Classic presentation
The classic presentation of appendicitis is abdominal pain that is initially diffuse and then intensifies and migrates toward the right lower quadrant (RLQ) to McBurney point (1.5–2 inches from the anterior superior iliac crest toward umbilicus).
It should be mentioned that the textbook presentation of nausea, vomiting, and pain migration is present only in 50–65% of patients, while fever is present in only 40% of patients with perforated appendices.
Also, patients often complain of bloating and anorexia.

Investigation
The migration of pain to the RLQ is the most useful clinical finding.
Other clinical findings like guarding and rebound tenderness increase the likelihood of appendicitis.

The WBC count and CRP, although always done, but cannot reliably rule in nor rule out acute appendicitis.

Urinalysis may be misleading and reveal pyuria and hematuria due to bladder inflammation from an adjacent appendicitis.

CT scanning is the best test at ruling out appendicitis when the diagnosis is uncertain (Sensitivity 92%, specificity 97%).

Ultrasound or MRI, although less reliable, but can be used as alternatives in cases of pregnancy or unavailability of CT.

If the patient is a female at child-bearing age, you should do a pregnancy test to rule out ruptured ectopic pregnancy.

There are 2 "rules" that can help in clinical decision:
• The Alvarado score
• The appendicitis inflammatory response (AIR) score

Hamburger sign:
To check for anorexia. Ask the patient if they would like to eat their favourite food, if yes, then they don't have anorexia, therefore it's unlikely to be appendicitis.

Treatment

Surgery remains the treatment of choice.
Broad-spectrum antibiotics can be used as alternatives, but they are not very reliable and have a 30% chance of recurrence within 1 year.

Absent bowel sounds, guarding, and rebound tenderness (Blumberg sign) all point to peritoneal involvement secondary to appendicitis.

Fever, jaundice, and right-upper quadrant abdominal pain (sometimes epigastric)

This triad of signs & symptoms suggests cholengitis (inflammation of the common bile duct) and is present in about two thirds of patients

Leukocytosis, elevated conjugated bilirubinemia, and elevated ALP are also present in a lot of patients.

Bacteremia is also very common is this disease.

Classic presentation
Patients often present with chronic and nonspecific epigastric pain.
A history of chronic use of NSAIDs, Smoking, alcohol consumption, and chronic stress are all suggestive of PUD.
Other less frequent signs and symptoms include melena and hematemesis (from a bleeding ulcer), signs and symptoms of anemia (also from bleeding), vomiting, and gastric outlet syndrome (due to chronic untreated duodenal ulcer).

You mostly won't be able to distinguish between duodenal ulcer and gastric ulcer based on history and exam alone, but some SSx can help:
Pain from gastric ulcer is usually diffused and unlocalized. Pain from duodenal ulcer is usually more localized and specific. It can also awaken patients at night.
In gastric ulcer, pain starts briefly after meals, and is not relieved by food, while duodenal ulcer pain starts about 2 hours after eating and can be usually relieved by food.
Another problem is that gastric ulcer is a risk factor for gastric cancer. There's a wide variation in the literature about the rate of gastric cancer in gastric ulcer patients which ranges between 3% up to 20%.
Duodenal ulcer on the other hand does not increase the risk for cancer.

One of the complications of PUD is a perforated ulcer which usually presents with a sudden, severe, and sharp abdominal pain. The pain is mostly diffuse all over the abdomen, although some patients present with severe epigastric pain. Pain worsens with movement (so patients often assume a fetal position to minimize movement).
Signs of peritoneal involvement like rebound tenderness and guarding are usually present, but this depends on many factors.
Patients of perforated ulcer may also present with SSx of septic shock; tachycardia, hypotension, and anuria.
They also may present with radiological signs of pneumoperitoneum (air in the peritoneum) and shoulder pain.

There's also Curling ulcer, which is usually seen in patients with severe burns. Because burns decrease plasma volume, which in turn decreases gastric blood flow and causes hypoxia and this decreases mucus secretion and can precipitate an ulcer.

Another type is Cushing ulcer in which a head injury causes vagal overstimulation and therefore increasing HCl to pathological levels.

Investigation

Patient's history will contain clues for the diagnosis of PUD; chronic use of NSAIDs, smoking (which decreases gastric emptying), stress, alcohol use, excessive spices in food, and H. Pylori infection.

Nevertheless, patient history and clinical exam alone are not conclusive enough to diagnose a patient with PUD. Endoscopy remains the test of choice to exclude malignancy as well, alongside radiography (Barium swallow and CT).
Any patient suspected to have PUD must also be checked for H. Pylori infection, because it causes recurrence even after the complete treatment and healing of the ulcer. A urease test is widely used to detect the bacteria. Fecal antigen (which is more sensitive that the antibody test) & urea-breath test are good alternatives.

Treatment
It aims at relieving the pain, curing the ulcer, and eradicating the infection, via:-

- A change in lifestyle and habits

- Decreasing gastric acid production

- Buffering the acidity of the stomach

- Increasing mucus secretion

- Antibiotics to get rid of the bacteria to prevent recurrence and complications like malignancy.

Decreasing gastric acid production:-

• Anti-muscarinics, like pirenzepine (they target M1 receptors in the stomach). nobody really uses them because of their low efficacy and atropine-like effects at higher doses.

• anti-histamines, like cimetidine (they target H2 receptors). They do a great job. Cimetidine, being the prototype, has more side effects than the newer drugs like famotidine; it has anti-androgenic effects (like gynecomastia), causes some CNS problems especially in the elderly, and is a potent inhibitor of CYP450. It also has weaker effect on acid secretion than famotidine.
Some guidelines suggest using them for 6 weeks as initial treatment, and then lowering the dose by half for 6 months (in addition to antibiotics, obviously).

• Protein-Pump Inhibitors (PPIs), like Omeprazole and pentoprazole. They are great, we love them, and they work fine.
Their side effects are usually diarrhea (due to decreased HCl level), deficiency in intrinsic factor (and therefore B12 deficiency), and osteoporosis (because osteoclasts also use K/H ATPase pump, which the PPIs inhibit). Also, omeprazole, but not the others, is an inhibitor of CYP450. Anyway, all PPIs change the bioavailability of drugs because the alter the acidity of the stomach.
The guideline is to take them initially for 4 weeks, then lower the dose by half for 4 months because they are more effective than cimetidine and his cousins.

It should be noted that all the drugs that decrease gastric acid secretion must not be discontinued suddenly, because this may increase HCl levels to terrible levels and causes a rebound ulcer.