gi for isces lorna roden. what we’re covering… 0 history and examination 0 3 cases –...

GI for ISCEsLorna Roden

What we’re covering…

0History and examination03 cases – differentials, investigations and

management0Common ‘lists’ of differentials

Mrs Gladys Brown is a 69-year-old retired lawyer. She has been referred to your outpatient clinic complaining of tiredness and loss of energy. She initially thought this was due to looking after her grandchildren twice a week, but since stopping this the symptoms have persisted. She describes loose bowel motions for the last few months and has lost 12.5kg in weight

What questions should you ask?0 Fatigue/ tiredness – duration of symptoms, relationship to work, preceding infection, intense exertion, stressful life

events

0 Loose stool – colour, consistency, odour

0 Presence of blood mixed in with or separate to stool0 Tenesmus (feeling of incomplete evacuation of stool)0 Weight loss – intentional or unintentional

0 Abdo pain/discomfort – SOCRATES

0 Bloating, distension and excessive passing of flatus – malabsorption

0 Heartburn and reflux – upper GI

0 Systemic features – recurrent mouth ulcers, arthritis, rash

0 Medications – recent changes

0 Recent travel abroad – Giardia causes chronic diarrhoea

0 Smoking – negative impact in Crohn’s disease but affords protection in UC

0 Alcohol – pancreatic insufficiency as a result of misuse

0 Diet - intolerance

0 HIV-risk – health-compromising behaviours

0 Family history – inflammatory bowel or colorectal cancer

Describe these dermatological signs

0Dermaitits herpetiformus – intensely itchy on the elbows/buttocks and associated with coeliac disease

0Errythema nodosum – tender, palpable, erythematous nodules on the shins associated with inflammatory bowel disease

History

Mrs Brown has been tired and lethargic for the last monthShe describes a 6 month history of watery loose stools, up to 3 times per day, associated with bloating and flatulence. There is no blood. She has had abdominal cramps intermittently for the last few years on most days.She has lost 12.5 kg in weight over 6 months unintentionally. She suffers from mouth ulcers every winter but not regularly. There have been no new rashes or additional symptoms.She takes aspirin, lisinopril and levothyroxine and beclometasone and salbutamol inhalers and is compliant with these.She is retired, drinks 2 units of alcohol per month and has never smoked.There is no recent travel history and no relevant family history.

Malabsorption and malnutrition

Iron deficiency

Angular stomatitis

Corneal Arcus

Ileostomy

Colostomy

Signs of chronic liver disease

0 Hepatomegaly0 Jaundice0 Ascites0 Circulatory changes – spider telangiectasia, palmar errythema0 Endocrine – loss of libido, hair loss, gyanecomastia, testicular

atrophy, impotence, irregular menses, ammenorrhoea0 Haemorrhagic tendency – bruises, purpura, epistaxis0 Portal hypertension – splenomegaly, colateral vessels, variceal

bleeding, fetor hepaticus0 Hepatic encepahlopathy0 Pigmentation, leukonychia

Causes of hepato-splenomegaly

Hepatomegaly Splenomegaly0 Parenchymal liver disease

0 Alcoholic liver disease0 Autoimmune hepatitis0 Viral hepatitis0 Primary biliary cirrhosis

0 Malignancy0 Primary HCC0 Secondary metastatic cancer

0 Right heart failure0 Haematological disorders

0 Lymphoma0 Leukaemia0 Myelofibrosis0 Polycythaemia

0 Rare0 Amyloidosis0 Budd-chiari syndrome

0 Haematological0 Lymphoma0 Leukaemia (CML)0 Myelofibrosis0 Polycythaemia0 Haemolytic anaemia

0 Portal hypertension0 Infections

0 Glandular fever0 Malaria0 Brucellosis0 Leishmaniasis0 Subacute bacterial endocarditis

0 Rheumatological0 RA (Felty’s Syndrome)0 SLE

0 Rare0 Sarcoidosis0 Amyloidosis

Examination

Examination reveals angular stomatitis and a few mouth ulcers. The abdominal examination was unremarkable with no palpable organomegaly or mass. The DRE was normal with good anal tone and no masses.

What is the differential diagnosis?

0Coeliac disease0Chronic pancreatitis and pancreatic insufficiency0Thyrotoxicosis0Colorectal cancer0 IBD0Microscopic colitis

Coeliac disease0 Immune-mediated disorder resulting in small intestinal villous

atrophy which resolves on gluten withdrawal from the diet0 Main toxic component of gluten is α-gliadin

0 Causes a T-cell mediated inflammatory response0 Anti-tissue tranglutaminase (anti-TTG) antibody, anti-gliadin antibody

0 Peaks in 3rd decade

Clinical features0 Children: abdominal pain, anaemia, short stature, delayed puberty0 Adults: abdominal bloating, lethargy, weakness, diarrhoea or

constipation, iron-deficiency anaemia, malabsorption, oral ulcers0 Associations

0 Dermatitis herpetiformus0 Small bowel lymphoma

Investigations?AIMS: Confirm diagnosis, look for consequences, supportive factors0 Confirm diagnosis

0 Duodenal biopsy - GOLD STANDARD – villous atrophy and crypt hyperplasia and intraepithelial lymphocytosis

0 IGA antibodies to tissue transglutaminase (TTG), endomysial and gliadin antigen – used to MONITOR treatment response

0 Consequences0 FBC0 Haematinics (low folate, B12, iron status)0 Clotting screen (Vit K)0 Bone investigation (low Ca2+, Vit D, albumin; osteopenia on DEXA scan)0 BMI

0 Supportive factors0 Liver enzymes (sometimes raised transamminases)0 Intestinal permeability (increased)0 Faecal fat (increased)

Management?

0Life-long gluten-free diet0Correct deficiencies0Aggressive management of any bone disease0 If patient remains refractory:

0 Check compliance with diet0 Consider additional diagnosis (giardiasis, lactase

deficiency)0 Consider complications (small intestinal bacterial

overgrowth, small intestine T-cell lymphoma)

CASE 3

Emma Ritchie is a 24 year old secretary. She has suffered with increased frequency of bowel opening, up to 5 times a day, abdominal pain and feeling generally unwell for the last 6 months.

Bowel habit?

0How has it changed?0What is ‘normal’ for you?0Nature of the stool?0Unusual contents of stool (watery, blood-stained,

mucous?0Colour change?0Odour change?0Urgency?

Poo!

Pale, oily, malodorous and difficult to flush

Watery and liquid; high frequency

Black, tarry and malodorous

Malabsorption of fat

Bacterial overgrowth or

microscopic colitis

Upper GI bleeding

Differentials?

0Crohn’s disease0Ulcerative colitis0Chronic parasitic infection i.e. giardiasis0 Irritable bowel syndrome0Coeliac disease0Chronic pancreatitis

Weight loss, anaemia and

sustained ill health can rule this out

Travel history

Alcohol history and family history

Differentials for chronic diarrhoea and malabsorption?

0Coeliac disease0Tropical sprue0Parasitic infections0 Immunodeficiency syndromes0Crohn’s disease0Whipple’s disease0 Irritable bowel syndrome0 Inflammatory bowel disease0Microscopic colitis

Inflammatory bowel diseaseUC Crohns

Area affected Colon only Mouth to anus

Distribution Continuous Skip lesions

Histologic features

Mucosa/submucosa, crypt abscesses, superficial ulcers

Transmural granulomas, apthoid ulcer

Macroscopic features

Mucosal friability, pseudopolyps, loss of haustra (chronic)

Cobblestoning, fistulas, fissures

Symptoms Rectal bleeding; Diarrhoea – often bloody, abdominal pain, weight loss

Abdominal pain, diarrhoea, fever, weight loss, fistulas

Presentation Diarrhoea + malaise Diarrhoea, malaise + abdominal pain

Extra-intestinal features of inflammatory bowel disease

0Most common: arthritis (10-35%)0Occur at roughly the same rates in Crohn’s and UC0These features are either related to disease activity or

not

What extra-intestinal features can you think of?

Arthritis is more common in Crohn’s than in UC

Extra-intestinal features related to disease activity

0 Pauci-articular arthritis• <5 joints• Asymmetric• Acute and self-limitting (weeks rather than months)

0 Errythema nodosum• Tender, red or violet subcutaneous nodules

0 Apthous ulcers• Painful, clearly defined round or ovoid, shallow ulcers of the smooth surfaces of the mouth

and underside of the tongue0 Episcleritis

• Red eye with injected sclera and conjunctiva, ± pain0 Metabolic bone disease

• Osteo –penia/-porosis/-malacia• Occurs in 30%

0 Thromboembolism and UC• Hospitalisation, malnutrition and immobilisation contribute• Platelets can also be high (acute phase reaction)

Extra-intestinal features not related to disease activity

0 Axial arthritis• Sacroiliac and spine• Pain in buttocks and back

0 Polyarticular arthritis• Symmetrical• Persistent• Damaging to affected joints

0 Pyoderma gangrenosum• Errythematous papules develop into deep ulcers containing sterile pus• Occurs on the shins most commonly• Sometimes where there has been previous trauma

0 Uveitis (irits)• Bilateral, insidious onset• Painful red eye, injected conjunctiva, blurred vision, photophobia, headaches• REFER URGENTLY any patients with occular pain, redness and visual disturbance

0 Hepatobiliary conditions• Primary sclerosing cholangitis (PSC), cholangitis, pericholangitis, steatosis, chronic hepatitis, cirrhosis, gallstones• May be a complication or an adverse effect of drugs• Present as incidental finding• PBC is more common in UC

0 Rare: bronchiectasis, bronchitis, hyperhomocysteinaemia, pancreatitis, renal stones

Complications

Crohn’s disease0 Perforation0 Abscess0 Fistulae0 Obstruction0 Malabsorption0 Low bile salt reabsorption0 Malnutrition0 Bacterial overgrowth

Active small bowel disease/extensive small

bowel resection

Deficiencies?Iron, folate, B12, fat-soluble

vitamins (ADEK)

Complications?Osteoporosis, anaemia

Predilection of Crohn’s for the ileum – bile salts spill into the

colon and cause bile-salt induced diarrhoea

Further disease/resection?Fat maldigestion and steatorrhoea

This leads to predilection for renal calculi – calcium readily binds unabsorbed fatty acids,

allowing oxalate to be taken up by the bowel in greater quantity

Result from disease itself or the treatments given…

From extensive resection

UC0Colorectal cancer

Risk factors?Duration, extent of disease, severity of

inflammation, family history of CRC,

concomittant PSC

Examination of the patient with IBDNow that you know the features, extra-colonic features and

complications of the disease what would you examine in the ISCE station if you suspected IBD?

Investigation0 Initial presentation – DIAGNOSIS is with history + histology + imaging

0 Bloods• FBC – anaemia, raised platelets (surrogate sign of inflammation)• WCC – infection• Electrolytes – diarrhoea• Liver chemistry – complications i.e. PSC (liver switches out of making albumin and makes inflammatory

mediators like CRP)• CRP – elevated in inflammatory conditions• Haematinics – iron, folate, B12• Calcium, magnesium and zinc – malabsorption, important for wound healing• Autoantibodies – gliadin peptides to rule out coeliac disease

0 Imaging• Endoscopy (Crohn’s) – mucosal biopsy and balloon dilation• Colonoscopy (UC) – to determine extent of disease• CT and barium studies• US – useful for detecting thickened bowel, abscess and fistulae

0 Special• Examination of the stool - macroscopic , microscopic and culture (to exclude infective diarrhoea)

0 Chronic disease investigation0 Assess disease activity – simple markers of inflammatory activity (CRP).

• ‘Activity Indices’ – Crohn’s Disease Activity Index0 Complications – AXR, bloods, stool cultures0 Severe colitis – recognize early

Management?0 GOALS:

0 Relief of clinical symptoms0 Medical therapy is a 3-pronged approach…

0 Remission from symptoms of active disease0 Maintaining remission0 Preventing complications

0 Also consider – RISK vs BENEFIT of toxic treatments

For both UC and Crohn’s suggest an MDT approachDieticianSurgeons

PhysiciansPsychological support

Management – Crohn’s0 Pharmacological therapies

0 5-Aminosalicylates (5-ASA) – do not alter disease course, favourable ‘safety profile’, used more commonly for UC

0 Antibiotics – Ciprofloxacin and metronidazole, study data varies0 Corticosteroids – achieve remission but don’t sustain it, PO Prednisolone

for most, IV methylprednisolone for those with poor absorptive states, side-effect profile if used long term is poor, can cause non-healing fistulae

0 Thiopurines (azathioprine and 6-mercaptopurine) – purine analogues, immunosuppressive agents, achieve and maintain remission

0 Methotrexate – can achieve remission and maintain it, not for women of childbearing age

0 Anti-TNF agents (infliximab, adalimumab) – anti-TNF (pro-inflammatory cytokine important in Crohns)

0 Surgical management – 75% of patients will have surgery within 20 years of diagnosis

0 Needed to address: stricturing, penetrating or fistulating disease0 Recurrence at anastomotic sites is common – surgery not recommended

as a primary treatment

Skin/soft tissueCushingoid appearance

Abdominal striaeAcne

HirsutismOedema

PsychiatricSleep disturbance/activation

Mood disturbancePsychosis

Neurologic Neuropathy

Pseudomotor cerebriMSK

OsteoporosisAsceptic necrosis of bone

MyopathyEndocrine

Diabetes mellitusAdrenal cortex suppression

ImmunologicLymphocytopenia

ImmunosuppressionFalse-negative skin test

CVHypertension

OpthalmicCataract

Narrow-angle glaucomaDevelopmental

Growth retardation

Complications?Infection – especially TB (screen for this

prior to administration), Hep B↑ risk of lymphoma

Management - UC0 Pharmacological therapies

0 5-ASA – mainstay of treatment, sulfazalazine is main drug in this class, SE’s: Nausea, vomitting, dyspepsia, headache, malaise, achieve and maintains remission, ask about adherence as 3-4 doses/day are required

0 Corticosteroids – achieve remission but do not maintain it, heavy SE profile0 Thiopurines – not as good in UC as in Crohn’s0 Infliximab0 Cyclosporine – calcineurin inhibitor, last-line in hospitalised patients, induces short-term response

0 Surgical management0 Offers a THERAPEUTIC option0 Colectomy with ileo-anal pouch formation – removes diseased tissue and the need for further medical

therapy0 Indications: severe disease, disease refractory to medical therapy, complications of a severe attack

(perforation, acute colonic dilation), colitis associated dysplasia/malignancy, impaired quality of life (unacceptable symptoms despite maximal therapy)

0 Surveillance of complications0 Colorectal carcinoma → colonoscopies with biopsies every 2 years initially (every year if +PBC/long-

standing disease)

ACUTE COLITISIV steroidsCiclosporin for disease not responding to steroids

“random 4-quadrant biopsies

every 10cm throughout the

colon”

CASE 4

Betty Smith is a 45 year-old teacher who presents to her GP with itching for a few years that has gradually got worse. Her neighbour has also noticed a yellow tinge to her eyes. She has a past medical history of hypothyroidism.On examination the sclera are yellow and her chest and abdomen are mildly excoriated.

Differentials

0Primary Biliary Cirrhosis0Autoimmune hepatitis0 Iron deficiency0Hypothyroidism

PBC0 Chronic0 Progressive destruction of small bile ducts

eventually leading to cirrhosis0 Women (90%), 40-50 years old0 Thought to be an immunological mechanism

involved0 Serum anti-mitochrondrial antibodies

(AMA) present0 E. Coli

0 Clinical features0 Incidental finding - ↑ALP, AMA autoantibodies0 Pruritis precedes jaundice by years0 Fatigue0 Hepatomegaly

0 Associations – autoimmune disorders occur with more frequency0 Sjogrens0 Scleroderma0 Thyroid disease0 Renal tubular acidosis, membranous glomerulonephritis,

coeliac disease, interstitial pneumonitis

0 Chronic0 Cholestatic liver disease

characterised by fibrosing inflammatory destruction of both intra- and extra-hepatic bile ducts

0 Men (70%), 40 years old0 Thought to be an immune-mediated

0 Serum pANCA in 60%0 Clinical features

0 Incidental finding - ↑ALP0 Fluctuating pruritis 0 Jaundice0 Cholangitis

0 Associations – with ulcerative colitis in 75% of cases

PSC

Investigations?

0Bloods0 Mitochondrial antibodies – measured by ELISA0 Liver profile – ALP raised, no others0 Serum cholesterol – raised

0 Imaging0 US – diffuse alteration in liver architecture0 MRCP0 Biopsy – portal tract infiltrate, granulomas, loss of small

bile ducts

Management?

0Pharmacological0 Ursodeoxycholic acid – improves bilirubin and

aminotransferase levels, does not improve prognosis0 Supplementation of fat-soluble vitamins (ADEK)0 Cholestyramine – for pruritis

0Complications – cirrhosis

0PSC – the only proven treatment is liver transplantation