Chronic gastritis is often silent; when symptoms appear, recurrent upper-abdominal discomfort dominates:
Vague pain, burning or bloating in the epigastrium or left upper quadrant, sometimes worse or better after meals
Early satiety: feeling full after only a few bites, preventing completion of a normal meal
Post-prandial fullness lasting >1 h, scarcely relieved by belching or position change
Frequent belching, often sour or bitter
Nausea or occasional retching; vomitus is gastric content without bile or blood
Upper epigastric heat: a heartburn-like sensation located higher, easily confused with reflux
Loss of appetite, thick tongue coating, halitosis and other ancillary complaints
Symptoms may be intermittent or persist for weeks, often linked to meals, emotion or fatigue and usually remit at night. Warn the doctor if steady weight loss, repeated vomiting, melena or anaemia appears.
Indigestion centers on recurrent upper-abdominal discomfort. Common features include:
Vague pain, burning, or bloating in the epigastrium or left upper quadrant, starting within 1 h after meals or sometimes worsening when the stomach is empty
Early satiety: feeling full after only a few bites, preventing completion of a normal meal
Post-prandial fullness: bloating persists >1 h after eating and is scarcely relieved by belching or position change
Epigastric distension and belching: a subjective sense of abdominal swelling with frequent sour-tasting eructations
Nausea or occasional retching; vomitus is usually gastric content without bile or blood
Upper epigastric heat: a heartburn-like sensation located higher, easily confused with reflux
Loss of appetite, thick tongue coating, halitosis and other ancillary complaints
Symptoms may be intermittent or persist for weeks, often linked to meals, emotion or fatigue and usually remit at night. Warn the doctor if steady weight loss, repeated vomiting, melena or anaemia appears.
The clinical picture differs between acute and chronic disease, but both revolve around upper-abdominal pain and disturbed digestion.
Acute pancreatitis begins with sudden, severe epigastric or left-upper-quadrant pain that bores through to the back; eating worsens it and antispasmodics give little relief. Most patients vomit repeatedly yet still feel bloated. Fever > 38 °C, tachycardia and, in severe cases, hypotension or shock may appear within 48 h. Bluish periumbilical (Cullen) or flank (Grey-Turner) bruising signals haemorrhagic-necrotic pancreatitis.
Chronic pancreatitis causes recurring or persistent upper-abdominal pain that is aggravated by meals and by lying supine; sitting forward or hugging the knees slightly eases it. Progressive loss of pancreatic enzymes leads to steatorrhoea: bulky, pale, greasy, foul-smelling stools that float and leave an oil film. Weight loss and malnutrition follow. Destruction of β-cells can produce “pancreatic” diabetes (polyuria, polydipsia, polyphagia, weight fall). Some patients present only when complications such as a pseudocyst or biliary obstruction develop.
Seek immediate care if pain lasts > 6 h, high fever, intractable vomiting or a rigid, board-like abdomen develops.
Type
Key symptoms
Typical signs
Red-flag alarms
Acute
Sudden severe epigastric pain → back, nausea, vomiting, fever
Chronic diarrhea means >3 loose or watery stools per day for more than four weeks. It is not a disease itself but a common end-point of many mechanisms. Here is a rapid overview from cause to clinic.
1. Osmotic diarrhea
Unabsorbed solutes (lactose, fructose, sorbitol, Mg-antacids) hold water in the lumen; stool output falls markedly when the patient stops eating the offending sugar or salt.
2. Secretory diarrhea
The mucosa actively pours water and electrolytes into the gut; fasting does not stop the flood. Think hyperthyroidism, adrenal insufficiency, gastrinoma, VIPoma, bile-acid malabsorption or chronic alcohol abuse.
3. Malabsorption / steatorrhoea
Insufficient pancreatic enzymes, bile acids or damaged villi (coeliac, short-bowel) leave fat and protein undigested. Stools are bulky, greasy, foul-smelling and often accompanied by weight loss.
Rapid transit gives contents too little contact time with the mucosa. Causes include hyperthyroidism, diabetic autonomic neuropathy, post-infectious IBS and pro-kinetic drugs.
Broad-spectrum antibiotics, long-term acid suppression or altered anatomy allow colonic-type bacteria to colonise the small bowel, producing gas, altering bile salts and generating watery, bloating diarrhea.
7. Food intolerance & dietary factors
Lactose, fructose, FODMAPs, caffeine, chilli or high-fat meals can trigger osmotic or secretory episodes; true food allergy may add urticaria or eosinophilic infiltrate.
8. Drugs & chronic toxins
NSAIDs, metformin, ACEI/ARB, colchicine, PPIs, Mg-containing antacids, heavy metals, organic phosphorus compounds and chronic alcohol all have “drug-induced or toxic diarrhea” on their label.
9. Systemic disease
Diabetes, hyperthyroidism, adrenal insufficiency, SLE, scleroderma and hypogammaglobulinaemia disturb electrolyte transport or neuromuscular control through endocrine, immune or neural pathways.
10. Neoplasia
Colorectal cancer, lymphoma, VIPoma, medullary thyroid cancer and villous adenoma may secrete peptides, cause partial obstruction or bleed, leading to nocturnal pain, weight loss and anaemia.
Stomach-ache is not just “tummy hurt”. The same spot can mean opposite diseases depending on how the pain feels and what comes with it. Here is a rapid field-map.
Pain ≥ 3 months, weekly episodes, normal tests → think irritable bowel or functional dyspepsia; night-pain absent, weight stable, pain relieved by defaecation or flatus.
6. Red-flag call-999 list
Sudden excruciating pain with rigid board-like abdomen, lasting > 6 h, plus high fever, haemodynamic instability, melaena or visible abdominal wall bruising – suspect perforation, massive bleeding, severe pancreatitis or gut necrosis.
Gastroenteritis doesn’t “fall from the sky.” It happens when the lining of your stomach and intestines is overwhelmed by one or more “attack factors.” Below are the common routes and culprits, followed by a one-page table so you can spot your own risk points at a glance.
1. Microbes: public enemy No. 1
Viruses – norovirus, rotavirus, adenovirus; spread faeco-orally or by droplets; famous for cruise-ship, school or nursing-home outbreaks.
Bacteria – Salmonella, pathogenic E. coli, Shigella, Campylobacter; linked to under-cooked poultry, eggs, raw seafood or contaminated water.
Parasites – Giardia, Cryptosporidium; hide in wild water, swimming pools or pet fur and can cause weeks of diarrhoea.
2. Chemical & drug injury: self-inflicted damage
Spirits, strong tea/coffee or super-spicy hot-pot scald the mucosa directly.
Regular NSAIDs (aspirin, ibuprofen, diclofenac) weaken the protective barrier and let gastric acid leak in.
Broad-spectrum antibiotics wipe out friendly flora, opening the door for C. difficile and pseudomembranous colitis.
3. Eating pattern: the stomach hates “feast-and-famine”
One huge meal → acid overshoot and delayed emptying.
Skip the next two meals → bile stasis and reflux. Repeat the cycle and mucosal inflammation is guaranteed.
4. Reflux & motility disorders: back-flow from the “drain”
Post-surgical anatomy, gall-bladder disease or chronic constipation can drive bile and pancreatic juice backward into the stomach; if the pylorus is lax, the mix reaches the oesophagus and creates a double acid–alkali burn.
5. Stress & psyche: the brain writes its worry on the gut
Major surgery, trauma, overnight deadlines or chronic anxiety reduce gastric mucosal blood flow and mucus secretion while raising acid output—perfect conditions for erosions and bleeding.
6. Auto-immunity & IBD: friendly fire
Auto-antibodies against parietal cells lead to chronic atrophic gastritis; Crohn’s or ulcerative colitis can ulcerate any part of the GI tract. These “non-infectious” forms tend to relapse for years.
7. Age & radiation: time and the environment gang up
After 60 the stomach makes less acid but also repairs itself more slowly; pelvic or abdominal radiotherapy and some chemo drugs can cause a direct radiation enteritis with diarrhoea and tenesmus.
Repeatedly ignoring the urge or “holding it in” lowers rectal sensitivity.
Distractions (phones) or bad posture on the toilet weaken the defecation reflex.
2. Diet & fluid changes
Low-calorie or low-residue diets, or < 25 g fibre day, reduce stool bulk.
Drinking < 500–1 000 mL day lets the colon re-absorb too much water → hard, dry stool.
3. Sedentary lifestyle
Long hours of sitting / bed rest lower abdominal-wall tone and colonic high-amplitude contractions → slow-transit constipation.
4. Stress & mood
Anxiety, depression or high stress act through the brain–gut–microbiome axis to slow colonic motility and raise anal-sphincter tone → outlet-obstruction or mixed type.
5. Drugs & diseases (always rule these out first)
Common culprits: calcium/iron supplements, opioids, some antidepressants, calcium-channel blockers.
Symptoms of gastric ulcer are highly variable. The most typical is a burning epigastric pain that usually begins 30–60 min after meals and may last from a few minutes to several hours. Patients often report accompanying dyspepsia, weight loss, nausea or vomiting, and complications such as bleeding or perforation may occur. Severity parallels ulcer depth; some individuals have no symptoms (“silent ulcer”), while others present initially with haemorrhage or perforation.
Typical pain characteristics
Onset: 0.5–1 h post-prandial
Relief: temporary with antacids
Duration: minutes to hours
Pattern: recurs over days or weeks
Associated symptoms
Post-prandial fullness, early satiety, belching
Loss of appetite and unexplained weight loss
Nausea, occasionally vomiting (fresh red or coffee-ground blood)
Melaena (tarry black stools) or dark-red blood per rectum
Disease course Malignant transformation is rare (<1%). Endoscopy with biopsy is performed only when endoscopic or histological features raise suspicion for cancer.
Summary of Gastric-Ulcer Symptoms
Category
Key Features (English)
Cardinal symptom
Burning epigastric pain, 30–60 min after meals, lasts minutes–hours; temporarily relieved by antacids; recurs over days–weeks.
Associated upper-GI symptoms
Post-prandial fullness, early satiety, belching, nausea, vomiting (clear or blood-stained).
Systemic / nutritional
Loss of appetite, unexplained weight loss.
Bleeding indicators
Hematemesis (fresh red or coffee-ground), melaena (tarry black stools), occasional dark-red rectal blood.
Complications
Silent ulcer (no symptoms), acute presentation with haemorrhage or perforation.
Malignant potential
<1 % risk of progression to gastric cancer; endoscopy + biopsy if suspicion arises.
Neuropsychiatric features: some patients report nervous tension, irritability, insomnia, palpitations, or poor memory; these symptoms may exacerbate the gastric complaints and create a vicious cycle.
Upper-abdominal discomfort and fullness: typically worse after meals and minimal when fasting; patients feel full after small portions.
Associated symptoms: frequent belching, acid regurgitation, epigastric burning, loss of appetite, generalized indigestion, nausea, and occasional vomiting.
Pain: usually mild, vague, or burning and well tolerated.
Neuropsychiatric features: some patients report nervous tension, irritability, insomnia, palpitations, or poor memory; these symptoms may exacerbate the gastric complaints and create a vicious cycle.
Category
Main Symptoms
Timing / Character
Associated Features
Acute Gastritis
Epigastric pain
Sudden onset; colicky, dull or burning; intensity varies from mild to severe
—
Nausea & vomiting
Chief complaint; may retch violently with little vomitus
Hypersalivation, early satiety
Dyspepsia
Immediate
Belching, upper-abdominal fullness
Chronic Gastritis
Upper-abdominal discomfort & fullness
Predominantly post-prandial; small meals induce fullness
Intestinal adhesions can be caused by abdominal surgery, intraperitoneal infection, abdominal trauma, abdominal radiotherapy, congenital factors, etc., and can be relieved by medication or surgery. Prompt medical attention is recommended so that an appropriate treatment plan can be chosen under a doctor’s guidance.
Abdominal surgery Abdominal surgery is the most common cause. Surgical manipulation may injure the bowel or peritoneum, triggering a local inflammatory reaction and fibrous tissue overgrowth. Appendectomy, hysterectomy, and other abdominal procedures carry a high risk. Patients may complain of abdominal pain, distension, or altered bowel habits. Amoxicillin capsules or cefixime dispersible tablets are often prescribed to prevent infection; severe cases may require adhesiolysis.
Intraperitoneal infection Infections such as peritonitis or pelvic inflammatory disease produce hyperemic, edematous peritoneum; after the inflammation subsides, fibrous adhesions remain. Tuberculous peritonitis is particularly prone to extensive adhesions. Fever and abdominal tenderness are common. Therapy targets the primary infection with antibiotics such as levofloxacin or metronidazole; surgical drainage is sometimes necessary.
Abdominal trauma Blunt or crush injuries can damage bowel or peritoneum, and adhesions form during healing. High-speed collisions or falls carry the greatest risk. Persistent pain and diminished bowel sounds may appear. Early symptoms can be controlled with ibuprofen sustained-release capsules; complete obstruction mandates surgery.
Abdominal radiotherapy Radiation for pelvic or abdominal tumors may injure the serosal layer of the bowel, leading to chronic inflammation and fibrosis. Gynecologic or rectal cancers are the most frequent settings. Radiation enteritis with secondary adhesions presents as diarrhea or tenesmus. Doctors may prescribe montmorillonite powder or live combined Bifidobacterium capsules; severe cases can require a diverting stoma.
Congenital factors A minority of patients have congenital maldevelopment of the mesentery or peritoneal defects that predispose to spontaneous adhesions. Intestinal malrotation is the classic example. Infants may present with recurrent pain or vomiting. Imaging confirms the diagnosis, and corrective surgery is performed when indicated.
Daily care Patients should eat soft, low-fiber foods in small, frequent meals and avoid binge eating. Gentle abdominal massage and light exercise promote peristalsis, but strenuous activity should be avoided. Maintain regular bowel habits. Seek immediate care if pain worsens, vomiting develops, or flatus and stool cease—signs of possible obstruction. Postoperative patients must follow prescribed rehabilitation programs and attend scheduled follow-ups to monitor for recurrent adhesions.
No.
Cause
Mechanism / Typical settings
Common symptoms / signs
Medical treatment
Surgical treatment
Special notes
1
Abdominal surgery (most common)
Surgical trauma → local inflammation → fibrous overgrowth (e.g. after appendectomy, hysterectomy)
Abdominal pain, distension, altered bowel habits
Amoxicillin, cefixime (infection prophylaxis)
Adhesiolysis for severe obstruction
Highest incidence within first post-operative year
Diverting stoma or resection for refractory stricture
Dose-dependent; may present months to years after RT
5
Congenital factors
Maldevelopment of mesentery or peritoneal fixation defects (e.g. intestinal malrotation)
Neonatal/infantile recurrent pain, vomiting, failure to thrive
Supportive (NG decompression, fluids)
Corrective surgery (Ladd procedure, adhesiolysis)
Diagnose with upper-GI contrast series or US
Daily care for all patients
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—
—
Low-fiber, easily digested diet; small frequent meals; gentle abdominal massage & light exercise; prompt medical review if pain ↑, vomiting, or no flatus/stool
