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PT1 B3 > Lecture 84/85 - Diseases and Path of the Small Bowel > Flashcards

Lecture 84/85 - Diseases and Path of the Small Bowel Flashcards

1
Q

Normal Small Bowel –

what vitamins and minerals are absorbed at the Duodenum and Jejunum

which are absorbed at the terminal ileum ?

A

D&J: Iron, Ca, Zn, folate -

Ileum: Fat soluble, bile, b12

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2
Q

Achlorydia impairs the absorption of what?

what may be deficient in the malabsorption of fat?

A

iron, Ca, B12

Ca, Mg – bind to fat in the gut

Vitamins: A, D, D, K

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3
Q

General approach to Diarrhea:
- which is more common – acute vs chronic?

  • What are differences between diarrhea of the large bowel vs small bowel?
A

Acute is more Common

SB: large volumes and due to malabsorption and maldigestion

Large bowel: less fluid overall; more nuisance sympatoms

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4
Q

Inflammatory vs non inflammatory diarrhea

  • characteristics
  • Cuases
A

Inflammatory: Mucoid, tenesmus, +/- blood, fever, small volume and more frequent

Cause: invasive infeciton, IBD, ischemia

Non Inflammatory: Watery, higher volume, no blood, dehydration

Causes: non invasive infection, IBS, medications

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5
Q

• Non inflammatory – Secretory vs Osmotic vs Fatty

  • characteristics/causes
  • which are improved by fasting?

what is the osmotic gap of an osmotic diarrhea

A

Secretory – excessive fluid secretion into the lumen (high volume);
Causes: Toxins (cholera), detergents, secretagogues, some laxatives
Not improved with fasting

Osmotic – due to non absorbable ions and solutes in the lumen (eg lactose interolerance)
Lower Volumes
Osmotic gap > 50
Causes: sugar substitutes, PEG, lactose interolace
Improved with fasting

Fatty – Oil droplets, foul smelling,
Causes; Pancreatic insufficiency, decreased bile acid, (Crohn’s terminal ileium destruction – decreased bile)

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6
Q

what tests can be done to help determine cauases of diarrhea?

A

Stool Osmotic Gap: (290 - (2x( Stool Na + Stool K))…nl < 50

fat testing
Carbs – breath testing; lactose tolerance test

Protein
BIle salts
VItamin levels
Schilling test (for b12)

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7
Q

Name 7 (exhaustive?) malabsorptive disease of the Small bowel?

A

Celiacs – immune

Infectious – tropical sprue, whipples disease, Giardia, HIV associated MAC, Cryptosporidia

Disaccharidease Deficiency –

Short Gut Syndrome

Other non infectious – PUD, NSAID enteritis, Crohns,

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8
Q

Celiac’s DIsease –

describe the pathogenesis:

(what is the susceptible HLA haplotype?)

A

Gliadin (a portion of Gluten) disrupts the mucosal tight junction

Tissue transglutaminase alters the Gliadin to make it negatively charged

Persons with suceptibility (aka HLA DQ2/8) mount vigorous immnune response and inflammatory cascade.

T cells recruited and damage the small bowel mucosa

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9
Q

Celiac’s

  • genetically susceptible populations?
  • Symptoms:
  • extra colonic manfestations

Associatd conditions (in particular , which disease of the skin?)

A

Europeans – irish, italians

diarrhea, bloating, abd pain, malabsorption symptoms

– anemia, osteopenia, neuropathy, amenorrhea, infertility

– Dermatitis hepatoformins; but also – Down’s, T1DM, Sjogren’s

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10
Q

Celiac’s diagnosis:
Macropathology
Micropathology

Name 3 serologic markers used
name 1 genetic test that might help

A

Scalloped villi

Micro: Intra-Epithelial Lymphocytes; Blunted villi

serology: Anti-Endomysial Abs
Anti-tissue transglutaminase Abs
Deaminated Gliadin Peptide

Genetic: HLA haplotyping

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11
Q

Celiac’s Complications:

A

Refractory Celiac – non responsive to GFD

Collagenous sprue
Ulcerative Jejuno-Ileitis Sprue
Osteopenia

30% more likely to get Small bowel Lymphoma

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12
Q

Treatment of Celiac

what is the #1 cause of refractory celiac’s

A

1 cause of refractory celiacs — not being on a true GFD

Gluten free diet

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13
Q

Tropical Sprue:

  • what is it?
  • Presentation/Timing?
  • What does a biopsy look like?
  • how does it differ from celiacs?
  • treatment?
A
  • Uncommon (thought to be infectious) cause of malabsorption –

Onset is usually after a bout of gastroenteritis, in persons who have travelled to the tropics

Bx – looks like Celiacs

But there are no positive serologies

Tx – Tetracycline, Folate

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14
Q

Whipple’s Disease

etiology: 
Symptoms 
Common Extra -GI symptoms 
Histo findings
treatment:
A

T. whipplei -

GI symptoms: diarrhea, weight loss

Extra GI: ARTHRALGIAS, CNS symptoms (+cardiac = per first aid)

Histo – organisims within macrophages; PAS+, Acid Fast Negative

Treat: long term ABX

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15
Q

compare histo stains of Whipple’s disease and MAC ?

A

Whipple’s: organisims within macrophages; PAS+, Acid Fast Negative

MAC: organisims within macrophages; PAS-, Acid Fast Positive

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16
Q

Infectious malabsorption – Giardia:

  • how is it commonly acquired
A
    • person to person
    • classically – camper drinking contaminated water

– histo findings: tear drop shaped organisim with two eyes

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17
Q

what are two HIV associated infections?

which is the #1 cause of diarrhea in HIV patients?

how do they appear histologically

A

Cryptosporidia –#1 cause of diarrhea in HIV patients
- Histo – tiny dots along the villi

Mycobacterium Avium Complex (MAC)
histo: PAS negative; AFB positive

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18
Q

Disaccharidase deficiency

  • what is it?
    -Symptoms
    what type of diarrhea does it lead to?
    -
A

inability to digest disaccharides (such as lactose)

bacteria are able to digest the disaccharides, producing methane, water, hydrogen etc

leading to bloating, indigestion and diarrhea after consumption

Osmotic diarrhea

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19
Q

what are the three forms of lactose intolerance?

which is the most common?

A

Congenital lack of lactase – rare

Primary – some populations lose the enzyme with age (Native Americans, Aftican Americans, Hispanics) (MOST COMMON)

Secondary – after bout of Gastroenteritis, mucosa is temporarily destroyed and cannot yet digest the dissarcharide

20
Q

Short Gut Syndrome

  • what is it?

Treatment:

A

Malabsorption due to loss of the small reason for any reason (congential, previous resection etc)

Treatment: Symptomatic managemnet;
can try parenteral nutrition
however this disease is notoriously hard to treat

21
Q

SIBO

  • what is it?
    Symptoms
  • Risk factors:
A

SMALL INTESTINAL BACTERIAL OVERGROWTH (SIBO)

  • Colonization of the SB (normally gram positive aerobes), by colonic flora (gram negative anaerobes)
  • Symptoms; bloating, diarrhea, malabsorption, Macrocytic Anemia (B12 deficinecy)

Risk factors: DM (slows motility), intestinal injury, GI surg, diverticuli (bacterial stasis), motor disorders

22
Q

SIBO

  • Pathology:
    Dx:
    Treatment
A

bacteria deconjagate bile salts and consume B12, damage mucosa

DX: Cultural jejunal aspirate; breath test

Treatment: treat vitamin deficiencies; help underlying cause; use abx to reset the gut flora

23
Q

• EOSINOPHILIC GASTROENTERITIS

  • what is it?
  • how does it present?
  • Diagnosis:
    Treatment:
A

Atopic d/o – abnormal eosinophilic infiltrates and degranulation in the gut leading to tissue destruction

thought to be food allergy

Presnetation: symptoms of diarrhea, distention, etc with exposure to the allergen

Dx: HIgh eosinophilia and degranulation (in the absence of other organisms)

Treatment: steroids; avoid the food allergen

24
Q

• SMALL INTESTINAL TUMORS

- what is the most common SB tumor ?

A

Metastasis –

Primary: Adenocarcinoma

25
Q

carcinoid (NET) Tumors of the SB

Locations:
which is typically worse?

Characterstics of NETs?

A

an epithelial tumor

§ Deuodenal (usually benign)
ileum (more malignancy than dueodenum)

		§ Growth/function/secretion  -- indolent and slow growing but produce and secrete things such as serotonin, histamine, bradykinin, dopamine
26
Q

what is carcinoid syndrome ?

A

§ Midgut Symptoms: (80% of carcinoids)
□ Asymptomatic –> abd pain –> obstructions
□ <10% get carcinoid syndrome — mets of the NET from midgut to the liver; therefore no metabolism of the liver; the secreted hormone/protein is now acting in the circulation (bc not deactivated by the liver) — flushing, diarrhea, SOB etc…

27
Q

Morphology of Carcinoid tumors?

stains for…

A

§ Salt and pepper nuclei with abundant chromatin

§ NET markers — Synpatophysin and chromogranin — confirmatory of NET

28
Q

carcinoid tumor:

Treatment

A

Treatment:
If not mets – resection

If mets – somatostatin analgons and other symptomatic control

29
Q

Adenocarcinomas of the SB

Risk factors

treatment

histo features?

A

most common primary SB cancer

Risks: Celiac, Crohn’s, colon polyp syndromes

Rx: surgery if not mets

malignant glands with desmoplastic stroma. same as other adenocarcinomas

30
Q

what is the most common mesenchymal tumor of the GI ?

genetic characteristics?

Treamtment;

A

GIST – GI stromal tumor

Stain positive for CD34 and c-kit (CD117) immunostains

				® Surgery

Glevac/Imatinib (anti BCR/ABL)

31
Q

what are two benign mesenchymal tumors of the GI?

A

○ Lipomas – benign

○ Leiosmas – benign

32
Q

EALT – what is it?
what is it a/w?
what isthe prognoss?

A

○ Enteropathy Associated T cell Lymphoma – (EATL)
§ Celilac associated
§ Prognosis is terrible – weeks to months survival :(

33
Q

kaposi’s sarcoma –

cause?
systemic features?
GI featurs?

A

○ Intermited grade angiosarcoma – making vessels but they are not functioning effectively, leaking blood, giving a bruise like appearance
○ Systemic Disease – Gi Tract, Skin, Pulmonary
○ Driven by HHV8 – typically associated with HIV/AIDS

34
Q

common region of metastasis to the gut?

common types of cancers that met to the sb?

A

○ Peri-ampullary region is a common region for mets

○ Common: Colon, Melanoma, Breast

35
Q

Chronic Mesenteric Ischemia:

  • frequency
  • causes:
  • symptoms
  • dx
  • treatment:
A

5% of all mesenteric ischemias

gradual loss of flow to celiac, SMA, IMA; — usually related to atherosclerosis

– symptoms: post prandial pain (intestinal angina), sitophobia, weight loss

  • Dx - Angiogram showing occlusion of 2/3 mesenteric vessels

Treatment
vascular reconstruction/bypass; angioplasty/stent.

36
Q

Acute mesenteric ischemia (AMI):

what is it? 
causes? 
Risk factors? 
Presentation? what is the pathognomonic symptom 
Dx:
A

sudden loss of flow to celiac, SMA, IMA (~a stroke of the gut)

Usually thrombo-emolic,

Risk factors: age, hypercoag, PVD, CHF, arrythmias, vasoactives (cocaine)

Presentation: acute, severe peri-umbilical pain that is out of proportion to the physical exam

Dx: angiogram

Treat: angiography/papaverine vasodilation, surgery

37
Q

Histology of ischemia small bowel

  • acute
  • chronic
A

acute – necrotic; dead vili first then the entire wall

chronic – fibrosis, short and stubby villi

38
Q

What are the 5 developmental GI conditions of infancy

what are the two acquired GI conditions of infancy

A

Malrotation, Atreisia, Meckel’s, Heterotopia, Duplicaitons

necrotizing entero-colitis, intusception

39
Q

Malrotation of the gut –

predisposes to…
treatment …

A

defect of embryology

§ Predisposes to Volvulus -- twisting of the bowel around the vascular supply leading to ischemia or infarct 
		§ Treatment: Surgery; resection; pin it down so it doesn't cause volvulus
40
Q

Atresia

  • what is it?
    possible cause?
    presentation?
A

§ Narrowing or disapperance of a segment of bowel, small or colonic

		§ Causes: possibly due to uterine ischemia insult during embryogenesis

presentation: as soon as child starts eating they will have vomiting;

41
Q

○ Meckel’s Diverticulum
- what is it?

– complications:

  • how is it detected? whats the reason behind this?
  • treatment
A

a true diverticulum (all layers)
remnant of the vitelline duct ( connected the yolk sac to mid gut)

Complications
– Gastric acid secretion – peptic ulcer disease
Heterotopias (gastic and pancreatic)
Obstruction —> diverticulitis

Dx – Technetium 99 scan (tracer taken up by gastric mucosa); see if its taken up anywhere outside the stomac

• Treatment: surgery
42
Q

• MECKEL’S DIVERTICULUM

rule of 2’s

A

2% of population,
2 inches long,
2 feet proximal to IC valve.

Contains 2 possible tissue types (gastric and pancreatic; 1/2 contain gastric).

2% symptomatic,
most by age 2.

Males 2x as likely to have symptoms

43
Q

○ Heterotopias

what is it?

A

§ Ectopic tissue

§ Eg – pancreatic tissue or gastric mucosa in the small intesntine

44
Q

Necrotizing Entero-colitis –

what is it?
histo

treatment

A

Immature GI Tract – most common in premature infants; uncertain etiology

Histology – Necrotizing enterocolitis (full thick necrosis through the bowel, typically perforation)

		§ Treatment: 
			□ Resection of the necrotic region
45
Q

○ Intussception –

what is it?
who?
where?

treatment?

A

Telescope folding of the bowe
sometimes due to the bowel

somtimes associated with a mass

Most common in infancy and at the Ileo-cecal junction

		§ Treatment: EMERGENT before ischemia 
			□ May be reduced by enema -- air or barium; but at risk for recurrence 
			□ May require surgery

PT1 B3 (16 decks)

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