(GI!) Panic Deck Flashcards

1
Q

Describe the structures of the foregut

A

esophagus –> first half of duodenum, including accessory organs

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2
Q

Describe structures of midgut

A

second half of duodenum –> first 2/3 of transverse colon

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3
Q

Describe structures of hindgut

A

Last 1/3 of transverse colon –> upper anal canal

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4
Q

Describe arterial supply to the fore-, mid-, and hindgut

A
Fore = Celiac a
Mid = Superior mesenteric a
Hind = Inferior mesenteric a
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5
Q

Where are the sympathetic preganglionic cell bodies for the fore-, mid-, and hindgut located?

A
Fore = T5-T9
Mid = T19-T12
Hind = T12 - L2
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6
Q

What are the sympathetic splanchinc nerves for fore-, mid-, hindgut?

A
Fore = Greater
Mid = Lesser
Hind = Least
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7
Q

What are the preaortic ganglions for sympathetic innervation to the fore-, mid- and hindgut?

A
Fore = Celiac
Mid = Superior mesenteric
Hind = Aortico-renal***
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8
Q

What paths do sympathetic axons to the fore-, mid-, and hind-gut follow?

A
Fore = Celiac artery
Mid = Superior mesenteric a
Hind = Infeior mesenteric a
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9
Q

Describe the location of the preganglionic cell bodies, the nerve, and the ganglia location for parasympathetic innervation to the fore, mid, and hindgut

A

Fore and Midgut share PNS innervation patterns:
Preganglionic cell bodies in the brainstem; CN X; ganglia in organ walls

Hindgut is slightly different:
Preganglionic cell bodies in S2-S4; pelvic splanchnic n.; ganglia in organ walls

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10
Q

What is the cellular change that occurs in Barrett’s esophagus?

A

Cells change from stratified squamous epi –> simple columnar, producing mucous to try to protect from acid

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11
Q

What are the portal-caval anastamoses that occur in esophageal varices?

A

L gastric (branch of portal) + azygos (branch of SVC)

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12
Q

What are the portal-caval anastamoses that are present in Caput Medusae?

A

Paraumbilical vv + throacoepigastric + superior epigastric (branch of portal) and inferior epigastric (branch of IVC)

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13
Q

What is the deficient enzyme in non-classical galactosemia?

A

Galactokinase

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14
Q

What product accumulates in non-classical galactosemia?

A

Galactose

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15
Q

What is the deficient enzyme in classical galactosemia?

A

Galactose-1-phosphatase

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16
Q

What product accumulates in classical galactosemia?

A

Hepatotoxic galactose-1-phosphate

17
Q

What is the route intermediates that accumulate in non/classical galactosemia take?

A

Polyol pathway –> cataracts, kidney damage

18
Q

What is the deficient enzyme in fructose intolerance?

A

Aldolase B

19
Q

What product accumulates in fructose intolerance?

A

Fructose-1-phosphate (hepatotoxic)

20
Q

What is responsible for the unpleasant effects of drinking alcohol?

A

Acetaldehyde

21
Q

What systems are responsible for the metabolism of alcohol?

A

Alcohol dehydrogenase and, in heavy drinking, MEOS

22
Q

What is the intermediate produced by the metabolism of alcohol?

A

Alcohol –> acetaldehyde via alcohol dehydrogenase and/or MEOS

23
Q

How is acetaldehyde metabolized?

A

Aldehyde dehydrogenase –> acetate

24
Q

What ratio is disrupted in alcohol metabolism, and what effects does this have?

A

Low NAD+ (consumed during metabolism with no regulation)
High NADH

Alters hepatic metabolism:

  • B-oxidation of fatty acids is inhibited (steatosis, hyperlipidemia)
  • TCA cycle is inhibited (ketoacidosis)
  • Lactate can’t be converted to pyruvate in liver (lactic acidoses, hypoglycemia, hyperuriecmia)
25
Q

What enzyme is deficient in Maple Syrup Urine Disease?

A

Alpha-keto acid dehydrogenase (accumulation of alpha-keto acids)

26
Q

What is the deficiency in PKU?

A

Phenylalanine hydroxylase or its cofactor, tetrahydrobioterin