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Unit 10 PBL cases > Crohn's disease > Flashcards

Crohn's disease Flashcards

1
Q

What factors can cause IBD?

A

Genetic - issues with antimicrobial peptides, autophagy (removing damaged cell parts), cytokines, response to bacteria
Environmental - diet, infections, microenvironment, stress, NSAIDs, smoking, antibiotics use

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2
Q

What maintains the gut wall barrier?

A

Commensal bacteria
Paneth cells - secrete antimicrobial peptides
Goblet cells - secrete mucous
M cells - in Peyer’s patches, transport pathogens and antigens to macrophages

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3
Q

What is the pathophysiology of Crohn’s?

A

Translocation of microbial products through M cells, or through the barrier due to impaired function - which activates immune cells
Macrophages phagocytose the bacteria and present the antigens to CD4 T cells
Macrophages and CD4 t cells release cytokines: TNF-A, IL-1, IL-6
Continuously released > chronic inflammation
TNF-A stimulates angiogenesis, induces paneth cell necrosis - antimicrobial cells destroyed, IEC death - impaired barrier function, increases immune response - further damage

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4
Q

What occurs in lactose intolerant patients?

A

Lactase enzymes not expressed, lactose does not break down, continues through to colon
Gut flora ferment lactose into H2, CO2 and CH3 gases and short chain fatty acids which aren’t absorbed
Unabsorbed lactose and fatty acids increase osmotic pressure -> influx of water -> diarrhoea

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5
Q

What tests can be used to detect lactose intolerance?

A

Hydrogen breath test: drink lactose drink, hydrogen in breath measured at regular intervals. Breathing out excessive H2 shows lactose isnt being absorbed
Lactose tolerance test: 2hrs after lactose drink, bloods taken to measure glucose levels. If levels havent risen, shows lactose isnt being absorbed > broken down into glucose and galactose

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6
Q

How is lactose normally processed in the body?

A

Lactase breaks down lactose into glucose and galactose
Lactase enzyme expressed in enterocytes in SI
Glucose and galactose then absorbed into epithelium, and into bloodstream via SGLT2 and GLUT2 co-transporters

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7
Q

How may IBD affect absorption?

A

Inflammation and damage to intestinal lining can disrupt SGLT1 and GLUT2 and other transporter function -> impaired glucose absorption

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8
Q

How are lipids absorbed into the gut?

A

Monoglycerides and fatty acids combine with bile salts -> micelles
Water soluble and diffuse to brush border and absorbed by endocytosis
Lipids combine with fatty acids, reassembled into triglycerides on SER
Packaged into chylomicrons in golgi apparatus, enter lymphatic system, then bloodstream

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9
Q

How are amino acids absorbed into the gut?

A

Via specific amino acid transporters across apical membrane
Di and tri peptides absorbed via H+ dependent cotransporters
Form complete proteins before moving into bloodstream by facilitated diffusion

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10
Q

How is fructose absorbed in the gut?

A

Fructose is transported across apical membrane into cell via GLUT5 receptor
Transported into interstitial space across basolateral membrane via GLUT2 receptor

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11
Q

How are glucose and galactose absorbed in the gut?

A

Glucose and galactose transported with sodium across apical membrane through the sodium/glucose cotransporter (SGLT1) - two Na2+ for one monosaccharide
Glucose and galactose enter interstitial space via GLUT2 receptor across basolateral membrane

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12
Q

What are the diagnostic tests for Crohn’s disease?

A

Colonoscopy
Biopsy
Blood tests: FBC, serology test, ferritin/transferrin, U&E
Hydrogen breath test
Barium swallow
Stool test

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13
Q

What is shown in the barium swallow for diagnosis of Crohn’s?

A

Cobblestone appearance on the x-ray due to fissures and ulceration in the intestine
String sign of Kantor - stricturing of the intestine and ‘creeping fat’ pushing intestine away

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14
Q

What is tested in a stool test to diagnose Crohn’s disease?

A

Calprotectin is a calcium and zinc-binding protein found in neutrophils
Prescence of calprotectin in faeces is a result of neutrophil migration into the GI tissue due to the inflammatory process
Faecal calprotectin levels correlate with inflammation, so used as a biomarker

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15
Q

What is analysed in a blood test to test for Crohn’s? 5

A

Can’t directly diagnose IBD, but looks for inflammation in the body looks at:
Serum FBC: Higher WBC count / higher platelet count
Serology test (serum inflammatory markers): antibodies, autoantibodies and microbial antigens, high CRP and ESR.
Ferritin and transferrin (anaemia), vitB12, folate, vit D levels - nutritional deficiencies
U&Es - signs of dehydration: high sodium, low potassium
Serum LFTs: low albumin

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16
Q

How can a hydrogen breath test be used to identify Crohn’s?

A

Hydrogen breath test can identify or rule out lactose intolerance

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17
Q

What is the prevalence and incidence of Crohn’s disease?

A

Prevalence: 145 in 100,000
Two age peaks - 20-30 yrs and 50 yrs
Incidence: 3-20 per 100,000

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18
Q

What are the risk factors for Crohn’s disease?

A

Family history: 20% have affected family member
Age: majority diagnosed before 30
Smoking: increases risk by x3, mor aggressive disease
Medications: NSAIDs - cause bowel inflammation
Other medications: upper resp tract infections, enteric infections

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19
Q

What is the difference between IBS and IBD?

A

IBD= structural (can be observed in scans, examinations) can be positively diagnosed
IBS= functional (affects function, cannot be observed visually) diagnosed by exclusion

20
Q

What are the differences between UC and Crohn’s?

A

UC is limited to large intestine, Crohn’s can be anywhere in the GI tract
UC inflammation only involves mucosa, Crohn’s inflammation extends through all layers of the gut wall
UC has continuous inflammation, Crohn’s has discontinuous inflammation
Crohn’s shows longitudinal ulcers, cobblestone mucosa

21
Q

What would be the endoscopy findings for ulcerative colitis?

A

Edematous mucosa - fluid accumulation
Erythema - redness
Loss of vascular markings
Mucosal friability (easily damaged by touch)

22
Q

What are the non-GI symptoms of ulcerative colitis?

A

Mouth ulcers
Shortness of breath
Irregular heart rate
Finger clubbing
Uveitis
Arthritis

23
Q

What are the symptoms of ulcerative colitis?

A

Bloody diarrhoea > 6 weeks
Rectal bleeding
Faecal urgency
Nocturnal defecation
Tenesmus - feel need to defecate, but can’t
Abdominal pain
Weight loss
Fatigue

24
Q

What is ulcerative colitis?

A

Chronic, relapsing, remitting, non-infectious inflammatory GI tract disease
Inflammation limited to mucosa
Usually effects rectum and extends proximally continuously

25
Q

What are the types of Crohn’s?

A

Gastroduodenal
Small bowel
Terminal ileal and ileocaecal
Colonic
Perianal

26
Q

What may the endoscopy find in Crohn’s?

A

Longitudinal aphthous ulcers
Cobblestone mucosa
Patchy inflammation
Strictures - due to lesions or acute inflammation

27
Q

What are the potential complications of Crohn’s disease?

A

History of UTIs
Passing gas or faces through vagina or urine due to fistula to vagina or bladder
Perianal discharge of mucus or pus due to fistula to perianal skin
Partial bowel obstruction due to intestinal stricture

28
Q

What may be observed in examination on a patient with Crohn’s?

A

Abdominal mass
Finger clubbing
Pallor
Perianal skin tags, fissures, fistulas or abcesses
Signs of malnutrition or malabsorption
Abnormalities to the skin, joints or eyes

29
Q

What are the symptoms of Crohn’s disease?

A

Recurring diarhhoea, abdominal pain, extreme tiredness, unintended weight loss, blood/mucus in stool
If symptoms are experienced for 4-6 weeks, Crohn’s should be suspected

30
Q

What are the potnetial causes of Crohn’s?

A

Genetics, environment, immunological factors
Patients usually have fewer varieties of gut flora

31
Q

What is Crohn’s disease?

A

Chronic, relapsing-remitting, non-infectious, discontinuous inflammatory disease of the GI
Inflammation extends through all the layers of the gut wall
Inflammation can occur anywhere within the GI tract from the mouth to the anus
Discontinuous so usually occurs in patches

32
Q

What are the two conditions within IBD?

A

Ulcerative colitis and Crohn’s disease

33
Q

What are the non GI symptoms of IBS?

A

Mouth ulcers - angular chelitis
Eye problems:
- episcleritis - no pain inflammation of sclera
- scleritis - painful inflammation of sclera
- uveitis - inflammation of uvea
- dry eye disease

34
Q

What are the GI symptoms of IBS? (11)

A

Stomach cramps, bloating, diarrhoea/constipation, excessive wind, occasional urgency to move bowels, passing mucus out of anus, fatigue, nausea, blood in stool, reduced appetite, right iliac fossa mass

35
Q

What are the different classifications of IBS?

A

Determined by the predominant stool type:
IBS-D: diarrhoea
IBS-C: constipation
IBS-M: mixed
IBS-U: unclassified

36
Q

What are the histological features of a gut biopsy from a patient with UC?

A
  • Crypt abscesses: inflammation of mucosa with accumulation of neutrophils in the lamina propria and colonic crypts
  • Paneth cell metaplasia: protect damaged colonic epithelium against bacterial invasion
  • Inflammatory pseudopolyps: in non ulcerated areas, can project above ulcerated areas
  • Lymphocyte infiltration: lymphocytes, plasma cells and eosinophils infiltrate the lamina propria
37
Q

What are the histological features of a gut biopsy from a patient with Crohn’s?

A
  • Skip lesions: patches of inflammation
  • Transmural inflammation: affects all layers
  • Non-caseating granulomas: contains giant cells formed by fusion of macrophages, lymphocytes and macrophages/monocytes
38
Q

What are the different treatments of Crohn’s?

A

Medications:
- Anti-inflammatory drugs (control inflam)
- Corticosteroids (treat moderate-severe inflam, treat acute flare ups)
- Immunosuppressants
- Antibiotics (treat infections that can occur during Crohns, exacerbating inflam)
Surgery

39
Q

What are the different drugs that may be used to treat Crohns?

A

Anti-inflam: mesalamine, balsalazide, olsalazine, sulfalazine
Corticosteroids: prednisolone, prednisone
Immunosuppressants: adalimumab, infliximab, JAK inhibitors, methotraxate, cyclosporine

40
Q

Prednisolone - pharma and physiol

A

Bind to glucocorticoid receptor, mediating changes to gene expression causing many downstream effects
Inhibit neutrophil apoptosis
Inhibit phospholipase A2, which inhibits formation of arachidonic derivatives like PGs, reducing inflammation
Inhibit inflammatory TF, upregulate anti-inflammatory genes

41
Q

Prednisolone - clinical uses and side effects

A

Uses: many including IBD, asthma, arthritis
Side effects: weight loss, insomnia, osteoporosis, mood changes, increased risk of infection

42
Q

Ferrous sulphate - pharma and physiol

A

Iron supplement
Enters macrophage via DMT1 channel
Incorporated into ferritin and stored within macrophage
Ferroportin transports iron out of the macrophage to be oxidised to Fe3+
Transferrin carries Fe3+ to many different sites

43
Q

Ferrous sulphate - clinical

A

Treats iron deficiency anaemia e.g. from IBD malabsorption
Side effects: black tarry stools, vomiting

44
Q

What are potential surgical options to treat Crohn’s?

A

Small bowel resection: removal of affected SI and reconnecting healthy parts
Subtotal colectomy (L bowel resection): removal of affected LI and reconnect healthy parts
Strictureplasty: widening of section of colon
Colectomy: removal of entire colon, SI connected to rectum
Ileostomy/colostomy: ileum attached to external opening, waste is collected in a pouch

45
Q

What MDT members are involved in the care of a Crohns patient?

A

-Consultant gastroenterologist
- Dietician
- Clinical nurse specialist
- Pharmacist
- GP
- Colorectal surgeon
- Psychologist
- Histopathologist
- Administrator
- Radiologist

46
Q

What are the impacts of having Crohn’s?

A

Learn to be selective about food
Flare ups can leave people unable to move
Constantly trying to mitigate stress
Worried families
Constantly constricting diet
Needing to know where the nearest toilet is
Impact of several surgeries and consequences of treatment

Unit 10 PBL cases (6 decks)

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