Review clinical manifestations of gastrointestinal dysfunction

Explain the pathophysiology and clinical presentation of achalasia, hiatus hernia and GERD. Distinguish symptoms among those conditions

Explain the pathophysiology of pyloric and intestinal obstruction

Explain the classification of peptic ulcer disease

Explain the pathophysiology and types of gastrointestinal bleeding

Explain the pathophysiology of appendicitis

Explain the pathophysiology of inflammatory bowel disease (IBD); Crohn’s disease, ulcerative colitis (UC), inflammatory bowel syndrome (IBS)

Explain the pathophysiology of malabsorption syndrome; various types eg. pancreatitis, celiac disease, gall bladder diseases

Explain the pathophysiology of diverticular diseases

Explain the pathophysiology of liver cirrhosis and portal hypertension

Classify the different types of jaundice and describe causes and the clinicopathological features of each

Explain the pathophysiology of viral hepatitis and diagnostic markers

Explain briefly the pathophysiology of obesity and malnutritionredispose an individual to the development of thrombosis.

Anorexia

– Lack of desire to eat despite physiologic stimuli that would normally produce

hunger

Nausea

– Subjective experience associated with a number of conditions

Vomiting

Projectile vomiting

– Spontaneous vomiting that does not follow nausea

Retching

– Nonproductive vomiting

Constipation

– Infrequent or difficult defecation

o Due to:

• Low-residue diet

• Sedentary lifestyle

• Changes in bowel habits

• Disease conditions:

o GI diseases

o Neurogenic disorders

• Medications

Diarrhea

– Increased frequency of bowel movements

– Alterations in volume, fluidity, weight of stools…etc

o Due to:

• Infection

• Malabsorption syndromes

• Autoimmune disease

• Medications

Abdominal pain

– Symptom of a number of gastrointestinal disorders

– Occurs in many forms, including:

o Parietal pain

o Visceral pain

o Referred pain

– Some GI diseases have distinctive pain patterns, such as rebound tenderness in appendicitis, however, often abdominal pain is a vague symptom that requires other diagnostic and clinical investigations to determine the cause

Gastrointestinal bleeding

– Upper GI

o Esophagus, stomach, or duodenum

– Lower GI

o Jejunum, ileum, colon, or rectum

– Forms of bleeding:

o Hematemesis: Vomiting of blood

o Melena: Passage of black, tarry stools (digested blood)

o Hematochezia: Passage of fresh blood through the anus usually with stools

• Indicates colonic origin

o Occult bleeding: Hidden blood in stool

• Detected using special techniques in the laboratory

o Bleeding per rectum

• Passage of fresh blood through the anus due to fissure or hard stools

– Dysphagia/ odynophagia: Difficulty/ pain in swallowing

o Mechanical obstructions

o Functional obstructions

Achalasia

Failure of relaxation of smooth muscle fibers (SMF) of the lower esophageal sphincter (LES)

Etiology & Pathophysiology:

A normal functioning LES maintains a zone of high pressure to prevent chyme reflux

Angle of His acts as a valve to prevent backflow

A balance of excitatory/ inhibitory impulses to SMF regulates muscular coordination required in the esophagus and LES

– The GI tract is stimulated (excited) by the neurotransmitter acetylcholine and inhibited by nitric oxide and vasoactive intestinal peptide

– Imbalance in these impulses result in failure of relaxation and subsequent obstruction causing food to build-up in the esophagus behind the obstruction

Clinical manifestations/diagnosis:

Dysphagia to both solids and liquids

Regurgitation

Chest pain

Obstruction appear in esophageal manometry, barium studies

– On x-ray the esophagus appears massively dilated

Similar conditions: GERD, hiatus hernia, psychosomatic disorders

Gastroesophageal Reflux Disease (GERD)

Reflux of chyme from the stomach to the esophagus

Leads to inflammation (reflux esophagitis)

Etiology & Pathophysiology:

Hiatal hernia due to mechanical and motility factors

Impaired esophageal motility

– Eg. Multiple sclerosis

Increased gastric acidity:

– Eg. Zollinger-Ellinson syndrome

Increased abdominal pressure

Obesity increases the severity

Clinical manifestations:

Heartburn

Regurgitation of chyme

Mid-epigastric pain within 1 hour of eating

Others:

– Increased salivation

– Chest pain

o This can be very intense and present similar to a myocardial infarction

o Patients presenting with central, epigastric pain require an ECG to rule out cardiac involvement, however, in the absence of other risk factors acid reflux should be considered as part of the differential diagnosis and the administration of an antacid to alleviate the pain

Complications:

Strictures and narrowing (reflux-induced inflammation), Barrett’s esophagus (Figure 4)

Hiatal hernia

Protrusion (or herniation) of the upper part of the stomach into the thorax through a tear or weakness in the diaphragm

Etiology & Pathophysiology:

Defect/ weakness in the diaphragm

Increased intra-abdominal pressure

– Eg. Straining, severe violent cough

Types:

Sliding hiatal hernia (Figure 5-A)

Para-esophageal (rolling) hiatal hernia (Figure 5-B)

Clinical manifestations:

– No symptoms

– Chest pain

– Symptoms of acid reflux

– Shortness of breath (hernia’s pressure on the diaphragm)

– Palpitations (from irritation of the vagus nerve (cranial nerve X)

Pyloric Obstruction

Blocking or narrowing of the opening between stomach & duodenum

Etiology & Pathophysiology:

Can be acquired or congenital (pyloric atresia)

Obstruction impairs emptying of gastric contents into the duodenum

Persistent vomiting leads to hypochloremia and subsequent metabolic alkalosis

– Compensatory respiratory acidosis → hypoventilation (pCO2)

Hypovolemia (decreased fluid volume) leads to dehydration and electrolyte disturbance, and secondary hyperaldosteronism

Manifestations:

Epigastric pain and fullness

Nausea

Vomiting

Succussion splash (gastric splash)

Malnutrition, dehydration, and extreme debilitation (with prolonged obstruction)

Intestinal Obstruction

Mechanical or functional obstruction of the intestine, preventing the normal transit of products of digestion

Etiology:

Adhesions post abdominal surgery (most common cause)

Hernias containing bowel

Inflammatory strictures

– E.g. Crohn’s disease

Intussusception (telescoping bowel into distal segment causing ischemia and necrosis)

Foreign bodies

Intestinal atresia

Neoplasms

Diverticulitis / Diverticulosis

Fecal impaction

Functional obstruction

– E.g. Paralytic ileus:

o Impairment of normal propulsive ability of the GI tract

o A common post-surgery side effect

Pathophysiology and Clinical Manifestations:

Can occur at any level distal to the duodenum

– Mechanical obstruction of chyme flow through the intestinal lumen

– Functional obstruction related to poor intestinal motility without an obstructing lesion

A medical emergency

Distension and colicky pain

Nausea and vomiting

Hypovolemia, dehydration, shock

Electrolyte imbalance

Silent abdomen (in complete obstruction)

Diagnostic Testing and Evaluation

Radiology

– Abdominal imaging by x-ray, computed tomography, and ultrasound can assist in determining presence and location of obstruction

– Endoscopy can confirm

Gastritis

Inflammatory disorder of the gastric mucosa

Etiology:

Peptic ulcer/H pylori and NSAIDs are the most common

Others:

– Alcohol, severe illness, pernicious anemia

Pathophysiology:

Can be acute or chronic (review pathophysiology of inflammation)

NSAIDs (consider mechanism of action)

– Eg. NSAIDs inhibit prostaglandins which stimulate mucus production to protect the lining of the stomach

Sites: fundal or antral

Clinical manifestations:

– Abdominal pain: central, dull aching

– Gastric ulcer and its complications (see Figure 8)

Peptic Ulcer Disease

A break or ulceration in the protective mucosal lining of stomach, or duodenum

Etiology and risk factors:

Main pathology: increased gastric acid secretion

High gastrin levels

Use of NSAIDs

Cigarette smoking

Zollinger-Ellison syndrome

– Excess secretion of the hormone gastrin from one or more tumors located in the pancreas and/or duodenum

– Causes increase in gastric acid secretion

H pylori toxins promote inflammation and ulceration

Pathophysiology:

Duodenal ulcers are the most common

– Gastric ulcers tend to develop in antral region

Acute or chronic

Superficial erosions or deep true ulcers

Clinical manifestations:

Pain

Manifestation of hyperacidity

Stress ulcer: A peptic ulcer that is related to severe illness, sepsis, neural injury, or systemic trauma, eg. TBI, burns

Pathophysiology:

Physiologic stress of a serious illness

Ischemia and hypoxic injury

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