Gastrointestinal Flashcards

Question

Histamine

Answer 1

1. Releasing Cells: * Enterochromaffin-like cells * Mast cells 2. Releasing structures: * Stomach 3. Functions: * Increases gastric acid secretion

Answer 2

1. Releasing Cells: * Cells lining GI tract 2. Releasing structures: * Mucosa 3. Functions: * Increase blood flow * Increase mucus secretion * Increase HCO₃^- secretion

Answer 3

1. Releasing Cells: * D cells 2. Releasing structures: * Stomach * Pancreas 3. Functions: * Inhibits peptide hormones * Inhibits gastric acid secretion

Answer 4

* Smooth muscle cells electrically coupled * Resting membrane potential oscillates ⇒ **slow waves** or **basic electric rhythm** * Slow waves generated by **Interstitial Cells of Cajal (ICC)** * Located in muscularis externa * Connected by gap junctions to smooth muscle cells * Drives AP of the entire muscle * Amplitude & frequency of slow waves altered by: * ANS * SNS input decreases or abolishes slow waves * PNS input increases amplitude * Hormones * Paracrines * Weak contractions can occur without AP if slow wave amplitude reaches contraction threshold * If AP fires contractile force enhanced

Answer 5

Both a **voluntary and involuntary** process. **Functions:** * Mixing food with saliva to lubricate and facilitate swallowing * Exposing starches to salivary α-amylase to initiate digestion * Reducing size of food particles

Answer 6

**Initiated voluntarily then becomes mostly a reflex action.** 1. Initiated when **touch receptors** of **pharynx** stimulated by **presence of food**. 2. **Afferent sensory impulses** sent to **swallowing center** of **medulla** and **lower pons**. 3. **Efferent motor neurons** transmit impulses to: * musculature of the **pharynx** and **upper esophagus** via **cranial nerves** * **remainder of the esophagus** via **vagal motor neurons**

Answer 7

Divided into 3 phases: 1. **_Oral Phase_** (voluntary process) * **Tip of tongue** seperates food bolus * **Tongue** presses against **hard palate** then sweeps backwards forcing bolus into **pharynx** * Bolus stimulates **touch receptors** triggering **swallowing reflex** 2. **_Pharyngeal Phase_** (takes \< 1 sec) * Respiration inhibited * **Nasopharynx** closed * prevents food entering nasopharynx * opens passage for food to pass into pharynx * **Vocal cords** and **larynx** move forward and upward against **epiglottis** * prevents food from entering trachea * opens **upper esophageal sphinchter (UES)** * **UES relaxes** to receive bolus * Contraction of **upper constrictor muscles** moves food deep into pharynx * **Peristaltic wave** initiated by contraction of **pharyngeal superior constrictor muscles** * Wave moves towards the esophagus forcing bolus through relaxed UES 3. **_Esophageal phase_** (controlled by **swallowing center**) * Once bolus past UES, **esophagus** contricts by a **reflex action** * **Primary peristaltic wave** begins **below UES** * Travels entire esophagus in \< 10 secs * Moves food bolus in front of it * If 1° wave insufficient, resulting **esophageal distension** triggers a **secondary peristaltic wave** **above** point of distention * Peristaltic waves modulated by input of **sensory fibers** to **CNS** and **enteric NS**

Answer 8

**_Structure_** * **Upper 1/3** * Composed of **skeletal muscle** * Innervated by **somatic motor fibers** * **Lower 2/3** * Composed of **smooth muscle** * Fed by branches **vagus nerve** * **Myenteric plexus** neurons directly innervate smooth muscle cells **_Transit_** * **Peristatic wave** propels food along esophagus * Associated **pressure wave** moves downward * Detected by manometer * **Relaxation of lower esophageal sphincter (LES)** allows food into stomach

Answer 9

* Tonic contraction of LES regulated by intrinsic and extrinsic nerves & hormones. * Most of the **resting tone of LES** mediated by **excitatory vagal cholinergic nerves** * **SNS** stimulation **contracts LES** * **LES relaxes** with initiation of peristalsis * **Vagus nerve** → **enteric nerves** → inhibit circular muscles of LES via: * **neurocrines** * **VIP** * **nitric oxide (NO)**

Answer 10

* Failure of LES to completely relax with swallowing and esophageal peristalsis * Symptoms: * dysphagia * regurgitation * aspiration pneumonia * Treat by stretching or sweakening LES with surgery or drugs

Answer 11

* Reflux of acidic gastric contents into esophagus * Caused by: * inadequate closure of LES * hiatal hernia which reduces ability of diaphragm to act as additional sphincter * Sx include heart burn and regurgitation * Sequela: * erosions and ulcerations of epithelium * esophageal stricture * columnar epithelium metaplasia (Barrett's esophagus) * Treatment: * PPI * hernia repair * LES closure

Answer 12

* Disorder of peristalsis * Simultaneous contractions of long duration of high amplitude * Dysphagia and chest pain * Treat with calcium channel blocks

Answer 13

1. Lubricate food 2. Facilitate speech 3. Protection against xerostomia (dry mouth), dental carries, and infections

Answer 14

1. **HCO₃^-** * maintains basic pH 2. **sIgA** against oral flora 3. **Mucins** * responsible for viscosity * most abundant protein in saliva 4. **Lysozyme** * disrupts bacterial cell walls 5. **Lactoferrin** * iron-binding protein to inhibit bateria 6. **Salivary α-amylase** * breaks down starches by cleaving α-1,4-glycosidic bonds * destroyed by stomach pH 7. **Lingual lipase** * hydrolyzes lipids * remains active throughout GI tract

Answer 15

Three pairs of salivary glands: 1. **Parotid** * mostly serous * contains mainly water and salt 2. **Submandibular** * mixed secretions 3. **Submaxillary / Sublingual** * mixed secretions

Answer 16

* **Salivon**: basic unit of a salivary gland * Contains: * **Acinus** * **Serous cells**: * secrete watery isotonic fluid * contains proteins such a α-amylase * **Mucous cells**: * secrete mucins * gives saliva its viscosity * **Intercalated duct** * **Striated duct** * **Excretory duct**

Answer 17

* **_Flow increased by:_** * smell and taste of food * mechanical pressure in mouth * various reflexes * **_Flow decreased by:_** * stress * dehydration * sleep * **Rate of secretion proportional to glandular blood flow.** * _Blood flow under ANS control:_ * **_Parasympathetic_** * Leads to **vasodilation** * **Ach → M₃ muscarinic** * **Substance P** * **VIP** * Increases fluid secretion by **acinar cells** * Increases synthesis of **salivary α-amylase** and to lesser extent mucins * Increases transport in **striated and excretory duct cells** * Net result is increased production of **watery** saliva rich in **electrolytes** and **salivary α-amylase.** * **_Sympathetic_** * Norepi → **β-adrenergic receptors** * Increases salivary flow by stimulating **contraction** of **striated duct cells** * Results in slightly increased production of **viscous** saliva richer in **proteins** and **mucins**

Answer 18

**Iso-osmotic to plasma.** * **_Basolateral_** * **Na/K-ATPase** * 3 Na⁺ out to interstitium * 2 K⁺ into cell * **Na/H exchanger** * Na⁺ into cell * H⁺ out to interstitium * **Na/K/Cl cotransporter** * Na⁺ into cell * K⁺ into cell * 2 Cl^- into cell * **_Apical_** * **Cl/HCO₃ cotransporter** * HCO₃^- out to lumen * Cl^- out to lumen * **_Paracellular_** * Cl/HCO₃ cotransporter established transepithelial potential with lumen negative * Favors **Na⁺** movement **into lumen** via paracellular pathway * **_Intracellular_** * ***Carbonic anhydrase*** * HCO₃^- and H⁺generated from CO₂ * **H₂O** moves **into lumen** due to **osmotic forces**

Answer 19

Electrolyte content altered as saliva travels down **intercalated and striated ducts**. Cells relatively **water-impermeant**. **Na⁺ and Cl^- absorbed.** **K⁺ and HCO₃^- secreted.** Net movement of salt without water produces **hypotonic saliva**. * **_Basolateral_** * **Na/K-ATPase** * 3 Na⁺ out to interstitium * 2 K⁺ into cell * **Na/H exchanger** * H⁺ out to interstitium * Na⁺ into cell * **Na/HCO₃ cotransporter** * Na⁺ out to interstitium * 2 HCO₃^- into cell * **Cl^- channel** * Cl^- out to interstitium * **_Apical_** * **Na/H exchanger** * H⁺ out to lumen * Na⁺ into cell * **Epithelial Na⁺ channel (ENaC)** * Na⁺ into cell * **Cl/HCO₃ exchanger** * HCO₃^- out to lumen * Cl^- into cell * **CFTR Cl^- channel** * Cl^- out to lumen * **H/K exchanger** * K⁺ out to lumen * H⁺ into cell

Answer 20

The slower the movement of saliva through the duct system the longer the time for electrolyte exchange. * Inc. secretion rate ⇒ dec. Na⁺ and Cl^- absorption & dec. K⁺ excretion * Inc. rate of secretion ⇒ inc. HCO₃^- levels * Due to inc. secretion by acinar cells * Ensures saliva remains slightly alkaline

Answer 21

**_Acinar Cells_** **Apical Cl^- channels** & **Basolateral K⁺ channels** _Increased_ by: **Ach** via M₃ receptors **Norepi** via α-adrenergic receptors **Substance P** via NK-1 receptors **_Ductal Cells_** Cl^- excretion by **CFTR** _increased_ by **Norepi** via β-adrendergic receptors **Na⁺ and Cl^- absorption** _decreased_ by **Ach** via M₃ receptors **Na⁺** and (indirectly) **Cl^-** **absorption** _increased_ by **aldosterone** through **ENaC** activity.

Answer 22

Four anatomical regions: 1. **Cardia** * Where esophageal contents 2. **Fundus** * Forms the upper curved region 3. **Corpus** (body) * Main region 4. **Pylorus** * Lower section * Facilitates emptying of gastric contents to duodenum

Answer 23

Consists of two functional regions: 1. **_Gastric reservoir_** * Fundus and top 1/3 of corpus * Muscles maintain a **continuous tone** * **No phasic contractions** 2. **_Antral pump_** * Distal 2/3 of corpus, antrum, and pylorus * Distal antrum undergoes **phasic contractions** * Breaks up food increasing SA and aiding digestion * Provides propulsive force to move contents into gastroduodenal junction

Answer 24

* **_Three layers of smooth muscle_** * **outer longitudinal layer** with **tonic** smooth muscle * **middle circular layer** with **phasic** smooth muscle * **inner layer** formed by **two bands** of smooth muscle: * radiates from LES * fuse with circular muscle at caudal area * **_Layers of muscularis externa_** * thin in the fundus and body * become thicker in the antrum * **_Mucosa_** * Contains various secretory cells * **Corpus** * **Parietal cells** * acid * intrinsic factor * **Chief cells** * pepsinogen * **Antrum** * **Chief cells** * Various **endocrine cells** * G & D cells

Answer 25

* **_Parasympathetic_** * **Vagus** **nerve** * Leads to motility and secretion * **_Sympathetic_** * **Celiac plexus** * Inhibits digestive functions * **_Sensory fibers_** * Some leave via vagus and other with celiac plexus * Some afferent links between sensory receptors and intramural plexuses * Relay information about: * intragastric pressure * gastric distention * pH * pain

Answer 26

1. **_Receptive relaxation_** * **Act of swallowing** activates a _vagovagal reflex_ * Relaxes LES and fundus * Anticipates food entering stomach 2. **_Adaptive relaxation_** (or **gastric accommodation**) * **Distention of gastric reservoir** by food activates a _vagovagal reflex_ * Large increase in stomach volume with little increase in intraluminal pressure * Lost after vagotomy

Answer 27

a.k.a. migrating myoelectric complex * Occurs during **fasted state** * Stomach **quiescent for 75 - 90 mins** * Followed by **vigours contractions in the antrum lasting 5-10** * **Pylorus is relaxed** * Cyclical activity sweeps from **stomach to terminal ileum** * Functions to **move undigested contents** from stomach → small intestine → colon * Maintains **low bacterial count** in upper intestine * MMC in stomach terminated by eating → fed pattern emerges * Initiated by **Motilin** * Propagated by **enteric NS**

Answer 28

* Eating terminates MMCs in stomach * In **fed state**, gastric contractions ~ 3/min * **Slow waves driven by ICC pacemakers** * Propagates towards pylorus * Gastric smooth muscle contractions occur when threshold crossed * Body has slow waves without AP's * AP in atrum occurs during plateau phase of slow wave * Contractions in atrum much stronger than in body * **Frequency and amplitude** of slow waves modulated by neural and hormonal input: * **Ach** and **gastrin** _stimulate_ contractions * **Norepi** _diminishes_ contractions

Answer 29

Liquids readily move from stomach into duodenum. Solids must be reduced to ~ 2 mm before moving to small intestine. * **_Propulsion_** * gastric contractions originate in the middle of the body * travel towards pylorus increasing in force and velocity * **_Grinding_** * majority of mixing activity occurs in the antrum * as peristaltic wave → antrum, pyloric sphincter shuts * small amount of chyme enters duodenum * **_Retropulsion_** * remaining chyme propelled back to fundus and body for more mixing * cycle repeats until particles ~ 2mm

Answer 30

* Functions of gastroduodenal Junction: * regulation of gastric emptying * prevention of regurgitation * **Pylorus** seperates antrum and proximal duodenum * **Neural control** * **Sympathetic** input increases pyloric constriction * **Parasympathetic** (vagal) input mixed: * **excitatory** (constriction) ⇒ **cholinergic** * **inhibitory** (relexation) ⇒ **VIP** and **NO** * **Hormonal control** * Promote **pyloric constrictio**n ⇒ slow gastric emptying * **CCK** * **gastrin** * gastric inhibitory peptide (**GIP**) * **secretin** * **Proximal Duodenum** * Influenced by slow waves of: * stomach (3-5/min) * duodenum (11-13/min) * **Contracts irregularly** * When antrum contracts, proximal duodenum often relaxed.

Answer 31

~ 3 hrs to empty 1,500 ml Tightly controlled by neural and hormonal mechanisms. * Sensory receptors in duodenal and jejunal mucosa sense: * osmotic pressure * pH * fats and fat digestion products * peptides * amino acids * Distention promotes emptying. * The greater the ingested volume, the faster the rate of emptying. * Relative rate based on **dominant nutrient class**: liquids \> carbs \> proteins \> fats * **Amino acids and proteins** * Stimulate **gastrin** from G cells in antrum and duodenum * Inc. antral contractions * Inc. pyloric contractions * Net dec. in gastric emptying * Stimulates **GIP** and **CKK** secretions * Inhibits gastric emptying * **Fats and monoglycerides** in _jejunum_ * Stimulates CCK and GIP * Both slow gastric emptying * **Hypertonic solutions** slow gastric emptying * Chyme becomes more hypertonic in duodenum * Added digestive enzymes * Increased # particles * Acid slows gastric emptying * Secretin released d/t acid in duodenum * Inhibits antral contractions * Stimulates pyloric sphincter contraction

Answer 32

Hormones released from the intestine which affects gastric secretions.

Answer 33

Expulsion of gastric/duodenal contents via the mouth. **Reflex behavior** controlled by **vomiting center** in medulla. Triggered by gastric distention, throat tickle, GU injury, dissiness. 1. Stimulus sent to **vomiting center**. 2. May begin with wave of **reverse peristalsis**, duodenum → stomach. * Severe obstruction primary stimulus for this 3. **Pylorus** and **stomach** _relax_ to accomodate contents. 4. **Forced expiration** occurs against a **closed glottis**. * Dec. intrathoracic pressure * Inc. intra-abdominal pressure 5. Strong contration of **abdominal muscles** * Further inc. intra-abdominal pressure * Forces **gastric contents into esophagus** * Accompanies **relaxation of UES** 6. **LES relaxes** while **pylorus and antrum contract**. 7. Gastric contents ⇒ esophagus, with **relaxation of UES**. 8. Emesis **_Retching_** * Gastric contents forced into esophagus but not pharynx * Because UES closed * Respiratory and abdominal muscles relax * Secondary peristalis returns contents to stomach * Typically, series of retches precedes vomiting.

Answer 34

* kills microorganisms * cleaves pepsinogen → pepsin * maintains low pH needed for pepsin activity * secreted by **parietal cells**

Answer 35

* secreted by **chief cells** as pepsinogen precursor * activated by acid in stomach * digests **proteins and peptides**

Answer 36

* secreted by **parietal cells** * binds **Vit B₁₂** allowing absorption in the **ileum**

Answer 37

* Secreted by **mucous neck cells** → serous thinner mucous * Secreted by **surface epitheliam cells** → thicker mucous * protects stomach epithelium from damage

Answer 38

* mixture of secretions from gastric epithelial cells and glands * **Non-parietal cells** * Secretion **constant and low volume** * Mostly **Na⁺ and Cl^-** * **K⁺, and HCO₃^-** at plasma concentration * **Parietal cells** * Secrete 150 mM **HCl** solution with 10-20 mL **KCl** * Secrete acid and Cl^- against gradient * ionic composion depends on rate of secretion * **slow → hypotonic** * primarily NaCl with pH ~ 2 * **fast → almost isotonic** * Na⁺ decreases * H⁺ increases * K⁺ always higher than plasma → prolonged vomiting = hypokalemia * as **rate increases** parietal cell compnent increases while non-parietal stays constant → approaches **pure parietal secretion**

Answer 39

Secretes acid against 10⁶ concentration gradient. * **_Intracellular_** * CO₂ converted to **H⁺** and HCO₃^- by **carbonic anhydrase** * **_Apical_** * **_H⁺/K⁺ exchanger_** * H⁺ into lumen while K⁺ enters cell * main acid transporter * target for PPIs * **_Cl_****^-** **_channel_** * Allows Cl^- to move down gradient into lumen * Combined with H⁺ to form HCl * **K⁺ channel** * K⁺ out on both apical and basolateral membranes * Luminal K⁺ recycled to drive movement of H⁺ into lumen * **_Basolateral_** * **Na/K-ATPase** * Moves Na out and K in * Sets up intracellular K gradient * **Cl/HCO₃ exchanger** * Bicarb into interstitium * Causes alkaline venous blood * Cl^- into cell * **K⁺ channel** * K⁺ out on both

Answer 40

* **_Directly stimulated by:_** * **Ach** * **Vagus nerve** → **M₃ muscarinic** → Ca⁺⁺ → **PKC** * **Gastrin** * **G cells** → **CCK_B receptors** → Ca⁺⁺ → **PKC** * In response to * PNS stimulation * amino acids and peptides in chyme * **Histamine** * Enterochromaffin-like **(ECL) cells** → **H₂ receptors** → Adenylate cyclase → **PKA** * In response to **Ach & gastrin binding ECL cells** * Receptor target for **H₂ blockers** * Synergistic response ⇒ **potentiation** * **_Inhibited by:_** * **Somatostatin** * **Prostaglandins** (E and I) * **Epidermal growth factor** (EGF) * All 3 act through inhibit of adenylyl cyclase → dec. cAMP

Answer 41

1. **_Cephalic phase_** * **Triggered** by **food** * **Vagovagal reflex** to **parietal and G cells** * ~40% of total gastric secretion 2. **Gastric phase** * _Triggered by:_ * **stomach distention** * **mechanoreceptors** → enteric & CNS → **Ach** → direct stimulation of **parietal cells (acid)** and **G cells (gastrin)** * **Gastrin** stimulates acid release * presence of **amino acids and peptides** * other chemicals like alcohol and caffeine * ~50% of gastric secretions 3. **_Intestinal phase_** 1. Triggered by **protein digestion** **products** in chyme in **duodenum** 1. **Duodenal distention** triggers **vagovagal reflex** → stimulates **parietal and G cells** 2. **Peptides and AA** stimulate **G cells** of **duodenum and proximal jejunum** → **Gastrin** 1. Also stimulates **duodenum** to release **entero-oxyntin** → stimulates **acid** secretion 2. Inhibited by **acid, fatty acids, monoglycerides, hypertonic chyme** in duodenum and proximal jejunum 3. Stimulated with **chyme pH \> 3**

Answer 42

Stimulated by: * PNS → **vagal stimulation** during **cephalic and gastric phases** → Ach → chief cells → pensinogen * **Acid** → enteric NS → **local cholinergic reflex** → Chief cells → pepsinogen * Secretion **increased when luminal pH low** * **Duodenal mucosa** → **Secretin and CCK** → pepsinogen

Answer 43

* **_Soluble mucous_** * PNS → **vagus** nerve → Ach → **mucous neck cells** → soluble mucous * **_Insoluble mucous and HCO₃^-_** * Secreted by **surface epithelial cells** * In response to **chemical or physical irritation** * Insoluble mucous traps dead cells and bicarb

Answer 44

* Villi increase surface area * Epithelial cells and globlet cells * Capillaries and lacteals * **Crypts of Lieberkuhn** * openings at base of villi * mostly in duodenum and jejunum * secrete **salts and water** * **Goblet cells** secrete **mucous** * **Paneth cells** secrete **defensins**

Answer 45

1. **Peristaltic contractions** * **vectoral** movement * propels chyme * slow waves generated by **ICCs** control contractions * duodenal contractions follow stomach contractions 2. **Segmental contractions** * most common movement * small sections rhythmically contract and relax * **mix chyme** with secretions 3. Codeine and opiates inhibit contractions

Answer 46

* MMCs during fasted state for housekeeping * Slow waves generated by ICCs * Limited to small areas * Can have APs superimposed * responsible for segmentation and peristaltic contractions * Smooth muscle cell excitability influiced by: * direct effects from enteric NS * inditect effects from CNS via enteric NS and ICCs * PNS increases excitability * SNS decreases

Answer 47

When a material placed in the small intestine, it will contract behind it and relax ahead of it. Responsible for movement of chyme in proper direction.

Answer 48

Overdistension of one segment of the intestine relaxes smooth msucle in the rest of the intestine. Protects from potential reupture. Does not faciliate movement.

Answer 49

Elevated stomach activity increases movement of chyme from the terminal ileum into the colon through the ilealcecal sphincter.

Answer 50

* Found in the beginning of the duodenum between pylorus and sphincter of Oddi * Secretes HCO₃^- and mucus * Protects epithelial cells from acid in chyme

Answer 51

* Epithelial cells secrete **isotonic fluid** * Up to 1.8 L/day * Keeps chyme in aqueous solution * Several transporters involved: * _Basolateral_ * **Na/K-ATPase** * sets up Na⁺ gradient * **NKCC1 cotransporter** * Na⁺, K⁺, and 2 Cl^- moved into cell * Uses Na⁺ gradient * _Apical_ * **CFTR Cl^- channel** * Cl**^-** into lumen * Activity increased by secretagogues * **Secretin and VIP** → cAMP → **PKA** → phosphorylates and **opens CFTR** * Cl^- movement increases luminal negatvity * **Na⁺** moves into lumen via **paracellular** pathways * **Water follows.**

Answer 52

Hormones released from the gut that increase insulin secretion in a glucose-dependent manner. Released in response to glucose in the lumen of small intestine. Act on β-cells of the endocrine pancreas to stimulate insulin release. * **Gastric inhibitory peptide (GIP)** * Secreted by K cells in duodenum and jejunum * **Glucagon-like intestinal peptide (GLP-1)** * Secreted by L cells in ileum and colon

Answer 53

* Secretion of **pancreatic juice** * Aids in digestion * Composed of **water, salts, and enzymes** * HCO3 neutralizes stomach HCl * Enzymes degrade carbs, proteins, and lipids * **Secretin** stimulates **bicarb** secretion * released in response to **acid in chyme** * **CCK** stimuates **digestive enzyme** secretion * released in response to **protein and fat in chyme**

Answer 54

**_Structure_** * **Pancreatic acinar cells** * specialized for **protein secretion** * **Ductal columnar epithelial cells** * specific membrane transporters * **bicarb excretion** **_Innervation_** * **PNS** * innervated by branches of the **vagus nerve** * synapse with neurons in pancreas * use **Ach** * * _directly_ stimulates **pancreatic juice secretion** * **SNS** innervate pancreatic **blood vessels** * activation → **vasoconstriction** * **indirectly decreases secretion** * no direct sympathetic effect on secretions

Answer 55

Secreted by **ductal columnar epithelial cells**. * Contains entirely water and salts * Initially hypertonic but water during duct movement making **isotonic** * **Na⁺ and K⁺** concentrations similar to plasma * **HCO₃^-** much higher than plasma * **concentration increases as rate of secretion increases** * **Cl^- concentration reciprocal to bicarb** * when bicarb high Cl low and vice versa

Answer 56

* **_Sources:_** * made by **carbonic anhydrase** * transported into cell from basolateral membrane by **Na⁺/HCO₃^- co-transporter** * **_Ductal Cell transporters_** * **Basolateral** * **Na⁺/K⁺-ATPase** sets up gradient * **Na⁺/HCO₃^- co-transporter** brings in bicarb * **Na⁺/H⁺ counter transporter** and **H⁺ pump** * removes H⁺ generated by carbonic anhydrase * favors splitting of water needed for bicarb production * **Apical** * **CFTR Cl^- channel** * moves Cl^- into lumen * **_Secretin_** ⇒ cAMP ⇒ PKA ⇒ **activates CFTR** * **Cl^-/HCO₃^- exchanger** * uses Cl^- gradient * exchanges luminal Cl^- for HCO₃^- * **Na⁺ and water** follows Cl^-/HCO₃^- into lumen via **paracellular** path * **Ach** ⇒ **Ca⁺⁺** ⇒ Ca⁺⁺-and-calmodulin dependent protein kinase II (**CaMK II**) ⇒ **increases HCO₃^- secretion** via unknown mech

Answer 57

Released from the **pancreatic acinar cells**. Isotonic and similar ion concentration to plasma. Exocytose Zymogen granules into lumen when stimulated * Proteases * **Trypsinogen** * Cleaved by **enterokinase** in _duodenum_ * Trypsin **cleaves other zymogens** * **Trypsin inhibitor** secreted from acini to inhibit prematurely formed trypsin * **Chymotrypsinogen** * **Procarboxypeptidase** * **Pancreatic α-amylase** * Degrades starches * Secreted in active form * **Lipase** * Requires **co-lipase** coenzyme to function * Fat degradation * **RNAse & DNAse** * degrade nucleic acids

Answer 58

Secretin and CCK secreted by duodenal mucosa. * **Ach** and **CCK** ⇒ **Ca⁺⁺** mechanism * **Secretin** and **VIP** ⇒ **cAMP**-mediated * **PNS** **vagal stimulation** activates secretion of pancreatic juices * **SNS** stimulation decreases in blood flow * indirectly inhibits pancreatic secretion

Answer 59

1. Cephalic Phase * Triggered by food * Vagus stimulation via muscarinic Ach receptors on acinar cells * Volume of pancreatic juice secreted low * Predominantly enzymatic 2. Gastric Phase * Triggered by food entering stomach * Vagovagal reflex starts in stomach * Induces pancreatic secretion * Gastrin released by stomach in response to AA * Activates CCK receptors on pancreatic acinar cells * Stimulates pancreatic secretion * Predominant effect on enzyme secretion 3. Intestinal Phase * Vagovagal reflexes stimulate pancraetic secretion * Acid in chyme stimuates Secretin * Secretin stimulates production of large volumes of pancreatic juice * Low enzyme concentration * High bicarb * AA and peptides in chyme in duodenum * Stimulate release of CCK from duodenal mucosa * CCK stimulates pancreatic enzyme release * Fatty acids and monoacylglycerols in duodenum * Stimulates CCK release * CCK stimulates pancreatic enzyme release * CCK and secretin work synergistically

Answer 60

* **Starch (**glucose, α-1,4- linkages with α-1,6 branches) * main dietary carbohydrate * ***salivary α-amylase*** in mouth * breaks _α-1,4-linkages only_ * ***pancreatic α-amylase*** in duodenum * _glucose polymers_ * _limit dextrin_ * **oligosaccharidases** * membrane bound at brush border * break down into _glucose monomers_ * ***α-dextrinase*** for limit dextrin * ***glucoamylase*** (maltase) for glucose polymers * **Lactose** (glucose-galactose) * ***Lactase*** breaks down to monomers * **Sucrose** (glucose-fructose) * ***Sucrase*** breaks into monomers

Answer 61

* Greatest absorption in **duodenum** * Decreasing as chyme travels down small intestine * All mono and di-sacch. absorbed in small intestine * 80-90% of start absorbed * remainder to colon where degraded by bacteria * Na⁺-dependent glucose transporter **(SGLT1)** * **glucose** and **galactose** into cell * secondary active transport * **GLUT 5** * **fructose** into cell * facilitated transporter * **GLUT 2** * facilitated transporter * move **all monosaccharides** out of basolateral membrane

Answer 62

* Deficiency of lactase after childhood * normal occurance * Lactose not degraded * Enters colon where degraded by bacteria * Causes gas and diarrhea

Answer 63

Complete loss of lactase at all life stages. Rare.

Answer 64

* Due to **defect in SGLT1** * Cannot absorb glucose or galactose * All carbs from fructose * Avoid starch, sucrose, and lactose

Answer 65

* Pancreactic Proteases * ***Trypsin*** * Activated by ***enterokinase*** * cleaves other inactive enzymes * ***Chymotrypsin*** * ***Carboxypeptidases*** * In duodenum: * Proteases degrade proteins into peptides containing **3-8 AA and free AA** * On brush border: * Membrane bound ***oligopeptidases*** and ***peptidases*** * Cleave most small peptides to free AA * Almost all protein cleaved to **free AA, di- and tri-peptides** in small intestine lumen

Answer 66

* Greatest amount in **duodenum** * Decreases as chyme moves down small intestine * **Na⁺/amino acid cotransporters** * primary **free AA** transporter * uses Na⁺ gradient * **H⁺/peptide cotransporter (PepT1)** * transport **di- and tri-peptides** * uses H⁺ gradient set up by **Na⁺/H⁺exchanger** on apical membrane * Inside the cell * di- and tri-peptides broken down into **free AA** by ***peptidases*** * Free AA transported into blood by **basolateral AA transporters** * two Na⁺dependent * three Na⁺ independent * each has **specificity** towards specific types of AA

Answer 67

* Small amount of protein absorbed by **phagocytosis** * important during first 6 months post-natal * aids in transfer of immunity * after 6 months, decreases to very low levels * primarily important for **antigen uptake and clearance**

Answer 68

* Ingest 2-2.5 L/day * Secrete ~ 7 L/day into GI tract * Only ~ 0.1 L excreted in feces * Absorb almost 9 L/day * no net water absorption in duodenum * most water absorbed in **jejunum and ileum** * ~ 2 L/day reaches **colon** * 1.9 L reabsorbed

Answer 69

* occurs throughout small intestine * little net absorption in duodenum * most occurs in **jejunum and ileum** * Basolateral **N⁺/K⁺-ATPase** * sets up gradient for other transport systems * Most Na reabsorbed by **sugar or AA linked co-transport systems** * **Na⁺/H⁺ exchanger** on apical membrane * Amiloride-sensitive Na⁺ channels (**ENaC**) * on apical membrane mainly in colon

Answer 70

* Little net absorption in duodenum due to excretions * Cl^- reabsorbed via **paracellular pathway** in **jejunum and ileum** * Direction of movement dependent on electrochemical gradient * Exchanged for bicarb by **Cl^-/HCO₃^- exchanger**

Answer 71

* In duodenum and jejunum: * **HCO₃^-** reacts with **H⁺** to form **H₂CO₃** * H⁺ pumped into lumen by **Na⁺/H⁺ exchanger** * H₂CO₃ broken down by *carbonic anhydrase* to **CO₂ and H₂O** * CO₂ **diffuses across epithelial cell** * **Net absorption of bicarbonate** * In ileum: * basolateral **Na⁺/K⁺-ATPase** * ****sets up gradient * basolateral **Na⁺/HCO₃^- co-transporter** * ****brings HCO₃^- into cell * apical **Cl^-/HCO₃^- counter-transporter** * **net excretion of HCO₃^-** * **net absorption of Cl^-**

Answer 72

* Small intestine * **Luminal [K⁺] progressively increases** * Due to movement of NacL, sugar, and AA from lumen * When [K⁺] becomes high enough it moves via **paracellular** path * Mostly through **solvent drag by water** * **Net absorption of K⁺ occurs** * No active transport of K⁺

Answer 73

Absorbed by both passive and active processes. * **Passive paracellular transport** * Occurs **throughout small intestine** * **Active Ca²⁺ transport** * Only in **duodenum** * Ca²⁺ moves down electrochemical gradient through **Ca²⁺ channel** * Inside cell: * Binds to **calbindin** * take up by **intracellular vesicles** * Bound Ca²⁺ excreted across basolateral membrane by: * **Ca²⁺-ATPase** * **N⁺/Ca²⁺-exchanger** * Active process regulated by **Vit D** (and indirectly by PTH) * Stimulates synthesis of calbindin, Ca²⁺-channels, and Ca²⁺-ATPases * Total Ca²⁺ absorption low in absence of Vit D

Answer 74

Lack of Ca²⁺ absorption can result in: **rickets** in children **osteomalacia** in adults Marked by softening of bones.

Answer 75

* Dietary iron in two forms: * Heme iron * Non-heme iron * Both poorly absorbed (10-20% dietary intake) * **_Heme Iron:_** * always in ferrous form * taken into cell by unknown mechanism * inside cell, **heme oxygenase**: * splits heme * oxidizes Fe²⁺to Fe³⁺ * Fe³⁺ treated like non-heme iron * **_Non-heme iron:_** * Ferric (Fe³⁺) or Ferrous (Fe²⁺) forms * Only absorbed in ferrous form * **Dcytb** * iron reductase on brush border * reduces ferric to ferrous form * **DMT** * H⁺/Fe²⁺- cotransporter * Moves Fe²⁺ into cell * Fe²⁺ binds **mobilferrin** inside cell * moved to basolateral membrane * **Ferroportin (IREG1)** transport out of cell * Oxidized to Fe³⁺ by **ferroxidase-hephaestin** * Binds to **transferrin** for transport through blood

Answer 76

* Disorder of **excess iron absorption** * Iron can accumulate in tissues causing damage * cirrhosis * hepatomas * Defect appears to involve **hepcidin** * normally downregulates DMT expression

Answer 77

* **Primary secretion (bile)** * Secreted by hepatocytes at the end of ducts * Contains bile acids, cholesterol, and PL * Stimulated by **CCK** * **Ductal cells** secrete fluid with **ions and bicar** * Stimulated by **secretin** * Stored and concentrated in the gallbladder * Post-prandial **CCK** stimulates **contration and excretion** * Bile acids emsulsifies fat in duodenum forming micells

Answer 78

* Concentrated x20 in gallbladder * Standing Osmotic Gradient Hypothesis * Transporters set up an osmotic gradient that drives water movement * _Apical_ **Na⁺/H⁺ counter-transporte**r moves Na⁺ into cell * _Basolateral_ **Na⁺/K⁺-ATPase** moves Na⁺ into interstitium * _Basolateral_ **K⁺ channel** acts as K⁺ shuttle for Na⁺/K⁺-ATPase * _Apical_ **Cl^-/HCO3^- exchanger** moves HCO3^- into lumen * HCO3^- neutralizes secreted acids * Cl^- enters cell * _Basolateral_ **Cl^- channel** moves Cl^- into insterstitium * Net Na⁺ and Cl^- movement into insterstitium establishes an _osmotic gradient_ * _Water_ follows Na⁺ and Cl^- into paracellular and instertitial space via **aquaporins**

Answer 79

* **During cephalic and gastric phases:** * Gallbladder contracts * Sphincter of Oddi relaxes * Allows **small amount of contents into duodenum** * Stimulated by: * **Vagus nerve** * **Gastrin** released from stomach * **During intestinal phase:** * **CCK** released from _duodenal cells_ * Strong gallbladder contractions * Complete relaxation of the Sphincter of Oddi * **Allows gallbladder to completely empty**

Answer 80

* **Bile acids reabsorbed in the terminal ileum:** * Cross _apical membrane_ via **Na⁺/bile salt transporter (ASBT)** * Leave basolateral membrane via **Na⁺-independent organic solute transporter** * Transported in the blood to liver by Na⁺-dependent process * Bound to **bile acid-binding proteins** * Secreted into canaliculi * Can be recycled \> 5 times with fatty mean

Answer 81

* Bile acids form micelles when concentration reaches **critical micellar concentration (CMC)** * **Phospholipid/cholesterol vesicles** from liver mix with micelles to form **mixed micelles** * **Monoacylglycerol and FA** from fat breakdown remain in mixed micelles until absorption * If cholesterol levels too high system **supersaturated** * Can form gallstones blocking bile duct

Answer 82

* Heme catabolized to **bilirubin** * Accumulates in blood ⇒ liver * Excreted in bile afte conjugation with **glucuronates**

Answer 83

* **Cholangiocytes** (bile duct cells) secrete aqueous solution * isotonic * higher HCO₃^- * lower Cl^- * Stimulated by **secretin** ⇒ cAMP ⇒ PKA ⇒ phosphorylation of **CFTR Cl^- channels** * initiates Cl^- recycling and Cl^-/HCO₃^- exchange * Also stimulated by: * glucagon * VIP * Inhibited by: * Somatostatin

Answer 84

Occurs in the **Duodenum and Jejunum**. * Mixed micelles increase SA of exposed lipids * ***Pancreatic lipases*** * requires **colipase** to remove inhibition by bile salts * ****break down TAG at water-micelle interface: * **two fatty acids** * **monoacyl glycerol** * ***Cholesterol ester hydrolase*** * pancreatic enzyme * degrades cholesterol esters to: * **cholesterol** * **fatty acid** * products remain in micelles until absorbed into epithelial cells * ***Phospholipase-A₂*** * pancreatic enzyme * degrades phospholipids to: * **fatty acids** * **lysolipid** (PL with only one FA)

Answer 85

* Micelles composed of monoacylglyerol, FA, lysolipids, and cholesterol. * Pass through **unstirred layer** at surface of epithelial cells * **Na/H exchanger** makes layer acidic * Causes **FA** to be **protonated** ⇒ **uncharged** * Movement through layer aided by: * segmentation contractions * contraction of muscularis mucosa * Hypdrophobic digestion products **diffuse through apical membrane** into cell. * **FA** transported to **ER** by **fatty acid binding proteins (FABP)** * **Glycerol** diffuses out into **blood**

Answer 86

* Lipids move to ER bound to **FABPs** * Converted back to **complex lipids**: * Monoacylglycerol + FA = **TAG** * Lysolipid + FA = **phospholipids** * Cholesterol + FA = **cholesterol ester** * In golgi, new lipids combine with **apolipoproteins** forming **chylomicrons** * **Abetalipoproteinemia** ⇒ inability to form chylomicrons * Steatorrhea * Secreted into **lacteals** ⇒ lymph ⇒ thoracic duct ⇒ blood

Answer 87

* Starts at **ileocecal sphincter** * Distension of distal ileum ⇒ peristalsis ⇒ sphincter relaxation ⇒ movement of chyme into proximal colon * Sphincter closes as proximal colon becomes distended * Smooth muscle * primarily **circular** smooth muscle * longitudinal smooth muscle in 3 band ⇒ **taenia coli** * **Anal canal** * end of the colon * closed by: * **internal anal sphincter** ⇒ smooth muscle * **external anal sphincter** ⇒ skeletal * innervated by somatic motor fibers from **pudendal nerve** * **Colonic contractions** * Mix chyme * Moves it along epithelial surface very slowly * **Mass movement** * Occurs 1-3 times / day * Colonic contents move a significant distance * Segments remain contracted for several minutes

Answer 88

* In proximal colon: * contractions segmental ⇒ **Haustra** process ⇒ Haustration * mixes chyme * little vectoral motion * slows movement of chyme so salt and water can be reabsorbed

Answer 89

* **Mass movements** move semi-solid feces to mid-colon * **Colonic contractions** continue to mix feces * Additional mass movements push feces towards end of the colon and into rectum

Answer 90

* **Direct control** of colonic contractions from **intramural plexus** * **Stimulatory** nerves ⇒ **Ach** and **substance P** * **Inhibitory** nerves ⇒ **VIP** and **nitric oxide** * Extrinsic nerves only have indirect effects.

Answer 91

* Colonic circular smooth cells rarely produces APs independently * **Interstitial cells of Cajal (ICCs)** * near inner border of smooth muscle * generates **slow waves** * **Enteric NS** ⇒ Ach ⇒ **stimulates ICCs** * **increase length of slow waves** * longer slow waves cause contraction * **Second class of ICCs** * near outer border * generates **myenteric potential oscillations** * lower in amplitude * higher frequency * may produce APs generating contractions

Answer 92

When one part of the colon is distended, the other parts relax. Reflex initiated by sympathetic nerve fibers.

Answer 93

When food enters the stomach, colonic smooth muscle contracts producing a mass movement. Sometimes of sufficient pressure to produce need to defecate.

Answer 94

* Mass movement in sigmoid colon fills rectum with feces * Triggers a **rectosphincteric reflex**: * **relaxes internal anal sphincter** * **constricts external anal sphincter** * interpreted as urge to defecate * Defecation starts with **voluntary relaxation of the external anal sphincter** * Other voluntary actions include: * deep breathing to increase abd pressure * contracting abnormal wall muscles * relaxation of pelvic floor * Involves strong contractions of the descending and sigmoid colon * **Reflex** controlled by **sacral spinal cord** with **PNS** fibers

Answer 95

Two different mechanisms: 1. **Early or proximal colon** * Na⁺/H⁺ exchanger * Cl^-/HCO₃^- exchanger 2. **Distal colon** * Aldosterone senstitive Na⁺ channel (ENaC) on apical membrane * Produces large transepithelial potential with lumen negative * Cl^- movement via paracellular path

Answer 96

Colon is a net secretor of K⁺. Occurs over entire length of colon. * **Passive K⁺ secretion** * Responsible for overall net K⁺ loss * **Paracellular** path * Driven by **negative transepithelial potential** * most negative at distal end of colon * passage the greatest there * **Active K⁺secretion** * **pump-leak mechanism** * K⁺ crosses basolateral membrane via: * **Na⁺/K⁺-ATPase** * **Na⁺/K⁺/Cl^- cotransporter (NKCC1)** * Intracellular K⁺ uses a **K⁺ channels** to either: * be **recycled** back across **basolateral** membrane * be **secreted** across **apical** membrane * Whether secretion takes place _depends on amount of K⁺ channels_ on apical membrane * **Aldosterone** and **VIP** (via **cAMP)** increases channel density thus secretion * **Active K⁺ Absorption** * Only takes place in the **distal colon** * Driven by **apical H⁺/K⁺-ATPase** * K⁺ then crosses basolateral membrane by unknown process

Answer 97

* HCO₃^- exchanged for Cl^- * Mucus secreted from goblet cells throughout colonic mucosa * Stimulated by mechanical irritation of mucosal surface

Answer 98

* Mostly nitrogen and oxygen from swallowed air * Normally expelled by belching * Gases not expelled move into small intestine * **Borborygmi** = sounds produced by movement of gas in stomach antrum & small intestine

Answer 99

* Normally very little gas in small intestine * Usually just oxygen and nitrogen from stomach * CO₂can build up if reaction between gastric acid and bicarb too rapid * Ability to reabsorb gas then exceeded * Gases usually make noise * Silent abdomen suggestive of intestinal immobility

Answer 100

* Gases mostly derived from bacterial action * Includes: * CO₂ * H₂ * odoriferous gases like indole * sulfur-containing compounds * Worse with carbs or high fiber diet * Worse with sudden diet changes * Excess gas expelled as flatus

Gastrointestinal Flashcards

(124 cards)