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Physio II (mine) > Hepatobiliary and GI Function > Flashcards

Hepatobiliary and GI Function Flashcards

1
Q

Progression steps of digestion

Mouth to anus

A
  1. Mouth: taste, chewing, bolus formation
  2. Esophagus: transport
  3. Stomach: Storage, grinding, mixing, digestion, acid secretion
  4. Small intestine: digestion, absorption
  5. Large intestine: fluid and electrolyte absorption
  6. Rectum: Storage and excretion
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2
Q

Accessory organs to digestions

A

Pancreas: Digestions and HCO3- buffer
Liver: Metabolism, detoxification, bile formation
Gallbladder: Bile Storage

Pancreas buffers stomach acid / Bile helps digest lipids

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3
Q

Transit time of food to excretion

A
  • Esophagus transit time: 10 s
  • Time to small intestine: 1-3 h
  • Time to ileocecal valve: 7-9 h
  • Time to decending colon: 25-30 h
  • Excretion: 30 h
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4
Q

what are the 5 functions of the liver?

A

carb metabolism
synthesis of plasma proteins
synthesis of lipoproteins
immunity
inactivation of toxins

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5
Q

what is the liver triad?

A
  • hepatic artery
  • portal vein
  • bile duct
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6
Q

what does the liver do for immunity?

A

kupffer cells produce lymph

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7
Q

liver blood supply

A

25% from celiac artery
75% from portal vein (drains from GI system)

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8
Q

how much blood pools in the liver

A

10%, 500mL

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9
Q

how much nutrients does the liver take (first pass)

A

1/3-1/2 of nutrients

not fat or suppositories

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10
Q

How to avoid first pass effect?

Different ways to administer drugs?

A

Topical
Inhaled
Sublingal
Injectable

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11
Q

Liver metabolism: Lipids

A
  • Fatty acid oxidation: Acetyl-CoA
  • Ketone formation: (Keto acidosis)
  • Synthesize lipoproteins, cholesterol, phospolipids
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12
Q

Liver metabolism: Carbs

A
  • Glucogenesis (Amino Acids)
  • Glycogensis (glycogenolysis)
  • Hormonal control of glucose release
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13
Q

Liver metabolism: Proteins

A
  • Synthesizes plasma proteins
    • Cirrhosis decreases albumin and clotting factors
    • Increase of unbound fraction of drugs (larger impact systemically)
  • Urea
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14
Q

Liver metabolism on anesthesia

A

Surgery is stressful. Relases of catecholamines, glucagon, and cortosol. Results in mobilization of carb and protein storage causing hyperglycemia and negative nitrogen balance

Iso and Sevo increase blood glucose levels, Propofol does not (lipid based)

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15
Q

Liver and Urea Recycling

A
  1. Deamination = Ammonia (NH3) [85% enters via portal circulation]
  2. Uptake and Ureagenesis
  3. GFR (75% of systemic flow after exit from liver)
  4. GI (25% of systemic flow after exit from liver) Ammonia and Ammonium Ion (NH4)
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16
Q

Liver detox

What toxins? MIDCAP-MF

A

Metabolic end products
Insecticides
Drugs
Contaminants / Pollutants
Alcohol
Pesticides
Mico-organisms
Food additives

*fat-soluble

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17
Q

Liver Detox: Phase 1

A

P450’s

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18
Q

Liver Detox: Phase 2

A

conjugation

ionize, to make water soluble

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19
Q

Liver Detox: Waste Products

Two paths of elimination

A
  1. Gallbladder→Bile→Stool
  2. Kidneys→Urine
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20
Q

Bilirubin production and excretion

A
  • Hemoglobin degraded to bilirubin by the reticuloendothelial system
  • Bilirubin is carried in circulation by albumin (bound to it)
  • Hits liver: bilirubin is conjugated with glucuronic acid by UDP glucuronyl transferase
  • Part of the conjugated bilirubin (glucuronide and bilirubin sulfate) is H2O soluble and excreted into bile
  • In the intestine conjugated bilirubin is converted to urobilinogen
  • 18% returned to the liver via the enterohepatic circulation then excreted in urine as urobilin (2%)
  • 80% is excreted in feces as urobilin and stercobilin
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21
Q

Obstructive / Conjugated / Direct

A

Bulirubin in Plasma? Yes
Bilirubin in Urine: Yes
Hepatobiliary dx (Cholestasis)

obstruction of the bile ducts, can not be released into the digestive tract

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22
Q

Hemolytic / Unconjugated / indirect

A

Bilirubin in plasma? Yes
Bilirubin in Urine? No
Impaired conjuction or overproduction

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23
Q

Albumin and bilirubin

A

Unconjgated bilirubin tighhtly binds to albumin creating an excess in the system

Conjugated bilirubin does not bind as tightly therefore can be excreted in the urine

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24
Q

Markers of liver inflammation / injury

A
  • Asparate transaminase (AST)
  • Alanine transaminse (ALT)
  • Alkaline Phosphatase (AP)
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25
Q

Markers of liver function

A
  • Total bilirubin
  • Albumin
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26
Q

Most liver disease lab values

A

ALT > AST

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27
Q

Alcholic liver disease lab values

A

AST > ALT

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28
Q

Gallbladder disease lab values

A

AP +/- TB

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29
Q

Cirrhosis / Ascites loop

A

Cirrhosis causes:
* Lowered albumin which lowers colloid oncotic pressure (pushes fluid out)
* Increased liver sinusoids resistance which increases portal pressure
* This causes fluid loss and decreased venous return
* This increases RAAS and ADH to compensate for hypovolemia
* Increases BP which pushes out more fluid…cycle continues

Bam ascites

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30
Q

what are the three things that control GI blood supply

A

arteriole control (vasodilators)
ANS command (PNS and CNS)
local events

local events, metabolic and myogenic mechanisms

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31
Q

what are the vasodilators for the GI arterioles?

A

NO
VIP
Ach
Substance P

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32
Q

when you are in shock what does that do to your absorption

A

ischemic villus (impaired)

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33
Q

what are the two local events that can change blood supply?

A

metabolic (changes in oxygen)

myogenic (stretch/tension)

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34
Q

Three control machanisms of GI function

A
  1. Hormonal regulation
  2. Neurogenic Innervation
  3. Myogenic pacing
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35
Q

Hormonal regulation of GI tract

A
  • Endocrine
  • Paracrine (can effect neighbor cells, chain reaction)
  • Exocrine
36
Q

Neurgenic Innervation of the GI tract

A
  • Extrinsic (Autonomic NS)
  • Intrinstic (Enteric NS)
37
Q

Myogenic pacing of the GI tract

Autonomous smooth muscle contractions

A
  • Pacemaker activity
  • electrical coupling
38
Q

GI Hormone: Gastrin

A

Source
* G Cells (antrum stomach, duodenum)

Stimulation:
* Peptides / Amino Acids
* Distention of stomach
* Vagal Stimulation (GRP)

Action
* Increased gastric acid (H+)
* Increased growth of gastric mucosa (to protect stomach lining)
* Increased gastric motility (emptying)

GRP = Gastrin releasing peptide

39
Q

GI Hormone: CCK

CCK: Cholecystokynin

A

Source:
* I Cells (duodenum and jejunum)
Stimulation:
* Peptides / Amino Acids
* Free Fatty Acids
Action:
* Increased gallbaldder contraction / relaxation of sphicter of Oddi
* Increased pancreatic enzyme / HCO3- sectretion (weaker than secretin)
* Increased trophic effects on pancreas and galbladder
* Decreased gastric emptying

40
Q

GI Hormone: Secretin

“Natures antacid”

A

Source:
* S Cells (duodenum and jejunum)
Stimulation:
* H+ (pH under 4.5)
* Free Fatty Acids
Action:
* Increased pancreatic and biliary HCO3- secretion
* Increased trophic effects on pancreas
* Decreased gastic acid (H+)
* Decreased growth of gastic mucosa

41
Q

GI Hormone: GIP (GLIP) / GLP

A

Source:
* GIP = K Cells (duodenum and jejunum)
* GLP = L Cells (duodenum and jejunum)
Stimulation:
* Oral glucose
* Peptides / Amino Acids
* Free Fatty Acids
Actions
* Increased pancreatic insulin secretion
* Decreased gastic acid (H+)

42
Q

GI Hormone: Motilin

A

Source:
* M-Cells (duodenum and jejunum)
Stimulation:
* Neural
* Decreased vagus signaling (fasting)
Action:
* Increased migrating motor complex during fasting to clear excess debris from GI system
* Helps prevent small intestinal bacterial overgrowth (SIBO)

43
Q

GI Hormone: Somatostatin

A

Source:
* Delta Cells (D Cells) from pancreatic islets and GI mucosa
Stimulation:
* Acid (H+)
Action:
* Decrease release of GI hormones (Gastrin, CCK, Secretin, GIP etc)
* Decreased gastric acid (H+)
* Decreased pacncreatic enzyme / HCO3- release
* Decreased gallbladder contractions

Off switch for GI tract, fight or flight mode

44
Q

GI Neurotransmitter: NE

A

Sympathetic innervation
* Decreased motility
* Decreased secretions
* Increased constriction of sphincters
* Vasoconstriction

45
Q

GI Neurotransmitter: ACh

A

Parasympathetic / Enteric
* Increased motility
* Increased secretions
* Decreased constriction of sphincters
* Vasodilation

46
Q

GI Neurotransmitter: VIP

A

Enteric
* Increased smooth muscle relaxation

47
Q

GI Neurotransmitter: GRP

A

Enteric
* Increased gastrin secretion

48
Q

An increase in sympathetic activity does what?

GI Tract

A

Slows digestion and absoption

49
Q

An increase in parasympathetic activity does what?

Gi Tract

A

Promotes digestion and absoption

50
Q

What are ICC cells

A
  • Interstital Cells of Cajal
  • Pacemaker cells of the gut
  • Partially innervated by Enteric NS but not a part of it
51
Q

Myogenic pacing via BER

Basal Electrical Rhythm aka slow waves

A

Always there at a slow pace and low rate
On graph depole is spikes

More spikes = more contractions

52
Q

does sympathetic or parasympathetic make saliva more protein rich?

A

sympathetic

53
Q

Which system produces more saliva? Symp or Parasymp?

A

Parasympathetic

54
Q

Saliva formation

A
  • Interstitial fluid (isotonic) flows into acinar cells
  • While it flows along ductal cells electrolytes flow in and out
  • In: K+ and HCO3- (concentration verse plasma? increased)
  • Out: NA+ and Cl- (concentration verse plasma? decreased)
  • Saliva is secreted (hypotonic)
55
Q

what 3 things stimulate gastric acid (HCl) release?

A

ECL Cells (Histamine): Strongest
ACh (Vagus): Strong
G cells (Gastrin): Weakest

56
Q

What two things inhibit gastric acid?

A
  1. Somatostatin
  2. Prostaglandins
57
Q

What recepors are used for gastric acid release?

A
  • Vagus→ACh→M3
  • G cells→Gastrin→CCK-B
  • ECL Cells→Histamine→H2
58
Q

All three work together to secret gastric acid. How?

ACh / Histamine / Gastrin

A

Vagal - ACh
* Release is stimulated by sight and smell
* Reflexivity to stomach stretch (vago-vagal)
* Parietal Cell + ACh = HCl
* ECL Cell + ACh = Histamine → Parietal Cell + Histamine = HCl

ECL Cell - Histamine
* Stimulated by ACh and Gastrin
* Parietal Cell + Histamine = HCl

G Cell - Gastrin
* Stimulated from ENS by GRP
* ECL Cell + Gastrin = H+ release = HCl
* Parietal cell + Gastrin = HCL

59
Q

What is the most important stimulant for pancreatic enzyme secretion?

A

CCK

60
Q

The effects of secretin are potentiated by what?

Two

A
  1. CCK
  2. ACh
61
Q

Pancreatic secretions are what?

A
  • More alkaline than saliva (pH 8.6)
  • Isotonic to plasma

Food is isotonic at this point; hypotonic secretions are not needed

62
Q

Pancreatic enzyme: Amylase

A

Secreted as:
* Active enzyme

Function:
* Starch digestion

63
Q

Pancreatic enzyme:
* Trypsinogen
* Chymotrypsinogen
* Procarboxypeptidase
* Proelastase

A

Secreted as:
* Proenzymes

Activation:
* Enteropeptidase to trypsin
* Proelastase activated by trypsin

Function:
* Protein digestion

64
Q

Pancreatic enzyme:
* Lipase
* Cholesterol esterase
* Phospholipase

A

Secreted as:
* Active enzyme

Function:
* Fat digestion
* Cholesterol esters
* Phospholipids

65
Q

Pancreatic enzyme:
* Deoxyribonuclease
* Ribonuclease

A

Secreted as:
* Active enzyme

Function:
* Nucleic acid digestion

66
Q

Circulation of bile

A
  1. Hepatocytes (formation)
  2. Gallbladder (storage and concentration)
  3. Release into system (CBD into duodenum)
  4. Reabsorption (95% by ASBT in gut)
  5. Return to liver via portal vein
67
Q

ASBT

A

Active absoption:

Apical sodium-dependent bile salt transporter

68
Q

what 2 things cause bile to go into gallbladder?

A

hepatic secretion pressure

pressure from closure of oddi

69
Q

how is the bile concentrated?

A

Cl- and bicarb are pumped out with water

70
Q

what is the ideal bile ratio?
bile salts: lecithin: cholesterol

A

10:3:1

71
Q

How do we get gall stones?

A

Too much cholesterol
Too little bile salts
Too little lecithin

72
Q

GI secretions: Saliva

A

Major characteristics:
* High HCO3-
* High K+
* Hypotonic
* Amylase
* Lingual lipase

Stimulated by:
* Parasympathetic
* Sympathetic

Inhibited by:
* Sleep
* Dehydration
* Atropine

73
Q

GI secretions: Gastric

A

Major characteristics:
* HCl
* Pepsinogen
* Intrinsic factor

Stimulated by:
* Gastrin
* Histamine
* Parasympathetic

Inhibited by:
* low stomach pH
* chyme in duodenum
* somatostatin

74
Q

GI secretions: pancreas

A

Major characteristics:
* Secretin
* CCK
* parasympathetic

75
Q

GI secretions: Bile

A

Major chaacteristics:
* Bile salts
* Bilirubin
* Phospholipids
* Cholesterol

Stimulated by:
* CCK (GB contraction / Oddi relaxation)
* parasymapathetic (GB contraction)

Inhibited by:
* Ileal resection

76
Q

peristalsis? where does this occur?

A
  • propulsion through the area
  • esophagus
  • stomach
  • Small intestine
  • large intestine
77
Q

segmentation? where does this occur?

A
  • used for mixing
  • stomach
  • small intestine
  • large intestine
78
Q

tonic contraction? where does this occur?

A

just a held contraction of sphincters

79
Q

How is swallowing controlled?

A
  1. Medulla (swallowing center)
  2. Upper Esophageal Sphincter (Skeletal muscle)
  3. Esophagus (first 3rd striated, last 2/3 smooth)
  4. Lower esophageal sphincter (smooth muscle)
80
Q

Swallows are blank , the response of peristalsis is blank?

A
  • voluntary
  • reflexive
81
Q

Antiperistalsis?

A

Opposite direction of peristalsis
can being as low as ilium
prelude to vomiting
pushes GI contents into duodenum
distentions excite vomiting act

82
Q

Vomiting act

A
  1. Deep breath
  2. UES opens
  3. Glottis closes
  4. Elevation of soft palate
  5. Diaphram contraction + abdominal muscles contract
  6. LES relaxes
  7. Expulsion of contents
83
Q

CTZ

Chemoreceptive Trigger Zone

A
  • postrema of medulla
  • Dopamin and Saratonin receptors
84
Q

what does a vagotomy impair in the stomach

A

relaxation of the stomach (cant eat as much)

85
Q

roux en Y gastric bypass

A

gold standard for weight loss surgery
60% weight gone
correct T2D

86
Q

what are the 6 probelms with RYGB surgery?

A

1 faster food motility so less dig/abs
2 dumping diarrhea
3 intake less water because feel full constantly
4 decrease glucose absorption
5 vitamin B12 deficiency
6 mineral (iron and calcium) deficiency

Physio II (mine) (6 decks)

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