High Yield pt6 PDF

    Acid Base  Normal blood pH is 7.4  Respiratory acidosis: too much CO2, hypoventilation would cause respiratory acidosis, kidneys compensate by increasing bicarbonate reabsorption, excreting H+  Respiratory alkalosis: too little CO2, hyperventilation would cause respiratory alkalosis, ki...

    Acid Base  Normal blood pH is 7.4  Respiratory acidosis: too much CO2, hypoventilation would cause respiratory acidosis, kidneys compensate by increasing bicarbonate reabsorption, excreting H+  Respiratory alkalosis: too little CO2, hyperventilation would cause respiratory alkalosis, kidneys compensate by increasing bicarb secretion, reabsorbing H+  Metabolic acidosis: too little bicarb creates acidic environment sensed by peripheral and central chemoreceptors, respiratory compensation by increasing ventilation to blow off CO2  Metabolic alkalosis: too much bicarb creates a basic environment sensed by central chemoreceptors to decrease ventilation rate, however respiratory compensation is limited because peripheral chemoreceptors will sense low O2 environment and increase ventilations 43: Respiratory Controls and Reflexes (Mayrovitz)  Respiratory control  Medullary cell groups:  DRG=dorsal respiratory group, mediates inspiration by stimulating phrenic nerve to contract diaphragm(contraction of diaphragm flattens it, enlarging the chest cavity and decreasing intrathoracic pressure) Nucleus tractus solitarius (NTS) is in the DRG, it is the site of input by glossopharyngeal and vagus  VRG=ventral respiratory group, mediates forced expiration (normal respiration is passive, mediated by relaxation of inspiratory muscles) by recruiting the inner intercostals and the abdominal muscles, VRG helps with inspiration as well by flaring nostrils and dilating larynx  Pontine Respiratory group: pneumotaxic center: turns off inspiration by inhibiting apneustic center, damage to the pneumotaxic center removes limitations on apneustic center, inspiration will be prolonged and expiration shortened  Basic Rhythm  Basic respiratory rhythm is generated in the medulla by the central pattern generator(CPG)  Nerve impulses to inspiratory muscles increase in frequency during inspiration, the impulses are absent in expiration  This ramping up rhythm can be modulated by changing inspiration time, afferent input from mechano/chemoreceptors, actions of pneumotaxic center  The lungs inflate throughout the time the nerve impulse ramps up(the lungs fill when we inspire), more nerve impulses will increase tidal volume  Chemoreceptors  Peripheral chemoreceptors in the carotid bodies and aortic bodies depolarize when faced with low PO2, high PCO2, low pH  Carotid body->hering n->glossopharyngeal nerve->NTSin the DRG>increase RR and tidal volume  Aortic body->aortic n->vagus nerve->NTS in DRG->increase RR and tidal volume  Central chemoreceptors live in brain parenchyma, monitor CSF  High PCO2 or low pH will depolarize central chemoreceptors, transmit signal to DRG->increase ventilation Mechanoreceptors  Slowly adapting receptors: among smooth muscle cells in the airway, increase their activity when they are increasingly stretched, send signals to reduce tidal volume  Rapidly adapting receptors: among airway epithelial cells, respond to irritants by bronchoconstricting, coughing, sneezing. They also respond to large lung deflations by triggering increased tidal volume and RR  C-fibers: sensitive to distention of capillaries next to alveoli, if the capillaries distend, ventilation will increase to match, if capillaries deflate the ventilation will decrease to match Hering-Breuer Reflexes  Hering-Breuer Inflation: reflex against overinflation  1. Too much lung expansion 42: Ventilation-Perfusion Matching (Mayrovitz)      Anoxia= no O2 Hypoxemia= low arterial blood PO2, hypoxic hypoxia Hypoxia: inadequate O2 available for tissue needs, 3 types  Hematologic hypoxia: low Hb carrying ability, examples are anemia or carbon monoxide poisoning  Ischemic hypoxia: low blood flow causing low tissue O2, arterial PO2 is normal  Histotoxic hypoxia: normal O2 supplied but can’t be utilized, example is cyanide poisoning(cyanide arrests the ETC yielding O2 ineffective) Ventilation-perfusion matching  Arterial blood gas stability is determined by the ventilation: perfusion ratio  The optimal ratio is 0.84  Decreasing this ratio shows the perfusion to the alveoli exceeds the ventilation, too much blood is flowing to the alveoli it is unable to pick up oxygen. The system will be hypoxemic, hypercapnic, respiratory acidosis  Increasing this ratio shows ventilation outweighs blood flow, too much CO2 leaves the system, too much O2 enters the system, it will become hyperoxemic, hypocapnic, respiratory alkalosis Clinical Correlations  Pulmonary embolism: Occlude the blood supply to a region of alveoli, the alveoli without blood supply will turn into alveolar dead space. There will be increased blood flow to the ventilated alveoli, increasing Q. Therefore, the V/Q ratio decreases. There is hypoxemia, hypercapnia, respiratory acidosis  Hyperventilation: Increase the alveolar ventilation, no change in the CO to the lungs, increase the V/Q ratio leading to hyperoxemia, hypocapnia, respiratory alkalosis Shunts  Mixing deoxygenated/lower oxygenated blood with oxygenated blood drops arterial PO2  The diluting blood can come from:  alveoli with low V/Q  bronchial veins  pleural veins  thebesian veins  patent foramen ovale A-a gradient  Alveolar O2-Arterial O2, this is an index of the amount of shunting going on in the body  This number is supposed to be less than the patient (age+10)/4, someone who is 30 should have A-a=10. Someone who is 60  Calculate the arterial O2 using FIO2(Patm-47)-PaCO2/R Vocab Terms     2. Smooth muscle is stretched, SARs depolarize  3. SARs transmit signal through vagus to the DRG  4. DRG sends less signal to inspiratory muscles  5. Decreased TV, decreased inspiration duration  Hering Breuer Deflation: reflex against rapid deflation  1. Rapid lung deflation causes lack of stretch on RARs  2. RARs signal to DRG via the vagus  3. Inspiration is promoted increasing tidal volume(hyperpnea) and respiratory rate (tachypnea) Mountain Sickness 44: Respiratory Physiology Applications     Watch lecture. 45 and 46: Endocrine Physiology I and II (Panavelil)         Endocrine System  Functions to integrate cell activity by regulating cellular and organ function to maintain homeostasis  Chemical Messengers can be neurotransmitters or Hormones  Hormones travel through the blood to a distant target  Endocrine = gland that releases hormones into blood steam for a distant site  Exocrine = gland that releases substances into ducts  Neuroendocrine = special neurons release neurotransmitters into blood for a distant site  Paracrine = secreted into ECF and affects local cells of a different type  Autocrine = secreted into ECF and affects itself  Target cell = cell receiving the messenger Hormones  Peptide = hydrophilic and can be stored, travel freely in blood  Synthesis is via Gs or Gq Steroid = transported via plasma proteins in blood  Synthesis from cholesterol  Can affect gene transcription Amines = derived from tyrosine, some are hydrophilic and some hydrophobic  Carried by thyroid binding globulin Binding globulins increase the half-life and hormones Regulated by Feedback Mechanisms  Negative Feedback = directly or indirectly inhibits secretion of hormones  Ultra-short inhibits its own secretion  Short = anterior pituitary inhibits the hypothalamus  Long loop = end hormone inhibits the whole hypothalamic - pituitary axis  Positive Feedback = stimulates further hormone release  Ex: estrogen and oxytocin both increase their own hormone release Hypothalamus and Pituitary  Hypothalamus = regulates the pituitary gland through hormones released into hypothalamic portal supply which feeds the anterior pituitary  Thyroid releasing hormone  Corticotropin releasing hormone  Gonadotropin releasing hormone  Growth hormone releasing / inhibiting hormones  Prolactin releasing / inhibiting hormones  Pituitary  Anterior (adenohypophysis) = glandular, releases hormones  Regulates reproduction, growth, energy and stress  Somatotrophs ----> Growth hormone  Thyrotrophs ----> Thyroid stimulating hormone  Corticotrophs ----> Adrenocorticotropic hormone  Gonadotrophs ---> Follicle stimulating hormone  Gonadotrophs ----> Luteinizing hormone  Lactotrophs ----> prolactin  Posterior (neurohypophysis) = neural, releases neurotransmitters  Oxytocin  Antidiuretic hormone (aka: anti-vasopressin hormone)  All together forms the Hypothalamic - Pituitary Axis Thyroid Axis  Synthesized in the thyroid gland and requires Iodide for its processing and function   T3 and T4 are the hormones released into the bloodstream  T3 is the active form  Use negative feedback on anterior pituitary and hypothalamus as regulation  Increases metabolism, HR, contractility, produces heat, required for brain maturation, and permits epi and NE  Hypothyroid = dry coarse hair, slow HR, weight gain, depression etc.  Hyperthyroid = hair loss, rapid HR, weight loss, heat intolerance, nervousness Adrenal Axis  Steroid hormones come from the cortex  GFR = Glomerulosa, fasciculata, reticularis  “GFR ---> Salt, sugar, sex”  Steroids are synthesized from cholesterol  Cholesterol desmolase (CYP 11A1) is the RLS and requires the Star protein!  Catecholamines secreted from medulla  Axis  Hypothalamus (CRH) ---> anterior pituitary (ACTH) ----> adrenal cortex ----> cortisol  Cortisol = Increases glucose, promotes protein and fat breakdown, stress response, suppress immune response  Aldosterone = Na and water balance, blood pressure regulation  Androgens = secondary sex characteristics Growth Hormone and Prolactin  Growth Hormone:  Synthesized by Somatotrophs  Stimulates lipolysis, inhibits glucose uptake, stimulates gluconeogenesis, anti-insulin  Long-term effects: promotes growth of tissues (highest in puberty)  Prolactin:  Peptide hormone made by lactotrophs in anterior pituitary  Hypertrophies during pregnancy  Principal hormone for lactation  Stimulates breast development during pregnancy  Regulated by positive and negative feedback mechanisms  TRH from hypothalamus stimulates ant. Pituitary (dopamine inhibits)  Ant. pituitary releases prolactin for breast tissue  Release of prolactin from ant. Pituitary stimulates hypothalamus to release more TRH or stimulates hypothalamus to release dopamine (inhibitory) Axises  Hypothalamic - Pituitary Axis  Hypothalamus releases GnRH which binds gonadotroph receptors on the ant. Pituitary  Ant. pituitary releases FSH and LH (glycoproteins)  LH is released more heavily in Males ----> testosterone  FSH ----> spermatogenesis  Inhibin inhibits FSH  Hypothalamic - Ovarian Axis  Hypothalamus releases GnRH which binds gonadotrophs on the ant. Pituitary  Ant. Pituitary releases FSH and LH  LH ---> theca cells  FSH --> granulosa cells  Both help regulate menstrual cycle Posterior Pituitary Hormones  Synthesized by hypothalamus and stored in post. pituitary  DOES NOT require a releasing hormone ---> release is triggered by physiologic stimuli  Vasopressin (ADH)  V2 receptors (Gs) regulate osmolarity by increasing H2O reabsorption  V1 receptors (Gq) constrict smooth muscle cells  Oxytocin  Causes let down of milk from breasts  Uterine contractions during birth  Up regulated during childbirth  Can also be used to control postpartum bleeding 47: Overview of Gastrointestinal Physiology (Nguyen)  Digestion  Smell  Activates salivary glands which release bicarb, amylase and lipase  Activates stomach acid, pancreas and gallbladder  All controlled by CNS  Bicarb neutralizes the acid  Clinical Correlation:  Sjogren’s Syndrome = autoimmune destruction of salivary glands ---> dry mouth and eyes  Taste  Salivary glands release mucous, amylase and lipase    Swallow  Tongue and skeletal muscle move food bolus ---> goes down esophagus  Stomach  stores and degrades food  Releases pepsinogen ---> pepsin  Small intestine  Pancreas adds digestive enzymes and bicarb, liver makes bile, water is reabsorbed  Absorption through enterocytes  Large Intestine  Dehydration, compaction, and elimination  Accessory Glands  Salivary Glands  Amylase breaks down starch  Lipase breaks down lipids  Pancreas  Release digestive enzymes (lipase) and bicarb  Insulin and glucagon  Cystic Fibrosis: decreased production of lipase ----> fat malabsorption  Liver  Makes bile ---> dissolves fats  Receives and stores CHO and other building blocks for making proteins  Gallbladder  Stores and concentrates bile  All this process contributes to the gut-brain axis  Hepatic Portal System  Detoxifies the substances absorbed from the gut  post -prandial state makes you sleepy because blood is diverted from skeletal muscles to small intestine GI Regulation  GI tract is regulated by endocrine (hormonal) and neurocrine (parasympathetic) control  Paracrine and autocrine regulation  Local regulation through hormones that act on nearby cells  Histamine release from stomach increases gastric acid secretion from stomach  Somatostatin from the GI tract inhibits the release of all GI hormones and gastric acid secretion  Gastrin from G cells in the stomach  Increases H+ secretion  Stimulated by distention of the stomach, GRP, tryptophan  Inhibited by H+ and somatostatin  Zollinger Ellison: endocrine tumor that leads to excess gastrin production ---> excess H+ secretion ---> ulcers and many of them (PUD)  Secretin  Stimulates bicarb secretion, increases bile production and inhibits H+ release  Released by S cells  Stimulated by too much H+ or too many fatty acids  CCK  From I cells  Contraction of the gallbladder ---> relaxes sphincter of Oddi --> bile secretion  Stimulates secretin ---> bicarb  Inhibits gastric emptying  Stimulated by small peptides and amino acids, fatty acids and monoglycerides  GIP  Stimulates insulin secretion, inhibits H+ secretion  Release is due to fat, protein and carbs  GLP 1  Stimulates insulin and decreases glucagon  Neurocrine  Substances are made in neurons in GI tract and are typically VIP, GRP and enkaphalins  VIP  Produces relaxation of GI smooth muscle including lower esophageal sphincter  Stimulates pancreatic bicarb secretion VIPoma: endocrine tumor ---> excess VIP secretion ---> watery diarrhea and  hypokalemia Nervous System Effects  Enteric Nervous System  Myenteric plexus ---> gut motility  Submucosal plexus ---> secretion  ACh is the primary excitatory Neurotransmitter  ATP, VIP and NO are the primary inhibitory neurotransmitters  NO and VIP ---> smooth muscle relaxation  Substance P ---> smooth muscle contraction  Parasympathetic  Stimulates motility and secretion  Inhibits sphincter tone   Sympathetic  Stimulates (increases) sphincter tone  Slows motility and secretion Ghrelin  Hormone from gastric cells  Stimulates orexigenic (tell you you’re hungry) neurons and inhibits anorexigenic (tell you you’re full) neurons 48: Gastrointestinal Motility (Nguyen)    Mastication, Salivation and Swallowing  Mastication = chewing  Breaks down food into small pieces and exposes it to salivary amylase enzymes for digestion  Salivary Glands  Secrete saliva  Water, bicarb, mucins, amylase, lysozyme, growth factors  Regulation  Parasympathetic ---> stimulates watery, abundant saliva production and secretion  Sympathetic ---> reduces saliva production and produces thick mucus saliva  Xerostomia (Dry Mouth)  Destruction or atrophy of the salivary glands  Ex: Sjogren’s Syndrome  Treatment: pilocarpine ---> improves salivary flow  Swallowing  Buccal phase = food pushed into pharynx from mouth  Pharyngeal phase = food passes through the pharynx into the esophagus  Breathing is inhibited during this process (epiglottis covers airway to prevent aspiration)  Esophageal phase = food passes into stomach by peristalsis Esophageal Disorders  Esophagus has an upper and lower sphincter ---> lower sphincter must relax for food to pass into stomach  Esophagitis is inflammation of the esophagus due to acid from stomach refluxing up as a result of little LES tone  Pill esophagitis  Older people have trouble swallowing large pills ---> they get stuck and cause inflammation  Common agents = Potassium tablets  Fungal esophagitis  Candida albicans infection  Viral esophagitis  Without dysphagia and without thrush  GERD  Incompetent lower esophageal sphincter ---> acid from stomach backflows into esophagus  Heartburn is the main symptom  Treat with proton pump inhibitor ---> reduces H+ content in the stomach  Esophageal Strictures  Narrowing of the esophagus due to thickened wall  Zenker’s Diverticulum  Herniation of esophageal mucosa through wall due to weak cricothyroid muscle  Barrett’s Esophagus  Result of chronic GERD ---> breaks down the squamous epithelium and replaces it with columnar epithelia  Pre-cancer disease  Achalasia  Inability to swallow both solids and liquids bc of denervation of the LES  This results in INCREASED tone ---> food can’t pass to stomach  Different from cancer which is progressive swallowing problem from liquids to solids  Esophageal Carcinoma  Can be squamous cell or adenocarcinoma Stomach and Small Intestine  Motility  Migrating Motor Complex  Constant sweeping of contractions that continually move through the stomach to prevent large amounts of indigestible materials from accumulating  Initiated by Motilin  If you have a motility disorder then you are deficient in motilin  Gastric secretion, bile flow and pancreatic secretion increase  Patterns  Propulsive = peristalsis (ring like contractions) that move food forward  Mixing = segmentation that helps chop food up  Gastric Emptying  Pyloris has a sphincter that controls rate of emptying  Influenced by CCK, GIP and secretin  Slow Wave    Oscillating resting membrane potentials of GI smooth muscle Rhythmic depolarizations initiated by pacemaker cells that move food from mouth to anus Large Intestine  Motility  Segmentation  Mass Movement = propels contents of one segment to the next  Defecation = evacuation of colon  Irritable Bowel Syndrome = cramping, abd pain, bloating and gas due to large intestine inflammation  Ileus = direct inhibition of motility due to trauma to the intestines  Hirschsprung disease = no innervation of large intestine in infant leads to distention, anorexia and lassitude  Dumping Syndrome  After bariatric surgery where the stomach is made smaller, the patient has to eat small frequent meals  If large meals are eaten, glucose is absorbed too fast leading to hyperglycemia  The hyperglycemia results in a secretion of insulin that leads to hypoglycemic symptoms  Weakness, dizziness, and sweating after meals  50: Small Intestines and Pancreas (Nguyen)  49: Gastric Secretions (Nguyen)       GI Secretions  GI secretions originate from specialized cells lining the GI lumen, as well as the pancreas, liver and gallbladder  The functions of the secretions based on the components  Water lubricates  Mucus lubricates and protects  HCl sterilizes  Bicarb neutralizes  Enzymes digest Saliva  Produced by parotid, submandibular, sublingual glands  Hypotonic solution with high bicarb concentration, amylase(starch breakdown), lingual lipase  Saliva is secreted by parasympathetic stimulation, when we see/smell/ think about food, when we have food in our mouth we secreted more saliva  Sleep, fatigue and fear inhibit saliva secretion Stomach Secretions  Gastric pits have multiple cell types with different secretions  Mucosal neck cells: secrete mucus and bicarb to protect stomach lining from acidic environment  Parietal Cells secrete HCl to kill bacteria and activate pepsin, and Intrinsic factor to help with vitamin B12 absorption. Destruction of parietal cells or intrinsic factor causes pernicious anemia, a type of macrocytic anemia.  Chief cells release pepsinogen, when it activates in the acidic stomach it begins digesting proteins. Chief cells also secrete gastric lipase for fat digestion  G cells respond to the presence of food in the stomach and secrete gastrin, which acts on the parietal cells to secrete HCl  In the stomach somatostatin reduces gastric acid secretions H+ secretions  In the stomach, acid production is the end result of 3 pathways  Vagal stimulation releasing Ach on M3 receptors of the parietal cell  Gastrin stimulating enterochromaffin cells to release histamine, which binds H2 receptors on parietal cells  Gastrin binding its CCK2 directly on the parietal cell  H+ flows out of the parietal cell via the H+/K+ pump  Treat acid overproduction with H+ pump inhibitors(omeprazole), or H2 antagonists  If the pH falls below 3 in the stomach, there is negative feedback to inhibit further gastrin secretion  Somatostatin decreases H+ secretion directly by acting on Gi proteins of the parietal cell, or indirectly by inhibiting histamine and gastrin secretion  Prostaglandins also inhibit H+ secretion by binding Gi proteins. NSAIDs decrease prostaglandin production and decrease mucus cells, contributing to peptic ulcer disease. Phases of GI stimulation  Cephalic phase: sight, thought, smell, taste of food stimulates the stomach to begin secreting acid, priming the system  Gastric phase: G sense presence of food, secrete gastrin, enhancing acid. Pepsinogen is activated and protein breakdown begins Clinical Correlations  D-xylose absorption test: to distinguish if the pancreas or the small intestine is the cause of malnutrition. D-xylose is a simple monosaccharide that does not need pancreatic digestion, and is absorbed exclusively in the small bowel. After drinking D-xylose, urine is collected and concentration of D-xylose is analyzed. If concentration >5g that shows the small bowel works (the sugar absorbed into blood then was filtered out as urine)so the pancreas must be the problem. If the concentration <5gm, that shows the small bowel is the problem.  Peptic ulcers: hostile factors outbalance protective factors. Can be caused by H. Pylori(use urea breath test) NSAIDs(give misoprostol for NSAID ulcers EXCEPT if pregnant) excess acid production-proton pump inhibitor, H2 antagonist  Duodenal ulcers: pain is alleviated while eating, patient will gain weight  Gastric ulcers: pain is aggravated by eating, patient will lose weight Clinical Correlations  Gastrinoma: Zollinger-Ellison syndrome, it is a neuroendocrine tumor that secretes gastrin without regulation. Excessive gastrin increases acid production overwhelming the mucosal barrier. Patients will have multiple ulcers in unusual spots throughout the small bowel.  H Pylori: leading cause of peptic ulcer disease, flagellated bacteria burrow into the mucosal lining of the stomach, and create a neutral environment for themselves using urease (produces ammonia and carbon dioxide which is sensed on urea breath test). Infiltration of the mucosal layer disrupts its protective ability causing peptic ulcers.  Smoking increases risk of peptic ulcers     Small intestine  Site where most digestion and absorption occurs. There is a combination of secreting neutralizing compounds to counteract the HCl in Chyme, and enzyme secretion to break molecules down to absorbable parts  Secretion occurs in crypts, absorption occurs in villi  Small intestine is lined by enterocytes with a brush border (increases absorptive surface area). Proteins, carbs, nucleic acids get absorbed into portal circulation going toward liver, fats are absorbed into lacteals and enter lymphatic flow  There is continuous regeneration of enterocytes, turning over every 3 days  Celiac sprue: malabsorption due to inflammation and autoimmune destruction of villi. This is caused by hypersensitivity to gliadin components of gluten, and is treated by avoiding gluten containing foods such as wheat Absorption  Passive diffusion, co transport, and exchange of Na and Cl creates a osmotic gradient for water to follow into the body. Absorption of water is dependent on osmosis  Pedialyte provides rapid hydration by creating osmotic gradient through Na, Cl, and dextrose(dextrose is absorbed quickly because it does not require digestion, absorbed through SGLT1)  Glucose is absorbed by SGLT1, once in the body it enters cells via GLUT transporters(GLUT4 is insulin dependent)  Fructose is absorbed by facilitated diffusion  Acarbose is a diabetes medication that blocks disaccharide enzyme function, leading to less glucose absorption  Peptides are cotransported with Na into enterocytes(these peptides are diand tri- peptides) larger peptides need endocytosis  Micelle formation aids in the absorption of triglycerides and fat soluble vitamins  Iron: absorbed in duodenum  B12: absorbed in ileum  Folate: absorbed in small bowel Diarrhea  Pedialyte is good for hydration and treatment of diarrhea  Osmotic: high amounts of solutes present in bowel inhibit water absorption, lactose intolerance is the absence of lactase in the bowel inhibiting the absorption of lactose causing bloat, flatulence, diarrhea  Secretory: Secretion of fluids into the lumen caused by pathogenic toxins, or neuroendocrine tumors (VIPoma). Vibrio cholerae causes Cl- secretion from intestinal crypts, leading to secretory diarrhea  Inflammatory: Inflammation and damage to mucus and intestinal lining leading to bloody diarrhea(hematochezia) Bile and fat digestion  Fat is hydrophobic, accumulates as large fat drops in the intestine. Bile and bile salts emulsify the large fat drops, turning them into smaller, easily absorbable micelles  Micelles are formed due to the hydrophobic interactions of the fat molecules, they have a hydrophilic shell and hydrophobic core  Cholestyramine is a drug for hyperlipidemia that reduces the amount of free bile acids, reducing the amount of triglyceride absorption. Patients taking cholestyramine need vitamin supplementation of fat soluble vitamins (ADEK)  Secretin is released from S cells in the duodenum, and stimulates bile secretion Pancreas  Endocrine function: Glucagon and insulin secreted into the blood from islets of Langerhans  Exocrine function: Secretion of neutralizing compounds (bicarb is secreted by duct cells) and digestive enzymes (trypsin, chymotrypsin, lipase, amylase are secreted by acinar cells)  Most of the pancreatic enzymes are inactive until they reach the intestinal lumen, inactive enzymes are zymogens and have the ending -ogen  Trypsinogen is activated by enterokinase at the brush border, turning it into trypsin, which goes onto activate the other pancreatic enzymes  CCK (cholecystokinin) and Ach stimulate pancreatic secretion. CCK is released by I-cells in the duodenum in response to fat. Ach is from vagus