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gastrointestinal_week_2_20190518174132 Flashcards

1
Q

what is jaundice (icterus)

A

yellowing of sclera (white of eyes) and skin

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2
Q

what causes jaundice

A

increase in blood levels of bilirubin

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3
Q

what is bilirubin

A

normal by-product of breakdown of RBC which occurs in spleen and is used to form bile in liver

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4
Q

what is the role of biliary tree

A

connects liver to 2nd part duodenum

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5
Q

what is the role of gallbladder

A

storage and concentration of bile

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6
Q

what is role of bile

A

normal absorption of fats from small intestine

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7
Q

what is role of pancreas

A

excretes digestive enzymes into 2nd part of duodenum - necessary for digestion of food

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8
Q

what is functions of liver (largest organ)

A

glycogen storage, bile secretion and other metabolic functions

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9
Q

what is the surface anatomy of the liver

A

mainly in RUQ, protected by ribs 7-11 and location changes in breathing

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10
Q

where is gallbladder in relation to liver

A

posterior and inferior

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11
Q

where is hepatic flexure in relation to liver

A

inferior

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12
Q

where is right kidney, right adrenal gland, IVC and abdominal aorta in relation to liver

A

posterior

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13
Q

where is stomach in relation to liver

A

posterior at mid/left side

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14
Q

what are the 4 anatomical lobes of liver

A

right lobe and left lobe (seen anterior)quadrate lobe and caudate lobe (seen posteriorly)

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15
Q

there are 8 functional segments which allow for segmentectomy. What does each segment contain

A

branch of hepatic artery, branch of hepatic portal vein, bile drainage (to bile duct) and venous drainage (to IVC)

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16
Q

IVC and hepatic veins lack valves - what is the consequence of this

A

increase in central venous pressure is directed to liver

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17
Q

what happens to the hepatic veins directing deoxygenated blood from liver before entering IVC

A

come together as 3 veins

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18
Q

what is contents of the portal triad

A

hepatic portal veinhepatic artery properbile duct

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19
Q

the structures of the portal triad run within which ligament

A

heptaduodenal

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20
Q

what is the coeliac trunk

A

first of 3 midline branches of aorta - leaves aorta at T12 and supples organs of foregut

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21
Q

the coeliac trunk trifurcates into 3 branches - what are these

A

splenic artery, left gastric artery and common hepatic artery

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22
Q

when does common hepatic artery become hepatic artery proper

A

when it gives off the gastroduodenal artery

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23
Q

where does the splenic artery run

A

superior to border of pancreas

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24
Q

where is spleen located

A

it is an intraperitoneal organ within left hypochondrium

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25
Q

what is the spleen anatomically related to

A

posteriorly to diaphragm anteriorly to stomachinferiorly to splenic flexuremedially to left kidney

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26
Q

what ribs protect spleen

A

9-11

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27
Q

what is the major blood supply to stomach

A

right and left gastric arteries and right and left gastro-omental arteries

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28
Q

where do right and left gastric arteries run

A

along junction of lesser curvature and lesser omentum - anastomose together

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29
Q

where do right and left gastro-omental arteries run

A

along junction of greater curvature and greater omentum - anastomose together

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30
Q

where does majority of blood received by liver come from

A

hepatic portal vein

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31
Q

where is the rest of blood supply to liver from

A

right and left hepatic arteries and branches of hepatic proper

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32
Q

what are the 2 clinically important areas of peritoneal cavity related to liver

A

hepatorenal recess (morisons pounch) and sub-phrenic processboth within greater sac

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33
Q

what can peritonitis result in in relational to these areas

A

collection of pus in recesses leading to abscess formation

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34
Q

which recess is one of lowest parts of cavity when patient supine and thus pus will drain if patient bedridden

A

hepatorenal recess

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35
Q

what is the role of hepatic portal vein (HPV)

A

drains blood from foregut, midgut and hindgut to liver for first pass metabolism

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36
Q

what forms the HPV

A

splenic vein (drains foregut) and superior mensenteric vein (drains midgut)

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37
Q

how does the HPV drain blood from hindgut then

A

because inferior mensenteric vein drains blood from hindgut to splenic vein

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38
Q

what is the role of interior vena cava in relation to HPV

A

drains cleaned blood from hepatic vein into right atrium

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39
Q

what structures are within portal triad

A

bile ducthepatic artery proper hepatic portal vein

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40
Q

where does the gallbladder lie

A

on the posterior aspect of liver and anterior to duodenum

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41
Q

what is function of gallbladder

A

stores and concentrates bile in between meals

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42
Q

bile flows in and out of gallbladder via what

A

cystic duct

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43
Q

what is three sections of gallbladder

A

neck (at cystic duct), body and fundus

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44
Q

what is the blood supply to gallbladder

A

cystic artery - branch of right hepatic artery an located in cystohepatic triangle (of calot)

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45
Q

what is the consequence of a gallstone

A

inflammation of gallbladder or cystic duct

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46
Q

gallblader is foregut - where does visceral afferents enter spinal cord and where is pain felt

A

T6-T9pain felt in epigastric region

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47
Q

where is can gallbladder pain present

A

hypochrondrium (top left and right)with or without pain referral to right shoulder as result of anterior diaphragmatic irritation

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48
Q

what is cholecystectomy

A

surgical removal of gall bladder

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49
Q

the common hepatic duct (combination of right and left hepatic) unites with cystic duct to form what

A

bile duct (common bile duct)

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50
Q

what is the 4 parts of duodenum

A

superior (duodenal cap - intraperitoneal), descending, horizontal and ascending

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51
Q

what is pyloric sphincter (where flow of chyme begins)

A

controls flow of chyme from stomach to duodenum

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52
Q

where does flow of chyme end

A

duodenojejunal flexure

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53
Q

what peptide hormones does duodenum secrete into blood

A

gastrin, CCK

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54
Q

where is pain from duodenal ulcer felt

A

epigastric region

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55
Q

where is pancreas located

A

retroperitoneal organ that lies transversely across te posterior abdomen

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56
Q

what is 4 parts of pancreas

A

head (with uncinate process), neck, body, tail

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57
Q

what lies posteriorly to pancreas

A

right kidney and adrenal gland, IVC, bile duct, abdominal aorta, superior mesenteric vessels, left kidney and adrenal gland, part of portal venous system

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58
Q

what lies anterior to pancreas

A

stomach

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59
Q

what lies superoposteriorly to pancreas

A

splenic vessels

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60
Q

what is exocrine function of pancreas

A

acinar cell (pancreatic digestive enzymes into main pancreatic duct)

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61
Q

what is endocrine function of pancreas

A

islets of langerhans (insulin and glucagon into bloodstream)

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62
Q

how does the biliary system drain

A

bile duct descends posteriorly to 1st part of duodenum, travels into groove onto posterior aspect of pancreasthen joints with main pancreatic duct forming ampulla of vaterboth then drain into 2nd part of duodenum

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63
Q

what smooth muscle sphincters are present in biliary system

A

bile duct sphincter pancreatic duct sphincter sphincter of Oddi

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64
Q

what is ERCP (endoscopic retrograde cholangiopancreatography)

A

investigation used to study biliary tree and pancreas and treat some pathologies associated with it

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65
Q

what are 2 main causes of jaundice

A

gall stones carcinoma at head of pancreas

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66
Q

how does this cause jaundice

A

flow of bile back up to the liver results in overspill into the blood of its constituents (including bilirubin)

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67
Q

what is one of the reasons for pain arising from pancreas

A

secondary to inflammation - pancreatitis

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68
Q

what is one cause of pancreatitis

A

blockage of ampulla by gallstone - bile is then diverted into pancreas leading to irritation and inflammationin more advanced cases, vascular haemorrhage can occur leading to blood/fluid accumulation in retroperitoneal space

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69
Q

where is pancreatic pain felt

A

foregut and midgut organ - presents in epigastric region and/or umbilical region can also radiate to back

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70
Q

where is grey-turners sign (in pancreatitis)

A

right or left flanks

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71
Q

where is cullens sign (in pancreatitis)

A

around umbilicus via falciform ligament

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72
Q

where are parts of small intestine located

A

1st and 2nd part of duodenum are foregut organs the rest of SI are midgut organs

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73
Q

where is jejunum and ileum found (make up most of SI)

A

all 4 quadrants jejunum begins at duodenaljejunal flexureileum ends at ileocaecal junction

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74
Q

what is colour difference between jejunum and ileum

A

jejunum is deep red, ileum is lighter pink

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75
Q

what is wall difference

A

jejunum is thicker and heavy, ileum thinner and lighter

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76
Q

what is vascularity difference

A

jejunum more vascular, ileum less vascular

77
Q

what is difference in mesenteric fat

A

jejunum has less, ileum has more

78
Q

what is difference in circular folds (L, plicae circularis)

A

jejunum has large, tall and closely packed fold ileum has low and sparse folds (absent distally)

79
Q

what is different in lymphoid tissue (peyers patches)

A

present in ileum

80
Q

what is arterial blood supply of jejunum and ileum

A

superior mesenteric arteries via jejunal and ileal arteries

81
Q

what is course of superior mesenteric vessels

A

leaves aorta at L1 vertebral level, posterior to neck of pancreastravels inferiorly, anterior to uncinate process of pancreas to enter the mesentery proper

82
Q

how is fat absorbed

A

bile absorbs fats from GI tract lumen into intestinal cellsfats (within chylomicrons) then absorbed from intestinal cells into specialised lymphatic vessels of SI called lactealsthey travel via lymphatic system to eventually drain into venous system at left venous angle

83
Q

what are the main groups of lymph nodes draining abdominal organs

A

celiac (forgut organs)superior mesenteric (midgut organs)inferior mesenteric (hindgut organs)lumbar (kidneys, posterior abdo wall, pelvis and lower limbs)

84
Q

what are peyers patches

A

distinctive structures within specialised epithelial lining, containing B and T lymphocytes and antigen presenting cells

85
Q

where are peyers patches most numerous

A

terminal ileum

86
Q

which specialised epithelial cells do peyers patches contain

A

M cells - lack microvilli and contain membranous folds enclosing lymphocytes, macrophages and dendritic cells these trap antigens and transport them across epithelium to interact with immune cells

87
Q

what is the function of M cells

A

transport intact peptides, viruses and bacteria across epithelium and pass them on to antigen-processing and antigen-presenting cells

88
Q

what mediates homing to the mucosa

A

cell surface molecules that interact with receptors on blood vessels in GI tract

89
Q

what molecule does lymphocytes homing to the intestine express

A

a4B7 which interacts with MAD-CAM (mucosal addressin cell adhesion molecule)

90
Q

what is an example of specific cytokines (chemokines) attracting subsets of lymphocytes to different parts of intestine

A

thymus and epithelial expressed chemokine (TECK) attracts cells to intestine via surface receptor CCR9

91
Q

what is the most abundant immunoglobulin in bronchial, reproductive tract and intestinal secretions

A

IgA

92
Q

how is secretory dimeric immunoglobulin A (sIgA) created and released

A

two IgA, joined to form polymeric IgA, binds to receptor called secretory component (SC) on basolateral surfaces of epitheliaThe complex is transported across cytoplasm and sIgA is released at luminal surface by proteolytic cleavage of SC

93
Q

which prions, viruses and pathogenic bacteria (respectively) are taken up by M cells allowing spread of infection

A

bovine spongiform encephalopathy (BSE) agentHIVShigella

94
Q

selective IgA deficiency affects how many people, without much effect on enteric immunity

A

1 in 500

95
Q

which diseases cause chronic immune stimulation which can lead to excess proliferation of immune cells, neoplastic change and intestinal lymphoma

A

helicobacter pylori or coeliac disease

96
Q

what occurs when IgA binds to poly-Ig receptors

A

endocytosis

97
Q

what is the role of poly-Ig receptors

A

allows IgA replacement by IgM as it recognises any polymers

98
Q

death caused by T cells causes flattened epithelial cell in coeliacs - what is consequence of this

A

decreased absorption -malabsorption is key symptom

99
Q

what happens when mucosal immunity becomes dysregulated

A

infected dendritic cells shuttle virus from the site of exposure to the regional lymph nodes where they concentrate virus particles and infect CD4+ T cells

100
Q

what is selective IgA deficiency

A

2/3 asymptomatic remainder recurrent sinopulmonary infections (coeliac disease 10x)

101
Q

what is CVID

A

failure to differentiate into Ig secreting cellsrecurrent sinopulmonary and GI infections

102
Q

what is XLA

A

no B cellssinopulmonary and GI infections plus devastating systemic manifestations

103
Q

what is CGD

A

failure of phagocyte respiratory burststaphylococcus aureus/inflammatory granulomas

104
Q

what is SCID

A

profound defect in T and B cell immunity oral candidiasis, chronic diarrhoea, interstitial pneumonitis

105
Q

how is a food allergy caused

A

type 1 hypersensitivity reaction initiated by crosslinking of allergen specific IgE on surface of mast cells with specific allergen

106
Q

how is coeliac disease diagnosed

A

biopsy serology useful as screening test

107
Q

what is crohns disease

A

focal and discontinous inflammation with deep and eroding fissures +/- granulomas commonly affects distal ileum and colon

108
Q

what is the immunology of crohns disease

A

mediated by Th1 CD4+ T cells / gamma interferon / IL-12 / TNF alpha

109
Q

what is ulcerative colitis

A

restricted to rectum and colon -distortion of crypts with infiltration of monocytes / neutrophils and plasma cells

110
Q

what is the cause of ischaemia of small bowel

A

mesenteric arterial occlusion (atheroscleorisis or thromboembolism from heart)non occlusive perfusion insufficiency (shock, strangulation eg hernia, drugs eg cocaine and hyperviscosity)

111
Q

which is most metabolically active part of bowel wall

A

mucosa - most sensitive to effects of hypoxia

112
Q

what is the complications of ischaemia of small bowel

A

resolutionfibrosis, structure, chronic ischaemia, mesenteric angina and obstruction gangrene, perforation, peritonitis, sepsis and death

113
Q

what is meckels diverticulum

A

small bulge in SI - result of incomplete regression of vitello-intestinal duct

114
Q

what is consequence of meckels diverticulum

A

bleeding, perforation or diverticulitis which mimics appendicitis

115
Q

what is incidence of tumours in small bowel

A

primary tumours raresecondary tumours (metastases) much more common eg in ovary, colon or stomach

116
Q

what primary tumours found in small bowel

A

lymphomas, carcinoid tumours, carcinomas

117
Q

characteristics of lymphomas of small bowel

A

rare, maltomas (b cell) derivedenteropathy associated T cell lymphomas (associated with coeliac disease)treated by surgery and chemo

118
Q

characteristics of carcinoid tumours

A

rare, common site is appendixsmall, yellow, slow growing tumourslocally invasive

119
Q

what is complication of carcinoid tumour

A

can cause intussusception, obstructionif metastases to liver occur, a carcinoid syndrome occurs producing flushing and diarrhoea

120
Q

characteristics of carcinoma of small bowel

A

rare, associated with crohns and coeliacsidentical to colorectal carcinoma in appearance presents late metastases to lymph nodes and liver

121
Q

what are symptoms of appendicitis

A

vomiting, abdominal pain, RIF tenderness and increased WCC

122
Q

what is that pathology of acute appendicitis

A

acute inflammation (neutrophils - must involve muscle coat), mucosal ulceration, serosal congestion - exudate - and pus in lumen

123
Q

what are complications of appendicitis

A

peritonitis, rupture, abscess, fistula, sepsis and liver abscess

124
Q

what is coeliac disease

A

abnormal reaction to constituent of wheat flour, gluten, which damages enterocytes and reduces absorptive capacity

125
Q

what does coeliac disease have strong associations with

A

HLA-B8, dermatitis herpetiformis and childhood diabetes

126
Q

what is cause of coeliac disease

A

gliadin in gluten - tissue injury may be bystander effect mediated by T cells which exist within SI epithelium (making them IELS)

127
Q

what happens to enterocytes in coeliac disease

A

increasing loss of them due to IEL mediated damage - leads to loss of villous structure, loss of surface area, reduction in absorption and flat duodenal mucosa

128
Q

what is the morphology of coeliac disease

A

increased inflammation in lamina propriaincreased intraepithelial lymphocytes

129
Q

biopsy results of coeliac disease

A

mucosa may be endoscopically normal or appear attenuated lesion worse in proximal bowel so duodenal biopsy very sensitive

130
Q

serology results of coeliac disease

A

antibodiesanti TTG, anti endomesial and anti gliaidin

131
Q

what is the metabolic effects of coeliac disease

A

malabsorption of sugars, fats, amino acids, water and electrolytes - leads to steatorrheareduced intestinal hormone production leads to reduced pancreatic secretion and bile flow (CCK) leading to gallstones

132
Q

what is the effects of malabsorption (can be managed by diet)

A

loss of weight, anaemia (Fe, Vit B12, folate), abdominal bloating, failure to thrive, vitamin deficiences

133
Q

what are other complications of coeliac disease

A

T cell lymphomas of GI tract, increased risk of small bowel carcinoma, gall stones, ulcerative - jejenoilleitis

134
Q

what is intestinal failure

A

inability to maintain adequate nutrition or fluid status via intestines

135
Q

what causes intestinal failure

A

obstruction, dysmotility, surgical resection, congenital defect or disease associated loss of absorption

136
Q

what is intestinal failure characterised by

A

inability to maintain protein-energy, fluid, electrolyte or micronutrient balace

137
Q

what are the different kinds of intestinal failure

A

acute (type 1&2 - 2 weeks) - eg mucositis post chemotherapychronic long term (type 3) - eg short gut syndrome

138
Q

how is type 1 intestinal failure treated

A

replace fluid, correct electrolytesparenteral nutrition if unable to tolerate oral food/fluids >7 days post opacid suppression - proton pump inhibitorsoctreotide alpha hydroxycholecalciferol to preserve Mg

139
Q

what is parenteral nutrition

A

provision of nutrients by IV route - ultrasound guided

140
Q

what is complications of parenteral nutrition

A

pneumothorax / arterial puncture / misplacementsepsis, SVC thrombosis, metabolic bone disease, liver disease

141
Q

what is type 2 IF

A

occurs in septic patients, abdominal fistulae and perioperative who may develop complication of feeding

142
Q

what is treatment for type 2 IF

A

weeks/months of care (ICU/HDU)Parenteral +/- some enteral feeding

143
Q

what is the treatment options for type 3 IF

A

home parenteral nutrition (treatment of choice, esp in SBS), intestinal transplantation, GLP2 (teduglutide) treatment for SBS or bowel lengthening

144
Q

what is malabsorption

A

defective mucosal absorption caused by defective luminal digestion, mucosal disease and structural disorders

145
Q

what are common causes of malabsorption

A

coeliac disease, crohns disease, post infectious, biliary obstruction, cirrhosis

146
Q

what are uncommon causes of malabsorption

A

pancreatic cancer, parasites, bacterial overgrowth, drugs, short bowel

147
Q

E/O of coeliac disease

A

intestinal antigen-presenting cells in people expressing HLA-DQ2, or HLA-DQ8, bind with dietary gluten peptides in their antigen binding grooves activate specific mucosal T lymphocytes cytokines mucosal damage

148
Q

symptoms of coeliac disease

A

spectrum asymptomatic to nutritional deficiencies - weight loss, diarrhoea, excess flatus and abdominal discomfort

149
Q

how is coeliac disease diagnosed

A

IgA anti-tissue transglutaminase test (tTGA)biopsy confirmative

150
Q

treatment for coeliac disease

A

gluten free diet

151
Q

E/O of lactose malabsorption

A

deficiency of lactase

152
Q

symptoms of lactose malabsorption

A

history of induction of diarrhoea, abdominal discomfort and flatulence following ingestion of dairy product

153
Q

how is lactose malabsorption diagnosed

A

the diagnosis is confirmed by lactose breath hydrogen test alternative is oral lactose intolerance test

154
Q

treatment for lactose malabsorption

A

lactose free diet

155
Q

E/O of tropical sprue

A

colonisation of the intestine by an infectious agent or alterations in the intestinal bacterial flora induced by exposure to another environmental agent

156
Q

what is symptoms of tropical sprue

A

diarrhoea, steatorrhea, weight loss, nausea and anorexia, anaemia

157
Q

how is tropical sprue diagnosed

A

biopsy

158
Q

what is treatment of tropical sprue

A

tetracycline and folic acid

159
Q

E/O of whipple’s disease

A

tropheryma whippleimultisystem involvement increase in frequency of HLA-B27

160
Q

symptoms of whipple’s disease

A

weight loss, diarrhoea, steatorrhoea and absominal distention, arthritis, fever, nutritional defect symptoms

161
Q

how is whipple’s disease diagnosed

A

diagnosis is established by demonstration of T.whipplei in involved tissues by microscopy

162
Q

what is treatment of whipple’s disease

A

antimicrobial

163
Q

what is E/O of crohns disease

A

crohns disease patients with extensive ileal involvement, extensive intestinal resections, enterocolic fistulas and structures leading to small intestinal bacterial overgrowth may develop significant and occasionally devastating malabsorption

164
Q

what is symptoms of crohns disease

A

abdominal pain and diarrhoea, fever and weight loss, abdominal tenderness, most classically in right lower quadrant

165
Q

how is crohns disease diagnosed

A

endoscopybarium imaging of small bowel mucosal disease, including strictures, ulcerations and fistulaeCT, MRIcolonoscopy - punched out lesions

166
Q

what is treatment for crohns

A

steroids, immunosuppressants, azathioprine 6-MP, biological therapy (and TNF)

167
Q

what is the risk factors for parasitic infections - giardia lamblia

A

travel to areas where water supply may be contaminated, swimming in ponds

168
Q

what is symptoms of parasitic infections

A

diarrhoea, flatulence, abdominal cramps and epigastric pain and nauseasignificant malabsorption with steatorrhea and weight loss may develop

169
Q

how is parasitic infections diagnosed

A

stool examination for ova and parasites

170
Q

what is treatment for parasitic infection

A

metrondiazole - 1 week

171
Q

what other parasites apart from giardia lambila can cause parasitic infection

A

coccidial, strongyloides

172
Q

what bacteria is involved in small bowel bacterial overgrowth

A

E.coli or bacteroids

173
Q

what is E/O of small bowel bacterial overgrowth

A

diverticula, fistulas and strictures related to crohns disease, bypass surgeries, functional stasis

174
Q

how is small bowel bacterial overgrowth diagnosed

A

low cobalamin and high folate levels

175
Q

what is treatment for small bowel bacterial overgrowth

A

surgical correction of anatomical blind looptetracyclines 2-3 weeks

176
Q

what is malnurition

A

deficit of energy, protein, vitamins and minerals with measurable adverse effects on body

177
Q

what are the disease related causes of malnutrition

A

decreased intake, impaired digestion/absorption, increased nutritional requirements, increased nutrient losses

178
Q

what is consequences of malnutrition

A

increased infection rate decreased wound healing physical weakness

179
Q

what acute events can cause GI dysfunction and malnutiriton

A

sepsis, pneumonia etc fever surgery trauma radiotherapy chemotherapy

180
Q

what chronic events can cause GI dysfunction and malnurtrition

A

anorexiaasthenia, depressiondysphagia malabsorption, fistula, diarrhoeainfection (TB, HIV etc)immobility

181
Q

what are the effects of starvation

A

decreased metabolic rateslow weight lossdecreased nitrogen lossesearly increases in catecholamines, cortisol, GH then slow fall - insulin decreasedinitial loss of water and sodium, late retention

182
Q

what are the effects of injury

A

increased metabolic rate rapid weight loss increased nitrogen losses increase in catecholamines, cortisol, GH - insulin increasedretention

183
Q

what is used to assess malnutrition

A

malnutrition universal screening tool (MUST) - look this up

184
Q

how is anthropometry used to assess nutrition

A

mid-arm muscle circumference, triceps and grip strength

185
Q

what biochemical assesments can be used o assess nutritional status

A

albumin (reduced), tansferrin (reduced), transthyretin (reduced), retinol binding protein, urinary creatinine, IGF-1 (reduced) and micronutrients

186
Q

what biochemical measures are used in older people in community

A

vitamins A, C, D and E, albumin and zinc all statistically significantly lower in high risk group compared with low risk group

187
Q

what is enteral tube feeding

A

the delivery of nutritionally complete feed directly into gut via tube (nasogastric NG or nasojejunal NJ)used if poor oral untake but functional, accessible GI tract

188
Q

what is contradictions for ETF

A

lower GI obstruction, prolonged intestinal ileus, severe diarrhoea or vomiting, high enterocutaneous fistula, intestinal ischaemia

189
Q

what are the indications for parenteral nurition

A

poor oral intake (or enteral nutritional intake) and non functional GI tract (eg by IBD, radiation enteritis, short bowel syndrome, motility disorders)

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