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Patient Sem 1 > Diabetes > Flashcards

Diabetes Flashcards

1
Q

What are the blood glucose ranges?

A

Hypoglycaemia: < 2.5 mmol/L
Normonglycaemia Fasted/Fed: 3 -5/7-8 mmol/L
Hyperglycaemia: > 10 mmol/L

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2
Q

What is proinsulin?

A 
product of translation 
A, C, B chain 
23 AAs of the C Peptide cleaved off
= biologically active insulin 
A and B chain linked together by disulphide bonds
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3
Q

Why would you measure blood concentration of C protein rather than Insulin?

A

because insulin has a short half life of 3 - 5 minutes

C Peptide is released at the same time as the insulin

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4
Q

What is insulin complexed in secretory granules?

A

complexed with Zinc to form a crystal structure
Zn will dissolve on release
this will release the insulin

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5
Q

What are the Islets of Langerhans?

A

a small cluster of endocrine (hormone producing) cells
make up 1% of the pancreas
highly vascularised and innervated, each islets has their own blood supply

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6
Q

What are the different cells of the Islets of Langerhans?

A 
alpha cells - secrete glucagon 
beta cells - secrete insulin 
delta cells - secrete somatostatin 
e cells - secrete ghrelin 
PP cells - secrete pancreatic peptide
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7
Q

What is the principle signal for insulin release?

A

a rise in blood glucose

  • mainly food intake and digestion
  • endogenous glucose production
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8
Q

What are the two different pathways for insulin releasE?

A
  • glucose metabolism

- incretin pathway

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9
Q

What is an incretin?

A

a hormone that causes the release of insulin

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10
Q

How is insulin released via glucose metabolism?

A
  • glucose transported into the B cell via the GLUT 2 transporter
  • glucose metabolism causes the K Channel to close
  • this causes DEPOLARISATION
  • this causes an influx of Ca ions
  • this causes the release of insulin via exocytosis

calcium dependent exocytosis

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11
Q

What drugs act on the K Channels of the B cells to cause insulin release?

A

Sulfonylureas - Gliclazide
Meglitinides

act on the K Channels to shut them, they cause secretion of insulin regardless of what the actual BG is, and therefore may cause hypoglycaemia

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12
Q

How is insulin released via the incretin mechanism?

A
  • release of gut hormones due to the presence of food
  • hormone GLP 1 released (glucagon like peptide)
  • GLP 1 is an incretin
  • acts on receptors of B cells to release insulin

THIS PATHWAY WILL NOT TAKE PLACE UNLESS THE GLUCOSE METABOLISM PATHWAY IS HAPPENING

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13
Q

What drugs act on the GLP 1 receptor of the B cells to cause insulin release?

A

GLP 1 AGONISTS (incretin mimetic)

they have LESS of a risk of a hypo as they will only work if pathway 1 is working, i.e. with the presence of food in the gut

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14
Q

What are examples of GLP 1 agonist drugs?

A
  • Duraglutide (Trulicity)

- Liraglutide (Victoza)

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15
Q

What type of receptor is the insulin receptor?

A

tyrosine kinase receptor

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16
Q

Where are insulin receptors found?

A
  • liver
  • muscle
  • fat
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17
Q

What does binding of insulin to insulin receptors cause?

A
  • activation of GLUT 2/4 on the cell membrane
  • increases expression for GLUT 2/4, and translocates new transporters to the cell membrane to facilitate uptake of glucose
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18
Q

What drugs act on the insulin receptor?

A

insulin sensitisers

- pioglitazone

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19
Q

What are the general effects of insulin on the body?

A

anabolic

  • increases transport of glucose into cells
  • converts glucose to glycogen in the liver
  • decreases glycogen breakdown
  • increases fat stores
  • increases protein production
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20
Q

What is leptin?

A

a hormone that regulates appetite

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21
Q

What are the autonomic symptoms of a hypo?

A
  • hunger
  • sweating
  • shaking
  • increased heart rate
  • headache
  • nausea
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22
Q

What are the neuroglycopenic symptoms of a hypo?

A
  • confusion
  • drowsiness
  • odd behaviour
  • incoherent speech
  • poor coordination
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23
Q

What are the treatment options available for a hypo after oral glucose?

A
  • Glucagon IM/IV/SC injection (reconstituted)

- Diazodixde Therapy (oral), stops influx of Ca to the B cell

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24
Q

What are the symptoms of Type 1/Type 2 diabetes?

A
  • Toilet
  • Thirsty
  • Tired
  • Thinner

Type 1: more extreme, difficult to spot, result in DKA
Type 2: slower onset, increased episodes of thrush and slower wound healing

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25
Q

What is DKA?

A

Diabetic Ketoacidosis

where the body has switched entirely to lipid metabolism which produces ketones that are acidic, because there is no insulin available

usually affects Type 1

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26
Q

There are diet restrictions for both Type 1 and Type 2 diabetes, true or false?

A

FALSE

only for Type 2, can be reversed if patients lose 20% of their body weight

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27
Q

Type 1 patients are more likely to develop complications than Type 2, true or false?

A

TRUE

but Type 2 are still at risk of developing complications

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28
Q

What are the risk factors for developing Type 2 Diabetes?

A
  • ethnicity
  • age
  • obesity
  • genetics
  • smoking/alcohol
  • raised BP
  • polycystic ovary syndrome
  • poor sleep
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29
Q

What do DPP 4 Inhibitors do, and what are some examples?

A

they inhibit the enzyme that breaks down incretin

  • saxagliptin
  • sitagliptin
  • linagliptin
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30
Q

What do SGLT 1 Inhibitors do, and what are some examples?

A

reduces the amount of glucose reabsorbed by the kidney, so that more glucose is excreted from the body

  • canaglifozin
  • dapaglifozin
  • empaglifozin
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31
Q

METFORMIN

A

1st Line Treatment

  • decreases amount of glucose produced in the liver
  • decreases insulin resistance
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32
Q

What are the advantages of metformin?

A
  • cheap
  • weight neutral
  • low risk of a hypo (makes the muscle MORE sensitive to the insulin, not making more insulin than what is needed)
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33
Q

What are the disadvantages of metformin?

A
  • GI side effects (avoid by initiating treatment slowly with meals)
  • Don’t use in lactic acidosis (at risk of heart attack/respiratory disease/sepsis)
  • Short Half Life (TDS, weeks to titrate up)
  • eGFR <45 cautioned, <30 contraindicated
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34
Q

What are the advantages of Sulfonylureas (gliclazide)?

A
  • OD or BD
  • quickly lowers blood glucose
  • therefore good for symptomatic diabetes patients
  • fewer GI side effects than metformin
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35
Q

What are the disadvantages of Sulfonylureas (gliclazide)?

A
  • causes hypos (needs to be taken with food)
  • causes weight gain
  • need residual pancreas function
  • unpredictable in renal impairment/elderly
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36
Q

What are the advantages of Pioglitazone?

A
  • OD
  • low risk of hypo
  • suitable in renal impairment
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37
Q

What are the disadvantages of Pioglitazone?

A
  • associated with heart failure (fluid retention)
  • increased risk of bladder cancer/fractures/osteoporosis
  • weight gain (fluid, 1 stone)
  • liver toxicity
  • 3 - 6 months to show benefit, not good for symptomatic
38
Q

What are the advantages of DPP 4 Inhibitors?

A
  • OD
  • no weight gain gain
  • low risk of hypo
  • some used in renal impairment
39
Q

What are the disadvantages of DPP 4 Inhibitors?

A
  • GI side effects, rash, UTI
  • pancreatic inflammation
  • not overly effective
40
Q

What are the advantages of SGLT 2 inhibitors?

A
  • can be used in Type 1
  • reduced blood pressure
  • weight loss, 200 calories of glucose urinated out
  • low risk of hypo
41
Q

What are the disadvantages of SGLT 2 inhibitors?

A
  • thrush and UTIs (glucose in the urine)
  • reasonable renal function needed to be effective
  • lower BP = fall risk
  • risk of DKA in Type 1
  • risk of kidney injury and foot ulcers
42
Q

What is the NICE pathway for Type 2 oral therapies for someone that can tolerate metformin?

A
  1. Exercise and Diet
  2. Metformin (HbA1C 48)
  3. Metformin + Other Oral Drug (HbA1C 58)
    • Metformin + SU + Any Other Oral Drug (HbA1C 58)
    • Metformin + Pg + Any other Oral Drug EXCEPT DPP4
  5. GLP 1 Mimetic / Insulin
    • insulin makes you gain weight, GLP 1 makes you lose (BMI over 30 - 35)
43
Q

What are the advantages of GLP 1?

A
  • weight loss
  • once a day/weekly injection
  • rarely causes hypos
44
Q

What are the disadvantages of GLP 1?

A
  • injections
  • severe GI side effects
  • suitable in moderate renal impairment
  • pancreatitis
  • have to have a BMI greater than 35/30
45
Q

What is the NICE pathway for Type 2 oral therapies for someone that CAN’T tolerate metformin?

A
  1. DPP 4/ SU/ Pg OR an SGLT 1
  2. DPP 4 AND any other drug bar Pg (SGLT 1 and Pg)
  3. Insulin
46
Q

What are the two different insulin regimes available for a Type 1 diabetic?

A

Basal Bolus - 1st Line Therapy

  • 1 Long Acting ON (or 2, OM & ON)
  • 3 Short Acting with each meal

Biphasic

  • 2 biphasic insulin doses (OM & ON)
  • doses split depending on how big the meal is (breakfast/tea)
47
Q

What are the different types of insulin available?

A
  • Rapid Acting (acts immediately)
  • Short Acting (takes 3 hours to work - more planning)
  • Intermediate Acting
  • Long Acting
  • Superlong Acting
48
Q

What is an example of a rapid acting insulin?

A
  • Novorapid = Insulin Aspart
  • Apidra = Insulin Glulisine
  • Humalog = Insulin Lispro
49
Q

What is an example of a short acting insulin?

A
  • Actrapid (used for diabetes emergencies)
  • Humulin S
  • Inhuman Rapid
50
Q

What is an example of an intermediate acting insulin?

A
  • Insulatard
  • Humulin I Kwikpen
  • Inhuman Basal
51
Q

What is an example of long acting insulin?

A 
Insulin Glargine OD: 
- Lantus
- Abasglar
Insulin Determir BD:
- Levemir
52
Q

What is an example of a super long acting insulin?

A

Insulin Degludec:
- Tresiba
Insulin Glargine (300units/mL, super concentrated)
- Toujeo

53
Q

What are the most expensive insulins available?

A
  • Superlong Acting
  • Rapid Acting

this is also the BEST way to mimic normal pancreatic insulin release

54
Q

Rapid Acting Insulin Analogues

A
  • onset 5 - 15 mins
  • peak 30 - 90 mins
  • duration 4 - 6 hours
55
Q

Short Acting Insulin

A
  • onset 30 - 60 mins
  • peak 2 - 3 hours
  • duration 8 - 10 hours
56
Q

Intermediate Acting Insulin

A

Isophane (Neutral Protamine Hagedorn NPH)

  • stuck the insulin to a protamine to make them last longer
  • cloudy, shake before use
  • onset 2 - 4 hours
  • peak 4 - 10 hours
  • duration 12 - 18 hours
57
Q

Long Acting Insulin Analogue

A

Insulin Glargine (OD) or Detemir (BD)

  • onset 2 - 4 hours
  • duration 20 - 24 hours
  • no peak
58
Q

Ultra-Long Acting Insulin Analogue

A

3rd Line Regime when other treatments have failed
Insulin Glargine or Degludec
- OD
- duration up to 42 hours
- benefit for patients that are shift workers/non-adherent/forget to take insulin

59
Q

What is a biphasic insulin?

A

a short/rapid acting insulin in a protamine suspension

  • onset 30 mins
  • peak 1 - 2 hours
  • duration 12 hours
60
Q

What is an example of a biphasic insulin?

A
  • Humulin M3
  • Insuman Comb 15, 25, 50
  • Humalog Mix 25, 50
  • Novomix 30
61
Q

For which type of patients is the biphasic insulin regime most suitable?

A

Type 2
Type 1:
- where the number of injections is problematic or struggle to carb count
- doesn’t offer the best control as its difficult to adjust the dose
- not first line for type 1

62
Q

Which types of insulin can be even without food?

A
  • Long Acting

- Super Long Acting

63
Q

For which patients is a continuous SC insulin infusion pump suitable for?

A
  • attempts to achieve HbA1c result in disabling hypoglycaemia
  • HbA1c levels have remained high (>69) on the multiple daily injection therapy
  • patient is demonstrated commitment and competency
64
Q

Why is reducing the HbA1c levels important?

A

to reduce these diabetic complications:

  • proliferative retinopathy
  • nephropathy
  • cardiovascular disease
65
Q

What are the macrovascular complications of diabetes?

A

larger vessels

  • heart attacks
  • strokes
66
Q

What are the microvascular complications of diabetes?

A

small vessels

  • amputations / diabetic neuropathy
  • kidney failure / diabetic nephropathy
  • retinopathy / diabetic retinopathy
67
Q

What does DKA cause?

A 
a lack of insulin means that there is:
hyperglycaemia (> 11 mol/L) 
- increased glucogenesis and glycogenolysis
- reduced glucose uptake 
dehydration 
- increased urine output 
ketoacidosis (pH < 7 - 7.4)
- fatty acids being metabolised to ketones
68
Q

What are the symptoms of DKA?

A
  • tachypnoea
  • altered mental state (drowsiness/coma)
  • nausea, vomiting, abdominal pain
69
Q

What is the management of DKA in the first 4 hours?

A
  • applies to children and adults
  • fluid resuscitation (1st hour)
  • insulin variable rate infusion (1 - 2 hours)
70
Q

What fluids are used in the fluid resusitation in DKA?

A
  • isotonic fluids (0.9% sodium chloride)

- given slowly because rapid replacement would cause oedema, coma, death

71
Q

What does the insulin variable rate infusion management step of DKA involve?

A
  • sliding scale 0.05 - 0.1 unit of insulin/kg/hour
  • monitor the blood glucose hourly (cBG)
  • cBG < 15 mmol/L move to maintenance management
72
Q

What is the maintenance management of DKA in adults?

A

maintenance fluid (2L / day maximum)

  • glucose containing fluid (sodium chloride + 5% glucose AND potassium chloride (as insulin will cause hypokalaemia)
  • continue sliding scale insulin

titrate the doses according to ketone levels:
> 3 mmol/L - give more glucose or increase insulin
< 3 mmol/L - reduce insulin

73
Q

What happens in the management of DKA in adults once the patient is ready to eat?

A
  • eat
  • give SC insulin 30 mins before stopping infusion insulin
  • then stop the glucose infusion
74
Q

What is the maintenance management of DKA in children?

A

fluid restriction

  • 10kg = 2mL/kg/hr
  • 10 - 40kg = 1mL/kg/hr
  • > 40kg = 40mL an hour
replace fluid deficit over 48 hours
start s/c insulin when:
- cBG < 14 mmol/L
- ketones < 3 mmol/L 
- resolved acidosis
- oral fluids tolerated
75
Q

What is the most common cause of fatality with DKA?

A

cerebral oedema

  • caused by rapid movement of water into the cells in the brain
  • > 4mL/kg/hour - too much fluid
  • hypotonic fluid
76
Q

What are the signs and symptoms of cerebral oedema?

A
  • bradycardia
  • dilated pupils
  • altered mental state/unconsciousness
77
Q

What is HHS?

A

hyperosmolar hyperglycaemic state

where there is a lack of insulin effect and results in severe hyperglycaemia

78
Q

What does HHS cause?

A
  • severe hyperglycaemia > 50mmol/L
  • hyperosmolality
  • increased urination and dehydration
  • little to NO acidosis - as insulin is present, just cannot exert its effect so there is NO lipid metabolism
79
Q

Insulin is only required when eating, true or false?

A

FALSE
insulin is required for normal body functions
patients may think this, and may lead to DKA due to poor understanding

80
Q

What are the aims of treating HHS?

A
  • normalise osmolality
  • replace fluids
  • balance electrolytes
  • prevent clots due to thickened blood
  • prevent foot ulcers
  • prevent cerebral oedema
81
Q

What is the treatment for HHS?

A
  • lots of physiological fluid (not just sodium chloride) to correct blood pressure
  • target systolic > 90
  • start slow variable rate insulin infusion (no faster than 5mmol/L/min)
  • replace potassium as required
  • give clot preventing medication
82
Q

What is defined as hypoglycaemia in people with medication controlled diabetes?

A

< 4 mmol/L

83
Q

What is the treatment for hypoglycaemia?

A

short acting carbs followed by long acting carbs
at home:
- lucozade/sweets
- meal

in hospital:

  • dextrose tabs/glucogel then meal
  • glucagon IM then 10% glucose 100mL/hr if unconscious
84
Q

Diabetic Retinopathy

A
  • high blood sugar causes micro-thrombi in the retina
  • causes the capillaries to become blocked
proliferative = new vessels form and leak blood 
non-proliferative = no new vessels form
  • no drug treatment
  • irreversible
85
Q

Diabetic Neuropathy

A
  • high blood sugar causes reduced blood flow and death of nerves
  • peripheral neuropathy most common
  • diabetic foot ulcers common
  • treat symptoms
  • gastroparesis
  • erectile dysfunction
  • diabetic diarrhoea
  • loss of bladder control
  • arrhythmias
  • lack of/excessive sweating
86
Q

What are the symptom treatments available for diabetic neuropathy?

A
  • Antidepressants
  • Anti-convulsants
  • Topical Treatments
87
Q

Diabetic Foot Ulcers

A
  • lack of sensation increases risk of damage to feet
  • high blood sugars increase infection risk and reduce healing
  • require prolonged antibiotic courses
  • may result in amputations
88
Q

Diabetic Nephropathy

A
  • linked to poor glucose control/poor blood pressure control
  • nephrons = thickened, scarred and less effective
  • kidney function becomes progressively worse
89
Q

What are the treatment options available for diabetic nephropathy?

A
  • control of blood pressure with ACE/ARB
  • mindful of which oral diabetic medication, these are cautioned in renal impairment:
  • Metformin
  • Sulfonylureas
  • SGLT 2
90
Q

How do microvascular complications of diabetes occur?

A

high insulin levels associated with atherosclerosis

  • myocardial infarctions
  • ischaemic strokes
  • vascular disease
91
Q

Control of blood pressure in diabetes

A

target: 140/80mmHg
- start with ACE inhibitor/ARB if dry cough
- then add CCB/thiazide like diuretic

92
Q

Control of cholesterol in diabetes

A

atorvastatin 20mg
type 1:
- older than 40 years OR
- had diabetes for more than 10 years OR
- have established nephropathy or other CVD risk factors
type 2:
- who have 10% risk or more of developing CV in the QRISK

aim to reduce HFL by 40% in 3 months

Patient Sem 1 (8 decks)

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