Diabetes Pharmacology and Guidelines Flashcards
(135 cards)
1
Q
Describe the chemical (primary) structure of insulin:
A
Two peptide chain
Chain A: 21 a.a residues
Chain B: 30 a.a residues
Chains linked by disulphide bridges between (A7 and B7) and (A20 and B19)- tertiary
Chain A is also internally bridged between A6 and A11
2
Q
What are the different types of insulin and their differences and which ones are used now?
A
Bovine
Porcine
Human
Very similar but different a.a residues on A8, A10 and B30
3
Q
Describe the physical (secondary) structure of insulin:
A
Alpha helix
Three segments
Intramolecular H-bonding between amide groups
4
Q
Describe the physical (tertiary) structure of insulin:
A
Disulfide bridges
5
Q
Describe the Dimer (quaternary) structure of insulin:
A
In solution exists as dimers
Anti-parallel B sheet formed between B23 and B30, with B28 proline which is important in weak hydrophobic interactions stabilised by H-bonding involving R24 and R26
6
Q
Describe the Hexamer (quaternary) structure of insulin:
A
Two Zn ions and three insulin dimers
Globular, not soluble
Interior is mainly non polar a.a side chains
Exterior is mainly polar a.a side chains
7
Q
What are the two forms of conformation of the B chain in insulin?
A
T (extended B1 to B8)
R (alpha helix B1 to B8)
8
Q
Which one of the conformation of the B chain in insulin is more predominant and stable?
A
R state found in presence of phenol or cresol
R state is more stable
9
Q
What does insulin need to be in order to be absorbed?
A
Dissolved
10
Q
What are the physical properties of insulin?
A
White powder
Can be amorphous or crystalline
Practically insoluble in water, ethanol and ethers
Dissolves in dilute mineral acids
Dissolves and decomposes in dilute solutions of alkali hydroxides
11
Q
Which structure of insulin will dissolve faster?
A
Amorphous
12
Q
What is the process in obtaining natural insulin?
A
Pig or cow, insulin from pancreas
Needs to be free from transmissible spongiform encephalopathies (TSF)
Long and involved purification process: extraction, purification, analysis
13
Q
Describe semi-synthetic human insulin?
A
Chemically identical to human insulin
Enzymatically modified porcine insulin
Label must state ‘emp’
14
Q
How is semi-synthetic human insulin made?
A
Generate purified porcine insulin as normal and then change the B30 residue from alanine to threonine by action of an enzyme
15
Q
What does ‘emp’ stand for on an insulin label?
A
Enzymatically modified porcine
16
Q
Describe biosynthetic human insulin:
A
Chemically identical to human insulin
Recombinant DNA tech
Label must contain the method of preparation :
‘Prb’ ‘Crb’ ‘Pyr’
17
Q
How is biosynthetic human insulin made?
A
Identify gene codes for insulin in humans
Insert gene into the plasmid of a bacterial or fungal vector
Grow the modified bacterium/fungus
Harvest and purify the human insulin
18
Q
What does ‘Prb’, ‘Crb’ and ‘Pyr’ stand for on an insulin label?
A
Prb and Crb= purified recombinant bacterial
Pyr= purified yeast recombinant
19
Q
What is one unit equivalent to in human insulin?
A
0.0347mg
20
Q
How is insulin administered?
A
Normally Subcutaneously
Occasionally IM
IV in emergencies
21
Q
Where is the absorption of insulin fastest when it is injected and what can also increase the rate of absorption?
A
Fastest at abdominal wall
Exercise and heat will increase rate
22
Q
Name the five types of insulin formulations:
A
Soluble insulin (neutral insulin)
Insulin Zinc suspension
Isophane insulin (NPH-neutral protamine hagedorn)
Protamine zinc insulin
Biphasic isophane insulin
23
Q
Describe soluble insulin:
A
Insulin is all in solution in the dimer form, fast acting and clear
24
Q
Describe Insulin zinc suspension:
A
Crystalline/ amorphous/ mixed (70:30 C:A)
Insulin is all as solid particles so it takes time to go from hexamers to dimers as in complex
25
Describe Isophane insulin:
Insulin in complex with protamine
Protamine sulfate= the sulphates of the basic peptides extracted from the sperm of roe of fish, usually salmon or herring
Slow dissolution as in complex
26
Describe protamine zinc insulin:
Complexed with both protamine and zinc
27
Describe Biphasic isophane insulin:
Mix of protamine insulin with soluble insulin
28
What is the onset of action, peak action and DoA time for soluble insulin?
SC:
- Onset- 30-60 mins
- Peak action- 2-4 hours
- DoA- 8 hours
IV:
- Onset- imediate
- Peak action: none
- DoA- 30 mins
29
What is the onset of action, peak action and DoA time for Zinc suspension?
Crystalline:
- Onset- 4-6 hours
- Peak action- 8-24 hours
- DoA- 28-36 hours
Amorphous:
- Onset- 1-2 hours
- Peak action- 2-4 hours
- DoA- 6-12 hours
Mixed:
- Onset- 1-3 hours
- Peak action- 6-12 hours
- DoA- 18-24 hours
30
What is the onset of action, peak action and DoA time for Isophane insulin?
- Onset- 1-2 hours
- Peak action- 4-12 hours
- DoA- 24 hours
31
What is the onset of action, peak action and DoA time for protamine zinc insulin?
- Onset- 4-6 hours
- Peak action- 10-20 hours
- DoA- 24-36 hours
32
Name three short acting new human insulin analogues:
Insulin Aspart (NovoRapid)
Insulin Glulisine (Apidra)
Insulin Lispro (Humalog)
33
Describe and explain the features of Insulin Aspart:
Produced using recombinant yeast
B28 proline in human insulin is replaced by aspartic acid
Aspartic acid is negatively charged at physiological pH whereas proline is non-ionisable:
-Increase in charge repulsion between neighbouring molecules
-Self aggregation reduced to decrease in dimer formation so increase in dissolution
-molecules act more independently
-molecules diffuse more rapidly to give a quicker clinical effect
-receptor interaction unchanged
34
What is the onset of action, peak action and DoA time for Insulin Aspart?
- Onset- 10-20mins
- Peak action- 1-3 hours
- DoA- 3-5 hours
35
Describe and explain the features of Insulin Glulisine:
Produced using recombinant bacteria (Ecoli)
B3 asparagine in human insulin replaced by lysine
B29 lysine in human insulin replaced by glutamic acid:
-Increased charged repulsion between neighbouring moleucles
-self aggregation reduced
-moluecules diffuse more rapidly to give a quicker clinal effect
Receptor interaction unchanged
36
What is the onset of action, peak action and DoA time for Insulin Glulisine?
- Onset- 5-10mins
- Peak action- 1 hour
- DoA- 2-4 hours
37
Describe and explain the features of Insulin Lispro:
Produced using recombinant bacteria (E coli)
B28 proline and B29 lysine in human insulin are reversed
Reversal of lysine and proline reduces potential for hydrophobic interactions between molecules (dimer formation due to hydrophobic):
-increased charge repulsion between neighbouring molecules
- decreasing self aggregation, molecules act more independently
-molecules diffuse more rapidly to give a quicker clinical effect
Receptor interaction unchanged
38
What is the onset of action, peak action and DoA time for Insulin Lispro?
- Onset- 10-20 mins
- Peak action- 1-2 hours
- DoA- 2-5 hours
39
In which way can insulin lispro be changed in order to make it have a longer DoA?
Complexed with protamine
40
Name three long acting new human insulin analogues:
Insulin Glargine (Lantus, Sanofi, Elililly)
Insulin Detemir (Levemir)
Insulin Degludec (Tresiba)
41
Describe and explain the features of Insulin Glargine:
Produced using recombinant bacteria (Ecoli)
A21 asparagine in human insulin replaced by glycine
Two arginine residues are added at the C terminus of the B chain (positions B31,B32)
Isoelectric point is changed (zero charge )
-completely soluble at pH 4
-low solubility at pH 7, so precipitates after SC injection, so it dissolves more slowly so prolonged absorption
Receptor interaction unchanged
42
What is the onset of action, peak action and DoA time for Insulin Glargine?
- Onset- 1 hour
- Peak action- NO PEAK
- DoA- 24 hours
43
Describe and explain the features of insulin Detemir:
Produced using recombinant yeast (saccharomyces cerevisiae)
B30 threonine removed and C14 fatty acid chain (myristic acid) added to B29 lysine
Strong molecular self association (not in monomer form as increase in hydrophobic interactions) leads to slow and prolonged absorption
Extensive binding to plasma albumin leads to consistent low plasma levels of monomer for absorption
Receptor interaction unchanged
44
What is the onset of action, peak action and DoA time for Insulin Determir?
- Onset- 1 hour
- Peak action- slight peak after 6 hours
- DoA- 24 hours
45
Describe and explain the features of insulin Degludec:
Produced using recombinant yeast (saccharomyces cerevisiae)
B30 threonine removed and C16 fatty diacid (hexadecanoic acid) linked to lysine B29 via a glutamate acid linker (increase hydrophobic)
Strong molecular self association of dihexamers to form linear multihexamers, which precipitate in the SC tissue
Extensive binding to albumin in the blood stream like insulin detemir
Receptor interaction unchanged
Clear even if long acting
46
What is the onset of action, peak action and DoA time for Insulin Degludec?
- Onset- 30-90 mins
- Peak action- NO PEAK
- DoA- 24 hours
47
Name an intermediate acting insulin:
NPH insulin- Humulin N
48
What is the NICE guidance on insulin therapy for T1D?
1,2 or 3 injections per day, usually injections of short acting + intermediate acting (biphasic regimen)
No regiment suits all
49
What is the NICE guidance on insulin therapy for T2D?
NPH insulin, injected once or twice a day
NPH+ short acting insulin should be considered especially if pts HbA1c is 75mmol (9%) or more
Insulin detemir/glargine should be considered as an alternative to NPH
50
What are the 3 aims of insulin therapy?
To ensure the pt has a normal lifestyle
To treat hyper without causing hypo
Reduce risk of long term complications
51
Describe rapid acting analogues of insulin:
Novorapid, Humalog
Injected 5-15 mins before eating or immediately after eating
52
Describe short acting insulin:
Actrapid, Humulin
Injected 15-30 mins before eating
Can act in the body for up to 8 hours
53
Describe medium acting insulin:
Insultard, Humulin I
Groups of insulin known as NPH
Injected usually at night and work up to 24 hours to keep blood glucose control between meals
54
Describe long acting insulin:
Levemir, Lantus
Injected usually at night and work up to 24 hours to keep blood glucose control between meals
55
Describe analogue mixture insulin:
Novomix 30
Injected 5-15 mins before eating or immediately after eating
They last 14-16 hours so usually injected 2x daily
56
Describe mixture insulin:
Humulin M3, Insuman Comb 15,25,50
Injected 20-30 mins before food
They last for 12 hours so injected 2x daily
57
Describe the vial and syringe for injecting insulin:
Syringes graduated in units
1ml=100units (for most)
Fixed needle, available in 1ml, 0.5ml and 0.3ml
58
What are the names of the insulin that aren't 100units/ml and give their strengths:
Insulin Glargine 300IU/ml Toujeo
Insulin Lispro 200IU/ml Humalog 200
Insulin Degludec 200IU/ml Tresiba
59
What are the ways of administering insulin?
Vial and syringe
Reusable pen and cartridge (most common)
Disposable pen and cartridge
Insulin pump- constant basal insulin, pts can activate bolus doses themselves
60
When are insulin pumps prescribed on the NHS?
For uncontrolled hypos
61
What are the features of needles to help with insertion?
Fine
Sharp
Coated in silicone oil so its less painful
Single use, must be disposed as needle can become hooked after multiple use
62
What are the lengths that needles come in?
5,6,8 (most common),12,12.7mm
63
What are the gauges that needles come in?
25G, 26G, 27G, 28G, 29G, 30G (most common)
64
What does the gauge of a needle mean?
Thickness of the needle, the higher the gauge, the finer the needle
65
What would determine which needle size is used for the patient?
The build of the patient:
Slim build: 5-6mm
Moderate build: 6-8mm
Large build: 12-12.7mm, as they have a thicker layer of SC fat
66
What are the features of needles which you can get for pen devices?
29G, 30G, 31G
5-12.7mm
67
Name reusable pens with cartridges:
Autopen, Clikstar
Novopen
68
Name disposable pens:
FlexPen, Solostar, Humalog Kwikpen
69
Where would you administer insulin in the body and which is fastest?
Abdomen (fastest)
Thighs (slower)
Upper arms (medium fast)
Buttocks (slowest)
70
Why would you rotate the site of injection?
To avoid lipohypertrophy- where there is thickening/ hardening of the tissue so erratic insulin absorption
71
Describe how you would inject insulin:
Prime the insulin needle by pressing it facing up until a little insulin comes out, to remove air, using 2IU
Inject insulin into clean skin with clean hands, do not use alcohol wipes (more painful)
Inject into soft fat, not muscle, at a 90º angle
'Pinch up' if slim or injection site with little SC fat or use shorter needle
Push needle all the way in and leave for 5-10 seconds to avoid leakage
72
What is the multiple insulin regime?
First line, most common
Intermediate/ long acting basal once daily at night+ short acting at meal times
e.g Lantus + Novorapid
73
What are the advantages and disadvantage of the multiple insulin regime?
+ Flexible if need to delay meal/ adjust for exercise, suitable for shift workers/busy jobs
- More injections, at least 4
74
What is the twice daily insulin regime?
Short+ intermediate acting premixed (rarely sometimes separated)
e.g Novomix 30, Humulin M3
75
What are the advantages and disadvantages of the twice daily insulin regime?
+ Simple, good control, fewer injections (good when admin is by other people)
- inflexible, fixed time, timed and constant food intake and lifestyle
76
What is the once daily regime?
Not for T1D
Intermediate/ long acting basal once daily at night, often used in combo with oral hypoglycaemics where max oral therapy doesnt give control
e.g Lantus
77
What is the sliding scale regime?
In hospital, given by IV
Used for medical emergencies or peri-operatively, during labour or unstable diabetes
Given by continuous IV infusion (with IV fluids) and rate of infusion adjusted according to blood glucose levels
78
What are the guidelines for the dosing routine for starting insulin?
Start with very low doses and very slowly to prevent hypos
Often 'honeymoon' period when some recovery of endogenous insulin production
Twice daily: 6-10 units BD
Multiple: Short 60% and long 40% (4 IU TDS and 8IU at night)
Patients can be taught to adjust dose according to pre-prandial BG
79
What are the rules for storing insulin?
Long term storage in fridge (loss of 5-10% potency at room temp over 2-3 months)
Current use keep out of fridge- cold temp takes longer to be absorbed and stings
Max 1 month out of fridge
Avoid freezing as decreases activity- keep insulin in salad draws in fridge to avoid this
80
What are the sick day rules for both T1 and T2 diabetics?
Don't stop taking insulin or tablets
Test blood more often- x4 daily more
Test for ketones
Drink plenty of fluids
Replace normal meals with carb containing drinks if necessary
81
Name 4 classes of drug that increases insulin production from pancreatic B cells:
Sulphonylureas - gliclazide
Meglitinides - nateglinide
GLP-1 agonists - exenatide
DPP-4 inhibitor - alogliptin
82
Name 4 sulfonylureas:
Tolbutamide - 1st gen
Glibenclamide (long acting)- 2nd gen
Gliclazide (short acting) -2nd gen
Glimepiride (long acting) -3rd gen
83
What is the pharmacological target for sulphonylureas?
ATP- sensitive K+ channels
84
How do sulphonylureas work?
Sulphonylureas block the Katp Channel (which has four SUR1 subuinits) causing depolarisation, as its closed, of the membrane potential and consequent downstream actions can cause hypoglycaemia as insulin secretion is increased because there is an influx of Ca2+ even in the absence of glucose as they have the same effect as glucose
85
What are the major side effects of sulphonylureas and why?
Hypoglycaemia and weight gain
Hypo as directly effecting insulin release
86
What are the difference between sulfonylureas and meglitinides?
Meglitinides have weaker binding and faster dissociation
Similar SEs but less pronounced
87
How do meglitinides work?
Same as sulphonylureas
Meglitinides block the Katp Channel (which has four SUR1 subuinits) causing depolarisation, as its closed, of the membrane potential and consequent downstream actions can cause hypoglycaemia as insulin secretion is increased because there is an influx of Ca2+ even in the absence of glucose as they have the same effect as glucose
88
Name 2 meglitinides:
Nateglinide
Repaglinide
89
What is the pharmacological target of the GLP-1 agonists?
The glucagon-like peptide 1 receptor
90
What is GLP-1?
GPCR, signals via Gas, activate adenylate cyclase, ATP-> cAMP, signal via PKA and Epac
Both of these further regulate insulin secretion by increasing intracellular calcium, proliferation of B cells and suppression of apoptosis
91
What is the consequence of the activation of GLP-1?
Decreases gastric emptying after a meal so takes longer for stomach to empty so slows down absorption of glucose form gut
Induces satiety so weight loss
Decreases glucagon secretion so decreases amount of glucose so decreases glycolysis
92
How do GLP-1 agonists work?
Activate the GLP-1 receptor and increase glucose dependent insulin release
GLP-1 is a peptide hormone released from the ileum that acts on the GLP-1 GPCR in pancreatic B cells
93
What are three ways to increase the lifetime of GLP-1 signalling?
Modify the structure of GLP1 so less easily hydrolysed- replace alanine by glycine so decreases cleavage by DPP4
Modify the structure so that it hides from DPP4- binding GLP1 to albumin or other proteins increases stability
Inhibits the protease DPP-4
94
How is lixisenatide an effective GLP1 agonist?
Adding a hexalysine increases stability and half life 2-4 hours
1x daily SC injection as large structure
95
How does Liraglutide work as an effective GLP1 agonist?
Similar key residues kept same for binding and conformation
Binds to albumin for stability
A lipophilic C16 fatty acid is added through a Glu spacer to K26
Half life is 11-15 hours, OD SC administration
96
How does Dulaglutide work as an effective GLP1 agonist?
An IgE conjugate of GLP1
Conjugated with IgG4 Fc fragment
1x weekly admin SC as half life 5 days
97
Name 3 GLP-1 agonists:
Liraglutide, lixisenatide, dulaglutide
98
What does DPP-4 stand for?
Dipetidyl Peptidase 4
99
How do DPP-4 inhibitors work?
GLP-1 has a very short half life (2 mins)
It is rapidly inactivated by DPP-4
DPP-4 inhibitor increase glucose dependent insulin secretion as they inhibit DPP-4 so decreases the breakdown of GLP-1 and therefore GLP-1 can perform its biological actions for longer
100
How did cyanpyrrolidines work as a DPP-4 inhibitor and why weren't effective?
DPP4 preference for proline a.a
Cyanpyrrolidines found to be proline mimetic that covalently bind to DPP4 via the a/s sereine
Not very stable due to intramolecular cyclisation (neutrophile and electrophile in same place)
101
Name 2 irreversible DPP4 inhibitors and how are they irreversible?
Vildagliptin- steric shielding of amine, attach bulky group to amine
Saxagliptin- add bulky group next to amine on carbon
Both given orally
102
Name 3 reversible DPP4 inhibitors:
Sitagliptin
Linagliptin
Alogliptin
103
Describe GLP1 agonists and DPP4 inhibitors together as drugs:
Dual effect of promoting insulin production in B cells and inhibiting glucagon production in alpha cells
Small chance of hypo
GLP1 injectable
DPP4 orally
Small bit statistically sig risk of pancreatitis and pancreatic cancer
104
Name two classes of drugs which affect energy metabolism of cells?
Meformin -biguanides (only one that used)
PPARgamma agonists - pioglitazone
105
Why does metformin not cause hypoglycaemia?
It doesn't involve an increase in insulin
106
Why can metformin only be used in T2D?
It requires endogenous insulin for action, only effective in functional pancreatic islet cells are present
107
What are the actions of Metformin?
Decreases gluconeogenesis in the liver
Increase peripheral glucose uptake and utilisation (skeletal muscle, adipose tissue), so decreases blood glucose as a result
Improves insulin sensitivity/ receptor function
Decreases carb absorption from GIT
Decreases lipid synthesis (dual action, decreases weight gain)
Reduces VDLs and LDLs in the blood, reduces CV risk
Increases GLP-1 secretion from GIT
108
What are VDLs and LDLs?
Very low density lipoproteins
Carry cholesterol and triglycerides to places that need them, help body gain energy and store it
109
What is the pharmacological mechanism of action of Metformin?
Metformin enters the liver cell via OCT then -> mitochondria and inhibits complex 1 in resp chain so decreases ATP production, so it increases AMP:ATP ratio
Increase in AMP has a direct effect on enzymes for gluconeogenesis
Glucagon acts at a GPCR which activates adenylate cyclase and increases cAMP
ATP is needed for more cAMP, with a decrease in cAMP so inhibitory effect on gluconeogenesis
Activation of AMPK stimulated by an increase in AMP, AMPK controls energy metabolism by an increase in breakdown of cAMP, so no gluconeogenesis
AMPK inhibits fat synthesis as it increases fat oxidation
AMPK decreases transcription for genes for gluconeogenesis, so a decrease in blood glucose
110
What are the side effects of Metformin and what can be done to reduce this?
GI side effects- change to MR formulation
Lactic acidosis (rare)
111
What are alternative potential benefits to metformin?
Against cancer and ageing
112
What is the pharmacological target of PPARg agonists?
The Peroxisome Proliferator Activated Receptor gamma (PPARgamma) receptor
113
How do PPARg receptors work?
PPARg is a nuclear receptor (transcription factor)
Found mainly in adipose tissue but also elsewhere including liver and skeletal muscles
Endogenous ligands are lipids
Together with the retinoid X receptor, it regulates effects on lipid metabolism and lowers BG levels
114
What is the pharmacological mechanism of action of PPARg agonists?
Ligand binds to PPARg and associates with Retinoid X receptor with its ligand
They come together and translocate to nucleus and bind to specific DNA sequence, "PPAR response element" effects gene transcription:
-regulate transcription in genes involved in fatty acid storage and glucose metabolism
-increase insulin sensitivity by increasing transcription on genes involved in insulin signalling and enhancing the effectiveness of insulin
115
What are the side effects of PPARg agonists and why doesn't it cause hypos?
Weight gain/ fluid retention
Doesn't cause hypos as effect is independent of insulin secretion
116
Name the two classes of drugs which affect the absorption and reabsorption of glucose:
Sodium Glucose Co-transporter 2 SGLT2 inhibitors- dapagliflozin
Alpha- glucosidase inhibitors -acarbose
117
What is the pharmacological target of SGLT2 inhibitors?
Sodium Glucose Co transporter 2 in proximal convoluted tubule
118
Describe the function of the SGLT2 transporter:
Major transporter that mediates the reabsorption of glucose in the kidney tubule , so glucose is reabsorbed back in the body
Has a low affinity and high capacity
119
Name the other sodium glucose co-transporter and how does it work?
SGLT1 found in the proximal straight tubule (main form in gut)
High affinity, low capacity
120
Describe the mechanism of action of SGLT2 inhibitors:
They will decrease reabsorption and increase excretion of glucose in urine
Hence plasma conc of glucose reduced
121
How is some glucose still reabsorbed when SGLT2 inhibitors are present?
SGLT1 still works as they are mainly found in the gut so can still absorb there
122
Name 3 SGLT2 inhibitors:
Canagliflozin
Dapagliflozin
Empagliflozin
123
What are common side effects of SGLT2 inhibitors and why?
Urinary disorders like UTIs or thrush
This is due to an increase in glucose (glycosuria >50g day) being excreted out in the urine so an increase in glucose for bacteria to thrive in
Tiredness, dehydration, weight loss due to reduced glucose
124
Do SGLT2 inhibitors cause hypos?
No- effect is independent from insulin
125
What is the pharmacological target of alpha-glucosidase inhibitors?
a-glucosidase (maltase)
126
What is the function of a-glucosidase?
An enzyme that breaks down short chain oligosaccharides, including maltose (disacc) into glucose in the GIT via SGLT1
Required before glucose can be absorbed from the gut into blood stream
127
How does a-glucosidase inhibitors work?
Inhibition would lead to a decrease in glucose absorption after a meal, so post-prandial glucose conc decreases
In the transition state of starch, the six membered ring is flattened with SP2 like hybridisation and partial positive change
a-glucosidase inhibitors resemble this transition state and act as a competitive inhibitor as has an N and a positive charge, so the NH is stable and isn't cleaved by the enzyme
128
Acarbose has a Mr higher than 500 (646), a polar logP and lots of HBA's and HBD's, why is it still okay to take orally?
Looks like it won't be orally bioavailable but that's okay as doesn't need to be absorbed into cell and transported to other parts of the body as sits in cell membrane of GI tract
129
What is the main side effect of a-glucosidase inhibitors and why?
Diarrhoea and flatulence due to buildup of oligosaccharides in the colon and their bacterial digestion
130
What would be the initial treatment for T2D?
Lifestyle:
-diet, weight, physical activity
131
What is a glucose tolerance test?
Give pt a significant amount of glucose and see how long the in vivo clearance takes
132
Describe the structure of starch:
Starch is joined by a-1,4 glycosidic bonds in chains
Chains joined together by a-1,6 glycosidic bonds
Polymerisation through theses linkages give starch
133
Which enzymes hydrolyse starch?
a-amylase
a-glucosidase
134
What does ADLS mean in medical notes?
Activates of daily living
135
What are the guidelines when starting a T1D on long acting insulin?
Start with determir BD
Alternative insulin glargine OD
Insulin Decludec OD
