10.3 - Pathological Conditions of the ______

Question 1

Types of Ulcerative Colitis

Answer 1

1) Ulcerative Proctitis
- Involves only the rectum
- Milder symptoms (i.e., rectal bleeding & urgency)

2) Proctosigmoiditis
- Involves the rectum & sigmoid colon
- More pronounced symptoms (i.e., cramping & bloody diarrhea)

3) Left-sided Colitis (Distal Colitis)
- Affects the rectum, sigmoid, & descending colon
- Symptoms = L abdominal pain, diarrhea, & significant bleeding

4) Pancolitis
- Throughout entire colon
- Associated with severe symptoms, higher complication rates, & ↑ colon cancer risk

Question 2

Cause of Ulcerative Colitis

Answer 2

Cause
- immune cells attack mucosal lining and cause inflammation
- genetic component: increased risk with first degree relatives

Question 3

Pathophysiology

Answer 3

• mucosal immune dysregulation

1) Autoimmune Activation
- abnormal immune response triggered by the gut microbiome = mucosal inflammation

2) Continous inflammation
- unlike crohns, UC involves continuous lesions

Question 4

Structural Changes of Ulcerative Colitis

Answer 4

• inflammation only attacks mucosal layers

1) Mucosal Ulcerations
- Inflammation = erosions & ulcers in mucosa = bleeding = bloody diarrhea

2) Loss of Goblet Cells
Chronic inflammation = ↓ in mucin-producing goblet cells = compromised protective mucus layer

3) Pseudopolyps
- Mucosa heals in patches = irregular areas of regenerating tissue = pseudopolyps formation =malignant potential

4) Crypt Abscesses and Distortion
- Immune cells (e.g., neutrophils) invade intestinal glands or crypts = disrupting normal architecture = crypt distortion & abscesses

5) Mucosal Atrophy and Fibrosis
- Structural atrophy
- Fibrosis
- Mild because inflammation is confined to mucosa and does not penetrate to deep layers (like in crohns)

Question 5

Clinical Significance of Ulcerative Colitis

Answer 5

S&S
- Chronic diarrhea
abdominal pain
- rectal bleeding
- tenesmus (a feeling of incomplete evacuation)
weight loss
- anemia, & dehydration

Disease Fluctuations
- Relapsing-remitting disease = periods of active inflammation & symptoms followed by remission

Risk of Colon Cancer
- Pancolitis & long-standing UC ↑ colorectal cancer risk
- Surveillance colonoscopy to monitor for dysplasia & early cancer detection

Question 6

What is Crohns Disease?

Answer 6

• Inflammatory bowel disease that is characterized by patchy inflammation that can affectc any part of the GIU tract from mouth to anus
• Crohn’s disease is marked by transmural inflammation - can penetrate all layers of the GI wall
  ○ Can lead to severe complications like fistulas, strictures, and abscesses

Question 7

Causes of Crohns Disease

Answer 7

1) Genetic Predisposition
- Strong hereditary component (genetic mutations in NOD2/CARD15 gene)
- NOD2/CARD15 gene play a role in immune response

2) Immune System Dysregulation
- Immune system attacks harmless bacteria in the GI tract = tissue damage = chronic inflammation
- Immune dysregulation is mediated by T cells and release of inflammatory cytokines

3) Environmental Triggers
- Smoking, diet, stress, & infections

Question 8

Pathophysiology of Crohns Disease

Answer 8

1) Immune Activation
- Immune system attacks normal gut microbiota = T-helper cells release pro-inflammatory cytokines (TNF-α, IL-12, IL-23) = inflammation = macrophage & neutrophil recruitment = tissue damage

2) Transmural Inflammation
- Inflammation extends all layers of bowel wall = fistulas, abscesses, and strictures

3) Patchy or Skip Lesions
- Discontinuous areas of inflamed tissue interspersed with healthy tissue
- mostly located = terminal ileum & proximal colon (can occur anywhere in tract)

Question 9

Distinguishing feature bw Crohns and Colitis

Answer 9

Crohns
- transmural inflammation; can extend though all walls of bowel

Colitis
- mucosal limited inflammation

Question 10

Types of Crohns Disease

Answer 10

1) Ileocolitis
- Most common
- Location = ileum & colon
- Symptoms = diarrhea, cramping, & weight loss

2) Ileitis
- Location = ileum
- Symptoms = diarrhea, cramping, weight loss, & nutrient malabsorption (i.e., vitamin B12)

3) Gastroduodenal Crohn’s
- Location = stomach & duodenum
- Symptoms = nausea, vomiting, & upper abdominal pain

4) Jejunoileitis
- Location = jejunum (patchy areas of inflammation)
- Symptoms = malnutrition & severe abdominal pain after meals (bc of increased peristalsis that occurs after eating in inflamed jejunum)

5) Crohn’s Colitis
- Location = colon
- Symptoms = bloody diarrhea & rectal bleeding

Question 11

Structural Changes of Crohns Disease

Answer 11

1) Mucosal Ulcers and Cobblestoning
- Deep ulcers in the mucosa =- “cobblestone” appearance of intestinal lining
- Ulcers can be longitudinal or serpiginous = fissures extend into deeper layers of bowel

2) Granuloma Formation
- Formation of non-caseating granulomas [clusters of immune cells (macrophages, T-cells)]
- form in response to persistent inflammation

3) Fistulas and Abscesses
- Fistulas = abnormal connections between segments of intestine OR between intestine & other organs (bladder, skin, or vagina)
- fistula creates the risk of developing abscesses
- Abscesses = collections of pus, forms around fistulas  infection requiring surgical intervention

4) Strictures and Obstructions
- Chronic inflammation = scar tissue & fibrosis (thickens walls) = strictures (narrowed segment of intestine) = obstruction of bolus = cramping, vomiting, & potential bowel obstruction

5) Fat Wrapping
- Mesenteric fat encircles inflamed intestine = “creeping fat”
- contributes to ongoing inflammation

Question 12

Clinical Significance of Crohns Disease

Answer 12

S&S
- Chronic diarrhea
- abdominal pain
- fatigue
- weight loss
- malnutrition
- Malabsorption (small intestine involvement) = nutrient deficiencies (e.g., vitamin B12, iron, folate)

Chronic and Relapsing Course
- Relapsing-remitting pattern = periods of remission & active disease (flare-ups)

Risk of Complications
1) Intestinal Complications
- Fistulas, abscesses, strictures, & perforation (disruption of walls_
- perforation is a concern bc non-sterile content from intestines enters abdominal cavity

2) ↑ Colon Cancer Risk

Extraintestinal Manifestations
- bc it is immune related, body has immune issues in other places
- Arthritis
- uveitis (eye inflammation)
- erythema nodosum (skin inflammation)
- pyoderma gangrenosum (ulcerative skin lesions)
- liver disorders (e.g., primary sclerosing cholangitis)

Psychosocial and Quality of Life Impact
- Impact on daily functioning
- diet
- social interactions can lead to emotional distress, anxiety, & depression

Treatment Implications
- Immunosuppressive therapy, biologics (e.g., anti-TNF agents)
- surgery (severe cases)
(try not to do surgery bc healing process is not normal; leads to delayed healing)

Question 13

Cause of Diverticulitis

Answer 13

Diverticulitis: Inflammation of diverticula; small pouches that can form in the GI tract (esp colon)

Cause
- Esp the result of diverticulosis - condition where diveritucla form in walls of intestine (sigmoid colon)
- Common in older adults
- Due to age-related weakening of intestinal wall

• Low-fiber diet (leads to harder stools and increased colonic pressure) , chronic constipation (increases pressure in colon), age, genetics, lifestyle factors (i.e., smoking, obesity, & low physical activity)

Question 14

Pathophysiology of Diverticulitis

Answer 14

• inflammation is caused by blocked diverticular or infection usually by fecal matter and undigested food particles
• Fecal material trapped in diverticula = creates microenvironment prone to bacterial growth = bacteria proliferate = localized infection & inflammation = cytokine release = ++ inflammation

Risk of Complications
1) Rupture = peritonitis
2) Abscesses formation around diverticula

Question 15

Types of Diverticulitis

Answer 15

Types (severity)
1) Uncomplicated Diverticulitis
- Localized inflammation without complications

2) Complicated Diverticulitis
- Abscess formation, perforation, peritonitis, fistula formation, or obstruction

Question 16

Structural Changes of Diverticulitis

Answer 16

Microscopic Changes
- Mucosal Damage
- Inflammatory Infiltration (i.e., neutrophils & macrophages)
- Fibrosis  narrowing the lumen = obstruction risk

Macroscopic Changes
1) Diverticula Formation
- Sac-like pouches protruding through weak points in the colon wall (found in clusters)

2) Inflamed Diverticula
- Swelling, redness = signs of infection

3) Abscesses or Perforation
- perforation can allow bowel content to enter abdominal cavity

4) Fistula Formation
- Connections between the colon & other structures, such as the bladder (colovesical fistula) or the vagina (colovaginal fistula)

Question 17

Clinical Significance of Diverticulitis

Answer 17

Symptoms of Uncomplicated
Diverticulitis
- Lower abdominal pain (LLQ pain due to diverticula in sigmoid colon)
- fever and malaise (from localized infxn)
- changes in bowel Habits (i.e., constipation or diarrhea)
- nausea and vomiting (due to irritation in GI tract)

Complications of Complicated Diverticulitis
1) Abscess Formation
- Collection of pus due to localized infection
- may require drainage & antibiotics

2) Peritonitis
- Perforation = bacteria & fecal contents enter peritoneal cavity = inflammation of the peritoneum (pertonitis)

3) Fistula Formation
- abnormal connections between colon & nearby structures = recurrent UTIs (colovesical fistulas)

4) Bowel Obstruction
- Fibrosis & narrowing = colon obstruction
- requires surgical intervention

Long-Term Management
- experience recurrent episodes
- Surgical removal of affected colon segment (sigmoid)
- Dietary changes (↑ fiber intake)
- Lifestyle modifications (weight management & smoking cessation)

Question 18

What is Intestinal Obstruction

Answer 18

• Passage of intestinal contents is partially or completely blocked

1) Mechanical - physical blockage
2) Mon-Mechanical - intestinal muscles can not contract

Question 19

Mechanical Causes of Intestinal Obstruction

Answer 19

Mechanical Obstruction = Physical blockage

1) Adhesions
- Bands of fibrous tissue form between intestinal loops after surgery or inflammation
- Most common cause of small bowel obstruction

2) Hernias (inguinal, femoral, or incisional)
- Abdominal contents protrude through weakened muscle walls = trapping section of intestine

3) Tumors
- Cancerous or benign masses
- Most common in large intestine

4) Intussusception
- Portion of the intestine telescopes into an adjacent section
- Most common in children
- common after surgical repair

5) Volvulus
- Twisting of intestine around itself = cutting off blood supply and causing obstruction
- More frequent in sigmoid colon or cecum

Question 20

Non-Mechnical Causes of Intestinal Obstruction

Answer 20

Functional (Non-Mechanical)
- Obstruction = paralytic ileus  intestinal muscles cannot effectively contract

1) Postoperative Ileus
- ileus common after surgery

2) Surgical Trauma and Inflammation, Autonomic Nervous System Disruption & Medications

a) Common after abdominal surgery from surgical trauma
- abdominal surgeries trigger inflammatory response, affecting bowels nerves and smooth muscle
- surgical handling activates immune cells which impair normal contraction (disrupts peristalsis)

b) Autonomic Nervous System Disruption
- surgery activates SNS and reduced PSNS tone
- PSNS stimulation is required for normal peristalsis (reduced PSNS slows digestion)

c) Medications
- opiods reduce peristalsis by inhibiting release of ACH needed for smooth muscle contraction (why they cause constipation)
- ACH is primary NT for GI contraction
- general anesthetics depress CNS

3) Infection or Inflammation
- Peritonitis or pancreatitis (inhibits intestinal motility)
- appendicitis can also inhibit smooth muscle by disrupting the enteric nervous system and altering neurohormonal balance of the gut

4) Neuromuscular Disorders
- Hirschsprung’s disease: lead to absent nerve cells in the colon
- chronic high blood glucose levels can damage persons nerves that innervate intestines which can reduce peristalsis
- Multiple Sclerosis .(demyelination of axons)
- can affect any part of NS (autonomic NS of GI tract)
- due to autonomic dysregulation; patients experience constipation and reduced motility

Question 21

Pathophysiology of Intestinal Obstruction

Answer 21

1) Fluid and Gas Accumulation
- Gasses & fluids to accumulate proximal to site of obstruction
- Contents build up = intestine becomes distended = abdominal pain & bloating

2) ↑ Intraluminal Pressure
- ↑ pressure in intestinal lumen = blood vessel compression = ↓ blood flow to affected segment (ischemia) = tissue death (necrosis) = perforation

3) Bacterial Overgrowth and Translocation
- Stagnant intestinal contents foster bacterial proliferation = infection & bacterial translocation across bowel wall

4) Systemic Effects
- Loss of fluids into the intestinal lumen (third-spacing) & vomiting = electrolyte imbalances, dehydration, & shock

Question 22

Structural Changes of Intestinal Obstruction

Answer 22

1) Proximal Dilation
- Segment of intestine above obstruction dilates due to accumulation of fluids, gases, and ingesta

2) Bowel Wall Thickening
↑ pressure & inflammation = edema & thickening of bowel wall

3) Mucosal Damage
- Prolonged distention & ischemia  mucosa damage = ulceration & ↑ permeability = bacterial translocation

4) Necrosis and Perforation
Necrosis of the bowel wall = perforation (bc impaired tissue integrity) = bowel contents enters peritoneal cavity = peritonitis

5) Intussusception
- Telescoped (folded in) segment appears shortened & thickened

6) Volvulus
- Twisted and narrowed segment of intestine (“whirl” pattern on imaging)

Question 23

Types of Intestinal Obstruction

Answer 23

1) Partial vs. Complete Obstruction
- Partial Obstruction = Some intestinal contents can pass, intermittent symptoms (allows for conservative management)

• Complete Obstruction = Complete blockage, severe symptoms, surgical intervention

2) Simple vs. Strangulated Obstruction
- Simple Obstruction = Blood flow intact, no ischemia, less severe symptoms

• Strangulated Obstruction = Impaired blood supply to affected section, ischemia, necrosis, high perforation risk, surgical emergency

3) Small vs. Large Bowel Obstruction
- Small Bowel Obstruction = Associated with adhesions, hernias, or volvulus; symptoms of early-onset emesis (vomiting) & electrolyte imbalance

• Large Bowel Obstruction = Associated with tumors or volvulus in older adults, symptoms of late-onset vomiting & progressive abdominal distention

Question 24

Clinical Significance of Intestinal Obstruction

Answer 24

Signs and Symptoms
1) Abdominal Pain
- Cramping & colicky pain that corresponds to peristalsis
- Pain in strangulated obstruction is more constant & severe

2) Vomiting
- Common in small bowel obstruction = leads to electrolyte disturbances
- Vomiting may be fecal matter (reverse peristalsis to prevent this)

3) Constipation and Obstipation
- Absence of flatus & stool suggests a complete obstruction
- why nurses are happy when clients pass gas after surgery

4) Abdominal Distention
- More pronounced in large bowel obstructions due to gas & fluid accumulation

Complications
1) Ischemia and Necrosis
Strangulated obstructions: Ischemia = necrosis = perforation = peritonitis

2) Sepsis and Shock
- Bacterial translocation & necrosis = systemic infection & septic shock

3) Chronic Obstruction and Malnutrition
- Partial obstruction: prolonged malabsorption = weight loss & nutritional deficiencies

Management
- fluid and electrolyte replacement
- decompression of bowel
- surgery (severe, strangulated)

Question 25

Causes of Colorectal Cancer

Answer 25

• malignancy arising in large intestine, colon, or rectum

1) Genetic Factors
a) Familial Adenomatous Polyposis (FAP)
- APC gene mutation
- Numerous polyps in the colon = progresses to cancer if untreated

b) Hereditary Non-Polyposis Colorectal Cancer (HNPCC) or Lynch Syndrome
- Mutations in DNA mismatch repair (MMR) genes ↑ cancer risk by disrupting DNA repair = accumulation of genetic mutations

2) Environmental & Lifestyle Factors
- Diets high in red and processed meats, low fiber, sedentary lifestyles, smoking, & excessive alcohol intake = ↑ colon cancer risk

3) Inflammatory Bowel Disease (IBD)
- UC or CD = chronic inflammation & ↑ risk of colon cancer due to DNA damage & accelerated cell turnover

Question 26

Pathophysiology of Colorectal Cancer

Answer 26

• typically follows progression from benign polpys to invasive adenocaorncomoa through genetic mutations

1) Adenoma-Carcinoma Sequence
- Begins with formation of a small adenomatous polyp [mutations in APC gene, as additional mutations accumulate (KRAS & TP53 genes) = polyp grows larger & undergoes dysplasia = carcinoma

2) Microsatellite Instability (MSI)
- common in Lynch syndrome = mutations in DNA mismatch repair (MMR) genes = microsatellite instability = accelerated mutation rates = hallmark of a subset of colon cancers

3) CpG Island Methylator Phenotype (CIMP)
- Sporadic cases = hypermethylation of specific DNA regions = gene silencing = uncontrolled cell proliferation

Question 27

Structural Changes of Colorectal Cancer

Answer 27

1) Polyp Formation
- Benign adenomatous polyps develop in the mucosal lining
- Polyps can be tubular, villous, or tubulovillous
- Villous polyps carry the highest cancer risk

2) Dysplasia and Invasive Cancer
- Dysplastic changes within polyps = adenocarcinoma (cancerous cells invade mucosal, submucosal, & muscular layers of colon wall)

3) Metastasis
- Invasion of blood vessels & lymph nodes = METS to liver, lungs, & peritoneum (cells enter circulation through lymph or blood)
- Structural changes at metastatic sites reflect primary tumor’s histological pattern

Question 28

Types of Colorectal Cancer

Answer 28

1) Adenocarcinoma
- Most common (> 90% of cases)
- Originates in glandular cells
- Progresses from polyps, various subtypes

2) Mucinous Adenocarcinoma
- Mucus-producing cancer cells
- associated with poor prognosis & high METS

3) Signet Ring Cell Carcinoma
- Rare & highly aggressive
- Cells with prominent intracellular mucin
- Presents at an advanced stage

4) Small Cell Carcinoma
- Rare & highly aggressive
- Neuroendocrine cancer
- Distinct treatment approach

Question 29

Clinical Significance of Colorectal Cancer

Answer 29

S&S
- Changes in bowel habits (diarrhea or constipation)
- rectal bleeding
- unexplained weight loss
- abdominal pain
- anemia
- Right-sided tumors (ascending colon) present with anemia & weight loss
-ascending colon has large lumen (does not cause obstruction unless very large, instead bleed overtime)
- Left-sided tumors (descending and sigmoid colon) cause obstructive symptoms

Staging
Colon cancer staging uses the TNM (Tumor, Node, Metastasis)
- Stage I: Limited to colon wall
- Stage II: Extends beyond muscular layer, no lymph node involvement
- Stage III: Involves regional lymph nodes
- Stage IV: Distant metastasis (e.g., liver or lungs bc highly vasculated)

Diagnosis
- Colonoscopy with biopsy
- resection surgery (removal of bowel)

Question 30

Causes of Hernias (Inguinal and Abdominal)

Answer 30

• occurs when organ tissue protrudes through weak spot in surrounding muscle or tissue

Causes
- Increased intra-abdominal pressure (e.g., coughing, constipation
- heavy lifting, or obesity) weakness in the abdominal wall [congenital or acquired (e.g., surgical scars or aging)],

Risk Factors
- family history/genetics
- Increasing age
- male gender (anatomy of inguinal canal)
- smoking (impairs tissue repair & collagen synthesis = weakens connective tissue)
- previous surgery or injury (scar tissue)

Question 31

Pathophysiology of Hernias

Answer 31

• develop due to imbalance bw increased intra-abdominal pressure and resistance of the abdominal wall structure resulting from:
• Weak connective tissue (genetic or acquired)
• Failure of embryologic closure (e.g., incomplete closure of processus vaginalis in inguinal region)
• Chronic straining or trauma (weakens abdominal muscles or fascia)
• Inguinal hernias occur through the inguinal canal, which has structures such as the spermatic cord (males) or round ligament (females), can be
  - Indirect = congenital
  - Direct = acquired

Question 32

Structural Changes of Hernias

Answer 32

1) Protrusion of viscera
Small intestine, omentum, or bladder

2) Weakness of muscle and fascial layers
- Sites of weakness (e.g., inguinal canal, umbilicus, or surgical scars)

3) Hernial sac
- Peritoneum & may contain bowel or other abdominal contents (meaning more severe bc has abdominal contents)

4) Inguinal hernias
-a) Indirect inguinal hernia
- Protrudes through deep inguinal ring, follows path of inguinal canal, reaching scrotum (males)

b) Direct inguinal hernia
- Protrudes directly through posterior wall of inguinal canal due to weakness in transversalis fascia

5) Abdominal hernias
a) Umbilical hernia
- Protrudes through umbilical ring

b) Incisional hernia
- Protrudes via site of previous abdominal surgery

c) Femoral hernia
- Protrudes through femoral canal (women more common)

Question 33

Clinical Significance of Hernias

Answer 33

S&S
- Visible or palpable bulge [worse with standing, coughing, or straining (↑ intra-abdominal pressure)]
- reducible hernia (reduce spontaneously) - happens when intrabdominal pressure goes back to normal
- pain or discomfort
- nausea or vomiting (obstructed hernia)
- localized edema

Complications
1) Incarceration
- Hernia contents become trapped = unable to return to abdominal cavity
- Symptoms: Pain, swelling, nausea

2) Strangulation
- Compromised blood supply to herniated tissue = ischemia & necrosis
- Symptoms: Severe pain, redness, fever, signs of sepsis

Surgical emergency
1) Bowel obstruction
- Larger hernias
- Symptoms: Abdominal distension, constipation, vomiting

Management
- surgical repair
- mesh implant to reinforce abdominal wall
- if mild hernia, you can wait for complications

Question 34

Cause of Anal Fissure

Answer 34

• small tear or ulcer in lining of anal canal
• occurs at posterior midline

Causes
1) Trauma during defecation (hard stools or chronic constipation)

2) Prolonged diarrhea or repeated straining

3) Inflammatory conditions (e.g., Crohn’s disease), childbirth, or anal infections

Question 35

Pathophysiology of Anal Fissure

Answer 35

• ↑ anal sphincter tone causes spasm = ↓ blood flow to tear & slowed healing
• Repeated trauma leads = chronic fissures, fibrosis, and hypertrophy of surrounding tissues

Question 36

Structural Changes of Anal Fissure

Answer 36

Acute fissure = Clean tear in mucosa

Chronic fissure = Thickened edges, presence of a sentinel skin tag, & hypertrophic anal papillae.

Question 37

Clinical Significance of Anal Fissure

Answer 37

S&S
- Pain during & after defecation (sharp, burning)
- bleeding (bright red on stool or tissue)
- anal spasm
- Chronic fissures = surgical intervention (e.g., lateral internal sphincterotomy)

Question 38

Cause of Anal Fistula

Answer 38

• abnormal epithelialized track connecting anal canal to perianal skin
• common for ppl with crohns

Cause
1) Abscess from infected anal glands (cryptoglandular theory)

2) Associated with Crohn’s disease, tuberculosis, trauma, or malignancy

Question 39

Pathophysiology of Anal Fistula

Answer 39

• Infected anal glands develop into an abscess = drains into perianal skin = fistula tract formation
• Chronic inflammation perpetuates cycle of infection & drainage

Question 40

Structural Changes of Anal Fistula

Answer 40

• Tract lined with granulation tissue & epithelium
• Surrounding tissues may show fibrosis & chronic inflammation

Question 41

Clinical Significance of Anal Fistula

Answer 41

S&S
- Persistent drainage of pus or stool from fistula opening
- pruritus (itchiness)
- discomfort, & pain

Complications
- Risk of abscess recurrence, fecal incontinence (sphincter muscles involvement), & impaired wound healing (common in crohns who have challenges in healing)

• Surgical correction (fistulotomy or seton placement)

Question 42

Cause of Hemorrhoids

Answer 42

• swollen, inflammed veins in anal canal (internal or external)
• ↑ venous pressure due to straining during defecation, constipation, prolonged sitting, pregnancy, obesity, or portal hypertension

Question 43

Pathophysiology of Hemorrhoids

Answer 43

• Chronic pressure = dilation of vascular cushions in anal canal
• Internal hemorrhoids arise from superior rectal vein
• External hemorrhoids arise from inferior rectal vein
• Prolonged pressure weakens connective tissues = prolapse

Question 44

Structural Changes of Hemorrhoids

Answer 44

Internal hemorrhoids
- Occur above dentate line
- Covered by mucosa

External hemorrhoids
- Occur below the dentate line
- Covered by skin
- Prolonged inflammation = thrombosis or fibrosis

Question 45

Clinical Significance of Hemorrhoids

Answer 45

S&S
- Internal: Painless rectal bleeding
- External: pain and swelling
- pruritus
- prolapse

Complications
- Thrombosis (causing severe pain)
- anemia (chronic bleeding)
- strangulation (prolapsed)

Question 46

Celiac Disease

Answer 46

Autoimmune disorder triggered by ingestion of gluten

Cause
- HLA DQ2 or HLA DQ8 (not everyone with this marker has it, but u need this marker to have it)
- ingestion of gluten: triggered immune system to attack itself

Patho
1) T cell Activation
- modified gluten peptides = produce inflammatory cytokines = intestinal damage
2) B cells generate antibodies
3) Inflammation damages mucosa and causes villous atrophy (flattened villi)

Types
1) Classic - classic GI symptoms (diarrhea, pain, bloating)
2) Non-classis: subtle symptoms (anemia, fatigue)
- diagnosed later
3) Silent - no symptoms

S&S
- diarrhea, bloating, abdominal pain

Complications
- osteoparesis
- anemia

Question 47

Irritable Bowel Syndrome (IBS)

Answer 47

Cause
1) Gut microbiome Imbalance
- ↑ permeability = inflammation

2) Dysregulation of Gut-Brain Axis
- miscommunication between CNS and ENS

3) Fool intolerances

Patho
1) Visceral Hypersensitivity
- enhanced response to pain and distention
- overactive pain signalling and release of neurotransmitters

Changes
1) Gut microbiome imbalance
2) Mucosal permeability
- ↑ mucosal permeability = leaky gut = allows pathogens and allergens to activate the immune response = inflammation (low-grade)

S&S
- abdominal pain
- bloating and gas