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Internal Med > GI > Flashcards

GI Flashcards

1
Q

Define dyspepsia

A

Pain or discomfort centered in the upper abdomen associated with fullness,early satiety, bloating or nausea.
intermittent or continuous, (+/-) meal related

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2
Q

If you are concerned about duodenal ulcers, what additional history do you want to know?

A
  • characterization of pain (burning)
  • relation to food (worse 2-5 hrs after meal)
  • do you wake up from sleep (around 1am)
  • relief with antacids
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3
Q

What are “alarm features” with dyspepsia?

A 
weight loss
recurrent vomiting
dysphagia
evidence of bleeding
anemia
***refer for endoscopy
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4
Q

How can H.pylori be diagnosed?

A
  • urea breath test (current infection)
  • H.pylori ab test (any previous infection)
  • biopsy with endoscopy
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5
Q

How do NSAIDs increase risk of ulcers?

A

NSAIDs inhibit gastroduodenal prostaglandin synthesis:

1) reduced secretion of mucus and bicarbonate
2) reduced mucosal blood flow

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6
Q

What is Zollinger-Ellison syndrome?

A

gastrin-producing tumor (usually pancreatic) that causes acid hypersecretion, peptic ulcers and diarrhea
***suspect if PUD w/o NSAID use or H.pylori

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7
Q

How can you diagnose Zollinger-Ellison syndrome?

A

serum gastrin levels: markedly elevated (>1000)

CT to localize tumor

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8
Q

What are some complications of PUD?

A

1) hemorrhage: hematemesis, melena
2) perforation: sudden onset pain, peritonitis, poss. pancreatitis*
3) gastric outlet obstruction: persistent vomiting and weight loss w/o abd distension*
* ** require surgery

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9
Q

What diseases are associated with H.pylori infection?

A

1) duodenal/gastric ulcers
2) chronic active gastritis
3) gastric adenocarcinoma
4) gastric mucosa-associated lymphoid tissue lymphoma (gastric MALToma)

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10
Q

What is Plummer-Vinson syndrome?

A

Upper esophageal webs with:

1) microcytic hypochromic (iron deficiency) anemia
2) atrophic glossitis
3) spoon shaped fingernails (koilonychia)

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11
Q

What is the molecular pathogenesis of colorectal cancer?

2 pathways

A

1) Microsatellite instability pathway: (~15%)
DNA mismatch repair –> sporadic and HNPCC syndrome

2) Chromosomal instability (~85%)
loss of APC gene –> K-RAS mutation –> loss of tumor suppressor genes (p53, DCC)

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12
Q

What does cholecystokinin do?

A

**works on neural muscarinic pathways to cause pancreatic secretion in response to fatty acids and amino acids

increases:
- pancreatic secretion
- gallbladder contraction
- sphincter of Oddi relaxation
decreases:
- gastric emptying
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13
Q

Where is cholecystokinin come from?

A 
I cells
(duodenum, jejunum)
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14
Q

Where is gastrin come from?

A

G cells

antrum of stomach

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15
Q

What does gastrin do?

A

increases:

  • gastric H+ secretion
  • growth of gastric mucosa
  • gastric motility
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16
Q

What affects gastrin secretion?

A

Increases production:

  • stomach distension
  • alkalinization (chronic PPI use)
  • amino acids (Tryptophan, Phenylalanine)
  • peptides
  • vagal stimulation
  • *Zollinger-Ellison syndrome has very high gastrin levels

Decreases production:
- stomach pH <1.5

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17
Q

What is Zollinger-Ellison syndrome?

A

Gastrin secreting tumor of pancreas or duodenum
Causes ulcers in distal duodenum and jejunum
- abd pain
- diarrhea/malabsorption
May be associated with MEN1

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18
Q

What is MEN1?

A

3 P’s: (Wermer syndrome)

1) Parathyroid tumors
2) Pituitary tumors (prolactin or GH)
3) Pancreatic endocrine tumors (Zollinger-Ellison, insulinomas, VIPomas, or glucagonomas)
* **often presents with kidney stones and stomach ulcers

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19
Q

What is MEN2A?

A

2 P’s: (Sipple syndrome)

1) Medullary thyroid carcinoma (secretes calcitonin)
2) Pheochromocytoma
3) Parathyroid hyperplasia
* *Associated with ret gene mutation

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20
Q

What is MEN2B?

A

1 P:

1) Medullary thyroid carcinoma (secretes calcitonin)
2) Pheochromocytoma
3) Oral/intestinal ganglioneuromatosis (mucosal neuromas)
* **Associated with marfanoid habituss
* *Associated with ret gene mutation

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21
Q

What does GIP do?

A

Gastric inhibitory peptide
Exocrine: decrease gastric H+ secretion
Endocrine: increase insulin release
*** Increased by fatty acids, amino acids and oral glucose

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22
Q

Where does GIP come from?

A 
K cells
(duodenum, jejunum)
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23
Q

What does motilin do?

A

Produces migrating motor complexes (MMCs)

increased in fasting state

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24
Q

Where does motilin come from?

A

small intestine

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25
Q

What does secretin do?

A

Increases pancreatic bicarbonate secretion (neutralizes gastric acid in duodenum for pancreatic enzymes to work)
Decreases gastric acid secretion
Increases bile secretion

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26
Q

Where does secretin come from?

A 
S cells 
(duodenum)
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27
Q

What does somatostatin do?

A

Decreases:

  • gastric acid and pepsinogen secretion
  • pancreatic and small intestine fluid secretion
  • gallbladder contraction
  • insulin and glucagon release
  • ***increased secretion when acid increased
  • ***decreased secretion with vagal stimulation
28
Q

Where does somatostatin come from?

A

D cells

pancreatic islets, GI mucosa

29
Q

What does nitric oxide do?

A

Relaxes smooth muscle including LES

if no NO then no opening of LES –> achalasia

30
Q

What does VIP do?

A

Vasoactive intestinal polypeptide

  • increases intestinal water and electrolyte secretion
  • relaxes intestinal smooth muscle and sphincters
31
Q

What does VIP do?

A

Vasoactive intestinal polypeptide
increases intestinal water and electrolyte secretion
relaxes intestinal smooth muscle and sphincters

32
Q

What does VIP do?

A

Vasoactive intestinal polypeptide
increases intestinal water and electrolyte secretion
relaxes intestinal smooth muscle and sphincters

33
Q

What affects VIP secretion?

A

Increases with distention and vagal stimulation

Decreases with adrenergic input

34
Q

What is a VIPoma?

A 
non alpha, non beta pancreatic tumor that secretes VIP
Causes:
- copious watery diarrhea
- hypokalemia
- achlorhydria
35
Q

What are some clinical features of portal hypertension?

A

ascites
peripheral edema
splenomegaly
varices (esophageal, gastric, hemorrhoids)

36
Q

What are the two main stigmata of cirrhosis

A

1) portal HTN

2) hepatocellular dysfunction

37
Q

What happens with hepatocellular dysfunctoin?

A

Decreased albumin production

Decreased clotting factor production

38
Q

How is cirrhosis classified?

A

Child’s classification
A: no ascites, bili 3.5
B: controlled ascites, bili 2.0-2.5, minimal encephalopathy, good nutrition, albumin 3.0-3.5
C:uncontrolled ascites, bili >3.0, severe encephalopathy, poor nutrition, albumin >3.0

39
Q

What are causes of cirrhosis?

A
  1. alcoholic liver disease
  2. chronic hepatitis (B&C)
  3. drugs (tylenol, mtx)
  4. autoimmune hepatitis
  5. primary biliary cirrhosis
  6. inheritied metabolic disease (hemochromatosis, Wilson disease)
  7. hepatic congestion from HFrEF, constrictive pericarditis
  8. alpha1 anti-trypsin deficiency
  9. hepatic veno-occlusive disease
  10. NASH
40
Q

What are signs of chronic liver disease?

A 
ascites
varices
gynecomastia/testicular atrophy
palmar erythema
spider angiomas on skin
hemorrhoids
caput medusae
41
Q

What is the biochemical cause of ascites?

A
  • increased hydrostatic pressure (Portal HTN)

- reduced oncotic pressure (hypoalbuminemia)

42
Q

What are the complications of liver failure?

A 
AC,9H
Ascites
Coagulopathy
Hypoalbuminemia
portal HTN
hyperammonemia
Hepatic encephalopathy
Hepatorenal syndrome
Hypoglycemia
Hyperbilirubinemia/jaundice
Hyperestrinism
Hepatocellular carcinoma
43
Q

What is hepatorenal syndrome

A

renal failure due to advanced liver disease that causes renal hypoperfusion from vasoconstriction of renal vessels

44
Q

What are some clinical features of hepatorenal sydrome?

A 
azotemia
oliguria
hyponatremia
hypotension
low urine Na (<10mEq/L)
45
Q

What do you find on LFTs for a cholestatic pattern?

What diseases do you think of?

A 
Elevated AST and ALT
Elevated T bili 
Elevated Alk Phos
- gall stones/blockage
- Med-induced blockage (MTX)
- NASH
46
Q

What do you find on LFTs for a hepatocellular pattern?

What diseases do you think of?

A

Very highly elevated AST/ALT

  • acute hepatitis (A usually)
  • acute autoimmune hepatitis (AMSA+, PSC, PBC)
  • shock liver
  • alcohol/toxin (tylenol)
  • NASH
  • Infiltrate: Wilsons/hemochromatosis
47
Q

What do you find on LFTs for an isolated bilirubin pattern?

What diseases do you think of?

A

Elevated indirect bili
- hemolysis of RBCs
Elevated direct bili
- congenital diseases: Gilbert, Criegler-Najjar, Roter, Dubin-Johnson

48
Q

What is the Charcot Triad?

What is disease does it indicate?

A
  1. RUQ pain
  2. Jaundice
  3. Fever
    * **Cholangitis
49
Q

What are the main functions of the liver? (6)

A
  1. Make bile
  2. Make proteins (albumin and clotting factors)
  3. Toxin metabolism
  4. Drug metabolism
  5. Lipid metabolism
  6. Gluconeogenesis
50
Q

What is in the hepatic triad?

A
  1. Hepatic artery
  2. Portal vein
  3. bile duct
51
Q

What are indications that diarrhea is inflammatory?

A
  • blood
  • mucus
  • small volume
  • **IBD (UC, Crohns), infection, malignancy
52
Q

What are indications that diarrhea is osmotic/secretory?

A
  • watery
  • large volume
  • **Carbohydrate metabolism, VIPoma, carcinoid, laxatives, DM neuropathy, Meds, GI bypass, gastroporesis
53
Q

What are indications that diarrhea is malabsorptive?

A
  • fatty/floats
  • foul-smelling
  • bloating
  • **mucosal (Celiac) or maldigestive (Pancreatic insufficiency)
54
Q

What are risk factors for colorectal cancer?

A
  1. age
  2. adenomatous polyps
  3. hx of cancer/adenomatous polyps
  4. IBD (UC > Crohns)
  5. family hx (esp. if age s, Peutz-Jeghers, FJPC, HNC)
55
Q

What is Familial adenomatous polyposis

A

AD disease with hundres of adenomatous polyps in the colon and usually duodenum
(sometimes jejunum, ileum, and stomach)
Will get CRC by age 40
Treat with prophylactic colectomy

56
Q

What is Gardner’s syndrome?

A

Polyps with osteomas, dental abnomalities, benign soft tissue tumors, desmoid tumors, sebaceous cysts
Will get CRC by age 40

57
Q

What is Turcot’s syndrome?

A

AR

plyps plus cerebellar medulloblastoma or glioblastoma multiforme

58
Q

What is Peutz-Jeghers disease?

A

Single or multiple hamartomas scattered through GI tract
(small bowel > colon > stomach)
Associated with pigment spots around lips, oral mucosa, genitals, palmar surfaces
May have intussusseption or GI bleeding but low risk for CRC

59
Q

What is Reynold’s pentad?

What disease does it make you think of?

A
  • Fever
  • Jaundice
  • RUQ pain
  • Septic shock
  • altered mental status (CNS depression)
    (Charcot’s triat + septic shock and CNS depression)
    ***Severe Cholangitis
60
Q

What is Mallory-Weiss syndrome?

A

mucosal tear at GE junction from forecul vomiting or retching

  • associated with binge drinking in alcoholics
  • hematemesis (slight streaking to bright red blood)
61
Q

What is a Schatzki’s Ring?

A

Distal esophageal web: circumferential ring in lower esophagus with sliding hiatal hernia
- usually due to ingestion of substance in a suicide attempt (bleach, detergent, alkali, acids)

62
Q

Where is a Zenker diverticulum located?

A

Upper 1/3 of esophagus

63
Q

What is the Rome III criteria for IBS?

A
  1. recurrent abd pain/discomfort and changed bowel habits for >6mo
  2. sypmtoms atleast 3 days/mo for 3 months
  3. two or more of:
    - pain releived by bowel movement
    - onset of pain is related to a change in frequency of stool
    - onset of pain is related to a change in stool appearance
    * **recommend high fiber diet
64
Q

What are some symptoms of C.diff infection?

A
  • diarrhea (10-15 per day)
  • lower abd pain/tenderness
  • cramping
  • fever
  • leukocytosis
  • *high suspicion if previou Abx use
65
Q

What are symptoms of Crohn disease

A

Symptoms over a period of months or years:

  • abd pain
  • diarrhea
  • wt loss
66
Q

What are symptoms of diverticulitis?

A

-abd pain
- fever
- LLQ tenderness
- leukocytosis
- diverticula of the colon
**associated with age
NO PAIN OR DIARRHEA

67
Q

What are symptoms of ischemic colitis?

A

Self-limited symptoms: (usually within 48hrs)

  • LLQ pain
  • bloody diarrhea

Internal Med (6 decks)

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