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GI Flashcards

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0
Q

Symptoms of upper GIT diseases

A

Haematemesis and Melaena,
Nausea & vomiting,
Dysphagia, odynophagia (difficult and painful swallowing),
Heartburn, acid regurgitation & belching,
Chest pain,
Epigastric pain.

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1
Q

General symptoms of Digestive disorders.

A

Anorexia,
Weight loss,
anaemia.

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2
Q

Odynophagia is..

A

Painful swallowing.

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3
Q

Symptoms of liver and biliary diseases

A 
RUQ pain,
Biliary Colic,
Jaundice,
Dark Urine / pale stool,
Abdominal distension (Ascites).
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4
Q

Symptoms of mid GIT and pancreas diseases

A

Abdominal pain,
Diarrhoea / steatorrhoea,
Distension.

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5
Q

Symptoms of lower GIT diseases

A 
Abdominal pain,
Bleeding,
Constipation,
Diarrhoea,
Incontinence.
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6
Q

General signs of digestive diseases

A 
Cachexia,
Obesity,
Lymphadenopathy,
Anaemia,
Jaundice,
Stigmata of chronic liver disease.
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7
Q

Hand signs of digestive diseases

A 
Koilonychia - Spoon nails,
Leuconychia - white nails,
Clubbing
Palmar erythema,
Dupytrens contracture,
Tremor,
Tachycardia.
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8
Q

Dupuytren’s contracture

A

fixed flexion contracture of the hand where the fingers bend towards the palm and cannot be fully extended.

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9
Q

Palmar erythema

A

reddening of the palms at the thenar and hypothenar eminences.

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10
Q

Abdominal signs of digestive diseases

A

Organ enlargement,
Mass,
Tenderness,
Distension.

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11
Q

Anal and rectal signs of digestive diseases

A 
Haemorrhoids,
Fistula,
Fissure,
Rectal masses,
Proctitis.
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12
Q

Proctitis

A

an inflammation of the anus and the lining of the rectum, affecting only the last 6 inches of the rectum.

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13
Q

The major cause of death in alcoholics is…

A

Complications of cirrhosis.

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14
Q

What are the percentages of outcome from HBV infection?

A

90% self-limiting, 10% persistent infection. Of those persistent infections: 70% symptomatic carriers, 30% Cirrhosis +/- Hepatocellular carcinoma.

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15
Q

What are the percentages of outcome from HCV infection?

A

20% self limiting, 80% persistent infection. Of those persistent infections: 80% non-progressive, 20% progressive.

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16
Q

What % of adults suffer dyspepsia?

A

40% - indigestion.

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17
Q

Helicobacter pylori

A

Gram-negative, spiral bacterium that colonises the gastric mucosa.

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18
Q

95% of pancreatic cancers are what type?

A

Adenocarcinomas of the pancreatic duct

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19
Q

Prevalence of gall stones in UK

A

1 in 10, especially women, overweight, middle aged or over

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20
Q

Which cells secrete gastric lipase?

A

Fundic cells.

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21
Q

What stimulates parietal and chief cell secretion?

A

Vagal activity, gastric distension, gastrin and histamine.

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22
Q

Major constitute of bile acid micelle.

A

Cholic acid

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23
Q

How many essential amino acids are there?

A

8

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24
Q

Trypsinogen is converted to what by what?

A

Trypsin by enteropeptidase

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25
Q

Example of exopeptidases

A

Carboxypeptidase

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26
Q

Example of endopeptidases

A

Trypsin, chymotrypsin, elastase.

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27
Q

5 levels of human needs (Maslow’s Hierarchy of Needs)

A 
Self-actualisation
Ego (esteem)
Social (belonging)
Safety/security
Physiological
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28
Q

During a short fast, majority of change is seen in which tissues?

A

Liver and gut (small loss in muscle and fat)

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29
Q

During a long fast, majority of change is seen in which tissues?

A

Muscle and fat (50%), same effect in liver and gut as short fast.

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30
Q

Ascorbic acid aka …..? Deficiency causes …..?

A

Vitamin C. Deficiency causes scurvy.

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31
Q

Vitamin B3 aka ….? Deficiency causes …..?

A

Niacin. Deficiency causes Pellagra.

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32
Q

Deglutition

A

Swallowing food

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33
Q

The three layers of the GIT from lumen outwards…

A

Mucosa, circular muscle, longitudinal muscle. Between the mucosa and circular muscle is the submucosal plexus, and between the two layers of muscle is the myenteric plexus.

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34
Q

Responsible for segmental contractions and peristaltic movements through the GIT.

A

Muscularis externa - inner circular SM + outer longitudinal SM.

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35
Q

Parasympathetic stimulation of GIT causes…

A

Smooth muscle contraction.

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36
Q

Achalasia

A

Lack of peristalsis of the lower oesophagus and incomplete relaxation of the lower oesophageal sphincter

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37
Q

What triggers swallowing reflex?

A

Pressure of bogus of pharynx

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38
Q

An increase in .. what?.. firing to the lower oesophageal sphincter causes it to….?x

A

Vagal inhibitory fibre firing causes relaxation, combined with decrease in vagal excitatory fibres.

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39
Q

Lower two thirds of oesophagus is composed of…

A

Smooth muscle and squamous mucosa, whereas the upper third is striated muscle and columnar mucosa.

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40
Q

The angle of hiss

A

Oblique angle of entry of oesophagus into stomach that forms a valve to prevent reflux

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41
Q

Cellular substrate of gastric pacemaker…

A

Interstitial cells of Cajal (ICCs)

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42
Q

Most antral contractions are…

A

Retrograde - facilitates mixing of food

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43
Q

Factors determining gastric emptying

A 
Gastric volume (increase accelerates).
Osmolarity (high slows)
Nutrients (fat and protein slow via CCK)
pH (high accelerates)
Vagal stimulation (accelerates)
SNS stimulation (decelerates)
Dopamine (inhibits)
Opiates (inhibitis)
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44
Q

Gastroparesis

A

Delayed gastric emptying due to stomach paralysis. Commonly caused by diabetic autonomic neuropathy.

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45
Q

Sphincter of oddi

A

Aka sphincter of hepatopancreatic ampulla, controls the flow of bile and pancreatic juices into the duodenum.

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46
Q

3 phases of fasting motility in the small intestine.

A

Phase I - contractile quiescence (15-30 mins).
Phase II - irregular phasic contractions (60-90 mins).
Phase III - migrating motor complex (MMC) (3-8 mins).

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47
Q

Which muscle is involved in voluntarily delaying deification?

A

Puborectalis - it alters the anorectal angle

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48
Q

Muscularis mucosa

A

Smooth muscle layer outside the lamina propria mucosae, separating it from the submucosa.

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49
Q

Total surface area of intestines?

A

200 square metres

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50
Q

Where are the enterocytes which express genes for active transport located?

A

Tip of the villi

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51
Q

What are preferentially absorbed in the terminal ileum?

A

Bile salts and cobalamin (B12)

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52
Q

What is maximally absorbed in the duodenum?

A

Iron and Calcium.

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53
Q

Loss of APC increases activity in which pathway?

A

Wnt pathway.

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54
Q

Stool cultures are needed for IBD to…

A

Rule out infection.

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55
Q

Truelove and Witts Criteria

A

For acute severe colitis:

BO>6x/day, tachycardia, pyrexia >37.5, anaemia.

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56
Q

Treatment for acute severe colitis.

A

IV hydrocortisone, Cyclosporin after 3-4 days no improvement, colectomy after 5-7 days no improvement.

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57
Q

Treatment for mild to moderate active UC

A

5-ASA therapy (mesalazine, sulfasalazine), topical if left sided.

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58
Q

Treatment for moderate to severe active UC

A

Oral prednisolone.

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59
Q

Treatment for active CD

A

Steroid therapy and diet control.

Azathioprine for difficult disease, Infliximab for very difficult disease.

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60
Q

What effect does 5-ASA have on UC remission rate?

A

Reduces it by ~60%. Has little effect against Crohn’s Disease however.

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61
Q

Long term issue with IBD.

A

Malignancy - colorectal carcinoma.

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62
Q

Features of myenteric (Auerbach’s) plexus

A

Parasympathetic origin, releases ACh, duel innervation, excitatory action causing muscle contraction, secretion and vasodilation.

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63
Q

Features of submucosal (Meissner’s) plexus

A

Only parasympathetic innervation, provides secretor motor innervation to gut mucosa. Neurotransmitter NA.

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64
Q

IBS diagnosis Rome criteria III

A

Recurrent abdominal pain >3 months plus two of:

Relieved by defecation, onset associated with change in stool frequency or form/appearance.

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65
Q

Serotonin is released from which cells when stimulated by pain?

A

Enterochromaffin cells

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66
Q

ENS signals via afferents to which brain regions?

A

Midbrain, thalamus and cortex

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67
Q

IBS patients have a ….. pain threshold?

A

Reduced pain threshold.

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68
Q

Treatments for IBS

A

Dietary advice, antidepressants, biofeedback, psychotherapy, CBT, hypnotherapy

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69
Q

Pancreatic mass presents with..

A

Painful obstructive jaundice, loss of appetite, weight loss.

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70
Q

Pancreatitis bloods

A

Elevated amylase, alkaline phosphatase, ALT and bilirubin (if obstruction)

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71
Q

What endocrine hormones does the pancreas secrete?

A

Insulin, glucagon and somatostatin.

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72
Q

Acute pancreatitis diagnosis.

A

Acute upper abdo pain, nausea and vomiting, raised amylase.

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73
Q

Causes of acute pancreatitis

A

Gallstones, alcohol, drugs, hereditary, infection-mumps, trauma.

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74
Q

Acute pancreatitis results from…

A

Inappropriate activation of pancreatic enzymes - autodigestion, necrosis and immune response.

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75
Q

Causes of chronic pancreatitis.

A

Alcohol, gallstones, autoimmune, hereditary.

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76
Q

Types of chronic pancreatitis

A

Type A - recurrent pain
Type B - continuous pain
No pain.

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77
Q

Protein affected in high penetrance hereditary pancreatitis

A

Trypsin-1 (cationic Trypsinogen) (PRSS1)

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78
Q

Which duct becomes the main pancreatic duct in development?

A

Ventral duct.

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79
Q

Which part of the pancreas are islet cells most abundant?

A

In the tail.

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80
Q

Insulin

A

Anabolic hormone, promotes glucose transport into cells and storage as glycogen, reduces blood glucose, promotes protein synthesis and lipogenesis.

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81
Q

Glucagon

A

Increases gluconeogenesis and glycogenolysis hence increases blood glucose.

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82
Q

Acini secrete …..

Islets secrete …..

A

Acini - pancreatic juice

Islets - endocrine hormones

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83
Q

Which cells secrete glucagon?

A

Alpha islet cells

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84
Q

Which cells secrete somatostatin?

A

Delta islet cells

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85
Q

Two components of pancreatic juice

A

Low volume, viscous, enzyme rich secretions from Acinar cells.
High volume, watery, HCO3 rich secretions from duct and centroacinar cells.

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86
Q

As duodenal pH falls below 5….

A

There is a linear increase in pancreatic bicarbonate secretion, maximal secretion at pH 3

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87
Q

Why does bicarbonate secretion stop when pH is still acid?

A

Bile also contains bicarbonate and helps neutralise acid. Brunners glands secrete alkaline fluid (in small intestine).

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88
Q

Main enzyme involved in bicarbonate secretion.

A

Carbonic anhydrase.

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89
Q

Which ions are exchanged at which membranes in pancreatic bicarb secretion?

A

Cl/HCO3 exchange at luminal membrane.
Na/H exchange at basolateral membrane - bloodstream.
Na gradient maintained by Na/K exchange pump.
K and Cl return via channels.

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90
Q

Gastric venous blood is…

A

Alkaline

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91
Q

Pancreatic venous blood is…

A

Acidic

92
Q

Brushborder enterokinases cleave…

A

Trypsinogen between a valine and isoleucine.

93
Q

Which pancreatic enzyme is secreted in active form?

A

Lipase, requires colipase which is secreted as a precursor.

94
Q

Orlistat

A

Anti-obesity drug, inhibits pancreatic lipases - causes steatorrhoea.

95
Q

Cephalic phase of pancreatic secretion

A

Reflex response to food stimuli.

Enzyme-rich component only - low volume.

96
Q

Gastric phase of pancreatic secretion

A

Stimulation from food arrival in stomach

97
Q

Intestinal phase of pancreatic secretion

A

Hormonally mediated when gastric chyme enters duodenum. Both components of pancreatic juice stimulated.

98
Q

Bicarbonate secretion by pancreas is controlled by…

A

Secretin (cAMP)

99
Q

Enzyme secretion by pancreas is controlled by…

A

Vagal reflex and cholecystokinin (CCK) (Ca/PLC)

100
Q

H+ ions in duodenum stimulate release of….

A

Secretin into blood which stimulates pancreas to secrete bicarb.

101
Q

Peptides and fat in the duodenum stimulate release of…

A

CCK into blood, stimulating pancreas to secrete enzymes. CCK also potentates effects of secretin - more bicarb secretion.

102
Q

Gastrin is produced by which part of the stomach?

A

Antrum

103
Q

HCl and pepsinogen are produced by which parts of the stomach?

A

Body and fundus

104
Q

Stomach has a third smooth muscle layer called…

A

Oblique layer - produces powerful contractions to grind food into small particles

105
Q

Mucosa of stomach

A

Simple epithelium one cell thick, secretes protective mucus-HCO3 blanket. Glands secrete into ‘pits’

106
Q

Gastric glands of body and fundus contain..

A

Chief cells (bottom) and parietal cells. Proliferative neck region.

107
Q

Parietal cells secrete…

A

HCl, Intrinsic factor and R protein

108
Q

Protein digestion begins with which enzyme?

A

Pepsin, in the stomach. Inactivated in alkaline duodenum.

109
Q

Ion transporters In chief cells

A

K/H ATPase at lumen.

Cl/HCO3 exchange at serosal membrane.

110
Q

Resting parietal cell

A

Cytoplasmic tubulovesicles, internal canaliculi, many mitochondria.

111
Q

Secreting parietal cell

A

Elaborate bell-shaped canaliculus open to gland lumen. Tubulovesicles absent.

112
Q

Parietal cell H+ pump is inhibited by…

A

Omeprazole

113
Q

Parietal cells have receptors for…

A

ACh, Gastrin and Histamine. All stimulate acid secretion.

114
Q

Vagus nerve effect on parietal cells..

A

Directly stimulates parietal cell, also stimulates gastrin and histamine release.

115
Q

NERD stands for…

A

Non-erosive reflux disease - 70% of patients with reflux symptoms.

116
Q

Functional heartburn

A

Symptoms not due to acid reflux

117
Q

Bernstein test

A

Reproduces symptoms of heartburn by sending HCl down oesophagus with tube.

118
Q

GORD medical treatment

A

Antacids, H2 receptor antagonists, Proton pump inhibitors.

119
Q

Surgical treatment for GORD

A

Nissen’s fundoplication

120
Q

Proton pump inhibitors are a risk factor for…

A

Clostridium difficile-associated diarrhoea

121
Q

Consequences of GORD

A

Oesophagitis, stricture, Barrett’/s -> cancer

122
Q

Paneth cells are where and produce what?

A

At the base of crypts. Produce defensins and lysozyme.

123
Q

Gut Associated Lymphoid Tissue

A

Peyer’s patches, isolated lymphoid follicles, appendix.

124
Q

Peyer’s patches are located…

A

In the small intestine, mainly distal ileum.

125
Q

Peyer’s patches are covered by…

A

Follicle associated epithelium (FAE): no goblet cells, microvilli or IgA.

126
Q

Mature naive B-cells in peyer’s patches express.. and do what on exposure to antigen?

A

Express IgM, class switch to IgA upon antigen presentation.

127
Q

IgA secreting plasma cells populate…

A

The lamina propria

128
Q

IgA is transported into the epithelial lumen by..

A

Epithelial cells

129
Q

IgA in the lumen…

A

Binds luminal antigen, prevents invasion and adherence, does not activate complement or cytotoxic lymphocytes.

130
Q

Th1 adaptive response associated with which diseases?

A

Crohn’s disease and coeliac disease

131
Q

Th2 adaptive response associated with which diseases?

A

Food allergy and ulcerative colitis. Th2 normal gut response however.

132
Q

Th17 adaptive response associated with which diseases?

A

Crohn’s disease

133
Q

TReg cells associated with…

A

Tolerance

134
Q

Loss of immune tolerance in the gut may underlie…

A

IBD, Coeliac disease, food allergy.

135
Q

Eating red meat and cholecystectomy are associated with which-sided colorectal tumours?

A

Red meat - left sided tumours.

Cholecystectomy - right sided.

136
Q

Protective factors against colorectal cancer

A

High fruit/veg low red meat diet, NSAIDs, exercise, folic acid, HRT, statins, fibre?

137
Q

Risk factors for colorectal cancer

A

Age, alcohol, acromegaly, smoking, red meat, cholecystectomy, pelvic radiation.

138
Q

Risk of CRC with FAP

A

100%

139
Q

Risk of CRC with HNPCC

A

50-80%

140
Q

Adenomas preceded CRCs by..

A

10-15 yrs. Their removal decreases the incidence of cancer.

141
Q

Commonest mechanism for genetic defects in CRC…

A

Chromosomal instability (CIN) - causes physical loss of wild-type copy of tumour suppressor genes (APC, P53, SMAD)

142
Q

MSI-H stands for..

A

Micro satellite instability - high. Problem with mismatch repair system e.g. HNPCC results in frameshift mutation inactivating TSGs

143
Q

MYH-associated polyposis

A

Geraldine mutation in MYH gene - repairs oxidative damage to guanine. Recessive inherited CRC.

144
Q

APC mutation results in…

A

Accumulation of beta catenin.

145
Q

Ashkenazi Jews have a high incidence of..

A

CRC due to germline mutation in APC.

146
Q

SMAD mutations result in inactivation of…

A

TGF Beta signalling

147
Q

COX-2 inhibition and CRC…

A

Prevents new adenomas and mediates regression of established adenomas by reducing prostaglandin signalling.

148
Q

Cetuximab

A

Epidermal growth factor inhibitor

149
Q

Bevacizumab

A

Vascular endothelial growth factor A inhibitor

150
Q

K-Ras and BRAF mutations predict…

A

No response to Cetuximab

151
Q

Cause of Typhoid

A

Salmonella typhi

152
Q

Gut hormones are produced by…

A

Cells in the mucosa or submucosa of the stomach, intestine and pancreas.

153
Q

Somatostatin..

A

Universal inhibitor, secreted by D cells in gastric ad intestinal mucosa, pancreas and also hypothalamus.

154
Q

Octreotide

A

Somatostatin analogue with poor potent inhibitory action

155
Q

High concentrations of secretin…

A

Inhibit gastric acid and gastric emptying.

156
Q

The blood brain barrier of the arcuate nucleus is…

A

Incomplete, allowing access to peripheral hormones

157
Q

To neuronal populations of arcuate nucleus

A

NPY/Agrp neurons - stimulatory.

POMC neurons - inhibitory.

158
Q

Arcuate nucleus projects to…

A

Paraventricular nucleus of hypothalamus to affect feeding.

159
Q

PYY effect on arcuate nucleus neurons

A

Inhibits NPY release, stimulates POMC neurons -> decreases appetite

160
Q

Affects of Ghrelin on arcuate nucleus neurons

A

Stimulates NPY/Agrp neurons, inhibits POMC neurons -> increases appetite

161
Q

Livers blood supply

A

20% arterial from hepatic artery, 80% venous from hepatic portal vein

162
Q

Liver unit… consists of…

A

Lobule, consists of cords of liver epithelial cells (hepatocytes) radiating from central vein.

163
Q

Portal triads consist of..

A

Arteriole, branch of portal vein and a bile duct, all coming from main triad entering liver at hilum,

164
Q

Cholangiocytes

A

Line biliary structures

165
Q

Kupffer cells

A

Fixed liver macrophages

166
Q

Hepatic stellate cells store…

A

Vitamin A. May be activated to a fibrogenic myofibroblastic phenotype.

167
Q

Space of Disse (D)

A

Aka perisinusoidal space. Between hepatocytes and a sinusoid. Contains blood plasma.

168
Q

Hepatic lobule differs from portal lobule…

A

Hepatic lobule drains to common central vein. Portal lobule secretes bile to common bile duct at a triad. Portal acinus is where drainage, secretion and artery supply is all common.

169
Q

All liver functions are carried out by… Except….

A

Hepatocytes except breakdown of red cells which is by Kupffer cells.

170
Q

Cori cycle

A

Metabolic pathway in which lactate produced by anaerobic glycolysis in muscle moves to the liver and is converted to glucose.

171
Q

Transamination

A

Exchange of an amine group on one acid with a ketone group on another acid.

172
Q

Major components of bile

A

Bile salts, cholesterol, phospholipids, bile pigments, bicarbonate and water

173
Q

Secondary bile salts are formed by…

A

Bacteria in the ileum. They de-conjugate and de-hydroxylate primary bile salts.

174
Q

Bile is secreted by…

A

60% hepatocytes, 40% cholangiocytes.

175
Q

Role of biliary tree in bile production.

A

Glutathione is split and reabsorbed, glucose and organic acids reabsorbed, HCO3 and Cl actively secreted into bile by CFTR protein, H2O drawn into bile by osmosis.

176
Q

Main bile transporters

A

Bile salt excretory pump (BSEP), MDR related proteins.

177
Q

Bile acids are conjugated in the liver to..

A

Glycine and taurine.

178
Q

2 main primary bile acids

A

Cholic acid and chenodeoxycholic acid

179
Q

Cell membranes protected from concentrated bile salts by..

A

Other intraluminal lipids, and cholesterol and glycolipid plasma membrane content.

180
Q

Canal of Hering

A

Between bile canaliculi and interlobular bile ducts at outer edge of liver lobule. Partially lined by cholangiocytes and hepatocytes.

181
Q

Gall bladder contraction is stimulated by..

A

Cholecystokinin (CCK), released once fats and proteins enter duodenum.

182
Q

95% bile salts reabsorbed in the..

A

Terminal ileum

183
Q

Gall bladder functions

A

Stores, acidifies and concentrates bile.

184
Q

Oxidation of …. to …. causes faeces colour

A

Stercobilinogen oxidised to stercobilin

185
Q

Cholestasis

A

Cessation of bile flow

186
Q

Classification of causes of jaundice

A

Pre-hepatic: increased rate of BR formation,
Hepatic: damage to liver, failure to form bile, reflux of bile,
Post-hepatic: damage to intrahepatic bile ducts, obstruction of intra or extra hepatic bile ducts.

187
Q

Other substances excreted into bile

A

Adrenocortical and steroid hormones, drugs, cholesterol, alkaline phosphatase (ALP)

188
Q

Liver failure pathophysiology characterised by..

A

Centrilobular necrosis of hepatocytes and mononuclear cell infiltrate.

189
Q

Acute liver failure definition

A

Onset of liver dysfunction in a patient without know liver disease and an illness <6 months duration.

190
Q

Acute liver failure subdivided according to..

A

Interval between onset of jaundice and encephalopathy.
Hyperacute <7days,
Acute 1-4 weeks,
Subacute 5-28 weeks.

191
Q

Clinical features of acute liver failure

A

Hepatic encephalopathy, cerebral oedema, coagulopathy, infection, decreased glucose K Na, metabolic acidosis.

192
Q

Clinical features of cerebral oedema

A

Systolic hypertension, increased muscle tone, myoclonus, dysconjugate eye movements, loss of pupillary reflexes, resp arrest.

193
Q

Liver synthesises all coagulation factors except…

A

Factor VIII

194
Q

To assess coagulopathy, measure the…

A

Prothrombin time

195
Q

Budd-Chiari syndrome

A

Obstruction of hepatic veins at any site from lobule to entry of IVC into right atrium.

196
Q

Wilson’s disease

A

Autosomal recessive disease leading to accumulation of copper within the body. May present with acute or chronic liver failure. Treat with penicillamine - copper chelator.

197
Q

Penicillamine

A

Copper chelator used to treat Wilson’s disease

198
Q

Kayser-Fleischer ring

A

Ring of copper around the iris due to Wilson’s disease

199
Q

Acute fatty liver of pregnancy

A

Presents 3rd trimester, urgent delivery required as treatment.

200
Q

Child-Pugh grade/score is used to…

A

Assess prognosis of chronic liver disease/cirrhosis.

201
Q

Sengstaken Blakemore tube is used for…

A

Oesophageal varices

202
Q

Features of chronic liver failure

A

Portal hypertension -> varicies
Ascites,
Hepatorenal syndrome

203
Q

Types of hepatorenal syndrome

A

1 - rapidly progressive renal failure, very poor prognosis.

2 - slowly progressive, poor prognosis.

204
Q

Key presenting features of malabsorption.

A

Diarrhoea / steatorrhoea

Growth failure / weight loss

205
Q

Full range of nutrients

A 
Fats
Amino acids and protein
Carbohydrates
Electrolytes and water
Minerals
Trace elements
Vitamins
206
Q

Causes of maldigestion

A

Reduced gastric tissue / secretion,
Loss of pancreatic tissue,
Impaired bile secretion,
Reduction in intestinal brush-border enzymes.

207
Q

Malabsorption causes

A

Loss of functional enterocytes,
Pre- and post-mucosal effects,
Single gene disorders.

208
Q

Faecal test for exocrine pancreatic sufficiency

A

Faecal pancreatic elastase 1 < 200 micrograms/g

209
Q

Common specific causes of malabsorption.

A

Coeliac disease, small bowel bacterial overgrowth, pancreatic insufficiency (chronic pancreatitis, cystic fibrosis).

210
Q

Coeliac disease

A

Inflammatory disease of upper small intestine resulting from gluten ingestion in genetically susceptible individuals.

211
Q

Blood test for coeliac disease

A

IgA Anti-endomysial antibodies and / or anti-tissue transglutaminase antibodies.

212
Q

What skin disease is associated with coeliac disease?

A

Dermatitis herpetiformis

213
Q

Coeliac disease more prevalent in patients with..

A

Diabetes type I, thyroid disease, IBS, osteoporosis, and in anaemic blood donors.

214
Q

Complications of coeliac disease

A

Nutrient malabsorption and impaired nutritional status.
Small bowel malignancy.
Osteoporosis / osteopenia.

215
Q

Which malignancies are associated with coeliac disease?

A

Lymphoma - enteropathy-associated T-cell lymphoma (EATL)

Adenocarcinoma

216
Q

Biggest cause of end stage liver disease?

A

HBC/HCV, followed by alcohol.

217
Q

After injury, collagen is laid down by….then broken down by…

A

Stellate cells, broken down by matrix metalloproteinases.

218
Q

What important cytokine is involved in activating stellate cells?

A

TGF-beta

219
Q

Hepatic venous pressure gradient =

A

Wedged hepatic venous pressure - free hepatic venous pressure. If greater than 5 = portal hypertension.

220
Q

Causes of portal hypertension can be…

A

Pre-hepatic - splenic or portal vein thrombosis.
Hepatic - cirrhosis, granulomatous disease.
Post-hepatic - Budd-Chiari syndrome

221
Q

Complications of portal hypertension.

A

Varices and variceal bleeding, ascites, encephalopathy.

222
Q

Vasopressin lowers portal pressure by…

A

Splanchnic vasoconstriction, also causing reduction in hepatic blood flow.

223
Q

Terlipressin

A

Synthetic vasopressin analogue. Maintains hepatic blood flow whilst decreasing portal pressure.

224
Q

TIPS stands for..

A

Transjugular intrahepatic porto-systemic shunt.

225
Q

Upregulation of which enzyme causes tolerance to alcohol?

A

Cytochrome P-450 2E1

226
Q

Chronic viral hepatitis can be caused by…

A

Hep B,C and D viruses.

227
Q

Consequences of chronic hepatitis infection

A

Cirrhosis and hepatocellular carcinoma

From Flashcardlet (8 decks)

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