Aula 7 - Gastrointestinal Disease Flashcards
1
Q
The GI tract includes the pathway that connects the ________ to the ________.
A
mouth, anus
2
Q
What are the 4 main functions of the GI system?
A
- Digestion
- Secretion
- Motility
- Absorption
3
Q
What organs belong to the upper GI tract?
A
- Mouth
- Esophagus
- Stomach
4
Q
What organs belong to the lower GI tract?
A
- Small intestine
- Large intestine
- Anus
5
Q
What are the 6 parts of the large intestine?
A
- Cecum
- Ascending colon
- Transverse colon
- Descending colon
- Sigmoid colon
- Rectum
6
Q
What are the 3 parts of the small intestine?
A
- Duodenum
- Jejunum
- Ileum
7
Q
What other organs and glands (besides the upper and lower GI tract) belong to the GI system?
A
- Liver
- Pancreas
- Gallbladder
- Salivary glands
8
Q
Give examples of pathologies in the upper GI tract.
A
- Gastritis
- Esophageal achalasia (the muscles in the esophagus don’t relax)
- Peptic ulcer
- Gastroesophageal reflux
9
Q
Give examples of pathologies in the lower GI tract.
A
- Diarrhea
- Constipation
- Inflammatory bowel disease
- Diverticular disease
- Irritable bowel syndrome
10
Q
Give examples of pathologies in the other organs and glands that belong in the GI system.
A
- Cholelithiasis (gallstones, i.e., hardened pieces of bile that form in your gallbladder or bile ducts)
- Cirrhosis (advanced scarring of the liver)
- Hepatitis
- Liver carcinoma
11
Q
What is gastroesophageal reflux disease (GERD)?
A
It is characterized by passage of gastric contents into the
esophagus.
12
Q
What are the two types of gastrointestinal reflux disease? What is the most common?
A
Can be divided into gastroesophageal reflux
* Without esophageal erosion (~70% of patients).
* With esophageal erosion = reflux esophagitis (30%).
13
Q
What are the two main causes of gastrointestinal reflux disease?
A
- Gastroesophageal junction dysfunction (dysfunction of the lower esophageal sphincter, which allows reflux of gastric contents into the esophagus)
- Decreased acid elimination
14
Q
What are the four main causes of gastroesophageal junction dysfunction?
A
- Increased frequency of cardia relaxations
- Reflux associated with cardia relaxations
- Mechanical dysfunction of the cardia
- Increased intragastric pressure
15
Q
What is the cardia?
A
The part of the stomach that is closest to the esophagus.
16
Q
What are the two main causes of the mechanical dysfunction of the cardia?
A
- Hiatal hernia (occurs when the upper part of the stomach bulges through the diaphragm into the chest cavity)
- Neoplasia
17
Q
What are the three main causes of increased intragastric pressure?
A
- Pregnancy
- Obesity
- Delayed gastric emptying
18
Q
What are the two main causes of decreased acid elimination?
A
- Decreased saliva secretion
- Decreased peristalsis (involuntary muscle movement that moves food through your gastrointestinal tract)
19
Q
What is the main cause of decreased saliva secretion?
A
Smoking
20
Q
What are common food triggers of GERD?
A
Spicy foods, alcohol, fatty foods, and junk foods.
21
Q
How does smoking contribute to GERD?
A
Smoking relaxes the lower esophageal sphincter (LES), increasing the risk of acid reflux and symptoms like heartburn and chest pain.
22
Q
What is abnormal LES relaxation?
A
It is excessive or prolonged transient lower esophageal sphincter relaxation, which allows stomach acid to move into the esophagus.
23
Q
What factors increase intra-abdominal pressure and worsen GERD?
A
Exercise, obesity, and positional changes (e.g., lying down).
24
Q
How does delayed gastric emptying contribute to GERD?
A
Gas buildup in the stomach increases pressure on the cardia, which is sensed by pressure receptors, stimulating the vagus nerve, which leads to the lower esophageal sphincter relaxation, allowing acid to reflux into the esophagus.
25
What medication used for hypertension can worsen GERD?
Amlodipine, which is a calcium channel blocker. Calcium channels allow calcium ions flow into the muscle cell, causing the muscle to contract. By blocking these channels, Amlodipine impairs the lower esophageal sphincter from contracting, leading to its relaxation and, thus, to acid reflux.
26
What complications arise from repeated esophageal damage in GERD?
* Metaplasia (replacement of squamous epithelium with columnar cells)
* Barrett’s Esophagus (precancerous lesion)
* Adenocarcinoma (progression of Barrett’s Esophagus)
* Esophageal scarring and bleeding
* Mechanical dysphagia (difficulty swallowing solid foods)
27
What is Non-Erosive Reflux Disease (NERD)?
It's a form of GERD where heartburn persists despite treatment, but without visible esophageal damage.
28
What are the respiratory complications of GERD?
* Water regurgitation (water brash, which occurs when spit and stomach acid mix together and cause a sour taste)
* Aspiration of acid into the larynx and lungs
* Upper respiratory tract irritation
* Chronic cough (especially at night)
* Asthma
* Hoarse voice (rough voice, typical of a sore throat)
29
What are the 7 most frequent clinical manifestations of GERD?
1. Epigastric pain with a burning feeling
2. Regurgitation (vomiting)
3. Dysphagia (difficulty in swallowing)
4. Odynophagia (pain while swallowing)
5. Sialorrhea (excess saliva)
6. Halitosis (bad breath)
7. Teeth damage (due to gastric acid in mouth)
30
What are the 5 less frequent clinical manifestations of GERD?
1. Eructation (burping)
2. Bloating (sensation of so tightness due to fluid or gas accumulation)
3. Nausea
4. Anorexia
5. Chronic cough
31
What are the main triggers (e.g., factors and behaviours) that exacerbate symptoms in GERD?
* Lying down after meals or at night
* Bending over
* Intake of fluids with meals
* Intake of certain foods and drinks (Ex. Caffein, alcohol, fatty foods or spicy foods)
* Smoking
32
What are the 6 main complications of GERD?
1. Ulcer on the esophagus
2. Scarring and narrowing of the esophagus
3. Esophagitis
4. Changes in the esophagus cells linen (e.g., Barrett’s esophagus)
5. Asthma
6. Esophagus carcinoma
33
What are the main diagnostic methods for GERD?
* Anamnesis
* Physical examination
* Biochemical blood tests
* Endoscopy
* Esophagram
* Esophageal pH test
* Esophageal manometry
* CT or MRI
34
What is an endoscopy, and how is it used in GERD diagnosis?
Endoscopy involves inserting a flexible tube with a camera down the throat to visualize the esophagus and check for damage, inflammation, or Barrett’s esophagus.
35
What is an esophagram, and why is barium used?
An esophagram (also called a barium swallow/enema) is an X-ray of the esophagus where barium contrast helps highlight abnormalities like reflux or abnormal narrowings.
36
What does an esophageal pH test measure and why is it used in GERD diagnosis?
It records the pH level in the esophagus over 24 hours to determine acid exposure and diagnose GERD.
37
What is esophageal manometry, and why is it performed in GERD diagnosis?
It measures pressure and movement in the esophagus to evaluate the function of the lower esophageal sphincter (LES) and esophageal motility disorders, associated with GERD.
38
How can CT or MRI aid in GERD diagnosis? What are the most common findings?
These imaging techniques provide detailed views of the esophagus and surrounding structures.
In CT or MRI for GERD, we may see:
* Esophageal thickening (from inflammation or scarring)
* Hiatal hernia (if present, which can worsen reflux)
* Esophageal strictures (narrowing due to chronic acid exposure)
* Barrett’s esophagus (potential precancerous changes in the esophageal lining)
39
What are the most common findings in biochemical blood tests for GERD?
Possible findings include:
* low hemoglobin (if there is chronic bleeding from esophageal damage) and anemia
* elevated inflammation markers
40
What are the most common findings in an esophagram (barium swallow X-ray) for GERD?
* Reflux of barium back into the esophagus
* Esophageal strictures (narrowing due to acid damage)
* Hiatal hernia (if present)
41
What are the most common findings in an esophageal pH test for GERD?
* Low pH in the esophagus (acid reflux episodes)
* Prolonged acid exposure over 24 hours
* Worsening acidity when lying down or after meals
42
What are the most common findings in esophageal manometry for GERD?
* Weak lower esophageal sphincter (LES) (does not close properly)
* Abnormal esophageal motility (poor movement of food down the esophagus)
43
What is a peptic ulcer?
It is a lesion characterized by open sores in the inner lining of the gastric or duodenal mucosa that penetrates the muscularis mucosa layer.
44
Why is it called "**peptic**" ulcer?
“Peptic” means it’s related to digestion, as the word is derived from pepsin, the major digestive enzyme produced in the stomach.
45
What are the two main types of peptic ulcers? Which is more common?
* **Gastric ulcer (80%)**: typically in the lesser curvature, at the body-antrum transition.
* **Duodenal ulcer (20%)**: both at the anterior or posterior wall.
46
In what age and gender are peptic ulcers more common?
Middle-aged adults, male gender.
47
What is are the two main causes of peptic ulcers?
| (Etiology)
* Infection with Helicobacter pylori (H. pylori) bacteria
* Long-term use of nonsteroidal anti-inflammatory drugs (NSAIDs)
48
What are the other possible causes of peptic ulcers, beside H. pylori and NSAIDs?
| (Etiology)
* Corticosteroids
* Alcohol
* Tobacco
* Gastric hyperacidity
* Duodenal-gastric reflux
* Zollinger-Ellison syndrome (rare digestive disorder that occurs when tumors in the pancreas or small intestine cause the stomach to produce too much acid)
* Acute stress
* Malignancy
* Inflammatory diseases (e.g., Crohn's Disease)
49
How do peptic ulcers develop?
| (Pathophysiology)
Increased damage and/or impaired defense can lead to decreased mucus production, which exposes the inner lining of the gastric/intestinal mucosa to acid, leading to epithelial cell dead and open sores.
50
What are the normal protective factors present in the gastric and intestinal wall that prevent/repair damage?
* Surface mucus secretion
* Bicarbonate secretion into mucus (neutralizes acid)
* Mucosal blood flow (supports tissue repair)
* Epithelial barrier function
* Epithelial regenerative capacity
* Prostaglandins (stimulate mucus and bicarbonate production)
51
What are the harmful triggers that increase damage or impair defenses in peptic ulcer disease?
* H. pylori infection (produces urease, an enzyme that neutralizes acid and weakens the gastric lining)
* NSAID use (reduces prostaglandins)
* Tobacco & alcohol (increase acid, reduce mucus)
* Gastric hyperacidity
* Duodenal-gastric reflux
52
How does H. pylori contribute to peptic ulcer formation?
H. pylori bacteria, which is commonly present in the human stomach, can overgrow and colonize the gastric mucosa, by adhering to epithelial cells. These bacteria inhibits mucin protein synthesis, decreasing mucus production and dysrupting this protective layer of the inner lining of the gastric/intestinal mucosa. Additionally, H. pylori can produce urease, which elevates the pH, further damaging the mucosa and leading to ulcers.
In summary, H. pylori:
* Colonizes epithelial cells
* Decreases mucus production
* Increases acid exposure to the mucosa
53
What are the NIGS histological changes seen in peptic ulcers?
* Necrotic debris (N) (from epithelial cells death)
* Acute inflammation (I) (infiltration of neutrophils)
* Granulation tissue (G) (repair response)
* Fibrosis (S) (scar formation)
54
What are the most common clinical manifestations of peptic ulcers?
Peptic ulcers are often asymptomatic (in about 70% of the patients). However, some of the most common symptoms include:
* Epigastric pain with a burning sensation
* Indigestion
* Bloated stomach
* Burping
* Nausea and vomiting.
55
How do symptoms differ in gastric and in duodenal ulcers?
* In gastric ulcer, symptoms might worsen after food intake and felling night pain is common.
* In duodenal ulcer, symptoms might actually improve after food intake, and night pain is not as often.
56
What are the clinical manifestations of peptic ulcers associated with bleeding?
* Melena (blood in feces)
* Dizziness
* Pallor (paleness)
57
What are the 4 most common complications of peptic ulcers?
* Bleeding (most common)
* Perforation (life-threatening a tear in the stomach wall that allows gastric contents to leak into the peritoneal cavity, including acid and bacteria, which cause corrosion and infection)
* Fistulation (abnormal direct connection from the stomach to another organ, typically the colon or the gallbladder)
* Malignant evolution (which can cause obstruction of the GI tract by the mass)
58
What are the main diagnostic methods for peptic ulcers?
* Anamnesis
* Physical examination
* Biochemical blood tests
* Endoscopy
* Esophagram
* H. Pylori tests
59
What techniques can be used to detect the presence of excessive H. Pylori in order to diagnose peptic ulcers?
* Serology (Blood Test) – Detects elevated antibodies (Immunoglobulin M and G - IgM and IgG) but can’t distinguish past vs. current infection.
* Urea Breath Test – Detects active infection by measuring urease activity.
* Stool Antigen Test – Also detects active infection by looking for proteins (antigens) associated with H. pylori infection in the stool.
* Biopsy (via Endoscopy) – Gold standard for direct detection, but only done if ulcers are suspected.
60
How can a breath test detect the presence of H. pylori infection?
The H. pylori breath test, also called urea breath test, relies on a simple chemical reaction which is based on the natural behaviour of the bacteria.
Naturally occuring gastric urea is made up of 99% carbon isotope 12-C and 1% carbon isotope 13-C. The breath test uses urea enriched with 13-C.
The patient must consume a drink containing 13-C enriched urea and after some time they blow into a tube. If the level of 13-C is elevated, then the enriched urea provided by the testing kit must have been **broken down to produce high levels of 13-C in the breath** (i.e., it means that the 13-C was separated from the urea) and this implies the presence of **urease** excreting H pylori in the stomach (an enzyme produced by this bacteria that degrades urea).
61
What is inflammatory bowel disease?
It is a chronic inflammation of several sections of the gastrointestinal tract, resulting from the immunological action on the intestinal mucosa.
62
How does inflammatory bowel disease differ from other infectious pathologies?
It does not present positive culture results for known microbial/pathological agents (bacteria/virus/fungus) and does not respond to antibiotic treatments.
63
How is the prevalence of inflammatory bowel disease in terms of gender and age?
In terms of gender, it affects men and women equally.
In terms of age, there are two more evident incidence peaks: between 15 and 30 years and between 60 and 80 years.
64
What is the typical presentation of Inflammatory Bowel Disease symptoms?
It often presents with recurrent episodes (with phases of exacerbation and remission) of bloody mucopurulent diarrhea and abdominal pain.
65
What are the two main types of Inflammatory Bowel Disease?
The two main types are Crohn's disease and ulcerative colitis.
66
Distinguish Crohn's disease and ulcerative colitis in terms of affected regions and lesion extension.
Affected regions:
* Crohn's Disease may affect the entire GI tract (from mouth to anus);
* Ulcerative colitis is mainly limited the descending colon, rectum and anus.
Lesion extension:
* Crohn's Disease presents transmural lesions (which affect the entire intestinal wall: mucosa, submucosa, muscularis propria and serosa)
* Ulcerative colitis lesions are usually limited to the mucosa (most superficial/inner layer of the intestinal wall).
67
Which of the two types of inflammatory bowel disease is considered an autoimmune disease?
Crohn's Disease
68
What is the cause of Crohn's disease?
The exact cause of Crohn's disease is idiopathic (still unknown).
69
What factors have been correlated with the etiology of Crohn's Disease?
* **Immune dysregulation**: exacerbated autoimmune inflammatory response.
* **Diet and stress**: can worsen the condition, but it is not certain that they trigger the disease.
* **Genetic factors**: more common in people who have cases in the family and some correlation with the HLA-B27 gene.
70
What are the main risk factors associated with Crohn's Disease?
* Age (< 30 years)
* Smoking habits
* Appendicectomy (the appendix may contribute to intestinal immunity, helping protect the GI tract against infections)
* Stress
* Geographical factors (industrialized countries are associated with higher risk, especially in the northern hemisphere)
71
Describe the pathophysiology of Crohn's Disease.
The exact cause of Crohn's disease is unknown, but it is believed to be triggered by a viral or bacterial infection that initiates an inflammatory response. However, this response does not resolve, leading to persistent inflammation and granulomatous formation. A strong inflammatory response, often linked to hyperactivity of Th-17 lymphocytes, results in thickening and weakening of the gastrointestinal tract walls.
72
What are the main gastrointestinal clinical manifestations of crohn's disease?
* Abdominal pain and cramps
* Chronic diarrhea
* Blood in the stool
* Mouth ulcers
* Loss of appetite and weight
* Pain around the anus
73
What are the main clinical manifestations of crohn's disease outside of the gastrointestinal disease?
* Fatigue
* Fever
* Joint pain/arthritis
* Eye inflammation (e.g. uveitis and episcleritis)
* Osteoporosis
74
What are the main complications of crohn's disease, due to constant aggression to the gastrointestinal walls?
* **Intestinal occlusion**: thickening of the walls and the formation of scar tissue can lead to stenosis in the digestive tract, making it difficult for food to pass through.
* **Ulcers**: small lesions appear on the mucosa of the digestive system (most commonly the mouth, anus and genital region).
* **Fistulas**: when mucosal lesions become deeper, they can connect two parts of the body that are not normally connected (e.g. between the rectum and the skin around the anus).
* **Abscesses**: accumulation of pus.
75
What other complications may arise from crohn's disease?
* Anemia
* Malnutrition
* Skin problems
* Artritis
* Colon cancer
76
What are the main diagnostic methods for crohn's disease and the most common findings in each one?
* **Anamnesis**: family history, abdominal pain and cramps, loss of weight and apetite.
* **Physical examination**: tenderness to abdominal palpation, for example.
* **Endoscopy and/or colonoscopy**: thickening of the walls and the formation of scar tissue can lead to narrowing of the digestive tract.
* **Computed Tomography (CT) or Magnetic Resonance Imaging (MRI)**: MRI is relevant for detecting fistulas and CT helps examine bowel wall.
* **Biochemical analysis of blood and/or feces**: includes complete blood count and inflammation panel (e.g. inflammatory markers – C-reactive protein, ESR, etc.). Additionally, microbial culture tests may be relevant to exclude infectious pathologies.
* **Biopsy**: the presence of clusters of inflammatory cells, called granulomas, will help to confirm a diagnosis of Crohn's disease.
77
A positive microbial culture helps to ________ (confirm/rule out) crohn's disease.
rule out
## Footnote
Crohn's disease is a result of an autoimmune inflammatory response, not derived from a pathogen.
78
Finding granulomas in a colon biopsy helps to ________ (confirm/rule out) crohn's disease.
confirm
## Footnote
It also allows to differentiate Crohn's disease from ulcerative colitis, as the latter does not present granulomas.
79
What is the cause of ulcerative colitis?
The exact cause of ulcerative colitis is idiopathic (still unknown).
80
What factors have been correlated with the etiology of Ulcerative colitis?
* Immune dysregulation (exarcebated autoimmune inflammatory response)
* Diet and stress
* Genetic factors (HLA-B27 gene)
81
T/F: The etiology and risk factors of crohn's disease and ulcerative colitis are all the same.
True
82
Explain the pathophysiology of ulcerative colitis.
Even though the exact cause is unknown, it is believed that it may be triggered by a viral or bacterial infection that leads to an inflammatory response. Typically, this inflammation begins in the anorectal area and extends proximally. Therefore, inflammation is generally limited to the mucosa, and foci of ulceration and abscesses may be seen.
83
What are the main signs and symptoms (clinical manifestations) of ulcerative colitis?
* Abdominal pain and cramps
* Diarrhea with blood, pus and/or mucus
* Urgency to defecate, but unable to do so
* Pain when defecating
* Loss of appetite and weight
84
What symptoms outside the gastrointestinal system are usually observed in ulcerative colitis?
* Fatigue
* Fever
* Joint pain/arthritis
* Eye inflammation (e.g. uveitis and episcleritis).
85
What specific symptoms of ulcerative colitis help to distinguish it from crohn's disease?
* Fecal urgency
* A feeling that the bowels haven't emptied completely
* Significative blood in stool
86
What are the main complications of ulcerative colitis?
* Severe bleeding
* Sudden perforation of the colon (fulminant or toxic colitis): may lead to fistulas and/or peritonitis.
* Osteoporosis
* Lithiasis (kidney stones)
* Colon cancer
87
What other complications may arise from ulcerative colitis?
Same as Crohn's Disease:
* Malnutrition
* Anemia
* Skin problems
* Artritis
* Colon cancer
88
What are the main diagnostic methods for ulcerative colitis and the most common findings in each one?
* **Anamnesis**: abdominal pain and cramps, diarrhea, urgency to defecate.
* **Physical examination**: tenderness to abdominal palpation, for example.
* **Endoscopy and/or colonoscopy**
* **Computed Tomography (CT) or Magnetic Resonance Imaging (MRI)**: MRI is relevant for detecting fistulas and CT helps examine bowel wall.
* **Biochemical analysis of blood and/or feces**: includes complete blood count and inflammation panel (e.g. inflammatory markers – C-reactive protein, ESR, etc.). Additionally, microbial culture tests may be relevant to exclude infectious pathologies.
* **Biopsy**: the presence of clusters of inflammatory cells, called granulomas, will help to confirm a diagnosis of Crohn's disease and rule out ulcerative colitis.
89
How can diagnostic techniques help to differentiate crohn's disease and ulcerative colitis?
In ulcerative colitis, fistulas are usually absent, as well as granulomas, and lesions are limited to the mucosa of the colon, normally presenting with bleeding.
In Crohn's disease, fistulas are common, as well as granulomas, and lesions are transmural (i.e., affect all layers of the walls) can affect the whole GI tract (i.e., from the mouth to the anus), usually without bleeding.
90
What is the irritable bowel syndrome (IBS)?
Hypersentivity of the intestinal muscle tissue to stimuli (triggers) that affects the frequency of bowel movements, as well as the consistency and/or shape of stool.
91
What is the prevalence of IBS in terms of age and gender?
In terms of gender, it affects more women than men.
In terms of age, it is most often diagnosed in young adulthood.
92
What is the etiology (cause) of IBS?
The exact cause of irritable bowel syndrome is idiopathic (still unknown).
93
What factors have been associated with the etiology of IBS?
* **Eating habits**: eating meals too quickly, high-calorie meals, foods rich in wheat, dairy, chocolate, coffee, spicy foods, etc.
* **Somatic pain syndromes** (pain in the musculoskeletal structures or skin): fibromyalgia, chronic fatigue, functional heart pain, etc.
* **Emotional and/or psychiatric disorders**: depressive disorders, anxiety, stress, fear, etc.
* **Other gastrointestinal disorders**: bacterial gastroenteritis, etc.
94
Describe the possible pathophysiology of IBS.
**Changes in the sensitivity of nerve pathways, both intrinsic and extrinsic to the intestine** (including neuron necrosis), can lead to exaggerated sensations of pain (hyperalgesia) and/or alterations in secretion, absorption, and intestinal motility, such as **decreased peristalsis**. This slowed motility can cause feces to be retained longer, potentially leading to **intestinal dysbiosis**, which is an imbalance in the intestinal microbiota. Dysbiosis may alter the permeability of the mucus layer, allowing pathogens to invade the intestinal lining, potentially causing inflammation and impairing normal nutrient absorption
95
What are the main clinical manifestations of IBS?
* Diarrhea alternating with constipation
* Changes in intestinal transit
* Presence of mucus in the stool
* Abdominal pain
* Abdominal distension (due to excess gas)
* Flatulence
* Nausea, reflux and early satiety
96
What are the main complications of IBS?
* **Malnutrition and dehydration**: result of possible electrolyte dysregulation caused by diarrhea or by dietary habits that involve avoiding certain essential foods (by triggering flareups).
* **Anxiety disorders and depression**: symptom and crisis management can generate additional anxiety.
* **Hemorrhoids**: in the case of recurrent constipation.
* **Sleep perturbations**: abdominal discomfort and pain, associated with changes in intestinal transit, can affect the quality of sleep.
* **Impact on quality of life**: management of the urge to defecate and management of pain/discomfort in a social environment.
97
What are the main diagnostic methods for IBS and the most common findings in each one?
* **Physical examination and anamnesis**: may show tenderness in the abdomen, especially in the lower abdomen, and signs of bloating or discomfort. The patient may appear thin and pale. There might be complaints of the urgency to defecate.
* **Biochemical analyses of blood and/or feces**: typically normal, with no signs of infection or inflammation, and may show mild anemia or altered electrolyte levels in some cases.
* **Endoscopy and/or colonoscopy**: usually normal, with no visible damage or inflammation in the intestinal lining.
* **Computed tomography (CT) or Magnetic Resonance Imaging (MRI)**: typically show no structural abnormalities, but may reveal signs of bloating or gas accumulation.
* **Psychological evaluation exams**: may indicate anxiety, depression, or stress-related factors that can exacerbate IBS symptoms.
98
What is diverticular disease?
It is characterized by the presence of dilations in the mucosa that form a type of balloon-shaped sac, the diverticula.
99
Distinguish diverticulosis and diverticulitis.
The presence of diverticula is called diverticulosis. When inflammation of the diverticula occurs, it is a condition called diverticulitis.
100
What are the main risk factors of diverticular disease?
* Sedentary lifestyle
* Smoking habits
* Eating habits (high-calorie meals, meals rich in wheat, dairy products, chocolate, coffee, spicy foods, etc)
101
What is the probable cause of diverticulosis?
The exact cause of diverticulosis is still uncertain (idiopathic). However, it may be linked to **muscle layer spasms**. Some studies indicate that the origin of diverticula may be related to spasms in the muscular layer of the intestine, since the inner layer of the wall is pushed through weak spots in the muscular wall, leading to the formation of diverticula.
102
What is the probable cause of diverticulitis?
The causes behind diverticulitis are still unknown, but it is thought that it may be related to **mechanical forces**, such as increased pressure in the colon or the closing of the diverticulum opening by feces, which can lead to its infection and inflammation. Diverticulitis is also considered in light of the **existence of small holes in the wall of the diverticulum** that allow the entry of microbial agents that trigger an inflammatory process.
103
What are the clinical manifestations of diverticulosis?
Diverticulosis is usually **asymptomatic** but is sometimes associated with:
* abdominal discomfort/pain (in the lower left quadrant) that is relieved by defecation
* diarrhea
* cramping
* changes in bowel habits
* occasionally rectal bleeding
104
What are the clinical manifestations of diverticulitis?
* Abdominal pain/tenderness
* Fever and chills
* Change in bowel habits
* Nausea and vomiting
105
What are the main complications of diverticular disease?
* Bowel obstruction
* Intestinal stenosis and necrosis
* Fistulas
* Abscesses
* Peritonitis
* Inflammation of adjacent organs
* Intestinal bleeding
106
What are the main diagnostic methods for diverticular disease and what are the most common findings in each one?
* **Physical examination and anamnesis**: atients may present with left lower quadrant abdominal pain, tenderness, bloating, and possible signs of mild fever in diverticulitis.
* **Biochemical blood tests**: may show elevated white blood cell count (leukocytosis) and increased C-reactive protein (CRP) in cases of inflammation or infection (diverticulitis), but are usually normal in diverticulosis.
* **Colonoscopy**: visible diverticula (small pouches in the intestinal wall), but colonoscopy is generally avoided during acute diverticulitis due to the risk of perforation.
* **Computed tomography (CT) or Magnetic Resonance Imaging (MRI)**: CT scan is the gold standard in acute cases, showing inflamed or thickened bowel walls, diverticula, abscesses, or signs of perforation. MRI can also detect inflammation but is used less frequently.
