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Conjoint > Final (Rachael's Contribution) > Flashcards

Final (Rachael's Contribution) Flashcards

1
Q
  • Macronutrients
  • Micronutrients
A
  • Macronutrients: carbohydrates, fats, and proteins
  • Micronutrients: vitamins, minerals
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2
Q

Actions of the Digestive System (4)

A
  • Digestion
    • Chemical and Mechanical
  • Absorption
    • Epithelial transport
  • Secretion
    • Digestive enzymes, water, mucus, bile, acid, bicarbonate
  • Motility
    • Progression, mixing, regulated passage
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3
Q

Internal vs. External Environment

A
  • NOT excretion on the list.
    • Removal of cellular waste products
    • What passes out of anus was never part of the internal environment
    • The respiratory and urinary system does some excretion
      • Exception: excretion via bile
        • Cholesterol, bile pigments (breakdown of heme)
  • Digestive secretions are: exocrine secretions
    • Released into the lumen
    • Digestive tract is not regulatory in what it absorbs. Wants max absorption. Other factors regulate things like how many calories are taken it.​
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4
Q

Peritoneum

A
  • Serous membrane
  • Delicate membrane that suspends digestive organs in the abdomen
  • Consists of tiny layer of connective tissue and then simple, squamous epithelium
  • Releases fluid
  • Around organ=visceral peritoneum
  • Again body wall=**parietal peritoneum **
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5
Q

Peritoneal Cavity

A
  • Potential space that is created by peritoneum
  • This is where the fluid is released
  • In the internal environment of the body
  • Break of GI tract and bacteria into peritoneal cavity is bad-news-bears
    • Called peritonitis
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6
Q

Retroperitoneal

A
  • Organ not completely surrounded by peritoneum
  • Ascending and descending colon
    • Have adventitia instead (aka: connective tissue)
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7
Q

Mesentery

A
  • Two peritoneum that come together
  • Suspend the organs
  • Place where there is a lot of adipose tissue
  • Blood vessels
    • Superior and Inferior mesenteric arteries
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8
Q

Peritoneum Figure

A
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9
Q

Components of the Digestive Tract

A
  • Gastrointestinal tract: Tube from mouth to anus
    • Accessory organ: Organs that attach to GI tract to release secretions
  • Mouth and Pharynx:
    • ​Salivary Glands: Moisten, lubricate, polysaccharide digestion
  • Esophagus:
  • Stomach: HCl, pepsin, mucus, store, mix, solubalize, protein digestion, lubricate and protect liquid suspension
    • **Liver: **bile salts, bicarbonate
    • **Gallbladder: **stores bile
  • **Small Intestine **(duodenum, jejunum, ileum): digestion and absorption, maintain fluidity of luminal contents, lubrication
    • **Pancreas: **digestive enzymes, bicarbonate
  • **Large Intestine: **tiny bit of nutrient absorption, water absorption, concentrating undigested/bacterial material
  • Rectum
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10
Q

What is Bacteria in GI Tract called?

A

gut microbiome

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11
Q

Gut Microbiome: Function

A
  • A bit of digestion; nutrient extraction
    • Release of vitamin K
  • Protective
    • Vast numbers/competition protect from colonization by pathogenic bacteria
  • Role in development of immune system
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12
Q

Gut Microbiome: Who are they?

A
  • Characterized by DNA sequencing
  • Different species based on what DNA sequences that they are finding
  • About 400 species
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13
Q

Gut Microbiome: How do they get there?

A
  • Colonization during birth
  • Twin have a different pattern of microbiome
  • Composition influenced by host and by diet
  • Trends associated with disease
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14
Q

Definition: Dysbiosis

A

Imbalance in gut microbiome that could lead to/exasperate disease

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15
Q

Antibiotic Associated Colitis

A
  • Wipe out your microbiome
    • Also known as C. diff.
  • Infection with bacterium Clostridium difficile
  • Pseudomembranous colitis
    • Patches on colon that ooze pus
  • Treat person by replacing with normal fecal microbiota
    • Fecal microbiota transplant (FMT)
    • 90-95% are cured in one treatment
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16
Q

Inflammatory Bowel Disease

A
  • Abnormal inflammatory response to gut microbiome
  • No smoking gun bacteria, might be a host genetic factor
  • Genes linked to IMD
    • Genes involved in innate immunity
    • Genes involved in barrier function (characteristics that prevent mucosa from being leaky)
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17
Q

Ulcerative Colitis

A
  • Is an inflammatory bowel disease
  • Restricted to the colon
  • Mucosal inflammation
  • Continuous lesions
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18
Q

Crohn’s Disease

A
  • Inflammation anywhere in the GI tract
  • Interspersed with normal mucosa
  • Affects mainly the ileum, and anal region
  • Lesions are transmural
    • go through all the layers
  • Develop fistula
    • abnormal connections between GI compartments
  • Treatments: anti-inflammatory drugs; biologic therapies
    • anti-TNFalpha
  • May be from abnormality in the bacteria that is living in their gut
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19
Q

Irritable Bowel Syndrome (IBS)

A

Like fibromyalgia where people are affected but no one knows why. Increased pain and discomfort

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20
Q

Which of the following are continuous with the external environment?

  • Rectum
  • Common Bile Duct
  • Pancreatic Duct
  • Liver Sinusoid
  • Peritoneal Cavity
A
  • Rectum: Yes
  • Common Bile Duct: Yes
  • Pancreatic Duct: Yes
  • Liver Sinusoid: No (It’s a capillary)
  • Peritoneal Cavity: **No **
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21
Q

Tissue structure of the digestive tract

A
  • ​Layer closest to lumen is mucosa
    • 3 subdivisions
  • Serosa is the peritoneum
  • Main thing that changes along GI tract is in the mucosa
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22
Q

Changes in Mucosa along GI Tract

A
  • Esophagus:
    • Protective: stratified squamous epithelium, MALT
  • Stomach:
    • Secretory: glands, highly folded simple columnar epithelium
  • Small Intestine:
    • Absorption: highly folded simple columnar epithelium, expanded surface area with villi
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23
Q

Why is there absorption in the small intestine?

A
  • Very long
  • Highly folded
    • Plicae circulares: see with eyes, folding of entire musocsa
    • Villi and crypts: folding of the epithelium
    • Enterocyte: (epithelium intestinal cell) apical membrane has microvilli. Individual cell. Only see with electron microscope. Brush border
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24
Q

Lacteal

A
  • Poking into the villi are capilaries and lacteal
  • Lacteals:
  • Lymphatic capillary
  • Involved in absorption of fats
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25
Q

Intestinal Crypts

A
  • Where cell division occurs
  • Some stem cells in the basement of the crypt
  • Travel up as they age
  • Cells in the crypt are secretory
  • Cells on villus are absorptive
    • Die at the villus
    • Whole epilthelium is renewed every 4-5 days.
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26
Q

Carbohydrates: Digestion by A**mylase **

A
  • Release by salivary glands and pancreas
  • Brush Border Enzyme
  • Undigestable Carb: Fiber
    • Hold water, creates bulk, helps motility in the large GI
  • Poly and disaccharides need to be converted to monosaccharides for absorption
    • Start in oral cavity
      • Polysaccharide: acted on by salivary amylase
    • Stomach
      • salivary amylase inactivated by low pH
    • Small intestine
      • pancreatic amylase, break things down to be small polysaccharides
      • brush border enzymes break down to monosaccharide (sucrase, lactase, etc.)
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27
Q

People with no Lactase

A
  • Lactose maldigestion, lactose ends up in large intestine
  • Large intestine:
    • Lactose digested by bacteria
    • Cause gas
    • More solute in large intestine (holds water and generates diarrhea)
  • Lots of symptoms, call lactose intolerance
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28
Q

Carbohydrate Absorption

A
  • Co-transport coupled to Na+
  • Absorption of monnosaccharide and amino acids
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29
Q

Protein: Digestion in Stomach

A
  • Pepsin just in stomach
    • Works best at stomach pH
    • Good at taking apart collagen
    • Turns proteins into peptides
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30
Q

Protein: Digestion in Small Intestine

A
  • trypsin, chymotrypsin, carboxypeptidase (pancreatic) and brush border enzymes
  • Pepsin inactivated (above pH 5)
  • Enzymes from pancreas
    • Digest down to very small peptides
  • Brush border enzymes
    • Down to the amino acid
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31
Q

Protein: Absorption

A
  • Co-transport coupled to Na+
  • Co-transport may be couple with a specific amino acid
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32
Q

Protein: Endocytosis

A
  • Mechanism for passive immunity in infants
  • Transcytosis
    • To absorb intact polypeptides
    • Endocytosis at apical surface to bring in protein
    • Travel to basolateral membrane and exocytose
  • Ig-A secreted into breast milk and then absorbed by the infant via transcytosis
  • Also how antigens travel into the MALT
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33
Q

Activation of zymogens

A
  • Inactive enzyme precursor
  • Ex: Chief cell makes pepsinogen
  • Pepsinogen + Acid → change confirmation and open active site
    • Then cleaves pepsinogen to make pepsin
  • Activation of pancreatic zymogens
  • Gall stone
    • Enzymes get inappropriately activated in pancreas.
    • Results in inflammation of pancreas called pancreatitis
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34
Q

Fats

A
  • Main fat is TAG
  • When fat digested, TAG goes to monoglyceride and 2 FA
    • Via lipase, this enzyme is water soluable
  • Fat want to associate with itself
    • Need to break up fat droplet into many little products
    • **Emulsification **
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35
Q

Fats: Emulsifying agents

A
  • Bile salts, phospholipids
  • Keeps fat from associating
  • Bile salt are made from cholesterol in the liver
  • Amphipathic molecules coat the small emulsion droplets
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36
Q

Fats: Digestion

A
  • ​Lipase
  • Lipase bound to emulsion droplets via amphipathic protein called co-lipase
  • Co-lipase
    • amphipathic, secreted by pancreas, binds lipase, anchors lipase to the surface of emulsion droplets
  • Digestion occurs in emulsion droplets
  • Lipase digests TAG to monoglycerides and FA
  • Fat digestion products associate with bile salts and phospholipids to form micelles
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37
Q

Fats: Micelle Formation

A
  • Micelles: fatty acids, monoglycerides, bile salts, phospholipids, cholesterol, fat-soluble vitamins
  • Fat digestion products
  • At the top are the amphipathic molecules that are in pancreas
  • 4-7 nm→1/200th the size of an emulsion droplet
  • Micelles ferry fat digestion products to the apical plasma membrane of enterocytes.
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38
Q

Fat Emulsion/Digestion Figure

A
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39
Q

Fat: Absorption into Enterocytes

A
  • Simple diffusion of freely dissolved monoglycerides and FA
  • Carrier proteins
  • Cholesterol absorption
    • Cholesterol in SI comes from cholesterol in bile and dietary cholesterol.
    • 50% cholesterol in SI is reabsorbed into body and 50% eliminated
    • Drug increases cholesterol elimination
      • Ezetimibe: blocks carrier protein for cholesterol (reduces absorption)
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40
Q

Fat: Chylomicrons

A
  • Lipoproteins
  • TAG
    • Cholesterol
    • Fat soluble vitamins
    • Phospholipids
    • Apolipoproteins
  • Chylomicrons: lipoproteins produced by enterocytes
    • Way that fat is carried around in the circulation
  • Get into circulation by entering leaky lymphatic capillaries (lacteals), flow via lymphatic vessels and get into circulation
  • TAG in lipoprotein digested by lipoprotein lipase→monoglyceride and 2 FA that can go into cells
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41
Q

Vitamin B12 Absorption

A
  • Requires intrinsic factor
  • Water soluble
  • Important for cell division, affects RBC products, anemia occurs
  • Parietal cells in stomach produce intrinsic factor
  • IF bind to vitamin B12 to make complex
  • Complex travels to bottom of the SI
  • Ileum: absorption via receptor-mediated endocytosis
  • Lack of intrinsic factor (causes B12 deficiency)→prenicious anemia
  • Autoimmune cells destroys parietal cells
  • Crohn’s disease causing inflammation in ileum, causing decreased absorption of B12 (causes deficiency)
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42
Q

Vitamin Absorption

A
  • Fat soluable vitamins→tag along with fat absorption
  • Water soluable vitamins→carriers, diffusion
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43
Q

Iron Absorption

A
  • No efficient way to get rid of iron, so needs to be efficiently recycled.
  • Iron deficiency→anemia
  • Too much ion: free radical formation→tissue damage
  • Into enterocyte via DMT-1
    • Then can go into 2 different pathways (ferritin or ferroportin)
      • Ferritin
        • not actually in the body because enterocytes overturn readily
  • Regulated iron absorption occurs in the duodenum
  • Transferrin: figure out how much iron in body by looking at saturation
    • <25% saturated (normally)
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44
Q

Regulation of Iron Absorption Responding to 2 Signals

A
    1. Is there a need for iron (w/ regard to bone marrow)
      * Needed because making RBC
      * Don’t know what that signal is
    1. Body iron stores (mostly liver, some spleen)→signal (hormone: hepcidin)→act of enterocytes to allow iron absorption
      * When body iron stores full
      • increased hepicidin by liver, travels to duodenum, bind ferroportin, ferroportin internalized and degraded
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45
Q

Hemochromatosis

A
  • Disorder of iron overload
  • Mutation in HFE gene
    • most common cause
  • Unregulated iron absorption
    • Accumulation of iron in tissue
    • form free radicals
    • tissue damage
      • Liver, pancreas, heart, joint
  • Symptoms arise in middle age
  • Treatment:
    • Bleeding to remove iron, phlebotomy
  • HFE protein thought to be involved in sensing the amount of iron
    • When defective
      • iron isn’t sensed properly
      • deficient secretion of hepcidin
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46
Q

Iron Absorption: Figure

A
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47
Q

Disruption of Absorption: Celiac Disease

A
  • Inappropriate immune response to gluten
    • Involves CD4+ helper T Cells
  • Not an allergy b/c not atopic disorder
  • Duodenal biopsy to diagnose celiac disease
    • Flattened mucosa (no villi)
    • Inflammation
    • Increased lymphocytes
  • Normal small intestine mucosa
  • Decreased iron absorption
  • Decreased folate
  • Anemia will occur
  • In lamina propia MALT engulf those peptides and display them on their surface
  • Consequences:
    • Malabsorption
    • Diarrhea
    • Anemia (iron deficiency)
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48
Q

Celiac Disease: Figure

A
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49
Q

Disruption of Absorption: Bariatric Surgery

A
  • Weight loss surgery
  • The two most common bariatric surgery procedures are Roux-en-Y gastric bypass and **adjustable gastric banding **
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50
Q

Adjustable Gastric Banding

A
  • Small pouch created so person feels full more quickly
  • Restricted procedure
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51
Q

Roux-en-Y (RYGB)

A
  • Combine restrictive and malabsorptive
  • Small pouch at fundus is created; piece of SI is brought up and joined to the pouch. Creates a tiny stomach and channel that food flows down.
  • Stomach left there so that secretions from liver, stomach and pancreas still go SI
  • Duodenum is powerhouse of absorption, so food bypasses this.
    • can cause micronutrient deficiency (like anemia)
  • Alimentary channel is where the food is. The biliopancreatic channel is where the secretions are.
  • Length of common channel determines the degree of absorption/malabsorption
  • For reasons not well understood endocrine changes occur that can achieve remission from Type 2 diabetes
    • 75-80% who have DM2 achieve remission
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52
Q

Hypothesis of RYGB Endocrine Alteration

A
  • Start to have changes in responsiveness and occur even before the profound weight loss
  • Hypothesis #1:
    • There might be an upper GI hormone that is involved in glucose homeostasis
  • Hypothesis #2:
    • Food quicker to lower small intestine
      • Stimulates **endocrine L cells **
      • Release GLP1 and PYY
      • GLP1 increases insulin secretion, decreases glucagon secretion, increasing satiety
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53
Q

Digestive Tract Enteric Nervous System

A
  • Branch of autonomic nervous system
  • Neurons in wall of GI tract controlling behavior
  • Can work in isolation from the CNS
  • Afferent neurons responding to changes in GI tract
    • Chemical sensors
    • Stretch sensitive sensors
  • Efferent neurons→projecting to secretory cells, smooth muscle
  • Interneurons: connecting and coordinating neurons
  • Vagus nerve inputs (parasympathetic part of ANS)
  • submucous plexus
    • deeper than the myenteric plexus
  • myenteric plexus
    • Between muscle layers regulating motility
    • More neurons
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54
Q

Digestive Tract Electrical Activity in Smooth Muscle

A
  • Cells are spontaneously active in smooth muscle
  • Cells are electrically coupled into groups so that they work in concert.
    • Via gap junctions
  • Spontaneous activity in specialized smooth muscle cells (pacemaker cells) produces the basic electrical rhythm
    • Spontaneous activity makes the slow waves (“basic electrical rhythm”)
    • Electrical coupling causes region to have the oscillating membrane potential
  • Slow waves with spikes of action potentials
    • In the stomach there are 3 waves/min
    • Duodenum: 12/min
    • Ileum: 9/min
  • Action potential lets calcium in that regulates muscle contractions (More calcium, stronger contraction)
  • Slow wave frequency: contraction frequency
  • Number of action potentials (@ peak): contraction strength
  • Excitatory input makes the cell more depolarized so that when slow wave reaches the peak, there will be more action potentials
  • Skeletal muscle only input is somatic efferent
  • Smooth muscle can have a variety of inputs (more complex):
    • Neurons
    • Hormones
    • Excitatory or inhibitory
    • Spontaneous activity
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55
Q

Digest Tract Electrical Rhythm Figure

A
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56
Q

gastrointestinal hormones and paracrines

A
  • Endocrine cells are generally in the epithelium
  • Internal secretion, hormone going to the blood stream
  • Important hormones: gastrin, cholecystokinin (CCK), secretin, incretins (GLP-1, GIP)
  • Important paracrines: histamine, somatostatin, serotonin
  • Change in lumen→triggers secretion
    • Causes feedback regulation of lumen of GI tract
  • Often act as growth factors
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57
Q

phases of gastrointestinal control

A
  • phase=location of stimulus
  1. cephalic phase (cephalic=head)
    • stimuli: sight, smell, taste, chewing
  2. gastric phase (gastric=stomach)
    • food in stomach
    • stimuli: stomach distension, acidity, peptides
  3. intestinal phase
    • stimuli: distension, acidity, osmolarity, digestive products
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58
Q

salivation

A
  • Release saliva in response to food in the mouth
  • Amylase to digest carbohydrate (from serous acinus)
  • Also antibacterials
  • Mucus from mucus acinus
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59
Q

Swallowing: 3 Phases

A
  1. Oral (buccal) Phase
  2. Pharyngeal Phase
  3. Esophageal Phase
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60
Q

Oral Phase of Swallowing

A
  • Food in mouth
  • Swallowing is voluntarily initiated
  • Retracted tongue: push food to the pharynx
    • Food in pharynx triggers pharyngeal sensory neurons that project to brainstem nuclei that coordinate the other two phases
  • Elevation of soft palate so no food up the nose
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61
Q

Pharyngeal Phase of Swallowing

A
  • Area common to breathing and eating
  • Inhibit respiration
  • Glottis muscles close breathing
  • Larynx elevated to tip the epiglottis down so the trachea is covered
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62
Q

Esophageal Phase of Swallowing

A
  • Esophageal sphincters relax to allow food to pass
    • One at top and one at bottom
  • Smooth muscle engages in propulsive movement
    • peristalsis
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63
Q

Swallowing Picture

A
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64
Q

Vomiting Figure

A
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65
Q

Vomiting Overview

A
  • Technical term is emesis
  • Nausea not well understood (can’t use animal models and ask how they feel)
  • Strong contractions of abdominal muscle to increase abdominal pressure
  • Relaxation of esophageal muscle
  • Reverse peristalsis
  • automatic behavior controlled by nuclei in the brainstem, referred to as the vomiting center
  • During retching, the lower esophageal sphincter relaxes, abdominal skeletal muscles contract, and strong peristaltic contractions of the muscularis externa operate in reverse of the normal pattern, forcing the contents of the stomach and even the small intestine upward into the esophagus
  • Emesis occurs when these contractions are strong enough to expel the contents of the GI tract past the upper esophageal sphincter.
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66
Q

Regualtion of Vomiting

A
  • Irritant in GI tract affects cells that release serotonin
    • Serotonin acts as paracrine
    • Excites afferents in vagus nerve
    • Up to the vomiting center in brain
  • Toxin in circulation
    • Act of area postrema in the brain
      • project to and activate vomiting center
    • Also the chemoreceptor trigger zone
    • At the posterior end of the 4th ventricle
    • Outside the BBB
  • CNS
    • Blow to head can trigger vomiting
    • Vestibular mismatch
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67
Q

Clinical Application of Vomiting

A
  • Post operative nausea and vomiting
    • opiods and anethestics
    • activate opiod receptors in area postrema
  • Chemotherapy induced nausea and vomiting
    • serotonin release of intestinal epithelium
    • Free radical formation release serotonin
  • Treated prophylactically with antiemetic
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68
Q

Antiemetics

A
  • Serotonin antagonist: Zofran and palonosetron (Aloxi®)
    • Bind to serotonin receptors 5HT3 antagonists
  • Substance P antagonists: Aprepitant (Emend)
    • P involved in inflammatory pain pathways
    • Very effective in limiting vomiting
  • Antagonists for dopamine, histamine and acetylcholine
    • dopamine antagonists promethazine (Phenergan®) and prochlorperazine (Compazine®)
    • histamine anatagonist dimenhydrinate (Dramamine®)
    • muscarinic anatagonist scopolamine
  • Cannabinoid agonists such as tetrahydrocannabinol (THC; the principal psychoactive ingredient in marijuana) are also used to reduce nausea and vomiting
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69
Q

Heartburn

A
  • Upper sphincter limits air into the GI tract (if gets in there, belching)
  • Factors that increase risk of gastroesophageal reflux:
    • decreased tone in lower esophageal sphincter
    • increased abdominal pressure (pregnancy, obesity, overeating )
    • hiatal hernia
      • When a piece of the stomach fundus goes through the “hiatus” (the hole in the diaphragm)
      • Diaphragm normally reinforces lower esophageal sphincter
  • GERD Treatments:
    • Suppression of acid secretion
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70
Q

Barrett’s Esophagus

A
  • The mucosa changes with continual exposure to acid
  • Columnar epithelium appears reddish (abnormal appearance)
  • Confirmation:
    • Biopsy to look for intestinal metaplasia: mucosal change where you see columnar epithelium where it should be stratified squamous. Will see goblet cells
  • Increased risk for esophageal adenocarcinoma
    • May need increased surveillance if known Barrett’s esophagus
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71
Q

Stomach: Secretion of Acid

A
  • Functions:
    • Solubilizes food
    • Pepsin activity
    • Kills bacteria
  • Parietal cells secrete HCl acid
    • H+/K+ ATPase-“proton pump”
    • Apical plasma membrane
  • Stimulation of acid secretion: translocation of proton pumps to apical plasma membrane
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72
Q

Stomach Acid Secretion Figure

A
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73
Q

Regulators of Gastric Acid Secretion

A
  • Stimulation of acid secretion: translocation of proton pumps to the apical plasma membrane
  • Regulators:
    • Neurotransmitter: acetylcholine
      • ​Released from enteric neurons
    • Paracrine: histamine
      • Released from ECL cells
    • Hormone: gastrin
      • ​Released by G cells in gastic epithelium
      • Stimulates ECL cells to increase histamine (indirect effect)
      • Stimulates proliferation of parietal cells (direct effect)
    • Negative Regulator:** Somatostatin**
      • ​secreted by endocrine cells of the gastric epithelium
      • Acts as both a paracrine and a hormone
74
Q

Cephalic Phase Gastric Acid Secretion Regulation

A
  • taste, small, sight
  • stimulate parasympathetic preganglionic neuron (in vagus nerve) to eneteric neurons to stimulate parietal cell, ECL and G cell.
  • Only a little acid secretion
75
Q

Gastric Phase Gastric Acid Secretion Regulation

A
  • With food in the stomach, get the most acid secretion
  • Distends stomach, activates neural reflex to stimulate acid secretion
  • Peptides in food stimulate acid secretion from G cells
  • Food acts as a buffer to bind hydrogen ions. Lots of hydrogen ions, somatostatin turned on.
    • Relieves inhibition
76
Q

Intestinal Phase Gastric Acid Secretion Regulation

A
  • Want to limit acid
  • As food reaches duodenum stimulates factors to feed back inhibits enteric neurons and stimulate enterogastrones
  • Enterogastrones: hormones that inhibit stomach processes
77
Q

Gastric Acid Secretion Regulation Figure

A
  • Acetylcholine and histamine directly stimulate parietal cells to increase acid secretion
  • Gastrin stimulates acid secretion by stimulating histamine release from ECL cells
78
Q

Figure of Stomach And Where Endocrine Cells Are

A
79
Q

Peptic Ulcers

A
  • Gastric ulcers (stomach)
  • Duodenal ulcers
  • Mucus in the stomach is protective
  • Use of NSAIDs can block prostaglandin production
    • Prostaglandins: promote mucus formation and inhibit acid secretion
80
Q

Helicobacter pylori

A
  • Causes peptic ulcer disease
  • Bacteria colonize by burrowing into the mucus and have enzymes that neutralize stomach acid near the bacteria
  • Causes gastritis (inflammation in the stomach)
  • Only certain individuals that have H. pylori will have ulcer
81
Q

Gastritis in stomach pylorus vs. stomach body

A
  • Gastritis setting up in pylorus
    • Causes endocrine deregulation
    • Decreased somatostatin, increase in gastrin
    • Acid hyper-secretion and no inhibits from somatostain
    • Overwhelms protective mechanisms in the duodenum
  • Gastritis setting up in body
    • Atrophy in the glands, decreased parietal cells
    • Decreased acid secretion: hypochlorhydria
    • Get change in mucosa: intestinal metaplasia: pre-malignant lesion
82
Q

Treatment of Peptic Ulcers

A
  • Goal is to eradicate bacteria
  • Give a couple of antibiotics to really make sure bacteria gone as well as giving drugs to decrease acid secretion
    • Histamine antagonists: H-2 receptors, Cimetidine, Ranitidine
    • Proton Pump Inhibitors: Omeprazole, Lansoprazole
83
Q

Gastric Motility: Receptive Relaxation

A
  • During eating
  • Expand during ingestion
  • Neural reflex response to eating
84
Q

Gastric Motility: Peristalsis

A
  • Basic propulsive movement
  • Inside is circular muscle, outside is longitudinal muscle
  • In segment, two parts: propulsive segment and receptive segment
    • Squeeze in propulsive segment and open in receptive segment
      • Contraction in circular muscle and relaxation of longitudinal muscle in propulsive segment
      • Reverse in receptive segment
  • Stronger peristalsis in pylorus
  • Once in food pylorus
  • Rate determined by BER (basic electrical rhythm) (3/min)
  • Gastric phase stimuli (stomach distension and/or gastrin) increase strength of contractions
  • Intestinal phase stimuli decrease strength of contractions; slow stomach emptying
85
Q

Gastric Motility: Stomach Emptying

A
  • Rate determined by BER (basic electrical rhythm) (3/min)
  • Gastric phase stimuli (stomach distension and/or gastrin) increase strength of contractions
  • Intestinal phase stimuli decrease strength of contractions; slow stomach emptying
  • Strong contraction in stomach smooth muscle, increase stomach emptying
  • Weak contraction in stomach smooth muscle, decrease stomach emptying
  • Enterogastrones: inhibit acid secretion and inhibit smooth muscle
  • Neural and hormone inputs to GI smooth muscle change the strength, but not the timing of contractions.
86
Q

Pancreatic Secretion

A
  • Providing digestion enzymes and bicarbonate
  • Exocrine secretion in the pancreas: acinar cells and duct cells
  • Acinar cells secreting digestive enzymes
  • Duct cells secreting bicarbonate and fluid
  • Regulated by hormones
  • Chyme in duodenum stimulate hormones
    • Low pH stimulate secretin release
      • Acts on duct cells to stimulate bicarbonate and fluid release
    • Fats and peptides stimulate CCK release
      • Travels in circulation to stimulate secretion from acinar cells
  • Some stimulation during cephalic and gastric phase via vagus nerve to cause secretions
87
Q

Pancreatic Secretion: Figure

A
88
Q

regulation of bile release into duodenum

A
  • Bile salts, phospholipids, bicarbonate, cholesterol, bile pigments, trace metals. Last three are targeted for excretion
  • Smooth muscle closing outlet: Sphincter of Oddi
    • Basically at the duodenal papilla
    • Regulates whether or not bile will enter duodenum
  • No meal: interdigestive period.
    • No need to for bile in duodenum, sphincter contracts
    • Pressure builds up and bile flow to gallbladder for storage
  • Digestive period. About 2 hours
    • Sphincter relaxed and bile flows into duodenum
  • Secretin stimulated by H ions
  • CCK stimulated by digestive products
    • Cholecystokinin
    • Cholescyst: gallbladder, kinin: to move
    • Triggers smooth muscle contraction in gallbladder
    • In SOO relaxes smooth muscle
    • Enables bile to flow out
    • Amount of bile not sufficient to digest all meal so bile salts need to be recycled…enteroheaptic circulation
89
Q

Regulation of Bile Release: Figure

A
90
Q

Enterohepatic circulation

A

Transporters take up bile salts in ileum and back to intestinal capillaries

91
Q

Gall Stones

A
  • Too much cholesterol in gallbladder precipitates to gallstones
    • Need enough bile salts to keep it soluable
  • Female (estrogen promotes cholesterol into bile), age (enzymes producing bile salts less active
    • Can be completely asymptomatic
92
Q

Location of Gallstones and Consequences

A
  • When problem is gallstone moved into bile duct.
    • Cystic bile duct: painful gallbladder contractions
    • Common bile duct: pain and nausea, lack of bile release, failure to excrete bilirubin leads to jaundice
    • Duodenal papilla: block pancreatic enzymes leading to inappropriate activation of pancreatic zymogens, acute pancreatitis
93
Q

Gallstone Treatment

A
  • Cholecystectomy→Removal of gallbladder
  • Endoscopic removal
  • Nonsurgical: give oral bile salts
    • Delivered to bile ducts via enterohepatic circulation
  • Shockwaves to break up stones
94
Q

Enterohepatic Circulation: Figure

A
95
Q

Small Intestine Secretion

A
  • Villus: absorptive
  • Crypt: secretory enterocytes
    • Depends upon activity of CFTR
    • Sodium follows chloride passively
  • Digestive pathologies of cystic fibrosis
    • Can cause intestinal blockage
    • Pancreatic insufficiency (digestive enzymes not produced/getting to duodenum)
    • Chronic pancreatitis
  • Excessive activation
    • Excessive secretion of fluid
    • Secretory diarrhea (cholera)
96
Q

Small Intestine Motility: Segmentation

A
  • Occurs during the digestive period
  • Turned on by cephalic phase stimuli
  • Alternating contractions and relaxations of smooth muscle
  • Helps mix things up
  • Cephalic phase stimuli switches on segmentationàcontinues during digestive period
  • Bi-directional movement: things going back and forth
  • Thing goes forward with gradual propulsion (net movement towards cecum) because BER has gradient: faster in duodenum (12/min) and slower in ileum (9/min)
97
Q

Small Intestine Motility: Migrating Motor Complex

A
  • During inter-digestive period
  • Get segment of pertalsis that travel down upper GI and then stops
  • Migrating segment of peristaltic activity
  • Like sweeping floor. Go forward and then backwards, etc.
  • Clears out what is left in the small intestine
    • Indigestible, un-absorbable, bacteria
    • Stomach growling: disrupts bubbles
  • Turns off when eat, because switches to segmentation
98
Q

Segmentation: Figure

A
99
Q

Functions of Large Intestine

A
  • absorption of fluid
  • secretion of mucus
  • bacterial digestion
  • storage of feces
  • defecation
100
Q

Large Intestine: Types of Motility

A
  • Slow mixing movement
    • Slow irregular contractions of circular muscle
  • Mass movement
    • Propulsive movement
    • Sustained contraction of circular muscle (squeeze and hold)
    • Provides stimulus for defecation
101
Q

Defecation

A
  • External anal sphincter to maintain continence
  • Anorectal angle during rest and defection. Contraction of puborectalis establishes more acute anorectal angle that keeps feces from leaking out
    • When defecation occur, conscious relaxation to allow feces passage
  • Mass movement puts feces in sigmoid colon and rectum and causes stretch
    • Triggers responses that causes more pressure inside the rectum (see course website)
      • The urge to defecate
    • If spinal injury or infants, pressure increases to a point where there is reflective defecation
  • Valsalva maneuver is pushing to increase abdominal pressure and push feces out
    • Contraction of abdominal muscles
102
Q

Liver Blood Flow

A
  • Hepatic portal vein, deoxygenated put nutrient rich
  • If water soluble in the diet, then first goes to the liver
  • Role in nutrient homeostasis
  • Makes lots of plasma proteins
    • Good reason to take amino acids there
103
Q

Liver Blood Flow: Figure

A
104
Q

Hepatocytes

A
  • Cells arranged in rows with sinusoids inbetween
    • Place where blood flows through
  • Look at sinusoid via EM
    • In sinusoid are some other cells
      • Enothelial cells
  • Hepatocytes making bile to go into own distinct secretory pathway
  • Green guys are canaliculi that hook up to bile ductule to let things flow out of the liver
105
Q

Liver Endothelial Cells

A
  • No basement membrane and not tightly linked
  • Liver secretion and taking things out of blood in sinusoids
    • Need lipoproteins to get in and out so need gaps
106
Q

Liver Cells: Figure

A
107
Q

Kupffer cells

A
  • (reticuloendothelial cells)
  • macrophages; consume aged RBC’s
  • iron recycling and storage
108
Q

Stellate Cells

A
  • AKA Ito cells
  • Connective tissue cells
  • Involved in situation with disorders causing injury to liver cells
  • Liver can regenerate (with limited capacity)
  • Chronic Liver injury:
    • Stimulates stellate cells
    • Can get too much connective tissue…fibrosis
    • Can reach terminal stage of fibrosis called cirrhosis
    • Connective tissue making islands of isolated hepatocytes that no longer function properly
109
Q

Hepatocyte Functions

A
  • Bile synthesis and secretion
  • Nutrient homeostasis
    • Absorptive state: synthesis of glycogen, TAG
    • Post absorptive state: glycogenolysis, gluconeogenesis, ketogenesis
  • Biotransformation
    • Metabolism of drugs, hormones, etc. to promote excretion via the urine
    • Convert to more soluble forms
  • Synthesis of plasma proteins
    • albumin, binding proteins, clotting factors, complement
    • Albumin is making sure that there is enough osmotic pressure to keep fluid in circulatory system
    • When not enough plasma proteins, can get edema
  • Cholesterol homeostasis
110
Q

lipids are transported in the circulation as lipoproteins

A

Apolipoprotein is also a label for cells to read

111
Q

chylomicrons

A
  • Are synthesizes in enterocytes from absorbed lipids
  • Synthesis of TAG in ER
112
Q

VLDL=very low density lipoprotein

A
  • TAG rich
  • Liver makes with extra glucose
  • Deliver TAG to cells
  • TAG extracted by lipoprotein lipase, on the surface of endothelial cells and acting of lipoprotein so FA and glycerol can be taken up by cells
  • When stripped of TAG, becomes more dense and then get taken up by liver and remodeled and sent out as LDL
113
Q

LDL=low density lipoprotein

A
  • Cholesterol delivery
  • LDL uptake into cells is via receptor mediated endocytosis
  • LDL receptor is really important in cell using cholesterol and in liver
  • Liver using LDL receptor to see how much LDL is out in circulation
114
Q

HDL=high density lipoprotein

A
  • Cleanup, reverse cholesterol transport
  • Empty bag that scavenges and picks up extra cholesterol to take back to liver
  • When high levels of LDL and low HDL cholesterol, increases risk of atherosclerosis
    • Fatty plaques inside blood vessels that lead to clots and blockage of blood
  • Lipid panel measure cholesterol but really we carry about the particles.
  • Familial hypercholestolemia
    • VERY high levels of LDL and have heart attacks at young ages
    • Major cause is mutation in gene for LDL receptor
    • Defective LDL reecptors means that liver can’t take up LDL and see how much is out there
      • Keeps pumping out LDL
115
Q

Lipoprotein Movement: Figure

A
116
Q

functions of the liver in cholesterol homeostasis

A
  • synthesis of cholesterol
    • HMG-CoA reductase: rate limiting enzyme for cholesterol synthesis; increases cholesterol in the hepatocyte decreases HMG-CoA reductase activity
  • synthesis of HDL
  • LDL uptake
    • Regulates levels of cholesterol in the circulation
  • synthesis of bile salts
  • secretion of cholesterol in bile (some in feces)
    • Cholesterol elimination from the body
117
Q

drugs for dyslipidemia

A
  • Altered levels of lipids that predispose to atherosclerosis
  • **statins: ** inhibit HMG-CoA reductase
    • Reduce LDL cholesterol
    • Shown in clinical trials to reduce cardiovascular events
    • May have anti-inflammatory effect
  • **ezetimibe: **inhibits GI cholesterol uptake
    • Blocks cholesterol transporter in the small intestine
  • Fibrates
  • Niacin
118
Q

Zymogen Definition

A
  • Digestive enzymes released in inactive form
  • to prevent digesting the cells that create them
  • Peptide blocks active site of enzyme
  • Cleave the peptide to activate the enzyme
119
Q

Activation of pepsinogen in the stomach

A
  • Peptidase in the stomach is pepsin
  • Active at pH 2-3 and inactive at pH 5
  • **Chief cells **at the base of gastric glands secrete the zymogen
    • called pepsinogen
  • Partially activation by HCl secreted by parietal cells
  • Then cleaves the peptide in other pepsinogens to activate them
120
Q

Pepsinogen Activation: Figure

A
121
Q

Activation of pancreatic zymogens in the small intestine

A
  • Brushborder enzyme enterokinase cleaves **trypsinogen **forming the active enzyme trypsin
  • **Trypsin **then activates other enzymes
  • Pancreatitis
    • inapropriate activation
    • Acinar cell secrete trypin inhibitor within the pancreas
    • Trypsin also has **autolysis **(self-digestion)
  • Fluid by duct cells flushes zymogens out
    • can get blocked by gallstone
  • Fluid secretion in pancreas depends upon chloride channel CFTR
  • Increased Risk for pancreatitis
    • Mutation in trypsin inhibitor
    • Cystic Fibrosis
    • Alchol consumption
    • hyperlipidemia
122
Q

Pancreatic Enzyme Activation: Figure

A
123
Q

Digestion and absorption of fats

A
  • Most dietary fat is TAG
  • hydrolyzed by lipase to release FFA and glycerol
124
Q

Emulsification and digestion

A
  • Key issue in digestion and absorption of fats is their solubility
  • **lipase **is water soluable and only work at surface of fat droplet
  • Digestion aided by **emulsifaction **of fat into emulsion droplets
  • **Bile salts **and cholesterol are ampipathic and are present in the bile
  • SI motility breaks up fats and then coats them with bile salts and phospholipids to prevent them from sticking together
  • Digestion occurs in emulsion droplets
    • Increases surface area for lipase
  • Colipase is ampipathic and anchors lipase to surface of emuslion droplet
125
Q

Micelles: Figure

A
126
Q

Micelles

A
  • Monoglycerides and glycerol associate with bile salts and phospholipids to form micelles
  • 200 times smaller than emulsion droplets
    • small enough to fall between the microvilli
  • Transport to surface of enterocyte for absorption
  • Micelle contains **fat soluable vitamins **and cholesterol
  • Constant forming and breaking down
  • Only freely dissolved monoglycerides and FFA can be absorbed by diffusion across membrane
  • Some have facillitate transport proteins
127
Q

Chylomicrons

A
  • Monoglycerides and FA resynthesized back into TAG inside the cell
  • TAG, cholesterol, fat solubale vitamin packaged into chylomicrons
    • are lipoproteins
  • Released from basal membrane of enterocytes
  • Enter lacteals and then drained into blood in chest
  • TAG in chylomicrons is hydrolyzed by **lipoprotein lipase, **found in capillary endothelial cells
128
Q

Cholesterol Absorption

A
  • Some cholesterol in SI is dietary and other is put there by the liver via bile
  • Only half of cholesterol is absorbed and rest eliminated in the feces
  • Ezetimibe: blocks transport of cholesterol across apical membrane. Reduced LDL levels, especially when combined with **statins **that inhibit cholesterol synthesis in liver
    • Lowers MI and stroke risk as well
129
Q

Cholesterol Handling: Figure

A
130
Q

Iron Absorption

A
  • Iron absorption matches iron loss (1-2 mg)
  • Iron is necessary component for many enzymes but plays important role in binding oxygen in Hb
    • anemia: reduced oxygen carrying capacity of blood
  • Too much iron can lead to free radical formation
  • Most iron in RBC, rest in **liver’s hepatoctyes **and Kupffer cells (aka reticuloendothelial cells)
    • Macrophage that ingest RBC to release iron
  • Iron brought into cell by active transporter DMT-1 (divalent metal transporter 1)
    • in duodenum
    • zinc, copper, cobalt, manganese, cadmium or lead
    • also absorb heme iron
  • Two fates of iron once inside cell:
    • leave the enterocyte and enter the body via the basolateral transporter known as ferroportin
    • bound to** ferritin, an intracellular iron-binding protein**
      • ​iron lost when enterocyte dies
  • ​Iron in the internal environement is rapidly bound by transferrin
    • delivered to RBC precursors and taken up by receptor-mediated endocytosis
  • Generally more transferrin than iron but, **transferrin saturation **determines if too much iron in the blood (normal 20-45%)
131
Q

Signals Affecting Iron Absorption

A
  • One signal reflects the need for iron due to erythropoiesis
    • hormone erythropoietin stimulates red blood cell production (another signal for iron absorption)
  • second signal depends upon the amount of iron in body stores
  • Regulate iron absorption in the proximal duodenum
  • ** Hepcidin** is produced by hepatocytes when iron stores are full. Inflammation can also stimulate hepcidin production.
    • causes ferroportin to be internalized and degraded
    • more iron in enterocyte, stimulating ferratin synthesis, more iron loss
132
Q

Hepcidin Action: Figure

A
133
Q

Hemochromatosis

A
  • severe juvenile form of hemochromatosis is due to a homozygous deletion of the gene for hepcidin
  • HFE functions in the process of sensing body iron levels and regulating hepcidin secretion
  • deficient secretion of hepcidin, iron absorption by duodenal enterocytes continues even when body iron stores are full
  • Half a liter of blood contains approximately 200-250 mg of iron
134
Q

Celiac Disease

A
  • also known as** gluten enteropathy** or celiac sprue
  • malabsorption because of inappropriate immune response to gluten
  • not atopic becuase not involve IgE
  • immune response in celiac disease is mediated by CD4+ helper T-cells
  • All individuals who develop celiac disease express particular alleles of one type of MHC molecule
135
Q

Celiac Disease: Pathogenesis

A
  • Peptides derived from gluten contain many proline and glutamine residues, making them **resistant to digestion **by pancreatic and brush border enzymes.
  • peptides gain access to the lamina propria (where MALT is located) either by transcytosis or by a paracellular route
    • paracellular by breakdown of tight junctions and increase intestinal permeability
  • in the lamina propria, an enzyme modifies these peptides, making them even more antigenic
  • displayed on the surface of antigen presenting cells (APC’s) by MHC II molecules
  • stimulate CD4+ helper T-cells, which secrete cytokines that orchestrate the inflammatory response that leads to tissue damage
  • One cytokine in particular (IL-15) stimulates intraepithelial lymphocytes, promoting their recruitment, survival, and cell-killing properties
136
Q

Celiac Tissue Damage

A
  • observed in a duodenal biopsy, which is a key test in the diagnosis of celiac disease
  • flattened mucosa
  • greatly decreases the surface area of the small intestine, causing** malabsorption of nutrients**, which can cause diarrhea and malnutrition
  • Duodenal tissue also shows increased numbers of lymphocytes
  • In adults, primary symptom is **iron deficiency anemia **
  • get a skin rash, which is termed dermatitis herpetiformis
137
Q

Celiac Treatment

A
  • Avoidance
  • bacterial and plant enzymes capable of digesting the immunostimulatory peptides that resist digestion by human digestive enzymes
  • block the breakdown in the epithelial barrier of the intestine
    • Peptides derived from gluten stimulate the release of** zonulin**, a regulatory molecule that causes tight junctions to open up
    • A drug that is in development blocks zonulin receptors
138
Q

Bariatric Surgery: Figure

A
139
Q

Bariatric Surgery

A
  • often performed** laparascopically**
  • adjustable gastric banding
    • band around fundus
    • restrictive procedure because weight loss from limited intake
    • More gradual weight loss
  • RYGB
    • both restrictive and malabsorpative
140
Q

Y of RYGB: Figure

A
141
Q

Cephalic Phase Stimuli on Acid Secretion: Figure

A
142
Q

Gastric Phase Stimuli on Acid Secretion: Figure

A
143
Q

Intestinal Phase Stimuli on Acid Secretion: Figure

A

CCK, secretin, GLP-1, and GIPact as enterogastrones.

144
Q

What does bright red blood tell you?

A
  • ​Bleeding in the lower GI, left colon
  • Bleeding from upper GI would cause black, tarry stools
  • Passage of recognizable blood is called hematochezia
  • Passage of tarry stools is called melena
145
Q

What parts of colon are on the left side of the body?

A

Descending and sigmoid colon.

146
Q

What bacterial infection is associated with recent antibiotic use?

A

Infection with Clostridium difficile. Treatment with broad-spectrum antibiotics kills off many bacteria, allowing overgrowth with C. difficile, which causes pseudomembranous colitis.

147
Q

erythrocyte sedimentation rate (ESR)

A

Increased ESR is indicative of inflammation.

148
Q

Colonoscopy reveals a uniformly inflamed mucosa in the rectum and sigmoid colon. The mucosa has a granular, reddish appearance, with occasional patches of spontaneous bleeding in shallow ulcerations. A biopsy shows that the inflammation is restricted to the mucosa. What type of inflammatory bowel disease does this patient have?

A

Ulcerative colitis. Shallow ulcerations that are limited to the mucosa are indicative of ulcerative colitis. Another characteristic feature is the uniform granular appearance seen with colonoscopy.

149
Q

Inflammatory bowel diseases are treated with drugs that suppress the immune system

A
  • standard treatment to achieve remission is with drugs containing 5-aminosalicylate (5-ASA)
150
Q

This patient is treated with the drug balsalazide, which consists of 5-ASA linked to an inactive carrier molecule. The 5-ASA is not released (and the drug is not active) until the drug gets metabolized in the colon. What do you suppose is responsible for metabolizing balsalazide?

A

Bacteria in the large intestine.

151
Q

Other treatments for ulcerative colitis

A

If a patient does not achieve remission with a 5-ASA drug, then he might be treated with glucocorticoids. A newer drug for ulcerative colitis treatment is a sort of topical glucocorticoid treatment for the colon. The glucocorticoid drug is contained in a matrix designed to allow steady release once it reaches the colon. This avoids the side effects associated with systemic use of glucocorticoids. More serious cases of inflammatory bowel disease are treated with biologic therapies such as infliximab, a monoclonal antibody drug that inhibits the action of TNF-alpha.

152
Q

What is the normal type of epithelium found in the esophagus, which gives the pale and glossy appearance in endoscopy?

A

Stratified squamous epithelium.

153
Q

What protein, found in parietal cells, is the target of omeprazole?

A

The H+/K+-ATPase, or proton pump. Proton pump inhibitors are the most potent antisecretory drugs (drugs that decrease acid secretion).

154
Q

What type of epithelium is seen with intestinal metaplasia? In particular, what mucus-secreting cell would be seen in this biopsy?

A

The intestinal epithelium is a simple columnar epithelium. A characteristic feature of intestinal metaplasia is the presence of goblet cells, the mucus-secreting cells that are found in the intestines.

155
Q

dysplasia

A

cellular abnormalities that indicate the beginnings of malignant transformation leading to cancer.

156
Q

Peptic Ulcer Disease

A
  • Acid in the stomach kills many bacteria, but H. pylori can evade destruction by burrowing into the protective mucus layer. H. pylori also expresses urease, an enzyme that hydrolyzes urea to produce ammonia, which is used to buffer acid in the immediate environment of the bacterium.
  • Infection with H. pylori causes chronic** gastritis**, which is inflammation of the stomach lining
  • Inflammation causes the recruitment of white blood cells and the production of cytokines, which have effects on the physiology of cells in the stomach epithelium
157
Q

duodenal ulcer

A
  • excessive quantities of acid
  • gastritis is localized in the pyloric region
  • cytokines released in response to inflammation disrupt the regulation of the endocrine cells located in the pylorus
  • G cells are stimulated to secrete more gastrin, while somatostatin secretion is inhibited
  • Gastrin stimulates **parietal cell proliferation **and increased parietal cells along with decreased somatostatin leads to acid hypersecretion
  • acid-neutralizing mechanisms become overwhelmed, and the duodenal tissue becomes damaged.
158
Q

Duodenal Ulcer: Figure

A
159
Q

atrophic gastritis

A
  • gastritis is located predominantly in the body of the stomach
  • inflammation induces apoptosis of parietal cells, and there is eventual atrophy of the gastric glands
  • hyposecretion of acid, or** hypochlorhydria**
  • Continued tissue damage may lead to development of a gastric ulcer
  • H. pylori is classified as a carcinogen because infection increases the risk of developing certain types of gastric cancer
  • atrophic gastric glands undergo a further change known as** intestinal metaplasia**
    • begins to resemble an intestinal epithelium, with villi and goblet cells
160
Q

Atrophic Gastritis: Figure

A
161
Q

drugs that reduce acid secretion

A
  • Reducing the acidity in the stomach lumen promotes healing, and it also increases the effectiveness of the antibiotics (for treating H. pylori)
  • Histamine blockers: these drugs are histamine antagonists that block the stimulatory effect of histamine released by ECL cells
  • Proton pump inhibitors: these drugs bind to and inactivate the H+/K+-ATPase on the apical membrane of the parietal cell
162
Q

Pancreatic Secretion

A
  • Acinar cells produce digestive enzymes: amylase, lipase, and peptidases
  • Pancreatic peptidases are produced as inactive zymogens that are only activated after they reach the duodenum
  • other major secretion is bicarbonate (HCO3-), which is produced by the** duct cells**
    • neutralize acidic chyme coming from the stomach
    • fluid that is produced by duct cells flushes enzymes and zymogens out into the large pancreatic duct.
  • intercalated duct
    • receive the acinar cell secretions, and secrete bicarbonate and fluid
    • connect to larger ducts that eventually lead to the large pancreatic duct that has its outlet at the duodenal papilla
163
Q

Regulation of Pancreatic Secretion

A
  • small amount of pancreatic secretion occurs due to neural inputs that are triggered by cephalic phase and gastric phase stimuli
  • majority of pancreatic secretion arises from **intestinal phase stimuli **(when chyme reaches the duodenum)
  • hormones secretin and cholecystokinin (CCK) are released by endocrine cells that are located in the duodenal epithelium.
  • secretin release is triggered by H+ ions
    • Secretin then travels via the circulation to stimulate bicarbonate secretion by duct cells
  • CCK release is triggered by digestive products (fats and peptides)
    • CCK then travels via the circulation to stimulate secretion by acinar cells.​
164
Q

Defect in duct cell secretion in cystic fibrosis

A
  • Secretion of bicarbonate by duct cells depends upon the protein** CFTR**
  • CFTR protein is also a bicarbonate channel
  • When the CFTR protein is defective, as it is in patients with cystic fibrosis, duct cell secretion is disrupted
    • causes a lack of fluid secretion to flush out pancreatic zymogens, blockage of pancreatic ducts, and inappropriate activation of trypsin in the pancreas
  • damage to acinar and duct cells, which may be replaced by connective tissue
  • Patients with severe mutations of CFTR (little or no CFTR function) are often born with pancreatic insufficiency, meaning their pancreas does not release sufficient quantities of digestive enzymes
    • failure to thrive, and need to be treated with digestive enzyme supplements​
  • Less severe mutations in CFTR (with some channel function) still increase the risk for **pancreatitis. **
165
Q

Bile

A
  • produced in the liver by hepatocytes
  • ** **contains phospholipids and bile salts, emulsifying agents that are necessary for fat absorption and digestion
  • bile is also a route for excretion of **cholesterol **and bile pigments
  • Bile pigments are metabolic breakdown products of hemoglobin and cytochromes that give bile its yellow-green color
  • Bile pigments are further metabolized by bacteria in the colon, causing feces to have a characteristic brown color
  • bile contains water and bicarbonate ions that are secreted by duct cells that line the bile ducts within the liver.
166
Q

Bile Storage in the Gallbladder

A
  • Whether or not bile is released into the small intestine depends upon the activity of the sphincter of Oddi
  • interdigestive period, the sphincter of Oddi is contracted, preventing bile from flowing out into the duodenum
  • pressure increases in the** common bile duct**, and bile flows into the gallbladder
  • gallbladder, epithelial cells reabsorb water and electrolytes, causing the bile to become more concentrated.
167
Q

Bile Flow Interdigestive/Digestive Period

A
168
Q

Bile release into the small intestine

A
  • During the digestive period, **intestinal phase **signals stimulate the release of bile into the small intestine.
  • Fatty acids in the lumen of the duodenum stimulate endocrine cells to release the hormone cholecystokinin (CCK)
    • stimulates contractions in the smooth muscle of the gallbladder
    • causes relaxation of the sphincter of Oddi, allowing bile release into the duodenum.
  • Acidic chyme in the lumen of the duodenum stimulates other endocrine cells to release the hormone secretin
    • Secretin stimulates duct cells in the liver to release bicarbonate into the bile.
169
Q

Enterohepatic circulation

A
  • bile salts present in the body are not sufficient to fully process the fats in a typical meal, thus they need to be recycled
  • Specific transporters in the terminal ileum move bile salts from the lumen of the digestive tract to the intestinal capillaries
  • transported directly to the liver via the hepatic portal vein
  • Hepatocytes take up bile salts from the blood, and increase the secretion of bile salts into the bile canaliculi
  • 95% of the bile that is released to the small intestine is recycled via the enterohepatic circulation,while 5% of the bile salts are lost in the feces
170
Q

Gallstone Location and Consequences: Figure

A
171
Q

Fecal Continence

A
  • maintained by two sphincters that surround the anal canal
  • internal anal sphincter
    • ​extension of the muscularis externa, and thus is smooth muscle innervated by enteric neurons found in the myenteric plexus
  • external anal sphincter
    • skeletal muscle that can be consciously controlled, and is innervated by somatic efferent neurons
  • puborectalis muscle
    • loops around the rectum like a sling, pulling it forward to create a more acute angle between the rectum and the anal canal
      • anorectal angle
  • ​During defecation, there is conscious relaxation of the puborectalis muscle, which creates a more open anorectal angle and allows for a straigther passage through the anal canal
172
Q

Anal Sphincters: Figure

A
173
Q

puborectalis muscle: Figure

A
174
Q

Defecation: Flow Chart

A
175
Q

Steps to Defecation

A
  • mass movement triggers a defecation reflex
    • mass movement is a maintained, high-intensity contraction of the circular muscle in the colon, which will propel feces toward the rectum
  • sufficient volume is deposited in the rectum, the increased pressure will stimulate a reflexive contraction in the sigmoid colon and rectum, relaxation of the internal anal sphincter and contraction of the external anal sphincter
  • With delay, continued contraction of the external anal sphincter and high pressure eventually trigger reverse peristalsis in the rectum
  • Defecation involves the relaxation of the external anal sphincter (as well as relaxation of the puborectalis muscle, to create a broader anorectal angle)
  • Expulsion of Feces
    • Valsalva maneuver
    • closure of the glottis along with **contraction of abdominal muscles **to increase abdominal pressure
176
Q

Cholesterol Synthesis Regulation

A
  • in hepatocytes
  • under** negative feedback regulation**
  • increased cholesterol in the cell decreases the activity of HMG-CoA reductase
    • rate-limiting enzyme in cholesterol synthesis.
177
Q

Chylomicrons and VLDL deliver TAG to cells in the body

A
  • Two types of lipoproteins are triglyceride-rich: the chylomicrons and VLDL
  • Chylomicrons are synthesized by enterocytes from lipids absorbed in the small intestine
  • VLDL is synthesized in the liver
  • deliver energy-rich triacylglycerol (TAG) to cells in the body
  • TAG is stripped from chylomicrons and VLDL through the action of lipoprotein lipase
  • TAG to fatty acids and monoglycerides, which can then diffuse into the cell to be oxidized, or in the case of an adipose cell, to be re-synthesized into TAG and stored in the cell
178
Q

LDL delivers cholesterol to cells in the body

A
  • As VLDL particles are stripped of triacylglycerol, they become more dense
  • deliver cholesterol to cells, where it is used in membranes, or for the synthesis of steroid hormones
  • Cells take up cholesterol by receptor-mediated endocytosis. LDL binds to a specific** LDL receptor** and is internalized in an endocytic vesicle
  • Receptors are recycled to the cell surface, while hydrolysis in an endolysosome releases cholesterol for use in the cell
179
Q

HDL is involved in reverse cholesterol transport

A
  • Excess cholesterol is eliminated from the body via the liver, which secretes cholesterol in bile or converts it to bile salts
  • liver removes LDL and other lipoproteins from the circulation by receptor-mediated endocytosis
  • excess cholesterol from cells is brought back to the liver by HDL in a process known as reverse cholesterol transport
  • HDL is synthesized and secreted by the liver and small intestine
  • travels in the circulation where it gathers cholesterol to form mature HDL, which then returns the cholesterol to the liver via various pathways
180
Q

Niacin (Nicotinic Acid)

A
  • essential nutrient of the vitamin B complex
  • niacin increases HDL levels and decreases triglyceride and LDL levels
  • inhibit an enzyme in the liver that is involved in triacylglycerol synthesis, causing a decrease in VLDL production
  • prolong the half-life of HDL particles by preventing HDL breakdown
  • Niacin is indicated when HDL is low, as it is the most effective drug for raising HDL levels.
181
Q

Fibrates

A
  • bind to the nuclear receptor PPAR-alpha
  • receptor works as a transcription factor to alter gene expression in target cells
  • increase HDL levels and decrease triglyceride levels
  • primarily used when the primary problem is high levels of triglycerides.

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