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DEMS > Unit I, week 2 > Flashcards

Unit I, week 2 Flashcards

1
Q

Tumors of the Appendix (3)

A

Neuroendocrine tumor (carcinoid) - most common

Epithelial tumors (adenocarcinoma)

Cystadenomas (mucinous tumor)

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2
Q

Appendix

A

arises off cecum (average 9 cm length), tubular structure

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3
Q

Types of watery diarrhea (2)

A

Osmotic

Secretory

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4
Q

Osmotic diarrhea

mOsm gap?
due to what 2 things?

A

type of watery diarrhea

gap > 50 mOsm

Carbohydrate malabsorption: Lactose intolerance, Sorbitol, Fructose

Osmotic laxatives: Magnesium containing laxatives

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5
Q

Secretory diarrhea

mOsm gap?
5 common causes

A

gap < 50 mOsm

1) Bacterial toxins (V. Cholera, E. Coli.)
2) Neuroendocrine tumors (Gastrinoma, VIPoma, Carcinoid)
3) Bile salt (e.g. terminal ileal resection)
4) Stimulant laxatives
5) Motility disorders (diabetes, IBS)

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6
Q

Differentiating osmotic vs. secretory diarrhea:

A

Normal stool osmolality = 290 mOsm

Osm gap = 290 - 2x(stool sodium + potassium)

→ greater than 50 mOsm → osmotic diarrhea

→ less than 50 mOsm → secretory diarrhea

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7
Q

Types of diarrhea (4)

A

1) Watery
2) Steatorrhea
3) InflammatoryExudative
4) Functional

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8
Q

Steatorrhea can be caused by what 2 main things?

A

(fecal fat+)

1) Malabsorption
2) Maldigestion

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9
Q

Diseases that cause steatorrhea via malabsorption (4)

A

1) Pancreatic insufficiency
2) Celiac
3) Whipple’s disease
4) Small bowel bacterial overgrowth
5) Short gut (small bowel) from surgery

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10
Q

Diseases that cause steatorrhea via maldigestion (2)

A

Pancreatic insufficiency

Biliary obstruction

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11
Q

3 main causes of inflammatory/exudative diarrhea

A

1) IBD - Crohn’s, UC
2) Ischemia
3) Invasive infections (colon)

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12
Q

Diagnosis of inflammatory diarrhea

Infection –> ?
Ischemia –> ?
Inflammatory –> ?

A

Infection → stool culture, PCR, ELISA, endoscopy with biopsy

Ischemia → CT scan, endoscopy-colon

Inflammatory → endoscopy

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13
Q

How does pancreatic insufficiency cause malabsorption and what kinds of malabsorption? (3)

A

1) → impaired lipolysis due to decreased lipase and colipase → fat malabsorption → steatorrhea
2) → decrease secretion of trypsinogen, chymotrypsinogen, proteases, pro carboxypeptidases A and B → protein malabsorption
3) → decreased pancreatic amylase → carbohydrate malabsorption

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14
Q

What are the pain causes of pancreatic insufficiency malabsorption

A

chronic pancreatitis, Cystic Fibrosis - insufficiency results when 90% of pancreas burned out

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15
Q

How does liver disease cause malabsorption?

A

alcoholic cirrhosis→, primary biliary cirrhosis, biliary obstruction

→ fewer hepatocytes with decreased function

→ decreased bile formation

→ lipid malabsorption

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16
Q

How does gastric bypass surgery cause malabsorption?

what deficiencies are common?

A

surgical rerouting results in inadequate mixing of food with biliary and pancreatic secretions

B12, Fe, Ca, Vit D deficiencies common

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17
Q

What causes predispose to small intestinal bacterial overgrowth (SIBO)? (5)

A

Hypomotility (scleroderma, diabetes, narcotics)

Partial intestinal obstruction

Small bowel diverticula

Decreased gastric acid secretion

Enterocolonic fistula (Crohn’s)

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18
Q

What problems to SIBO cause? (5)

A

1) Fat soluble vitamin and B12 deficiency
- Bacteria de-conjugate bile salts and consume B12

2) Folate levels will be normal to high
3) Catabolizing disaccharides in microvilli
4) Reducing effectiveness of enterokinase
5) Disrupting small bowel motility

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19
Q

How do you diagnose small intestinal bacterial overgrowth (SIBO) (3)

A

Aspiration of duodenum with culture

Glucose-Hydrogen breath test

Empiric treatment with abx (e.g. Ciprofloxacin)

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20
Q

What are the symptoms of SIBO? (6)

A

diarrhea, steatorrhea, abdominal pain, flatulence, bloating, weight loss

Deficiencies of fat soluble vitamins (A, D, E, B12)

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21
Q

Fat malabsorption vitamin deficiencies:

Vitamin A → ?
Vitamin D → ?
Vitamin E → ?
Vitamin K → ?

A

Vitamin A → night blindness, xerophthalmia

Vitamin D → osteomalacia (bone mineralization defects)

Vitamin E → hemolytic anemia (rare in adults)

Vitamin K → clotting dysfunction (PT/INR)

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22
Q

Celiac disease

A

inflammatory disease of small intestine

Immune response to peptides of gluten (gliadin) → loss of villi due to presence of increased intraepithelial lymphocytes and crypt hyperplasia leading to malabsorption

Mostly affects proximal small intestine → iron and folate deficiency

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23
Q

Symptoms of celiac disease

typical signs (8)

atypical signs (6)

A

steatorrhea, diarrhea, weight loss, bloating, abdominal pain, flatulence, failure to thrive, vomiting

Atypical signs: dermatitis herpetiformis, iron deficiency anemia, LFTs (AST, ALT elevations), cerebellar ataxia, osteoporosis, oral ulcers

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24
Q

Diagnosis of celiac disease

Intestinal biopsy (3 findings)

Serologic testing (what ab?)

What two HLA alleles?

A

Intestinal biopsy → villous flattening, intraepithelial lymphocytes, crypt hyperplasia

Serologic anti-tissue transglutaminase (tTg) IgA antibody test

HLA-DQ2, HLA-DQ8 → REQUIRED to have celiac disease (but not everyone with this will have celiac disease)

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25
Q

Tropical sprue

cause
presentation

A

Residents or visitors to tropics

Cause: bacterial toxins or colonization of aerobic coliform bacteria

Classic presentation: megaloblastic anemia (B12 and folate deficiency)

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26
Q

Tropical sprue

diagnosis
treatment

A

Diagnosis: intestinal biopsy with villous flattening and travel history

Treatment: abx, B12, folate

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27
Q

Symptoms of chronic vs. acute mesenteric ischemia

A

Chronic: 2-3 major vessels occluded

  • Symptoms: postprandial abdominal pain, weight loss, sitophobia, malabsorption
  • Causes: Atherosclerosis, clot, radiation stenosis of vessel

Acute: embolus, severe abdominal pain

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28
Q

Small Intestinal Tumors

A

VERY rare cause of primary tumors

Present with symptoms of obstruction: abdominal pain, distension, decreased stool output

Neuroendocrine tumor→ endocrine symptoms

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29
Q

Irritable Bowel Syndrome (IBS)

A

abdominal pain and altered bowel habits in absence of an organic cause

Pain improved with defecation

Pain onset with change in stool frequency

Pain onset with change in stool appearance

Constipation and/or diarrhea

10-15% of population in North America

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30
Q

Function of normal colon

A

resorption of water and electrolytes from chyme, bacterial fermentation of unabsorbed nutrients, storage and elimination of waste and indigestible materials

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31
Q

5 layers of normal colon

A

mucosa → muscularis mucosae → submucosa → muscularis propria → serosa (no villi)

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32
Q

Muscularis propria of colon and innervation of colon

A

Muscularis propria = inner circular smooth muscle + outer longitudinal smooth muscle layer

Muscle innervated by: afferent/efferent parasympathetic (stimulatory) and sympathetic (inhibitory)

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33
Q

Mucosa of colon

A

glandular epithelium with cylindrical indentations (crypts) with epithelial stem cells at base and columnar enterocytes, goblet cells, and neuroendocrine cells throughout

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34
Q

Anatomic pathway of the colon

A

ileocecal valve → cecum → ascending colon → hepatic flexure → transverse colon → splenic flexure → descending colon → sigmoid colon → rectum → anus

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35
Q

Blood supply to the colon

A

SMA → right colon (IC valve → distal transverse colon)

IMA → left colon

Inferior rectal and hemorrhoidal arteries → Distal rectum

*Splenic flexure and rectum = watershed areas (susceptible to ischemia)

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36
Q

Inflammatory Bowel Disease

A

disorderly immune function involving small and large intestines (immune dysregulation)

HLA-B27 associated with IBD

Chronic inflammation of mucosa and submucosa

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37
Q

Pathogenesis of Crohn’s and UC

A

immune dysregulation (not strictly autoimmune)

Can result from:
1) Host interactions with intestinal microbiota

2) Intestinal epithelial dysfunction with tight junction barrier dysfunction

3) Aberrant mucosal immune responses
- TH1 skewed response → Crohn’s disease
- TH2 skewed response → Ulcerative colitis

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38
Q

IBD and cancer?

A

IBD Increases cancer risk → adenocarcinoma

Increased risk with: duration of disease, extent of disease, family history, and extra-intestinal manifestations

Requires regular endoscopic surveillance for dysplasia

Ulcerative colitis has higher risk of colon cancer than Crohn’s

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39
Q

Defining features of Ulcerative colitis (6)

A

1) *Location limited to COLON, usually rectosigmoid
- -> Cure via surgical resection

2) Improves with tobacco use
3) Inflammation confined to mucosa/submucosa
4) *DIFFUSE inflammation (friability, edema, bleeding, punctate ulcerations)
5) Circumferential ulceration
6) Formation of pseudopolyps

  • No strictures, no fistulae or abscess
  • Increased risk of colon cancer
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40
Q

Defining features of Crohn’s (7)

A

1) *ENTIRE GI TRACT - Occurs from distal oropharynx to anus, most common in terminal ILEUM and right colon
2) *TRANSMURAL inflammation (extends to muscle and serosa)
3) → spread of disease outside GI tract → *FISTULA FORMATION
4) Can cause *marked FIBROSIS, narrowing, and *STRICTURES of small bowel common
5) *Patchy inflammation / ulceration with relative sparing of mucosa in between (“SKIP LESIONS”)
6) *Linear/focal ulceration - Deep ulcers
7) Exacerbated by tobacco use

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41
Q

Symptoms of Ulcerative Colitis (8)

A

1) *LOWER abdominal pain, crampy - LLQ > RLQ
2) *HEMATOCHEZIA
3) *MUCUS in stool
4) *Tenesmus
5) *Urgency
6) Chronic diarrhea, fatigue, weight loss
7) **No problems with malabsorption or obstruction
8) Extra-intestinal manifestations more common in UC than Crohn’s → *Primary sclerosing cholangitis

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42
Q

Symptoms of Crohn’s (5)

A

1) *LOWER OR MID abdominal pain
2) *Nausea/vomiting
3) *Steatorrhea
4) *FISTULA symptoms
5) Weight loss, chronic diarrhea, fatigue

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43
Q

Microscopic appearance of UC

A

Chronic inflammation restricted to mucosa

Bowel wall is thinned

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44
Q

Microscopic appearance of Crohn’s (4)

A

1) Transmural chronic inflammation and lymphoid aggregates
2) Bowel wall thickening
3) *Granuloma formation - NOT in UC
4) *Fissuring ulcers - UC has broad based ulcers

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45
Q

Extra-intestinal manifestations of IBD (6)

A

1) Uveitis: eye pain, redness
2) Pyoderma gangrenosum: large, painful, ulcerative condition over lower extremities
3) Erythema nodosum: painful raised erythematous nodules
4) Ankylosing spondylitis: stiffness and pain in lumbar spine
5) Primary sclerosing cholangitis
6) Osteoporosis and osteopenia

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46
Q

Primary sclerosing cholangitis

A

fibrosing condition of intra/extrahepatic bile ducts → cirrhosis or cholestasis

More common in UC

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47
Q

Ischemic colitis

A

inflammatory condition of colon that develops as a result of severely impaired regional blood flow (low CO or occlusive disease of vascular supply to bowel)

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48
Q

2 typical areas where ischemic colitis occurs

A

Typically occurs in watershed vascular areas (splenic flexure, rectosigmoid junction)

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49
Q

Risk factors predisposing to ischemic colitis

A

older individuals with peripheral vascular disease or CHF, or younger patients (long distance runners, oral contraceptive use)

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50
Q

Presentation of ischemic colitis

A

sudden onset crampy lower abdominal pain, diarrhea, and/or hematochezia

Weight loss or severe bleeding NOT present

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51
Q

Diagnosis of ischemic colitis

A

gold standard is colonoscopy or flexible sigmoidoscopy with biopsy
→ mucosal edema, friability, ulceration, hemorrhage

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52
Q

Infectious colitis

presentation? without what?

A

common cause of acute diarrhea

Inflammatory diarrhea caused by invasion or destruction of mucosa by microbe

Presentation: crampy lower abdominal pain, diarrhea, small volume, frequent, bloody or mucoid without caloric malabsorption

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53
Q

Diagnosis of infectious colitis

A

Leukocyte stain of stool (nonspecific)

Stool cultures or stool toxin assays

History: travel, undercooked beef, contaminated poultry, eggs, milk, lettuce, recent abx use (c.diff)

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54
Q

C. Diff/Pseudomembranous Colitis

A

results in formation of necrotic, mucopurulent debris adherent to inflamed colonic mucosa

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55
Q

Diverticulosis

A

outpouching of colon wall composed of mucosa and submucosal layers that herniate outward through muscularis propria but are contained by serosa

Benign in 80% of patients

VERY common - 60% in Western adult populations over 60

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56
Q

Pathogenesis of diverticulosis

A

low fiber diet → decreased stool bulk → increase peristaltic squeeze pressure and intra-colonic pressure → mucosal herniation through focal defects in bowel wall

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57
Q

What is a symptom of diverticulosis but not diverticulitis?

A

Diverticulosis → possible diverticular hemorrhage (diverticula can penetrate colon wall and vasa recta)

Painless hematochezia, often heavy, typically stops within 2-3 days

NOT a feature of diverticulitis

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58
Q

4 complications of diverticulosis

A

infection, perforation, abscess formation, hemorrhage

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59
Q

Diverticulitis

A

fecalith obstruction of diverticulum → distension from bacterial gas and neutrophils, micro perforation, abscess, or frank perforation with peritonitis

Infiltration of diverticulum with acute, then chronic inflammatory cells

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60
Q

Symptoms of diverticulitis

A

Typically occur in sigmoid → rapid onset, lower abdominal pain (LLQ), fever, nausea/vomiting

NO diarrhea, NO bleeding

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61
Q

Treatment of diverticulitis (uncomplicated vs. complicated)

A

Oral/IV abx for uncomplicated diverticulitis

Percutaneous drainage, surgery for complicated diverticulitis (perforation, stricture, recurrent disease)

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62
Q

Complications of diverticulitis (3)

A

1) Perforation: rupture of diverticulum due to multiplication and expansion of bacteria
2) Obstruction
3) Abscess formation

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63
Q

Microscopic colitis

A

autoimmune inflammatory condition of colon associated with mild-moderate diarrhea

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64
Q

Presentation of microscopic colitis (3)

A

Females > males, after age 50

Mild, chronic, watery, non-bloody diarrhea WITHOUT weight loss

Endoscopic and imaging normal

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65
Q

Diagnosis of microscopic colitis

A

Diagnosis by endoscopic biopsy → two types (lymphocytic or collagenous)

NORMAL on endoscopy, diagnosis on BIOPSY

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66
Q

Lymphocytic colitis (microscopic colitis) appearance on biopsy

A

increased intraepithelial lymphocytes

Strong association with celiac disease, lymphocytic gastritis, and other autoimmune diseases (thyroiditis)

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67
Q

Collagenous colitis (microscopic colitis) appearance on biopsy

A

thickened subepithelial collagen layer

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68
Q

Colonic hemorrhage

presentation
common causes

A

lower GI bleeding

Presentation: hematochezia (red/maroon blood per rectum)

Causes: diverticulosis (most common), AVMs, IBD, neoplasia, internal hemorrhoids

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69
Q

Symptoms of colonic obstruction (5)

A

1) Diffuse or upper abdominal discomfort
2) Distension
3) Nausea/vomiting
4) Emesis may be feculent
5) Absence of stool passage (obstipation) or low grade diarrhea

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70
Q

Diagnosis of colonic obstruction

A

Abdominal radiographs show dilated loops of colon and/or small intestine

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71
Q

Causes of colonic obstruction

A

adenocarcinoma of colon or rectum, volvulus, strictures, volvulus, foreign body

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72
Q

KEY POINTS - KNOW THESE!!!

Chronic abdominal pain and diarrhea → ?

Weight loss, new constipation → ?

Painless, heavy bleeding in otherwise healthy elderly patient → ?

Hematochezia after major surgery or MI → ?

A

1) Chronic abdominal pain and diarrhea → IBD
2) Weight loss, new constipation → Neoplasia
3) Painless, heavy bleeding in otherwise healthy elderly patient → Diverticulosis
4) Hematochezia after major surgery or MI → ischemic colitis

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73
Q

KEY POINTS - KNOW THESE!!!

Acute dysentery, travel, ill contracts, or abx use → ?

Chronic microcytic anemia → ?

NSAIDS → ?

History of pelvic radiation → ?

A

5) Acute dysentery, travel, ill contracts, or abx use → infectious diarrhea
6) Chronic microcytic anemia → AVMs or neoplasia
7) NSAIDS → drug induced colitis
8) History of pelvic radiation → radiation proctitis

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74
Q

Gliadin - what is it, what does it do to celiac people

A

(glycoprotein extract from gluten)

Effects:
Directly toxic to enterocytes
Stimulates lymphocyte mediated response and formation of autoantibodies

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75
Q

Pathophysiology of celiac disease

A

Gliadin deamidated by tissue transglutaminase (tTG)

→ deamidated gliadin presented by APCs via MHC class II to helper T cells → helper T cell mediated tissue damage

→ Villous atrophy, tissue damage, loss of mucosal and brush border surface area → malabsorption, diarrhea

*Typically involves duodenum

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76
Q

Presentation of Celiac disease

A

Bulky fat diarrhea, flatulence, weight loss, anemia, nutritional deficiencies, growth failure in children

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77
Q

Extra-intestinal complications of celiac disease

A

Dermatitis herpetiformis**

Other extra-intestinal complaints:

Fatigue, iron-deficiency anemia, pubertal delay, short stature, aphthous stomatitis
Lymphocytic gastritis, lymphocytic colitis

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78
Q

Dermatitis herpetiformis

A

small, herpes-like vesicles on skin that arise due to IgA deposition at tips of dermal papillae

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79
Q

What malignancies are associated with Celiac disease

A

Enteropathy-Associated T-Cell Lymphoma (EAT Lymphoma happens when you eat gluten)

Small intestinal adenocarcinoma

Both present as refractory disease despite good dietary control

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80
Q

Endoscopy and serology of Celiac disease

A

Endoscopy: loss of surface villi

Serology: IgA antibodies to tTG, anti-endomysial antibodies

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81
Q

Tissue biopsy: 3 characteristic findings

*****KNOW THIS

A

1) Villous blunting
2) Increased intraepithelial lymphocytes
3) Lymphoplasmacytosis of lamina propria

*Histologic severity does not always correlate with symptoms

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82
Q

Whipple’s Disease

Pathogenesis

A

gram (+) bacilli, Tropheryma whippelii (actinomycete) absorbed by lamina propria macrophages

Organism laden macrophages accumulate in small intestinal lamina propria and mesenteric lymph nodes → lymphatic obstruction

→ impaired lymphatic transport → malabsorptive diarrhea

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83
Q

Whipple’s Disease

Presentation

A

Triad: diarrhea, weight loss, malabsorption

  • Arthritis, lymphadenopathy, neurologic disease
  • Middle-aged/elderly white males
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84
Q

Whipple’s Disease

Diagnosis

A

tissue biopsy demonstrates presence of Tropheryma whippelii

PAS+ Macrophages filled with Whipple bacilli on biopsy

PCR based assay

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85
Q

Whipple’s Disease

Treatment

A

one year of abx

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86
Q

Giardia lamblia

what type of bug is it?
how do you get it?
incubation period?
causes what?

A
  • noninvasive flagellated parasite
  • can cause sporadic or epidemic diarrhea
  • cysts present in stool
  • Waterborne or food borne (cysts resistant to chlorine, need filter)

7-14 day incubation period

-diarrhea due to malabsorption / hyper-secretion with villous atrophy

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87
Q

Symptoms of Giardia Lamblia GI infection

A

chronic diarrhea, malabsorption, flatulence, weight loss

Sx may be intermittent

Can persist for years

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88
Q

Giardia Lamblia GI infection on duodenal biopsy

A

identification of organisms in lumen = “schools of fish”

Tear-drop shaped with two nuclei on each side of axoneme

Cyst in stool by immunofluorescence

villous atrophy

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89
Q

Giardia Lamblia GI infection microscopic findings

A

Villous blunting but no ulceration

Intraepithelial lymphocytes

Numerous protozoa bound to brush border, but no invasion

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90
Q

Bacterial infections and diarrheal illness

A

Mostly related to ingestion of contaminated water, food, foreign travel

Typically acute, self-limited colitis

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91
Q

Campylobacter spp diarrheal illness

A

gram negative, comma shaped, motile
-major cause of diarrhea worldwide

Inflammatory diarrhea - watery diarrhea at first –> progress to bloody

WBCs present in stool

Found in contaminated meat (poultry), water, and unpasteurized dairy

-complications: reactive arthritis, Guillan-Barre

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92
Q

Salmonella diarrheal illness

2 main types

A

gram negative bacilli, transmitted through food (uncooked chicken), reptiles (turtles), and water

Typhoid (enteric) fever = S. typhimurium
-or-
Non-Typhoidal Salmonella species

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93
Q

Typhoid (enteric) fever = S. typhimurium

A 
Fever
Abdominal pain
Bacteremia
"Pea soup" diarrhea
"Rose spots" rash on trunk
Hepatosplenomegaly

Peyers Patch hyperplasia –> perforation/intestinal bleeding

Abx treatment does not help

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94
Q

Non-Typhoidal Salmonella species:

A

Mild, self limited gastroenteritis

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95
Q

4 kinds of E. Coli diarrheal illness

A

1) Enteroadherent
2) Enterotoxigenic E. Coli (ETEC) and Enteropathic E. Coli
3) Enteroinvasive E. Coli
4) Enterohemorrhagic E. Coli

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96
Q

Enteroadherent E. Coli diarrheal illness

A

non-invasive, non-bloody diarrhea

Chronic diarrhea and wasting in AIDS

Form a coating of adherent bacteria on surface epithelium of enterocytes

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97
Q

Enterotoxigenic E. Coli and Enteropathic E. Coli diarrheal illness

A

Non-invasive, non-bloody diarrhea

Enterotoxigenic = major cause of traveler’s diarrhea

Enteropathic = infection of infants and neonates

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98
Q

Enteroinvasive E. Coli diarrheal illness

A

Invasive (similar to Shigella), non-bloody diarrhea, dysentery-like illness, bacteremia

Contaminated cheese, water, person-person contact

Cause of traveler’s diarrhea

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99
Q

Enterohemorrhagic E. Coli (EHEC) diarrheal illness

A

O157:H7 strain

Non-invasive, toxin-producing, bloody diarrhea
-Severe cramps, mild or no fever

From contaminated hamburgers

Sometimes renal failure = HUS

Deadly outbreaks

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100
Q

Rotavirus diarrheal illness

A
  • most common cause of severe childhood diarrhea and diarrheal mortality worldwide
  • Children 6-24 months most vulnerable

Selectively infects and destroys mature enterocytes → villus surface repopulated by immature secretory cells → loss of absorptive function → net secretion of water and electrolytes → osmotic diarrhea → DEHYDRATION = DEATH

Vaccines available

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101
Q

Protozoal infections of GI tract

1 example

A

typically in subtropical and tropical areas, dx via stool sample examination

Entamoeba histolytica

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102
Q

Entamoeba histolytica

A

infects 10% of world’s population

  • Symptoms: abdominal pain, bloody diarrhea, nausea, vomiting
  • can spread to liver –> elevated LFTs, liver abscesses

Cecum most commonly affected → “Flask shaped” ulcers in mucosa/fecal matter

cysts found in stool

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103
Q

Helminthic Infections of GI tract

1 example

A

Dx via stool examination for ova and parasites

Serious disease in nations with deficient sanitation systems, hot, humid, climate, and poverty

Can cause severe and life-threatening nutritional deficiencies

EX) Ascaris lumbricoides (roundworm)

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104
Q

Ascaris lumbricoides (roundworm)

A

In tropics, one of most common parasites in humans

Ingested from soil contaminated feces

Obstruction, perforation, growth retardation (malnutrition)

Giant worms up to 20 cm can be identified

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105
Q

Pathogenesis of pseudomembranous colitis

A

disruption of normal colonic flora by antibiotic allows C. difficile overgrowth → toxins released caused disruption of epithelial cytoskeleton, tight junction barrier loss, cytokine release, and apoptosis

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106
Q

Pseudomembranes

A

adherent layer of inflammatory cells and mucinous debris at sites of colonic mucosal injury

Eruption of neutrophils and mucinous debris attached to surface epithelium

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107
Q

Appendicitis

clinical features
treatment

A

Most common in adolescents and young adults

M > F

McBurney’s sign = tenderness located ⅔ of distance from umbilicus to R anterior superior iliac spine

Often presents as an acute abdomen

TX: appendectomy

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108
Q

Appendicitis

pathogenesis

A

luminal obstruction by stone-like mass of stool (fecalith) → ischemic injury and stasis of luminal contents → inflammatory response

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109
Q

Appendicitis

microscopic findings

A

Mucosal ulceration

Transmural acute and chronic inflammation

Extension of inflammation into mesoappendix

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110
Q

Bile

A

amphipathic liquid that contributes to excretion of various components (cholesterol, copper, medications) and lipid digestion within the small bowel

Synthesized by hepatocytes

Secreted into canaliculi → drain into peripheral intrahepatic bile ducts → right and left hepatic ducts → common hepatic duct

Main components = bile acids/salts, bilirubin, cholesterol

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111
Q

What happens to your bile in the fasting state

A

Storage and concentration of bile in gallbladder

Parasympathetic vagal tone and cholecystokinin levels decreased → sphincter of Oddi remains closed, gallbladder and bile duct peristalsis inhibited

  • Bile flows proximally up cystic duct into gallbladder = reservoir
  • Bile becomes 5-10x more concentrated during fasting
  • -> Na+ actively transported from lumen into bloodstream
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112
Q

What happens to your bile in the fed state

A

Bile is released into duodenum

Cholecystokinin levels and vagal tone increased → gallbladder/bile duct peristalsis → transport of bile into duodenal lumen

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113
Q

Gallbladder

A

columnar epithelium, thin fibromuscular layer, and serosa

Stores and concentrates bile (fasting state)

Contracts to deliver bile to duodenum (fed state)

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114
Q

When is the pathogenesis of cholesterol stone formation

A

cholesterol supersaturation or decreased bile acid synthesis

Supersaturation of cholesterol → cholesterol crystals

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115
Q

When do cholesterol stones form (4)

A

Bile duct/gallbladder dysmotility (stasis)

Hereditary mutations in cholesterol chain structure

Bile acid hypersecretion

Inflammation of gallbladder

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116
Q

Cholesterol stones - composition, appearance

A

made up of cholesterol, bile acids, phospholipids, lecithin

White or yellow in color

Soft and greasy consistency

Develop within the gallbladder but may spill into bile duct/duodenum

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117
Q

Brown stones - develop when?

A

develop as a result of infection in patients with prostheses or downstream obstruction

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118
Q

Pigment stones appearance and composition

A

composed of calcium bilirubinate salts that coalesce around mucin nidus

Black and hard consistency

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119
Q

Risk factors for pigment stone formation (4)

A

Asian, rural

Chronic hemolytic syndromes (SICKLE CELL)

Biliary infection

Ileal disease

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120
Q

When do pigment stones form?

A

increased concentration of bilirubin in bile (hemolytic state), and obstructed gallbladder/bile duct as a result of stasis

Can also develop in Asia due to chronic inflammation within biliary tree, (parasitic infections, oriental cholangiohepatitis)

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121
Q

Risk factors for stone formation

A

5 F’s = Fat, Female, Fertile, Forties, Family hx

Others:

  • rapid weight gain or weight loss
  • Latin American or Native American ethnicity
  • Estrogen/contraceptive use, pregnancy
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122
Q

Abdominal ultrasound and diagnosis of stones in biliary tree/organs

A

Abdominal ultrasound (>90% accuracy for cholelithiasis or cholecystitis)

Less accurate for bile duct stones (50%) → CT scan considered

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123
Q

Gallstone related complications (5)

A

1) Biliary Colic
2) Cholecystitis
3) Choledocholithiasis
4) Acute gallstone pancreatitis
5) Biliary Strictures

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124
Q

Biliary colic

A

gallstone can move downstream and obstruct gallbladder neck, cystic duct, or common bile duct

Intermittent gallbladder occlusion, e.g. after eating = Biliary colic

*complications of cholelithiasis

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125
Q

Presentation of biliary colic and treatment

A

Dull crampy pain in epigastrium or in RUQ which occurs within an hour of eating and resolves spontaneously within 3-5 hours

Timing corresponds to rise in cholecystokinin and decline

TX = cholecystectomy

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126
Q

Acute (calculous) cholecystitis

Pathophysiology

A

90% due to stone obstruction of neck/cystic duct → accumulation of toxic products in lumen → disruption of protective mucus layer

→ Severe inflammation and/or ischemia of gallbladder

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127
Q

Acute (calculous) cholecystitis

Symptoms and exam finding

A

Symptoms: Severe pain in RUQ, radiating to flank or shoulder, nausea, fever

Exam: focal tenderness to deep palpation during exhalation = Murphy’s sign

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128
Q

Acute (calculous) cholecystitis

treatment

A

admit, pain control, NPO, IV fluids, IV abx, cholecystectomy

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129
Q

Acalculous Cholecystitis

Pathophysiology

A

no obstructive stone, no infection, only inflammation and/or necrosis of gallbladder due to ISCHEMIA (vascular insufficiency)

Typically due to generalized hypoperfusion (sepsis, trauma, burns, MI)

Can be caused by vasculitis of cystic artery (Polyarteritis Nodosa)

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130
Q

Treatment of Acalculous Cholecystitis

A

drainage of gallbladder, or cholecystectomy if stable (typically since this is due to hypoperfusion, these patients are pretty sick and not surgery candidates)

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131
Q

Chronic cholecystitis

A

chronic inflammation in gallbladder, marked thickening and fibrosis of gallbladder wall

Clinically silent, follows repeated episodes of mild cholecystitis

*Increases risk of gallbladder cancer

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132
Q

Choledocholithiasis

A

stones travel into common bile duct, but too large to pass through ampulla → cause BILE DUCT OBSTRUCTION and/or acute pancreatitis

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133
Q

Choledocholithiasis

Symptoms

A

epigastric or RUQ pain, jaundice, dark urine

Liver chemistries elevated

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134
Q

Choledocholithiasis

Treatment
Possible complication?

A

ERCP with extraction or surgery

Ascending cholangitis

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135
Q

Ascending Cholangitis:

A

infection develops within bile duct above obstructing stone = LIFE THREATENING

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136
Q

Ascending Cholangitis:

presentation and treatment

A

Presentation:

  • Charcot’s Triad: RUQ pain, jaundice, fever
  • Progress to sepsis or death if untreated

Treatment: urgent IV abx and URGENT ERCP with stone extraction/stent

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137
Q

Biliary strictures

symptoms
causes

A

fixed narrowing or blockage of bile duct

Symptoms are more chronic and persistent - cholestasis (jaundice, dark urine/choluria, acholic stools, pruritus), RUQ pain, LFTs elevated

Can be benign or malignant causes

138
Q

Benign biliary strictures (BBS)

what is it?
symptoms?

A

caused by edema and fibrosis, fixed narrowing or blockage of bile duct

Can cause cholestasis –>

Symptoms: jaundice, dark (bilirubin rich) urine, pruritus (from systemic retention of bile acids), acholic stool (gray/white color)
RUQ pain, fever

139
Q

Causes of benign biliary strictures

A

1) Chronic chledocholithiasis (chronic inflammation of bile duct wall adjacent to stone or iatrogenic)
2) Chronic pancreatitis → narrowed distal common bile duct due to severe fibrosis of pancreatic head
3) Autoimmune pancreatitis
4) Primary sclerosing cholangitis (PSC)

140
Q

Primary sclerosing cholangitis (PSC)

A

idiopathic intra/extra hepatic inflammatory disorder causing numerous BBS throughout biliary tree

  • *Associated with IBD (UC)
  • *High risk for cholangiocarcinoma (bile duct cancer) **KNOW THIS
  • Progress to cirrhosis and liver fibrosis
  • No medical therapy, treat symptoms only
141
Q

Diagnosis of Biliary stricture

A

Ultrasound, CT → dilation of bile duct proximal to stricture

Confirm with MRCP or ERCP

Liver biopsy: assess decree of liver damage, may see concentric fibrosis around bile ducts (onion skinning)

Biopsy to determine if benign or malignant

142
Q

Treatment of biliary strictures

A

ERCP, dilation of BBS

143
Q

Sphincter of Oddi

A

muscular sphincter that regulates opening and closing of biliary orifice

Normal: sphincter relaxed during fed state (NO or B-adrenergic control) and contracts (cholinergic control) in fasting state

144
Q

Sphincter of Oddi Dysfunction (SOD)

Clinical features (4)

A
  • episodic epigastric or RUQ pain
  • elevations in liver/pancreatic chemistries
  • recurrent pancreatitis
  • dilation of bile or pancreatic duct by imaging

DX confirmed by ERCP

145
Q

Sphincter of Oddi Dysfunction (SOD)

treatment

A

ERCP guided biliary, pancreatic, or combined sphincterotomy

146
Q

Gallbladder cancer

type?
prognosis?
treatment?

A

Typically adenocarcinoma

rare, but poor survival

Treatment:
Surgical removal of gallbladder and surrounding lymph nodes
Palliative with advanced disease (pain control, ERCP w/stent)

147
Q

Gallbladder cancer histology

2 major risk factors?

A

Adenocarcinoma - gland forming epithelial cancer that usually develops in patients with *gallstones and *chronic cholecystitis (infection)

Produce desmoplasia (thick stroma of connective tissue)

148
Q

Choledochal Cysts

A

congenital dilation of common bile duct

Typically discovered in infancy and early childhood

Increases risk for bile duct carcinoma

149
Q

Bile Duct Carcinoma

prognosis, histology, 4 risk factors

A

nearly all adenocarcinomas, very rare, poor prognosis

Risk factors:

1) Choledochal cyst in older adults
2) Primary sclerosing cholangitis**
3) Infections (liver flukes)
4) Cholelithiasis

150
Q

Pancreatic ductal adenocarcinoma

A
  • most common form of pancreatic cancer
  • Very poor prognosis

Appearance: Firm, white mass with irregular borders

Typically at head of pancreas and blocks common bile duct and pancreatic duct → painless jaundice

151
Q

Pancreatic Endocrine Neoplasia

A

Better prognosis than ductal adenocarcinoma

Most clinically relevant tumor are: Nonfunctional and Well-differentiated

Functional tumors:
Insulinoma 42% → low blood sugar
Gastrinoma 24% → Peptic ulcers
Glucagonoma 14%

Appearance: well circumscribed fleshy tumor, arranged in “string of pearls” arrangement on histology

152
Q

Ondansetron, Granisetron

mechanism

clinical use (3)

A

5HT3 antagonist

Clinical uses: greatest efficacy of antiemetic classes

  • Prevention of chemo-induced N/V
  • Post-op emesis
  • N/V associated with post-op use of opioid analgesics
153
Q

Side effects of Ondansetron, Granisetron

A

well tolerated, occasional GI upset (constipation, diarrhea) and headaches

154
Q

Promethazine, Meclizine, Diphenhydramine

mechanism?

A

antihistamines

First generation H1 antagonist → good CNS penetration and muscarinic receptor blocking actions

155
Q

Promethazine, Meclizine, Diphenhydramine

clinical use (2)

A

motion sickness, postoperative emesis

156
Q

Scopolamine

mechanism?
clinical uses (2)
A

anticholinergic

Clinical use: prevention and treatment of motion sickness, some post-op N/V prevention

Administered transdermally (duration of action 72h)

157
Q

Metoclopramide, Prochlorperazine, Droperidol

mechanism?

A

D2 receptor antagonists

158
Q

metocloparmide vs. prochlorperazine?

A

Botha re D2 receptor antagonists used as antiemetic

Metoclopramide: also blocks 5HT3 → used for N/V of chemo

Prochlorperazine: cross BBB poorly

  • Less effective against emetic stimuli in gut which are mediated via 5HT3 receptors
  • Additional block of M and H1 receptors increases utility in nausea with motion sickness
  • Block a1 receptors increases potential for HTN
159
Q

Side effects of Metoclopramide, Prochlorperazine, Droperidol (5)

A

Extrapyramidal symptoms, restlessness, fatigue, drowsiness, diarrhea

160
Q

Best treatment of nausea/vomiting in pregnancy (2)

A

Pyridoxine (B6) and doxylamine (H1 antagonist) first line treatment

161
Q

What are some causes of drug induced constipation (6)

A

1) Antimuscarinic agents
2) Drugs with antimuscarinic side effects (1st gen antihistamines, TCAs, typical antipsychotics)
3) Antacids: calcium carbonate, Aluminum
4) Ca2+ channel blockers (especially Verapamil)
5) Opioid analgesics
6) 5HT2 Antagonists (Ondansetron)

162
Q

Management of simple constipation

A

proper diet (high fiber, 20-30g daily), exercise, adequate fluid intake (6-8 8oz glasses/day)

163
Q

Types of laxatives (4)

A

1) Fiber/Bulk Forming Laxatives
2) Saline (osmotic) Laxatives
3) Stimulant/Irritant Laxatives
4) Stool-Wetting Agents and Emollients

164
Q

Psyllium

A

Fiber/Bulk Forming Laxatives

First line treatment

Approximates physiological mechanism - facilitates passage, stimulates peristalsis via H2O absorption → bulk expansion

Effective in 12-24 hours to 3 days

May combine and interact with other drugs (digoxin/salicylates)

165
Q

Saline (osmotic) Laxatives

4 examples

A

non absorbable ions → osmotic retention of intestinal water → increased peristalsis

Used for purging doses for food/drug poisoning

1) Milk of Magnesia, Magnesium Citrate
2) Phosphate enemas
3) Polyethylene Glycol
4) Lactulose

166
Q

Milk of Magnesia, Magnesium Citrate:

A

most used for mild/moderate constipation

Avoid in renal dysfunction (can cause electrolyte imbalances)

167
Q

Phosphate enemas

A

primarily used for fecal impaction

168
Q

Polyethylene Glycol

A

Electrolyte solutions

High volume solutions → bowel cleansing prior to medical procedures, contain Na+/K+ salts to prevent net transfer of electrolytes

Small volume solutions → for difficult to treat constipation
-Excessive use may lead to electrolyte depletion

169
Q

Lactulose

A

disaccharide metabolized by colonic bacteria to low MW acids → osmotic diarrhea → increased peristalsis

Alternate for acute constipation (useful in elderly)

170
Q

Stimulant/Irritant Laxatives

3 examples

A

try if fiber/saline fail

1) Bisacodyl
2) Senna
3) Castor Oil

171
Q

Bisacodyl

mechanism
side effects?

A

increased peristaltic activity via local irritation (PG-NO) → accumulation of water and electrolytes → increased motility

Potentially dangerous side effects = electrolyte/fluid deficiencies, severe cramping

Most widely abused class

Safe for chronic use in recommended doses

172
Q

Castor Oil

mechanism of action?

A

contains triglyceride hydrolyzed in gut to ricinoleic acid

Acts primarily in small intestine → stimulate fluid/electrolyte secretion and speed intestinal transit

Castor bean also contains ricin an extremely TOXIC glycoprotein

173
Q

Stool-Wetting Agents and Emollients

2 examples

A

Docusate

Lubricant (mineral oil, olive oil)

174
Q

Docusate

mechanism
use

A

surfactant that acts as stool softener (facilitates admixture of aqueous and fatty substances)

Primarily used for prevention

Often combined with stimulant laxative during opioid therapy

175
Q

Lubricant (mineral oil, olive oil)

mechanism?

A

coats fecal contents - prevents colonic absorption of fecal water

Potential for aspiration in very young/elderly

176
Q

Treatment of opioid-induced constipation

A

stool softener (docusate)
+ stimulant laxative (bisacodyl-senna)
+ osmotic laxatives (milk of magnesia)

177
Q

What are two peripherally acting opioid antagonists that can be used to treat opioid induced constipation?

A

Methylnaltrexone (does not cross BBB) - very expensive

Naloxegol (primarily binds opioid receptors in GI tract only) - cheaper

178
Q

Activated charcoal

A

Prevention of Absorption-Chemical Adsorption

binds drug in gut to limit absorption

Effective without prior gastric emptying
Can even reduce elimination half-lives of drugs given IV

Given with Sorbitol 70%: recommended given with charcoal to prevent briquet formation

179
Q

Treatment of watery diarrhea:

ETEC
EHEC

A

E. Coli (ETEC) → quinolones, azithromycin, rifamaxin

EHEC → DO NOT treat with abx (increases risk of HUS) or anti peristaltics (increase risk of systemic disease)

180
Q

Treatment of watery diarrhea:

Giardia lamblia
C. diff
rotavirus

A

Giardia lamblia → metronidazole

C. Difficile → metronidazole, oral vancomycin
**Risk INCREASED with fluoroquinolones, clindamycina dn broad spectrum penicillin/cephalosporins

Rotavirus → rehydration

181
Q

Loperamide

mechanism
uses (2)
A

opioid receptor agonist affecting intestinal motility (mu), intestinal secretion (delta), and absorption (mu and delta)

Uses:
Anti-secretory activity against cholera toxin (blocks cAMP)
Effective against traveler’s diarrhea

182
Q

Side effects of loperamide (3)

A

Low addiction potential (BUT can be injected IV)

CNS (euphoria)

Cardiac toxicity (increased QT)

183
Q

Polycarbophil

A

antidiarrheal agent

binds free fecal water

Used for diarrhea and constipation

184
Q

Avoid use of ________ in children under 12 years old

A

Avoid use of bismuth subsalicylate in children under 12 years old (salicylate risk for Reye’s Syndrome)

185
Q

Drugs used to treat IBS (4)

A

1) TCAs
2) Drugs to improve bowel function (anti-diarrheals and anti-constipation)
3) 5HT-3 Antagonists
4) 5HT-4 Agonists

186
Q

TCA use in IBS

A

TCAs → relieve abdominal pain and discomfort

Pain in IBD due to functional pain - abnormal operation of nervous system

187
Q

Alosetron

mechanism
use?
side effects?

A

5HT3 Antagonists

→ reduces pain and inhibits colonic motility

*Used for severe IBS in women with diarrhea as prominent symptom

Can cause constipation

188
Q

Tegaserod

mechanism?
use?
side effects?

A

5HT4 Agonists → increase release of NTs → peristaltic reflex → gastric emptying and intestinal motility

Used for IBS patients with predominant constipation

Can cause diarrhea and linked to heart attacks, strokes, and unstable angina

189
Q

Leading causes of death from infectious disease worldwide

mainly effects who?

A

pneumonia and diarrhea

Mainly affects the young and old

190
Q

Leading cause of morbidity and mortality with diarrhea?

what is the mainstay of therapy?

A

Dehydration: leading cause of morbidity and death associated with diarrheal disease

Rehydration is the mainstay of therapy

191
Q

Pathogens that cause inflammatory diarrhea (6)

A 
C. Jejuni
Shigella
Salmonella
E. Coli O157:H7
C. Difficile
E. Histolytica

**Campylobacter is #1 cause of diarrhea in children and adults in US

192
Q

Composition of inflammatory diarrhea and where?

A

increase T cells, WBC, and RBC

in colon

193
Q

Noninflammatory diarrhea pathogens (5)

A 
Norwalk
Rotavirus
Giardia lamblia
Vibrio cholerae
Enterotoxigenic E. Coli (ETEC)
194
Q

Composition of noninflammatory diarrhea and location

A

watery, in small bowel

195
Q

Cholera

type of diarrhea?
mechanism?

A

non-inflammatory watery diarrhea that affects the small bowel

Once cholera toxin has infected, cells must slough off for them to stop secreting fluid due to cAMP → abx not very effective

196
Q

Presentation of cholera

A

18h to 5 day incubation

Abrupt diarrhea (rice water stool), vomiting

NONBLOODY

Normal histology (noninflammatory)

197
Q

Signs of dehydration

how do you rehydrate?

A

Decreased pulse volume, low BP

Poor skin turgor, sunken eyes, decreased urine, decreased MS

Metabolic acidosis, hypoglycemia, hypokalemia

Rehydration: give fluids with Na+ and glucose

198
Q

ETEC

A

noninflammatory watery diarrhea

traveller’s diarrhea

199
Q

Rotavirus

leading cause what?

A

Leading cause of: prolonged diarrhea, dehydration from diarrhea, hospitalization from diarrhea, and death from diarrhea (US and world)

200
Q

Epidemiology of rotavirus

what ages are typically effected?

how is it transmitted?

incubation and duration of illness?

A

Epidemiology: sporadic cases, usually winter, occasionally epidemic

Age affected: infants, young children

Transmission: Fecal-oral

Incubation period: 1-3 days

Duration of illness: 5-8 days

201
Q

Norwalk viruse (norovirus)

epidemiology?

what ages are typically effected?

how is it transmitted?

incubation and duration of illness?

A

Epidemiology: family and community epidemics, often winter

Age affected: older children, adults

Transmission: fecal-oral, contaminated shellfish and water

Incubation period: 1-2 days

Duration of illness: 1-2 days

202
Q

Giardia Lamblia

typically caused by what?
presentation?

A

typically water contamination

-Protozoan

Diarrhea, fatigue, abdominal cramps, bloating (borborygmi), fat malabsorption

203
Q

E. Coli O157:H7 (EHEC)

A

causes bloody inflammatory diarrhea

Causes vast majority of HEMORRHAGIC colitis (and HUS) in US

Can cause hemolytic uremic syndrome and thrombotic thrombocytopenic purpura (TTP)

Illness lasts 2-4 days (less than 7 days)

Highest rates in young children and elderly

204
Q

Toxin involved in EHEC

A

verotoxin, Shiga-like toxin (SLT-I/II)

Binds especially to human renal endothelial cells

Inhibits protein synthesis

205
Q

Where is EHEC typically found?

A

Reservoir in intestines of beef and dairy cattle

206
Q

C. Difficile

presentation?
associated with what?

A

leading, and almost only cause of nosocomial infectious diarrhea

Most commonly associated with antibiotic use

Symptoms may be mild diarrhea, watery or bloody, or may have fever, leukocytosis with severe colitis

207
Q

Salmonella typhi

risks of infection

A

enteric fever

Risks: fecal contamination, food/water (poor handling) contact with carrier

208
Q

Where is free air/gas typically found on an abdominal XR

A

Free air: will always be located in the most non-dependent space

Upright CXR → look under diaphragm

cross table (left lateral decubitus) look → air is anterior, pushing against liver on right side

209
Q

Systematic approach for interpreting abd XRs

A 
Free air/Gas
Bones
Stones
Calcifications
Mass
210
Q

Imaging modalities used to evaluate GI tract

A

1) Abdominal XR

2) Fluoroscopy
- Biphasic esophagram
- Upper GI
- Small bowel follow through (SBFT)
- Enteroclysis
- Barium enema

3) Ultrasound
4) CT
5) MRI
6) Nuclear medicine
7) Angiography/interventional radiology

211
Q

Barium Swallow test

what is it?
what is it used to evaluate?

A

fluoroscopic-radiographic contrast exam of oral, pharyngeal, and/or esophageal swallowing

Used to evaluate: 3 phases of swallowing (oral, pharyngeal, esophageal), structural, and functional abnormalities of oral cavity, pharynx, and esophagus

212
Q

Biphasic esophagram

Evaluates what 4 areas?

A

Evaluates: oropharynx, hypopharynx, esophagus, GE junction

213
Q

Biphasic esophagram

looks at what pathology?

A

reflux (common), hiatal hernia (very common), aspiration, neoplasm, esophagitis, stricture

214
Q

Upper GI

evaluates what 3 areas?
sees what pathology?

A

Evaluates: esophagus, stomach, duodenum

Pathology: gastritis/duodenitis, gastric or duodenal ulcers, diverticula, benign or malignant tumors

215
Q

Small bowel follow through (SBFT)

evaluates what area of GI tract?

sees what pathology?

A

Evaluates: distal duodenum, duodenojejunal junction to ileocecal valve

Pathology: Crohn’s disease, lymphoma, TB, sprue, adhesions, partial/intermittent obstruction

216
Q

Enteroclysis

A

gold standard of small bowel imaging, double contrast exam of jejunum and ileum (contrast + air)

Not well tolerated by patients, expensive, high radiation

217
Q

Barium Enema

A

fluoroscopic-radiographic test to evaluate colon and rectum (single or double contrast)

Requires bowel prep - stool can obscure/mimic pathology

Contraindicated in acute perforation, toxic megacolon, or immediately after biopsy

218
Q

Ultrasound used to evaluate what in GI tract?

A

evaluate abdominal organs and biliary system

Use: suspected appendicitis, cholecystitis, solid organ lesions (solid vs. cystic differentiation), vascular flow evaluation

Not widely used to evaluate GI tract

219
Q

Computed Tomography (CT) used to evaluate what in GI tract?

with vs. without contrast

A

Without IV contrast → detection of renal stone or hemorrhage

With Iv contrast → ischemic, infectious, or inflammatory disease, trauma, or tumor

220
Q

When is barium contraindicated?

A

DO NOT give orally upstream of a colon obstruction

221
Q

Contrast agents

A

used to opacify the lumen and include air, thin (low density), thick (high density) barium, and water soluble contrast

air
barium
Iodinated water soluble contrast
IV contrast
Enteric contrast
222
Q

When would iodinated water soluble contrast be given?

A

give if possible gut perforation

223
Q

what are the risks of IV contrast?

what about gadolinium based IV contrast?

A

Risks: nephrotoxic, allergic reactions

Gadolinium-based: IV contrast agent used in MRI

  • No nephrotoxicity
  • allergic reactions rare
224
Q

What is the composition of salivary gland secretions during HIGH FLOW RATES?

A

Saliva slightly hypotonic

  • HIGH bicarb
  • LOW Cl-

Moving too fast for significant exchange - limits action of duct cells on ionic/water content

Parasympathetic AND sympathetic input modifies secretion and changes in blood flow

225
Q

What is the composition of salivary gland secretions during LOW FLOW RATES?

A

-Saliva highly hypotonic because striated duct has time to modify secretion

  • Absorb Na+ and Cl- and secrete K+ and HCO3-
  • *→ Decrease NaCl, increase KHCO3-

-Movement of water in ducts restricted by tight junctions, leaving saliva hypotonic

226
Q

What is the composition of pancreatic juice in relation to flow rate?

A

Increase flow → increase [HCO3-], and decrease [Cl-] in pancreatic secretions, but Na+ (high) and K+ (low) always constant

**→ High NaHCO3-

227
Q

Regulation of salivary secretions

A

Via SNS and PNS input

228
Q

Parasympathetic regulation of salivary secretions

A

input from higher brain centers: vagal ACh

INCREASES acinar cell secretion and VASODILATION of blood vessels surrounding acini (results in protein rich and fluid/ion rich solution)

→ increased blood flow around acinus → increased fluid content of saliva by moving ions and water into acinar lumen

229
Q

Sympathetic regulation of salivary secretions

A

increased sympathetic input –> increased acinar cell secretion (results in high protein, low fluid solution

230
Q

Regulation of pancreatic secretion (3)

A

ANS input and hormonal input

1) ACh
2) CCK
3) Secretin

231
Q

ACh regulation of pancreatic secretion

  • released from where?
  • stimulates release of what and from where?
A

released from vagus and ENS nerves, stimulates release of digestive enzymes from acinar cells

232
Q

Cholecystokinin (CCK) regulation of pancreatic secretion

  • released from where?
  • stimulates release of what and from where?
A

released from endocrine cells in proximal small intestine in response to fat and proteins

Stimulates release of digestive enzymes from acinar cells

233
Q

3 main effects of CCK release

A

1) Stimulates release of digestive enzymes from acinar cells
2) Causes gallbladder contraction and Sphincter of Oddi relaxation
3) Reduces stomach emptying

Matches nutrient delivery to digestive and absorptive capacity

234
Q

Secretin regulation of pancreatic secretion

  • released from where in response to what?
  • stimulates release of what and from where?
A

released from endocrine cells in proximal small intestines in response to acid

Stimulates bicarb-rich fluid secretion from pancreatic duct cells

Acts by increasing cAMP levels in duct cells

235
Q

Main components of saliva

A

1) Mucins - lubricate food, facilitate swallowing
2) Amylase, lingual lipase - begin digestion of starches and fats
3) NaHCO3 - maintain optimal pH for enzyme activity, reduce Ca2+ solubility
4) IgA, lysozyme (destroys bacterial cell walls), lactoferrin (chelates iron, preventing bacterial growth that requires iron) → innate and acquired immune protection
5) Water - facilitates taste and dissolution of nutrients, aid in swallowing/speech

236
Q

Saliva

A

1-2 L of saliva secreted per day - 70% from submaxillary or submandibular gland, 25% from parotid gland, 5% from sublingual gland

Formed by passive filtration

Dependent on blood flow

237
Q

Acinar cells of salivary gland do what?

A

make saliva

Contain leaky tight junctions that allow increased blood flow to move more ions and water into acinar lumen

238
Q

Intercalated duct of salivary gland

A

between acinus and striated duct - contains myoepithelial cells to facilitate active secretion

239
Q

Striated duct of salivary gland

A

modifies ionic composition of saliva as it exits

240
Q

Main goals of striated duct of salivary glands

what channels and enzyme make this happen? (5)

A

Goal: NaCl reabsorption, K+ secretion, bicarbonate secretion

Cl-/HCO3- exchanger
+ H+/K+ exchanger
+ Na+/H+ cotransport

  • Na+/K+ ATPase establishes concentration gradient
  • Carbonic anhydrase uses H2O + CO2 to produce H+ + HCO3-
241
Q

Acinar cells vs ductal cells of pancreas

A

Acinar cells: produce variety of enzymes
-Acinar cells produce and excrete full complement of pancreatic enzymes via secretory granules released via exocytosis

Ductal cells: produce bicarb solution to help liquefy and neutralized acidic chyme in duodenum

242
Q

What is the aqueous component of pancreatic secretions

A

Aqueous component: water and bicarb

Produced by duct cells

Acid in small intestine triggers secretin release from duodenal endocrine cells → stimulus for NaHCO3 release

Secretin and CCK both inhibit gastric acid/fluid production and delay gastric emptying

243
Q

Pancreas does NOT contain what? (as compared to salivary gland)

A

MYOEPITHELIAL CELLS

244
Q

Similarities of pancreas and salivary gland

A

Both have acinar and ductal cells, both produces slightly hypertonic solution that is modified by ductal cells before release

245
Q

Comparing regulation of secretion between pancreas and salivary gland

A

Salivary secretion regulated by ANS

Pancreatic secretion regulated by both ANS and hormones

246
Q

How does increase in blood flow effect the salivary gland vs. pancreas

A

Salivary acinus is very vascular and increased blood flow results in a dilute saliva that is modified by duct cells

Pancreatic acini are not as vascular and respond to ACh and CCK

247
Q

How would you compare the ducts of the salivary glands and pancreas?

A

Pancreas: Ductal cells actively secrete a water and bicarbonate rich solution in response to secretin

Salivary: Salivary ducts on the other hand are fairly impermeable to water

248
Q

Saliva is rich in _______, where as pancreatic juice is rich in _______

A

**Saliva is rich in KHCO3-, whereas pancreatic juice is rich in NaHCO3-

249
Q

Categories of Salivary gland diseases (5)

A

1) Reactive lesions
2) Infectious sialadenitis
3) Benign neoplasms
4) Malignant neoplasms
5) Rare tumors

250
Q

Eight infectious/reactive diseases of salivary gland

A

1) Mumps
2) CMV Sialadenitis
3) Bacterial Sialadenitis
4) Sarcoidosis (granuloma)
5) Sjogren’s Syndrome
6) Salivary Lymphoepithelial Lesion
7) Xerostomia (dry mouth)
8) Halitosis

251
Q

Benign neoplasms of salivary gland (4)

A

1) Mixed Tumor (pleomorphic adenoma):
2) Monomorphic Adenomas
3) Ductal papilloma
4) Warthin’s Tumor: Warthin’s has abundant lymphoid and epithelial components (WHALE)

252
Q

Features suggesting malignancy in a salivary neoplasm (7)

A 
Induration (hard)
Fixed to overlying skin or mucosa
Ulceration of skin or mucosa
Rapid growth, growth spurt
Short duration
Pain, often severe
Facial nerve palsy
253
Q

Tracheo-esophageal fistula

A

connection of distal esophagus and trachea in setting of proximal esophageal atresia (ends in a blind pouch)

Presentation: polyhydramnios, choking with feeds, inability to swallow oral secretions

254
Q

Infantile hypertrophic pyloric stenosis

A

hypertrophy and hyperplasia of smooth muscle of gastric wall at level of pylorus → narrowing of antrum → causes near complete obstruction

Symptoms: dilation of stomach, projectile nonbilious vomiting, olive mass in RUQ, presents around 3 weeks of life

255
Q

Meckel diverticulum

what is it?
how do you diagnose it?

A

partial persistence of vitelline duct or yolk sac → blind pouch protrudes from terminal ileum

Wall may contain gastric mucosa → can cause gastric diseases (PUD)

Rule of 2’s: in 2% of population

Diagnosis: Technetium-99 scan (detects gastric mucosa) or other imaging (US/CT)

256
Q

Omphalocele

A

failure of intestines to return from extraembryonic celom to abdominal cavity at 10 weeks of gestation

Defect in abdominal wall at attachment site of umbilical cord → large sac composed of amniotic membranes filled with loops of bowel

Intestines have peritoneal AND amniotic covering

Typically associated with other congenital malformations

257
Q

Gastroschisis

A

bowel protruding from abdomen, but by different mechanism

Due to defect in anterior abdominal wall

NO amniotic covering

Usually an isolated defect, no other malformations

258
Q

Omphalocele vs Gastroschisis

A

Omphalocele: intestines have peritoneal AND amniotic covering
-associated with other congenital malformations

Gastroschisis: intestines do NOT have amniotic covering
-Isolated defect

259
Q

Intestinal malrotation

A

abnormal rotation and fixation of intestinal tract

Anomaly of large intestine during development

Typically occurs at 10 weeks when intestines returning to abdominal cavity

Present with volvulus of large bowel → obstruction (bilious vomiting)

260
Q

Gastrointestinal duplications/cysts

A

saccular (cystic) or tubular structures containing all layers of normal bowel wall and gastrointestinal lining, which may or may not communicate with bowel

261
Q

Intestinal stenosis

A

congenital narrowing of bowel

262
Q

Intestinal atresia

associated with with what congenital abnormality?

A

complete failure of development causing a blind ending

Associated with down syndrome (duodenal atresia)

263
Q

Imperforate anus/rectal agenesis

A

malformation ranging in severity from thin membrane of tissue covering the anus to complete agenesis of rectum

264
Q

Hirschsprung Disease

A

Causes congenital megacolon (massive dilation of intestinal lumen) due to failure of bowel nerve plexi (both auerbach and Meissner) to form in a segment of the bowel wall → absence of ganglion cells (ENS neurons)

TX: surgical resection of segment of bowel

265
Q

Necrotizing Enterocolitis

A

Complication of prematurity typically associated with hypoxemia

Blood shunted away from intestines to provide scarce oxygen to vital organs → ischemic damage to bowel wall → perforation and peritonitis

266
Q

Symptoms and treatment of necrotizing entorcolitis

A

SX: abdominal distension and bloody stools, feeding intolerance

TX: bowel rest, abx, surgical resection if meds fail

267
Q

Allergic esophagitis: aka eosinophilic esophagitis

what is it?
acid probe test results?
histology?

A

Immune reaction to dietary allergens

Normal pH probe testing, no response to acid block

Histology: severe eosinophilic infiltrate, typically involves entire length of esophagus with relative uniformity

268
Q

Reflux Esophagitis

what is it?
acid probe test results?
histology?

A

inadequate gastroesophageal sphincter function

Abnormal esophageal pH probe testing due to reflux of gastric acid
-Responds to treatment with PPIs

Histology: typically in distal esophagus, mild intraepithelial infiltrate with eosinophils

269
Q

Sessile vs. pedunculated polyp

A

Sessile → no stalk, flat base

Pedunculated → polyp on a stalk

270
Q

Inflammatory polyps

benign or malignant?
how does it form?
How does it present?

A

benign

Present with bleeding

Cycles of injury and healing result in “polyp” formation = inflamed colonic mucosa with ulceration/erosion, epithelial hyperplasia

Not a precursor to malignancy

271
Q

Hamartomatous polyps

benign or malignant?
associated with what?
how does it form?

A

benign - but can increase risk of future GI carcinoma

typically associated with syndromes (juvenile polyposis, Peutz-Jeghers) –> extra-GI symptoms

“tumor-like” overgrowth of mature or developing tissue where it is NORMALLY present

272
Q

Juvenile polyposis

A

Type of hamartomatous polyp

sporadic and syndromic

Often have foci of dysplasia

Increase risk of future GI carcinoma

Onset at under 5 years old

273
Q

Symptoms of Juvenile polyposis

associated with what other cancers?

A

Symptoms: arborizing polyps (small intestine > colon > stomach), colonic adenocarcinoma

Extraintestinal:

  • mucocutaneous pigmented lesions
  • increased risk thyroid, breast, lung, pancreas, gonadal and bladder cancers
274
Q

Peutz-Jeghers Syndrome

A

increases risk of future GI carcinoma

Onset between 10-15 years

Symptoms: juvenile polyps with increased risk of gastric,small intestinal, colonic, and pancreatic adenocarcinoma

Extraintestinal: pulmonary AVMs, digital clubbing

275
Q

Hyperplastic polyps

typical location and size?
need to distinguish it from what?

A

Location: left colon and rectum (90%)

Increased incidence with age

Small in size (less than 0.5 cm)

Need to distinguish from “sessile serrated polyp/adenoma” (SSP) which are premalignant**

276
Q

Histology of hyperplastic polyps

A

delayed maturation with overgrowth of superficial epithelium (hyperplasia) resulting in SERRATED architecture

No dysplasia, NOT pre-malignant

277
Q

Sessile Serrated Polyps/Adenomas

benign or malignant?
typical size and location?
genetic pathway to get these?

A

Premalignant - can progress to adenocarcinoma

Location: right side of colon most common, larger

Alternate pathway to carcinoma that the usual adenomatous polyp
–> Microsatellite instability pathway

278
Q

Adenomas

A

Variable size (can be 10 cm or more)

VERY common - in 50% of Western adults by age 50

Precancerous lesion that can lead to adenocarcinoma

279
Q

Signs of dysplasia in an adenoma

A 
Increased number of cells piling up on each other
Loss of basal-orientation of nucleus
Reduced mucin production
Reduced cytoplasm
Increased mitotic activity
280
Q

Risk of malignancy in an adenoma

_______ adenomas more invasive then ______ adenomas

_______ is the most important characteristic that correlates risk of malignancy overall

A

Villous adenomas contain foci of invasion more frequently than tubular adenoma

SIZE

281
Q

Main molecular pathways associated with colon cancer (4)

A

1) WNT/APC/B-catenin
2) K-Ras/MAP kinase
3) K-Ras/PI3 kinase
4) Microsatellite Instability: defects in mismatch repair

282
Q

WNT/APC/B-catenin pathway for colon cancer

A

classical adenoma-carcinoma sequence

WNT critical for development - WNT ligands drive proliferation of their target tissues/organs

WNT pathway regulates levels of cytoplasmic B-Catenin

283
Q

Classic pathway from nothing to adenoma to colon cancer?

4 steps

A

1) Germline (inherited) or somatic (acquired) mutation in APC tumor suppressor gene
2) → 2nd APC inactivation
3) → KRAS proto oncogene mutation
4) → p53 tumor suppressor gene loss with overexpression of COX-2 → Cancer

284
Q

Risk factors for colorectal carcinoma

A 
Advanced age
Obesity
FAP/HNPCC
Long standing UC
Smoking
Excessive alcohol
285
Q

Familial Adenomatous Polyposis (FAP)

A

APC mutations that are hereditary (AD), Chr5 (polyp has 5 letters!)

APC = component of Wnt signaling pathway, “destruction complex” that turns over B-catenin in absence of WNT ligand signaling
-Mutation in APC –> constiutively active B-catenin –> polyp formation

  • 100% develop invasive colon adenocarcinoma by age 30
  • Numerous colon polyps

Treatment: preventative colectomy

286
Q

Hereditary Non-Polyposis Colorectal Cancer (HNPCC)

A

(aka Lynch Syndrome), AD

-Develop colon cancer at an earlier age than sporadic forms - not associated with numerous polyps

Tend to be right sided

Inherit mutation of mismatch repair gene allele → acquire second allele mutation over time leading to MICROSATELLITE INSTABILITY

–> formation of sessile serrated polyps (adenomas) and eventually cancer

287
Q

Detection of colon cancer (3)

A

Visualization +/- Biopsy: colonoscopy

Blood detection in stool

DNA/mutation detection in stool

288
Q

Colorectal carcinoma

invasion of ________ cells beyond ___________

_______ is biggest risk for invasion

A

invasion of dysplastic epithelial cells into and beyond the lamina propria

SIZE is biggest risk (>4cm = high risk of invasive component in lesion)

289
Q

Most important prognostic features for colorectal carcinoma

A

Depth of invasion
Presence or absence of lymph node metastasis
Distant metastasis -

MOST COMMONLY METS TO LIVER***

290
Q

Cetuximab

A

EGFR receptor inhibitor that can be used to treat colon cancer with WILD TYPE KRAS tumors

-If KRAS is constitutively activated, inhibiting EGFR will have no effect

KRAS = signaling molecule downstream of EGFR tyrosine kinase receptor

291
Q

Blood flow through liver (4)

A
  1. Hepatic portal vein supplies 75% of (DEOXYGENATED) blood and hepatic artery (branch from celiac trunk) supplies (OXYGENATED) 25% of blood
  2. Drained by hepatic vein into IVC
  3. All vessels enter/exit from porta hepatis (hilar region)
  4. Blood supply completely separated from biliary secretion via tight junctions
292
Q

Lobes of the liver

A

Four lobes - each surrounded by fibrous connective tissue (Glisson’s capsule)

Each lobe maximizes contact with blood

293
Q

Fibrous connective tissue that surrounds liver

A

Glisson’s capsule

294
Q

Liver lobules

A

smallest functional unit within liver, generated by repeated branching of hepatic portal vein and hepatic artery

295
Q

3 types of liver lobules

A
  1. Classic lobule
  2. Portal lobule
  3. Acinar lobule
296
Q

Classic lobule

A

hexagonal-shaped arrangement of hepatocytes around central vein
Interlobular vessels between lobules carry incoming blood from hepatic portal vein and hepatic artery

  • Each vertex has a bile duct and lymphatic space (space of Mall)
  • Interlobular vessels + bile duct = portal triad
297
Q

Portal lobule

A

triangular shape between three central veins, zone of tissue around a bile duct into which a group of bile canaliculi feed

Bile secretory functional unit

298
Q

Acinar lobule

A

short axis between two portal triads and long axis between two central veins

  • Defines liver tissue in terms of blood delivery

Distributing branches of interlobular vessels run along “edges” of classic lobule, but run along short axis of acinar lobule

299
Q

Significance of acinar lobule (3)

A
  1. Toxin exposure → degeneration nearest to distributing vessels
  2. Lack of oxygenation or nutrients → affect hepatocytes nearest central vein
  3. Most glycogen accumulation in hepatocytes near central acinar lobule (nearest blood supply)
300
Q

Function of liver

A

first organ receiving blood from GI system → gets nutrients and toxins

Synthesizes blood proteins, glycoproteins, and lipoproteins, stores glucose from gut (temporarily as glycogen), metabolizes lipid soluble molecules and toxins, involved in urea formation

301
Q

Arrangement of hepatocytes

A

Arranged in anastomosing plates or sheets with two sides facing blood sinusoids → every hepatocyte exposed to plasma components

302
Q

Components of hepatocytes

A

Contain rough/smooth ER, golgi network, and secretory vesicles + abundant lysosomes, peroxisomes, and lipid droplets

  • Smooth ER hypertrophies upon exposure to toxins/alcohol
  • Extensive microvilli aiding in absorptive process
303
Q

Function of hepatocytes (4)

A

1) Take up glucose after a meal, store it as glycogen, convert glycogen to glucose during fasting periods for reentry into blood
2) Produce major blood proteins (albumin, clotting glycoproteins - fibrinogen/prothrombin, and lipoproteins)
3) Take up lipid soluble toxins, bilirubin from spleen, etc. → detoxify them by biochemically conjugating them
4) Excess cholesterol elimination in bile

304
Q

Sinusoidal endothelial cells of liver

A

outside microvillar surface of hepatocytes facing sinusoids
Fenestrated, allow large plasma components and lipoproteins to pass freely

DO NOT permit RBCs to contact hepatocyte surface

305
Q

Perisinusoidal space

A

(space of Disse) = space between endothelial cells and hepatocyte

Space contains fine meshwork of reticular fibers → support for sheets of hepatic cells + endothelial cells on top of them

306
Q

Kupffer cells

A

derived from monocytes, part of fenestrated endothelial layer adjacent to hepatocytes

Large nuclei, rapidly phagocytose particulate materials

Key role in defense and general removal of particulate material from blood

307
Q

Bile canaliculi (2)

A

Formed in between grooves of adjacent hepatocytes forming circumferential belt around each hepatocytes with microvilli extending into canaliculi lumen

Hepatocytes have tight junctions to prevent leakage of bile

308
Q

Canals of Hering

A

Small bile ducts where bile canaliculi come together within liver lobule

Surrounded by cuboidal epithelial cells with microvilli projecting into lumen

309
Q

Interlobular bile ducts

A

Formed by canals of Hering coming together at the portal triad

Has cuboidal epithelial lining initially → columnar epithelium as ducts fuse toward the porta hepatis to for lobar ducts which connect to form common hepatic duct

310
Q

Gallbladder

A

attached to liver surface, connected to common hepatic duct via cystic duct

311
Q

Common hepatic duct + cystic duct →

A

Common bile duct

312
Q

2 bile sphincters

A

Sphincter chledochus (sphincter of Boyden) - controls bile before entry of pancreatic duct

Sphincter of Oddi - controls bile entry after pancreatic duct

313
Q

Histology of gallbladder (4)

A
  1. Mucosa of the gallbladder: extensively folded
  2. Columnar epithelium: numerous microvilli, tight junctions, numerous mitochondria, folded basolateral surface (actively transport salt into space between cells, water follows by osmosis → concentration of bile)
  3. Lamina propria → lymphocytes and plasma cells, loose CT
  4. Muscularis externa → adventitia and adipose tissue
314
Q

Jaundice (icterus)

A

yellowish pigmentation of skin/sclerae, due to abnormally high levels of bilirubin in blood (hyperbilirubinemia)

315
Q

Normal bilirubin metabolism

A

RBCs broken down → heme → biburdin → bilirubin released into circulation from spleen

Bilirubin → carried in complex with albumin, into liver → conjugated in liver → makes bilirubin water soluble → excreted in feces

316
Q

Physiologic jaundice

A

babies unable to adequately conjugate bilirubin before 2 weeks of age and increased breakdown of fetal RBCs → increased unconjugated bilirubin

Develops gradually in first week of life

Most common cause of neonatal jaundice

317
Q

Tx of physiologic jaundice

A

Self-limited, phototherapy can be used to transform bilirubin into isomers that can be excreted in bile and urine

318
Q

Kernicterus

A

toxic accumulation of unconjugated bilirubin in neonatal brain

319
Q

Differential for neonatal jaundice

A
  1. Physiologic
  2. Metabolic disorders
    Bile obstruction
  3. Choledochal cyst
  4. Hereditary
  5. Idiopathic neonatal hepatitis
  6. Infection, medication
320
Q

Metabolic disorders that can cause jaundice

A

(alpha-1 antitrypsin deficiency, CF, metabolic storage disorders)

321
Q

Choledochal cyst

A

congenital dilation of biliary tree and bile stasis

Present before age 10 + jaundice ,abdominal pain, RUQ mass

322
Q

4 types of hereditary hyperbilirubinemia

A
  1. Crigler-Najjar Syndrome
  2. Gilbert Syndrome
  3. Dubin-Johnson Syndrome
  4. Rotor Syndrome
323
Q

Biliary atresia and two types

A

causes neonatal cholestasis, number one pediatric disorder requiring liver transplantation

  1. perinatal
  2. congenital structural anomaly of biliary tree
324
Q

Perinatal form of biliary atresia

A

extrahepatic biliary tree normal at birth and undergoes progressive destruction, more common

325
Q

Presentation of perinatal biliary atresia

A

late onset jaundice with progressively acholic stools

No associated anomalies

326
Q

Diagnosis of perinatal biliary atresia

A

cholangiogram to assess patency of biliary tree

327
Q

Treatment of perinatal biliary atresia

A

hepatoportoenterostomy (Kasai Procedure):

  • Excise extrahepatic biliary system and loop of small bowel connected to hepatic hilum to allow for bile drainage
  • Best if performed before 2 months
  • No non-surgical therapeutic options - liver transplant only
328
Q

Congenital structural anomaly of biliary tree

A

abnormal development of biliary tree, associated with other anomalies

Presentation: progressive jaundice immediately AT BIRTH

329
Q

Hereditary disorders with increased unconjugated bilirubin (20

A
  1. Crigler-Najjar (type I and II)

2. Gilbert syndrome

330
Q

Crigler-Najjar Syndrome

A

mutation leads to lack of Type I or decrease in Type II UDP-glucuronyltransferase (UGT1A1)

  • UDP-Glucuronyltransferase typically conjugates bilirubin to glucuronic acid making water soluble bilirubin glucuronides that are excreted in bile

Type 1 = fatal without liver transplant, no functional enzymes
Type 2 = jaundice, normal life expectancy, decreased enzyme activity

331
Q

Gilbert syndrome

A

mild, benign, fluctuating serum bilirubin due to decrease in UGT1A1 activity

Episodic jaundice during physiologic stress (e.g. illness)

332
Q

Disorders causing increased conjugated bilirubin (2)

A
  1. Dubin-Johnson syndrome

2. Rotor syndrome

333
Q

Dubin-Johnson syndrome

A

hereditary defect in excretion of bilirubin glucuronides across canalicular membrane due to absence of multidrug resistance protein 2

→ episodic jaundice, normal life expectancy

334
Q

Benign neoplasms of liver (4)

A

1) Mesenchymal Hamartoma:
2) Teratoma
3) Hepatocellular adenoma
4) Focal nodular hyperplasia

335
Q

Mesenchymal hamartoma

A

Nontender abdominal enlargement over days to months

Vomiting, decreased appetite, respiratory distress

Alpha fetoprotein levels NOT increased

336
Q

Malignant neoplasms of liver (3)

A
  1. Hepatoblastoma
  2. Hepatocellular carcinoma
  3. Undifferentiated/embryonal sarcoma
337
Q

Hepatoblastoma

A

tumor recapitulates hepatogenesis and arises in an otherwise NORMAL liver (unlike hepatocellular carcinoma)

338
Q

Presentation of hepatoblastoma (4)

A
  1. Enlarged abdomen, anorexia, weight loss, nausea, vomiting, pain
  2. Elevated alpha-fetoprotein (unlike mesenchymal hamartoma)
  3. Presents before age 5
  4. **NOT associated with underlying liver disease
339
Q

Activation of what pathway is seen in hepatoblastoma

A

Activation of Wnt/B-Catenin pathway present

340
Q

Hepatoblastoma incidence increased in which two syndroms

A

Beckwith-Wiedemann Syndrome and FAP

341
Q

Tx of hepatoblastoma

A

preop chemo and surgical resection

342
Q

MOST important prognostic factor of malignant neoplasms of the liver

A

STAGE at time of resection

DEMS (10 decks)

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