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Diabetes Mellitus Flashcards

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1
Q

What is the relevant epidemiology of diabetes?

A

4.4 million in the UK
Estimated 1.2million undiagnosed type 2
People of Asian and Black Caribbean descent are 2-4x more likely to have diabetes compared to white populations
90% type 2
8% type 1
2% other forms

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2
Q

What is the epidemiology/genetics of type 1 DM?

A

Usually diagnosed in childhood
Peak around puberty
Worldwide incidence increasing
10-15% affected 1st degree relative
36% concordance in MZ twins
Lower genetic link than type 2 DM

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3
Q

What is the relevant epidemiology and genetics of Type 2 diabets?

A

Risk: Age, obesity, FH, ethnicity, sedentary lifestyle, low socio-economic status
Increasing prevalence in under 40s in the UK
40% lifetime risk with 1st degree relative
60-100% concordance in MZ twins
Stronger genetic link than T1

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4
Q

What is the ideal blood glucose range?

A

4.4 to 6.1 mmol/L

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5
Q

Where is insulin produced?

A

Beta cells
Islets of langerhans in the pancreas

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6
Q

What is the role of insulin?

A

Anabolic hormone - reduce blood glucose
Cells in the body absorb glucose from blood
Muscles and liver absorb glucose from the blood and store it as glycogen (glycogenesis)

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7
Q

Where is glucagon produced?

A

By alpha cells in the islets of Langerhans in the pancreas

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8
Q

What is the role of glucagon?

A

Catabolic -> increase blood glucose
Liver -> glycogenolysis
Liver -> gluconeogenesis -> protein and fats into glucose

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9
Q

What is the key pathophysiology of T1DM?

A

Autoimmune destruction of beta cells in the islets of Langerhans in the pancreas
No longer able to produce adequate insulin
T cell-mediated response

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10
Q

What is the key presentation of T1DM?

A

4Ts
Toilet - frequent urination
Thirsty -
Tired
Thinner - weight loss

May also present with diabetic ketoacidosis

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11
Q

At what blood glucose levels can type 1 DM be diagnosed?

A

Must also have clinical suspicion
Random >=11.1mmol/L
Fasting >=7.0mmol/L
OGTT >=11.1mmol/L

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12
Q

What autoantibodies may be tested for in DM type 1?

A

Anti-GAD
Anti-islet cell
Anti-insulin

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13
Q

How does serum C peptide relate to insulin?

A

Connects alpha and beta chains of pro-insulin
Reflects levels of insulin
Not routinely measured
Longer half life than insulin

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14
Q

What are the different aspects of managing T1DM?

A

Blood glucose monitoring
Subcutaneous insulin
Monitoring dietary carbohydrate intake and ‘carb counting’
Monitoring for complications, both short term and long term.
Patient/carer education
Support and individualised care
Physical activity
Hypoglycemia awareness and management
DKA awareness and ketone monitoring
Optimisation of cardiovascular risk
DVLA /occupational implications

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15
Q

What are the main methods that diabetics monitor their blood glucose?

A

BM machines - capillary blood glucose
Continuous glucose monitors - conc in interstitial fluid

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16
Q

Who manages the insulin prescription in a MDT for diabetics?

A

A diabetic specialist nurse

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17
Q

What are the different types of insulin available?

A

Rapid-acting - ActRapid
Short acting - NovoRapid
Intermediate acting - Humulin 1
Long-acting - Levemir and Lantus

Can be given as combination with rapid and intermediate insulin
Humalog 25
Humalog 50
Novomix 30

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18
Q

Why might diabetics need to contact the DVLA?

A

When on insulin therapy - risk of Hypos
Needs assessment and medical risk evaluation

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19
Q

What are the three characteristics of insulin?

A

Onset - lenght of time before reaches bloodstream and stars to lower blood glucose
Peak time - insulin at maximum activity
Duration - how long continues to lower blood glucose

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20
Q

Compare the peak and duration of different types of insulin

A
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21
Q

What is the once daily regime of insulin?

A

Long or intermediate acting insulin given at bedtime
Suitable in T2 - combined with oral hypoglycemic drugs
Used if dependent on others for injection

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22
Q

What is the twice daily insulin regime?

A

Biphasic insulin - before breakfast/evening meals
Assumes three meals a day
Peak action varies with solubility of insulin
Difficult to get glycemic control - risk of hypos

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23
Q

What is the basal bolus insulin regmie?

A

Long acting insulin at bed for overnight requirements
Combined with rapid/short acting for meals
Most common regime
May suffer hypos between meals and at nigh

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24
Q

Why must the insulin injection site be rotated?

A

Lipodystrophy - subcuntaneous fat hardens if repeated injected
Prevents insulin absorption

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25
Breifly describe how continuous sub-cut insulin infusions work?
Canula - subcut injection (must be rotated 2-3days) Pump of rapid acting insulin - continuous low dose (mimic long acting insulin), larger doses bolused for mealtimes and hyperglycemia Must have back up prescription of insulin pens just in case
26
What are the pros/cons of a continuous sub-cut insulin infusion?
+ better glycaemic control + inc flexibility + fewer injections - technical difficulties (must have back up prescription of insulin pens) - wearing a device - blockages in the line
27
What is a closed loop system for insulin control for diabetics?
Continous blood glucose monitoring measures glucose and sends signal to glucose pump (Bluetooth) Glucose control algorithm automatically determines insulin dose Insulin pump delivers dose This reduced hypos however may still need to carb count for meals/snacks and adjust for exercise
28
How can a pancreas transplant be used to treat T1DM?
Donor pancreas produce insulin Host pancreas remain insitu to produce digestive enzymes Risky and requires life long immunosuppression Reserved for patients with severe hypos and having kidney transplants
29
How is an islet transplant used to treat T1DM?
Inserting donor islet cells into liver to produce insulin Patients still often require insulin therapy after this
30
What is the relevant pathophysiology of T2DM?
Combination of peripheral insulin resistance and relative secretory failure Hyperglycemia has secondary affect on liver -> glycogenolysis -> further raises levels Progressive decline in B cell function - B cell apoptosis - often have 50% function remaining at diagnosis
31
What is metabolic syndrome?
A group of condition that often occur together and increase your risk of heart disease, T2DM and stroke
32
What conditions are included within metabolic syndrome?
Increase BP (130/85) High triglycerides Large waistline (central obesity) Low HDL cholesterol Elevated fasting blood sugar
33
What is the sub-acute presentation of T2DM?
Excessive tiredness Polyuria Excessive thirst Unintended weight loss Many are asymptomatic
34
What are the late established complications of T2DM?
Diabetic retinopathy Polyneuropathy Erectile dysfunction Arterial disease Susceptible to infections e.g thrush Slow healing skin wounds Acanthosis nigricans (signs of insulin resistance)
35
What is the reliance on blood glucose for diagnosis of T2DM?
Symptomatic and single abnormal blood glucose - can diagnose but should repeat the test Asymptomatic - do not diagnose based on a single result, repeat the test in one month
36
What can cause transient hyperglycemia?
Acute infection Trauma Circulatory stress
37
What are the different diagnostic ranges for HbA1c?
In mmol/mol >=48 is T2DM 42-47 pre-diabetes <42 is normal
38
What is the diagnostic range for fasting plasma glucose?
mmol/L >7.o is T2DM 6.1-6.9 is Pre-diabetes <= 6.o is normal
39
What is the diagnostic range of random plasma glucose?
mmol/L >=11.1 T2DM 7.8 to 11.0 is pre-diabetes <7.8 is normal
40
What is the HbA1c?
Glycated haemoglobin - made when glucose sticks to red blood cells Average blood glucose levels for the last 2-3 months
41
When should HbA1c not be used as a test?
Children <18yrs Pregnant or <2months post partum People with symptoms for <2months or acutely unwell Taking medications that cause hypers e.g steroids Acute pancreatic damage or end stage renal disease People with HIV infection or rbc turnover/Hb type
42
How often is HbA1c measured in adults with T2DM?
A. 3-6months until stable on unchanging therapy B. 6 months once stable
43
What is the target HbA1c for diabetics?
48mmol/mol if manafed by lifestyle/diet/single drug not associated with hypos 53mmol/mol is drug associated with hypos
44
What HbA1c level is concerning in Diabetics and what changes are made?
>58mmol/mol reinforce lifestyle advice Discuss drug compliance Intensify drug treatment
45
What management plan for T2DM include?
Structured education program Low glycaemic index, high fibre diet Exercise and weight loss (if overweight) Anti-hyperglycaemic drugs Monitoring and managing complications
46
What is the first line medical management for T2DM?
Metformin
47
How does metformin benefit diabetics?
A biguanide medication increases insulin sensitivity and decrease glucose production by the liver Note acts only in the presence of endogenous insulin so some functioning beta cells must remain
48
What is the relevant side effect profile of metformin?
Gastrointestinal upset (can reduce by trying modified release metformin) Lactic acidosis (secondary to AKI) DOES NOT cause weight gain or hypos
49
What is the second line treatment for T2DM?
Already on metformin Add a sulfonylurea, pioglitazone, DPP-4 inhibitor or SGLT-2 inhibitor
50
Example SGLT2 inhibitors
(gliflozin) Dapagliflozin, empagliflozin
51
What is the basic mechanism of action of SGLT2 inhibitors in diabetics?
Block SGLT-2 in proximal tubule of the kidney = more glucose excreted in urine Causes weight loss and reduce BP to lower cardiovascular risk Also used in HF and CKD Used alongside metformin as first line if high risk CVD
52
What are the side effects of SGLT2 inhibitors for treating T2DM?
Glycosuria Increased urine output Gential/UTI Fourniers gangrene Weight loss Euglycaemic ketoacidosis
53
What is an example of a thiazolidinediones? How do they treat T2DM?
(glitazone) Pioglitazone Increase insulin sensitivity and decrease liver production of glucose
54
What is the side effect profile of thiazolidenodiones?
Weight gain Heart failure Increased risk of bone fracture Small increased risk of bladder cancer
55
What is sulfonylureas example? How does it treat T2DM?
Gliclazide Stimulate insulin release from the pancreas
56
What is the side effect profile of sulfonylureas/gliclazide?
Weight gain Hypoglycaemia
57
How do DPP-4 inhibitors (gliptin) treat T2DM?
DPP-4 inhibits incretins (produced after large meal) Incretins - increase insulin, inhibit glucagon and slow absorption from GI -> this would decreased blood glucose DPP-4 inhibitors -> lead to unopposed incretins action Examples = sitagliptin, algoliptin
58
What is the side effect profile of DPP_4 inhibitors? (sitagliptin, alogliptin)
Headaches Acute pancreatitis
59
How do GLP-1 mimetics treat T2DM?
GLP-1 is a type of incretin Released after a large meal Decreases blood glucose by stimulating insulin secretion, inhibiting glucagon production and slowing absorption by the GI tract Mimetics also cause this effect Given as a subcut injection Examples = semaglutide, liraglutide
60
What is the side effect profile for GLP-1 mimetics?
Reduced appetite Weight loss Gastro-intestinal upset
61
What is the third line treatment for T2DM?
Triple therapy - metformin + two others If triple therapy fails and BMI >35kg/m2 add a GLP-1 mimetic Insulin therapy
62
What other medications (not directly for blood glucose) might a T2DM receive?
ACEi - for HTN control Statins - lipid-lowering drugs Treatment of specific complications - retinopathy, neuropathy
63
What influences the chance of complications from diabetes?
Duration and degree of hyperglycaemia Compliance with extensive screening programmes - eye screening, podiatry, annual diabetes reviews, routine bloods.
64
What are the macrovascular complications of diabetes?
Coronary artery disease Peripheral ischaemia Diabetic foot ulcers Stroke HTN
65
What are the microvascular complications of DM?
Peripheral neuropathy Diabetic retinopathy Kidney disease (glomerulosclerosis)
66
What are some other complications of DM?
Depression Infection risk Lipohypertrophy
67
In a healthy person how is glucose handled by the kidneys?
Produce 20-25% of total endogenous glucose All filtered glucose is re-absorbed into the blood by SGLT2/1
68
How is glucose reabsorbed in the kidenys?
SGLT2 - proximal tubules - 90% - high capacity low sensitivity SGLT1 - further along proximal tubule - 10% - low capacity - high sensitivity
69
What enzyme is important for endogenous glucose production? Where is it found?
Glucose-6-phosphatase enzyme Liver, cortex of kidney, intestinal epithelium
70
What is the relationship between the kidney and insulin?
25% daily insulin from pancrease is cleared by kidneys Increased insulin - suppress gluconeogenesis in the kidney and enhance glucose re-uptake
71
How does hyperglycaemia drive diabetic nephropathy?
1. activates protein Kinase C and growth factors leading to tubulointerstitial injury 2. Accelerates RAAS -> HTN -> Glomerular damage 3. AGEs form -> overproduction of mesnagial cell matrix -> glomerular damage All lead to nephron loss and proteinuria.
72
How does HTN cause diabetic nephropathy?
1. intraglomerular HTN 2. Glomerulosclerosis 3. Reduce funcationing glomeruli = decline in renal function 4. Increased blood flow to remaining neprhons Process repeats
73
How does obesity drive diabetic nephropathy?
A. Inc risk of HTN = CKD B. Increased insulin resistance/visceral adiposity -> (point c) and altered adipokines -> CKD C. glomerular hyperfiltration and hypoperfusion -> glomerular hypertrophy and proteinuria -> CKD D. CDK = glomerulosclerosis and end stage kidney disease
74
How is chronic kideny disease diagnosed in adults?
1. Estimate GFR using CKD-EPI creatine equation, urine dip for proteinuria and measure ACR is risk factor present 2. eGFR annually is taking medication that affect kidney 3. If below 60 repeat eGFR within two weeks - treat as AKI and test for haematuria 4. If still <60 repeat after 3months diagnose CKD is ACR >3mg/mmol or eGFR<60
75
What blood glucose is considered hypoglycaemia? What is meant by severe hypoglycaemia?
4.0 Severe - when requires help from another person
76
What are the signs of hypoglycaemia?
Asymptomatic Sweating Trembling Feeling of hunger Anxiety Poor concentration Palpitations Tingling of lips Pale Vague/confusion Convulsions Coma
77
How should hypolgycaemia be treated?
IV insulin should be stopped Mild - fast acting carbs (dextrose tables or glucojuice) Moderate - disorientated or aggressive -glucose gel Both - retest in 10mins - repeat above up to 3 times If BM above 4 give long acting carb Severe = NBM or less than 2.6mmols/L Check ABCDE, secure IV access - 100ml 20% glucose over 10-15mins, recheck after 10mins
78
How do most children with unknown T1DM tend to present?
In diabetic ketoacidosis
79
What is the process of ketogenesis?
Insufficient glucose and glycogen e.g prolonged fasting, low carb diets Liver converts fatty acids to ketones Ketons are soluble fatty acids than can be used as fuel and cross the BBB Not harmful in healthy individuals
80
How can ketone levels be measured?
Urine dipstick Blood ketone meter
81
What is the mechanism behind DKA?
1. Cells in body have no fuel as unable to process glucose due to insulin resistance (despite hyperglycaemia). 2. Ketogenesis initiated for fool 3. Bicarb is produced by kidenys to buffer ketone acids in blood. 4. Bicarb runs out - blood becomes acidic - ketoacidosis
82
What is the mechanism behdin dehydration in DM?
1. Hyperglycemia - not all glucose reabsorbed in kidney -. glucosuria 2. Osmotic diuresis 3 Polyuria, severe dehydration and polydispsia
83
How does DM lead to potassium imbalance?
1. Insulin drives potassium into cells - does not happen as insulin resistance 2. Some potassium excreted in urine 3. Total body potassium is low because not potassium is stored in cells 4. Insulin can trigger severe hypokalemia, leading to data arrhythmias.
84
How does DKA present?
Signs of dehydration, potassium imbalance and acidosis Polyuria and polydipsia Nausea and vomiting Weight loss Pear drop breath Dehydration and subsequent hypotension Symptoms underlying trigger e.g infection
85
What is the triad for DKA diagnosis?
Ketonaemia - blood >3.0mmol/L, ketonuria 2+ Acidosis pH<7.3 or bicard <15mmol/L Hyperglycaemia - BM >11.0mmol/L
86
How is DKA managed?
Fluid resuscitation Followed by IV insulin infusion - take up potassium, glucose and stop producing ketones Long acting insulin if taken should be continued Treat underlying trigger for infections
87
What is the link between DKA and cerebral oedema?
High risk in children Hyperglycaemia and dehydration cause water to move from intra to extracellular space -> brain cells shrink due to dehydration Rapid correction causes rapid shift back into intracellular space Brain becomes oedematous -> brain cell destruction/death
88
What are the signs of cerebral oedema in DKA?
GCS decline Headache Altered behaviour Bradycardia
89
How should cerebral oedema due to childhood DKA be managed?
Senior paediatrician Slowing rate of IV fluids and administering IV mannitol and IV hypertonic saline
90
What is hyperglycaemic hyperosmolar state (HHS)?
Rare but potentially fatal complication of T2DM. Characterised by hyperosmolarity, hyperglycaemia and absence of ketones
91
How does hyperglycaemic hyperosmlar state present?
Polyuria and dehydration Polydyspia Weight loss Tachycardia and hypotension Confusion
92
What is the treatment for hyperglycaemic hyperosmolar state?
IV fluids and careful monitoring
93
What is gestational diabetes?
Diabetes triggered by pregnancy - resolves after birth Caused by reduced insulin sensitivity Anyone with risk factors should be screened with an OGTT
94
What are the complications of gestational diabetes?
Large foetus Macrosomia (higher risk of should dystocia) Women remain at higher risk of T2DM in the long term
95
What is the treatment regarding pre-existing diabetes in pregnant women?
Pre-conception - optimise glycaemic control - folic acid 5mg until 12w gestation Oral medications should be stopped Retinopathy screening after booking and at 28w NICE planned delivery 37-38+6 weeks Sliding scale insulin and dextrose infusion is considered during labour
96
What is the post-natal care for diabetes during pregnancy?
If gestational - stop all medication immediately after birth Pre-existing - lower insulin doses and be wary of hypoglycaemia Babies need close monitoring for neonatal hypoglycaemia

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