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Clin Med 2 > GI Path and Phys > Flashcards

GI Path and Phys Flashcards

1
Q

What is the function of the stomach?

A

storage, grinding, mixing, digestions, acid secretion

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2
Q

What is the function of the exocrine pancreas?

A

digestions, HCO3- buffer

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3
Q

What is the function of the liver?

A

metabolism, detox

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4
Q

What is the function of the small intestine?

A

ABSORPTION

digestions

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5
Q

What is the function of the large intestine?

A

water reabsorption

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6
Q

What is the function of the gallbladder?

A

stores bile

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7
Q

For embryologic development, which structures arise from the foregut?

A

pharynx
esophagus
stomach
respiratory tract

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8
Q

For embryologic development, which structures arise from the midgut?

A

small intestine

primordium of live and pancreas

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9
Q

For embryologic development, which structures arise from the hindgut?

A

colon

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10
Q

What does the salivary gland produce and what is its function?

A

amylase

-digestion of starch

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11
Q

What does the stomach produce and what is its function?

A

pepsin
HCL
-digestion of proteins

Gastrin
Intrinsic Factor
-mediates absorption of vitamin B12

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12
Q

What does the small intestine produce and what is its function?

A

enterokinase
-activates pancreative enzymes

cholecystokinin
-stimulates GB contraction and pancreatic secretion of bicarbs

secretin
-stimulates secretion of pancreatic trypsin and chymotrypisin

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13
Q

Sialadenitis: infectious

A

infectious (viral or bacterial)
stap or strep viridans
obstruction

mumps (paramyoxviridae) - most common viral; children > adults

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14
Q

Sialadenitis: autoimmune

A

sjogren’s disease

xerostomia (dry mouth) and xerophthalmia (dry eyes) with enlargement of the salivary glands

destruction of the parenchymal cells affects their function and results in decreased production of saliva and tears

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15
Q

Salivary gland Neoplasms epi

A

W > M
all age groups –peak incidence in 6th - 7th decade of life

MC parotid gland –epithelial origin

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16
Q

What is the most common salivary gland to get neoplasms?

A

parotid gland

majority of salivary gland neoplasms are of epithelial origin, representing 80% to 90% of all neoplasms

75% benign

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17
Q

What is the most common benign neoplasms of the salivary glands?

A

pleomorphic adenoma

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18
Q

What is the most common malignant tumors of the salivary glands?

A

mucoepidermoid carcinoma

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19
Q

Which salivary glands are more likely to be benign and which ones are more likely to be malignant?

A

major salivary gland neoplasms –mc benign

minor salivary gland neoplasms – mc malignant

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20
Q

How long is the human esophagus?

A

25cm long

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21
Q

What is considered a definitive anatomic landmark for the tubular esophagus?

A

identification of a squamous duct and submucosal mucous glands

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22
Q

Achalasia

A

spasm of lower esophagus sphincter with esophageal dilation proximal to the site of spasm

pts present with dysphagia

typically idiopathic

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23
Q

What is the most common esophagitis?

A

reflux of gastric juice (“peptic esophagitis”), with pepsin and HCl leading to ulcerations and epithelial metaplasia

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24
Q

Esophageal atresia

A

lack of lumen, with or without esophagotracheal fistula

babies vomit ingested milk

without repair, babies die of hunger or aspiration PNA

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25
Q

What are the 2 types of hiatal hernias?

A

sliding vs paraesophageal

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26
Q

What is the most common cause of hiatal hernia?

A

reflux esophagitis

tone of LES can decrease d/t smoking and caffeine; pregnancy

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27
Q

What is a chemical cause of esophagitis?

A

Lye in suicide attempts

pts taking NSAIDs and not drinking water

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28
Q

What is the common cause of esophageal varices?

A

liver cirrhosis
or any disease causing portal HTN

among MC causes of UGI bleeds

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29
Q

What is a common cause of UGI bleeds?

A

esophageal varices

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30
Q

What is Mallory Weiss syndrome?

A

laceration of small vessels at GE junction during strenuous vomiting

MC in EtOHers

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31
Q

Who is more likely to have Mallory Weiss Syndrome?

A

pts with hx of severe vomiting

EtOHers

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32
Q

What is Barrett’s Esophagus?

A

characterized by the conversion of normal squamous epithelium of the esophagus into metaplastic columnar epithelium

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33
Q

What is the most common cause of Barrett’s esophagus?

A

chronic GERD

familial predispositions forBE and esophageal adenocarcinoma (EAC) has been documented in familial clusters

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34
Q

Epi of esophagus carcinoma

A

accounts for 4% of all cancers
M > W
correlates with EtOH + tobacco

bad survival

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35
Q

At dx of esophageal carcinoma, where is the tumor?

A

most have spread through adventitia to lymph nodes and adjacent organs

“locally invasive”

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36
Q

What is the most important developmental abnormality?

A

congenital pyloric stenosis

appears during neonate periods

M > F

projectile vomiting

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37
Q

What are causes of acute gastritis?

A

stress, shock, food, exogenous chemicals, drugs (aspirin)

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38
Q

What is peptic ulcer?

A

related to an underlying chronic gastritis (typically caused by H. pylori)

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39
Q

What does an H2 blocker do?

A

inhibits gastric sections and promotes healing in peptic ulcer pts

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40
Q

“Punched out round defects of the mucosa extending into deep layers”

A

macroscopic features of peptic ulcers

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41
Q

What are complications of peptic ulcer diseases?

A

hemorrhage (most common): hematemesis, melena, iron deficiency anemia
penetration into the pancreas: acute pancreatitis
perforation: peritonitis
cicatrization: stenosis after healing of ulcers leads to scaring

42
Q

Where are peptic ulcers most common?

A

duodenal 4x more common than gastric

43
Q

What age group presents with peptic ulcers?

A

depends on the type

gastric - >40 age
duodenal - any age

44
Q

When/how do peptic ulcers present?

A

pain 1-3 hrs after a meal or during the night

nausea, vomiting, weight or appetite loss, Melena, iron deficiency

45
Q

What are the clinical features of gastric carcinoma?

A

nonsepcific sxs - weight loss, anemia, weakness, vomiting, loss of appetite, dysphagia, bleeding

46
Q

Hirschsprung’s Disease

A

developmental abnormality in the innervation of the rectum and sigmoid colon
intramural ganglion cells don’t develop making the colon in permanent spams and thus fecal matter can’t pass –> megacolon

tx. resection and end-to-end anastomosis

47
Q

Atresia

A

developmental abnormality
complete obstruction of the lumen of the intestine
tx. end-to-end anastomosis

48
Q

Congenital diverticula

A

out pouchings of the intestine

the best known one is MECKEL’S DIVERTICULUM

49
Q

Meckel’s Diverticulum

A

a congenital diverticula
incompletely obliterated omphalomesenteric duct –connection between small intestine and umbilicus
sxs similar to acute appendicitis but w/ LLQ pain instead

50
Q

older pts with chronic constipation

A

think diverticulosis

51
Q

Where are the most significant diverticuli?

A

sigmoid colon

commonly occur at point of arterial entry through muscle

52
Q

Hemorrhoids

A

varicosities of the anal and perianal region

5% of adults

53
Q

What determines if a hemorrhoid is internal or external?

A

the anorectal line
above = internal
below = external

i think you can have internal hemorrhoids protrude outside of the anus

54
Q

Hemorrhoids are associated with what?

A

lower extremity varicose veins

some hereditary component of looseness of connective tissue

commonly seen in pregnant pts

55
Q

Angiodysplasia

A

localized vascular lesion of the colon (cecum and ascending colon MC)
in elderly pt

56
Q

unexplained rectal bleeding

A

think about angiodysplasia (these can rupture)

especially if the pt is older

57
Q

Mesenteric thrombosis

A

MC in elderly pts

thrombosis of mesenteric vessels - MC superior mesenteric artery

frequently a complication of atheroscleorsis

58
Q

Common infectious pathogens of the small-intestine

A

E. coli
vibrio cholerae
giardia lambila
rotavirus

59
Q

Common infectious pathogens of the large-intestine

A

E. coli
shigella
Norwalk virus
Entamoeba

60
Q

How does the diarrhea differ between small and large intestine?

A

small intestine

  • large volume
  • watery appearance
  • rarely ever blood

large intestine

  • small volume
  • mucoid appearance
  • commonly blood
  • +/- leukocytes
    • proctoscopy
61
Q

What is the MC pathogen causing pseudomembranous colitis?

A

> 90% of cases = C. difficile

62
Q

What causes the diarrhea in pseudomembranous colitis?

A

the c.diff bacteria makes exotoxin that acts on epithelial cells causes necrosis and superficial ulcers

63
Q

Strawberry gallbladder

A

cholesterolosis

d/t cholesterol

64
Q

What are the 4 Fs of cholelithiasis?

A 
risk factors 
Female
Fat
Fertile
Forties
65
Q

What can cholelithiasis cause?

A

cholecystitis
pancreatitis
gall bladder carcinoma

66
Q

What is the most common composition of gallstones?

A

cholesterol

67
Q

pigment stones

A

derived from hemoglobin/bilirubin

68
Q

Rokitansky-Aschoff sinuses

A

hallmark of chronic cholecystitis

69
Q

Lipase

A

produced exclusively by the pancreas

used to breakdown fat

70
Q

Common causes of acute pancreatitis?

A

EtOH
Gallstones
Idiopathic

71
Q

Hallmark of acute pancreatitis

A

necrosis (not fat necrosis)

72
Q

What is the vast majority of lesions in the pancreas?

A

pseudocysts

73
Q

Pancreatic Neoplasms

A

most are malignant

more commonly exocrine derived from the ductal system

74
Q

What is the 4th major cause of cancer death in men and women?

A

adenocarcinoma of pancreas

75
Q

Epi of adenocarcinoma of pancreas

A

rare before age of 40
incidence increases with age
4th major cause of cancer death in men and women
prognosis is poor (most die within 2 years)

76
Q

Where are ductal adenocarcinoma most common?

A

60-70% in the head (upper half)

77
Q

Courvoisier

A

painless jaundice
tumor in the head
seen with ductal adenocarcinoma

78
Q

How do you dx ductal adenocarcinoma?

A

ERCP

endoscopic retrograde cholangiopancreatography

79
Q

What predicts the survival of adenocarcinoma?

A 
size 
site
stage
margins
recurrence
80
Q

Acinar cell carcinoma

A 
very rare (more rare than ductal carcinoma) 
worse prognosis --present metastatic typically

7th generation
M&raquo_space; F

81
Q

Where do pancreatic endocrine neoplasms arise from?

A

arise from the ducts

82
Q

What is the 6th leading cause of death?

A

diabetes

83
Q

When does gluconeogenesis occur?

A

once glycogen stores are depleted–synthesized from amino acids

84
Q

What produces insulin?

A

Beta cells in the pancreatic islets
as pro-insulin

when needed they are cleaved into insulin and inactive C-peptide

85
Q

What is the half life of insulin?

A

4 minutes

86
Q

Which type of diabetes has sweet urine?

A

DM

87
Q

Type 1 vs Type 2 DM?

A

Type 1 - insulin dependent

Type 2 - non-insulin dependent

88
Q

What is the pathophys behind type 1 DM?

A

autoimmune destruction of islets so no production of insulin

89
Q

How does glucose get into the cell?

A

with the help of insulin

90
Q

How does glucose leave the cell?

A

glucagon, epinephrine, cortisol, growth hormone

91
Q

What age group is most common for type 2 DM?

A

> 40 years

92
Q

Honeymoon period

A

in adult pt dx with type 1 have this period in which they are still producing insulin, and might not need insulin for a few years

93
Q

Amyloid deposition

A

can be seen with DM type 2

94
Q

Family history is more prominent with type 1 or type 2 DM?

A

Type 2 surprisingly

95
Q

How does the speed of onset differ between type 1 and type 2 DM?

A

Type 1 is sudden onset while 2 is gradual

96
Q

Antibodies to islet cells

A

seen in DM type 1

97
Q

Gestational Diabetes

A

hyperglycemia developing during pregnancy

leads to neonate hypoglycemia and bigger birth weights

these babies have a 50/50 chance of developing DM type 2 later in life

98
Q

What should a random glucose reading be?

A

<200 mg/dL

99
Q

What should a normal fasting glucose reading be?

A

<126 mg/dL

100
Q

What is a normal hemoglobin A1c?

A

<6.5%

101
Q

_____ is required for fat absorption?

A

Emulsification

102
Q

What enzyme is produced in the intestinal mucosa?

A

enteropeptidase/
enterokinase

substrate: trypsinogen

Clin Med 2 (13 decks)

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