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Work sessions Flashcards

1
Q

What five things should be the focus of an assessment of readiness to lose weight?

A
  1. How they’re feeling about losing weight (previous attempts, motivation etc)
  2. How life would be different if they did (expectations)
  3. Advantages and disadvantages of weight loss
  4. Barriers to weight loss (eg binge eating)
  5. Support mechanisms
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2
Q

Which two things are used to calculate daily energy expenditure?

A
  1. Basal metabolic rate

2. Physical activity ratios

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3
Q

What is gastric acid secretion stimulated by?

A

Acetylcholine and gastrin binding to receptors on parietal cells. They also indirectly stimulate it by stimulating the release of histamine from ECL cells.

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4
Q

What is gastric acid inhibited by?

A
  1. Somatostatin
  2. Prostaglandin binds to a receptor on the parietal cell and activates an inhibitory G protein that inhibits adenylate cyclase so decreases gastric acid production.
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5
Q

A peptic ulcer is a break in epithelial cells that penetrates to the _____________ (which layer?) in the _________ or ___________

A

Muscluaris mucosa, stomach, duodenum

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6
Q

What are the symptoms of a peptic ulcer?

A
  1. burning/gnawing pain in upper left abdomen, maybe after eating, worse at night.
  2. indigestion, heart burn
  3. loss of appetite, weight loss
  4. vomiting
  5. melina
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7
Q

What are peptic ulcer symptoms relieved by?

A

Eating and antacid tablets

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8
Q

What are three potential complications of a peptic ulcer?

A
  1. Perforation
  2. Internal bleeding
  3. Scar tissue (makes digestion difficult)
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9
Q

What are two main causes of peptic ulceration?

A
  1. Helicobacter pylori

2. NSAIDS

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10
Q

Is H. Pylori gram negative or positive?

A

Gram negative

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11
Q

Which cells does H. Pylori adhere to?

A

Gastric mucosal cells

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12
Q

Which enzyme does H. Pylori express? What does this do? Why is this beneficial for H. Pylori?

A

Urease, catalyses the conversion of urea into water and ammonia. Ammonia is alkaline so neutralises stomach acid, aiding H. Pylori’s survival

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13
Q

Which toxins do some strains of H. Pylori express? What do they do?

A

CagA (induces apoptosis) and VacA (increases cell permeability and prevents normal immune responses.)
Both associated with higher levels of inflammation

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14
Q

Other than peptic ulcers, what upper GI disorders are associated with H. Pylori?

A 
Non ulcer dyspepsia
Stomach cancer (CagA)
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15
Q

How is H. Pylori diagnosed?

A
  1. Breath test
  2. Stool antigen test
  3. Blood test for antibodies
  4. Biopsy (usually if endoscopy being done anyway)
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16
Q

Which patients with dyspepsia might undergo an endoscopy?

A
  1. > 55yo with dyspepsia

2. Red flags for cancer (weight loss, melaena, anorexia, dysphagia, haematemesis)

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17
Q

How is H. Pylori treated?

A

PPI + 2 antibiotics (amoxycillin + clarithromycin/metronidazole)

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18
Q

What is the name of the proton pump that PPIs act on?

A

H+/K+ ATPase

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19
Q

What is the role of the enzyme COX?

A

Converts arachadonic acid into e.g. prostaglandin, prostacyclins, thromboxane.

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20
Q

What is the role of prostaglandins?

A

Promote inflammation, vasodilation and smooth muscle contraction. A paracrine hormone.

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21
Q

How do NSAIDs work?

A

Inhibit COX

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22
Q

What are the two isoenzyme forms of COX?

A

COX 1 (expressed all the time in a range of tissues including gastric mucosa) and COX 2 (in monocytes and macrophages in response to inflammation)

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23
Q

Why might aspirin use encourage secretion of excess gastric acid?

A

It inhibits COX which inhibits gastric acid via prostaglandins. So gastric acid secretion not inhibited.

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24
Q

Which isoenzyme of COX needs to be inhibited for NSAIDs to have their desired effect?

A

COX 2 - so want a drug specific to this.

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25
Q

What is a concern about COX 2 inhibitors?

A

They may increase risk of coronary heart disease

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26
Q

What is a further problem with taking aspirin if you already have a peptic ulcer?

A

Aspirin is an antithrombolytic so the ulcer is more likely to bleed.

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27
Q

How to H2 antagonists (another anti-ulcer drug) work? What are some names of these drugs?

A

Bind to histamine 2 receptors so histimine can’t bind- less stomach acid produced.
e.g. Ranitidine and Famotidine (available OTC)

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28
Q

Why can breathlessness be a symptom of a bleeding peptic ulcer?

A

Losing blood so become anaemic.

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29
Q

What can be done during an endoscopy to treat an ulcer?

A

inject adrenaline, thermocoagluation, seaking perforated ulcer

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30
Q

Describe the absorption of water, sodium, glucose, amino acids and chloride ions into the blood from the small intestine.

A
  1. Sodium rapidly exported from the cell by sodium pumps into the intercellular space so cell sodium concentration is low.
  2. Sodium is absorbed from the gut lumen down its concentration gradient by several mechanisms but in particular co-transport with glucose and amino acids, and by anti-port exchange with proteins.
  3. Cl- enters by anti-port exchange with bicarbonate ions.
  4. Water diffuses into the cell from the gut lumen due to osmotic gradient created by sodium. Mostly transcellular, some through tight junctions.
  5. Water and sodium diffuse into the blood.
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31
Q

Describe the lifecycle of an enterocyte

A

Begins life in the Crypts of Lieberkuhn as a secreting cell. It migrates up the walls of the crypt and ends life as an absorbative cell on the villi.

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32
Q

True or false water is only ever absorbed from the gut, never secreted into it.

A

False, water is secreted into the gut to disperse chyme, maximise contact with the epithelium and allow efficient enzymatic digestion to occur.

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33
Q

Which two processes establish an osmotic gradient that pulls water into the lumen of the intestine?

A
  1. Influx of food resulting in an increase in luminal osmotic pressure .
  2. Crypt cells serete electrolytes. e.g. CFTR (aka cyclic-AMP dependent chloride channel) which transports chloride ions out of the cell.
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34
Q

As digestion of foodstuffs proceeds, does the osmotic pressure of the gut lumen increase or decrease?

A

Increases (so more water flows in)

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35
Q

What are CFTR channels activated by?

A

Elevated levels of cAMP in the cell.

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36
Q

What are the four most common mechanisms causing diahoerra?

A
  1. Osmotic (macro-molecules aren’t broken down and absorbed so remain in the gut and draw fluid in)
  2. Secretory (lots of secretion of ions and therefore water to the lumen e.g. C. diff, cholera)
  3. Motility (abnormal motile function of gut)
  4. Infection and inflammation (damage to mucosal cells so fluid released)
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37
Q

What might cause osmotic diarrhoea?

A

Enzyme deficiency e.g. lactose intolerance.

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38
Q

Why might patients with glucose-galactose intolerance have flatulence and bloating?

A

The food is undigested so remains in the gut and is fermented which produces gas.

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39
Q

Other than enzyme deficiency, what is a cause of glucose-galactos intolerance?

A

Mutation in the SGLT1 gene (sodium/glucose transporter) so glucose absorption impaired.

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40
Q

What sort of diarrhoea results from lactose intolerance?

A

Osmotic

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41
Q

Why might lactose intolerance lead to malabsorption of other nutrients?

A

Causes diarrhoea so the passage of food through the gut is too rapid for much to be absorbed.

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42
Q

CFTR predominantly transports Cl- but what else can it transport?

A

Bicarbonate ions

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43
Q

What is meconium ileus?

A

Inability of a baby to pass meconium (first faeces)- occurs in cystic fibrosis because the meconium is too thick and sticky

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44
Q

How does cystic fibrosis affect digestion?

A

Pancreatic fluid and HCO3- secretion is reduced, leading to blockage of pancreatic ducts with mucus and limited delivery of pancreatic enzymes to the duodenum. This causes inadequate digestion leading to steatorrhea, diarrhoea and wasting.

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45
Q

What condition is meconium ileus indicative of?

A

Cystic fibrosis

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46
Q

Why does steatorrhea occur in cystic fibrosis?

A

Lack of pancreatic enzymes so fat not broken down so it is still present in stools.

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47
Q

Is cholera a gram negative or gram positive bacteria?

A

Gram negative

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48
Q

What are the three phases of cholera infection?

A
  1. Evacuation phase (profuse, watery diarrhoea)
  2. Collapse phase (caused by dehydration)
  3. Recovery phase (if the patient survives the collapse phase)
49
Q

Describe the action of the cholera toxin

A

Subunit of cholera toxin crosses the membrane of intestinal cells and permanently activates a G protein. This activates the enzyme adenyl cylcase which produces cAMP (2nd messenger) this activates a Cl- channel, large amounts of Cl-, HCO3-, K+, Na+ are secreted into the lumen of small intestines and water follows = diarrhoea

50
Q

How is cholera treated?

A

Oral rehydration / IV / intra peritoneal (

51
Q

True or false people with cystic fibrosis are unaffected by cholera

A

True

52
Q

Which antigens is coeliac disease associated with?

A

Human leukocyte MHC antigens DQ2 and DQ8

53
Q

What happens to the lining of the small intestine in coeliac disease?

A

Atrophy of villi, crypt hyperplasia- resembles colon and there is a reduction in surface area.

54
Q

What affect does coeliac disease have on patients?

A

poor growth, weight loss, deficiencies, diarrhoea

55
Q

What sort of diarrhoea is associated with cholera?

A

Secretory

56
Q

What sort of diarrhoea is associated with coeliac disease?

A

Osmotic

57
Q

Which type of diabetes is linked to coeliac disease?

A

Type 1

58
Q

Why might someone with coeliac disease experience tingling in their hands?

A

Reduced absorption of calcium, sodium and potassium which are needed for nerves.

59
Q

What are the five main components of the innate immune system?

A
  1. Physical barriers
  2. Phagocytic leukocytes
  3. Dendritic cells
  4. NK cells
  5. Circulating plasma proteins.
60
Q

How is the innate immune sytem activated?

A

Lectin, alternative and classical pathways.

61
Q

What are the three compartments of the mucosal immune system?

A
  1. Gut associated lymphoid tissue (peyer’s patches, adenoid, appendix)
  2. Intraepithelial lymphocytes (mainly CD8 cytotoxic T cells)
  3. Lamina propria lymphocytes (CD4 helper T cells, B lymphocytes, mast cells)
62
Q

What are the two factors thought to be involved in triggering the inflammatory response in IBD?

A

Alteration to enteric bacteria, genetic

63
Q

What is the difference between Ulcerative Colitis and Crohn’s in terms of location?

A

Crohn’s in any part of GI tract mouth to anus

UC only in colon

64
Q

What is the difference between Crohn’s and UC in terms of distribution?

A

UC is uninterrupted, Crohn’s is patchy

65
Q

What happens to the intestinal glands in ulcerative colitis? Is this the case with Crohn’s?

A

They are destroyed, but are preserved in Crohn’s.

66
Q

Where histologically does inflammation occur in UC and Crohn’s?

A

UC- mucosal and submucosal

Crohn’s- transmural (all layers)

67
Q

What are complications of Crohn’s?

A

Stricturing and fistulae

68
Q

What are complications of Ulcerative Colitis?

A

Colon cancer, colonic perforation, malnutrition, toxic megacolon.

69
Q

Is there a surgical cure for either Crohn’s or UC?

A

For UC can cure by removing colon. In Crohn’s can sometimes remove affected sections of the GI tract but no real cure.

70
Q

What symptoms might patients with IBD present with?

A 
Mucus/ blood in faeces/steatorrhea
Weight loss
Vomiting
Diarrhoea
Cramps/muscle spasms
Fatigue
Faecal urgency
71
Q

What signs might someone with IBD present with?

A
  1. Fistula
  2. Anaemia
  3. Mouth ulcer
  4. Abdominal tenderness
  5. Mass on palpitation
72
Q

What are the extra-intestinal manifestations of IBD?

A
  1. Musculoskeletal (arthritis, osteoporosis)
  2. Hepatobiliary (primary sclerosing cholongitis)
  3. Vascular (vasculitis)
  4. Dermatological (ulcers)
  5. Ocular (uvitis)
  6. Renal (kidney stones, glomerular nephritis)
73
Q

What type of granuloma is present in Crohn’s? Is it also present in UC?

A

Non-caseating granuloma. Not present in UC.

74
Q

What is the medical name for mouth ulcers?

A

Apthous ulcers.

75
Q

What drugs would you use to treat Crohn’s?

A
  • To induce remission: anti-inflammatories (corticosteroids)
  • To maintain remission: immune suppressants, methotrexate, antibiotics
  • In resistant cases: biological therapies e.g. TNF alpha antibodies.
76
Q

What is azathioprine?

A

An immunosuppressant drug. Pro-drug for mercaptopurine. Inhibits enzyme required for DNA synthesis and most strongly affects proliferating cells such as T and B cells.

77
Q

What is a monoclonal antibody?

A

Chimeric, mouse and human antibodies combined and it is specific to one antigen. e.g. infliximab binds to TNF and prevents it binding to its receptor. Drugs that are monoclonal antibodies always have the suffix ‘-mab’

78
Q

What are three common causes of liver disease in the UK?

A
  1. Viral hepatitis
  2. Alcohol consumption
  3. Non-alcoholic fatty liver disease (NAFLD)
79
Q

What are the routes of transmission of Hepatitis A, B and C?

A

A- Faeco-oral
B- Body fluids
C- Blood

80
Q

Of Hepatitis A, B and C, which are chronic and which are acute? Which is the most difficult to treat?

A

A acute, B acute but can become chronic, C chronic. B is hardest to treat- treatment rarely clears the virus.

81
Q

Which type of hepatitis is the most common infective agent globally?

A

Hepatitis A

82
Q

What system of the brain does alcohol initially inhibit?

A

Reticular activating system

83
Q

What might people who are alcohol dependent experience if they abstain from drinking?

A

Rebound hyperactivity.

84
Q

What is the daily recommended limit of alcohol intake for women and men?

A

Men: 3-4 units
Women 2-3 units
+ two days per week alcohol free

85
Q

What constitutes binge drinking?

A

Drinking more than twice the recommended limit in one session.

86
Q

What can be the effects of excessive drinking on the liver?

A 
Accumulation of triacylglycerols in hepatocytes
Alcoholic hepatitis (inflammation). Maybe with jaundice.
Fibrosis and cirrhosis long term.
87
Q

What is NAFLD?

A

Non-alcoholic fatty liver disease:

accumulation of triacylglycerides in hepatocytes not related to alcohol intake.

88
Q

What are risk factors for NAFLD?

A

Obesity, hypertension, type 2 diabetes, hyperlipidaemia.

89
Q

What are complications if NAFLD?

A

Inflammation (non-alcoholic steatohepatitis- NASH)

Fibrosis and cirrhosis.

90
Q

What structural changes occur at a gross level in liver cirrhosis?

A

Micro-nodular appearance
Enlarged
Mallory bodies

91
Q

What structural changes occur at a cellular level in liver cirrhosis?

A

Fibrosis
Stellate cells activated
Steatosis
Immune cell infiltration

92
Q

What conditions other than NAFLD, alcohol use and hepatitis can cause liver cirrhosis?

A

Hereditary haemachromatosis, alpha 1-antitrypsin deficiency, Wilson’s disease, galactosaemia, glycogen storage disease
Bile duct damage
Immune mediated damage
Drugs, toxins, infection

93
Q

What stage of haem metabolism occurs in the liver?

A

Conjugation

94
Q

What are the excretion products of haem metabolism?

A

Stercobilin in faeces and urobilin in urine.

95
Q

Why is albumin tested for in liver function tests?

A

It is synthesised by the liver so compromised liver function = low levels

96
Q

Why is bilirubin tested for in liver function tests?

A

It is broken down by the liver so builds up if liver function compromised.

97
Q

Why is alkaline phosphate tested for in liver function tests?

A

It is released by damaged liver/bile duct cells

98
Q

Why is gamma glutamyl transferase tested for in liver function tests?

A

It’s release is induced by alcohol and is an early indicator of liver dysfunction.

99
Q

Why might ALT and AST levels appear close to normal in advanced liver disease?

A

So little tissue function left that not much is produced.

100
Q

Why might liver damage result in vomiting blood?

A

Fibrosis of portal vein so hypertension- easier for the blood to exit through the gut.

101
Q

Why can patients with liver damage have itchy skin?

A

Built up bile salts stimulate nerve endings in the skin

102
Q

Why does bruising and bleeding occur in patients with liver damage?

A

Clotting factors 10, 9, 7 and 2 are normally produced by the liver.

103
Q

Why is hypoglycaemia more likely to occur in those with alcoholic liver disease?

A

Liver’s job to control glood glucose, can’t do this if compromised.

104
Q

Why are patients with hypoglycaemia due to alcoholic fatty liver disease given an injection of thiamine/vit B1 before administration of glucose?

A

They are likely to be deficient in vit B1 and this is a co-factor for the enzyme pyruvate dehydrogenase (used in processing of glucose during respiration.) If this enzyme can’t be used, lactic acidosis occurs and Wernicke’s syndrome (neurological damage) can follow.

105
Q

Alcohol should be avoided when taking drugs that involve which enzyme?

A

Cytochrome P450.

Drugs e.g. antibiotics, diazepam, some antihistamines, acetaminophen (pain killer.)

106
Q

What medication can be used to reduce alcohol dependence?

A

Benzodiazepine (enhances GABA neurotransmitter)
Acamprosate calcium
Diazepam
Disulfuram

107
Q

Which tissues rely particularly on glucose as an energy source?

A

Brain, RBCs

108
Q

What is glucagon’s effect on gluconeogenesis, glycolysis and glycogenolysis?

A

Promotes gluconeogenesis and glycogenolysis.

Inhibits glycolysis.

109
Q

How does insulin promote the uptake of glucose into cells?

A

GLUT4 inserted into cell membrane, PFK (phosphofructokinase) promoted- fructose-6-phosphate to fructose-1,6- bisphosphate (a step in glycolysis)

110
Q

How does insulin promote the storage of glucose as glycogen?

A

Stimulates glycogen synthase

Inhibits glycogen phosphorylase

111
Q

How does insulin promote the conversion of glucose to triacylglucerols?

A

Stimulates pyruvate dehydrogenase (pyruvate –> acetyl coA –> malanyl coA)

112
Q

Why does low blood glucose increase the availability of Acetyl CoA?

A

Low insulin and high glucagon activates hormone sensitive lipase (TAG–>fatty acids–>Acetyl CoA) so tisssues sensitive to this switch to fat for energy production to spare glucose for the brain.

113
Q

Why is muscle protein breakdown promoted in diabetes?

A

Cells can’t use glucose for energy so must use protein instead. Amino acids can enter the Kreb’s cycle.

114
Q

Why do diabetic patients get ketoacidosis?

A

Fat used as an alternative energy source to glucose, ketones are a product of fatty acid breakdown. Results in metabolic acidosis. Could result in cerebral oedema.

115
Q

What is HbA1c?

A

Glycated haemoglobin- reflects long term blood glucose levels.

116
Q

What are three longer term effects of diabetes at a cellular level?

A
  1. Increased use of minor metabolic pathways e.g. to convert glucose but products may be toxic e.g. sorbitol/lead to swelling.
  2. Glycation of proteins e.g. in lens
  3. Changes in insulin levels and insulin is involved in long term growth/proliferation of tissues.
117
Q

Why are diabetic patients more at risk of coronary heart disease?

A

Glycation of many proteins e.g. RBCs, body sees this as foreign so immune reaction. Cell membrane characteristics may change e.g. to be more sticky. Increased circulating fats as no insulin to activate lipoprotein lipase.
= atherosclerosis.

118
Q

Why does diabetic neuropathy occur?

A

Accumulation of sorbitol and fructose (products of alternative glucose breakdown) in schwaan cells disrupts function and structure - demyelation. Vascular degeneration also slows healing.

GI (13 decks)

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