Block 32 Week 3&4 Flashcards
Paget’s disease of the nipple?
- rare condition associated with breast cancer. It causes eczema-like changes to the skin of the nipple - It’s usually a sign of breast cancer in the tissue behind the nipple.
ductal vs lobular carcinomas?
- ductal carcinomas are more likely to present with a discreet lump but lobular carcinoma may be harder to detect
/PVD - lipodermatosclerosis
refers tochanges in the skin of the lower legs. It is a form of panniculitis (inflammation of the layer of fat under the skin)
UC?
- begins in rectum and extends proximaly
- Mostly pathological findings limited to mucosa and submucosa
Changes seen in UC?
- Muscularis propria only affected in fulminant disease
- Distorted crypt architecture
- Crypt abscesses
Who does UC affect more?
- less common in smokers
- increased in caucasians, jews and females
UC peaks?
15-25 and 55-65
histological changes seen in IBD?
Symptoms of UC?
- dominant Sx is diarrhoea
- often associated w bleeding PR
- often freq of small stools w urgency - inflamed rectum loses ability to distend and relax
Other findings of UC?
- fatigue
- malaise
- weight loss
- fever
- tachycardia
CD can affect…
- can affect anywhere from mouth to anus
- transmural inflammation
- granulomas but these are more common in submucosa
3 major patterns of CD?
- ileeocaecal disease - 40%
- confined to SI - 30%
- confined to colon - 25%
Who does CD affect more?
- Increased incidence in Caucasians, Jews and slight female preponderance
- More common in smokers
peaks in CD?
15-25 and 55-65 years of age
Symptoms of CD?
- diarrhoea
- abdominal pain
- weight loss
- fatigue
- low grade fever
CD activity index?
Harvey-bradshaw index?
- score <4 = in remission
- score 5-8 = moderate activity
- score >8 = severe active disease
- crohns
investigations?
- flexible sigmoidoscopy/ colonoscopy and biopsies
radiology?
- plain AXR - thumbprinting
- CT
- MR enterography
- small bowel follow-through meal
test for IBD?
- faecal calprotectin
Tx of IBD?
- aminosalicyclates
- mainly mesalazine
- others: olsalazine, sulphasalazine, balsalazide
UC scan
stovepipe sign
aminosalicyclates r used for?
- prevention of CRC
- high dose to prevent remission
side effects of aminosalicyclates?
- rashes
- headache
- diarrhoea
- reversible infertility
- intestinal nephritis
corticosteroid with a low first pass metabolism?
prednisolone
corticosteroids with a high first pass metabolism?
beclomethasone
nutrition for IBD?
- elemental or semi elemental diets
immunomodulators for IBD?
- Azathioprine
- mercaptopurine
- methotrexate
- ciclosporin
- mycophenolate
- cytokine modulators
azathioprine?
- Affects purine (A+G) synthesis
- Decreases T-lymphocytes
side effects of azathioprine?
- Side effects; up to 30% don’t tolerate
- Dangerous neutropenia
mercaptopurine?
- active metabolite of azathioprine
methotrexate?
- antifolate
- once weekly
- fibrosis
Tx pathway of IBD?
Ciclosporin?
- calcineurin inhibitor
- CN activates T cells
rescue therapy in UC?
Ciclosporin
mycophenolate?
- affects guanine (purine) synthesis in B and T lymphocytes
TNF-a?
activates NF-KB which induces apoptosis
drugs that inhibit TNF-a?
- infliximab and adalimumab inhibit TNFa
- used in severe crohns not responding to conventional drugs
Side effect of infliximab and adalimumab?
- hepatosplenic T cell lymphoma
- especially in young males
surgery for UC?
- toxic megacolon/ acute colitis
- failure to respond to medical therapy
- colectomy is curative
surgery for CD?
- High rate of disease recurrence after surgery
inducing remission in crohns?
- offer monotherapy of a conventional glucocorticoid to induce remission
- aminosalicyclates if ^ are CI or if the person can’t tolerate them
what should not be used to induce remission in CD?
azathioprine, mercaptopurine or methotrexate as monotherapy to induce remission
what to check for azathioprine?
TPMT activity
How is remission induced in UC?
in mild to moderate UC: aminosalicyclate
risk factors CD?
- Fhx
- smoking
- prev GE
- NSAIDs
Crohns vs UC?
- UC: continous inflammation of the mucosa starting in the rectum in most cases and is limited to the colon
- CD: transmural patchy inflammation throughout the GIT - MOUTH TO ANUS
genetics in CD?
- disrupted microflora-immune response
- association between SNP in NOD2 (CARD15) gene and crohns
increased risk of CD…
- smoking increases risk of CD but is protective in UC
- western diets, abs and contraceptive use increases risk of CD
Perianal CD?
- About a third of patients suffer from perianal CD - e.g. skin tags, fissures, fistulae, abcesses, or anal canal stenosis
Pathological changes of CD mneumonic?
CD - ? appearance of mucosa?
- cobblestone appearance which is caused by small superficial ulcers which become deep with a wavy margin
- bowel wall thickening, lumen narrowing, deep ulcers, fistulae and fissues may also occur
microscopic changes in CD?
- lymphoid hyperplasia and non-caseating granulomas
- skip lesions and transmural ulceration
Sx of CD?
- nausea and vomiting
- fatigue
- low grade fever
- weight loss
- abd pain
- diarrhoea (+/- blood)
- rectal bleeding
- perianal disease
Signs of CD?
- pyrexia
- Dehydration
- Angular stomatitis
- Aphthous ulcers
- Tachycardia
- Hypotension
- Abdominal pain, mass and distension
MSK manifestation of CD?
- peripheral arthiritis
Skin changes in CD?
- erythema nodosum
- pyoderma gangrenosum
Erythema nodosum?
- Erythema nodosum, a panniculitis, is characterised by reddened, raised, tender nodules.
pyoderma gangrenosum?
pyoderma gangrenosum presents with ulcerating nodules characterised by black (gangrenosum) edges and central pus (pyoderma).
eye changes in CD?
- episcleritis
- uveitis
- conjuncitivitis
which EIM can precede intestinal disease?
apthous ulcers
primary sclerosing cholangitis in CD?
- Primary sclerosing cholangitis may occur but is more common in UC
- fatty liver disease and gallstones are more common
other extra-intestinal mainfestations of CD?
- Renal calculi
- Osteoporosis
- B12deficiency
- Pulmonary disease
- Venous thrombosis
- Anaemia
investigations of CD?
- macroscopic assessment and histological evidence (e.g. biopsy) of inflammation typical of CD
- stool microscopy, culture, parasites, C diff toxin
- faecal calprotectin - released following degranulation of neutrophils
Endoscopic Ix of CD?
- colonoscopy - can do a tissue biopsy
- upper GI endoscopy - biopsy needed to differentiate CD from other pathology
inducing remission in CD?
- budesonide
- systemic corticosteroids if the patient doesn’t resond to budesonide or if they have moderate-severe crohns e.g. prednisolone
Inducing remission in M-S CD?
immunosuppressive therapy e.g. azathioprine or methotrexate
CD - maintenance therapy?
- thiopurines, methotrexate and biologics
- considered in patients with recurrent flares, moderate-to-severe disease, or poor prognostic features (e.g. extensive disease).
thiopurines mechanism?
azathioprine and mercaptopurine - purine synthesis inhibition in lymphocytes
* check TPMT levels!!
what to check b4 methotrexate use?
- check renal and liver function before use
side effects of methotrexate?
- bone marrow suppression, hepatotoxicity, pulmonary toxicity
management of perianal disease ?
- Control perianal sepsis(e.g. antibiotics)
- Evaluation(e.g. MRI or examination under anaesthesia)
- Surgical intervention(e.g. abscess drainage or seton for fistula)
surveillance colonoscopy?
- patients with IBD in the UK are offered surveillance ileocolonoscopy between 6-10 years following diagnosis to screen for dysplasia
- patients w primary sclerosing cholangitis are at a paticularly high risk of cancer
UC is more common in which populations?
Jewish
environmental factors contributing to UC?
milk consumption, bacterial microflora alteration and medications like OCP and NSAIDs
Pattern of UC?
- UC affects the rectum (proctitis) first and then extends proximally to the colon
- most patients (50%) suffer from proctitis only
pancolitis?
inflammation of the entire colon
what does pancolitis put you at risk of?
- backwash ileitis
- reflux of colonic contents into the distal few centimetres of the ileum through theileocaecal valve
macroscopic changes of UC?
- continuous inflammation that extends proximally along the colon
- may be inflammatory polyps
Microscopic changes of UC?
- crypt abcesses and goblet cell depletion
- increased inflammatory infiltration into the lamina propria, which is largelyneutrophilic.
Hallmark of UC?
bloody diarrhoea/ rectal bleeding
Symptoms of UC?
- Weight loss
- Fatigue
- Abdominal pain
- Loose stools
- Rectal bleeding
- Tenesmus(incomplete emptying)
- Urgency
Signs of UC?
- Febrile
- Pale
- Dehydrated
- Abdominal tenderness
- Abdominal distension/mass
- Tachycardic, hypotensive
Major complication of UC?
- toxic megacolon is a major complication
TMC?
medical emergency - toxic, non obstructive dilatation of the colon
When should TMC be suspected?
- UC + abdominal distension and tenderness -> suspect TMC
Systemic symptoms suggestive of TMC?
- Fever
- Tachycardia
- Hypotension
- Dehydration
- Altered mental status
- Biochemical abnormalities(e.g.leukocytosis,anaemia, andelectrolyte derangements)
most common manifestation of UC?
ARTHIRITIS - can be simple peripheral arthititis or spondylarthropathy e.g. ankylosing spondyliti
Eye related manifestation of UC?
- uveitis is strongly assoc w UC
- episcleritis
other MSK features of UC?
osteopenia/ osteoporosis, clubbing of hands and feet
mouth changes seen in UC?
Apthous ulcers
skin changes assoc w UC?
Erythema nodosum and pyoderma gangrenosum
hepatobiliary manifestation of UC?
- fatty liver disease and autoimmune liver disease
- most commonly: primary sclerosing cholangitis
Link between PSC and UC?
- up to 95% of patients w PSC have UC - suspect PSC in any UC patient who has an isolated rise in ALP
haem manifestations of UC?
- anemia
- thromboembolism
Ix of UC?
- Stool microscopy, culture & sensitivities
- Ova, cysts and parasites
- C. difftoxin(CDT)
- Faecal calprotectin(marker of intestinal inflammation)
bloods for UC?
- FBC
- LFTs
- U&Es
- magnesium
- autoantibodies - e.g. p-ANCA
Imaging for UC?
- abd X ray for looking at dilatation of the bowel and perforations
Endoscopy for UC?
- colonoscopy
- biopsies for histological assessment
- sigmoidoscopy can be used as an alternative
Truelove and Witts?
- scores UC severity
- into mild, moderate and severe
Inducing remission: mild to moderate UC?
- mild to moderate UC: initially 5-ASA agents - topically +/- orally
- Patients with extensive UC (e.g. pancolitis or left-sided colitis) should be treated with both oral and topical (e.g. enemas) 5-ASAs.
inducing remission for severe UC?
- patients who fail to respond to 5-ASAs or those w moderate to severe UC can be treated w systemic corticosteroids as a 6-8 wk course
Maintenance therapy for UC?
- thiopurines
- biologics
- in patients who don’t respond to remission therapy or steroid dependent or >2 flares in a 12 month period
surgery for UC?
- principle surgical option in UC is proctocolectomy followed by ileal pouch anal anastomosis (IPAA) or end ileostomy.
management of acute severe UC?
- High dose corticosteroids IV with PPI
- VTE prophylaxis: LMWH
- antibiotics: broad spectrum
- hydration and nutrition
How can an upper GI bleed present?
- severe bleeding w haematemesis, hametochezia and hypotension
- coffee ground vomiting (exclude bowel obstruction)
- gradual bleeding w melena
- occult bleeding detected by positive tests for blood in stool, anaemia
causes of UGIB?
Assessment of an UGIB?
- FBC, PT and PTT
If the patient is unstable with an UGIB…
- O2
- fluid of 500ml in less than 15 min
- continous monitoring - nEWS
- catheter and monitor urine output
UGIB - resus - transfusion?
- for patients w massive bleeding
- prothrombin complex concentrate or vitamin K -> Warfarin
- recomb factor 7a when other methods fail
warfarin reversal?
prothrombin complex concentrate or vitamin K
2 methods used to assess risk in an UGIB?
- Glasgow-Blatchford score
- Rockall score
Rockall score?
- incorporates clinical and endoscopic findings
- evaluates risk of re-bleeding or death
history with an UGIB?
- ulcers
- recent trauma
- liver disease
- varices
- alcoholism - MWT or oesophageal varices
- vomiting
UGIB history - medications?
- medications that interefere w coagulation - NSAIDS, aspirin, dipyridamol
physical exam w an UGIB?
- jaundice
- ascites and other signs of liver disease
- tumour mass
- bruit
NG aspiration?
- clear and bile stained - can have bleeding distal to pylorus
- bloody
Tx of an upper GIB is dependent on
whether it’s variceal or non variceal bleeding
Cirrhosis/ variceal bleeding Tx?
- IV Terlipressin - vasopressin analogue
- or somatostatin/ octreotide
- ECG >65 yrs
Terlipressin caution?
- Be careful w Telipressin in patients w IHD or PVD as it can worsen it
what else should be prescribed for an UGIB patient - variceal bleeding?
- IV ab as infections more common in ppts w cirrhosis and UGI bleeding
- 7 day broad spectrum abs
Other things to do during management of UGIB?
- fluid resus
- coagulopathy common and should be addressed
method of stopping bleeding for an UGIB?
- balloon tamponade to stop the bleeding - balloon at the G-E junction
- temporary method until patient stabilised
- sig risk of ischaemia if the tube is left for more than 24 hrs
endoscopy with an UGIB?
- endoscopy: looking for oesophageal gastric varices
- Gastroesophageal varices occur in ~30% of cirrhosis patients
Methods of stopping oesophageal varices from bleeding?
- band ligation - best option (during endoscopy)
- stent insertion - applies pressure
- TIPS (transjugular intrahepatic portosystemic shunts) if bleeding is not controlled by band ligation
when does endoscopy be done for an UGIB?
- endoscopy should be done immediately after resus for unstable patients w severe bleeding
- all other patients with UGI bleeding need one within 24hrs
how to stop gastric varices from bleeding?
- endoscopic injection of cyanoacrylate (sclerotherapy)
- TIPS (shunt) if bleeding isn’t controlled
main cause of non-variceal UGIB?
PUD
CT angiography for UGIB?
- for patients who are haemodynamically Unstable
- fastest and least invasive method
- catheter angiography -> source of bleeding can be embolised
If the source of bleeding can’t be identified with CT angiography?
immediate OGD
Sugery for UGIB?
- last resort
- shock
- failure of endoscopic manegement
- recurrent haemorrhages after intial stabilization
- continued slow bleeding with a transfusion
methods of dealing with non variceal bleeding - during endoscopy?
- Adrenaline injection plus
- thermal modalities e.g. heater probe
- mechanical modality (clips)
- haemostatic powders
Other management methods of non variceal bleeding?
- PPIs
- H pylori eradication
- antithrombin therapy interupted
How are oral AC reversed?
inhibitors (idarucizumab or andexanet)
when should AC be restarted for low vs high thrombotic risk patients?
- low thrombotic risk - restart warfarin in 7 days
- high thrombotic risk - LMWH after 48 hrs
Re-bleeding?
- related to size and location - posterior duodenum carries a higher risk
- repeat endoscopy for patients who re-bleed
MWT?
- Lower part of oesophagus/ lesser curvature
- lesion usually stops bleeding w/o therapy
Acute haemorrhagic gastritis is when?
- related to stress or medications like NSAIDs
- whole gastric mucosa bleeds
AHG treatment?
- stop NSAIDs
- give H2 receptor blockers, PPIs
- anti- H pylori therapy
if bleeding doesn’t stop w AHG then give?
IV somatostatin
last resort for AHG?
gastrectomy
lower GI bleeding?
- distal to LoT
- less frequent than UGI bleeding
- majority of cases from colon, and is more common in men
how to distinguish between an upper and lower GI bleed?
NG aspiration
causes of a LGIB
Oakland score?
- LGIB
- helps u decide if the patient needs admittance
- less than 8 means the patient can be seen as an outpatient
Tx pathway for a LGIB?
Ix of a LGIB?
- haemodynamic instability may indicate an upper GI bleed so
- CT angiography first
- if inconclusive -> OGD
LGIB - if a colonoscopy isn’t feasible then?
- If bleeding volume means that colonoscopy is not feasible or is ineffective -> selective mesenteric arteriography
Tx of LGIB?
- vasopression infusion and embolization of bleeding vessels
Acute UGIB?
- Medical emergency
- divided into variceal and non-variceal
- death from exsanguination is uncommon
Summary for management of an UGIB?
- history and exam
- resus
- investigation
Common causes of an UGIB?
- PUD
- gastritis
- gastric ulcer
- varices
- cancer - ooesephageal or gastric, duodenal is rare
Things to ask in an UGIB history?
- volume
- type of blood loss
- fresh haemetemsis
- coffee ground vomit
- maleana
- fresh PR blood
oesphagitis?
heartburn, occassionaly chest pain often worse on lying down
gastritis?
dyspepsia - e.g. epigastric often burning pain
gastric or duodenal ulcer?
dyspepsia, nausea, vomiting, weight loss
varices?
history of liver disease, excess alcohol
cancer?
malaise, weight loss, vomiting, early satiety
meds history for UGIB?
NSAIDs, steroids, AC meds including warfarin
Examination for an UGIB?
- pulse, BP, pallor, cap refill
- postural drop
- signs of anemia
- stigmata of CLD
- working out if the patient has shock
Ix for UGIB summary?
- FBC - hb, MCV
- U&Es - raised urea and creatine indicates UGIB
- clotting screen - espec if patient is on AC
- LFTs
- upper GI endoscopy - diagnostic test of choice
resus for a bleed?
- IV access
- catheter
- fluids
- blood
initial management of a non variceal bleed?
initial management of variceal bleeds?
- higher morbidity and mortality
- terlipressin - splenic vasoconstrictor, reduces portal hypertension
- IV broad spectrum ab
chronic LGIB - history?
- type of blood
- change in bowel habit
- mucus
- abd pain
- weight loss
- eye, joint or skin symptoms
overt GI bleed?
- if its on wiping - most likely an anal cause like haemorrhoids
anal causes of chronic GI bleeding ?
- piles
- fissure
- carcinoma
rectal causes of chronic GI bleeding?
- carcinoma
- inflammation
- polyps
colonic causes of chronic GI bleeding?
- cancer
- diverticular disease
- inflammation
- polyps
- angiodysplasia - fragile blood vessels
Severe overt lower GI bleeding is a ?
med emergency
assessment of a lower GI bleed
examination for lower GI bleeding?
investigations for LGIB?
- bloods
- colonoscopy
- alternatives - barium enema, CT colonography
What does chronic occult GI bleeding cause?
- causes iron deficieny anaemia
- microcyctic, hypochromic anaemia
- Fe can be falsely raised by inflammation
- faecal occult blood testing
diagnoses of upper GI Bleeds
fresh rectal bleeding commonly results from?
- fresh rectal bleeding commonly results from a source in a rectum or colon but large upper GI bleeds can also present w haematochezia
diverticulosis?
- most common cause of lower GI bleeding
- increases w age
Diverticular disease vs diverticulitis?
- Whilst diverticular diseasebleeds are often painless, any bleeds secondary todiverticulitiscan often bepainful, due to the localised inflammation.
haemorrhoids?
- pathologically engorged vascular cushions in the anal canal
- can present as a mass, with pruritus, or fresh red rectal bleeding
- blood is classically on thesurface of the stoolor toilet pan, rather than mixed in with it.
RF of CRC?
- Family history
- Hereditary syndromes - lynch syndrome and FAP
- Inflammatory bowel disease
- Ethnicity - white
- Radiotherapy
- Obesity
- Diabetes mellitus
- Smoking
CRC most commonly affects?
- Most commonly affects left side of the colon
- mets mostly to liver
which cancers mets to the lung?
- Rectal cancers are more commonly associated with lung metastasis (prior to liver metastasis) due to direct haematogenous spread via the inferior rectal vein and IVC
Summary of CRC mets?
left sided -> liver
rectal -> lung
also peritoneum, brain and bone
pres of CRC?
- change in bowel habit, anaemia, weight loss
- Diagnosis frequently follows the recognition of an unexplained (and typically iron deficient) anaemia - a key indication for endoscopy.
Symptoms of CRC?
- Change in bowel habit
- Weight loss
- Malaise
- Tenesmus
- PR bleeding
- Abdominal pain
Signs of CRC?
- pallor
- abd mass
signs of metastatic disease from CRC?
- Hepatomegaly
- Jaundice
- Abdominal pain
- Lymphadenopathy
Right sided CRC?
- right sides lesions tend to develop as masses arising from a dyplastc polyp -> iron deficieny anaemia
Left sided CRC?
- left sided lesions - grow circumferentially creating an apple core appearance -> narrowing of lumen and symptoms of changes in bowel habit and obstruction
Right vs left sided CRC?
- right: iron def anemia
- left: apple core apperance -> obstruction
Screening for CRC?
- FIT test
- 60-74
RF for an UGIB?
- NSAIDs
- Anticoagulants
- Alcohol abuse
- Chronic liver disease
- Chronic kidney disease
- Advancing age
- Previous PUD orH. pyloriinfection
macronutrients (3)?
- carbs
- proteins
- lipids
micronutrients?
- minerals
- vitamins
- trace elements
functions of proteins?
- Structural i.e. Collagen in bone
- Regulatory i.e. Hormones like insulin
- Contractile i.e. Myosin and actin in muscle cells
- Immunological i.e. Antibodies
- Transport i.e. Haemoglobin
- Catalytic i.e. enzymes
lipids?
- Most plentiful lipid in your body
- Provide more than twice as much energy as carbohydrates or protein
steroids?
- such as cholesterol, bile salts, adrenocortical hormones, sex hormones
eiconasoids?
- Lipids derived from arachidonic acid
- 2 principle subclasses are prostaglandins and leukotrienes
- Involved in inflammatory reactions, gastric protection, airway calibre, clotting
water soluble vitamins?
▪Vitamin B1, B2, B6, B12, C, Folate and Niacin
▪Absorbed along with water in the GI tract
fat soluble vitamins?
▪Vitamin A, D, E, K
- Absorbed with other dietary lipids in small intestine – dependent on bile salts
antioxidant vitamins?
Vitamins C, E and Beta-carotene act as antioxidants – they inactivate oxygen free radicals which would otherwise damage DNA, cell membranes and structures within a cell
what must equal to maintain weight?
- intake and output must equal to maintain weight
vitamin deficienies table
basal energy expenditure?
rest energy required for metabolism
nutritional assessments?
- BMI - body mass index (weight (kg)/height (m2))
- Mid - arm circumference = muscle mass
- Skin - fold thickness = body fat
enteral feedinf?
▪Oral
▪Tube feeding
- preferred as lack of enteral feeding atrophies the intestinal epithelium + inc risk of sepsis
when is enteral feeding used?
- Cannot eat sufficient food
- Unconsciousness (tube feed)
- Dysphagia (tube feed)
- Loss of nutrients from fistulas/stomas
- Major illness/postoperatively
tube feeding?
- For patients with inadequate or unsafe oral intake
- Via a fine bore nasogastric tube
- Nasojejunal tube can be inserted in presence of gastroparesis or pancreatitis
complications of tube feeding?
insertion of tube into lungs, aspiration, nasal erosion, refeeding syndrome
enterostomy feeding?
- feeding for more than 4-6 wks
- usually inserted using PEG
risks of enterostomy feeding?
perforation, peritonitis, buried bumper syndrome, infected site, aspiration
parenteral feeding?
IV
when is parenteral feeding used?
- for those w unsafe oral or enteral intake
- non-functional, inaccessible or perforated GI tract
- requires use of solution containing macros and micros
how can parenteral feeding be done?
- short term feeding - peripheal cannula if no need for CV access
- PICC line
- central venous catheters
picc line?
peripherally inserted central catheter via basilic vein
central venous catheters?
subclavian line
what is common with a peripheral cannula for parenteral feeding?
thrombophlebitis
risks of central venous catheter insertion?
- Catheter related infection, blockage, venous thrombosis, fatty liver disease
refeeding syndrome?
- too rapid intro of feed following starvation
- can occur after enteral or parenteral feeding
why does refeeding syndrome occur?
- Results from a reduced carbohydrate intake secondary to starvation producing low insulin levels.
- Once feeding restarted increased insulin secretion occurs, which increases cellular uptake of PO4.
RS - when phosphate levels fall?
rhabdomyolosis, leucocyte dysfunction, respiratory/cardiac failure, muscle weakness, seizures, coma.
when does RS occur?
usually around day 4 of refeeding
Patients at high risk of refeeding syndrome include:
- BMI < 16kg/m2
- History of alcohol abuse
- Little or no nutritional intake for last 10 days
- Low levels of potassium, phosphate or magnesium prior to commencing feed
- Unintentional weight loss of > 15% last 3-6 months
- Those at high risk require additional vitamin supplements – thiamine/vitamin B/trace elements
intestinal failure?
- intestinal failure is characterised by inadequate intake and absorption of nutrients
type 1 intestinal failure?
- post-op ileus or small intestinal obstruction, usually requires short term nutrition
type 2 intestinal failure?
- type 2 IF: greater than 28 days
- typical patients: complex CD, intestinal fistula, abd sepsis
type 3 intestinal failure?
- type 3: generally irreversible
- usually occurs as a consequence of massive bowel resection leading to short bowel syndrome
features of malabs - caloric?
weight loss with normal appetite
features of malabs - fat?
pale, greasy, offensive diarrhoea
features of malabs - protein?
edema, muscle atrophy, amenorrhea
features of malabs - carbs?
abd bloating, diarrhoea, flatus
features of malabs - B12?
- macrocytic anemia
- degeneration of SC
Features of malabs - folic acid?
- folic acid: macrocytic anemia
features of malabs - vitamin B?
glossitis, stomatitis, acrodermatitis, cheliosis
features of malabs - iron?
- iron: microcytic anemia
features of malabs - calcium and vitamin D?
osteomalacia, tetany
Features of malabs - vitamin A?
night blindness, follicular hyperkeratosis
features of malabs - vit K?
bleeding
CF of malabs
rationale for and practical implications of a gluten-free diet?
- coeliac disease
- demeatitis herpetiformis
- gluten ataxia
- wheat allergy
Haemorrhoids?
- H: piles
- painless rectal bleeding
- usually on wiping
fissures?
- fissues: tear in the lining of the anus or anal canal
- peak 15-40 yrs old
causes of fissures?
- commonly due to local trauma from constipation, diarrhoea, anal sex
management of rectal bleeding?
- low hb: transfusion
- reversal of anticoagulation
- endoscopic haemostatis methods
- arterial embolisation
Endoscopic haemostasis methods?
- include injection (typically diluted adrenaline), contact
- non-contact thermal devices (such as bipolar electrocoagulation or
- argon plasma coagulation),
- mechanical therapies (endoscopic clips and band ligation)
arterial embolisation?
possible in those with an identified bleeding point
UC vs CD pain?
- Ulcerative colitis patients tend to have pain in the lower left part of the abdomen, while Crohn’s disease patients commonly (but not always) experience pain in the lower right abdomen
UC vs CD
uc VS CD
marker
what is seen more commonly in UC?
P-ANCA
Mild to moderate acute ulcerative colitis is treated with:
- Aminosalicylate (e.g., oral or rectal mesalazine) first-line
- Corticosteroids (e.g., oral or rectal prednisolone) second-line
Severe acute UC is treated w:
Intravenous steroids (e.g., IV hydrocortisone) first-line
Other options for severe acute ulcerative colitis include:
- Intravenous ciclosporin
- Infliximab
- Surgery
Options for maintaining remission in ulcerative colitis are:
- Aminosalicylate (e.g., oral or rectal mesalazine) first-line
- Azathioprine
- Mercaptopurine
Inducing remission in an exacerbation of Crohn’s disease is with:
- Steroids (e.g., oral prednisolone or IV hydrocortisone) first-line
- Enteral nutrition as an alternative, particularly where there are concerns about steroids affecting growth
Other ways of inducing remission in CD when steroids alone don’t work?
- Azathioprine
- Mercaptopurine
- Methotrexate
- Infliximab
- Adalimumab
Maintaining remission in CD?
First-line for maintaining remission in Crohn’s is with either:
- Azathioprine
- Mercaptopurine
Methotrexate alt
