PBL Topic 4 Case 6 Flashcards
(174 cards)
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
2
Q
What is the role of the GLUT-1 transporter?
A
- Enables basal non-insulin stimulated glucose uptake into any cell
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
4
Q
What is the role of the GLUT-3 transporter?
A
- Enables non-insulin mediated glucose uptake into brain neurones and placenta
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
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)
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
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
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
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
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
12
Q
How many steps are there in glycolysis?
A
- 10
13
Q
What is the overall efficiency of ATP formation in glycolysis?
A
- 43%
- Remainder of energy is lost as heat
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
15
Q
Where in the cell does glycolysis occur?
A
- In cytoplasm
16
Q
Where does Link reaction occur?
A
- Mitochondrial matrix
17
Q
Where does citric acid cycle occur?
A
- Mitochondrial matrix
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
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
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
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
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
23
Q
Where does oxidative phosphorylation take place?
A
- Inner (shelf) mitochondrial membrane
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
25
What is the role of cytochrome A3 / cytochrome oxidase
- 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
26
Outline the process of hydrogen ions transport in the outer chamber of the mitochondria
- 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
27
Outline the process of ATP formation during oxidative phosphorylation
- 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
28
What is the total number of ATP molecules formed from each molecule of glucose?
- 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
29
What is the overall efficiency of energy transfer in the formation of ATP from glucose?
- 66%
30
What is the role of the citrate ion in controlling the rate of glycolysis?
- Inhibits phosphofructokinase
| - An enzyme involved in glycolysis
31
How is lactic acid formed during anaerobic glycolysis?
- Pyruvic acid reacts with NADH
- Catalysed by lactic dehydrogenase
- Which can then be reconverted to pyruvic acid and NADH
32
How can alanine be converted into pyruvic acid?
- Deamination
33
Identify a pathway by which amino acids can be converted into glucose
- Phosphogluconate pathway
34
Outline the role of the anterior pituitary gland in gluconeogensis
- 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
35
What is a normal fasted blood glucose?
- 90 mg/dl
36
Outline the formation of glycerol-3-phosphate from triglycerides
- Intracellular hydrolysis of triglycerides
- Into fatty acids and glycerol
- Glycerol is converted to glycerol-3-phosphate by intracellular enzymes
37
Where does beta oxidation of fatty acids occur?
- Mitochondria
38
How do fatty acids enter cytoplasm for beta oxidation?
- Carrier mediated process
| - That uses carnitine as the carrier substance
39
Outline the process of beta oxidation
- 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
40
Outline the process of acetoacetic acid formation in the liver
- 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
41
Name three ketones
- Acetoacetic acid
- Beta hydroxybutyric acid
- Acetone
- Latter two are formed from acetoacetic acid
42
What is ketosis?
- Rise in concentration of acidic ketone bodies
- When carbohydrates / insulin are unavailable
- Requiring metabolism of fats for energy
43
When does acidosis occur in ketosis?
- When there is oxaloacetate deficiency
| - Because acetyl-CoA(derived from ketone bodies) bonds with oxaloacetate
44
Identify a diagnostic criterion for ketosis that involves acetone
- Acetone is a volatile substance
- Which can be blown off in expired air of lungs
- Giving breath an acetone smell
45
Describe the synthesis of triglycerides from carbohydrates
- 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
46
Identify the importance of fat synthesis from triglycerides
- Excess of energy can be stored
| - Each gram of fat contains 2.5 times more calories than each gram of glycogen
47
Identify the four main cell types of the islets of langerhans and what each cell secretes
- B-cells: Insulin and amylin
- A cells: Glucagon
- D cells: Somatostatin
- PP cells: Pancreatic polypeptide
48
Outline the synthesis of insulin
- Insulin RNA is transcribed by ribosomes to form insulin preprohormone
- Proinsulin is cleaved from insulin preprohormone in Golgi apparatus
- To form insulin
49
Identify the three insulin chains
- A and B, which are connected by a disulphide bridge
| - C chain
50
Identify an enzyme that degrades insulin
- Insulinase
51
Identify the structure of the insulin receptor
- Two alpha subunits outside cell membrane
| - Two beta subunits that penetrate through cell membrane into cytoplasm
52
How is the insulin receptor activated?
- Insulin binds to alpha subunits
- Which causes autophosphorylation of beta units
- Which activates tyrosine kinase
- Which causes phosphorylation of insulin-receptor substrates (IRS)
53
Identify two conditions in which muscle cells take up large amounts of glucose, and how they take up this glucose
- During heavy exercise
- Following a meal
- Facilitated diffusion by GLUT-4 transporter
54
Why do insulin levels fall between meals?
- Following a meal blood glucose falls
| - So insulins role in glycogenesis is no longer necessary
55
Identify the mechanism by which insulin causes glucose uptake and storage in liver cell
- Facilitated diffusion of glucose by GLUT-2 transporter
- Phosphorylation of glucose by glucokinase
- Increase in glycogen synthase
- Inactivation of liver phosphorylase
56
When does insulin convert glucose to fatty acids? What happens to these fatty acids? What is the effect of insulin on gluconeogenesis?
- When excess glucose cannot be stored as glycogen in liver
- Fatty acids are packaged as triglycerides in VLD lipoproteins
- Insulin also inhibits gluconeogenesis
57
Identify the mechanisms of fat storage and synthesis by insulin
- Increases utilisation of glucose which spares fat
| - Inhibits lipase
58
Outline the effects of insulin on protein metabolism
- 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)
59
Identify the main pathological mechanism by which insulin deficiency causes diabetes
- Lipase releases fatty acids into blood
- Which are converted to cholesterol an phospholipids by liver
- Which are released as lipoproteins in blood
60
Why does insulin lack cause acidosis?
- 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
61
Why does insulin deficiency cause enhanced urea excretion in urine?Identify the effects of insulin deficiency on protein storage
- Increased catabolism of proteins
- Plasma amino acid concentration increases
- Increased formation of ammonia
- Which is then converted into urine and excreted in urine
62
Outline the mechanism of insulin secretion
- 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
63
Outline factors that enhance the exocytosis of insulin
- Gastric inhibitory peptide
- Glucagon
- ACh
- Rising blood glucose concentration
- Arginine and lysine
64
Outline factors that inhibit exocytosis of insulin
- Somatostatin
| - Noradrenaline (by alpha-adrenergic receptors)
65
Outline the two major effects of glucagon
- Glycogenolysis
- Increase gluconeogenesis
- Both of which enhance the availability of glucose to other organs
66
Outline the process by which glucagon causes glycogenolysis in the liver
- 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
67
Outline the process by which glucagon causes gluconeogenesis in the liver
- Activates enzymes required for amino acid transport for gluconeogenesis
- Especially enzyme system for converting pyruvate to phosphoenolpyruvate
68
Outline factors that stimulate glucagon secretion
- Decrease in blood glucose
- High concentrations of amino acids (L-arginine)
- Exercise (due to circulating amino acids, or beta-adrenergic stimulation)
69
Identify factors that stimulate somatostatin release from delta cells
- Increased blood glucose
- Increased amino acids and fatty acids
- Concentrations of GI hormones released in response to food intake
70
Identify the inhibitory effects of somatostatin
- 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
What is the principal role of somatostatin?
- 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
Outline 3 functions of amylin
- Delays gastric emptying
- Breakdown of glycogen to lactate in striated muscle
- Inhibition of insulin secretion
73
What is diabetes mellitus?
- 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
How is hyperglycaemia defined?
- 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
Outline the aetiology of type 1 diabetes
- 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
Outline the pathology of Type 1 diabetes
- T cell autoimmune disease
- Infiltration of islets with monocytes containing activated macrophages, T-cells, NKCs and B-cells
- Destruction of beta cells
77
Identify the three principal metabolic disturbances in type 1 diabetes
- Increased blood glucose
- Increased utilisation of fats for energy and cholesterol formation
- Depletion of proteins
78
Explain why polyuria and polydypsia occur in type 1 diabetes
- 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
Explain why retinopathy occurs in type 1 diabetes
- Chronic high glucose causes abnormal function of blood vessels
- With inadequate blood supply to tissues
80
Explain why neuropathy occurs in type 1 diabetes
- Chronic high glucose concentration causes damage to peripheral nerves
81
Explain why metabolic acidosis occurs in type 1 diabetes
- Increase fat metabolism
- Increases release of keto acids
- Which are oxidised and taken up by cells
82
Explain why atherosclerosis occurs in type 2 diabetes
- Increased fat utilisation in liver
- Increased amount of cholesterol formation
- Which is deposited in arterial walls
83
Explain why weight loss and asthenia occurs type 1 diabetes
- Increased utilisation and decreased storage of proteins as well as fats
84
Identify the four major determinants of type 2 diabetes
- Age
- Obesity
- Family history
85
What is the prevalence of type 2 diabetes in the UK
- 4-6%
86
What is metabolic syndrome?
- Group of conditions
- Such as obesity, hypertension, hypetriglyceridaemia
- That are associated with insulin resistance
87
Identify a genetic factor in the development of type 2 diabetes
- TCF7-L2
- Which increases risk of 35%
- Modulates pancreatic islet cell function
88
Explain the connection between low birth weight and development of type 2 diabetes
- Poor nutrition early in life impairs beta cell development and function
- Low birth weight predisposes to heart disease and hypertension
89
Identify the inflammatory changes in diabetes
- Elevated CRP
- Elevator PAI-1
- Elevated TNF-a
- Elevated IL-6
90
Outline the role of adipose tissue in the pathology of type 2 diabetes
- 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
Outline the role of physical inactivity in the pathology of type 2 diabetes
- 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
Outline the role of amyloid in the pathology of type 2 diabetes
- Inhibits insulin secretion
93
Outline the metabolic disturbances in type 2 diabetes
- Increased plasma insulin concentration
- Increased blood glucose
- Increased lipid accumulation in tissues
94
Identify different mutations in monogenic diabetes mellitus
- 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
Identify two pathological processes that cause secondary diabetes two examples of each
- Hypersecretion causing hyperglycaemia: Cushing's, acromegaly
- Destruction of the pancreas e.g. pancreatitis, haemochromatosis
96
How do symptoms differ between type 1 and type 2 diabetes?
- Type 1: Polyuria, polydipsia, nocturia
| - Type 2: Asymptomatic or non-specific complaints e.g. fatigue and malaise
97
Why does weight loss and ketoacidosis not occur in type 2 diabetes?
- Insulin resistance
| - Small amounts of insulin are required to suppress lipolysis and some glucose is maintained
98
What is pruritus vulvae?
- Itching of vulva
99
What is balanitis?
- Inflammation of glans or head of penis
100
Identify overlap in age between type 1 and type 2 diabetes
- Young people have MODY (type 2)
| - LADA in adults (type 1)
101
Why is testing urine for glucose used in the detecting
- 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
Why is testing urine for ketones not pathognomonic?
- 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
Outline the diagnosis of diabetes
- 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
Outline the dietary advice in the treatment of type 2 diabetes
- No different from that considered healthy for everyone
- Low in sugar
- Low in saturated fat
- High in fibre
- High in starch carbohydrates
105
What is the importance of foods with a low glycaemic index?
- Slower absorption
- Reduced glucose peak
- Pasta is recommended over white potato
106
What is the ideal HbA1c in diabetes?
- <7% (53 mmol/mol)
107
What is the ideal blood pressure in diabetes
- <130/80 mm Hg
108
What is the ideal total cholesterol in diabetes?
- <4.0 mmol/L
109
What are the ideal LDL and HDL values in diabetes?
- LDL: <2.0
| - HDL: >1.1 in men >1.3 in women
110
What is the ideal triglyceride value in diabetes?
- <1.7
111
Outline a drug course for the treatment of diabetes
- 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
Which class of drug does metformin belong to?
- Biguanide
113
Identify five biochemical effects of metformin
- Reduced carbohydrate absorption
- Increased glucose uptake and utilisation
- Reduced gluconeogenesis
- Increased fatty acid oxidation
- Reduced LDL and VLDL
114
Outline the mechanism by which metformin reduces hepatic gluconeogenesis
- Activation of AMPK
- Which increases expression of TR4
- Which inhibits expression of genes that are important for gluconeogenesis
115
Identify the main adverse effects of metformin
- GI effects, mainly diarrhoea
| - Lactic acidosis is rare but fatal (treated using rehydration and bicarbonate infusion)
116
Why is metformin advantageous in obese patients?
- Appetite suppression
117
Outline the mechanism of action of sulfonylureas
- Blocks K-ATP channels on beta cells
| - Which depolarises membrane and allows calcium entry and insulin secretion
118
Identify drug interactions of sulfonylurea
- Binds to albumin
| - Competes with binding sites for salicylates and sulfonamides (antibacterial)
119
Why are sulfonylureas only effective in achieving short term glucose control (1-3 years)
- Beta cell mass declines with disease progression
120
What is the main side effect of sulfonylureas and what prolongs this effect?
- Hypoglycaemia
- Related to potency and duration of action
- Highest incidence occurs in chlorpropamide and glibenclamide
- Lowest incidence in tolbutamide
121
Identify 3 other disadvantages of sulfonylureas
- 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
Identify two biochemical effects of glitazones
- Reduced hepatic glucose output
| - Increased glucose uptake into muscle
123
Outline the mechanism of action of glitazones
- Binds to a nuclear receptor PPARy-RXR complex
- Causes it to bind to DNA
- Promotes transcription and then insulin signalling
124
Identify the only glitazone in use and why this is the case
- Pioglitazone
| - As it does not cause severe hepatotoxicity
125
Describe the metabolism of pioglitazone
- Metabolised by CYP2c and CYP3A4
| - To active metabolites which are eliminated in bile
126
Identify adverse effects of glitazones
- Weight gain
- Fluid retention which precipitate or worsen heart failure
- Can cause ovulation because of insulin resistance
127
Identify an alpha-glucosidase inhibitor
- Acarbose
128
Outline the mechanism of action of acarbose
- Inhibits brush border enzymes
- Delays carbohydrate absorption
- Reducing postprandial increase in blood glucose
129
Identify adverse effects of alpha-glucosidase inhibitors
- Flatulence
- Loose stools and diarrhoea
- Abdominal pain
- Bloating
130
Identify an incretin mimetic
- Exenatide
131
Outline the mechanism of action of exenatide
- Mimics the effect of glucagon like peptide
- Which stimulates insulin secretion before absorbed glucose reaches islet cells
- And inhibits glucagon secretion
132
How and when is exenatide administered?
- Subcutaneous injection
| - Twice delay before first and last meal of day
133
Outline adverse effects of exenatide
- Hypoglycaemia
- GI effects
- Rarely pancreatitis
134
Identify two gliptins
- Sitagliptin
| - Vildagliptin
135
Outline the mechanism of action of gliptins
- Competitive inhibition of DPP4
- Therefore potentiate endogenous incretins (GLP-1 and GIP)
- Stimulating insulin secretion and reduced glucagon secretion
- Lowering blood glucose
136
Identify adverse effects of gliptins
- Nausea
| - Acute pancreatitis
137
Outline the mechanism of action of orlistat
- Lipase inhibitor
- Reduces absorption of fat from diet
- Promotes weight loss
138
Identify an averse effect of orlistat
- Steatorrhoea
139
How does a gastric band work?
- 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
How does a gastric bypass surgery work?
- 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
Identify four ways that insulin decreases blood glucose?
- Increases glucose uptake by GLUT-4
- Increases glycogen synthesis
- Decreased gluconeogenesis
- Decreased glycogenolysis
142
Identify an immediate-acting preparation of insulin
- Isophane insulin
143
Identify a long-acting insulin analogue and how it is made
- Glargine
| - Precipitating insulin with protamine or zinc
144
Identify a short-acting insulin analogue
- Lispro
145
How are insulin kinetics modified?
- Altering amino acid sequence
146
When is IV insulin given?
- Emergency treatment e.g. diabetic ketoacidosis
147
What is the most common complication of insulin therapy?
- Hypoglycaemia
148
What are the times of greatest risk of hypoglycaemia?
- Before meals
- During the night
- During exercise
149
What are the most common features of hypoglycaemia
- Sweating
- Tremor
- Pounding heartbeat
- Pallor
- Cold sweat
150
Which patients are at the highest risk of neuroglycopenia
- Those with hypoglycaemic unawareness
| - Who report loss of the main symptoms
151
Identify features of neuroglycopenia
- Patient appears pale, drowsy or detached
- Clumsy and inappropriate behaviour
- Irritable and aggressive
- Hemiparesis
152
Identify 3 ways of relieving nocturnal hypoglycaemia
- Snack before bed
- Separate evening dose to supper and before bed
- Insulin infusion pump
153
How can mild episodes of hypoglycaemia be relived?
- Sugary snack or drink
154
Why should excessive carbohydrate consumption be avoided in treatment hypoglycaemia?
- Causes rebound hyperglycaemia
155
How should an unconscious diabetic patient be treated?
- Intramuscular glucagon
- Or intravenous glucose (50%)
- Followed by a flush of 0.9% saline to preserve the vein (as glucose scleroses vein)
156
In what circumstances is diabetic ketoacidosis seen?
- Type 1 diabetes
- Previously undiagnosed
- Interruption of insulin therapy
- Stress of intercurrent illness
157
Identify the cardinal biochemical features of diabetic ketoacidosis
- Hyperglycaemia
- Hyperketonaemia
- Metabolic acidosis
158
Why does dehydration occur in diabetic ketoacidosis
- Hyperglycaemia causes osmotic diuresis and electrolyte loss
159
How does metabolic acidosis occur in diabetic ketoacidosis?
- Lipolysis
- Increased fatty acids to kidneys for ketogenesis
- Increased acidic ketones in blood
- H+ displaces intracellular K+
160
Identify the clinical features of ketoacidosis
- Loss of skin turgor, furred tongue, cracked lips
- Tachycardia, hypotension, reduced intra-ocular pressure
- Kussmaul respiration, fetid breath, acetone breath
- Confusion, drowsiness, coma
161
How is DKA diagnosed?
- Hyperglycaemia demonstrated by dipstick
| - Ketonaemia confirmed by centrifuging blood sample
162
Identify test results that indicate severe DKA
- 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
Identify the four components of treating DKA
- Administration of short acting soluble insulin
- Fluid replacement
- Potassium replacement
- Antibiotics if infection present
164
Outline the pathophysiology of diabetic foot
- 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
Identify how diabetic foot can be prevented
- Regular washing and moisturising feet
- Changing socks daily and avoiding barefoot
- Wearing appropriate footwear and checking it for foreign bodies
166
Outline the treatment of diabetic foot
- Removal of callus
- Antibiotics
- Measures to improve glycaemic control
- Amputation when there is ischaemic pain at rest in a limb
167
Outline PRIME Theory
- 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
Outline COM-B system
- 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
Outline the features of health belief model
- 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
Outline the seven concepts in Health Belief model
- Susceptibility
- Severity
- Benefits
- Barriers
- Cues to Action
- Self-Efficacy
171
Identify three reasons for poor self-management in a long term condition
- Information overload, too complex
- Unaware of strategies to activate readiness
- Ineffective action plans
172
Identify three psychological problems in adjusting to chronic illness
- Initial adjustment involves shock
- Later adjustment involves anger
- Motivational loss
173
Identify four factors that should be addressed by doctors in self management in chronic illness
- Coping
- Adherence
- Self management
- Motivation
174
What is meant by SMART goals?
- Specific
- Measurable
- Achievable
- Relevant
- Time-bound
