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Semester 4: Nutrition and Metabolism > PBL Topic 4 Case 6 > Flashcards

PBL Topic 4 Case 6 Flashcards

1
Q

Outline the process by which glucose is transported across cell membranes

A
  • Facilitated diffusion since it exceeds molecular weight for simple diffusion
  • Glucose binds to a channel
  • Channel undergoes conformational change
  • And releases glucose on the other side of the membrane
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2
Q

What is the role of the GLUT-1 transporter?

A
  • Enables basal non-insulin stimulated glucose uptake into any cell
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3
Q

What is the role of the GLUT-2 transporter?

A
  • Transports glucose in the beta cell
  • A prerequisite for glucose sensing
  • It is also present in the renal tubules and hepatocytes
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4
Q

What is the role of the GLUT-3 transporter?

A
  • Enables non-insulin mediated glucose uptake into brain neurones and placenta
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5
Q

What is the role of the GLUT-4 receptor?

A
  • Enables glucose to be taken up into muscle and adipose tissue cells following stimulation of the insulin receptor
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6
Q

Outline the process of phosphorylation of glucose when it enters the cell. Which enzyme(s) is/are involved?

A
  • Combines with a phosphate radical
  • To form glucose-6-phosphate
  • Catalysed by the enzyme glucokinase (in hepatocytes) or hexokinase (in non-hepatocytes)
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7
Q

What is the role of glucose-6-phosphatase in hepatocytes?

A
  • Reverses the phosphorylation of glucose

- Allowing glucose to diffuse back out of the cell

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8
Q

What is the importance of storing glucose as glycogen?

A
  • Glycogen has a high molecular weight

- Which limits changes in osmotic pressure of the intracellular fluid

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9
Q

Outline the process of glycogenesis

A
  • G6P is converted to G1P
  • G1P is converted to UDP-Glucose
  • UDP-Glucose is converted to glycogen
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10
Q

Outline the stimulus for, and process of, glycogenolysis

A
  • Decreased in blood glucose or increased cellular demand of glucose
  • Causes activation of phosphorylase by glucagon or adrenaline
  • Which splits individual glucose molecules from glycogen by phosphorylation
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11
Q

Outline the process of glycolysis

A
  • Glucose is converted glucose-6-phosphate
  • Which is converted to fructose-1,6-phosphate
  • Which is split into 2 molecules of glyceraldehyde-3-phosphate
  • Which eventually forms 2 molecules of pyruvic acid
  • As well as 2 molecules of ATP and 4 H
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12
Q

How many steps are there in glycolysis?

A
  • 10
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13
Q

What is the overall efficiency of ATP formation in glycolysis?

A
  • 43%

- Remainder of energy is lost as heat

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14
Q

Outline the formation of acetyl coenzyme A from pyruvic acid

A
  • 2 molecules of pyruvic acid
  • React with 2 molecules of CoA
  • To from 2 molecules of acetyl CoA,
  • As well as 2 molecules of CO2 and 4 H
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15
Q

Where in the cell does glycolysis occur?

A
  • In cytoplasm
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16
Q

Where does Link reaction occur?

A
  • Mitochondrial matrix
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17
Q

Where does citric acid cycle occur?

A
  • Mitochondrial matrix
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18
Q

Outline the citric acid cycle

A
  • Acetyl CoA combines with oxaloacetic acid to form citric acid
  • Addition of 6 water molecules
  • Which are degraded to 4 carbon dioxide molecules, 16 H and 2 molecules of CoA
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19
Q

During which step of the Citric Acid cycle are 2 molecules of ATP formed?

A
  • Change from alpha-ketoglutaric acid to succinic acid
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20
Q

Following the Citric Acid cycle, how many hydrogen atoms are released from each original glucose?

A
  • Glycolysis: 4
  • Link: 4
  • Citric Acid: 16
  • Total of 24
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21
Q

What happens to the majority of hydrogen atoms formed in the metabolism of glucose?

A
  • Removed in pairs
  • One reacts with NAD+ to form NADH
  • The other forms H+
  • Catalysed by dehydrogenase
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22
Q

What is the role of decarboxylases in the metabolism of glucose?

A
  • Cause release of carbon dioxide
  • Which is dissolved in body fluids
  • Transported to lungs
  • And expired from body
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23
Q

Where does oxidative phosphorylation take place?

A
  • Inner (shelf) mitochondrial membrane
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24
Q

What happens to the electrons that are removed from the hydrogen atoms to cause hydrogen ionisation?

A
  • Enter an electron transport chain
  • Which are shuttled between acceptors
  • Which are then oxidised or reduced by accepting or giving up electrons
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25
Q

What is the role of cytochrome A3 / cytochrome oxidase

A
  • Accepts an electron from electron transport chain
  • Which gives up two electrons
  • And reduces elemental oxygen to ionic oxygen
  • Which then combined with protons to form water
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26
Q

Outline the process of hydrogen ions transport in the outer chamber of the mitochondria

A
  • Electrons pass through electron transport chain
  • Which releases energy
  • Which pumps protons into outer chamber between the two membranes
  • Creating a high concentration of positively charged protons in the chamber
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27
Q

Outline the process of ATP formation during oxidative phosphorylation

A
  • Protons in outer chamber diffuse down a concentration gradient
  • Into inner mitochondrial matrix
  • Through ATP synthetase molecule
  • Which provides energy to convert ADP to ATP
  • Facilitated diffusion of ATP into cytoplasm
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28
Q

What is the total number of ATP molecules formed from each molecule of glucose?

A
  • Glycolysis: 4 (2 are expended to cause initial phosphorylation of glucose)
  • Citric Acid Cycle: 2
  • Oxidative phosphorylation: 30
  • Oxidation of the remaining four protons releases 2 more molecules of ATP
  • Total: 38
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29
Q

What is the overall efficiency of energy transfer in the formation of ATP from glucose?

A
  • 66%
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30
Q

What is the role of the citrate ion in controlling the rate of glycolysis?

A
  • Inhibits phosphofructokinase

- An enzyme involved in glycolysis

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31
Q

How is lactic acid formed during anaerobic glycolysis?

A
  • Pyruvic acid reacts with NADH
  • Catalysed by lactic dehydrogenase
  • Which can then be reconverted to pyruvic acid and NADH
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32
Q

How can alanine be converted into pyruvic acid?

A
  • Deamination
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33
Q

Identify a pathway by which amino acids can be converted into glucose

A
  • Phosphogluconate pathway
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34
Q

Outline the role of the anterior pituitary gland in gluconeogensis

A
  • Secretes CTRF
  • Which causes released of cortisol from adrenal cortex
  • Which mobilises cellular proteins, which can be broken down into amino acids
  • Which can be deaminated in the liver to be converted into pyruvic acid
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35
Q

What is a normal fasted blood glucose?

A
  • 90 mg/dl
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36
Q

Outline the formation of glycerol-3-phosphate from triglycerides

A
  • Intracellular hydrolysis of triglycerides
  • Into fatty acids and glycerol
  • Glycerol is converted to glycerol-3-phosphate by intracellular enzymes
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37
Q

Where does beta oxidation of fatty acids occur?

A
  • Mitochondria
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38
Q

How do fatty acids enter cytoplasm for beta oxidation?

A
  • Carrier mediated process

- That uses carnitine as the carrier substance

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39
Q

Outline the process of beta oxidation

A
  • Fatty acid combines with CoA to form acyl-CoA
  • 2nd carbon is oxidised
  • 1st two carbons are split from fatty acid to release acetyl-CoA
  • Acetyl-CoA then enters the citric acid cycle
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40
Q

Outline the process of acetoacetic acid formation in the liver

A
  • Fatty acid chains are split to form acetyl-CoA during beta oxidation
  • Two molecules of acetyl-CoA condense to form one molecule of acetoacetic acid
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41
Q

Name three ketones

A
  • Acetoacetic acid
  • Beta hydroxybutyric acid
  • Acetone
  • Latter two are formed from acetoacetic acid
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42
Q

What is ketosis?

A
  • Rise in concentration of acidic ketone bodies
  • When carbohydrates / insulin are unavailable
  • Requiring metabolism of fats for energy
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43
Q

When does acidosis occur in ketosis?

A
  • When there is oxaloacetate deficiency

- Because acetyl-CoA(derived from ketone bodies) bonds with oxaloacetate

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44
Q

Identify a diagnostic criterion for ketosis that involves acetone

A
  • Acetone is a volatile substance
  • Which can be blown off in expired air of lungs
  • Giving breath an acetone smell
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45
Q

Describe the synthesis of triglycerides from carbohydrates

A
  • Carbohydrate converted to acetyl-CoA
  • Acetyl-CoA converted to malonyl-CoA
  • Malonyl converted to fatty acyl-CoA
  • Fatty acyl-CoA converted to fatty acids
  • Alpha-glycerophosphate forms glycerol which reacts with fatty acids to form triglyceride
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46
Q

Identify the importance of fat synthesis from triglycerides

A
  • Excess of energy can be stored

- Each gram of fat contains 2.5 times more calories than each gram of glycogen

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47
Q

Identify the four main cell types of the islets of langerhans and what each cell secretes

A
  • B-cells: Insulin and amylin
  • A cells: Glucagon
  • D cells: Somatostatin
  • PP cells: Pancreatic polypeptide
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48
Q

Outline the synthesis of insulin

A
  • Insulin RNA is transcribed by ribosomes to form insulin preprohormone
  • Proinsulin is cleaved from insulin preprohormone in Golgi apparatus
  • To form insulin
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49
Q

Identify the three insulin chains

A
  • A and B, which are connected by a disulphide bridge

- C chain

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50
Q

Identify an enzyme that degrades insulin

A
  • Insulinase
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51
Q

Identify the structure of the insulin receptor

A
  • Two alpha subunits outside cell membrane

- Two beta subunits that penetrate through cell membrane into cytoplasm

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52
Q

How is the insulin receptor activated?

A
  • Insulin binds to alpha subunits
  • Which causes autophosphorylation of beta units
  • Which activates tyrosine kinase
  • Which causes phosphorylation of insulin-receptor substrates (IRS)
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53
Q

Identify two conditions in which muscle cells take up large amounts of glucose, and how they take up this glucose

A
  • During heavy exercise
  • Following a meal
  • Facilitated diffusion by GLUT-4 transporter
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54
Q

Why do insulin levels fall between meals?

A
  • Following a meal blood glucose falls

- So insulins role in glycogenesis is no longer necessary

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55
Q

Identify the mechanism by which insulin causes glucose uptake and storage in liver cell

A
  • Facilitated diffusion of glucose by GLUT-2 transporter
  • Phosphorylation of glucose by glucokinase
  • Increase in glycogen synthase
  • Inactivation of liver phosphorylase
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56
Q

When does insulin convert glucose to fatty acids? What happens to these fatty acids? What is the effect of insulin on gluconeogenesis?

A
  • When excess glucose cannot be stored as glycogen in liver
  • Fatty acids are packaged as triglycerides in VLD lipoproteins
  • Insulin also inhibits gluconeogenesis
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57
Q

Identify the mechanisms of fat storage and synthesis by insulin

A
  • Increases utilisation of glucose which spares fat

- Inhibits lipase

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58
Q

Outline the effects of insulin on protein metabolism

A
  • Stimulates transport of amino acids into cells
  • Increases translation of mRNA
  • Increases rate of transcription
  • Inhibits catabolism of proteins
  • Depresses gluconeogenesis (amino acids are substrate)
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59
Q

Identify the main pathological mechanism by which insulin deficiency causes diabetes

A
  • Lipase releases fatty acids into blood
  • Which are converted to cholesterol an phospholipids by liver
  • Which are released as lipoproteins in blood
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60
Q

Why does insulin lack cause acidosis?

A
  • Carnitine transport mechanism of fatty acids becomes increasingly activated
  • Beta oxidation occurs rapidly, releasing acetyl-CoA
  • Which is condensed to form acetoacetic acid
  • Which is not utilised due to lack of insulin
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61
Q

Why does insulin deficiency cause enhanced urea excretion in urine?Identify the effects of insulin deficiency on protein storage

A
  • Increased catabolism of proteins
  • Plasma amino acid concentration increases
  • Increased formation of ammonia
  • Which is then converted into urine and excreted in urine
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62
Q

Outline the mechanism of insulin secretion

A
  • Glucose enters cell through GLUT-2 transporter
  • Phosphorylation of glucose to glucose-6 phosphate
  • Which is oxidised to form ATP
  • Which inhibits ATP sensitive potassium channels
  • Which depolarises the membrane
  • Which opens voltage gated calcium channels
  • That simulate fusion of the docked insulin-containing vesicles with th cell membrane
  • And secretion of insulin by exocytosis
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63
Q

Outline factors that enhance the exocytosis of insulin

A
  • Gastric inhibitory peptide
  • Glucagon
  • ACh
  • Rising blood glucose concentration
  • Arginine and lysine
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64
Q

Outline factors that inhibit exocytosis of insulin

A
  • Somatostatin

- Noradrenaline (by alpha-adrenergic receptors)

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65
Q

Outline the two major effects of glucagon

A
  • Glycogenolysis
  • Increase gluconeogenesis
  • Both of which enhance the availability of glucose to other organs
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66
Q

Outline the process by which glucagon causes glycogenolysis in the liver

A
  • Activates of adenylyl cyclase, cAMP, PKA, and finally phosphorylase
  • Which converts glycogen into G1P
  • G1P converted to G6P
  • G6P is converted to glucose by glucose phosphatase
  • Allowing glucose to be mobilised from liver cells
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67
Q

Outline the process by which glucagon causes gluconeogenesis in the liver

A
  • Activates enzymes required for amino acid transport for gluconeogenesis
  • Especially enzyme system for converting pyruvate to phosphoenolpyruvate
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68
Q

Outline factors that stimulate glucagon secretion

A
  • Decrease in blood glucose
  • High concentrations of amino acids (L-arginine)
  • Exercise (due to circulating amino acids, or beta-adrenergic stimulation)
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69
Q

Identify factors that stimulate somatostatin release from delta cells

A
  • Increased blood glucose
  • Increased amino acids and fatty acids
  • Concentrations of GI hormones released in response to food intake
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70
Q

Identify the inhibitory effects of somatostatin

A
  • Depress the secretion of both insulin and glucagon
  • Decrease the motility of the stomach, duodenum, and gallbladder
  • Decreases both secretion and absorption in the gastrointestinal tract.
71
Q

What is the principal role of somatostatin?

A
  • To extend the period of which time the food nutrients are assimilated into blood
  • To decrease utilisation of absorbed nutrients by the tissues (preventing exhaustion of the food, making it available over a longer period fo time)
72
Q

Outline 3 functions of amylin

A
  • Delays gastric emptying
  • Breakdown of glycogen to lactate in striated muscle
  • Inhibition of insulin secretion
73
Q

What is diabetes mellitus?

A
  • Metabolic disorder
  • Characterised by a hyperglycaemia
  • Which is caused by either a lack of insulin secretion or decreased sensitivity of the tissues to insulin.
74
Q

How is hyperglycaemia defined?

A
  • Fasting plasma glucose greater than 7.0 mmol/l

- Plasma glucose greater than 11.1 mmol/l one to two hours after a meal.

75
Q

Outline the aetiology of type 1 diabetes

A
  • Autoimmune destruction (1A) with autoantibodies to islet cells
  • Genetic factors, e.g. HLA-DR4, HLA-B8 HLA-DR3
  • Viral infection e.g. Coxsackie B
76
Q

Outline the pathology of Type 1 diabetes

A
  • T cell autoimmune disease
  • Infiltration of islets with monocytes containing activated macrophages, T-cells, NKCs and B-cells
  • Destruction of beta cells
77
Q

Identify the three principal metabolic disturbances in type 1 diabetes

A
  • Increased blood glucose
  • Increased utilisation of fats for energy and cholesterol formation
  • Depletion of proteins
78
Q

Explain why polyuria and polydypsia occur in type 1 diabetes

A
  • Glucose does not enter cell
  • Increased osmotic pressure in extracellular fluid
  • Causes osmotic transfer out of cells
  • Loss of glucose in urine causes osmotic diuresis
79
Q

Explain why retinopathy occurs in type 1 diabetes

A
  • Chronic high glucose causes abnormal function of blood vessels
  • With inadequate blood supply to tissues
80
Q

Explain why neuropathy occurs in type 1 diabetes

A
  • Chronic high glucose concentration causes damage to peripheral nerves
81
Q

Explain why metabolic acidosis occurs in type 1 diabetes

A
  • Increase fat metabolism
  • Increases release of keto acids
  • Which are oxidised and taken up by cells
82
Q

Explain why atherosclerosis occurs in type 2 diabetes

A
  • Increased fat utilisation in liver
  • Increased amount of cholesterol formation
  • Which is deposited in arterial walls
83
Q

Explain why weight loss and asthenia occurs type 1 diabetes

A
  • Increased utilisation and decreased storage of proteins as well as fats
84
Q

Identify the four major determinants of type 2 diabetes

A
  • Age
  • Obesity
  • Family history
85
Q

What is the prevalence of type 2 diabetes in the UK

A
  • 4-6%
86
Q

What is metabolic syndrome?

A
  • Group of conditions
  • Such as obesity, hypertension, hypetriglyceridaemia
  • That are associated with insulin resistance
87
Q

Identify a genetic factor in the development of type 2 diabetes

A
  • TCF7-L2
  • Which increases risk of 35%
  • Modulates pancreatic islet cell function
88
Q

Explain the connection between low birth weight and development of type 2 diabetes

A
  • Poor nutrition early in life impairs beta cell development and function
  • Low birth weight predisposes to heart disease and hypertension
89
Q

Identify the inflammatory changes in diabetes

A
  • Elevated CRP
  • Elevator PAI-1
  • Elevated TNF-a
  • Elevated IL-6
90
Q

Outline the role of adipose tissue in the pathology of type 2 diabetes

A
  • It releases fatty acids which induce insulin secretion because they compete with glucose as a fuel supply for oxidation
  • It releases adipokines which reduce sensitivity of cells to insulin
91
Q

Outline the role of physical inactivity in the pathology of type 2 diabetes

A
  • Down-regulation of insulin-sensitive kinases
  • Promotes accumulation of fatty acids in skeletal muscle
  • Allows non-insulin-dependent glucose uptake into cells, reducing the demand of pancreatic beta cells
92
Q

Outline the role of amyloid in the pathology of type 2 diabetes

A
  • Inhibits insulin secretion
93
Q

Outline the metabolic disturbances in type 2 diabetes

A
  • Increased plasma insulin concentration
  • Increased blood glucose
  • Increased lipid accumulation in tissues
94
Q

Identify different mutations in monogenic diabetes mellitus

A
  • Insulin receptor mutations
  • Maternally inherited diabetes in deafness
  • Wolfram’s syndrome
  • Prader Willi, Bardet-Biedl, Alstroms
  • Disorders of insulins signalling
  • Beta cell glucose sensing mutation (GCK) beta cell transcription regulation (HNF)
95
Q

Identify two pathological processes that cause secondary diabetes two examples of each

A
  • Hypersecretion causing hyperglycaemia: Cushing’s, acromegaly
  • Destruction of the pancreas e.g. pancreatitis, haemochromatosis
96
Q

How do symptoms differ between type 1 and type 2 diabetes?

A
  • Type 1: Polyuria, polydipsia, nocturia

- Type 2: Asymptomatic or non-specific complaints e.g. fatigue and malaise

97
Q

Why does weight loss and ketoacidosis not occur in type 2 diabetes?

A
  • Insulin resistance

- Small amounts of insulin are required to suppress lipolysis and some glucose is maintained

98
Q

What is pruritus vulvae?

A
  • Itching of vulva
99
Q

What is balanitis?

A
  • Inflammation of glans or head of penis
100
Q

Identify overlap in age between type 1 and type 2 diabetes

A
  • Young people have MODY (type 2)

- LADA in adults (type 1)

101
Q

Why is testing urine for glucose used in the detecting

A
  • Normal people lose undetectable amounts of urine in glucose
  • Diabetics lose glucose in small to large amounts (glycosuria)
  • In proportion to severity of disease
102
Q

Why is testing urine for ketones not pathognomonic?

A
  • Found in normal people who have:
  • Been fasting or exercising strenuously for long periods,
  • Vomiting repeatedly
  • Been eating a diet high in fat and low in carbohydrate
103
Q

Outline the diagnosis of diabetes

A
  • Fasting glucose > 7 mmol/L
  • Random plasma glucose > 11.1 mmol/L
  • Both needed for asymptomatic, only one needed in symptomatic
  • HBA1c > 48 mmol/L
104
Q

Outline the dietary advice in the treatment of type 2 diabetes

A
  • No different from that considered healthy for everyone
  • Low in sugar
  • Low in saturated fat
  • High in fibre
  • High in starch carbohydrates
105
Q

What is the importance of foods with a low glycaemic index?

A
  • Slower absorption
  • Reduced glucose peak
  • Pasta is recommended over white potato
106
Q

What is the ideal HbA1c in diabetes?

A
  • <7% (53 mmol/mol)
107
Q

What is the ideal blood pressure in diabetes

A
  • <130/80 mm Hg
108
Q

What is the ideal total cholesterol in diabetes?

A
  • <4.0 mmol/L
109
Q

What are the ideal LDL and HDL values in diabetes?

A
  • LDL: <2.0

- HDL: >1.1 in men >1.3 in women

110
Q

What is the ideal triglyceride value in diabetes?

A
  • <1.7
111
Q

Outline a drug course for the treatment of diabetes

A
  • Lifestyle changes and metformin
  • Add sulfonylurea or basal insulin
  • If HbA1c still high add a DPP4 inhibitor
  • If HbA1c still high, intensify insulin treatment
112
Q

Which class of drug does metformin belong to?

A
  • Biguanide
113
Q

Identify five biochemical effects of metformin

A
  • Reduced carbohydrate absorption
  • Increased glucose uptake and utilisation
  • Reduced gluconeogenesis
  • Increased fatty acid oxidation
  • Reduced LDL and VLDL
114
Q

Outline the mechanism by which metformin reduces hepatic gluconeogenesis

A
  • Activation of AMPK
  • Which increases expression of TR4
  • Which inhibits expression of genes that are important for gluconeogenesis
115
Q

Identify the main adverse effects of metformin

A
  • GI effects, mainly diarrhoea

- Lactic acidosis is rare but fatal (treated using rehydration and bicarbonate infusion)

116
Q

Why is metformin advantageous in obese patients?

A
  • Appetite suppression
117
Q

Outline the mechanism of action of sulfonylureas

A
  • Blocks K-ATP channels on beta cells

- Which depolarises membrane and allows calcium entry and insulin secretion

118
Q

Identify drug interactions of sulfonylurea

A
  • Binds to albumin

- Competes with binding sites for salicylates and sulfonamides (antibacterial)

119
Q

Why are sulfonylureas only effective in achieving short term glucose control (1-3 years)

A
  • Beta cell mass declines with disease progression
120
Q

What is the main side effect of sulfonylureas and what prolongs this effect?

A
  • Hypoglycaemia
  • Related to potency and duration of action
  • Highest incidence occurs in chlorpropamide and glibenclamide
  • Lowest incidence in tolbutamide
121
Q

Identify 3 other disadvantages of sulfonylureas

A
  • Excreted in urine so action is prolonged in elderly/obese patients
  • Stimulates appetite and causes weight gain
  • Crosses the placenta and enters breast milk
122
Q

Identify two biochemical effects of glitazones

A
  • Reduced hepatic glucose output

- Increased glucose uptake into muscle

123
Q

Outline the mechanism of action of glitazones

A
  • Binds to a nuclear receptor PPARy-RXR complex
  • Causes it to bind to DNA
  • Promotes transcription and then insulin signalling
124
Q

Identify the only glitazone in use and why this is the case

A
  • Pioglitazone

- As it does not cause severe hepatotoxicity

125
Q

Describe the metabolism of pioglitazone

A
  • Metabolised by CYP2c and CYP3A4

- To active metabolites which are eliminated in bile

126
Q

Identify adverse effects of glitazones

A
  • Weight gain
  • Fluid retention which precipitate or worsen heart failure
  • Can cause ovulation because of insulin resistance
127
Q

Identify an alpha-glucosidase inhibitor

A
  • Acarbose
128
Q

Outline the mechanism of action of acarbose

A
  • Inhibits brush border enzymes
  • Delays carbohydrate absorption
  • Reducing postprandial increase in blood glucose
129
Q

Identify adverse effects of alpha-glucosidase inhibitors

A
  • Flatulence
  • Loose stools and diarrhoea
  • Abdominal pain
  • Bloating
130
Q

Identify an incretin mimetic

A
  • Exenatide
131
Q

Outline the mechanism of action of exenatide

A
  • Mimics the effect of glucagon like peptide
  • Which stimulates insulin secretion before absorbed glucose reaches islet cells
  • And inhibits glucagon secretion
132
Q

How and when is exenatide administered?

A
  • Subcutaneous injection

- Twice delay before first and last meal of day

133
Q

Outline adverse effects of exenatide

A
  • Hypoglycaemia
  • GI effects
  • Rarely pancreatitis
134
Q

Identify two gliptins

A
  • Sitagliptin

- Vildagliptin

135
Q

Outline the mechanism of action of gliptins

A
  • Competitive inhibition of DPP4
  • Therefore potentiate endogenous incretins (GLP-1 and GIP)
  • Stimulating insulin secretion and reduced glucagon secretion
  • Lowering blood glucose
136
Q

Identify adverse effects of gliptins

A
  • Nausea

- Acute pancreatitis

137
Q

Outline the mechanism of action of orlistat

A
  • Lipase inhibitor
  • Reduces absorption of fat from diet
  • Promotes weight loss
138
Q

Identify an averse effect of orlistat

A
  • Steatorrhoea
139
Q

How does a gastric band work?

A
  • Band around upper part of stomach
  • Slows and inhibits amount of food that can be consumed
  • Results in satiety with release of peptide YY
140
Q

How does a gastric bypass surgery work?

A
  • Stomach is divided into two pouches
  • Which come together in small intestine
  • Reduces volume and stretching of stomach
  • Less release of CCK, PYY, GLP-1 and ghrelin
141
Q

Identify four ways that insulin decreases blood glucose?

A
  • Increases glucose uptake by GLUT-4
  • Increases glycogen synthesis
  • Decreased gluconeogenesis
  • Decreased glycogenolysis
142
Q

Identify an immediate-acting preparation of insulin

A
  • Isophane insulin
143
Q

Identify a long-acting insulin analogue and how it is made

A
  • Glargine

- Precipitating insulin with protamine or zinc

144
Q

Identify a short-acting insulin analogue

A
  • Lispro
145
Q

How are insulin kinetics modified?

A
  • Altering amino acid sequence
146
Q

When is IV insulin given?

A
  • Emergency treatment e.g. diabetic ketoacidosis
147
Q

What is the most common complication of insulin therapy?

A
  • Hypoglycaemia
148
Q

What are the times of greatest risk of hypoglycaemia?

A
  • Before meals
  • During the night
  • During exercise
149
Q

What are the most common features of hypoglycaemia

A
  • Sweating
  • Tremor
  • Pounding heartbeat
  • Pallor
  • Cold sweat
150
Q

Which patients are at the highest risk of neuroglycopenia

A
  • Those with hypoglycaemic unawareness

- Who report loss of the main symptoms

151
Q

Identify features of neuroglycopenia

A
  • Patient appears pale, drowsy or detached
  • Clumsy and inappropriate behaviour
  • Irritable and aggressive
  • Hemiparesis
152
Q

Identify 3 ways of relieving nocturnal hypoglycaemia

A
  • Snack before bed
  • Separate evening dose to supper and before bed
  • Insulin infusion pump
153
Q

How can mild episodes of hypoglycaemia be relived?

A
  • Sugary snack or drink
154
Q

Why should excessive carbohydrate consumption be avoided in treatment hypoglycaemia?

A
  • Causes rebound hyperglycaemia
155
Q

How should an unconscious diabetic patient be treated?

A
  • Intramuscular glucagon
  • Or intravenous glucose (50%)
  • Followed by a flush of 0.9% saline to preserve the vein (as glucose scleroses vein)
156
Q

In what circumstances is diabetic ketoacidosis seen?

A
  • Type 1 diabetes
  • Previously undiagnosed
  • Interruption of insulin therapy
  • Stress of intercurrent illness
157
Q

Identify the cardinal biochemical features of diabetic ketoacidosis

A
  • Hyperglycaemia
  • Hyperketonaemia
  • Metabolic acidosis
158
Q

Why does dehydration occur in diabetic ketoacidosis

A
  • Hyperglycaemia causes osmotic diuresis and electrolyte loss
159
Q

How does metabolic acidosis occur in diabetic ketoacidosis?

A
  • Lipolysis
  • Increased fatty acids to kidneys for ketogenesis
  • Increased acidic ketones in blood
  • H+ displaces intracellular K+
160
Q

Identify the clinical features of ketoacidosis

A
  • Loss of skin turgor, furred tongue, cracked lips
  • Tachycardia, hypotension, reduced intra-ocular pressure
  • Kussmaul respiration, fetid breath, acetone breath
  • Confusion, drowsiness, coma
161
Q

How is DKA diagnosed?

A
  • Hyperglycaemia demonstrated by dipstick

- Ketonaemia confirmed by centrifuging blood sample

162
Q

Identify test results that indicate severe DKA

A
  • Pulse > 100 or <60 b.p.m
  • Systolic BP < 90 mm Hg
  • Glasgow Coma Score < 12
  • Blood ketones > 6 mmol/L
  • Bicarbonate < 12 mmol/L
  • Hypokalaemia <3.5 mmol/L
163
Q

Identify the four components of treating DKA

A
  • Administration of short acting soluble insulin
  • Fluid replacement
  • Potassium replacement
  • Antibiotics if infection present
164
Q

Outline the pathophysiology of diabetic foot

A
  • Somatic neuropathy: reduced pain perception, so trivial trauma causes infection
  • Autonomic neuropathy: Absent sweating, reduced blood flow causes callus formation
  • Tissue necrosis occurs and breaks through callus to surface
165
Q

Identify how diabetic foot can be prevented

A
  • Regular washing and moisturising feet
  • Changing socks daily and avoiding barefoot
  • Wearing appropriate footwear and checking it for foreign bodies
166
Q

Outline the treatment of diabetic foot

A
  • Removal of callus
  • Antibiotics
  • Measures to improve glycaemic control
  • Amputation when there is ischaemic pain at rest in a limb
167
Q

Outline PRIME Theory

A
  • Wants and needs are mental images of attractive goals
  • Wants are for pleasure or satisfaction
  • Needs are for anticipated relief of discomfort
  • Personal rules must generate wants or needs that can overcome competing wants or needs
168
Q

Outline COM-B system

A
  • Behaviour impacted by capability, motivation and opportunity
  • Capability: psychological and physical
  • Motivation: reflective and automatic processes
  • Opportunity: physical and social
  • Opportunity and capability influence motivation
  • Enacting a behaviour can alter capability, motivation and opportunity
169
Q

Outline the features of health belief model

A
  • Health related behaviour enacted if person:
  • Feels as though condition can be avoided
  • Has expectation taking a positive action will avoid negative condition
  • Believes they can successful take a positive action
170
Q

Outline the seven concepts in Health Belief model

A
  • Susceptibility
  • Severity
  • Benefits
  • Barriers
  • Cues to Action
  • Self-Efficacy
171
Q

Identify three reasons for poor self-management in a long term condition

A
  • Information overload, too complex
  • Unaware of strategies to activate readiness
  • Ineffective action plans
172
Q

Identify three psychological problems in adjusting to chronic illness

A
  • Initial adjustment involves shock
  • Later adjustment involves anger
  • Motivational loss
173
Q

Identify four factors that should be addressed by doctors in self management in chronic illness

A
  • Coping
  • Adherence
  • Self management
  • Motivation
174
Q

What is meant by SMART goals?

A
  • Specific
  • Measurable
  • Achievable
  • Relevant
  • Time-bound

Semester 4: Nutrition and Metabolism (17 decks)

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