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Clin Med II > GI General > Flashcards

GI General Flashcards

1
Q

How long does it take for food to get from your mouth to the bottom of the esophagus?

A

10 seconds

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2
Q

How long does it take for food to get from your mouth to exit the stomach?

A

1-3 hours

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3
Q

How long does it take for food to get from your mouth to the end of the small intestine?

A

7-9 hours

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4
Q

How long does it take for food to get from your mouth to the large intestine?

A

25-30 hours

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5
Q

How long does it take for food to get from your mouth to excretion?

A

3-5 days (30-120 hrs)

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6
Q

What are the modalities for GI regulation?

A

endocrine-stimuli associated with meal
neurocrine- connections to CNS and enteric nervous system
paracrine- local mediators

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7
Q

What happens when the parasympathetic nerves (enteric neurons) are stimulated?

A

cause general increase in activity of entire enteric nervous system which enhances GI functions

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8
Q

What happens when the sympathetic nerves in GI tract are stimulated?

A

inhibition of activity in GI tract
inhibition of smooth muscle fn
excitation/contraction of sphincters

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9
Q

Actions of Ach in GI function

A 
contraction of smooth muscle in wall
relaxation of sphincters
↑ salivary secretion
↑ gastric secretion
↑ pancreatic secretion
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10
Q

Actions of NE in GI function

A

relaxation of smooth muscle in wall contraction of sphincters
↑ salivary secretion

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11
Q

Actions of vasoactive intestinal peptide (VIP) in GI function

A

relaxation of smooth muscle
↑ intestinal secretion
↑ pancreatic secretion

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12
Q

Action of gastrin-releasing peptide (GRP) in GI function

A

↑ gastrin secretion

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13
Q

Stimulus for gastrin release

and site of production

A

AA and stomach distension
↓ with low pH
site: stomach

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14
Q

simuli and site of production for cholecystokinin

A

AA/FA

site: small intestine

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15
Q

simuli and site of production for secretin

A

H+/FA

site: small intestine

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16
Q

simuli and site of production for GIP

A

AA/FA/carbs

site: small intestine

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17
Q

simuli and site of production for motilin

A

↓ with feeding

site: small intestine

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18
Q

Macronutrients → absorptive units

carbohydrates →
proteins →
lipids →

A

carbohydrates →monosaccharides (glucose, fructose, galactose)
proteins → di and tri-peptides
lipids → monoglycerides and fatty acids

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19
Q

What do pepsins (pepsinogens) digest and how are they activated?

A

proteins and polypeptides

activated by HCl in the stomach

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20
Q

What does enteropeptidase/enterokinase digest and where is it excreted?

A

tyrpsinogen

excreted: intestinal mucosa

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21
Q

What does trypsin (tyrpsinogen) digest and how is it activated?

A

proteins and polypeptides

activated by enteropeptidase/enterokinase in exocrine pancreas

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22
Q

What does collipase (procolipase) digest and how is it activated?

A

fat droplets

activated by trypsin in exocrine pancreas

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23
Q

What does pancreatic lipase digest and where does it come from?

A

triglycerides

comes from exocrine pancreas

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24
Q

What does pancreatic amylase digest and how is it activated?

A

starch

activated by Cl- in exocrine pancreas

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25
Q

Where is iron and calcium absorbed?

A

duodenum

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26
Q

where are carbohydrates absorbed?

A

upper part of small intestine

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27
Q

where are fats and proteins absorbed?

A

throughout small intestine

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28
Q

where are bile salts and vitamin B 12 absorbed?

A

ileum

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29
Q

What is receptive relaxation?

A

the act of swallowing causes neurotransmitters too send signals to relax lower esophageal sphincter and stomach fundus

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30
Q

Define achalasia

A

inability of LES to relax during swallowing

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31
Q

What anatomical dysfunction allows for gastric reflux to occur

A

↓ LES tone

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32
Q

What is stimuli for gastrin release?
what is its effect?
inhibitory stimuli?

A

small peptides, AA, stomach distention, vagal stimulation-GRP
effect: H+ secretion
inhibitory-secretin H+ feedback loop

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33
Q

Rank rate of gastric emptying from slowest to fastest for proteins, carbs and fats

A

fat < protein < carb

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34
Q

Gastric pressures seldom rise above the levels that breach the lower esophageal sphincter even when the stomach is filled with a meal due to what process?

A

receptive relaxation

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35
Q

What is the major function of the duodenum?

A

neutralization to inactivate pepsin
biliary secretion
pancreatic secretion

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36
Q

What cells secrete secretin and why?

A

S cells of duodenum stimulated by H+ and fatty acids to increase pancreatic secretions of bicarb

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37
Q

What cells secrete cholecystokinin and why?

A

I cells of duodenum and jejunum stimulated by fatty acids and AA to increase pancreatic secretions and stimulate gallbladder to contract and inhibit gastric emptying

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38
Q

What is the 3rd MC cancer of internal organs?

A

carcinoma of large intestine

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39
Q

What is fn of fenestrated endothelium?

A

lines capillary sinusoids and provides easy access of nutrient delivery to hepatocytes

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40
Q

What is the fn of Kupffer cells within capillary sinusoids?

A

uniquely positioned to remove bacterial toxins coming from gut and to clear circulating Ag-Ab complexes

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41
Q

What is the function of Stellate cells within space of Disse?

A

fibroblasts activated to myofibroblasts
store Vit A
produce collagen, impt in scar formation during liver damage

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42
Q

What does LFT consist of?

A

bilirubin, albumin

Add: prothrombin time

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43
Q

What is included in hepatic panel?

A 
bilirubin
AST
ALT
AlkP
Albumin
Prothrombin time
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44
Q

If a patient is treated with a broad-spectrum antibiotic for several days or more, what might happen to the color of the stool – and why?

A

lighter bc bacteria are not there to conjugate bilirubin

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45
Q

What happens to albumin with liver injury?

A

decreases

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46
Q

What happens to prothrombin time with liver injury

A

increases

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47
Q

What clotting factors are affected by the liver?

A

1, 2, 5, 7, 9, 10

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48
Q

What is HL of albumin?

HL of prothrombin time?

A

albumin 20 days

prothrombin time ~6 hours

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49
Q

What happens to AST and ALT with liver injury?

A

increases
ALT>AST in most cases of liver inj

If alcohol related inj, cirrhosis /malnutrition or sudden acute liver necrosis → AST>ALT

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50
Q

What is HL of AST?

HL of ALT?

A

AST 8 hrs (mitochondrial AST is 10 days)

ALT 48 hrs

51
Q

What enzyme do we use to evaluate the biliary tract?

What is its HL?

A

alkaline phosphatase (AlkP)

HL 7 days

can also arise from bone, placenta, reticuloendothelial cells, intestine, kidney

52
Q

What tests do you use to detect cholestasis?

A

bilirubin
alkP
GGT

53
Q

What is jaundice usually due to?

A

hepatobiliary disease

54
Q

If urine is dark like tea what can it be?

A

blood (hemolysis)- if unconjugated bili

direct bilirubin- if conjugated (obstruction)

55
Q

What are causes of ↑ unconjugated bilirubin?

A

↑ RBC degradation
↓ albumin-bilirubin binding
↓ Hepatocyte internalization
↓ bilirubin conjugation (gilbert’s disease)

56
Q

What are causes of ↑ conjugated bilirubin?

A

↓ bilirubin excretion from liver-

cholestasis

57
Q

What causes increase in peritoneal fluid in cirrhosis?

A

low albumin
high portal HTN
renal retention
INC renin causing Na retention

58
Q

What is Child’s A for liver cirrhosis severity?

A

no abnormal parameters

~40 mos survival

59
Q

What is Child’s B for liver cirrhosis severity?

A

1-2 abnormal parameters

~32 mos survival

60
Q

What is Child’s C for liver cirrhosis severity?

A

> 2 abnormal parameters

~8 mos survival

61
Q

What parameters are considered for child-pugh’s severity score for cirrhosis?

A 
encepalopahty
ascites
bilirubin
albumin
prothrombin ratio
62
Q

When is patient considered for liver transplant with cirrhosis?

A

when they have approximately <1 yr survival

63
Q

What is MELDs score based on?

A

serum creatinine
bilirubin
INR prothrombin time

<10 is >1 yr survival
11-25 50% 1 yr survival
>25 <1 yr survival

64
Q

What are contraindications to liver transplant?

A

systemic infection or AIDS (HIV alone is not an absolute contraindication)
severe cardiopulmonary disease
metastatic malignancy

65
Q

What are the 3 criteria for the histopath grade of chronic hepatitis?

A
  1. Amount of lymphocytic infiltrate
  2. Amount of lobular necrosis and apoptotic bodies
  3. Amount of periportal necrosis
66
Q

What is the best gauge of diarrhea?

A

stool mass (>250 g)

also 70-95% water
>2x daily

67
Q

What is the foregut composed of?

A

pharynx, esophagus, stomach, respiratory tract

68
Q

What is the midgut composed of?

A

small intestine, primordium of liver and pancreas

69
Q

What is the hindgut composed of?

A

colon

70
Q

What does the Salivary Gland secrete and what is its fn?

A

Amylase

Fn: Digestion of starch

71
Q

What does the stomach secrete and what is its fn?

A

Pepsin & HCL→digest proteins

Gastrin Intrinsic Factor →mediates absorption of vit B12

72
Q

What does the small intestine secrete and what is its fn?

A

Enterokinase →activates pancreatic enzymes

Cholecystokinin →Stimulates GB contraction &pancreatic secretion of bicarbs

Secretin→Stimulates secretion of pancreatic trypsin and chymotrypsin

73
Q

The 3‐cm segment of proximal esophagus at the level of the cricopharyngeus muscle (15 to 18 cm from the incisors) is referred to as the

A

upper esophageal sphincter

74
Q

The 2‐ to 4‐cm segment just proximal to the anatomic GEJ (at 36 to 40 cm from the incisors), at the level of the diaphragm, is referred to as the

A

lower esophageal sphincter

75
Q

Dysphagia

A

difficulty swallowing

76
Q

What is the MC benign salivary gland tumor

A

Pleomorphic Adenoma

77
Q

What is the MC malignant salivary gland tumor

A

Mucoepidermoid Carcinoma

78
Q

What is MC type of carcinoma in upper and middle esophagous?

lower?

A

U & M = SCC

lower= adenocarcinoma

79
Q

How is insulin produced?

A

by β-cells in pancreatic islets as proinsulin → cleaved to insulin and inactive C-peptide

80
Q

How much does Hgb A1c increase for every 30 mg/dL rise in serum glucose?

A

1%

81
Q

Difficulty transferring food from the mouth to the upper esophageal sphincter

A

Oropharyngeal dysphagia

82
Q

Difficulty with the passage of ingested material from the hypopharynx to the stomach

A

Esophageal dysphagia

83
Q

Painful swallowing

A

odynophagia

84
Q

What does odynophagia usually represent?

A

inflammatory process

85
Q

Effect of H. pylori infection in duodenal antrum

A

increased gastric acid secretion from G cells which can cause gastric metaplasia in the duodenal bulb and colonization of these islands by H pylori leads to duodenitis or duodenal ulcers

86
Q

Effect of H. pylori infection in gastric body

A

decreased acid secretion as the chronic inflammation overwhelms the gastric mucosal defense mechanisms

87
Q

What is required for fat absorption?

A

emulsification

88
Q

What is the principal digestive enzyme in the stomach?
What activates it?
What are substrates?

A

Enzyme- pepsins (pepsinogens)

Activator- HCl

Substrates- Proteins and polypeptides

89
Q

What is the principal digestive enzyme in the intestinal mucosa?
What are substrates?

A

Enzyme- nteropeptidase/ enterokinase

Substrates-Trypsinogen

90
Q

What are the pancreatic digestive enzymes

A

Trypsin (trypsinogen)
Colipase (procolipase)
Pancreatic lipase
Pancreatic lipase

91
Q

Activator and substrates for Trypsin (trypsinogen)

A

Activator- Enteropeptidase/ enterokinase

Substrates- Proteins and polypeptides

92
Q

Activator and substrates for Colipase (procolipase)

A

Activator- Trypsin

Substrates- Fat droplets

93
Q

Substrates for Pancreatic lipase

A

Substrates- Triglycerides

94
Q

Activator and substrates for Pancreatic -amylase

A

Activator- Cl-

Substrates- Starch

95
Q

What does Migrating Motor Complex (MMC) do?

A

During fasting, sweeps periodically along the length of the stomach and small
intestine to clear them of undigested residues

96
Q

What is bile acid composed of?

A

Cholic acid and chenodeoxycholic acid

97
Q

What are micelles?

A

detergents formed by bile acids that emulsify the products of lipid digestion so fats can be absorbed

98
Q

What stimulates the gallbladder to contract after a meal?

A

CCK (also causes relaxation of sphincter of Oddi)

99
Q

Color of biliverdin?

unconjugated bilirubin?

A

biliverdin- green

unconjugated bilirubin- yellow

100
Q

What causes neonatal jaundice?

A

↓ UDP glucuronyl transferase

101
Q

Where does absorption of nutrients and electrolytes occur?

secretion?

A

abs- SI at villus tip (NaCl, nutrients)

sec- crypt (Cl-)

water follows Cl-

102
Q

What intestinal immunity defense do we have against GI infection?

A

Secretory IgA: lamina propria plasma cells
Mucosa-associated lymphoid tissue (MALT): Peyer’s patches
Phagocytes

103
Q

Enterotoxins

A

direct effect on intestinal mucosa to elicit net fluid & electrolyte secretion

Increased production of cAMP or cGMP

Classic = cholera toxin, E. coli LT and ST toxins

104
Q

Cytotoxins

A

mucosal destruction

Shiga toxin” – E. coli
Shigella dysenteriae
Clostridium difficile toxin B

105
Q

Neurotoxins

A

pre-formed toxins

Act on autonomic nervous system

Acute N/V/D within hours of ingestion

“Food poisoning” by Staph aureus, Bacillus cereus, Clostridium botulinum

106
Q

What bacteria has ability to adhere to and colonize mucosa

A

E. coli

107
Q

What bacteria invade and destroy epithelial cells?

A

Shigella, Salmonella

108
Q

What tests are true measures of liver function, becoming abnormal when liver cell function is impaired?

A

Bilirubin
Albumin
Prothrombin Time

109
Q

When is Unconjugated bilirubin increased?

A

hemlysis

110
Q

When is conjugated bili increased?

A

hepato-biliary disease

111
Q

What happens to albumin with liver inj?

PT time?

A

albumin decreases

PT increases

112
Q

When do alanine(ALT) aspartate(AST) increase?

A

injury to hepatocyte membrane allows release

113
Q

What is the only abnormality in majority of persons with liver disease?

A

Elevated liver enzymes

114
Q

What causes jaundice?

A

bilirubin excess

visible in adults > 2x normal
Visable in neonates > 5x normal

115
Q

What happens to urine and stool with hepatobiliary disease?

A

dark tea colored urine (urine bilirubin)

light stools (no stool pigments unless bilirubin reaches gut)

116
Q

What causes Cholestasis

A

static bile flow, due to biliary obstruction or hepatocyte loss of function

117
Q

What is the preferred site of absorption of iron and folate?

A

Duodenum

118
Q

Where does > 90% of nutrient absorption occur?

A

Jejunum

119
Q

Where is the site of vitamin B12 and bile salt absorption?

A

Ileum

120
Q

What are Manifestations of Malabsorption?

A 
Abdominal distension, flatulence
Anemia
Kidney stones
Peripheral neuropathy
Bone pain, osteomalacia, fractures
dermatitis
121
Q

What happens instead of losing carbs that are malabsorbed?

A

absorbed in the colon as short chain fatty acids

122
Q

What occurs as a result of Small Ileal Resection?

A

Fat Malabsorption
Significant bile malabsorption
Result is secretory diarrhea

123
Q

How do you test for CHO Malabsorption?

A

Malabsorbed CHO reaches intraluminal bacteria and H2 is produced, absorbed and measured in exhaled air

124
Q

How do you test for SBBO?

A

Lactulose is ingested (non-absorbable CHO) to test for SBBO. Excess H2 is exhaled and measured

Clin Med II (19 decks)

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