The Digestive System - Small Bowel/ Nutrition, Pancreas and GI Bleeding Flashcards

1
Q

Developmental diseases in small bowel

A

Atresia
Stenosis
Duplications
Meckel diverticulum

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2
Q

Atresia of small bowel

A

Complete occlusion of intestinal lumen or lack of continuity of ends

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3
Q

Stenosis of small bowel

A

Stricture of the intestinal lumen secondary to incomplete intraluminal diaphragm

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3
Q

Stenosis of small bowel

A

Stricture of the intestinal lumen secondary to incomplete intraluminal diaphragm

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4
Q

Duplications of small bowel

A

Enteric cysts that may communicate w/ the intestinal lumen (most common in ileum)
May cause gastric mucosa and cause peptic ulcer

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5
Q

Meckel divertiuclum

A

Partial persistence of the vitelline duct, 60-100cm before the ileocaecal valve, w/ all layers of intestinal or gastric mucosa

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6
Q

Development issues of large intestines

A

Abnormal positioning of colon in Abdominal cavity e.g. caecum in LUQ
May give rise to volvulus

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7
Q

Pathophys of coeliac disease

A

Reaction to gliadin
Gliadin binds to enterocytes, creating a hybrid antigen to which immune system responds

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8
Q

What is gliadin

A

Protein found in the gluten of wheat, rye and barely (oats are okay)

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9
Q

Condns causing intestinal obstruction

A

Herniation
Adhesions
Volvulus
Intussusception

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10
Q

Which autoantibodies are seen in coeliac disease

A

Reticulin
Endomysial transglutaminase
Most sensitive and spp - IgA endomysial ab

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11
Q

Histology seen in coeliac disease

A

Viili disappear along the small bowel and the crypts deepen (hyperplasia)
Activated cytotoxic killer T-cell invade epithelium

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12
Q

Endoscopy findings for coeliac disease

A

Abnormally smooth gut mucosa

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13
Q

Px of coeliac - GI

A

Diarrhoea and steatorrhea
Abdo pain
Bloating
Wt loss

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14
Q

Px of coeliac - extra intestinal

A

Anaemia (malabsorption of iron and folate)
Osteoporosis - Ca and vit D malabsorption
Mouth ulcers
Dermatitis herpetiformis
Infertility

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15
Q

Px of coeliac in young children

A

Diarrhoea and/ or constipation
FTT
Vomiting
Abdo protrusion

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16
Q

Epidemiology of coeliac

A

Prevalence is 1/100
Px at any age but small peak in 1-3yrs (when first exposed to gluten)

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17
Q

Risk factors for coeliac

A

Fhx
AI disease - T1DM, thyroid disease
IgA deficiency

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18
Q

Natural hx of coeliac

A

10% of pts eventually get 1’ lymphoma if not properly treated
Osteoporosis

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19
Q

Dx of coeliac

A

Anti-tTG IgA (can also use IgG)
Endomysial ab is more spp but less sensitive
Bx via upper endoscopy to confirm dx
HLA-DQ2/8 typing if dx unclear

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20
Q

What is is necessary for accurate coeliac ix

A

Pts should stay on gluten while under ix to ensure test accuracy

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21
Q

Extra tests for coeliac

A

FBC - anaemia
LFT - may see raised transaminases
Ca and albumin (low)
DEXA
Skin bx for dermatitis herpetiformis

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22
Q

Screening for coeliac

A

1st degree relatives w/ coeliac

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23
Q

Causes of villous atrophy

A

Whipple’s
Lymphoma
Peptic duodenitis
Acid damage to duodenum

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24
Mx of coeliac
Life-long gluten free diet Replace micronutrients if deficient
25
Monitoring for coeliac disease
Annual review DEXA 1-3yrs after dx, and at menopause (55 in men)
26
IBD
Infl bowel disease Incl Crohn's disease and ulcerative colitis
27
What is Crohn's disease
Systemic disease non which ulcers and fibrosis, often w/ granulomas, affect portion of the alimentary canal
28
Crohn's disease morphology
Transmural involvement (all three layers) Ulcers on mucosa - fissures and cobble stoning Wall is oedematous w/ narrowed lumen Fat tends to 'creep around' mesentery Increased goblet cells
29
Crohn's disease lesions
Lesions are sharply demarcated from normal regions (skip lesions) Most common site of involvement is terminal ileum
30
What are pt's w/ CD prone to, since any portion of the gut can be involved
Apthae in mouth Scleorosing cholangitis Perianal abscesses, fistulas and fissures
31
Systemic sx seen in CD
Same as infl enteropathy Arthritis Uveitis Erythema nodosum, pyoderma gangrenosum If HLA-B27, ankylosing spondylitis
32
Epidemiology of IBD
Prevalence is 1/600 in CD and 1/1000 in UC Bimodal onset: 15-30yrs and 60-80
33
Sx of CD
Diarrhoea - bloody in 25% RLQ pain Wt loss Fever Fatigue More likely to present acutely
34
Signs of CD
Perianal = abscesses, fistula, tags RIF mass from infl of terminal ileum
35
Hepatobilary signs of CD
Gallstones C/c hepatitis, NAFLD and cirrhosis
36
Risk factors for CD
Smoking Fhx NOD2 mutation Caucasians
37
Ix for IBD - blood's
Increased CRP/ ESR, platelets (low albumin) Anaemia LFT for associated hepatobiliary disease U&Es for nutritional deficiencies
38
Ix for IBD - stool
Culture to rule out infection Faecal calprotectin - marker of infl C. diff - poor prognostic marker
39
Endoscopy for CD
Skip lesions Cobblestoning appearance Apthous ulcers Bx - transmural disease w/ granulomas
40
Small bowel enema - radiological findings for CD
Strictures - Kantor's string sign Rose thorn ulcers Proximal bowel dilation
41
Complications of IBD
Obstruction - CD Fistula - CD Colorectal cancer - higher in UC than CD
42
Inducing remission in CD attack
Methylpred IV 3/7 then pred PO 2/52 If refractory: add azathioprine or add/ switch biologic May give enteral nutrition therapy
43
Indications for treatment for CD
Freq relapses >2 steroid courses per yr Relpase <6/52 after stopping steroids
44
Drugs for maintaining remission in CD
Azathioprine or mercaptopurine May give MTX or biologics
45
Use of biologics in treating CD
Can be used for induction and maintenance for refractory severe disease Examples incl infliximab or adalimumab
46
Drugs given for symptomatic relief of CD
Loperamide and an anti-spasmodic, but not during attacks PPi for upper GI problems
47
Drugs given for perineal disease in CD
Oral metronidazole and/ or cipro Topical mesalazine Seton insertion for fistulae
48
Indications for surgical mx of CD
Needed in 70% Medically refractory Obstruction or perforation Growth failure
49
What may extensive small bowel resection in CD cause
Short bowel syndrome
50
Features of short bowel syndrome
Diarrhoea Steatorrhea Electrolyte abnormalities Malnutrition incl vit deficiency Wt loss Fatigue
51
Post-op recurrence of CD
30% in 1yr Risk increased if smoker
52
Long-term surgical complications of CD procedures
Vit B12 deficiency, esp if >20cm removed Bile salt malabsorption
53
Ulcerative colitis
IBD beginning in rectum and may extend to caeca, Continuous pathology - NO skip lesions
54
Pathophys of UC
Continuous area of infl in rectum Inflammable, friable mucosa w. crypt changes, reduced goblet cells and psuedopolyps
55
Intestinal sx of UC
Diarrhoea - bloody in 25% Lower abdo cramps Rectal sx - urgency, tenesmus More likely to present gradually
56
Sx of UC attacks
Tender distended abdo Fever Anorexia and wt loss May be triggered by infection
57
Non-intestinal sx of UC
Uveitis Apthous ulcers (less than CD) Clubbing Erythema nodusum Pyoderma gangrenous Entero arthritis
58
Hepatobiliary sx of UC
PSC C/c hepatitis, NAFLD and cirrhosis
59
Shared sx in IBD
Diarrhoea Arthritis Erythema nodosum Pyoderma gangrenosum Uveitis
60
Toxic megacolon
Complication of severe colon disease or infection - UC more likely Bowel wall becomes paralysed due to lumen filled w/ toxins - increased release of NO, from inflamed bowel wall Transverse colon dilation of >6cm
61
Risk factors for UC
Not smoking - less common in smokers Fhx HLA-B27
62
Endoscopy for UC
Sigmoidoscopy usually sufficient Looking for mucosal granularity Bx - crypt abscesses, loss of goblet cells
63
Mx of mild to moderate attack of UC
1st line - PR mesalzine if distal (descending colon, rectosigmoid) and PO if proximal 2nd line - Add pred
64
Criteria for severe attack of UC
>6 stools/ day, usually bloody Plus one of: severe, tachycardia, anaemia, ESR > 30
65
Mx of severe attack of UC
Admit and give IV steroids Then ciclosporin, biologic or subtotal colectomy if refractory
66
Drugs to maintain remission in UC - mild/moderate attacks
Mesalazine PO +/or PR if rectosigmoid
67
Most serious complication of UC
Adenocarcinoma of the colon - screen w/ colonoscopy every 3yrs, starting 10yrs after dx Colectomy is probs advisable if mucosal cells begin to look dysplastic Cancer risk continues even if disease is quiescent, approaches 100% in 30 yrs
68
Backwash ileitis
Involvement of the terminal ileum in UC Small bowel is spared
69
Drugs to maintain remission in UC - severe attacks
Azathioprine or mercaptopurine PO
70
Drugs given for refractory moderate-severe disease
Anti-TNF alpha drugs JAK inhibitors - tofacitinib
71
Indications for surgery for UC
Medically-refractory c/c or a/c UC Toxic megacolon or perforation Dysplasia or malignancy
72
Complications of a/c surgery for UC
Sepsis Poor healing due to high dose steroids
73
Complications of UC
Perforation Toxic megacolon Colorectal cancer VTE
74
Arterial supply of cervical oesophagus
Inferior thyroid artery
75
Venous drainage of cervical oesophagus
Inferior thyroid vein
76
Arterial supply of thoracic oesophagus
Oesophageal branches of the thoracic aorta
77
Venous drainage of thoracic oesophagus
Azygous system
78
Arterial oesophagus of abdominal oesophagus
L gastric artery
79
Venous drainage of abdominal oesophagus
Portal system via L gastric vein
80
What vertebral level os the gOJ found at
T11
81
Blood supply of fundus
Short and posterior gastric branches of splenic artery
82
Blood supply of pylorus
Gastroduodenal artery, branch of common hepatic artery
83
Venous drainage of stomach
Vein run parallel to the arteries L & R gastric arteries drain into portal venous system The short gastric vein and the L & R gastro-omental veins drain in the superior mesenteric veins
84
What key structure is housed in the duodenum
Ampulla of Vater
85
Is there a clear demarcation between the jejunum and ileum
No Ileum is thicker and has more 'fatty mesentery' Ileum contains more LNs and Peyer's patches
86
Arterial supply of duodenum
Proximal to major duodenal papilla - (branches of coeliac trunk) gastroduodenal artery and superior pancreaticoduodenal artery Distal to the major duodenal papilla - (branches of SMA) inferior pancreaticoduodenal artery
87
Arterial supply of jejunum
Jejunal branches of SMA
88
Arterial supply of ileum
Ileal branches of the SMA Ileocolic artery supplies the distal ileum
89
Venous drainage of duodenum
Superior pancreaticoduodenal vein --> portal vein Inferior pancreaticoduodenal veins ---> SMV ---> portal vein
90
Venous drainage of jejunum and ileum
SMV ---> portal vein
91
Parts of the colon
Caecum Ascending colon Transverse colon Descending Sigmoid Rectum Anus
92
Arterial supply to the caecum and ascending colon
Midgut derived (SMA) Ileocolic artery ---> colic, anterior caecal & posterior caecal R colic artery
93
Arterial supply to transverse colon
Midgut & hindgut (SMA & IMA) R colic artery (SMA) Middle colic artery (SMA) L colic artery (IMA)
94
Arterial supply to descending colon
IMA - L colic artery
95
Arterial supply to sigmoid artery
Hindgut (IMA) Sigmoid arteries, branches of IMA
96
Venous drainage of the colon
Mesenteric veins parallel their corresponding arteries SMV and IMV drain their respective structures IMV fuses w/ splenic veins, which the fins SMV to form portal vein
97
Role of SMV in venous drainage of colon
Drains small intestine, caeca, and ascending and transverse colon Via jejunal, ill, ileocolic, R colic and middle colic veins
98
Role of IMV in venous drainage of colon
Drains descending colon through the L Drains sigmoid via sigmoid veins Drains rectum via superior rectal vein
99
How can we differentiate between upper and lower GI bleeding
Ligament of Treitz
100
Causes of upper GI bleeding
Peptic ulcer Oesophageal varices Oesohagitis Mallory Weiss tear Upper GI cancer AV malformation
101
Causes of lower GI bleeding
Diverticulosis Haemorrhoids Colorectal cancer Mesenteric ischaemia AV malformations
102
Haematemesis
Vomiting fresh or altered blood
103
Malaena
Passage of altered ("tarry") blood rectally
104
Haematochezia
Bright red rectal bleeding
105
Types of GI bleeding in relation to disease site
Haematemesis - proximal to ligament of Treitz Melaena - usually upper gI Haematochezia - usually oleo-colonic
106
Which layer do peptic ulcer usually penetrate
Muscularis mucosa
107
Where can HP survive
Gastric type mucosa in the stomach (metaplastic gastric mucosa in the duodenum, oesophagus (Barrett's)) Small bowel (Meckel's diverticulum)
108
How does HP survive in acid pH of stomach
Urease activity (converts urea to ammonia) Motility Proteases (digests protective mucus)
109
How does HP damage gastric type mucosa
Production of ammonia - increases pH Enzymes - proteases, lipases, mucinases
110
How does NSAID use contribute to PUD
Causes damage to gastric epithelium topically Causes systemic damage by inhibiting the production of prostaglandins by gasproduodenal epithelial cells
111
Ddx for PUD
Functional dyspepsia GORD Biliary pain Gastric/ duodenal malignancy Pancreatitis Ischaemia
112
Initial assessment for peptic ulcer bleeding
Haemodynamic status Risk stratification Looking for possible causes
113
Stages in mx of upper GI bleeding
Initial assessment - A-E IV fluid resus and transfusion (Hb < 7) Pt should be NBM and supplemental oxygen given Definitive treatment Appropriate follow-up - endoscopy once stable
114
Physiological changes w/ hypovolaemia
Tachycardia Peripheral shut down Hypotension (BP may be well preserved in young and fit) May see postural drop Confusion Oliguria
115
Grading haemorrhagic shock
(Hypovolaemic shock) Looks at blood loss, pulse, BP, RR, urine output
116
Risk stratification for gI bleeidng
Rockall score - predicts mortality Can be calculated pre endoscopy (max 7) or post-endoscopy (max 11)
117
Glasgow-Batchford score
Preferred by NICE pre-endoscopy for deciding upon timing of intervention Cut-off for intervention is >1 Parametres incl urea, Hb, SBP, pulse, tachycardia
118
Timing of endoscopy following upper GI bleed
Dx requires endoscopy Adequate resus required before endoscopy Usually, 24hrs of admission
119
What to do when endoscopic therapy fails for upper GI bleeding
Embolisation (interventional radiology) Surgery
120
When do you perform surgery for bleeding peptic ulcer
Minimal surgery necessary to control bleeding Severe uncontrolled bleeding
121
What constitutes as severe uncontrolled bleeding in PUD
After failed endoscopic pretreatment <60y, 2nd rebleed, 8 units transfused >60y, 1st rebleed, 4 units transfused
122
Portal hypertensive bleeding
Spectrum of condns encompassing oesophageal, gastric and ectopic varices and portal hypertensive gastropathy
123
What gradient of pressure between portal vein and iVC is needed for the devlopment of oeopshagela varices
10mmHg Normal gradient is 3-7 Pressure gradient and other factors within vary wall (Laplace's law) influence when varices bleed
124
Vasoactive therapy for variceal haemorrhage
Examples incl terlipressin (vasopressin analogue), octreotide Reduces splanchnic blood flow and pressures in varices
125
Abx for variceal haemorrhage
Bacteraemia and subsequent sepsis v common Prophylactic BSA reduce mortality - cipro, 3rd gen cephalosporin
126
Secondary prevention for varicella haemorrhagew
Treat liver disease Variceal obliteration Drugs - BB Determine cause of PHTN
127
Complications of Sengstaken tube
Aspiration Mucosal necrosis
128
What can be done if endoscopic therapy fails for bleeding varices
Confirm it is variceal in origin Balloon tamponade - sengstake tube Portosystemic shunting
129
TIPPS procedure
Transjugular intrahepatic portosystemic shunt Shunts blood from portal veins to hepatic vein 'Rescue' therapy for refractory a/c bleeding Definitive treatment for bleeding gastric varices
130
Complications of TIPSS
Procedural/ technical Infection Stent occlusion Rebleeding Encephalopathy
131
Structure of villi in small intestines
Epithelial cells in villi extend down into lamina proprietor to form crypts Important cells reside in more protected crypts Goblet cells produce mucous Paneth cells produce lysosomes
132
Appearance of distal jejunum on AXR
'Stack of coins' Because of valvular conniventes folds
133
Segmental contraction vs peristalsis
Segmental contraction - mixing bile and pancreatic enzymes w/ chyme, does NOT propel the chyme Peristalsis - advances chyme
134
Different foods and peristalsis
Solid foods induce greater activity than liquid meals Food high in glucose cause greater stimulation than ones high in FFA
135
What is digestion
The breakdown of large insoluble food molecules (proteins, lipids and carbs) to small water-soluble absorbable molecules
136
Production of gastric juice
Pepsinogen and HCl secreted into lumen HCl converts pepsinogen to pepsin Pepsin activates more pepsinogen, starting a chain reaction
137
Proteolytic enzymes from pancreas
Trypsin, chymotrypsin, carboxypeptidase Break down to peptides to AAs RNA/ DNA to nucleotides
138
Digestion of carbs
Salivary amylase Pancreatic amylase Glycoside hydrolyses e.g. maltose, sucrose Fibre is resistant to hydrolyses and isn't digested
139
Digestion of lipids
Emulsifies in stomach and then in duodenum and upper small bowel with action of bile Requires gastric lipase, pancreatic lipase, phospholipase and cholesterol esterase
140
Absorption of glucose
Requires transport proteins, GLUT in enterocytes Transporter binds Na and caused conformational change, moving sodium and glucose intracellularly Na dissociates into the cytoplasm so unloaded transporter reorients back into position
141
Inflow and outflow of GIT
IN - 2L food/fluid, 6.5-7L secretions OUT (to recirculate) - 8.4L per day Total loss - 100ml faeces
142
Vitamins and minerals absorbed in duodenum
Calcium Iron Fat soluble vitamins - ADEK, Mg
143
Vitamins and minerals absorbed in jejunum
Folate Vitamin B6 Vit C Thiamine Niacin
144
Vitamins and minerals absorbed in ileum
Bile slats and acids Vit C Vit B12 and folate Vit D Vit K
145
Vitamins and minerals absorbed in large intetsine
Water Sodium Potassium Chloride Vit K Biotin
146
Intestinal failure
Reduction of gut function to below minimum necessary for the absorption of macronutrients and/or water & electrolytes TPN required to maintain health
147
Intestinal insufficiency
Reduction of gut absorptive function that does NOT require IV supplementation
148
Functional classification of intestinal failure
Type 1 - self-limiting Type 2 - prolonged Type 3 - long term
149
Type 1 intestinal failure
Post-op ileus A/c infl
150
Type 2 intestinal failure
GI complictaion EC fistula Abdominal sepsis
151
Type 3 intestinal failure
Short bowel syndrome C/c obstruction Motility disorder
152
5 major condns causing intestinal failure
Short bowel syndrome Intestinal fistula Intestinal dysmotility Mechanical obstruction Extensive small bowel mucosal disease
153
Consequences of intestinal failure
Dehydration - treat w/ water & salt Malnutrition - nutrition
154
Treating mild intestinal failure
Nutrition - oral supplements, oral glucose/ saline Water & electrolytes - dietary adjustments, NaCl
155
Treating moderate intestinal failure
Enternal nutritiojn Enteral electrolytes
156
Treating severe intestinal failure
Parenteral nutrition
157
Causes of short bowel syndrome
Massive intenstinal rescetion Repeated intestinal resection EC fistuale Gastric bypass Paediatric - intetsinal atresia, midgut volvulus
158
Complications of intestinal failure
Dehydration Malnutrition Complications of IV support Psychological Stoma care
159
Short bowel syndrome
Less than 2m of small bowel
160
Mx of short bowel syndrome
St Marks solution Double strength dioralyte Loperamide Codeine Lanreotide S/c fluids and electrolytes IV fluids TPN
161
Intestinal failure operations
Reversal of stomas Putting bowel back into continuity Repair of fistulas Stricturoplasty Removal of obstruction
162
Intestinal failure operations
Reversal of stomas Putting bowel back into continuity Repair of fistulas Stricturoplasty Removal of obstruction
163
Pathophys of pancreatic cancer
Typically duct adenocarcinoma of the pancreatic head (80%)
164
Prognosis of pancreatic cancer
5-yr survival is 3.3% 15% are resectable at dx Median survival is 28-54 months
165
Histology of pancreatic cancer
V poor vascularity V fibrous - rich stroma in which cancer is embedded
166
Risk fcators for pancreatic cancer
Smoking, alcohol C/c pancreatitis Fhx Diabetes
167
Sx of pancreatic cancer
B sx - wt loss, anorexia, fatigue Worsening of DM/ new onset Head tumours - PAINLESS obstructive jaundice (bile ducts blocked) Body/ tail tumour - epigastric pain that radiates to back, relived leaning forward
168
Signs of pancreatic cancer
Palpable liver, GB and/or spleen - think Courvoisier's law Jaundice Ascites Trousseau's sign
169
Courvoisier's law
Palpable GB w/ jaundice is rarely gallstones, consider malignancy (pancreatic or cholangiocarcinoma)
170
Trousseau's sign of malignancy
Migratory thrombophlebitis and hypercoagulability May also be seen in gastric or lung cancer
171
Metastasis of pancreatic cancer
Presenting sx may be from mets Commonly affects liver, lungs, peritoneum
172
Referral for pancreatic cancer
Over 40 w/ new onset jaundice - 2WW Over 60 w/ wt loss and any of following - CT abdo: Diarrhoea Back pain N & V Constipation New onset DM
173
Importance of cancer associated fibroblasts
Immunosuppressive V dense fibrous tissue - hard for chemo to penetrate V hypoxic enviuronment
174
Ix for pancreatic cancer
CT - CAP CA19.9 Bx Bloods - FBC, LFTs, bone profile, U&Es Endoscopic ultrasound
175
General aspects of care for pancreatic cancer
Nutrition - PERT Mental health Psych support Pain control - v important Good palliative care
176
Chemo regimes for pancreatic cancer
Gemcitabine and Capecitabine FOLFIRINOX
177
Surgical treatment for pancreatic cancer
Whipple's procedure (Pancreaticoduodenectomy) if resectable Biliary stent insertion by ERCP Total pancreatectomy
178
Epidemiology of a/c pancreatitis
Increased incidence w/ age Common surgical emergency
179
Pathogenesis of a/c pancreatitis
Involves intra-pancreatic activation of pancreatic enzymes and auto-digestion Infl ---> oedema, fluid shifts and hypovolaemia
180
Causes of a/c pancreatitis
Idiopathic Gallstones (50%) Ethanol Trauma Steroids Malignnacy and mumps AI Scorpion bite Hyperlipidaemia and hyperCa ERCP Drugs
181
Px of a/c pancreatitis
Sudden-onset epigastric or LUQ pain and tenderness - radiates to back, better leaning forward N & V SIRS Pleural effusions and ascites if severe
182
What is required for a dx of a/c pancreatitis
2 out of 3 of: Typical pancreatic type pain Increased amylase or lipase (>3x ULN) Compatible CT, MRI or US findings
183
Other causes of a raised amylase
Renal insufficiency Salivary infl Macroamylaseamia Hereditary Intestinal infarction/ peritonitis Ectopic prehnancy an ovarian cyst Appendicitis
184
Bloods for a/c pancreatitis
FBC - increased WBC, deranged RBC (low - haemorrhage, high - dehydration) Increased CRP Increased LFTs Deceased Ca if severe
185
Imaging modalities for a/c pancreatitis
AXR CXR US Abdo CT or MRCP - gold standard but only needed if dx unclear
186
XR for a/c pancreatitis
AXR - Dilated gut ('sentinel loop') next to pancreas CXR - pleural effusion
187
US for a/c pancreatitis
May show pancreatic infl but mainly done to find gallstones Repeat after a/c phase if gallstones found
188
Drugs that may cause a/c pancreatitis
Azathioprine Valproate Thiazides Ceratin antimicrobials - metronidaxole, sulphonamides
189
Causes of pancreatic duct obstruction
Pnacreatic cancers Ampullary/ periampullary cancers Ascariasis Duodenal cancers/ lymphomas/ mets
190
What should be done for pts w/ unexplained pancreatitis
ALL should have a CT scan within 6/52 of dx to check no malignant ductal obstruction
191
Addn sx of haemorrhagic pancreatitis
Bruising over both flanks (Grey-Turner's sign) Bruising over peri-umbilicus (Cullen's sign)
192
Glasgow score to asses severity of pancreatitis
PaO2 < 8 kPa Age > 55 Neutrophilia (WBC > 15) Ca2+ < 2mmol/L Renal impairment (urea < 16) Enzymes (raised LDH, AST) Albumin < 32 Sigar (glucose) > 10mmol >3 is severe nd requires HDU admission
193
Initial mx of a/c pancreatitis
Supportive care - IV fluids (catheterisation and fluid balance chart), analgesia, antiemetics, nutritional support (NG or NJ tube) Abx if signs of infection Mx of aetiology
194
Complications of a/c pancreatitsi
Necrosis Abscess formation Peripancreatic fluid collections - seen by 2/52 Pseudocyts - 4/52 Pseudoaneurysm VTE
195
Systemic complications of a/c pancreatitis
ARDS Renal failure Shock
196
Prognosis of a/c pancreatitis
20% mortality if severe
197
Interventional treatment for a/c pancreatitis
Necrosectomy Drainage of pseudocyts If due to gallstones, offer cholecystectomy or ERCP after recovery
198
What should be done for recurrent a/c pancreatitis
Mx of aetiology Modify lifestyle Consider rare causes e.g. genetic causes PSS-1, SPINK1 or AI pancreatitis (IgG4 level may be raised) - steroid responsive
199
What is c/c pancreatitis characterised by
C/c, progressive pancreatic infl and scarring Resulting in the loss of exocrine and endocrine function
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Most common causes of c/c pancreatitis
Alcohol
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A/c vs c/c pancreatitis
C/c is less intense and longer lastlasting Presence of exocrine or endocrine dysfunction in c/c Lipase / amylase is typically NOT raised in c/c
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Clinical features of c/c pancreatitis
Recurrent or c/c epigastric pain radiating to back Exocrine pancreatic insufficiency ---> steatorrhea and malnutrition DM
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Ix for c/c pancreatitis
Blood glucose CT (ideally) or US: pancreatic calcification
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Mx of c/c pancreatitis
Lifestyle - avoidance of triggers e.. smoking Medical - pain relief, pERT Endoscopic - relief of obstruction, stone removal, coeliac nerve block Surgical - Whipple's, Frey
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Diagnostic test of pancreatic exocrine insufficiency
Faecal elastase - low levels
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Is 2' DM to pancreatitis common
No, relatively uncommon Behaves like T1DM (destroyed islets)
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Pancreatic cancer risk and c/c pancreatitis
CP increases risk Most significantly in those w/ genetic predispositions (SOPINK1) and cig smokers No evidence for screening except in genetic group - done w/ CT abdo
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Key complications of c/c pancreatitis
C/c epigastric pain Loss of exo/endocrine functions Damage to duct system --> obstruction of excretion Psudoecyts formation
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Risk stratification for GI bleeding
Rockall score - predicts mortality Can be calculated pre endoscopy (max 7) or post-endoscopy (max 11) Any pts w/ a score >0 erequire input
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Conservative mx of toxic megacolon
Bowel decompression - place pt NBM, insertion of NGT, IV fluids Surgery indicated if pt isn't responding to mx or develops complications
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What features constitute 'problem drugs' for ADR
Benefit-harm ratio critically balanced e.g. digoxin, anti-coag Poor kinetics (narrow range of safety) e.g. phenytoin Enzyme inducers/ renal effects e.g. anticonvulsant
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What features constitute 'problem diseases/ susceptible pts' for ADR
Serious consequences of therapeutic failure e.g. anti-arrythmics Disease required multiple drugs e.g. CHF Pt is elderly or has multiple pathology
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Examples of how mechanism of drug action predicts interactions
Blocked AVN conduction - bradycardia Arterial dilatation - hypotension CNS drugs - sedation Antiplatelets/ anti-coag - haemorrhage HF drugs - electrolyte abnormalities
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What to do when anticipating drug interactions
Monitor drug levels or response e,g, iNR Adjust dose if interactions e.g. reduce BB if on diltiazem Correct metabolic disturbances Monitor when using liver enzyme inducers or inhibitors
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What effect would an enzyme inducer cause if the enzyme breaks down drugs
Less drug in body, less drug action
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What effect would an enzyme inhibitor cause if the enzyme breaks down drug
More drug in body, more drug action
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What effects would an enzyme inducer cause if the enzyme activates drugs
More drug in body, more drug action
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What effect would an enzyme inhibitor cause if the enzyme activates drug
Less drug in body, less drug action
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Oral contraceptive interactions
Abx Anticonvulsants Encouraged to use barrier method
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Abx that potentiate the effects of warfarin
Metronidazole Co-trimoxazole
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Which electrolyte does ACEi increase and what problems can this cause
K Significant problem if given w/ K sparing diuretics, K supplements an drugs that worsen renal function
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Alcohol and CNS drugs
Potentates CNS depressants Sedating antihistanes Benzodiazepines
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Which drug class increases alcohol conc in body
H2RA e.g. ranitidine
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Alcohol as a vasodilator
GTN and alcohol Increased risk of hypotension & fainting Esp when GTN used within 1hr of alcohol
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What is an ADR
An unfavourable outcome that occurs during or after the use of a drug Could be: Abnormal sign, symptom or lab tests Any untoward or unplanned occurrence (e.g. accidental/ unwanted pregnancy) Unexpected worsening in a concurrent illness
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What is a side effect
Any unintended effects May be harmful or beneficial e..g alpha-blocker for HTN - improvement in prostatic symptoms
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When to consider ADRs - narrow benefit: harm margin
Limited benefit but some risk of harm e.g. HRT Some public health measures - flu vaccines Major benefit but substantial harm e.g. cancer chemo Older pts - multiple comorbidities and poly pharmacy
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Reporting ADRs
UK Yellow Card System Particularly important for black triangle drugs - newly launches or suspected to have sig problems
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Classification of ADR
Type A - dose dependent, predictable Type b - not dose dependent, cannot be predicted pharmacologically
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Limitation of classification of ADR
No account of duration e.g. steroid osteoporosis - dose and length of therapy are relevant Susceptibility - poor mobile elderly women more likely
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Examples of Type A ADR
BB causes bradycardia, higher dose, greater degree of bradycardia
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Examples of Type B ADR
Anaphylaxis to penicillin
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Monitoring and predicting ARDS
DoTS scheme Dose relatedness (at what dose does ADR happen) Time relatedness (when does it happen, should I monitor for it) Susceptibility factors (is pt at special risk)
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Digestion and GIT - mouth
Ground and mixed sallivary amylase
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Digestion and GIT - stomach
Mixing Acid proteases Reservoir w/ gradual release
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Digestion and GIT - small bowel
Bile Pancreatic enzymes Absorption
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Digestion and GIT - colon
Water absorption Bacterial flors [Short chain FA, vit K]
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Is the small intestine mobile or immobile
Mobile - attached by mesentery to posterior abdo wall
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Features of plicae semilunaris
Found in jejunum Circular folds are large, tall and closely packed in upper jejunum Gradually reduce until lower ileum where they are absent
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Where does the blood supply of the large intestine change
Proximal to splenic flexure - SMA Distal to splenic flexure - IMA
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What vertebral level is the rectum at
S3
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How is CT colonoscopy done
Cleanse bowel using laxatives Oral contrast agent Put pts on low residue agency CO2 via Foley catheter PR Scan in two positions
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Indications for imaging small bowel
Previous admission for SBO Unexplained IDA [OGD & colonoscopy normal] Malabsorption Unexplained pain/ diarrhoea/ wt loss esp w/ raised infl markers
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Crohn's disease radiological findings
Skip lesions Ulcers Fissures and oedema (cobble stoning) Stenosis Wall thickening and distortion Fistulation Infl mass and crypt abscesses
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Imaging suspected Crohn's
Barium studies - loss of haustrations, cobble-stoning, string sign Ultrasound - blood flow using Dopple CT enterography - infl fat wrapping MR enter-graphs
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Indications for imaging large bowel
CIBH PR bleeding IDA Palpable mas Carcinomas and polyps Dovertoculsar Colitis Volvulus
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What determines the premalignant potential of polyps (adenomas)
Size 1cm - 10% risk of being malignant 2cm polyps - 50% risk
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Types of colitis
IBD - UC, Crohn's Ischaemia Radiation Infections (incl abx related)
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Imaging for suspected colon cancer
Colonoscopy - gold standard Flexible sigmoidoscopy + CTC CT CAP
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Imaging for suspected colitis
Rigid sigmoidoscopy Colonoscopy CT
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Colonoscopy vs sigmoidoscopy
Coloscopy looks at entire colon but sigmooidoscopy is only lower 1/3rd
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Benefits of colonoscopy over CTC
Able to perform biopsies
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Benefits of CTC over colonoscopy
Minimal prep required Images can be reviewed after
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Anorexia
Reduced desire to eat
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How can we classify causes of intestinal ischaemia
Occlusive - thrombosis, embolus Non-occlusive - vasoconstriction, hypoperfusion
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Colonic ischaemia vs mesenteric ischaemia
Colin - large intestine Mesenteric - small intestine
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Ix for intestinal ischaemia
CT pelvis and abdo Erect CXR Echo - if source of embolism suspected Bloods - metabolic acidosis and raised lactate Endoscopy
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Sx of intestinal ischaemia
Non-spp abdo pain Diarrhoea Haematochezia N & V
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Signs of intestinal ischaemia
Tenderness Peritonism/ guarding Tachycardia/ hypotension (haemodynamic instability)
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Px of c/c mesenteric ischaemia
Triad of: Post-prandial abdo pain Wt loss - food avoidance Abdo bruit
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Mx of intestinal ischaemia - thromboembolic cause
Anticoagulant Broad spectrum abx due to bacterial translocation May need resections
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Mx of c/c mesenteric ischaemia
Similar to CDV mx Reduce modifiable risk factors Implement 2' prevention Revascularisation procedures may be performed
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Complications of intestinal ischaemia
Shock Peritonitis Sepsis Necrosis Perforation
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Barium enema findings for UC
Loss of haustrations Superficial ulcerations Psuedopolyps In long-standing disease, colon in narrow and short - ‘drainpipe colon’
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Proctitis
Infl of rectum
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Does UC affect the anus
No