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Medicine > Gastrointestinal > Flashcards

Gastrointestinal Flashcards

1
Q

-Hiatus hernia, describe the 2 types and which is most common? Where does the gastro-oesophageal junction (GOJ) lie in both?

A
  • 95% are sliding: GOJ slides through hiatus and lies above diaphragm, asymptomatic or +reflux
  • para-oesophageal: fundus rolls up through hiatus alongside oesophagus, GOJ remains below diaphragm.
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2
Q

A para-oesophageal rolling hernia is more rare than the classic sliding hernia and more serious, what are risks associated with a rolling hernia?

A
  • gastric volvulus (rotation and strangulation of stomach)
  • bleeding
  • respiratory complications
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3
Q

Acute hepatic failure is hepatic failure with ______.

  • It develops in less than __weeks in a pt with previously normal liver/in pts with an acute exacerbation of underlying disease.
  • Cases that evolve up to 12 weeks are known as ___ hepatic failure.
A
  • encephalopathy (a neuropsych condition in pts with liver disease)
  • <2 weeks
  • 2-12weeks = subacute hepatic failure
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4
Q

2 most common causes of acute hepatic failure in UK? It occurs as a result of massive liver cell ____ following acute liver damage of any cause.

A
  • viral hepatitis
  • paracetamol overdose
  • massive liver cell necrosis
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5
Q

Acute hepatic failure presents with encephalopathy (severity varies) and severe ____ and a marked _____.
Name 3 complications:

A
  • severe jaundice & marked coagulopathy

- complications: cerebral oedema, hypoglycaemia, severe bacterial/fungal infections, hypotension, renal failure

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6
Q

-What can be life-saving treatment for some acute hepatic failure but is offered solely based on severity of encephalopathy and reserved for the most severe cases of which 80% would die without it?

A

-emergency liver transplant

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7
Q

explain the grades of hepatic encephalopathy from 0 (completely fine) to 4 (coma)

A

0-no LOC, normal personality/behaviour
1-daytime somnolence, short attention span, mild asterixis
2-lethargic, time disorientated, obvious asterixis, inappropriate behaviour
3-asleep but rousable, confusion, incomprehensible speech
4-coma

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8
Q

Name 2 criteria for pts with acute livery injury to be transferred to specialist liver units?

A
  • INR > 3
  • hepatic encephalopathy present
  • Hypotension despite fluid resus
  • Metabolic acidosis
  • Prothromin time seconds > interval (hours) from OD ( in terms of paracetamol induced)
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9
Q

What blood test can be used to screen for problematic levels of alcohol intake?

A

-elevated serum gamma GT and raised MCV (also helpful to monitor progress)

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10
Q

Liver damage by alcohol is as a direct result of tissue toxicity and the effects of malnutrition and vitamin deficiency which often accompany excessive drinking, name a cardio and 2 neuro related complications (short term & long term) other than Wernicke’s and Korsakoffs

A
  • cardio: direct toxicity –> cardiomyopathy and arrhythmias
  • neuro: acute intoxication -> ataxia, falls, head injury + intercranial bleeds. Long term: polyneuropathy, myopathy, cerebellar degeneration, dementia and epilepsy.
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11
Q

Wernicke’s encephalopathy is a result of vitamin __ deficiency. Other than alcohol related, it can be secondary to sever ____ or prolonged ____

A
  • B1 thiamine

- severe starvation or prolonged vomiting

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12
Q

What is the classic triad in Wernicke’s encephalopathy? NB: its a clinical diagnosis

A
  • confusion (drowsiness, pre-coma..)
  • ataxia
  • ophthalmoplegia
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13
Q

What is the immediate treatment of Wernicke’s encephalopathy?

A

-IV injection of B-complex vitamins TDS for 3-5days

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14
Q

Pts at risk of Wernicke’s encephalopathy are treated prophylactically with IV B vitamins for 3-5days, suggest 2 pt groups that may be classed as “at risk”?

A
  • significant weight loss
  • signs of undernutrition
  • alcohol withdrawal symptoms requiring hospital admission
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15
Q

Administration of ____ may exacerbate an acute loss of thiamine hence it is essential that ___ is given before ___

A
  • glucose

- thiamine is given before glucose

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16
Q

Alcohols consequence on following, state 2 each:

  • GI
  • haem
  • Psych
  • Social
A
  • GI: liver damage, pancreatitis, oesophagitis, increased oeophageal carcinoma risk
  • Haem: thrombocytopaenia (platelet maturation inhibited and less release from BM), raised MCV and anaemia (from dietary folate deficiency)
  • Psych: increased depression and self-harm
  • Social: marital and sexual difficulties, employment, financial and homelessness issues
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17
Q

Alcohol withdrawal symptoms:

  • in 6-12 hrs
  • between 2 days-2weeks..
A
  • 6-12hrs: tremor, nausea, sweating (rx reducing dose chlordiazepoxide)
  • generalised tonic-clonic seizures
  • delirium tremens: fever, marked tremor, tachyC, agitation, visual hallucinations, treat urgently
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18
Q

Chlordiazepoxide dose in alcohol withdrawal:

A

-30mg four times daily decreasing to 0mg over 7 days

with heavy intake can increase up to 60mg QDS and reduce to 0mg over 10days

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19
Q

What is the drug of choice for alcohol detoxification in pts with severe liver disease?
(it is not metabolised by the liver) O____

A

Oxazepam

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20
Q

After alcohol withdrawal it’s essential that relapse is prevented, DALs, psych, counselling etc help. What oral GABA analouge reduces relapses by 50%? A______.

A

Acamprosate

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21
Q

Name 5 conditions affecting the small intestine that can cause malabsorption

A
  • coeliac disease
  • crohn’s disease
  • dermatitis herpatiformis
  • tropical sprue
  • bacterial overgrowth
  • intestinal resection
  • Whipple’s disease
  • radiation enteritis
  • parasite infection e.g. Giardia Intestinalis
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22
Q

Name 2 substances absorbed in the terminal ileum by specific receptors?

A
  • vitamin B12

- bile salts

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23
Q

Suggest 3 presenting symptoms of small bowel disease.
Investigation of suspected SB disease is initially with ____ serology, small bowel ____ swallow or ___ and endoscopic small bowel ____.

A
  • diarrhoea, steatorrhoea, abdo pain/discomfort, anaorexia–>weight loss
  • coeliac serology, small bowel barium swalow or MRI and endoscopic SB biopsy
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24
Q

What is coeliac disease aka gluten-sensitive enteropathy

A
  • an autoimmune condition
  • abnormal jejunal mucosa
  • improves when gluten is excluded from diet, relapses when included
  • 1% Europeans have it, most of whom are undiagnosed
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25
Q

coeliac disease is strongly associated with which 2 HLA class II molecules? Which peptide is the toxic portion of gluten?

A

HLA: DQ2 and DQ8

-alpha-gliadin peptide = toxic

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26
Q

How does alpha-gliadin of gluten cause bowel irritation in coeliacs?

  • it is resistant to ____ in SB lumen and passes through a damaged ___ barrier of SB where it is _______ by tissue _____ so increasing its immunogenicity.
  • Gliadin then interacts with ___ in the ___ ___ via HLA ___ and ___ and activated gluten-sensitive __-cells.
  • The resultant inflamm cascade contributed to villous ___ and crypt ____
A
  • proteases, epithelial, deaminated, transglutaminase
  • APCs, lamina propria, DQ2 and DQ8, T-cells
  • atrophy, hyperplasia
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27
Q

Presentation of coeliac disease of coeliac disease peaks at 2 ages-when? Symptoms/signs may include…. and there may be an increased incidence of ___ and ______ diseases.

A
  • infancy post-waning on to gluten containing foods
  • adults in 5th decade
  • diarrhoea, steatorrhoea, abdo pain/discomfort, anaorexia–>weight loss
  • non-specific: tiredness/malaise, physical signs from anaemia and nutritional deficiency
  • atopy and autoimmune disease
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28
Q

Investigations for coeliac disease, name 3

A
  • serum antibodies: IgA tTG - high sensitivity and specificity (IgA endomysial are less sensitive)
  • distal duodenal biopsies for definitive diagnosis
  • blood count: mild anaemia is common, rarely B12, and almost always folate deficiency
  • small bowel radiology or capsule endoscopy if a complication is suspected only
  • bone densitometry (DEXA) done at diagnosis due to increased risk of osteoporosis
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29
Q

Explain the findings of a distal duodenal biopsy on a pt with coeliac disease:

A
  • increase in number of intraepithelial lymphocytes
  • crypt hyperplasia
  • chronic inflammatory cells in the lamina propria
  • subtotal villous atrophy
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30
Q

What at risk patient groups should be screened with serological testing for coeliac disease? name 4

A
  • autoimmune disease: T1DM, thyroid disease, autoimmune liver disease, Addison’s disease
  • IBS with diarrhoea
  • unexplained osteoporosis
  • those with a 1st degree relative affected (10x increased risk)
  • Down’s syndrome (20x increased risk)
  • Turner’s syndrome
  • Infertility and recurrent miscarriage
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31
Q

Management of coeliac’ s disease:

  • diet?
  • correct any..?
  • __vaccine due to association with ??
A
  • lifelong gluten free diet
  • correct any vitamin deficiencies
  • pneumococcal vaccine (as coeliac’ s is associated w hyposplenism)

NB: symptoms and serological tests monitor recovery/compliance with diet and re-biopsy is reserved for pts who do not respond or in whom there is diagnostic uncertainty

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32
Q

Name 2 malignant complications of coeliac disease

A
  • increased malignancy risk esp.
  • –> intestinal T-cell lymphoma
  • –> small bowel cancer
  • –> oesophageal cancer
  • incidence may be reduced by a gluten free diet
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33
Q

Dermatitis herpetiformis is what?

  • rash description? which surfaces effected?
  • deposition of what? Where?
  • pts also have a what sensitive enteropathy?
A
  • an itchy, symmetrical eruption of vesicles and crusts over the extensor surfaces
  • with deposition of granular IgA at the dermoepidermal junction of the skin including areas not involved with the rash
  • pts also have a gluten-sensitive enteropathy (usually asymptomatic)
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34
Q

Treatment for Dermatitis herpetiformis?

A
  • the skin responds to dapsone

- both the skin and gut improve on a gluten-free diet

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35
Q

Tropical sprue is a progressive small intestine disorder presenting with: ____, ____ and _______ anaemia. Occurs in residents of the geographical areas of the ____ e.g. asia, caribbean, s.America islands) Aetiology is unknown but is likely to be ____

A
  • diarrhoea, steatorrhoea, megaloblastic
  • the tropics
  • infective
36
Q

Diagnosis of tropical sprue is based on demonstrating evidence of _____ esp. ___ and vit __ with a small bowel ___ showing …. also exclude infective causes of diarrhoea e.g. ______
Treatment is with __ __ and ____ for 3-6months and correction of ____ ___

A
  • malabsorption esp. fat and vitamin D
  • small bowel biopsy - shows fts similar to coeliac crypt hyperplasia and villous atrophy
  • Giardia intestinalis
  • folic acid and tetracycline
  • correct nutritional deficiencies
37
Q

What conditions may predispose to bacterial overgrowth of the small bowel?

A
  • anything causes stasis of intestinal contents due to abnormal motility
  • e.g. systemic sclerosis, structural abnormality e.g. previous SB surgery or a diverticulum
38
Q

In bacterial overgrowth of the small bowel the bacteria ______ ____ salts causing ____ and/or ____ and metabolise vitamin ___ which may result in deficiency. If clinical suspicion is high a therapeutic trial of abx is given, otherwise diagnosis is by what? Result?

A
  • bacteria deconjugate bile salts causing diarrhoea/steatorrhoea
  • metabolise vitamin B12
  • diagnosis by hydrogen breath test (measure hydrogen in exhaled air after oral lactulose)
  • result: early peak in breath hydrogen (abnormal) followed by the later colonic peak (normally present due to colonic bacteria metabolism of lactulose
39
Q

What does resection of the terminal ilium lead to malabsorption of?
There is increased _____absorption that can result in ____ stones.

A
  • vitamin b12 –> megaloblastic anaemia
  • bile salts which overflow -> colon, this causes secretion of water and electrolytes and diarrhoea, and increased oxalate absorption, which may result in oxalate stones
40
Q

Whipple’s disease is a rare disease caused by what bacteria? Features include: steatorrhoea, abdo pain, f___, l_____, a____ and n______ involvement. Small bowel biopsy shows ___ ___-___ (PAS)-positive m_____ which on EM are seen to contain the causative bacteria.

A
  • Tropheryma Whipplei
  • fever, lymphadenopathy, arthritis and neurological
  • periodic acid-Schiff + macrophages
41
Q

Treatment of Whipple’s disease is _______ for 1 year

A

Co-trimoxazole

42
Q

Crohn’s disease typically effects the ______ area. Small bowel disease causes ____ ___ usually with ___ ___. Can less commonly present with terminal ileum acute pain with ___ pain, mimicking _____. Colonic disease presents with _____, ____ and pain related to _____. In perianal disease there are anal ___, ____, ______ and ____ formation,

A
  • ileocaecal
  • abdo pain with weight loss
  • RIF pain, appendicitis
  • diarrhoea, bleeding, pain - defecation
  • anal skin tags, fissues, fistulae and abcess formation
43
Q

Ulcerative colitis presents with ____ often containing ___ and ___. Clinical course may be persistent ____, relapses and remissions or severe _____ colitits. +/-extra-intestinal manifestations.

A
  • diarrhoea, containing blood and mucus
  • persistent diarrhoea
  • fulminant colitis
44
Q

Give an example of extra-intestinal manifestations of IBD of the following:

  • Eyes:
  • Joints:
  • Skin:
  • Hepatobiliary:
  • Renal Calculi:
A
  • Eyes: uveitis, episcleritis, conjunctivitis
  • Joints: arthralgia, small joint arthritis, ank spond, inflamm back pain
  • Skin: erythema nodosum, pyoderma gangrenosum (necrotising ulceration of skin)
  • Hepatobiliary: fatty liver, sclerosing cholangitis, chronic hepatitis, cirrhosis, gallstones
  • Renal Calculi: oxalate stones in pts with SB disease or post-resection
45
Q

Medical management of IBD:

  • what is used for moderate/severe disease? dose? Reduced over approx _ weeks
  • what 2 medications are used to maintain remission in pts who require 2+ above med courses/year.
A
  • oral prednisolone 40mg/day, reduce over 8 weeks. Severe disease may need IV hydrocortisone
  • thiopurines e.g. azathioprine 2.5mg/kg/day or its metabolite 6-mercaptopurine 1.5mg/kg/day
46
Q
  • thiopurines e.g. azathioprine 2.5mg/kg/day or its metabolite 6-mercaptopurine 1.5mg/kg/day are used to maintain remission in IBD, name 2 sides effects of this medication class.
  • what enzyme involved in their metabolism must be measured on a blood sample before commencing the medication? Risk associated with it’s absence?
A
  • SEs: bone marrow suppression, acute pancreatitis, allergic reactions
  • TPMT (thiopurine methyltransferase) if absent, can’t metabolise drug(CI) as will –> pancytopenia
47
Q
  • thiopurines e.g. azathioprine 2.5mg/kg/day or its metabolite 6-mercaptopurine 1.5mg/kg/day are used to maintain remission in IBD, steroid are used for acute flares, what aspect of disease does metronidazole help with?
  • If a pt with Crohn’s is treatment resistant to steroids/thioprines, what IM drug can help acute/remission?
A
  • helps severe perianal crohn’s disease as a result of its antibacterial and immunosupressive action
  • rx resistant Crohn’s, give IM Methotrexate (also anti-TNF antibodies e.g. infliximab can be given)
48
Q

Oral ____ is first line for the treatment of ___ ulcerative colitis either left-sided or extensive in nature. For proctitis/proctosigmoiditis, the same medication is indicated _____. This medication is also used long-term to ___ ___. (Steroids and thiopurine are only given for pts who relapse frequently/have an inadequate response to ___)

A
  • 5-ASA (mesalazine)
  • rectally
  • maintain remission
  • 5-ASA
49
Q

2 SEs of 5-ASA

A
  • diarrhoea
  • Steven-Johnson’s syndrome
  • acute pancreatitis
  • renal impairment
50
Q

Acute severe colitis (!) should be managed as inpt with gastroenterologist + colorectal surgeon

  • Suggest 4 investigations
  • Suggest 3 rx
  • what 3 things should be closely monitored?
A
  • Ix: FBC, CRP, LFTs, serum albumin, U&Es
    • Blood cultures (gram - sepsis occurs)
    • Abdo X-ray: colonic dilatation ? transverse colon >5cm? mucosal islands
  • Rx: stop drugs that may precipitate colonic dilatation

-Monitor:

50
Q

Acute severe colitis (!) should be managed as inpt with gastroenterologist + colorectal surgeon

  • Suggest 3 investigations and poss findings of imaging and cultures
  • Suggest 3 rx
  • what 3 things should be closely monitored?
A
  • Ix: FBC, CRP, LFTs, serum albumin, U&Es
    • Blood cultures (gram - sepsis occurs)
    • Abdo X-ray: colonic dilatation ? transverse colon >5cm? mucosal islands
  • Rx: stop drugs that may precipitate colonic dilatation
    • give IV hydrocortisone 100mg 6-hrly, correct fluid/electrolyte imbalance
    • LMWH to reduce VTE risk
    • IV ciclosporin 2mg/kg over 24hrs or infliximab (if no response after 4days hydrocortisone)

-Monitor: stool chart for frequency, type and presence of blood, monitor vitals 4x/day+, daily bloods and abdo x-ray is admission film was abnormal

51
Q

Name 3 complications of IBD:

A
  • toxic dilatation of colon and perforation
  • stricture formation
  • abscess formation in Crohn’s
  • fistulae and fissures
  • Colon cancer
52
Q

Megaloblastic macrocytic anaemia = there are developing RBCs in the BM with delayed ___ ___ relative to that of the cytoplasm, the underlying mechanism is defective ___ synthesis which can also affect the WBCs (–>h____ n___) and platelets (–> th____)
Most common causes:

A
  • delayed nuclear maturation
  • defective DNA synthesis
  • hypersegmented neutrophils, thrombocytopenia
  • vitamin B12, folate of both deficiency
53
Q

Daily requirement of vitamin B12 is __. Only source is ____ products.

A
  • 1 microgram

- animal products

54
Q

Gastric acid and pepsin liberates b12 from protein complexes, and binds to a b12-binding receptor..
Free b12 is released by pancreatic enzymes, and is bound to ____ ___ which along with H+ ions, is secreted from gastric _____ cells. This complex is delivered to the ___ ___ where b12 is absorbed, it is transported by the carrier protein transcobalamin II . It is stored in the ___, which houses supply sufficient for ~___. B
ased on this suggest 4 causes of vitamin B12 deficiency:

A
  • intrinsic factor (IF)
  • parietal cells
  • terminal ileum
  • liver, 2 years+ supply
  • deficiency: vegans, pernicious anaemia, gastrectomy, IF deficiency, ileal resection/disease, tropical sprue, bacterial overgrowth, congenital transcobalamin II deficiency…
55
Q

What is pernicious anaemia?
-an _____ condition, with ____ gastritis (plasma and ____ cells infiltrate in the ____) with loss of ____ Cells and hence failure of ____ ___ production so vitamin __ _____.

A

-an autoimmune condition with atrophic gastritis (plasma and lymphoid cells infiltrate in the fundus) with loss of parietal cells and hence failure of intrinsic factor production and so vitamin B12 malabsorption.

56
Q

name some clinical features of pernicious anaemia (common in elderly women, fair haired, with other autoimmune conditions):

A
  • glossitis
  • angular stomatitis
  • mild jaundice (excess Hb breakdown)
  • neuro eg. polyneuropathy, subacute combined degen. of the cord)
  • dementia and visual disturbances from optic atrophy
  • gastric carcinoma risk
57
Q

subacute combined degen. of the cord if untreated presents with what? (caused by symmetrical damage to the peripheral nerves and posterior and lateral columns of the spinal cord).

A
  • progressive weakness
  • ataxia
  • paraplegia
58
Q

Vitamin B12 deficiency treatment is __ or __ vitamin B12, __mg/day

A
  • IM or oral

- 2mg/day

59
Q

Folate is found in __ ___ and offal eg. ___ & ___
It is absorbed in the ___ ___
Daily requirement is approx ___micrograms
Body stores last ~ __months

A

green vegetables, liver & kidney
Small intestine
100-200micrograms
4 months

60
Q

-main cause of folate deficiency is poor intake, investigation of choice is __ __ ___ (more accurate than serum folate in estimating tissue folate amounts)

A

-red cell folate (NR: 160-640mcgs)

61
Q

Folic acid deficiency treatment is oral folic acid __mg/day for __months

A

5mg/day, for 4months

62
Q

Most common cause of a raised MCV with macrocytosis with a normoblastic bone marrow is:

A

-alcohol excess in the UK

63
Q

Suggest causes of folate deficiency in the following categories:

  • poor intake
  • malabsorption
  • excess utilisation
  • drugs
A
  • poor intake: old age, poverty, alcohol excess, anorexia
  • malabsorption: coeliac’s, crohn’s, tropical sprue
  • excess utilisation: physiological - pregnancy, lactation, prematurity, pathological - chronic haemolytic anaemia, malignant and inflammatory illness, renal dialysis
  • drugs: phenytoin, trimethoprim, sulfasalazine, methotrexate
64
Q
  • vit D deficiency if profound leads to inadequate _____ of the osteoid framework –> ___ bones
  • so development of ____ in children and _____ in adults
  • main source of vit D is from ___ _____ following UVB sunlight exposure + small amount dietary
A
  • mineralisation -> soft bones
  • rickets or osteomalacia
  • skin photosynthesis
65
Q

5 RFs for vit D deficiency:

A
  • pigmented skin
  • use of sunscreen/concealing clothing
  • old age
  • institutionalisation
  • malabsorption
  • short bowel
  • renal disease
  • cholestatic liver disease
  • drugs: anti-convulsants, rifampicin, ART
66
Q

Clinical features of vit D deficiency:

A
  • proximal muscle weakness
  • low bone density on DEXA, osteopenia on X-rays
  • if severe –> hypocalcaemia, tetany and seizures
67
Q

Investigations for suspected vit D deficiency:

A
  • low vitamin D (25-hydroxyvitamin D3 less than 50nmol/L)
  • serum biochemistry: ALP often high, PTH high, phosphate and calcium can be normal or low
  • Radiology: defective mineralisation and Looser’s pseudofractures (low density bands running perpendicular to cortex)
68
Q

Treatment for vit D deficiency:

  • initial loading stage: dose oral vit D ____units per week for _ weeks or 2x IM 300,000units injection
  • subsequent maintenance dose: ~____units per day
    • give supplementary ___ ~1000mg/day
A
  • 50,000 units/week for 8 weeks
  • maintenance at ~1000units per day
  • also give Ca2+
69
Q

Vit B6 deficiency causes a mainly ___ ___
Can be precipitated during ____ therapy for TB in those who acetylate the drug slowly
Therefore treat with prophylactic pyridoxine (vit b6) 10mg daily with ____ drug treatment.

A
  • sensory neuropathy
  • isoniazid
  • isoniazid
70
Q

vit b12 deficiency causing subactue degeneration of the cord can present with:

A
  • distal sensory loss (posterior column esp)
  • absent ankle jerks
  • cord disease: exaggerated knee jerks, extensor plantar responses
71
Q

suggest a couple of principles for treating hepatic encephalopathy:

A
  • treat sepsis/dehydration
  • lactulose (reduced colonic pH, increased transit)
  • abx: rifaximin
  • (rarely: dietary protein restriction)
72
Q

What is the pathophys behind ascites?

NB: ..>12mmHg pressure in sinusoids is when risk of varices and ascites is likely

A
  • liver is scarred, pressure is higher, blood struggles to enter
  • back pressure causes veins to distend –> varices
  • this booling of blood in tributaries means it isn’t recirculated
  • body thinks its underfilled so activated RAAS
  • increased fluid and Na+ absorption –> ascites
73
Q

The Child Pugh Score gives 2 year estimated mortality for what condition?

A

Cirrhosis

74
Q

The Child Pugh Score gives 2 year estimated mortality for cirrhosis, name 4 parameters it takes into account?

A
  • high bilirubin
  • low albumin
  • ascites present
  • encephalopathy present
  • INR high
75
Q

West Haven criteria is used to grade what?

A

Encephalopathy severity

76
Q

ASUC (Acute Severe UC) Flare occurs in ~15% UC pts at the time of disease onset. what are 2+ of the sx? (known as Truelove and Witt’s Criteria)

A
  • > 6x stools/day
  • frequent blood in stools
  • Hb <75% normal
  • temp >37.5, HR >90bpm
  • ESR >30mm/h or CRP >30
77
Q

Acute Severe UC Flare what ix should you carry out? Suggest 4. NB: often 1st UC presentation..

  • e.g. what enzyme should you check
  • what electrolyte due to SE from some meds
  • why check lipids?
  • imaging?
A
  • TMPT enzyme (checks if pt has it to metabolise immunosuppressive meds)
  • check Mg2+ (SE of cyclosporin/tacrolimus) and lipid levels (lipids chelate meds, gives idea of med dose level)
  • screen for infection (as will be giving immunosuppressants
  • calprotectin (new pt confirms IBD, previous pt used to monitor response to rx)
  • abdo xray
  • endoscopy and biopsy after resuscitated pt
78
Q

For pain control in UC, opioids should be avoided. why? What is useful instead?

A
  • risk of ileus and perforation

- IV paracetamol, buscopan, entanox useful

79
Q

name 3 prophylaxis/protection things that can be used alongside the treatment of a UC flare

A

-LMWH prophylaxis (unless actively bleeding) as DVT->PE = highest mortality risk
-PPI prophylaxis
-ca2+/Vit D bone protection
-empirical abx e.g. metronidazole after stool cultures taken
-

80
Q

UC flare is treated with steroids initially, what route/dose/frequency?

A

-100mg IV hydrocortisone qds

81
Q

-100mg IV hydrocortisone qds is used to treat UC flare, what are the 2 medications that are the mainstays of salvage therapy in ASUC?

A
  • infliximab

- ciclosporin

82
Q

GI bleed management:

  • ABCDE
  • give
  • access insert
  • give IV ___ 1 unit ____ in each __
  • crossmatch __ units
  • ______ screen
  • put on _____ monitor
  • c______
A
  • give 02
  • access insert 2 large bore cannulae
  • give IV colloid 1 unit gelofusin in each arm
  • crossmatch 6 units
  • clotting screen
  • put on cardiac monitor
  • catheterise
83
Q

Blatchford Score is used pre-endoscopy to indicate who can be discharged post GI bleed, suggest 3 things it takes into account:

A
  • urea level
  • Hb level
  • systolic BP
  • pulse
  • meleana
  • syncope
  • HF
  • liver failure
84
Q

What does the Rockall Score use and what does it predict?

A
  • age
  • shock (HR and BP)
  • morbidity (e.g. HF. LF, RF, malignancy..)
  • post endoscopy: -diagnosis and major stigmata of the haemorrhage

-predicts rebleeding and mortality risk post upper GI bleed

Medicine (10 decks)

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