Salivary and Gastric Glands Secretions and functions.pptx

Salivary GLANDS and Gastric Glands Secretions and functions.pptx

1. Presented by – Dr. Amrit Kour PG Scholar 1 st year R.G.G.P.G.Ayu.Clg & Hospital Paprola Functions and Secretions of Salivary & Gastric Glands with their applied physiology

2. Salivary Glands

3. Introduction There are three pairs of salivary glands – Major salivary Glands- 1. Parotid Glands 2. Submandibular / Submaxillary glands. 3. Sublingual Glands. In addition there are tiny salivary glands are present – Minor Salivary Glands - buccal , labial, G lossopalatine glands

4. S.No . Salivary Glands Location Duct Opening 01. Parotid Glands Lie in the groove between the ramus of mandible and mastoid process i.e below the ear. Duct of Stensen Opens in the mouth cavity, near the crown of upper 2 nd molar tooth. 02. Submandibular / Submaxillary Glands Situated medial to the mandible in the submaxillary triangle. Duct of Wharton’s opens in the floor of mouth. 03. Sublingual Glands Beneath the tongue Saliva from these glands is poured into 5 to 15 small glands – Duct of Rivinus . One of the duct is larger and is called Bartholin’s Duct. Floor of mouth

5. Salivary ducts

6. Classification of salivary glands based upon the types of secretion - 1. Serous Glands 2. Mucus Glands 3. Mixed Glands Secretions are watery – contain enzymes(amylase) but negligible amount of mucus. Secretions are rich in mucous and also contains antibodies. So , provide lubrication and protection . Secretions contain both enzymes as well as mucus. PAROTID GLANDS SUBLINGUAL GLANDS Submandibular / Submaxillary Glands

7. Histology of Salivary Glands Two main components of Salivary glands – 1. Acini 2. Salivary Ducts

8. Acini – each acini is lined by a single layer of epithelial cells called acinar cells or end piece cells. Responsible for the production of saliva. Myoepithelial cells (which contain actin and myosin) surround the Acini and intercalated ducts. Contraction of myoepithelial cells leads to expulsion of fluid accumulated in the acini .

9. From acinus , a duct called intercalated duct arises Which opens into striated duct & several striated ducts open into excretory duct which opens into mouth .

10. PROPERTIES OF SALIVA In 24 hours, salivary secretion ranges from 1 to 1.5 litres . Contribution by different salivary glands Ph – 6.0 to 7.0 (favorable for digestive action of amylase.) Saliva is hypotonic to plasma. Parotid Glands Sublingual Glands Submandibular / Submaxillary Glands 25% 5% 70%

11. Composition of Saliva Water – 99.5% Solids – 0.5% NOTE - saliva contain large quantities of K + and HCO3 - Both sodium and chlorides ions are several times less in saliva than in plasma. Inorganic Organic Sodium Potassium Calcium Chlorides Bicarbonates Alpha – amylase/ Ptyaline Mucus Lingual lipase Lysozymes Immunoglobulins – IgA .

12. Mechanism of Secretion of Saliva Salivary secretion is a two- stage operation – First stage – Acini Second stage – Salivary Ducts Note – Acini secrete a primary secretion that contains ptyalin and/or mucin in a solution of ions with concentration similar to extracellular fluid. Primary Secretion – by Acini Contains Amylase Na + , K + , Cl - , HCO3 - similar to plasma

13. As the primary secretion flows through the ducts, two major active transport processes takes place that modify the ionic composition of the fluid in the saliva. 1 st }}– sodium ions are actively reabsorbed from all the salivary ducts and potassium ions are actively secreted in exchange for the sodium ions. Therefore the sodium ion concentration of saliva reduces whereas concentration of Potassium increases in the saliva. Excess sodium reabsorption creates a electronegitivity of -70mv in the salivary ducts. This causes chloride ions to be reabsorbed passively. Therefore concentration of chloride ions also decreases in the saliva. 2 nd bicarbonates ions are secreted by the ductal epithelium into the lumen of duct.

14. Net result of these transport processes Potassium and bicarbonate ions concentration is very much high in the saliva as compared to the plasma concentration.

15. Functions of Saliva Under basal awake conditions, about 0.5 mL of saliva is secreted each minute but little secretion occurs during sleep. There are main three functions of saliva 1. Lubrication 2. Protection 3. Digestion Mucin in the saliva lubricates food, help in speech, keeps the oral cavity moist. Lysozomes Lactoferrin IgA Immunoglobulin – secretory Amylase – carbohydrates digestion Lingual lipase – digestion of fats.

16. Nervous regulation of salivary secretion Salivary glands are controlled mainly by parasympathetic nervous signals arising from superior and inferior salivatory nuclei present in the brainstem(at the junction of Pons and Medulla) There are superior and inferior salivatory nuclei. These salivatory nuclei are stimulated by 1. Taste stimuli – mainly in sour taste (acids) more salivation occur 2. Tactile stimuli – due to presence of smooth objects in the mouth – causes marked salivation. Whereas presence of rough objects causes less salivation and even inhibit the salivation.

17. Stimulation of Parasympathetic nervous fibers causes 1. salivary secretion 2. Vasodilation of salivary secretion Acetylcholine Vasoactive polypeptide (VIP)- responsible for salivary vasodilation . Stimulation of sympathetic nerve fibers has little effect – it causes small amount of salivary secretion.

18. Taste reflxes are integrated in the brainstem From the nucleus of tracteus solitarus , many taste signals are transmitted within the brainstem itself directly into the salivatory nuclei. There are superior and inferior salivatory nuclei. Superior salivatory nuclei – transmit signals to submandibular and sublingual glands via Facial Nerve( chorda tympani branch). Inferior salivatory nuclei – transmit signals to parotid gland via glossopharyngeal nerve . Thus superior and inferior salivatory nuclei helps to control the secretion of saliva during the ingestion and digestion of food.

19. Reflex regulation of salivary secretion Salivary secretion is regulated by nervous mechanism through reflex action. S.No . Unconditional Reflex Conditional Reflex 01. It is the inborn reflex that is present since birth. This reflex is acquired by experience . 02. It does not need any previous experience. Presence of food in the moth is not necessary to elicit this reflex. 03 Example – when we put acidic food material in the mouth- salivation occurs. Example – this reflex is stimulated by sight, smell and thought of food.

20. APPLIED PHYSIOLOGY HYPOSALIVATION HYPERSALIVATION Reduction in the secretion of saliva. It is of two types, T emporary hyposalivation & Permanent hyposalivation . Excess secretion of saliva. Physiological hypersalivation occurs during pregnancy 1.Temporary hyposalivation occurs in: Emotional conditions like fear. Fever. Dehydration. Pathological conditions: 1. Decay of tooth or neoplasm in mouth or tongue due to continuous irritation of nerve endings in the mouth. 2. Permanent hyposalivation occurs in: Sialolithiasis (obstruction of salivary duct). Congenital absence or hypoplasia of salivary glands. iii. Bell palsy (paralysis of facial nerve) 2. Disease of esophagus, stomach and intestine. 3. Neurological disorders such as cerebral palsy, mental retardation, cerebral stroke and parkinsonism. 4. Nausea and vomiting.

21. OTHER DISORDERS In addition to hyposalivation and hypersalivation , salivary secretion is affected by other disorders also, which include: Mumps Sjögren syndrome

22. Mumps Mumps is the acute viral infection affecting the parotid glands. The virus - paramyxovirus . It is common in children who are not immunized. It occurs in adults also. Features of mumps are puffiness of cheeks (due to swelling of parotid glands), fever, sore throat and weakness. Mumps affects meninges , gonads and pancreas also.

23. Sjögren Syndrome autoimmune disorder. immune cells destroy exocrine glands such as lacrimal glands and salivary glands. Common symptoms of this syndrome are dryness of the mouth due to lack of saliva ( xerostomia ), persistent cough and dryness of eyes. In some cases, it causes dryness of skin, nose and vagina. In severe conditions, the organs like kidneys, lungs, liver, pancreas, thyroid, blood vessels and brain are affected

24. Gastric Glands

25. FUNCTIONAL ANATOMY OF STOMACH „ Stomach is a hollow organ situated just below the diaphragm on the left side in the abdominal cavity. Volume of empty stomach is 50 mL. Under normal conditions, it can expand to accommodate 1 L to 1.5 L of solids and liquids. However, it is capable of expanding still further up to 4 L.

26. PARTS OF STOMACH 1. Cardiac end 2. Fundus 3. Body or corpus 4. Pyloric region. Stomach has two curvatures. One on the right side is lesser curvature and the other on left side is greater curvature.

27. 1.Cardiac region OR cardiac end. is the upper part of the stomach where esophagus opens. The opening is guarded by a sphincter called cardiac sphincter, which opens only towards stomach. 2. Fundus Fundus is a small dome­shaped structure. It is elevated above the level of esophageal opening.

28. Body or Corpus Body is the largest part of stomach forming about 75% to 80% of the whole stomach. It extends from just below the fundus up to the pyloric region.

29. 4. Pyloric Region It has two parts, 1. Antrum and 2. Pyloric canal. The body of stomach ends in antrum . Junction between body and antrum is marked by an angular notch called incisura angularis . Antrum is continued as the narrow canal, which is called pyloric canal or pyloric end. Pyloric canal opens into first part of small intestine called duodenum. The opening of pyloric canal is guarded by a sphincter called pyloric sphincter. It opens towards duodenum.

30. 4 coats / layers of stomach 1. Serous coat 2. Muscular coat 3. Submucus coat 4. Mucous coat Outer most layer of stomach wall. Gastric muscles are smooth muscles. Thick muscularis externa . Formed by areolar tissues,blood vessels,lymph vessels and meissner nerve plexus. Inner . Formed by mucous secreting columnar epithelial cells. Formed by peritoneum. It is formed by 3 layers – a).outer – longitudinal b). Middle – circular c).Inner- oblique

31. 4. Mucous coat Inner surface of mucus layer is covered by 2 mm thick mucus. Gastric glands are situated in this layer. When the stomach is empty/under resting conditions- mucosa of the stomach is thrown into numerous longitudinal folds- RUGAE . When the stomach is full with meals, rugae disappears. Throughout the inner mucus layer, small depressions called gastric pits are present. Glands of the stomach open into these pits.

32. GASTRIC GLANDS Glands of the stomach or gastric glands are tubular structures made up of different types of cells. These glands open into the stomach cavity via gastric pits. Based upon the location – main 3 classes of gastric glands – 1. Cardiac glands – present in the cardiac end of stomach. Occupy less than 5% of total gastric glands. 2. Oxyntic Glands- present in the body of gastric mucosa. Accounts for about 75% of total gastric glands. 3. Pyloric Glands – present in the pyloric end. Accounts for about 20% of total gastric glands.

33. Each gastric Gland contains several types of cells Surface mucous cells – also known as Foveolar Cells – mucous producing cells. Note – intrinsic factor produced by parietal cells – help in Vit.B12 absorption.

34. Functions of stomach as whole In short, there are four major functions of stomach 1. it receives and retains food. 2. it grinds food to smaller segments. 3. It partly digest the food proteins and fats but no carbohydrates digestion occur. It propels chyme ( partially digested food).

35. Composition of gastric juice Volume – in 24 hrs, vol.of gastric juice is between 1 to 1.5 L. Ph – 0.8- 1.3(strongly acidic). Composition – 99% water , rest 1 % solid Organic solids Inorganic solids Enzymes – pepsinogen , intrinsic factor, mucus. HCL, HCO3 -, sodium, potassium

36. Functions of Gastric Juice 1. Digestive functions Chief cells of gastric glands – secrete pepsinogen and gastric lipase. Pepsinogen – inactive form . In acidic environment. It is converted into pepsin- which is a proteolytic enzyme. Breakdown food proteins into peptides and amino acids. Note – pepsin remain activated in very strong Ph 1 to 3 . And it gets inactivated at ph above 5. Acid – pepsin Mixture (APM) – means gastric juice in which both acid and pepsin are present and the medium is strongly acidic. Gastric lipase enzyme – help in lipids breakdown.

37. 2. Antimicrobial functions HCL of gastric juice kills the microbes coming in stomach along with food. Because of this reason, the contents of small intestine is almost bacteria free. Note – there is normally a very good bacterial flora in the large intestine.

38. 3. Protective Functions The gastric mucosa is exposed to two kinds of injury – 1. Mechanical injury – due to rubbing of food. 2.Autodigestion of gastric mucosa by Acid – Pepsin Mixture.

39. Protection against mechanical injury- There is continuous production of mucus by the surface epithelium which gives a mechanical protection. Mucus = mucin (glycoprotein) + water. So, even in very low conc. Mucus forms a stiff gel.

40. Protection against autodigestion -“Mucosal Barrier” Gastric mucosal surface epithelium cells secrete mucus and HCO3 - So, mucus is present above the gastric mucosa layer and below this mucus , HCO3- ions are present. In the gastric lumen , Ph is about 2.0 so that pepsin remains active and can digest food proteins. But in the region where a thick layer of mucus is present above the surface epithelium layer.ph is about 7.0 because i ).HCL cannot penetrate through this mucus covering rapidly ii). Reacts with HCO3- to produce C02 – Ph rises. At PH 7.0 – pepsin becomes inactive and therefore mucosal epithelium remains unharmed.

41. 4.Instrinsic factor(IF) Secreted by parietal/ Oxyntic cells. This is required for Vitamin.B12 absorption . In chronic gastritis, where gastric mucosa is severly damaged, IF may be deficient. Note – Except, the production of IF, no function of stomach is indispensible for life. Therefore, if vitamin B12 is given parenterally (by injection) patients of gastrectomy can kept alive.

42. Basic Mechanism of Hydrochloric Acid Secretion. Canaliculi - Parietal cell (also called an oxyntic cell),contains large branching canaliculi . The hydrochloric acid is formed at the villus like projections inside these canaliculi and is then conducted through the canaliculi to the secretory end of the cell.

43. About Parietal cell Membranes Apical membrane–towards lumen-1. H+-K+ ATPase . 2.chloride channels Basolateral membrane – 1.Na+-K+ ATPase 2. Cl − HCO3 − antiporter .

44. The H+ ions are produced as follows Intracellular H₂O is present in the Parietal cell cytoplasm . These parietal cells also produce CO₂ by metabolic activity. H2O + CO2 combine, the reaction is catalyzed by the enzyme carbonic anhydrase (which is naturally present in the parietal cell cytoplasm), to produce H2CO3. This H2CO3 is split spontaneously into H+ and HCO3 ions. The H+ ion enters, from the cytoplasm of the parietal cell, within the canaliculus → then the H⁺ ion, by the help of proton pump is excreted into the canal of i.e within the oxyntic gland.

45. In exchange of each H+ ion excreted, one K+ ion is drawn into the cytoplasm of parietal cell by the same proton pump. Thus the proton pump is also called H+ K+ ATPase . Simple Diffusion of K+ ion from cytoplasm to lumen occur. A Cl ion is drawn from ECF into the parietal cell cytoplasm and then pumped out of the cell via a chloride channel into the lumen of the oxyntic gland - where it unites with H⁺ ion to form HCl . The HCO3 ion of the parietal cell leaves the parietal cell cytoplasm → enters the ECF via basolateral membrane of the cell and in exchange of the HCO3-ion one Cl ion (from NaCl of ECF) is drawn into the cytoplasm.

46. From the cytoplasm, this Cl - is excreted via apical membrane to the lumen of the gland where it unites with H⁺ ion to form HCl . The exchange of HCO3 ion and Cl - ion (at the basolateral membrane) is mediated by an enyme , is naturally C l - HCO3- antiporter . )

47. Thus, the final secretion from the canaliculus contains water, Hcl at a concentration of about 150 to 160 mEq /L, Kcl at a concentration of 15 mEq /L, & small amount of Nacl

48. REGULATION OF GASTRIC ACID SECRETIONS The Basic Factors that Stimulate Gastric Secretion Are 1. Acetylcholine, 2. Gastrin , & 3. Histamine. secretion of this acid is under continuous control by both endocrine and nervous signals.

49. Stimulation of Acid Secretion by Acetylcholine Acetylcholine released by parasympathetic stimulation excites 1.secretion of Pepsinogen by peptic cells, 2. hydrochloric acid by parietal cells, and 3. mucus by mucous cells. In comparison, both gastrin and histamine strongly stimulate secretion of acid by parietal cells but have little effect on the other cells.

50. Stimulation of Acid Secretion by Histamine The parietal cells operate in close association with another type of cell called enterochromaffin -like cells ECL cells the primary function of which is to secrete histamine. The ECL cells lie in the deep recesses of the oxyntic glands and therefore release histamine in direct contact with the parietal cells of the glands . The rate of formation and secretion of hydrochloric acid by the parietal cells is directly related to the amount of histamine secreted by the ECL cells. In turn, the ECL cells are stimulated to secrete histamine by the hormone gastrin , which is formed almost entirely in the antral portion of the stomach mucosa in response to proteins in the foods being digested.

51. Stimulation of Acid Secretion by Gastrin Gastrin is itself a hormone secreted by gastrin cells, also called G cells. These cells are located in the pyloric glands in the distal end of the stomach. Gastrin is a large polypeptide secreted in two forms: a large form called G-34, which contains 34 amino acids, and a smaller form, G-17, which contains 17 amino acids. Although both of these forms are important, the smaller form is more abundant. When foods containing protein reach the antral end of the stomach, some of the proteins from these foods have a special stimulatory effect on the gastrin cells in the pyloric glands to cause release of gastrin . This gastrin act on ECL cells in the body of the stomach, causing release of histamine directly into the deep oxyntic glands, This histamine directly stimulate parietal cells for gastric hydrochloric acid secretion.

52. Phases of Gastric Secretion Gastric secretion is said to occur in three “phases” 1. Cephalic phase, 2. Gastric phase 3. Intestinal phase.

53. 1. Cephalic Phase The cephalic phase of gastric secretion occurs even before food enters the stomach, especially while it is being eaten. It results from the sight, smell, thought, or taste of food, and the greater the appetite, the more intense is the stimulation. This phase is purely regulated by Neurogenic signals . This phase of secretion normally accounts for about 30% of the gastric secretion associated with eating a meal.

54. Neural Regulation of Cephalic Phase S. No. Unconditional Reflex Conditional Reflex 01. It is the inborn reflex that is present since birth. This reflex response is acquired by experience . Presence of food in the moth is not necessary to elicit this reflex. 02. It does not need any previous experience. Example – when we put acidic food material in the mouth- salivation occurs. Sight, smell and thought of food induces salivary and gastric secretion. 03. HOW??? Taste buds and other receptors in the mouth are stimulated. Sensory impulse through afferent nerve fibers(7 th and 9 th CN – enter amygdala and appetite centre in the hypothalamus. Motor information through efferent NF pass through vagal nerve fibers – Ach – M3 receptors – HCL release. HOW ???? Sensory impulses from special sense organs (eye, ear, nose) through afferent nerve fibers - cerebral cortex.

55. Experimental Evidences Proving Cephalic Phase Conditional Reflex Unconditional Reflex Bell Dog Experiment - Conditional Reflex of gastric secretion is proved byBell dog experiment. Sham Feeding - After bilateral vagotomy , Sham Feeding does not cause gastric secretion.

56. 2. Gastric Phase In this phase gastric secretion occurs Once food enters the stomach. it excites the following: (1) long vagovagal reflexes from the stomach to the brain and back to the stomach; (2) local enteric reflexes; and (3) the gastrin mechanism, all of which cause secretion of gastric juice during several hours while food remains in the stomach. The gastric phase of secretion accounts for about 60% of the total gastric secretion associated with eating a meal and therefore accounts for most of the total daily gastric secretion of about 1500 ml.

57. Nervous regulation of Gastric Phase 1. Vagovagal Reflex – 2. Local Myenteric Reflex – when the food enter the stomach – distension of stomach – stimulate myenteric nerve plexus present in the wall of stomach. There is release of acetylcholine – stimulate parietal cell – HCL increases.

58. 3. Intestinal Phase. secretion of gastric juice when chyme enters the intestine. When chyme enters the intestine, initially, the gastric secretion increases but later it stops. Intestinal phase of gastric secretion is regulated by nervous and hormonal control. Initial Stage of Intestinal Phase- Chyme that enters the intestine stimulates the duodenal mucosa to release gastrin , which is transported to stomach by blood. There it increases gastric secretion. This secretion accounts for about 10% of the acid response to a meal. Later Stage of Intestinal Phase After the initial increase, there is a decrease or complete stoppage of gastric secretion. Gastric secretion is inhibited by two factors: 1. Enterogastric reflex 2. Gastrointestinal (GI) hormones.

59. APPLIED PHYSIOLOGY

60. Gastritis Inflammation of the Gastric Mucosa ETIOLOGY - certain ingested irritant substances (most common of these substances are excesses of alcohol or aspirin, H.Pylori , Trauma by nasogastric tubes )can be especially damaging to the protective gastric mucosal barrier—that is, to the mucous glands and to the tight epithelial junctions between the gastric lining cells—often leading to severe acute or chronic gastritis. COMPLICATION - It results in the atrophy of the gastric mucosa, with loss of chief cells and parietal cells of gastric glands. Therefore, the secretion of gastric juice decreases.

61. Features of gastritis are nonspecific. Common feature is abdominal upset or pain felt as a diffused burning sensation. It is often referred to epigastric pain. Other features are: i . Nausea ii. Vomiting iii. Anorexia (loss of appetite) iv. Indigestion v. Discomfort or feeling of fullness in the epigastric region vi. Belching (process to relieve swallowed air that is accumulated in stomach

62. GASTRIC ATROPHY Gastric atrophy is the condition in which the muscles of the stomach shrink and become weak. Gastric glands also shrink, resulting in the deficiency of gastric juice. Causes of Gastric atrophy - caused by chronic gastritis called 1.chronic atrophic gastritis. There is atrophy of gastric mucosa including loss of gastric glands. 2. Autoimmune atrophic gastritis also causes gastric atrophy. Features - Generally, gastric atrophy does not cause any noticeable symptom. However, it may lead to achlorhydria (absence of hydrochloric acid in gastric juice) and Pernicious anemia. Some patients develop gastric cancer

63. Gastric Atrophy May Cause Pernicious Anemia. Pernicious anemia commonly accompanies gastric atrophy and achlorhydria . It results in the atrophy of the gastric mucosa, with loss of chief cells and parietal cells of gastric glands. Parietal cells secrete HCL & Instrinsic factor. Chief cells secrete – Pepsingogen and gastric lipase Therefore, the secretion of gastric juice decreases. NOTE - Intrinsic factor must be present for adequate absorption of vitamin B12 from the ileum. Intrinsic factor combines with vitamin B12 in the stomach and protects it from being digested and destroyed as it passes into the small intestine. Then, when the intrinsic factor–vitamin B12 complex reaches the terminal ileum, the intrinsic factor binds with receptors ,then vitamin B12 is absorbed. In the absence of intrinsic factor, vitamin B12 is not absorbed. Then an adequate amount of vitamin B12 is not made available for newly forming red blood cells to mature in the bone marrow. The result is pernicious anemia.

64. Peptic ulcer Peptic ulcer means an ulcer in the wall of stomach or duodenum, caused by digestive action of gastric juice. If peptic ulcer is found in stomach, it is called gastric ulcer and if found in duodenum, it is called duodenal ulcer. Causes i . Increased peptic activity due to excessive secretion of pepsin in gastric juice ii. Hyperacidity of gastric juice iii. Reduced alkalinity of duodenal content iv. Decreased mucin content in gastric juice or decreased protective activity in stomach or duodenum v. Constant physical or emotional stress vi. Food with excess spices or smoking (classical causes of ulcers) vii. Long­term use of NSAIDs (see above) such as Aspirin, Ibuprofen and Naproxen viii. Chronic inflammation due to Helicobacter pylori.

65. Features of peptic ulcer Most common - severe burning pain in epigastric region. In gastric ulcer, pain occurs while eating or drinking. Other symptoms accompanying pain are: i . Nausea ii. Vomiting iii. Hematemesis (vomiting blood) iv. Heartburn (burning pain in chest due to regurgitation of acid from stomach into esophagus) v. Anorexia (loss of appetite) vi. Loss of weight.

66. Classification of clinical features Chronic Duodenal Ulcer Chronic Gastric Ulcer 1. Incidence Common Less common 2. site 1 st inch of 1 st part of the duodenum . Lesser curvature or the prepyloric region. 3. Pain It is due to the acid irritating the ulcer- hunger pain. It is relieved by taking food. After 1 to 2 hours of food, pain becomes severe. Pain occurs on taking food and is relieved by induced vomiting. Pain is burning in nature with retrosternal radiation(heart burn). Increased salivation. Pain is burning in nature. 4. Vomiting Never occur, till the patient develops pyloric stenosis . Frequent and it occurs immediately after the patient takes food. 5. weight Weight gain Weight loss. 6. On examination Tenderness in the RIGHT HYPOCHONDRIUM. Tenderness in the EPIGASTRIUM

67. ZOLLINGER-ELLISON SYNDROME is characterized by secretion of excess hydrochloric acid in the stomach. Cause - This disorder is caused by tumors called gastrinomas found often on the head of the pancreas and upper small intestines. These gastrinomas secrete gastrin . High levels of gastrin cause production of excess stomach acid, which leads to peptic ulcer. Features i . Abdominal pain ii. Diarrhea (frequent and watery, loose bowel movements) iii. Difficulty in eating iv. Occasional hematemesis

68. MANAGEMENT 1. Proton Pump Inhibitors(PPI)– H+ K+ ATPase /proton pump inhibitor. No HCL is formed . Absence of HCL – leads to healing of peptic ulcers. PPIs are extensively used in peptic ulcers. Example – Pantaprozole Omeprazole

69. 2. H2 Blockers – block Histamin combination with H2 recptors – no effect of histamin is produced – HCL secretion greatly reduces- hence very popular in peptic ulcer therapy. Example – Ranitidine

70. RESEARCH STUDIES 1}. Risk Factors for Recurrence of Peptic Ulcer Disease:  From 2016 to 2021, Among 223 patients, there were 187 (83.8%) diagnosed with endoscopy-proved PUD and 36 (16.2%) diagnosed with clinical PUD. Among them, 126 (56.5%) patients were males, and the mean age was 62±2 years. Possible risk factors including smoking, nonsteroidal anti-inflammatory drugs (NSAIDs), aspirin, alcohol, caffeine, and steroids . Treatment outcomes, 5-year recurrence rate, and mortality rate were assessed. The five years recurrence rate of PUD was 30.9%. There was no significant difference in the recurrence rate between the duodenal ulcer (33.3%) and the gastric ulcer (28.8%). The common complication of PUD was gastrointestinal bleeding (34.1%).

71. 2. Gastric cancer over 1 million new cases in 2018 worldwide. It is the 4 th most commonly occurring cancer in men and the 7 th most commonly occurring cancer in women.

72. THANK YOU