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GI pathophysiology > Embryo/Anatomy/Physiology > Flashcards

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
Q

Blood supply, parasympathetic innervation and vertebral level for Foregut

A

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)

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26
Q

Blood supply, parasympathetic innervation and vertebral level for Midgut

A

Blood supply: SMA

Parasympathetic innervation: Vagus (CN X)

Vertebral level: L1

Structures supplied: Distal duodenum to proximal 2/3 of transverse colon

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27
Q

Blood supply, parasympathetic innervation and vertebral level for Hindgut

A

Blood supply: IMA

Parasympathetic innervation: Pelvic nerve

Vertebral level: L3

Structures supplied: Distal 1/3 of transverse colon to upper rectum

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28
Q

Splenic flexure

A

watershed region btwn SMA and IMA -> highly susceptible to ischemic damage

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29
Q

SMA syndrome

A

transverse portion (3rd part) of duodenum is entrapped btwn SMA and aorta -> intestinal obstruction

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30
Q

What is the blood supply of the lesser and greater curvature of the stomach?

A

lesser curvature- L and R gastric arteries

greater curvature - L and R gastroepiploic arteries

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31
Q

What are the branches of the celiac trunk?

A

common hepatic artery
splenic artery
L. gastric artery

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32
Q

What are the branches of the common hepatic artery?

A

gastroduodenal artery
Hepatic artery proper
R. gastric artery

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33
Q

What are branches of the splenic artery?

A

L. gastroepiploic artery

Short gastric arteries (poor anastomoses if splenic artery blocked, unlike gastroepiploic)

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34
Q

What are the portosystemic anastomoses and what the clinical signs?

A
  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
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35
Q

What procedure is done to relieve portal HTN?

A

Transjugular intrahepatic portosystemic shunt (TIPS) between portal vein and hepatic vein relieves portal HTN by shunting blood to systemic circulation and bypassing liver

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36
Q

Pectinate (detate) line

A

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
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37
Q

Direction of blood flow through liver

A

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

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38
Q

Direction of bile flow through liver

A

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

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39
Q

What is located in the femoral sheath?

A

3-4cm below inguinal ligament

Contains femoral vein, artery and canal (deep inguinal LNs)

Does NOT contain femoral nerve

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40
Q

What are the layers of the spermatocord? What are the layers derived from?

A

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

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41
Q

What are the sites of protrusion of indirect and direct hernias?

A

indirect hernia- protrudes into internal inguinal ring

direct hernia protrudes into abdominal wall, usually medially to internal inguinal ring

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42
Q

Diaphragmatic hernia

A

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
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43
Q

Hiatal hernia

A

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

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44
Q

Paraesophageal hernia

A

Fundus of stomach protrudes into thorax, gastroesophageal junction normal

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45
Q

Indirect inguinal hernia

A

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

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46
Q

Direct inguinal hernia

A

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

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47
Q

Femoral hernia

A

Protrudes below inguinal ligament through femoral canal (below and lateral to pubic tubercle)

  • common in females
  • leading cause of bowel incarceration
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48
Q

What are the boarders of the inguinal (Hesselbach) triangle?

A

inferior epigastric vessels laterally
Lateral border of rectus abdominis medially
inguinal ligament inferiorly

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49
Q

Gastrin

A

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

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50
Q

Somatostatin

A

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

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51
Q

Cholecystokinin (CCK)

A

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

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52
Q

Secretin

A

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

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53
Q

Glucose-dependent insulinotropic peptide (GIP)

A

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

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54
Q

Motilin

A

Source: Small intestine

Action: Produces migrating motor complexes (MMCs)

Regulation: (+) fasting state

Notes: motilin receptor agonists (erythromycin) stimulate intestinal peristalsis

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55
Q

Vasoactive intestinal polypeptide (VIP)

A

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)

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56
Q

Nitric oxide

A

Action: Relaxes smooth muscle of lower esophageal sphincter (LES)

Notes: Loss of NO secretion implicated in higher LES tone of achalasia

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57
Q

Intrinsic factor

A

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

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58
Q

Gastric acid

A

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

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59
Q

Pepsin

A

Source: Chief cells (stomach)

Action: protein digestion

Regulation: (+) vagal stimulation, local acid

Notes: Pepsinogen -> pepsin in presence of H+

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60
Q

HCO3-

A

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

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61
Q

Pancreatic secretions

A

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
Q

What are the signaling pathway mechanisms of ACh, Gastrin, Histamine, Prostaglandins and Somatostatin on gastric parietal cells?

A

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
Q

How are glucose, galactose and fructose absorbed by enterocytes?

A

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
Q

Where is iron, folate and B12 absorbed?

A

iron- as Fe2+ in duodenum

folate- in small bowel

B12 - in terminal ileum with bile salts, requires IF

65
Q

Peyer patches

A

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
Q

Bile composition and function

A

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
Q

Bilirubin synthesis and breakdown

A

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
Q

Necrotizing enterocolitis (NEC)

A

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
Q

Dietary energy- how many Calories/1g for protein, carbohydrates, fat and alcohol?

A

protein and carbs: 4 kcal/1g
fat: 9 kcal/1g
EtOH: 7 kcal/1g

70
Q

Aphthous ulcer

A

painful superficial ulceration of oral mucosa

  • arises in relation to stress and resolves spontaneously but often recurs
  • Gray base (granulation) surrounded by erythema
71
Q

Behcet syndrome

A

Recurrent aphthous ulcers, genital ulcers and uveitis

  • Due to immune complex vasculitis involving small vessels, etiology unknown
  • Seen after viral infection
72
Q

Oral herpes

A

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
Q

Squamous cell carcinoma of the oral mucosa

A

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
Q

Oral leukoplakia

A

white plaque that cannot be scraped away; often squamous cell dysplasia

75
Q

Oral candidiasis

A

white deposit on tongue, easily scraped awa

associated with immunocompromised states

76
Q

Hairy leukoplakia

A

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
Q

Erythroplakia

A

red plaque-> vascularized leukoplakia suggests angiogenesis and highly suggestive of squamous cell carcinoma

78
Q

Mumps

A

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
Q

Sialadenitis

A

Inflammation of salivary gland (unilateral)

Commonly due to obstructing stone (sialolithiasis) leading to staph aureus infection

80
Q

Pleomorphic adenoma

A

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
Q

Warthin tumor

A

Benign cystic tumor w/ abundant lymphocytes and germinal centers (LN-like stroma)

Usually arises in parotid

82
Q

Mucoepidermoid carcinoma

A

Malignant tumor composed of mucinous and squamous cells; most common malignant tumor of salivary gland

Usually in parotid; commonly involves CN VII

83
Q

Esophageal web

A

Thin protrusion of esophageal mucosa, usually in upper esophagus

Presents w/ dysphagia for poorly chewed food

Increased risk for esophageal squamous cell carcinoma

84
Q

Plummer-Vinson syndrome

A

iron-deficiency anemia, esophageal web and beefy-red tongue from atrophic glossitis

85
Q

Zenker diverticulum

A

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
Q

Mallory-Weiss syndrome

A

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
Q

Boerhaave syndrome

A

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
Q

Esophageal varices

A

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
Q

Esophageal strictures

A

associated with lye ingestion and acid reflux

90
Q

Achalasia

A

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
Q

Gastroesophageal reflux disease (GERD)

A

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
Q

Barrett esophagus

A

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
Q

Eosinophilic esophagitis

A

Infiltration of eosinophil in the esophagus in atopic patients.

Food allergens -> dysphagia, heartburn, strictures. Unresponsive to GERD therapy

94
Q

Esophagitis

A

Associated w reflux, infection in immunocomproimsed (Candida: white pseudomembranes; HSV-1: punched-out ulcers; CMV: linear ulcers), or chemical ingestion

95
Q

Sclerodermal esophageal dysmotility

A

Esophageal smooth muscle atrophy -> decreased LES pressure and dysmotility -? acid reflux and dysphagia -> stricture, Barret esophagus and aspiration

Part of CREST syndrome

96
Q

Esophageal carcinoma

A

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
Q

Acute gastritis

A

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
Q

Chronic gastritis- Type A

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
Q

Chronic gastritis- Type B

A

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
Q

Menetrier disease

A

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
Q

Peptic ulcer disease

A

Solitary mucosal ulcer involving proximal duodenum (90%) or distal stomach (10%)

102
Q

Duodenal ulcers

A
  • 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
Q

Gastric ulcers

A
  • 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
Q

Gastric carcinoma

A

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
Q

Ulcer complications - hemorrhage

A

Gastric, duodenal (posterior>anterior)

Ruptured gastric ulcer lesser curvature -> bleeding from L gastric

Ruptured duodenal ulcer posterior wall -> bleeding gastroduodenal artery

106
Q

Ulcer complications - perforation

A

Duodenal ulcers (anterior>posterior)

See free air under diaphragm on CXR w/ referred pain to shoulder via phrenic nerve

107
Q

Meckel diverticulum

A

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
Q

volvulus

A

Twisting of bowel along mesentery -> obstruction and cut off blood supply -> infarction

Sigmoid colon (elderly)
Cecum (young adults)
109
Q

Intussception

A

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
Q

Small bowel infarction

A

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
Q

Lactose intolerance

A

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

112
Q

Celiac disease

A

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

113
Q

Tropical sprue

A

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)
114
Q

Whipple disease

A

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

115
Q

Pancreatic insufficiency

A

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
116
Q

Carcinoid tumor

A

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

117
Q

Acute appendicitis

A

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

118
Q

Crohn Disease

A

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

119
Q

Ulcerative colitis

A

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

120
Q

Colonic diverticula

A

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

121
Q

Angiodysplasia

A

Acquired malformation of mucosal and submucosal capillary beds

-usually cecum and R. colon due to high wall tension. Rupture -> hematochezia in older adult

122
Q

Ischemic colitis

A

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

123
Q

Irritable bowel syndrome (IBS)

A

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
124
Q

Hirschsprung disease

A

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

125
Q

Ileus

A

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

126
Q

Malrotation of gut

A

anomaly of midgut rotation -> improper positioning of bowel -> formation of fibrous bands (Ladd bands) -> can cause volvulus, duodenal obstruction

127
Q

Malignant potential of colonic polyps

A
  1. Dysplasia
  2. Villous > Tubular-villous > Tubular
  3. Size: >4cm 40% risk;
128
Q

Hyperplastic polyps

A

benign hyperplasia of glands; appears ‘serrated’ on microscopy

most common type of polyp; usually L colon

129
Q

Adenomatous polyps

A

Neoplastic proliferation of glands

Benign, but premalignant; may progress to adenocarcinoma via adenoma-carcinoma sequence

130
Q

Adenoma-carcinoma sequence

A
  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
131
Q

Microsatellite instability pathway

A

DNA mismatch repair gene mutations -> sporadic and Lynch syndrome. mutations accumulate but no defined morphologic correlates

132
Q

Familial adenomatous polyposis (FAP)

A

AD mutation of APC on chromosome 5q

2hit hypothesis

100% progress to colorectal carcinoma unless colon resected; pancolonic; always involves rectum

133
Q

Gardner syndrome

A

FAP + osseous and soft tissue tumors, congenital hypertrophy of retinal pigment epithelium, impacted/supernumerary teeth

134
Q

Turcot syndrome

A

FAP + malignant CNS tumor (medulloblastoma and glial tumors)

135
Q

Peutz Jeghers syndrome

A

AD. Numerous hamartomas throughout GI tract along w hyperpigmented mouth, lips, hands, genitalia

Increased risk of colorectal, breast, stomach, small bowel and pancreatic cancers

136
Q

Juvenile polyposis syndrome

A

AD syndrome in children

137
Q

Hamartomatous polyp

A

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

138
Q

Lynch syndrome

A

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

139
Q

Colorectal carcinoma

A

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

140
Q

Acute pancreatitis

A

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
141
Q

Chronic pancreatitis

A

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

142
Q

Pancreatic carcinoma

A

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

143
Q

Biliary atresia

A

Failure to form or early destruction of biliary tree -> biliary obstruction w/in first 2mo of life

Presents with jaundice and progresses to cirrhosis

144
Q

Cholelithiasis

A

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
145
Q

Spider angiomata

A

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

146
Q

Hemochromatosis

A

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

147
Q

Primary biliary cirrhosis

A

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

148
Q

Primary sclerosing cholangitis

A

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

149
Q

Reye syndrome

A

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

150
Q

Zollinger-Ellison syndrome

A

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)

151
Q

VIPoma

A

Pancreatic neuroendocrine tumor secreting VIP (vasoactive intestinal polypeptide)

  • diarrhea
  • metabolic acidosis
  • hypokalemia

GI pathophysiology (1 decks)

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