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Semester 4: Nutrition and Metabolism > PBL Topic 4 Case 3 > Flashcards

PBL Topic 4 Case 3 Flashcards

1
Q

Identify the two major types of tissues in the pancreas and what each secretes

A
  • Acini: Digestive enzymes into duodenum

- Islets of Langerhans: Insulin and glucagon into blood

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2
Q

Identify the three main pancreatic enzyme(s) for digesting proteins

A
  • Trypsin
  • Chymotrypsin
  • Carboxypolypeptidase
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3
Q

How does the splitting action of the pancreatic proteases differ?

A
  • Trypsin and chymotrypsin split proteins into peptides

- Carboxypolypeptidase splits peptides into amino acids

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4
Q

Identify the main pancreatic enzyme(s) for digesting carbohydrates

A
  • Pancreatic amylase
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5
Q

Identify two carbohydrates that are digested by pancreatic amylase and one that is not

A
  • Starches, glycogen

- Cellulose

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6
Q

Identify the three main pancreatic enzymes involved in fat digestion

A
  • Pancreatic lipase
  • Cholesterol esterase
  • Phospholipase
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7
Q

Identify the action of pancreatic lipase

A
  • Hydrolyses neutral fats into fatty acids and monoglycerides
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8
Q

Identify the action of cholesterol lipase

A
  • Hydrolysis of cholesterol esters
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9
Q

Identify the action of phospholipase

A
  • Splits fatty acids from phospholipids
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10
Q

In what form are proteolytic pancreatic enzymes stored when they are first secreted?

A
  • Inactive form (zymogens)
  • Trypsinogen
  • Chymotrypsinogen
  • Procarboxypolypeptidase
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11
Q

When and how is trypsin activated?

A
  • By the enzyme enterokinase
  • Which is secreted by the intestinal mucosa
  • When chyme comes into contact with the mucosa
  • Also activated by active trypsin
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12
Q

How are chymotrypsinogen and procarboxypolypeptidase activated?

A
  • By activated trypsin in the intestine
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13
Q

What is the role of trypsin inhibitor?

A
  • Prevents activation of trypsin, chymotrypsin and procarboxypolypeptidase
  • Both inside secretory cells and in acini and ducts of pancreas
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14
Q

From which region of the pancreas are bicarbonate ions secreted?

A
  • Ductules and ducts that lead from acini
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15
Q

What is the importance of bicarbonate ions secreted by the pancreas?

A
  • Neutralise the HCl of gastric acid

- That is emptied into the duodenum from the stomach

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16
Q

Outline the mechanism of bicarbonate secretion

A
  • CO2 diffuses to interior of cell from blood
  • Combines with water to form carbonic acid (catalysed by carbonic anhydrase)
  • Which dissociates into bicarbonate and hydrogen ions
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17
Q

What happens to the bicarbonate ions that are formed by dissociation of carbonic acid?

A
  • Transported in association with sodium ions through the luminal border of the cell into the lumen of the duct
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18
Q

What happens to the hydrogen ions that are formed by dissociation of carbonic acid?

A
  • Exchanged for sodium ions through active transport
  • Sodium ions are then transported through luminal border into pancreatic duct
  • To provide electrical neutrality for the secreted bicarbonate ions
  • Causing osmosis of water into pancreatic duct
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19
Q

Identify three stimuli that are involved in causing pancreatic secretion

A
  • ACh, released from the parasympathetic vagus nerve endings
  • CCK, secreted by I cells of the mucosa in the small intestine in response to proteins and fatty acids in chyme
  • Secretin. secreted from S cells of the duodenum, when highly acidic food enters small intestine
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20
Q

Which cells do ACh and CCK stimulate?

A
  • Acinar cells
  • Producing large quantities of pancreatic enzymes
  • And small quantities of water and electrolytes
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21
Q

Outline the process by which ACh and CCK cause enzyme release from acinar cells

A
  • Bind to G-alpha-Q receptor protein on acinar cells
  • Which activates phospholipase C
  • Which causes breakdown of phosphatidylcholine and phosphoinositide
  • Increasing calcium release from intracellular stores
  • Which activates calmodulin
  • Which causes activation of protein kinases and enzyme release
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22
Q

Which cell does Secretin stimulate?

A
  • Ductal epithelial cells
  • Secreting large amounts of water and bicarbonate
  • To wash the enzymes into the duodenum
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23
Q

Outline the process by which secreting causes water and bicarbonate release from ductal cells

A
  • Binds to G-alpha-S receptor on ductal cells
  • Which stimulates adenylyl cyclase
  • Leading to activation of protein kinase A
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24
Q

Identify the role of endocrine PP cells on pancreatic enzyme release?

A
  • Secretes pancreatic polypeptide

- Which has an inhibitory on acinar cells

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25
Q

Identify hormones involved in regulating pancreatic secretion

A
  • Somatostatin
  • Peptide YY
  • Glucagon-like peptide
  • Leptin
  • Ghrelin
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26
Q

Outline the cephalic phase of pancreatic secretion

A
  • ACh released by vagal nerve acting on M3 receptors on pancreatic cells
  • Accounting for 20% of pancreatic secretion
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27
Q

Outline the gastric phase of pancreatic secretion

A
  • ACh released by vagal nerve acting on M3 receptors on pancreatic cells
  • Accounting for 5-10% of pancreatic secretion
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28
Q

Outline the intestinal phase of pancreatic secretion

A
  • Mainly in response to secretin from S cells (water)

- Accounting for 70% of pancreatic secretion

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29
Q

Outline the process that occurs in the duodenum to neutralise HCl

A
  • Activation of secretin which causes copious amounts of pancreatic juice
  • Which contains large amounts of NaHCO3
  • Which reacts with HCl to form NaCl and H2CO3
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30
Q

What happens to the carbonic acid that is formed in the duodenum?

A
  • Dissociates into CO2 and H2O
  • CO2 is absorbed into blood and expired through lungs
  • Leaving a neutral solution of NaCl
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31
Q

What is the optimum pH for pancreatic digestive enzymes?

A
  • pH = 7.0 - 8.0

- Provided by bicarbonate ion secretion

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32
Q

Why is fat malabsorption considered a late manifestation of pancreatic disease?

A
  • It does not occur until there has been a reduction of 90% of pancreatic lipase
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33
Q

Outline a direct test of pancreatic function

A
  • Intravenous infusion of secretin and cholecystokinin
  • Aspiration is assessed for pancreatic enzymes and bicarbonate production
  • In response to the these hormones
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34
Q

Outline the faecal test of pancreatic function

A
  • Faecal elastase is present in faeces and diminished levels may suggest pancreatic insufficiency
  • Increased fat in faeces also suggests insufficiency
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35
Q

Outline the pancreolauryl test

A
  • Fluorescein dilaurate is hydrolysed by cholesterol esterase
  • With the release of fluorescein which is conjugated in the liver and excreted in the urine
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36
Q

Outline the NBT-PABA test

A
  • NBT-PABA is hydrolysed by pancreatic chymotrypsin to PABA

- Which is then is absorbed and excreted in the urine.

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37
Q

What is the role of plain abdominal radiography in pancreatic investigations?

A
  • Shows calcification
  • Associated with chronic pancreatitis
  • Particularly when alcohol is the aetiology
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38
Q

What is the role of CT scanning in pancreatic investigations?

A
  • Gold standard for investigation of pancreatic disease
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39
Q

What is the role of MRI scanning in pancreatic investigations?

A
  • Alternative to CT

- Can be used to identify gallstones (magnetic resonance cholangiopancreatography)

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40
Q

What is the role of ultrasound in pancreatic investigations?

A
  • Investigation of neoplasia and inflammation

- Endoscopic ultrasound provides fine-needle aspiration and biopsy of targeted lesions

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41
Q

What is the most common cause of acute pancreatitis? Identify three other causes

A
  • Alcohol
  • Infections
  • Tumours
  • Drugs
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42
Q

Identify four causes of activation of proenzymes in acute pancreatitis

A
  • Defective transport and secretion of pancreatic zymogens
  • Pancreatic duct obstruction
  • Hyper-stimulation by alcohol or fat
  • Reflux of infected bile or duodenal contents into pancreatic duct
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43
Q

Identify the clinical features of acute pancreatitis

A
  • Epigastric abdominal pain
  • That becomes more tense and leads to back pain
  • Nausea and vomiting
  • Tachycardia and hypotension
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44
Q

What do palpation and auscultation show in acute pancreatitis?

A
  • Tenderness with guarding

- Absent bowel sounds

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45
Q

What are Cullen’s sign and Grey Turner’s sign?

A
  • Cullen’s sign: bruising in periumbilical area

- Grey Turner’s sign: bruising in flanks

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46
Q

Identify two features of acute pancreatitis that are more likely to occur with gallstone aetiology

A
  • Jaundice

- Cholangitis

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47
Q

Identify the investigations involved in the diagnosis of acute pancreatitis

A
  • Urinary amylase (remains elevated longer than serum amylase)
  • CXR to exclude GI perforation (which also causes serum amylase to rise)
  • Contrast enhanced CT to detect complications (fluid collections, abscess or cyst development)
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48
Q

Why is IV access important in the treatment of acute pancreatitis?

A
  • Early fluid loss may be large
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49
Q

What is the importance of nasogastric suction in the treatment of acute pancreatitis?

A
  • Prevents abdominal distension and vomitus

- To reduce risk of aspiration pneumonia

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50
Q

What is imipenem and its role in the treatment of acute pancreatitis?

A
  • Beta lactam

- Reduces incidence of infected pancreatic necrosis

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51
Q

What is the purpose of fentanyl in the treatment of acute pancreatitis?

A
  • Patient-controlled system of pain control
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52
Q

Why is enteral nutrition preferred over parenteral nutrition in the treatment of acute pancreatitis?

A
  • Lower risk of infection
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53
Q

Why is LMWH used in the treatment of acute pancreatitis?

A
  • DVT prophylaxis
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54
Q

Which patients require positive pressure ventilation?

A
  • Small proportion of patients who develop multi-organ failure
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55
Q

What is a sphincterotomy and when is it performed in acute pancreatitis?

A
  • Incision made into the sphincter of ampulla

- In patients with gallstone related pancreatitis

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56
Q

What does the morbidity in acute pancreatitis reflect?

A
  • First 7 days: systemic inflammatory response

- Thereafter: extent of pancreatic necrosis

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57
Q

What is considered excessive necrosis?

A
  • Greater than 50%

- May require necrosectomy

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58
Q

Outline the prognosis of acute pancreatitis

A
  • Most patients make a full recovery
  • Recurrent episodes may occur
  • Patients with more severe acute pancreatitis may develop malabsorption and or diabetes
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59
Q

What is chronic pancreatitis?

A
  • Chronic inflammatory disease
  • Characterised by fibrosis and destruction of exocrine pancreatic tissue
  • Diabetes mellitus occurs in advanced cases because the islets of Langerhans are involved
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60
Q

What is the most common cause of chronic pancreatitis in the Western world?

A
  • Alcohol misuse
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61
Q

In the pathogenesis of chronic pancreatitis, what is the role of cationic trypsin mutations? Give an example of one.

A
  • Early activation of trypsinogen to trypsin

- PRSS1+

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62
Q

What is the effect of ethanol in the pathogenesis of chronic pancreatitis?

A
  • Ethanol dysregulates calcium levels
  • Which plays a role in controlling trypsin activation
  • Dysregulation causes early activation of trypsinogen to trypsin
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63
Q

What is the affect of Chymotrypsin C on pancreatic secretion? What is found in patients with chronic pancreatitis with regards to Chymotrypsin C?

A
  • Chymotrypsin C inactivates trypsin

- Loss of function mutations

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64
Q

What causes an acute inflammatory response in chronic pancreatitis?

A
  • Active trypsin within the pancreas leading to pancreatic injury
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65
Q

What is the effect of AIR on Kazal 1 (SPINK1)? What is the role of Kazal 1 (SPINK1)?

A
  • AIR upregulates Kazal 1
  • Which is a serine protease inhibitor
  • Which blocks active trypsin
  • Preventing further activation of trypsinogens
  • Limiting further tissue damage
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66
Q

What is the role of CFTR in the pathogenesis of chronic pancreatitis?

A
  • Expressed on apical surface of acinar cells
  • Responsible for maintaining a high volume bicarbonate rich pancreatic secretion
  • Responsible for flushing the activated trypsin into the duodenum
  • Mutations in CF (delta F508) result in exocrine failure
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67
Q

Identify five IgG4-related disroders

A
  • Chronic pancreatitis
  • Autoimmune cholangitis
  • Reidel’s thyroiditis
  • Aortitis
  • Tubule-interstitial nephritis
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68
Q

Why is chronic pancreatitis considered an IgG4-related disorder?

A
  • Raised IgG4 level

- IgG4-positive plasma cells

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69
Q

Identify the two types of autoimmune chronic pancreatitis

A
  • Type 1: Typically affects middle aged men with raised serum and tissue levels of IgG4
  • Type 2: Occurs in middle age with equal sex distribution and is seen in association with IBD
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70
Q

Outline the clinical features of chronic pancreatitis

A
  • Epigastric pain which radiates through back
  • Associated with anorexia and weight loss
  • Steatorrhoea
  • Malabsorption
  • Diabetes
  • Jaundice when there is obstruction of common bile duct
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71
Q

Outline the investigations involved in the diagnosis of chronic pancreatitis

A
  • Physical exam: thin, malnourished patient with epigastric tenderness, erythema ab igne
  • Elevated serum amylase (inflammation increased cell permeability allowing entry of amylase into blood) and faecal elastase
  • Gene mutation analysis: PSRSS1, SPINK1, CFTR
  • CT shows calcification and a dilated pancreatic duct
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72
Q

Outline the treatments involved in chronic pancreatitis

A
  • Short term pain: NSAID and opiate (tramadol)
  • Chronic pain: TCA (amitriptyline) and membrane stabilising agent (pregabalin)
  • Steatorrhoea: Pancreatic enzyme supplementation and an acid suppressor
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73
Q

What is the most common complication of chronic pancreatitis? How is this compilation treated?

A
  • Pancreatic pseudocyst surrounded by granulation tissue
  • Treatment of which involves endoscopic drainage using a direct fistula between the pseudocyst lumen and the gastric lumen which is kept patent by insertion of stents
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74
Q

Outline the epidemiology of carcinoma of the pancreas

A
  • Fifth most common cancer in Western world (with increasing incidence)
  • Men are affected twice as often as women
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75
Q

Identify four modifiable risks in the development of carcinoma of the panceas

A
  • Smoking (two-fold increase)
  • Excess alcohol
  • Coffee intake
  • Asprin
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76
Q

Identify two conditions that increase the incidence of pancreatic cancer

A
  • Diabetes

- Chronic pancreatitis

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77
Q

Outline the pathogenesis of pancreatic cancer

A
  • Mutations to DNA repair genes such as BRCA2
  • Activation of KRAS2 oncogene
  • Inactivation of tumour-suppressor gene TP53
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78
Q

Outline the clinical features associated with pancreatic cancer of the head and ampulla

A
  • Courvoisier’s Sign
  • Obstructive jaundice and palpable gall bladder
  • Is pancreatic cancer until proven otherwise
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79
Q

Outline the clinical features associated with pancreatic cancer of the body or tail

A
  • Abdominal pain
  • Weight loss and anorexia
  • Thromboembolic phenomenon
  • Polyarthritis and skin nodules
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80
Q

Outline the investigations used in the diagnosis of pancreatic cancer

A
  • Ultrasound: Bile duct obstruction + head mass

- CT: Exclusion of tumour invasion and lymph node involvement

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81
Q

What is the differential diagnosis of pancreatic cancer?

A
  • IgG4 related autoimmune pancreatitis
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82
Q

Outline the management of pancreatic cancer

A
  • Resection if tumour is localised
  • With adjunct chemotherapy
  • Palliative measures include stents for duodenal obstruction
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83
Q

What happens when a portion of the small intestine becomes distended by chyme?

A
  • Stretching of the intestinal wall elicits localised concentric contraction
  • Which are spaced at intervals along the intestine
  • Resulting in segmentation of the small intestine
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84
Q

Outline the process of segmentation of the small intestine

A
  • Intestine is divided into spaced segments
  • As one set relaxes, a new set begins at points between the previous two contractions
  • These contractions chop the chyme 2-3 times per minute
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85
Q

What determines the maximum frequency of segmentation contractions?

A
  • Slow waves in the intestinal wall

- Up to 12 per minute (only under extreme conditions)

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86
Q

Describe the propulsive movements that occur in the small intestine

A
  • Move 0.5-2 centimetres per second
  • Faster in proximal intestine and slower in terminal intestine
  • Doe out after 5 centimetres
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87
Q

What is the gastroenteric reflex?

A
  • Distension of stomach after ingestion
  • Excites local myenteric reflexes
  • Which increase peristaltic activity in small intestine
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88
Q

Identify five hormones that enhance intestinal motility

A
  • Gastrin
  • CCK
  • Insulin
  • Motilin
  • Serotonin
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89
Q

Identify two hormones that enhance intestinal motility

A
  • Secretin

- Glucagon

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90
Q

Aside from causing progression of chyme in the small, identify another cause of peristalsis in the small intestine

A
  • Spreads the chyme out
91
Q

What is the gastroileal reflex

A
  • Following a meal
  • Intensifies peristalsis in the ileum
  • To force remaining chyme through the ileocecal valve into the cecum
92
Q

What is peristaltic rush?

A
  • Rapid and powerful peristalsis
  • That occurs following intense irritation of the intestinal mucosa
  • Sweeping contents into the colon and thereby relieving the small intestine of the irritative chyme
  • As occurs in diarrhoea
93
Q

What are Brunner’s glands and where are they located?

A
  • Compound mucous glands

- Located in the proximal duodenum (between pylorus and hepatopancreatic ampulla)

94
Q

What type of mucous do Brunner’s glands secrete? What is the function of this mucous?

A
  • Alkaline mucus
  • Owing to bicarbonate content
  • Which protects duodenal wall from GI juice
  • By neutralising HCl
95
Q

Identify three stimuli that cause release of mucus from Brunner’s glands

A
  • Tactile or irritating stimuli
  • Vagal stimulation
  • Hormones (especially secretin)
96
Q

Why are emotional states associated with peptic ulcers?

A
  • Excitable states cause sympathetic stimulation
  • Which inhibits alkaline secretions from Brunner’s glands
  • Duodenum is unprotected form HCl
  • Resulting in inflammatory changes and ulceration
97
Q

What are Crypts of Lieberkuhn?

A
  • Small pits which lie between intestinal villi

- Composed of goblet cells or enterocytes

98
Q

What is the rate of intestinal secretions by the enterocytes of the crypts?

A
  • 1800 ml / day
99
Q

What is the pH of intestinal secretions by the enterocytes of the cyrpts?

A
  • pH = 7.5 - 8.0
100
Q

What is the role of the intestinal secretions by the enterocytes of the crypts?

A
  • Supplies a water vehicle for absorption of substances from chyme when it comes into contact with the villi
101
Q

What is the role of peptidases

A
  • Split small peptides into amino acids
102
Q

Identify four enzymes lining the villi of the small intestines that split disaccharides in the small intestine

A
  • Sucrase
  • Maltase
  • a-Dextrinase
  • Lactase
103
Q

What is the life cycle of an intestinal epithelial cell? What is the importance of mitosis?

A
  • 5 days

- Allows rapid repair of excoriations that occurs in the mucosa

104
Q

How does pancreatic alpha amylase differ to salivary alpha-amylase?

A
  • Several times as powerful
  • Digests all carbohydrates in chyme in duodenum with 30 minutes
  • Converts carbohydrates mainly to maltose
105
Q

Identify the role of lactase

A
  • Splits lactose into a molecule of galactose and a molecule of glucose
106
Q

Identify the role of sucrase

A
  • Splits sucrose into a molecule of fructose and a molecule of gluocse
107
Q

Identify the role of maltase

A
  • Splits maltose into two molecules of glucose
108
Q

What is the importance of the breakdown products of lactase, sucrase and maltase?

A
  • All are monosaccharides
  • Which are water soluble
  • And are absorbed immediately into the blood
109
Q

What is the role of elastase

A
  • Major pancreatic proteolytic enzyme

- Which digests elastin fibres that partially hold meat together

110
Q

Describe the structure of enterocytes in the small intestine

A
  • Bush border that consists of hundreds of microvilli

- Which are composed of multiple peptidases that protrude to the exterior

111
Q

Identify two proteolytic enzymes found in the brush border of enterocytes. What is their role?

A
  • Aminopolypeptidase
  • Dipeptidases
  • Split larger polypeptides into tripeptides and dipeptides (a few amino acids)
  • Which are transported through the microvillar membrane to the interior of the enterocyte
112
Q

What happens to the dipeptides and tripeptides in the cytosol of the enterocyte?

A
  • Broken down by peptidases that are specific for the remaining types of linkages between amino acids
  • To form single amino acids
113
Q

Why is fat broken down into very small sizes?

A
  • To allow water-soluble digestive enzymes to act on its surface (emulsification)
114
Q

Outline the first stage of fat digestion that occurs in the stomach

A
  • Agitation in stomach

- To mix fat with products of stomach digestion

115
Q

Identify two components of bile that are involved in fat digestion

A
  • Lecithin

- Bile salts

116
Q

Outline the process of emulsification of fats by bile

A
  • Polar parts of bile salts and lecithin dissolve in water
  • Fat soluble part of bile salts and lecithin dissolve in surface layer of fat
  • Which reduces interfacial tension of globule
  • Allowing easily hydrolysis
  • Increasing the surface area of the fat
117
Q

Identify the main enzyme involved in digestion of triglycerides

A
  • Pancreatic lipase
118
Q

What are the main breakdown products of triglycerides by pancreatic lipase?

A
  • 2-monoglycerides

- Free fatty acids

119
Q

What is the role of bile salts in the removal of monoglycerides and fatty acids

A
  • Formation of micelles

- Which act as a transport medium to carry these products to enterocytes

120
Q

Why do micelles develop?

A
  • Bile salt has a fat soluble sterol nucleus

- As well as a water soluble polar group

121
Q

Outline the process of micelle formation

A
  • Sterol nucleus encompasses fat digestate

- Polar groups project outward and dissolves in water

122
Q

What happens to the bile salts once the monoglycerides and fatty acids have dissolved?

A
  • Released back into chyme to be reused in formation of micelles and transport of fatty acids/monoglycerides
123
Q

Which enzyme is responsible for digesting cholesterol esters?

A
  • Cholesterol ester hydrolase
124
Q

Which enzyme is responsible for digesting phospholipids?

A
  • Phospholipase A2
125
Q

What is the total quantity of fluid that must be absorbed each day?

A
  • 8 to 9 litres

- Includes both that ingested and that secreted

126
Q

What volume of fluid is absorbed by the small intestine?

A
  • All but 1.5 litres

- Leaving 1.5 litres to pass through ileocecal valve into colon

127
Q

Identify two reasons why absorption in the stomach is poor?

A
  • Lack villi

- Tight junctions between epithelial cells

128
Q

What are plicae circulares?

A
  • Circular folds in the small intestine (mainly duodenum and jejunum)
  • Which form the absorptive surfaces of the small intestine
129
Q

Identify two other structures involved in the absorption of fluid from the small intestine

A
  • Villi located on epithelial cell surface the entire length of small intestine
  • Microvilli on brush border of each epithelial cell
130
Q

What are pinocytic vesicles and what is their function?

A
  • Small vesicles which are pinched off portions of unfolded enterocyte membrane
  • Which absorbed small amounts of substance by pinocytosis
131
Q

What is the role of actin filaments on the brush border?

A
  • Contract to cause continual movement of microvilli

- Keeping them constantly exposed to new quantities of intestinal fluid

132
Q

Describe the movement of water across the mucosa of the small intestine

A
  • Diffusion by osmosis from through mucosa in blood

- Can diffuse in opposite direction from blood to chyme when chyme is hyper-osmotic

133
Q

Describe the movement of sodium ions across the mucosa of the small intestine

A
  • Diffusion into epithelial cell down a concentration gradient (142 - 50 mEq/L)
  • Active transport into the blood
134
Q

What is the role of aldosterone in sodium absorption? What is the role of aldosterone is dehydration?

A
  • Increased activation of Na+K+-ATPase for sodium absorption
  • Increased sodium transport increases absorption of chloride ions and water by diffusion. Preventing water loss in dehydration
135
Q

Describe the process of active absorption of bicarbonate ions

A
  • Sodium ions are absorbed
  • Hydrogen ions are secreted into lumen in exchange
  • Which combine with bicarbonate ions to form carbonic acid
  • Which dissociated into water and carbon dioxide
  • Water remains as part of chyme
  • Carbon dioxide is readily absorbed into blood and subsequently expired through the lungs
136
Q

What is the importance of bicarbonate secretion into the ileum and large intestine?

A
  • Alkaline neutralises acid produced by bacteria in small intestine
137
Q

Outline the process of calcium absorption

A
  • Mainly from duodenum
  • PTH activates Vitamin D
  • Which greatly enhances calcium absorption
138
Q

Identify how the two different types of iron are absorbed into the epithelial cells of the small intestine

A
  • Haem iron: by a carrier protein called HCP1

- Non-haem iron, converted from ferric (Fe3+) to ferrous (Fe2+) by ferrireductase and absorbed by DMT1 or NRAMP2

139
Q

Identify how the body’s iron status determines the fate of iron that has been absorbed

A
  • Stored as ferritin

OR

  • Transported across basolateral surface by ferroportin 1 (+hephaestin) through its iron responsive element
140
Q

What is the role of hepcidin?

A
  • Regulates ferroportin by binding to it an causing its degradation
  • Thereby decreasing iron efflux
141
Q

Identify a cause of high levels of hepcidin and a cause of low levels of hepcidin?

A
  • High levels: inflammatory cytokines (IL-6) e.g anaemia of chronic disease
  • Low levels: iron-deficiency / hypoxia
142
Q

Outline the process of glucose absorption from small intestine

A
  • Via co-transport with glucose
  • Active transport of sodium into blood causes facilitated diffusion of sodium into epithelial cell
  • Via the sodium dependent glucose transport (SGLT)
  • Which also carries a glucose molecule into the cell
  • Facilitated diffusion of glucose into blood by transport protein e.g. GLUT-2
143
Q

How is galactose absorbed?

A
  • Same mechanism as glucose
144
Q

How is fructose absorbed?

A
  • Facilitated diffusion into cell but not coupled with sodium transport
  • Where it becomes phosphorylated and converted into glucose
  • Transported through basolateral surface by facilitated diffusion e..g GLUT-2
145
Q

Outline process of protein absorption?

A
  • Either by co-transport with glucose or by facilitated diffusion (like that of frucotse)
146
Q

Outline the process of fat absoprtion

A
  • Lipid diffusion into cell
  • Taken up by ER and converted into new triglycerides
  • Which are released in the form of chylomicrons through the basal surface
  • Through thoracic duct to empty into circulating blood
147
Q

How does the absorption of small and medium-chain fatty acids (e.g butterfat) differ to that of long-chain fatty acids?

A
  • Absorbed directly into portal blood

- Since they are more water soluble

148
Q

What is Coeliac disease?

A
  • Immunologically mediated inflammatory disorder of the small intestine that results in malabsorption
149
Q

Outline the epidemiology of Coeliac disease

A
  • Most common in Northern Europe
  • Prevalence of 1%
  • Most patients are asymptomatic
150
Q

What are prolamins?

A
  • Plant storage found in proteins
  • Mainly in cereals and grains
  • That are resistance to digestion by pepsin
  • Because of their high glutamine and proline content
151
Q

What is gliadin?

A
  • A type of prolamin present in wheat
  • That is deaminated by transglutaminase
  • Which increases its immunogenicity
152
Q

Outline the pathology of Coeliac disease

A
  • Gliadin is deaminated and binds to antigen presenting cells
  • APCs interact with CD4 T cells via HLA class II molecules DQ2 or DQ8
  • T cells interact with B cells to produce transglutaminase antibodies
  • Release of inflammatory cytokines, particularly INF-Y
  • Results in villous atrophy and crypt hyperplasia
153
Q

Identify 3 environmental factors implicated in Coeliac disease

A
  • Bread feeding at age of introduction of gluten into diet
  • Rotavirus
  • Adenovirus-12
154
Q

Outline the clinical features of Coeliac disease

A
  • Diarrhoea, steatorrhoea, abdominal pain, weight loss
  • Mouth ulcers and angular stomatitis
  • Abdominal distension, and growth delay in children
  • Anxiety and depression
  • Infertility
155
Q

Outline the investigations used in Coeliac disease

A
  • Endoscopic small bowel biopsy demonstrating blunting of villi and crypt hyperplasia
  • IgA anti-endomysial antibodies
  • tTg assay (tissue transglutaminase antibody)
  • Full blood count shows anaemia
  • Measurements of BMD
156
Q

Identify the treatments used in Coeliac disease

A
  • Vitamin and mineral replacement e.g. iron, folic acid, calcium, vitamin D
  • Gluten free diet for life
157
Q

Identify the complications of Coeliac disease

A
  • Twofold increased risk of malignancy (small bowel carcinoma)
  • Jejuna-ileitis (fever, pain, obstruction or perforation)
  • Osteoporosis and osteomalacia in poorly controlled disease
158
Q

Identify the cellular mechanisms postulated for the depressant effects of ethanol

A
  • Enhancement of GABA and glycine action
  • Inhibition of calcium channel opening
  • Activation of potassium channels
  • Inhibition of NMDA-type glutamate receptors
159
Q

Behavioural impairment of ethanol increases in relation to what measurement?

A
  • Blood alcohol concentration (BAC)

- Measured in mg/dL

160
Q

Identify three peripheral effects of ethanol

A
  • Self-limiting diuresis (reduced ADH secretion)
  • Cutaneous vasodilation
  • Delayed labour (reduced oxytocin secretion)
161
Q

Identify adverse effects associated with ethanol consumption

A
  • Dementia and peripheral neuropathy
  • Cirrhosis and liver failure
  • Impaired fetal development
  • Psychological and physical dependence
162
Q

Outline the process of ethanol metabolism

A
  • Ethanol metabolised by liver
  • First by alcohol dehydrogenase to acetaldehyde
  • Then by aldehyde dehydrogenase to acetate
  • Both processes involve reduction of NAD to NADH
163
Q

What is the maximum rate of ethanol metabolism?

A
  • 10 ml / hour
164
Q

Outline the effects associated with a BAC of 20-99 mg/dL (2)

A
  • Impaired coordination

- Euphoria

165
Q

Outline the effects associated with a BAC of 100-199 mg/dL (3)

A
  • Ataxia
  • Poor judgement
  • Labile mood
166
Q

Outline the effects associated with a BAC of 200-299 mg/dL (3)

A
  • Slurred speech
  • Nausea
  • Vomiting
167
Q

Outline the effects associated with a BAC of 300-399 mg/dL (2)

A
  • Stage 1 anaesthesia

- Memory lapse

168
Q

Outline the effects associated with a BAC of 400+ mg/dL

A
  • Respiratory failure
  • Coma
  • Death
169
Q

What is meant by alcohol misuse?

A
  • Drinking in such a way that causes problems to partners or others
170
Q

What is meant by a problem drinker?

A
  • Drinker who experiences or causes harm as a consequence of drinking
171
Q

What is meant by a heavy drinker?

A
  • Drinking more than is safe to do so
172
Q

What is meant by a binge drinker?

A
  • Drink excessively in short bouts separated by periods of abstinence
173
Q

What is meant by alcohol dependence?

A
  • Physical dependence or an addiction to alcohol
174
Q

Outline the epidemiology of alcohol misuse

A
  • 20% of men and 10% of women drink more than recommended limits
  • 4% of men and 2% of women report alcohol withdrawal symptoms suggesting dependence
  • Two to three times increased risk of dying
175
Q

What are the recommended limits of alcohol?

A
  • 3 units a day in men (24 g of pure ethanol) (21 units per week)
  • 2 units a day in women (14 g of pure ethanol) (14 units per week)
176
Q

Outline CAGE questionnaire

A
  • Have you ever felt you should CUT down?
  • Have people ever ANNOYED you by criticising your drinking?
  • Do you ever feel GUILTY about drinking?
  • Have you EVER had a drink first thing in the morning
  • Positive answer to two or more of these questions suggests a problem drinking
  • Confirm by asking amount the maximum taken
177
Q

What is alcohol dependence?

A
  • Repeated self-administration
  • That causes tolerance, withdrawal and compulsive drug taking
  • Despite significant substance-related problems
178
Q

Identify three genetic markers that are linked to alcohol dependence

A
  • D2 receptor allele A1
  • Alcohol dehydrogenase subtypes
  • Monoamine oxidase B activity
179
Q

Identify two other causes of alcohol dependence

A
  • Grow up around parents who drink

- Psychiatric illness e..g depression and anxiety

180
Q

Identify five symptoms of alcohol dependence

A
  • Strong overpowering desire to drink
  • Inability control starting or stopping drinking
  • Increased tolerance
  • Withdrawal state
  • Continuing to drink despite being aware of harmful consequences
181
Q

Identify the diagnostic criteria for alcohol withdrawal syndrome

A
  • Any three of the following:
  • Tremor of the hands, tongue or eyelids
  • Sweating
  • Nausea, retching, vomiting
  • Anxiety
  • Insomnia
  • Tachycardia or hypertension
182
Q

What percentage of cases of alcohol misuse lead to chronic alcohol dependence

A
  • 25%
183
Q

After how many years of drinking does alcohol dependence usually develop?

A
  • 10 years in men

- 3-4 years in women

184
Q

What name is given to most serious withdrawal state of alcohol dependence that occurs up to 3 days after alcohol cessation?

A
  • Delirium tremens
185
Q

What are the features of delirium tremens?

A
  • Disorientated
  • Agitated
  • Tremor
  • Visual hallucinations
  • Signs include tachycardia, tachypnoea and pyrexia
186
Q

Identify a complication of delirium tremens

A
  • Wernicke-Korsakoff syndrome
  • Damage to the mamillary bodies and dorsomedial nuclei of thalamus
  • Due to a deficiency in thiamin (B1) caused by a heavy drinking
187
Q

Identify non-pharmacological treatments for alcohol dependence syndrome

A
  • Motivational therapy
  • Cognitive behavioural therapy
  • 12-step facilitation
  • Group therapy (e.g. family, marital)
  • Education
188
Q

What is the mechanism of action of naltrexone?

A
  • Opioid antagonist

- Reduces alcohol-induced reward

189
Q

What is the mechanism of action of acamprosate?

A
  • Weak NMDA antagonist

- Used to reduce craving

190
Q

What is the mechanism of action of disulifram?

A
  • Alcohol dehydrogenase inhibitor

- Which accentuates nausea and renders alcohol consumption unpleasant

191
Q

Outline the treatment of delirium tremens

A
  • Treat electrolyte abnormalities (e.g. Pabrinex)
  • Sedate patient (chlordiazepoxide, a benzodiazepine)
  • Prophylactic antiepileptics with a history of withdrawal fits (e.g. phenytoin, carbamazepine)
192
Q

What is the cost of alcohol misuse for the NHS?

A
  • £3.5 billion
  • Accounts for 1 in 20 emergency admissions
  • Accounts for 10% of UK burden of disease
193
Q

Outline the Moral Modal of Addiction

A
  • Person is choosing to behave excessively

- And is therefore deserving of punishment

194
Q

Outline the First Disease Concept of Addiction

A
  • Substance was the problem

- Individual succumbs to its addictive influence

195
Q

Outline the Second Disease Concept of Addiction

A
  • Individual has the problem

- Requiring support and treatment

196
Q

How can classical conditioning explain alcohol addiction?

A
  • Person associated drinking with feeling relaxed so is likely to repeat the behaviour
197
Q

How can operant conditioning explain addiction?

A
  • Drinking removes the negative withdrawal symptoms

- So individual is more likely to repeat behaviour

198
Q

How can social learning theory explain addiction

A
  • People learn from role models

- Parents / friends drinking influences people to drink

199
Q

Outline the four stages of substance use

A
  • Initiation
  • Maintenance
  • Cessation
  • Abstinence
200
Q

Identify psychological predictors of drinking

A
  • Fun and pleasure
  • Calming nerves
  • Building confidence
201
Q

Identify social predictors of drinking

A
  • Parental drinking
  • Peer group pressure
  • Attitudes of school
202
Q

What is meant by revolving door schema

A
  • Cessation occurs in a dynamic manner across the five stages of cessation rather than a linear manner
203
Q

Identify the five stages of cessation

A
  • Pre-contemplation: not seriously considering quitting
  • Contemplation: having some thoughts about quitting
  • Preparation: seriously considering quitting
  • Action: Initial behaviour change
  • Maintenance: Maintaining behaviour change for a period of time
204
Q

Identify three types of intervention that help to promote cessation

A
  • Clinical interventions
  • Self help movements: therapy: aversion therapy/contingency contracting/cue exposure
  • Public health interventionsL government interventions, doctors advice, community-based programmes
205
Q

Outline the relapse prevention model

A
  • Addictive behaviours are learned and therefore can be unlearned,
  • Addictions are not ‘all or nothing’ but exist as a continuum
  • Lapses from abstinence are likely and acceptable, and are determined by good coping strategies and positive outcome expectancies.
206
Q

What is a high risk situation?

A
  • Situation that motivates individual to carry out addictive behaviour
  • External cues include someone else drinking
  • Internal cues include anxiety
207
Q

Outline two types of coping strategies employed when an individual is exposed to a high risk situation

A
  • Behavioural: avoiding situation, using a substitute behaviour
  • Cognitive: remembering to abstain
208
Q

What are positive and negative outcome expectancies?

A
  • Positive: Expectancies that drinking will make the individual feel better
  • Negative: Expectancies that drinking will be harmful to health
209
Q

What is the HARK Questionnaire?

A
  • Framework for helping identify people that have suffered domestic abuse in past year
  • Humiliate: Make you feel bad about yourself, that you can’t do anything right
  • Afraid: What is it that makes you scared of your partner
  • Rape: Raped, forced into sexual activity
  • Kicked: Physical abuse or threatened with physical abuse
210
Q

What is IRIS?

A
  • Support program to improve the general practice response to domestic violence
  • Through interventions to help clinicians recognise and respond to patients affected by domestic violence
211
Q

Outline the three components of the Theory of Planned Behaviour

A
  • Attitude towards a behaviour (positive or negative)
  • Subjective norm (perception of social norms and pressures to perform a behaviour)
  • Perceived behavioural control, including internal control factors (skills, abilities) and external control factors (obstacles and opportunities)
212
Q

Apply the Theory of Planned Behaviour to alcohol reducting

A
  • Attitude to behaviour: reduction would be beneficial to health
  • Subjective norms: family and friends would want them to cut down
  • Perceived behaviour control: capable of drinking less due to past behaviour and evaluation of internal and external factors
213
Q

What are odds?

A
  • Likelihood of an event occuring
214
Q

1 in 10 people develop pancreatitis. Calculate the odds of developing pancreatitis

A
  • 1/(10-1) = 0.11
215
Q

What are odds ratios?

A
  • Used to compare whether the likelihood of an event differs between two groups
216
Q

64 out of 256 people in the treatment group had the outcome. 45 out of 180 people in the control group had the outcome. Calculate the odds ratio

A
  • 64/(256-65) / 45/180-45) = 1
217
Q

What does an odds ratio of less than 1, 1 and greater than 1 mean?

A
  • Less than 1: Event was less likely in treatment group
  • 1: Event was equally likely in both groups
  • More than 1: Event was more likely in control group
218
Q

What does a Chi-square test test?

A
  • A null hypothesis stating that
  • Frequency distribution of observed findings
  • Is consistent a particular theoretical distribution
219
Q

Identify two types of Chi-square test

A
  • Goodness of fit: whether observed frequency distribution differs from a theoretical distribution
  • Independence: whether paired observation on two variables are independent of each other
220
Q

What is a confounding variable?

A
  • A variable that has an outcome on the effect and is also correlated to the exposure
  • E.g. alcohol consumption has an effect on disease X and is correlated with smoking (the exposure) because smokers tend to drink more
221
Q

Identify three common confuonders

A
  • Age
  • Socioeconomic status
  • Gender
222
Q

What is the purpose of multiple logistic regression?

A
  • Control for many potential confounders at one time
223
Q

How does simple logistic variation differ to multiple logistic variation?

A
  • Simple: Explore associations between one outcome and one exposure variable (E.g. how does smoking affect likelihood of pancreatitis)
  • Multiple: Explore associations between one outcome and two or more exposure variables (E.g. how does smoking affect likelihood of having pancreatitis, after accounting for alcohol smoking?’

Semester 4: Nutrition and Metabolism (17 decks)

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