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Year 3 > Block 32 Week 3&4 > Flashcards

Block 32 Week 3&4 Flashcards

1
Q

Paget’s disease of the nipple?

A
  • 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.
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2
Q

ductal vs lobular carcinomas?

A
  • ductal carcinomas are more likely to present with a discreet lump but lobular carcinoma may be harder to detect
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3
Q

/PVD - lipodermatosclerosis

A

refers tochanges in the skin of the lower legs. It is a form of panniculitis (inflammation of the layer of fat under the skin)

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4
Q

UC?

A
  • begins in rectum and extends proximaly
  • Mostly pathological findings limited to mucosa and submucosa
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5
Q

Changes seen in UC?

A
  • Muscularis propria only affected in fulminant disease
  • Distorted crypt architecture
  • Crypt abscesses
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6
Q

Who does UC affect more?

A
  • less common in smokers
  • increased in caucasians, jews and females
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7
Q

UC peaks?

A

15-25 and 55-65

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8
Q

histological changes seen in IBD?

A
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9
Q

Symptoms of UC?

A
  • dominant Sx is diarrhoea
  • often associated w bleeding PR
  • often freq of small stools w urgency - inflamed rectum loses ability to distend and relax
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10
Q

Other findings of UC?

A
  • fatigue
  • malaise
  • weight loss
  • fever
  • tachycardia
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11
Q

CD can affect…

A
  • can affect anywhere from mouth to anus
  • transmural inflammation
  • granulomas but these are more common in submucosa
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12
Q

3 major patterns of CD?

A
  • ileeocaecal disease - 40%
  • confined to SI - 30%
  • confined to colon - 25%
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13
Q

Who does CD affect more?

A
  • Increased incidence in Caucasians, Jews and slight female preponderance
  • More common in smokers
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14
Q

peaks in CD?

A

15-25 and 55-65 years of age

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15
Q

Symptoms of CD?

A
  • diarrhoea
  • abdominal pain
  • weight loss
  • fatigue
  • low grade fever
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16
Q

CD activity index?

A
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17
Q

Harvey-bradshaw index?

A
  • score <4 = in remission
  • score 5-8 = moderate activity
  • score >8 = severe active disease
  • crohns
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18
Q

investigations?

A
  • flexible sigmoidoscopy/ colonoscopy and biopsies
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19
Q

radiology?

A
  • plain AXR - thumbprinting
  • CT
  • MR enterography
  • small bowel follow-through meal
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20
Q

test for IBD?

A
  • faecal calprotectin
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21
Q

Tx of IBD?

A
  • aminosalicyclates
  • mainly mesalazine
  • others: olsalazine, sulphasalazine, balsalazide
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22
Q

UC scan

A
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23
Q

stovepipe sign

A
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24
Q

aminosalicyclates r used for?

A
  • prevention of CRC
  • high dose to prevent remission
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25
Q

side effects of aminosalicyclates?

A
  • rashes
  • headache
  • diarrhoea
  • reversible infertility
  • intestinal nephritis
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26
Q

corticosteroid with a low first pass metabolism?

A

prednisolone

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27
Q

corticosteroids with a high first pass metabolism?

A

beclomethasone

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28
Q

nutrition for IBD?

A
  • elemental or semi elemental diets
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29
Q

immunomodulators for IBD?

A
  • Azathioprine
  • mercaptopurine
  • methotrexate
  • ciclosporin
  • mycophenolate
  • cytokine modulators
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30
Q

azathioprine?

A
  • Affects purine (A+G) synthesis
  • Decreases T-lymphocytes
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31
Q

side effects of azathioprine?

A
  • Side effects; up to 30% don’t tolerate
  • Dangerous neutropenia
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32
Q

mercaptopurine?

A
  • active metabolite of azathioprine
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33
Q

methotrexate?

A
  • antifolate
  • once weekly
  • fibrosis
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34
Q

Tx pathway of IBD?

A
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35
Q

Ciclosporin?

A
  • calcineurin inhibitor
  • CN activates T cells
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36
Q

rescue therapy in UC?

A

Ciclosporin

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37
Q

mycophenolate?

A
  • affects guanine (purine) synthesis in B and T lymphocytes
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38
Q

TNF-a?

A

activates NF-KB which induces apoptosis

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39
Q

drugs that inhibit TNF-a?

A
  • infliximab and adalimumab inhibit TNFa
  • used in severe crohns not responding to conventional drugs
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40
Q

Side effect of infliximab and adalimumab?

A
  • hepatosplenic T cell lymphoma
  • especially in young males
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41
Q

surgery for UC?

A
  • toxic megacolon/ acute colitis
  • failure to respond to medical therapy
  • colectomy is curative
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42
Q

surgery for CD?

A
  • High rate of disease recurrence after surgery
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43
Q

inducing remission in crohns?

A
  • offer monotherapy of a conventional glucocorticoid to induce remission
  • aminosalicyclates if ^ are CI or if the person can’t tolerate them
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44
Q

what should not be used to induce remission in CD?

A

azathioprine, mercaptopurine or methotrexate as monotherapy to induce remission

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45
Q

what to check for azathioprine?

A

TPMT activity

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46
Q

How is remission induced in UC?

A

in mild to moderate UC: aminosalicyclate

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47
Q

risk factors CD?

A
  • Fhx
  • smoking
  • prev GE
  • NSAIDs
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48
Q

Crohns vs UC?

A
  • 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
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49
Q

genetics in CD?

A
  • disrupted microflora-immune response
  • association between SNP in NOD2 (CARD15) gene and crohns
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50
Q

increased risk of CD…

A
  • smoking increases risk of CD but is protective in UC
  • western diets, abs and contraceptive use increases risk of CD
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51
Q

Perianal CD?

A
  • About a third of patients suffer from perianal CD - e.g. skin tags, fissures, fistulae, abcesses, or anal canal stenosis
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52
Q

Pathological changes of CD mneumonic?

A
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53
Q

CD - ? appearance of mucosa?

A
  • 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
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54
Q

microscopic changes in CD?

A
  • lymphoid hyperplasia and non-caseating granulomas
  • skip lesions and transmural ulceration
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55
Q

Sx of CD?

A
  • nausea and vomiting
  • fatigue
  • low grade fever
  • weight loss
  • abd pain
  • diarrhoea (+/- blood)
  • rectal bleeding
  • perianal disease
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56
Q

Signs of CD?

A
  • pyrexia
  • Dehydration
  • Angular stomatitis
  • Aphthous ulcers
  • Tachycardia
  • Hypotension
  • Abdominal pain, mass and distension
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57
Q

MSK manifestation of CD?

A
  • peripheral arthiritis
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58
Q

Skin changes in CD?

A
  • erythema nodosum
  • pyoderma gangrenosum
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59
Q

Erythema nodosum?

A
  • Erythema nodosum, a panniculitis, is characterised by reddened, raised, tender nodules.
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60
Q

pyoderma gangrenosum?

A

pyoderma gangrenosum presents with ulcerating nodules characterised by black (gangrenosum) edges and central pus (pyoderma).

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61
Q

eye changes in CD?

A
  • episcleritis
  • uveitis
  • conjuncitivitis
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62
Q

which EIM can precede intestinal disease?

A

apthous ulcers

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63
Q

primary sclerosing cholangitis in CD?

A
  • Primary sclerosing cholangitis may occur but is more common in UC
  • fatty liver disease and gallstones are more common
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64
Q

other extra-intestinal mainfestations of CD?

A
  • Renal calculi
  • Osteoporosis
  • B12deficiency
  • Pulmonary disease
  • Venous thrombosis
  • Anaemia
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65
Q

investigations of CD?

A
  • 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
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66
Q

Endoscopic Ix of CD?

A
  • colonoscopy - can do a tissue biopsy
  • upper GI endoscopy - biopsy needed to differentiate CD from other pathology
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67
Q

inducing remission in CD?

A
  • budesonide
  • systemic corticosteroids if the patient doesn’t resond to budesonide or if they have moderate-severe crohns e.g. prednisolone
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68
Q

Inducing remission in M-S CD?

A

immunosuppressive therapy e.g. azathioprine or methotrexate

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69
Q

CD - maintenance therapy?

A
  • thiopurines, methotrexate and biologics
  • considered in patients with recurrent flares, moderate-to-severe disease, or poor prognostic features (e.g. extensive disease).
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70
Q

thiopurines mechanism?

A

azathioprine and mercaptopurine - purine synthesis inhibition in lymphocytes
* check TPMT levels!!

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71
Q

what to check b4 methotrexate use?

A
  • check renal and liver function before use
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72
Q

side effects of methotrexate?

A
  • bone marrow suppression, hepatotoxicity, pulmonary toxicity
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73
Q

management of perianal disease ?

A
  • Control perianal sepsis(e.g. antibiotics)
  • Evaluation(e.g. MRI or examination under anaesthesia)
  • Surgical intervention(e.g. abscess drainage or seton for fistula)
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74
Q

surveillance colonoscopy?

A
  • 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
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75
Q

UC is more common in which populations?

A

Jewish

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76
Q

environmental factors contributing to UC?

A

milk consumption, bacterial microflora alteration and medications like OCP and NSAIDs

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77
Q

Pattern of UC?

A
  • UC affects the rectum (proctitis) first and then extends proximally to the colon
  • most patients (50%) suffer from proctitis only
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78
Q

pancolitis?

A

inflammation of the entire colon

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79
Q

what does pancolitis put you at risk of?

A
  • backwash ileitis
  • reflux of colonic contents into the distal few centimetres of the ileum through theileocaecal valve
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80
Q

macroscopic changes of UC?

A
  • continuous inflammation that extends proximally along the colon
  • may be inflammatory polyps
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81
Q

Microscopic changes of UC?

A
  • crypt abcesses and goblet cell depletion
  • increased inflammatory infiltration into the lamina propria, which is largelyneutrophilic.
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82
Q

Hallmark of UC?

A

bloody diarrhoea/ rectal bleeding

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83
Q

Symptoms of UC?

A
  • Weight loss
  • Fatigue
  • Abdominal pain
  • Loose stools
  • Rectal bleeding
  • Tenesmus(incomplete emptying)
  • Urgency
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84
Q

Signs of UC?

A
  • Febrile
  • Pale
  • Dehydrated
  • Abdominal tenderness
  • Abdominal distension/mass
  • Tachycardic, hypotensive
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85
Q

Major complication of UC?

A
  • toxic megacolon is a major complication
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86
Q

TMC?

A

medical emergency - toxic, non obstructive dilatation of the colon

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87
Q

When should TMC be suspected?

A
  • UC + abdominal distension and tenderness -> suspect TMC
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88
Q

Systemic symptoms suggestive of TMC?

A
  • Fever
  • Tachycardia
  • Hypotension
  • Dehydration
  • Altered mental status
  • Biochemical abnormalities(e.g.leukocytosis,anaemia, andelectrolyte derangements)
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89
Q

most common manifestation of UC?

A

ARTHIRITIS - can be simple peripheral arthititis or spondylarthropathy e.g. ankylosing spondyliti

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90
Q
A
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90
Q
A
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91
Q

Eye related manifestation of UC?

A
  • uveitis is strongly assoc w UC
  • episcleritis
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91
Q

other MSK features of UC?

A

osteopenia/ osteoporosis, clubbing of hands and feet

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92
Q

mouth changes seen in UC?

A

Apthous ulcers

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93
Q

skin changes assoc w UC?

A

Erythema nodosum and pyoderma gangrenosum

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94
Q

hepatobiliary manifestation of UC?

A
  • fatty liver disease and autoimmune liver disease
  • most commonly: primary sclerosing cholangitis
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95
Q
A
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96
Q

Link between PSC and UC?

A
  • up to 95% of patients w PSC have UC - suspect PSC in any UC patient who has an isolated rise in ALP
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97
Q

haem manifestations of UC?

A
  • anemia
  • thromboembolism
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98
Q

Ix of UC?

A
  • Stool microscopy, culture & sensitivities
  • Ova, cysts and parasites
  • C. difftoxin(CDT)
  • Faecal calprotectin(marker of intestinal inflammation)
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99
Q

bloods for UC?

A
  • FBC
  • LFTs
  • U&Es
  • magnesium
  • autoantibodies - e.g. p-ANCA
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100
Q

Imaging for UC?

A
  • abd X ray for looking at dilatation of the bowel and perforations
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101
Q

Endoscopy for UC?

A
  • colonoscopy
  • biopsies for histological assessment
  • sigmoidoscopy can be used as an alternative
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102
Q

Truelove and Witts?

A
  • scores UC severity
  • into mild, moderate and severe
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103
Q

Inducing remission: mild to moderate UC?

A
  • 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.
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104
Q
A
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104
Q
A
105
Q

inducing remission for severe UC?

A
  • 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
106
Q

Maintenance therapy for UC?

A
  • thiopurines
  • biologics
  • in patients who don’t respond to remission therapy or steroid dependent or >2 flares in a 12 month period
107
Q

surgery for UC?

A
  • principle surgical option in UC is proctocolectomy followed by ileal pouch anal anastomosis (IPAA) or end ileostomy.
108
Q

management of acute severe UC?

A
  • High dose corticosteroids IV with PPI
  • VTE prophylaxis: LMWH
  • antibiotics: broad spectrum
  • hydration and nutrition
109
Q

How can an upper GI bleed present?

A
  • 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
110
Q

causes of UGIB?

A
111
Q

Assessment of an UGIB?

A
  • FBC, PT and PTT
112
Q

If the patient is unstable with an UGIB…

A
  • O2
  • fluid of 500ml in less than 15 min
  • continous monitoring - nEWS
  • catheter and monitor urine output
113
Q

UGIB - resus - transfusion?

A
  • for patients w massive bleeding
  • prothrombin complex concentrate or vitamin K -> Warfarin
  • recomb factor 7a when other methods fail
114
Q

warfarin reversal?

A

prothrombin complex concentrate or vitamin K

115
Q

2 methods used to assess risk in an UGIB?

A
  • Glasgow-Blatchford score
  • Rockall score
116
Q

Rockall score?

A
  • incorporates clinical and endoscopic findings
  • evaluates risk of re-bleeding or death
117
Q

history with an UGIB?

A
  • ulcers
  • recent trauma
  • liver disease
  • varices
  • alcoholism - MWT or oesophageal varices
  • vomiting
118
Q

UGIB history - medications?

A
  • medications that interefere w coagulation - NSAIDS, aspirin, dipyridamol
119
Q

physical exam w an UGIB?

A
  • jaundice
  • ascites and other signs of liver disease
  • tumour mass
  • bruit
120
Q

NG aspiration?

A
  • clear and bile stained - can have bleeding distal to pylorus
  • bloody
121
Q

Tx of an upper GIB is dependent on

A

whether it’s variceal or non variceal bleeding

122
Q

Cirrhosis/ variceal bleeding Tx?

A
  • IV Terlipressin - vasopressin analogue
  • or somatostatin/ octreotide
  • ECG >65 yrs
123
Q

Terlipressin caution?

A
  • Be careful w Telipressin in patients w IHD or PVD as it can worsen it
124
Q

what else should be prescribed for an UGIB patient - variceal bleeding?

A
  • IV ab as infections more common in ppts w cirrhosis and UGI bleeding
  • 7 day broad spectrum abs
125
Q

Other things to do during management of UGIB?

A
  • fluid resus
  • coagulopathy common and should be addressed
126
Q
A
126
Q
A
127
Q

method of stopping bleeding for an UGIB?

A
  • 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
127
Q

endoscopy with an UGIB?

A
  • endoscopy: looking for oesophageal gastric varices
  • Gastroesophageal varices occur in ~30% of cirrhosis patients
128
Q

Methods of stopping oesophageal varices from bleeding?

A
  • band ligation - best option (during endoscopy)
  • stent insertion - applies pressure
  • TIPS (transjugular intrahepatic portosystemic shunts) if bleeding is not controlled by band ligation
128
Q

when does endoscopy be done for an UGIB?

A
  • endoscopy should be done immediately after resus for unstable patients w severe bleeding
  • all other patients with UGI bleeding need one within 24hrs
129
Q

how to stop gastric varices from bleeding?

A
  • endoscopic injection of cyanoacrylate (sclerotherapy)
  • TIPS (shunt) if bleeding isn’t controlled
130
Q

main cause of non-variceal UGIB?

A

PUD

131
Q

CT angiography for UGIB?

A
  • for patients who are haemodynamically Unstable
  • fastest and least invasive method
  • catheter angiography -> source of bleeding can be embolised
132
Q

If the source of bleeding can’t be identified with CT angiography?

A

immediate OGD

133
Q

Sugery for UGIB?

A
  • last resort
  • shock
  • failure of endoscopic manegement
  • recurrent haemorrhages after intial stabilization
  • continued slow bleeding with a transfusion
134
Q

methods of dealing with non variceal bleeding - during endoscopy?

A
  • Adrenaline injection plus
  • thermal modalities e.g. heater probe
  • mechanical modality (clips)
  • haemostatic powders
135
Q

Other management methods of non variceal bleeding?

A
  • PPIs
  • H pylori eradication
  • antithrombin therapy interupted
136
Q

How are oral AC reversed?

A

inhibitors (idarucizumab or andexanet)

137
Q

when should AC be restarted for low vs high thrombotic risk patients?

A
  • low thrombotic risk - restart warfarin in 7 days
  • high thrombotic risk - LMWH after 48 hrs
138
Q

Re-bleeding?

A
  • related to size and location - posterior duodenum carries a higher risk
  • repeat endoscopy for patients who re-bleed
139
Q

MWT?

A
  • Lower part of oesophagus/ lesser curvature
  • lesion usually stops bleeding w/o therapy
140
Q

Acute haemorrhagic gastritis is when?

A
  • related to stress or medications like NSAIDs
  • whole gastric mucosa bleeds
141
Q

AHG treatment?

A
  • stop NSAIDs
  • give H2 receptor blockers, PPIs
  • anti- H pylori therapy
142
Q

if bleeding doesn’t stop w AHG then give?

A

IV somatostatin

143
Q

last resort for AHG?

A

gastrectomy

144
Q

lower GI bleeding?

A
  • distal to LoT
  • less frequent than UGI bleeding
  • majority of cases from colon, and is more common in men
145
Q

how to distinguish between an upper and lower GI bleed?

A

NG aspiration

146
Q

causes of a LGIB

A
147
Q

Oakland score?

A
  • LGIB
  • helps u decide if the patient needs admittance
  • less than 8 means the patient can be seen as an outpatient
148
Q

Tx pathway for a LGIB?

A
149
Q

Ix of a LGIB?

A
  • haemodynamic instability may indicate an upper GI bleed so
  • CT angiography first
  • if inconclusive -> OGD
150
Q

LGIB - if a colonoscopy isn’t feasible then?

A
  • If bleeding volume means that colonoscopy is not feasible or is ineffective -> selective mesenteric arteriography
151
Q

Tx of LGIB?

A
  • vasopression infusion and embolization of bleeding vessels
152
Q

Acute UGIB?

A
  • Medical emergency
  • divided into variceal and non-variceal
  • death from exsanguination is uncommon
153
Q

Summary for management of an UGIB?

A
  • history and exam
  • resus
  • investigation
154
Q

Common causes of an UGIB?

A
  • PUD
  • gastritis
  • gastric ulcer
  • varices
  • cancer - ooesephageal or gastric, duodenal is rare
155
Q

Things to ask in an UGIB history?

A
  • volume
  • type of blood loss
  • fresh haemetemsis
  • coffee ground vomit
  • maleana
  • fresh PR blood
156
Q

oesphagitis?

A

heartburn, occassionaly chest pain often worse on lying down

157
Q

gastritis?

A

dyspepsia - e.g. epigastric often burning pain

158
Q

gastric or duodenal ulcer?

A

dyspepsia, nausea, vomiting, weight loss

159
Q

varices?

A

history of liver disease, excess alcohol

160
Q

cancer?

A

malaise, weight loss, vomiting, early satiety

161
Q

meds history for UGIB?

A

NSAIDs, steroids, AC meds including warfarin

162
Q

Examination for an UGIB?

A
  • pulse, BP, pallor, cap refill
  • postural drop
  • signs of anemia
  • stigmata of CLD
  • working out if the patient has shock
163
Q

Ix for UGIB summary?

A
  • 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
164
Q

resus for a bleed?

A
  • IV access
  • catheter
  • fluids
  • blood
165
Q

initial management of a non variceal bleed?

A
166
Q

initial management of variceal bleeds?

A
  • higher morbidity and mortality
  • terlipressin - splenic vasoconstrictor, reduces portal hypertension
  • IV broad spectrum ab
167
Q

chronic LGIB - history?

A
  • type of blood
  • change in bowel habit
  • mucus
  • abd pain
  • weight loss
  • eye, joint or skin symptoms
168
Q

overt GI bleed?

A
  • if its on wiping - most likely an anal cause like haemorrhoids
169
Q

anal causes of chronic GI bleeding ?

A
  • piles
  • fissure
  • carcinoma
170
Q

rectal causes of chronic GI bleeding?

A
  • carcinoma
  • inflammation
  • polyps
171
Q

colonic causes of chronic GI bleeding?

A
  • cancer
  • diverticular disease
  • inflammation
  • polyps
  • angiodysplasia - fragile blood vessels
172
Q

Severe overt lower GI bleeding is a ?

A

med emergency

173
Q

assessment of a lower GI bleed

A
174
Q

examination for lower GI bleeding?

A
175
Q

investigations for LGIB?

A
  • bloods
  • colonoscopy
  • alternatives - barium enema, CT colonography
176
Q

What does chronic occult GI bleeding cause?

A
  • causes iron deficieny anaemia
  • microcyctic, hypochromic anaemia
  • Fe can be falsely raised by inflammation
  • faecal occult blood testing
177
Q

diagnoses of upper GI Bleeds

A
178
Q

fresh rectal bleeding commonly results from?

A
  • fresh rectal bleeding commonly results from a source in a rectum or colon but large upper GI bleeds can also present w haematochezia
179
Q

diverticulosis?

A
  • most common cause of lower GI bleeding
  • increases w age
180
Q

Diverticular disease vs diverticulitis?

A
  • Whilst diverticular diseasebleeds are often painless, any bleeds secondary todiverticulitiscan often bepainful, due to the localised inflammation.
181
Q

haemorrhoids?

A
  • 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.
182
Q

RF of CRC?

A
  • Family history
  • Hereditary syndromes - lynch syndrome and FAP
  • Inflammatory bowel disease
  • Ethnicity - white
  • Radiotherapy
  • Obesity
  • Diabetes mellitus
  • Smoking
183
Q

CRC most commonly affects?

A
  • Most commonly affects left side of the colon
  • mets mostly to liver
184
Q

which cancers mets to the lung?

A
  • 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
185
Q

Summary of CRC mets?

A

left sided -> liver

rectal -> lung

also peritoneum, brain and bone

186
Q

pres of CRC?

A
  • 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.
187
Q

Symptoms of CRC?

A
  • Change in bowel habit
  • Weight loss
  • Malaise
  • Tenesmus
  • PR bleeding
  • Abdominal pain
188
Q

Signs of CRC?

A
  • pallor
  • abd mass
189
Q

signs of metastatic disease from CRC?

A
  • Hepatomegaly
  • Jaundice
  • Abdominal pain
  • Lymphadenopathy
190
Q

Right sided CRC?

A
  • right sides lesions tend to develop as masses arising from a dyplastc polyp -> iron deficieny anaemia
191
Q

Left sided CRC?

A
  • left sided lesions - grow circumferentially creating an apple core appearance -> narrowing of lumen and symptoms of changes in bowel habit and obstruction
192
Q

Right vs left sided CRC?

A
  • right: iron def anemia
  • left: apple core apperance -> obstruction
193
Q

Screening for CRC?

A
  • FIT test
  • 60-74
194
Q

RF for an UGIB?

A
  • NSAIDs
  • Anticoagulants
  • Alcohol abuse
  • Chronic liver disease
  • Chronic kidney disease
  • Advancing age
  • Previous PUD orH. pyloriinfection
195
Q

macronutrients (3)?

A
  • carbs
  • proteins
  • lipids
196
Q

micronutrients?

A
  • minerals
  • vitamins
  • trace elements
197
Q

functions of proteins?

A
  • 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
198
Q

lipids?

A
  • Most plentiful lipid in your body
  • Provide more than twice as much energy as carbohydrates or protein
199
Q

steroids?

A
  • such as cholesterol, bile salts, adrenocortical hormones, sex hormones
200
Q

eiconasoids?

A
  • Lipids derived from arachidonic acid
  • 2 principle subclasses are prostaglandins and leukotrienes
  • Involved in inflammatory reactions, gastric protection, airway calibre, clotting
201
Q

water soluble vitamins?

A

▪Vitamin B1, B2, B6, B12, C, Folate and Niacin
▪Absorbed along with water in the GI tract

202
Q

fat soluble vitamins?

A

▪Vitamin A, D, E, K
- Absorbed with other dietary lipids in small intestine – dependent on bile salts

203
Q

antioxidant vitamins?

A

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

204
Q

what must equal to maintain weight?

A
  • intake and output must equal to maintain weight
205
Q

vitamin deficienies table

A
206
Q

basal energy expenditure?

A

rest energy required for metabolism

207
Q

nutritional assessments?

A
  • BMI - body mass index (weight (kg)/height (m2))
  • Mid - arm circumference = muscle mass
  • Skin - fold thickness = body fat
208
Q

enteral feedinf?

A

▪Oral
▪Tube feeding

  • preferred as lack of enteral feeding atrophies the intestinal epithelium + inc risk of sepsis
209
Q

when is enteral feeding used?

A
  • Cannot eat sufficient food
  • Unconsciousness (tube feed)
  • Dysphagia (tube feed)
  • Loss of nutrients from fistulas/stomas
  • Major illness/postoperatively
210
Q

tube feeding?

A
  • 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
211
Q

complications of tube feeding?

A

insertion of tube into lungs, aspiration, nasal erosion, refeeding syndrome

212
Q

enterostomy feeding?

A
  • feeding for more than 4-6 wks
  • usually inserted using PEG
213
Q

risks of enterostomy feeding?

A

perforation, peritonitis, buried bumper syndrome, infected site, aspiration

213
Q

parenteral feeding?

A

IV

214
Q

when is parenteral feeding used?

A
  • for those w unsafe oral or enteral intake
  • non-functional, inaccessible or perforated GI tract
  • requires use of solution containing macros and micros
215
Q

how can parenteral feeding be done?

A
  • short term feeding - peripheal cannula if no need for CV access
  • PICC line
  • central venous catheters
216
Q

picc line?

A

peripherally inserted central catheter via basilic vein

217
Q

central venous catheters?

A

subclavian line

218
Q

what is common with a peripheral cannula for parenteral feeding?

A

thrombophlebitis

219
Q

risks of central venous catheter insertion?

A
  • Catheter related infection, blockage, venous thrombosis, fatty liver disease
220
Q

refeeding syndrome?

A
  • too rapid intro of feed following starvation
  • can occur after enteral or parenteral feeding
221
Q

why does refeeding syndrome occur?

A
  • 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.
222
Q

RS - when phosphate levels fall?

A

rhabdomyolosis, leucocyte dysfunction, respiratory/cardiac failure, muscle weakness, seizures, coma.

223
Q

when does RS occur?

A

usually around day 4 of refeeding

224
Q

Patients at high risk of refeeding syndrome include:

A
  • 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
225
Q

intestinal failure?

A
  • intestinal failure is characterised by inadequate intake and absorption of nutrients
226
Q

type 1 intestinal failure?

A
  • post-op ileus or small intestinal obstruction, usually requires short term nutrition
227
Q

type 2 intestinal failure?

A
  • type 2 IF: greater than 28 days
  • typical patients: complex CD, intestinal fistula, abd sepsis
228
Q

type 3 intestinal failure?

A
  • type 3: generally irreversible
  • usually occurs as a consequence of massive bowel resection leading to short bowel syndrome
229
Q

features of malabs - caloric?

A

weight loss with normal appetite

230
Q

features of malabs - fat?

A

pale, greasy, offensive diarrhoea

231
Q

features of malabs - protein?

A

edema, muscle atrophy, amenorrhea

232
Q

features of malabs - carbs?

A

abd bloating, diarrhoea, flatus

233
Q

features of malabs - B12?

A
  • macrocytic anemia
  • degeneration of SC
234
Q

Features of malabs - folic acid?

A
  • folic acid: macrocytic anemia
235
Q

features of malabs - vitamin B?

A

glossitis, stomatitis, acrodermatitis, cheliosis

236
Q

features of malabs - iron?

A
  • iron: microcytic anemia
237
Q

features of malabs - calcium and vitamin D?

A

osteomalacia, tetany

238
Q

Features of malabs - vitamin A?

A

night blindness, follicular hyperkeratosis

239
Q

features of malabs - vit K?

A

bleeding

240
Q

CF of malabs

A
241
Q

rationale for and practical implications of a gluten-free diet?

A
  • coeliac disease
  • demeatitis herpetiformis
  • gluten ataxia
  • wheat allergy
242
Q

Haemorrhoids?

A
  • H: piles
  • painless rectal bleeding
  • usually on wiping
243
Q

fissures?

A
  • fissues: tear in the lining of the anus or anal canal
  • peak 15-40 yrs old
244
Q

causes of fissures?

A
  • commonly due to local trauma from constipation, diarrhoea, anal sex
245
Q

management of rectal bleeding?

A
  • low hb: transfusion
  • reversal of anticoagulation
  • endoscopic haemostatis methods
  • arterial embolisation
246
Q

Endoscopic haemostasis methods?

A
  • 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)
247
Q

arterial embolisation?

A

possible in those with an identified bleeding point

248
Q

UC vs CD pain?

A
  • 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
249
Q

UC vs CD

A
250
Q

uc VS CD

A
251
Q

marker

what is seen more commonly in UC?

A

P-ANCA

252
Q

Mild to moderate acute ulcerative colitis is treated with:

A
  • Aminosalicylate (e.g., oral or rectal mesalazine) first-line
  • Corticosteroids (e.g., oral or rectal prednisolone) second-line
253
Q

Severe acute UC is treated w:

A

Intravenous steroids (e.g., IV hydrocortisone) first-line

254
Q

Other options for severe acute ulcerative colitis include:

A
  • Intravenous ciclosporin
  • Infliximab
  • Surgery
255
Q

Options for maintaining remission in ulcerative colitis are:

A
  • Aminosalicylate (e.g., oral or rectal mesalazine) first-line
  • Azathioprine
  • Mercaptopurine
256
Q

Inducing remission in an exacerbation of Crohn’s disease is with:

A
  • Steroids (e.g., oral prednisolone or IV hydrocortisone) first-line
  • Enteral nutrition as an alternative, particularly where there are concerns about steroids affecting growth
257
Q

Other ways of inducing remission in CD when steroids alone don’t work?

A
  • Azathioprine
  • Mercaptopurine
  • Methotrexate
  • Infliximab
  • Adalimumab
258
Q

Maintaining remission in CD?

A

First-line for maintaining remission in Crohn’s is with either:

  • Azathioprine
  • Mercaptopurine

Methotrexate alt

259
Q
A

Year 3 (45 decks)

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