestive tract histology- duodenum, jejunum, ileum

A

duodenum: villi and microvilli, Brunner glands (secrete bicarb, in submucosa), crypts of Lieberkuhn (secretion, basal cells)
jejunum: plicae circulares (folds with villi) and cypts of Lieberkuhn
ileum: Peyer patches (lymphoid aggregates in lamina propria, submucosa, plicae circulares in proximal ileum, crypts of Lieberkuhn, Largest # of goblet cells in small intestine

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24
Q

Digestive tract histology- colon

A

crypts of Lieberkuhn, abundant goblet cells, NO villi

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25
Blood supply, parasympathetic innervation and vertebral level for Foregut
Blood supply: Celiac artery Parasympathetic innervation: Vagus nerve (CNX) Vertebral level: T12/L1 Structures supplied: Pharynx (vagus nerve only, blood from thyroid arteries) and lower esophagus (celiac artery only) to proximal duodenum; liver, gallbladder, pancreas, spleen (mesoderm)
26
Blood supply, parasympathetic innervation and vertebral level for Midgut
Blood supply: SMA Parasympathetic innervation: Vagus (CN X) Vertebral level: L1 Structures supplied: Distal duodenum to proximal 2/3 of transverse colon
27
Blood supply, parasympathetic innervation and vertebral level for Hindgut
Blood supply: IMA Parasympathetic innervation: Pelvic nerve Vertebral level: L3 Structures supplied: Distal 1/3 of transverse colon to upper rectum
28
Splenic flexure
watershed region btwn SMA and IMA -> highly susceptible to ischemic damage
29
SMA syndrome
transverse portion (3rd part) of duodenum is entrapped btwn SMA and aorta -> intestinal obstruction
30
What is the blood supply of the lesser and greater curvature of the stomach?
lesser curvature- L and R gastric arteries greater curvature - L and R gastroepiploic arteries
31
What are the branches of the celiac trunk?
common hepatic artery splenic artery L. gastric artery
32
What are the branches of the common hepatic artery?
gastroduodenal artery Hepatic artery proper R. gastric artery
33
What are branches of the splenic artery?
L. gastroepiploic artery Short gastric arteries (poor anastomoses if splenic artery blocked, unlike gastroepiploic)
34
What are the portosystemic anastomoses and what the clinical signs?
1. esophagus: left gastric and esophageal vein anastomosis -> can cause esophageal varices w portal HTN 2. Umbilicus: Anastomosis btwn paraumbilical vein and small epigastric veins of anterior abdominal wall -> causes caput medusae with portal HTN 3. Rectum: anastomosis btwn superior rectal vein with middle and inferior rectal veins -> causes anorectal varices
35
What procedure is done to relieve portal HTN?
Transjugular intrahepatic portosystemic shunt (TIPS) between portal vein and hepatic vein relieves portal HTN by shunting blood to systemic circulation and bypassing liver
36
Pectinate (detate) line
Endoderm (hindgut) meets ectoderm Above pectinate line - arterial supply: superior rectal artery (branch of IMA) - venous drainage: superior rectal v -> IMV -> portal system - lymphatic drainage - internal iliac LNs - internal hemorrhoids (visceral innervation --> NOT painful) Below pectinate line - arterial supply: inferior rectal artery (branch of internal pudendal artery) - venous drainage: inferior rectal v -> internal pudendal v -> internal iliac v -> common iliac -> IVC - lymphatic drainage: superficial inguinal nodes - external hemorrhoids (somatic innervation from inferior rectal branch of pudendal --> PAINFUL) - anal fissures - squamous cell carcinoma
37
Direction of blood flow through liver
Nutrient rich, low O2 blood enters via branch of portal vein and O2 rich blood enters via branch of hepatic artery into portal triad (zone I) and pass through basolateral surface of hepatocytes Portal vein -> sinusoids (zone II) -> central vein (zone III) -> hepatic vein -> IVC
38
Direction of bile flow through liver
bile flows in opposite direction of blood, from zone III (centrilobular) to zone I (periportal) via bile canaliculi into hepatic bile ducts -> common hepatic bile duct -> common bile duct -bile canaliculi face apical surface of hepatocytes
39
What is located in the femoral sheath?
3-4cm below inguinal ligament Contains femoral vein, artery and canal (deep inguinal LNs) Does NOT contain femoral nerve
40
What are the layers of the spermatocord? What are the layers derived from?
Outermost layer: External spermatic fascia, derived from external oblique aponeurosis Middle layer: Cremasteric muscle and fascia, derived from internal oblique muscle Inner layer: internal spermatic fascia, derived from transversalis fascia
41
What are the sites of protrusion of indirect and direct hernias?
indirect hernia- protrudes into internal inguinal ring direct hernia protrudes into abdominal wall, usually medially to internal inguinal ring
42
Diaphragmatic hernia
abdominal structures enter thorax - may occur due to congenital defect of pleuroperitoneal membrane or trauma - commonly left sided due to protection of right hemi-daphragm by liver
43
Hiatal hernia
Most common diaphragmatic hernia stomach herniates upward through esophageal hiatus of diaphragm -most common subtype: sliding hiatal hernia - gastroesophageal jxn is displaced upward, "hour glass stomach" on imaging
44
Paraesophageal hernia
Fundus of stomach protrudes into thorax, gastroesophageal junction normal
45
Indirect inguinal hernia
Enters through internal (deep) inguinal ring lateral to inferior epigastric artery, then goes through external (superficial) inguinal ring and into scrotum Occurs in infants from failure of processus vaginalis to close, covered by all 3 layers of spermatic fascia
46
Direct inguinal hernia
Protrudes through inguinal (Hesselbach) triangle -> bulges through abdominal wall medial to inferior epigastric artery Goes through external superficial inguinal ring only Covered by external spermatic fascia Usually older men
47
Femoral hernia
Protrudes below inguinal ligament through femoral canal (below and lateral to pubic tubercle) - common in females - leading cause of bowel incarceration
48
What are the boarders of the inguinal (Hesselbach) triangle?
inferior epigastric vessels laterally Lateral border of rectus abdominis medially inguinal ligament inferiorly
49
Gastrin
Source: Antrum of stomach, duodenum (G cells) Action: Increases gastric H+ secretion, growth of gastric mucosa and gastric motility Regulation: (+) stomach distention/alkalinization, amino acids, peptides, vagal stimulation (-) low pH
50
Somatostatin
Source: Pancreatic islets and GI mucosa (D cells) Action: Decreases gastric acid and pepsinogen secretion, decreases pancreatic and small intestine fluid secretion, decreases gallbladder contraction, inhibits release of hormones like insulin, GH and glucagon Regulation: (+) low pH, (-) vagal stimulation Notes: Octreotide is analog used to treat acromegaly, insulinoma, carcinoid syndrome and variceal bleeding
51
Cholecystokinin (CCK)
Source: Duodenum, jejunum (I cells) Action: Increases pancreatic secretion, gallbladder contraction and relaxes sphincter of Oddi. Decreases gastric emptying Regulation: (+) fatty acids and amino acids Notes: Acts on neural muscarinic pathways to cause pancreatic secretion
52
Secretin
Source: Duodenum (S cells) Action: Increases pancreatic bicarb secretion and bile secretion. Decreases gastric acid secretion. --> increases pH Regulation: (+) acid, fatty acids in duodenum Notes: bicarb neutralizes gastric acid in duodenum to allow pancreatic enzyme fxn
53
Glucose-dependent insulinotropic peptide (GIP)
Source: Duodenum, jejunum (K cells) Action: Exocrine: decreases gastric acid secretion. Endocrine: increases insulin release Regulation: (+) fatty acids, amino acids, *oral glucose* Notes: aka gastric inhibitory peptide. Oral glucose -> higher insulin compared to IV due to GIP secretion
54
Motilin
Source: Small intestine Action: Produces migrating motor complexes (MMCs) Regulation: (+) fasting state Notes: motilin receptor agonists (erythromycin) stimulate intestinal peristalsis
55
Vasoactive intestinal polypeptide (VIP)
Source: Parasympathetic ganglia in sphincters, gallbladder, small intestine Action: Increases: intestinal water and electrolyte secretion, relaxation of intestinal smooth muscle sphincters Regulation: (+) distention, vagal stimulation (-) adrenergic input Notes: VIPoma- non-alpha or -beta islet cell pancreatic tumor secretes VIP - copious water diarrhea, hypokalemia and achlorhydria (WDHA syndrome)
56
Nitric oxide
Action: Relaxes smooth muscle of lower esophageal sphincter (LES) Notes: Loss of NO secretion implicated in higher LES tone of achalasia
57
Intrinsic factor
Source: Parietal cells (stomach) Action: Binds Vitamin B12, required for uptake in terminal ileum Notes: Autoimmune destruction of parietal cells -> chronic gastritis and pernicious anemia
58
Gastric acid
Source: Parietal cells (stomach) Action: lowers stomach pH Regulation: (+) Histamine, ACh, gastrin (-) somatostatin, GIP, prostaglandin, secretin Notes: Gastrinoma: gastrin secreting tumor causes high levels of acid and ulcers refractory to PPIs
59
Pepsin
Source: Chief cells (stomach) Action: protein digestion Regulation: (+) vagal stimulation, local acid Notes: Pepsinogen -> pepsin in presence of H+
60
HCO3-
Source: Mucosal cells (stomach, duodenum, salivary glands, pancreas) and Brunner glands (duodenum) Action: neutralize acid Regulation: (+) pancreatic and biliary secretion with secretin Notes: bicarb is trapped in mucus covering gastric epithelium
61
Pancreatic secretions
Isotonic fluid; low flow -> high Cl-, high flow -> high bicarb (via Cl-/HCO3- exchanger) alpha-amylase: starch digestion (secreted in active form) lipases (colipase, phospholipase A): fat digestion Proteases: trypsin, chymotrypsin, elastase, carboxypeptidases (secreted as zymogens) Trypsinogen -> trypsin via enterokinase/enteropeptidase (brush-border enzyme on duodenal and jejunal mucosa) -activates other proenzymes including self
62
What are the signaling pathway mechanisms of ACh, Gastrin, Histamine, Prostaglandins and Somatostatin on gastric parietal cells?
ACh- released by vagus, stimulates H+ secretion via M3 receptor/Gq -> IP3/Ca2+ -> (+) H+/K+ATPase Gastrin- released by G cells, stimulates H+ secretion via CCKb receptor/Gq -> IP3/Ca2+ -> (+) H+/K+ATPase Histamine- released by ECL cells (enterochromaffin-like cells), stimulates H+ secretion via H2 receptor/Gs -> (+)cAMP -> (+) H+/K+ATPase Prostaglandins/misoprostol and Somatostatin- decrease H+ secretion via binding Gi receptor and (-)cAMP -> (-)H+/K+ATPase
63
How are glucose, galactose and fructose absorbed by enterocytes?
Glucose and galactose taken up by SGLT1 (Na+ dependent co-transporter) and fructose taken up by facilitated diffusion via GLUT5 All transported out of enterocytes to blood by GLUT-2
64
Where is iron, folate and B12 absorbed?
iron- as Fe2+ in duodenum folate- in small bowel B12 - in terminal ileum with bile salts, requires IF
65
Peyer patches
In lamina propria and submucosa of ileum - contain specialized M cells that are APCs - B cells stimulated in germinal centers- differentiate into IgA secreting plasma cells and reside in lamina propria IgA receives protective secretory component before being transported into gut
66
Bile composition and function
composed of bile salts, phospholipids, cholesterol, bilirubin, water and ions Cholesterol 7alpha hydroxylase catalyzes rate limiting step Functions: - digest and absorb lipids and fat soluble vitamins - cholesterol excretion - antimicrobial activity (membrane disruption)
67
Bilirubin synthesis and breakdown
Macrophages: RBCs-> heme -> unconjugated bilirubin (water insoluble) Blood: UB complexed with albumin Liver: UB-->conjugated bilirubin (soluble) via UDP-glucuronosyltransferase -> excreted in bile to gut Gut: Gut bacteria convert CB--> Urobilinogen 80% urobilinogen goes to feces and is excreted as stercobilin (brown) 2% goes to kidney-> excreted in urine as urobilin (yellow) 18% goes back to liver
68
Necrotizing enterocolitis (NEC)
Common GI emergency in newborns - Typically occurs with pre-term secondary to GI and immunologic immaturity. - Initiate enteral feeding -> bacteria introduced into bowel and proliferate due to compromised immune clearance -> invade bowel wall since impaired mucosal barrier fxn -> inflammation and ischemic necrosis of terminal ileum and colon -> bowel becomes congested and gangrenous w/ intramural gas collection Commonly presents as abdominal distention and bloody stools in an infant -pneumatosis intestinalis (air in bowel wall) w/ curvilinear areas of lucency seen on imaging
69
Dietary energy- how many Calories/1g for protein, carbohydrates, fat and alcohol?
protein and carbs: 4 kcal/1g fat: 9 kcal/1g EtOH: 7 kcal/1g
70
Aphthous ulcer
painful superficial ulceration of oral mucosa - arises in relation to stress and resolves spontaneously but often recurs - Gray base (granulation) surrounded by erythema
71
Behcet syndrome
Recurrent aphthous ulcers, genital ulcers and uveitis - Due to immune complex vasculitis involving small vessels, etiology unknown - Seen after viral infection
72
Oral herpes
Usually due to HSV-1, primary infection in childhood; lesions heal but remain dormant in trigeminal nerve ganglion - vesicles that rupture -> shallow painful red oral ulcers - Stress and sunlight cause reactivation -> vesicles on lips (cold sores)
73
Squamous cell carcinoma of the oral mucosa
Malignant neoplasm of squamous cells lining oral mucosa, usually floor of mouth Risk factors: tobacco and alcohol Oral leukoplakia and erythroplakia are precursor lesions
74
Oral leukoplakia
white plaque that cannot be scraped away; often squamous cell dysplasia
75
Oral candidiasis
white deposit on tongue, easily scraped awa associated with immunocompromised states
76
Hairy leukoplakia
white rough 'hairy' patch that arises on lateral tongue -often seen in immunocompromised individuals (AIDS ex) and is due to EBV-induced squamous cell hyperplasia; not premalignant
77
Erythroplakia
red plaque-> vascularized leukoplakia suggests angiogenesis and highly suggestive of squamous cell carcinoma
78
Mumps
infection w/ mumps virus -> bilaterally inflamed partoid glands -Orchitis, pancreatitis and aseptic meningitis may also present Lab findings: increased serum amylase due to salivary gland or pancreatic involvement
79
Sialadenitis
Inflammation of salivary gland (unilateral) Commonly due to obstructing stone (sialolithiasis) leading to staph aureus infection
80
Pleomorphic adenoma
Benign tumor composed of stromal and epithelial tissue; most common tumor of salivary gland - Presents as painless mobile mass in parotid (angle of jaw) - high rate of recurrence since extension of small islands of tumor through tumor capsule often leads to incomplete resection
81
Warthin tumor
Benign cystic tumor w/ abundant lymphocytes and germinal centers (LN-like stroma) Usually arises in parotid
82
Mucoepidermoid carcinoma
Malignant tumor composed of mucinous and squamous cells; most common malignant tumor of salivary gland Usually in parotid; commonly involves CN VII
83
Esophageal web
Thin protrusion of esophageal mucosa, usually in upper esophagus Presents w/ dysphagia for poorly chewed food Increased risk for esophageal squamous cell carcinoma
84
Plummer-Vinson syndrome
iron-deficiency anemia, esophageal web and beefy-red tongue from atrophic glossitis
85
Zenker diverticulum
Outpouching of pharyngeal mucosa through acquired defect in muscular wall - False diverticulum Arises above UES at junction of esophagus and pharynx Presents with dysphagia, obstruction, halitosis (bad breath)
86
Mallory-Weiss syndrome
Severe vomiting (alcoholism or bulimia) causes increased intraluminar P-> longitudinal laceration of mucosa at GE junction Presents w/ painful hematemesis Risk of Boerhaave syndrome
87
Boerhaave syndrome
Usually due to violent vomiting -> Rupture of esophagus -> air in mediastinum and subQ emphysema (air bubbles beneath skin and crackling sound - crepitis) Surgical emergency
88
Esophageal varices
Dilated submucosal veins in lower esophagus secondary to portal HTN -> L gastric vein backs up into esophageal vein -> dilation Asymptomatic, but risk of rupture-> - painless hematemesis - most common cause of death in cirrhosis
89
Esophageal strictures
associated with lye ingestion and acid reflux
90
Achalasia
Damaged ganglion cells in myenteric plexus (idiopathic or secondary to malignancy or T. cruzi (Chagas disease) infection) -> disordered esophageal motility and inability to relax LES -> progressive dysphagia solids -> liquids; barium swallow 'birds beak' Associated with increased risk of esophageal squamous cell carcinoma
91
Gastroesophageal reflux disease (GERD)
Reflux of acid from stomach due to reduced LES tone commonly presents as heartburn and regurg upon lying down. May also present with adult onset asthma, nocturnal cough and dyspnea Complications -ulceration with stricture and Barrett esophagus
92
Barrett esophagus
Glandular metaplasia of the lower esophageal mucosa from stratified squamous epithelium to nonciliated columnar epithelium w/ goblet cells -Response of lower esophageal stem cells to acidic stress (GERD) Associated with esophagitis, esophageal ulcers and increased risk of esophageal adenocarcinoma
93
Eosinophilic esophagitis
Infiltration of eosinophil in the esophagus in atopic patients. Food allergens -> dysphagia, heartburn, strictures. Unresponsive to GERD therapy
94
Esophagitis
Associated w reflux, infection in immunocomproimsed (Candida: white pseudomembranes; HSV-1: punched-out ulcers; CMV: linear ulcers), or chemical ingestion
95
Sclerodermal esophageal dysmotility
Esophageal smooth muscle atrophy -> decreased LES pressure and dysmotility -? acid reflux and dysphagia -> stricture, Barret esophagus and aspiration Part of CREST syndrome
96
Esophageal carcinoma
Presents: progressive dysphagia, weight loss; poor prognosis ``` Squamous cell carcinoma (more common worldwide) - usually upper 2/3 of esophagus -Risk factors: alcohol and tobacco (most common) hot tea (China and Iran) achalasia esophageal web esophageal injury ``` -Can present with hoarse voice and cough (recurrent laryngeal n and trachea involvement) Adenocarcinoma (more common in U.S.) - arises from preexisting Barrett esophagus - lower 1/3 of esophagus - Other risk factors: tobacco, achalasia, cigarettes, GERD LN spread depends on level of esophagus: upper 1/3 -> cervical nodes middle 1/3-> mediastinal or tracheobronch. lower 1/3-> celiac and gastric nodes
97
Acute gastritis
Acidic damage to stomach mucosa -> inflammation, erosion or ulcer Caused by: - NSAIDs -> decreased PGE2 -> decreased gastric mucosa protection - Burns (curling ulcer) -> decreased plasma volume -> sloughing of mucosa - Brain injury (Cushing ulcer) -> increased vagal stimulation -> increased ACh -> increased H+ production - Chemotherapy - Shock -> stress ulcers Common among alcoholics and patients taking daily NSAIDs
98
Chronic gastritis- Type A
Chronic inflammation of stomach mucosa caused by autoimmune destruction of gastric parietal cells-> Body and fundus Associated w/ autoab against parietal cells and/or intrinsic factor, pathogenesis mediated by T cells (type iv hypersensitivity) Clinical features: - Atrophy of mucosa w intestinal metaplasia - Achlorhydria (decreased H+ production) w/ increased gastrin levels and antral G-cell hyperplasia - pernicious Anemia (megaloblastic) due to lack of IF - increased risk of gastric Adenocarcinoma (intestinal type)
99
Chronic gastritis- Type B
H. pylori induced acute and chronic inflammation (most common form, 90%) H. pylori ureases and proteases + inflammation -> weakened mucosal defenses in antrum of stomach Presents: epigastric pain, increased risk for ulceration (peptic ulcer disease) and risk for gastric adenocarcinoma (intestinal type) and MALT lymphoma Triple therapy: 1. PPI (omeprazole) 2. Clarithromycin 3. Amoxicillin or metronidazole Confirm H. pylori with urea breath test and stool antigen
100
Menetrier disease
Gastric hyperplasia of mucosa -> hypertrophied rugae (look like brain gyri), excess mucus production w/ protein loss and parietal cell atrophy -> decreased H+ production Precancerous
101
Peptic ulcer disease
Solitary mucosal ulcer involving proximal duodenum (90%) or distal stomach (10%)
102
Duodenal ulcers
- H pylori in almost 100%, rarely ZE syndrome - Presents: epigastric pain improving w/ meals (gain weight) - Biopsy: ulcer with hypertrophy of Brunner glands - Usually anterior duodenum, posterior duodenum may cause bleeding from gastrodudoenal artery or acute pancreatitis - Mechanism: decreased mucosal protection (H.pylori) or increased gastric acid secretion (ZE gastrinoma) - benign risk of carcinoma
103
Gastric ulcers
- Caused by H.pylori (75%), NSAIDs and bile reflux - Mechanism: decreased mucosal protection - Presents: pain that is greater with meals (lose weight); usually lesser curvature of antrum - rupture-> bleeding from L gastric artery - biopsy margins to rule out malignancy --> benign gastric ulcer small malignant gastric ulcers- large and irregular w heaped up margins
104
Gastric carcinoma
Adenocarcinoma, presents late w weight loss, early satiety and some cases acanthosis nigricans or Leser-Trelat (seborrheic keratosis) Intestinal type (more common) - Large, irregular ulcer w/ heaped up margins - lesser curvature of stomach - Risk factors: intestinal metaplasia (H. pylori and autoimmune gastritis), nitrosamines in smoked food (Japan) and blood type A Diffuse type (rare) - Not associated w/ H. pylori, nitrosamines or intestinal metaplasia - Signet ring cells - stomach wall grossly thickened and leathery (linitis plastica) Spread to LN -> L supraclavicular node (Virchow node) Distant metastasis: - commonly liver - periumbilical region: Sister Mary Joseph nodule; INTESTINAL type - bilateral mets to ovaries: Krukenberg tumor w abundant signet ring cells; DIFFUSE type
105
Ulcer complications - hemorrhage
Gastric, duodenal (posterior>anterior) Ruptured gastric ulcer lesser curvature -> bleeding from L gastric Ruptured duodenal ulcer posterior wall -> bleeding gastroduodenal artery
106
Ulcer complications - perforation
Duodenal ulcers (anterior>posterior) See free air under diaphragm on CXR w/ referred pain to shoulder via phrenic nerve
107
Meckel diverticulum
True diverticulum - outpouching of all 3 layers Failure of vitelline duct to involute Rule of 2s - 2% of population - 2in long and located within 2ft of ileocecal valve in small bowel - presents first 2 yrs life w/ bleeding, volvulus, intussception or obstruction
108
volvulus
Twisting of bowel along mesentery -> obstruction and cut off blood supply -> infarction ``` Sigmoid colon (elderly) Cecum (young adults) ```
109
Intussception
Telescoping of proximal segment of bowel into distal via peristalsis -> obstruction and cut off blood supply -> infarction Current jelly stools and intermittent abdominal pain Usually occurs in children due to lymphoid hyperplasia, associated with tumors in adults
110
Small bowel infarction
small bowel susceptible to ischemic injury Presents with abdominal pain, bloody diarrhea and decreased bowel sounds transmural infarction - thrombosis/embolism of SMA (A. fib, vasculitis) or mesenteric vein (p. vera or lupus anticoagulant) Mucosal infarction - marked hypotension
111
Lactose intolerance
lactase breaks lactose -> glucose and galactose Enzyme deficiency -> abdominal distention diarrhea with milk product consumption due to osmotic gradient Deficiency acquired rare (AR) or acquired; temporary deficiency can arise after small bowel infection
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Celiac disease
Immune mediated damage of small bowel villi due to gluten (gliadin) exposure -> malabsorption and steatorrhea Associated with HLA-DQ2 and DQ8, N. European descent, dermatitis herpatiformis (IgA deposition at tips of dermal papillae) Lab findings: - IgA antibodies against endomysium, tTg or gliadin; IgG antibodies useful for diagnosis in those w/ IgA deficiency - Biopsy: flattened villi, hyperplasia of crypts and increased intraepithelial lymphocytes - Damage most prominent in duodenum Complications: -small bowel carcinoma and T-cell lymphoma present as refractory disease despite diet control
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Tropical sprue
Damage to small bowel cilli due to unknown organism -> malabsorption Similar to celiac disease except: * Tropical regions * Arises after infectious diarrhea and responds to antibiotics * Damage more prominent in jejunum and ileum (secondary vitamin B12 deficiency may occur)
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Whipple disease
Infection with Tropheryma whipplei (gram+) -> PAS+ foamy macrophages in intestinal lamina propria -> compress lacteals -> chylomicrons cannot be transferred to lymphatics -> malabsorption and steatorrhea Most often in older men Cardiac symptoms, arthralgias, LN involvement and neuro symptoms common
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Pancreatic insufficiency
Causes: CF Cancer - obstruction chronic pancreatitis Presentation: - Malabsorption of fat and fat-soluble vitamins and vitamin B12 - Increased neutral fat in stool - D-xylose absorption test: normal urinary excretion (decreased excretion with intestinal mucosal defects or bacteria overgrowth
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Carcinoid tumor
Malignant proliferation of neuroendocrine cells Can arise anywhere along gut, small bowel most common -Submucosal polyp-like nodule (+)chromogranin staining -Secretes serotonin -> metabolized by MAO in liver to 5HIAA and excreted -> NO CARCINOID SYNDROME Metastasis -> bypass liver --> no metabolism of 5HT--> goes into hepatic vein and systemic circulation -> CARCINOID SYNDROME: bronchospasm, diarrhea, flushing of skin triggered by etoh or stress Carcinoid heart disease -> right-sided valvular fibrosis -> tricuspid regurgitation and pulm. stenosis; NO L-sided lesions due to MAO in lungs
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Acute appendicitis
acute inflammation of appendix Children- obstruction from lymphoid hyperplasia Adults- obstruction from fecalith Features: periumbilical pain, fever, nausea -> goes to McBurney point (RLQ) Complications: Rupture-> peritonitis w/ guarding and rebound Periappendiceal abscess
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Crohn Disease
Location: Anywhere in Gi tract w/ skip lesions, terminal ileum most common, rectum least common Gross morphology: Transmural inflammation -> fistulas. Cobblestone mucosa, creeping fat, bowel wall thickening 'string sign' strictures, linear ulcers, fissures Micro morphology: noncaseating granulomas and lymphoid aggregates (Th1 mediatedO Complications: strictures, fistulas (enterovesical fistulae can cause UTIs), perianal disease, malabsorption, nutritional deficiency, colorectal cancer, gallstones, calcium oxalate nephrolithiasis Intestinal manifestation: RLQ pain, Diarrhea (usually non-bloody) Extraintestinal manifestations: *Migratory polyarthritis*, erythema nodosum, ankylosing spondylitis, pyoderma gangrenosum, aphthous ulcers, uveitis, *kidney stones* Treatment: Steroids, azathioprine, antibiotics, infliximab, adalimumab
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Ulcerative colitis
Location: Begins in rectum and extends continuously, proximally up to cecum Gross morphology: Mucosal and submucosal inflammation only. Friable mucosal pseudopolyps. Loss of haustra -> 'lead pipe' on imaging Micro morphology: Crypt abscesses and ulcers, bleeding, no granulomas (Th2 mediated) Complications: Malnutrition, sclerosing cholangitis, toxic megacolon, colorectal carcinoma (worse w/ right-sided or pancolitis) Intestinal manifestation: Bloody diarrhea Extraintestinal manifestations: Pyoderma gangrenosum, erythema nodosum, *Primary sclerosing cholangitis*,p-ANCA, ankylosing spondylitis, aphthous ulcers, uveitis Treatment: 5-aminosalicylic preps (mesalamine), 6MP, infliximab, colectomy
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Colonic diverticula
Outpouching of mucosa and submucosa through muscularis propria (false diverticulum) related to wall stress-> constipation, low-fiber, older adults; usually L colon (high stress in R colon -> angiodysplasia) -arise where vasa recta traverse -> weak point in wall; Sigmoid colon most comon location Complications: Rectal bleeding Diverticulitis- obstructing fecal matter causes appendicitis-like symptoms in LLQ Fistula - inflammed diverticulum ruptures -> colovesicular fistula presents with air or stool in urine
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Angiodysplasia
Acquired malformation of mucosal and submucosal capillary beds -usually cecum and R. colon due to high wall tension. Rupture -> hematochezia in older adult
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Ischemic colitis
Ischemic damage to colon, usually splenic flexure (watershed region btwn SMA and IMA) Atherosclerosis of SMA most common cause Presents: postprandial pain and weight loss; infarction -> pain and bloody diarrhea
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Irritable bowel syndrome (IBS)
relapsing abdominal pain with bloating, flatulence and change in bowel habits that improve with defecation - middle-aged females - related to disturbed intestinal motility, no path changes
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Hirschsprung disease
Congenital megacolon due to lack of ganglion cells/enteric nervous plexuses (Auerbach and Meissner) in segment of colon due to failure of neural crest cell migration (goes caudally, so rectum always involved) Associated with RET mutation, increased risk with Down syndrome Presentation: bilious emesis, abdominal distention, failure to pass meconium -> constipation Colon proximal to aganglionic segment is dilated. Diagnosis: rectal suction biopsy Treatment: resection
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Ileus
intestinal hypomotility without obstruction -> constipation, distended/tympanic abdomen with decreased bowel sounds Associated with abdominal surgeries, opiates, hypokalemia, sepsis Treatment: bowel rest, electrolyte correction, cholinergic drugs
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Malrotation of gut
anomaly of midgut rotation -> improper positioning of bowel -> formation of fibrous bands (Ladd bands) -> can cause volvulus, duodenal obstruction
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Malignant potential of colonic polyps
1. Dysplasia 2. Villous > Tubular-villous > Tubular 3. Size: >4cm 40% risk;
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Hyperplastic polyps
benign hyperplasia of glands; appears 'serrated' on microscopy most common type of polyp; usually L colon
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Adenomatous polyps
Neoplastic proliferation of glands Benign, but premalignant; may progress to adenocarcinoma via adenoma-carcinoma sequence
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Adenoma-carcinoma sequence
1. APC mutations increase risk for formation of polyp 2. Kras mutation leads to formation of polyp 3. p53 mutation, increased COX expression and DCC mutations allow progression to carcinoma
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Microsatellite instability pathway
DNA mismatch repair gene mutations -> sporadic and Lynch syndrome. mutations accumulate but no defined morphologic correlates
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Familial adenomatous polyposis (FAP)
AD mutation of APC on chromosome 5q 2hit hypothesis 100% progress to colorectal carcinoma unless colon resected; pancolonic; always involves rectum
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Gardner syndrome
FAP + osseous and soft tissue tumors, congenital hypertrophy of retinal pigment epithelium, impacted/supernumerary teeth
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Turcot syndrome
FAP + malignant CNS tumor (medulloblastoma and glial tumors)
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Peutz Jeghers syndrome
AD. Numerous hamartomas throughout GI tract along w hyperpigmented mouth, lips, hands, genitalia Increased risk of colorectal, breast, stomach, small bowel and pancreatic cancers
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Juvenile polyposis syndrome
AD syndrome in children
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Hamartomatous polyp
non-neoplastic; solitary lesions no significant risk of malignant transformation Growths of normal colonic tissue w/ distorted architecture Associated w/ Peutz-Jeghers syndrome and juvenile polyposis
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Lynch syndrome
Previously hereditary nonpolyposis colorectal cancer (HNPCC) AD mutation of DNA mismatch repair genes -> microsatellite instability -> 80% go to CRC Proximal colon ALWAYS involved (R sided) Associated with endometrial, ovarian and skin cancers
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Colorectal carcinoma
Epidemiology: most patients >50yo, 25% have family hx Most come from adenoma-carcinoma sequence, minority from microsatellite pathway Risk factors: Adenomatous and serrated polyps, familial cancer syndromes, IBD, tobacco, processed meats Presentation: Rectosigmoid>Ascending>Descending * Ascending (R sided): raised lesion, large exophytic mass -> bleeds -> iron deficiency anemia, weight loss and vague pain * Descending (L sided): infiltrating mass 'napkin ring' lesion-> decreased lumen-> colicky LLQ pain, hematochezia Association with increased risk for Streptococcus bovis endocarditis Diagnosis: iron deficiency anemia in men and postmenopausal females -Apple core lesion on barium enema x-ray -CEA tumor marker - good for monitoring, not screening Screen >50yo with colonscopy or stool occult blood test
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Acute pancreatitis
Inflammation and hemorrhage of pancreas Pathogenesis: Autodigestion of pancreatic parenchyma by premature activation of trypsin -> liquefactive hemorrhagic necrosis of pancreas and fat necrosis of peripancreatic fat Causes: - alcohol and gallstones -> obstruction of sphincter of Oddi (less drainage) - Trauma - Hypercalcemia - Hyperlipidemia - Drugs (sulfa drugs, NRTIs, protease inhibitors) - Scorpion stings - Mumps - Rupture of posterior duodenal ulcer Clinical features: - epigastric pain radiating to back - nausea and vomiting - periumbilical and flank hemorrhage (spreads into periumbilical soft tissue and retroperitoneum) - Elevated serum lipase (more specific) and amylase - Hypocalcemia (poor prognosis, Ca2+ consumed in saponification in fat necrosis) Complications: - Shock - Pancreatic pseudocyst- fibrous tissue surrounds liquefactive necrosis: mass w/ persistently elevated amylase - Pancreatic abscess (often due to E coli) - DIC and ARDS
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Chronic pancreatitis
Chronic inflammation, atrophy and calcification of pancreas Causes: - alcohol abuse (adults) - Cystic fibrosis (kids) - idiopathic Clinical features: - epigastric pain radiating to back - pancreatic insufficiency - malabsorption, steatorrhea, fat-soluble vitamins deficiency - Dystrophic calcification of pancreatic parenchyma on imaging- 'chain of lakes' pattern due to dilation of ducts *amylase and lipase NOT useful markers* Complications: DM-type2, risk of pancreatic carcinoma
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Pancreatic carcinoma
Adenocarcinoma from pancreatic ducts, poor prognosis; 1yr survival 20yrs) - Diabetes - Age >50 - Jewish and African American males Clinical features (usually presents late) - epigastric abdominal pain and weight loss - Obstructive jaundice w/ pale stools and palpable gallbladder (Couvoisier sign, tumor in head of pancreas) - Secondary DM; associated w tumors in body or tail - Pancreatitis - Migratory thrombophlebitis (Trousseau sign)- swelling, erythema, tenderness in extremities -Serum marker CA 19-9 Surgical resection - removal of head and neck of pancreas, prox. duodenum and gallbladder - Whipple procedure
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Biliary atresia
Failure to form or early destruction of biliary tree -> biliary obstruction w/in first 2mo of life Presents with jaundice and progresses to cirrhosis
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Cholelithiasis
Precipitation of cholesterol or bilirubin in bile due to: 1. supersaturation of cholesterol/ bilirubin, 2. decreased phospholipids or bile acids (normally increase solubility) or 3. stasis Cholesterol stones, yellow, most common - Usually radiolucent (10% radiopaque from associated Ca2+) - Risk factors: F, 40s, Fat, Fertile, clofibrate, NA ethnicity, Crohn disease and cirrhosis Bilirubin stones pigmented - Radiopaque - Risk factors: extravascular hemolysis and biliary tract infection - E.coli - Ascaris lumbricoides: roundworm fecal-oral transmission, infects biliary tract - Clonorchis sinensis: Chinese liver fluke; infects biliary tract increases risk for gallstones, cholangitis and cholangiocarcinoma Gallstones usually asymptomatic Complications: - biliary colic- 'waxing and waning' RUQ pain - cholecystitis - ascending cholangitis - gallstone ileus - gallbladder cancer
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Spider angiomata
small multiple dilated blood vessels radiating from single central vessel - found on trunk, face, upper extremities - not specific for cirrhosis but, quantity and size correlate with extend of liver damage (also see in pregnancy and malnutrition) -Caused by hyperestrogenemia Cirrhosis--> decreased metabolism of estrogen and decreased production of sex binding globulin -> increased estrogen in blood --> spider angiomas, palmar erythema, gynecomastia, testicular atrophy
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Hemochromatosis
Mutation of hemochromatosis gene (HFE) on chromosome 6, which encodes HLA-A3, affects iron absorption from GI tract -often missense mutation cysteine to tyrosine at 282 (C282Y) Increased frequency in caucasian population Classic triad: micronodular Cirrhosis, Diabetes mellitus, skin pigmentation Findings: high ferritin, iron and transferrin saturation, low TIBC Prussian blue stain shows iron deposition Complications: HF testicular atrophy Increased risk HCC Treatment: phlebotomy chelation with deferasirox, deferoxamine, deferiprone
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Primary biliary cirrhosis
Autoimmune granulomatous destruction of intrahepatic bile ducts w/ lymphocytic infiltration Associated w/ other autoimmune disease, classically seen in F, 40yrs Anti-mitochondrial antibody (AMA) (+) Presents w/ features of obstructive jaundice: - pruritis - HSM - xanthelasma - pale stools - malabsorption Complications: cirrhosis
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Primary sclerosing cholangitis
Inflammation and fibrosis of intrahepatic and extrahepatic bile duct Findings: - Periductal fibrosis w/ 'onion skin' appearance - Uninvolved regions are dilated -> 'beaded' appearance on contrast imagingin Etiology unknown; Associated with UC p-ANCA (+) Presents w/ obstructive jaundice: pruritis, HSM, xanthelasma, pale stools Complications: cirrhosis, increased risk of cholangiocarcinoma
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Reye syndrome
Liver failure and encephalopathy in kids who take aspirin for viral illness Related to mitochondrial damage of hepatocytes Presents: - Hypoglycemia - Elevated LFTs - Nausea and vomiting May progress to coma and death
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Zollinger-Ellison syndrome
Gastrinoma. Neuroendocrine tumor in pancreas (usually) or duodenum that secretes gastrin -> increase H+ secretion Presentation: - upper GI ulcers, duodenum and jejunal ulcers very suggestive - abdominal pain and diarrhea (+)secretin stimulation test: gastrin levels stay high after administering secretin Also measure Ca2+, PTH and pituitary hormones due to association with MEN 1 (pituitary, parathyroid and pancreatic tumors)
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VIPoma
Pancreatic neuroendocrine tumor secreting VIP (vasoactive intestinal polypeptide) - diarrhea - metabolic acidosis - hypokalemia