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Year 3 Medicine Block > ENDOCRINE: DM and Hypo/hyperglycaemia > Flashcards

ENDOCRINE: DM and Hypo/hyperglycaemia Flashcards

1
Q

What does diabetes predispose you to?

A

GI complication - gastroparesis
Neurological - autonomic neuropathy = can lead to falls, postural hypotension
Vascular - PAD
Foot - diabetic foot ulcerations and infections
Sexual dysfunction - e.g. ED
Cardiac complications - atherosclerosis, leading to CVD

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2
Q

How does diabetes affect your chance of getting renal disease?

A

1 in 3 T2Dm develops overt kidney disease and diabetes is the most common causes of ESRD.

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3
Q

What is the risk of amputation in a patient with diabetes?

A

15% lifetime risk of amputation

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4
Q

How is the life expectancy affected by diabetes?

A

Reduced by 5-10 years

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5
Q

What is the normal plasma glucose concentration?

A

4-6 mmol/l

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6
Q

How do you define diabetes?

A

Abnormally elevated plasma glucose concentration

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7
Q

How do you diagnose diabetes?

A

Symptoms + one abnormal result OR 2 abnormal results of ideally the same (but can be different) tests at least week apart.

Fasting glucose greater than or equal to 7mmol/l and/or
OGTT of 75g glucose, 2 hours after greater than or equal to 11.1mmol/l
Hba1c greater than or equal 6.5%

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8
Q

If the patient is asymptomatic, how far apart do diagnostic tests for diabetes have to be?

A

1 week

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9
Q

What is the classic triad of symptoms for diabetes

A

polyuria, polydipsia and weight loss

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10
Q

What is the treatment basis for T1DM?

A
  • Insulin therapy - individualised regimens - as basal bolus regime
  • tight glycaemic control
  • lifestyle intereventions - need advice on nutrition, exercise and alcohol consumption
  • regilar self monitoring of blood sugars - around meals and bedtime
  • education on hypoglycaemia and how to treat it
  • regular follow up - with DM specialist nurse /GP for HbA1c follow up
  • psychosocial support
  • screening for complications
  • blood pressure control
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11
Q

What other diseases is T1DM associated with?

A

Thyroid disease and adrenal insufficiency, coeliac disease due to its autoimmune nature

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12
Q

What is LADA syndrome?

A

Latent autoimmune diabetes adult, patient who has positive antibodies to beta cell function, indicative of T1DM, but insidious presentation with mild hyperglycaemia

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12
Q

Why don’t healthy people have ketone production?

A

It is suppressed by insulin, absence of insulin leads to gluconeogenesis and fat breakdown—> free fatty acid

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13
Q

What is the mechanism of ketone production in T1DM?

A

No insulin, therefore production of ketones by beta oxidation of free fatty acids.

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14
Q

What is the relevance of a diabetic patient with ketones in their urine?

A

They may be in DKA - so require fluids, fixed rate insulin infusion and potassium.

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15
Q

How is T1DM managed?

A

Insulin- SC injection–> different types of insulin available

Patient education
Lifestyle–> accurate carbohydrate counting -DAFNE course
Home blood glucose monitoring
Regular HbA1c testing and complications- foot check, renal assessment and retinal screening assessment

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16
Q

How is T2DM managed?

A 
Lifestyle 
Anti-obesity drugs 
Oral hypoglycaemic drugs 
GLP 1 agonists 
Insulins 
SGLT2s
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17
Q

What is first line therapy for T2DM?

A

Metformin
500mg once daily for at least 1 week, then twice daily for at least one week, then 500mg 3 times daily.
Maximum dose 2g per day.

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18
Q

What are contraindications of metformin?

A

eGFR< 30mL/min
Acute metabolic acidosis (including lactic and dka)

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19
Q

How does metformin work?

A

Decrease hepatic glucose production by inhibiting gluconeogenesis

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20
Q

What are the ADRs of metformin?

A

Abdominal pain
nausea
vomitting
diarrhoea
taste altered
Vit B12 deficiency
reduced appetitie

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21
Q

What are the drug-drug interactions with metformin?

A
  • ACEi, diuretics, NSAIDs- drugs that may impair renal function
  • loop and thiazide like diuretics- increase glucose so can reduce metformin action
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22
Q

A patient complains of diarrhoea with metformin, what would you suggest?

A

modified release preparations or temporarily decrease the dose.

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23
Q

How do sulphonylureas work?

A

Stimulate the beta cells to release insulin by blocking ATP dependent K+ channels

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24
What are the side effects of sulphonylureas?
Weight gai, mild GI upset, hypoglycaemia
25
What is GLP-1?
incretin hormone
26
What are the effects of GLP-1
Pancreas- Increase insulin secretion, decrease glucagon secretion, increase insulin biosynthesis Liver- decrease glucose production Stomach- decreases gastric emptying Muscle- increase glucose uptake Brain- increase satiety
27
When is GLP-1 release?
From the intestinal L cells, during meals
28
When do you use GLP-1 agonists?
NICE suggest add-on if triple therapy is ineffective, but evidence for their use is vey strong
29
What are the benefits of GLP-1 agonists?
Weight loss
30
When is using GLP-1 agonists contraindicated?
Renal impairment
31
When do you use sulphonyureas in diabetes management?
Used less now, but often used if patient with T2DM has low weight, to increase their weight.
32
What are DPP-4 inhibitors?
They inhibit DPP-4 activity which increases GLP-1 concentrations
33
What are the side effects of DPP-4 inhibitors?
GI symptoms, but quite well tolerated Acute pancreatitis Hypoglycaemia when prescribed with other hypoglycaemic drugs - SU, insulin
34
When are SGLT-2 inhibitors used?
In diabetes but also people who have comorbities such as congestive cardiac failure and CKD
35
What are the acute complications of type 1 DM?
DKA
36
How is DKA defined?
Hyperglycaemia, ketonaemia and acidosis
37
How is DKA diagnosed ?
``` Needs to have Ketonaemia greater than or equal to 3 mmol/L Blood glucose > 11mmol/L Bicarb < 15mmol/L and/or pH<7.3 ```
38
What are the key issues in DKA?
``` Hyperglycaemia Acidosis Dehydration due to osmotic diuresis and vomitting Electrolyte loss Cerebral oedema Hyperkalaemia ```
39
How do you manage DKA?
Rapid fluid administration 0.9% NaCl and insulin Restoration of circulatory volume Clearance of ketones Correct any electrolyte imbalance using crystalloids
40
What insulin therapy do you use for DKA?
Fixed rate IV infusion 0.1 units per kilo body weight per hour
41
What are your metabolic treatment targets for DKA?
Reduce ketones by 0.5mmol/l/hour Increase venous bicarb by 3.0mmol/l/hour Maintain potassium between 4-5.5mmol/l If blood glucose falls below 14mmol/l introduce dextrose with N saline until patient is eating
42
What do you measure hourly in patients admitted with DKA?
Blood glucose | Hourly ketones
43
What initial investigations should you do for a patient with DKA?
``` Blood ketones Cap blood glucose Venous plasma glucose Urea and electrolytes VBG FBC Blood cultures ECG continuous cardiac monitoring Urianalysis and culture ```
44
How many mmol/L in the blood do you start potassium therapy in patients with DKA?
Between 3.5-5.5mmol/L you add 40mmol/L of potassium into the infusion, any less than 3.5mmol/L need senior review
45
What must be done/considered in the first 6 hours of DKA treatment?
``` At least hourly review Clear blood of ketones and surprise ketogenesis, reduce at rate of 0.5mmol/l/hour Avoid hypoglycaemia Consider catheterisation Consider NG tubing Continuous cardiac monitoring Treat co-morbities ```
46
When can you stop the fixed rate insulin infusion (FRII) and convert back to subcut insulin in a patient with DKA?
Ketones <0.6mmol/L and ready to eat | No evidence of acidosis
47
What is hyperosmolar hyperglycaemic syndrome?
Marked water loss due to hyperglycaemia, without ketonaemia or acidosis. High osmolality--> v dehydrated Usually you get a mixed picture of both HHS and DKA
48
How do you diagnose HHS?
Hypovolaemia Marked hyperglycaemia (30mmol/L or more) with significant hyperkenonaemia (<3mmol/L) or without acidosis Osmolality usually 320 mosmol/kg or more
49
Who is most affected by HHS?
Elderly and frail people
50
What can trigger HHS?
Usually precipitated by something e.g. infection
51
How can you calculate plasma osmolality?
2Na + glucose +urea
52
What are the treatment goals for HHS?
Normalise osmolality Replace fluid and electrolyte losses Normalise blood glucose We also want to prevent Arterial or venous thrombosis Other potential complications e.g. Cerebral oedema, central pontine mylinolysis Foot ulceration
53
How do you treat HHS?
``` Crystalloids Aim to replace 50% of loss within first 12 hours FRIII 0.05units/Kg/hour Monitor potassium and renal function Glucose fall 4-6mmol/hour Co-morbities Anticoagulation ```
54
Name 5 RF for hypoglycaemia?
* Increased exercise (relative to usual), * renal failure, * strict glycemic control, * previous hx of severe hypoglycaemia, * long duration of type 1 diabetes, * food malabsorption, * inadequate glucose monitoring
55
What are the causes of inpatient hypoglycaemia?
acute discontinuation of long term steroid therapy, recovery from acute illness, mobilisation after illness, missed or delayed meals, less carbs than normal, reduced appetite
56
How do you treat hypoglycaemia in an adult who is conscious, orientated and able to swallow?
15-20g quick acting carbohydrate of patients choice e.g. 90-120ml go original lucozade, 3-4 heaped teaspoons of sugar dissolved in water, 150-200ml pure fruit juice
57
How do you treat hypoglycaemia in a patient who is confused but able to swallow?
1.5-2 tubes glycogen/dextrogel squeezed between teeth and gum OR give glucagon IM (less effective in pts prescribed sulfonylurea therapy or under influence of alcohol)
58
What are the chronic complications of diabetes?
neuropathy nephropathy retinopathy CVS
59
What 3 groups can the symptoms of hypoglycaemia be divided into?
Autonomic Neuroglycopenic General malaise
60
What are some autonomic symptoms of hypoglycaemia?
Sweating palpitations shaking hunger
61
What are some neuroglycopenic symptoms of hypoglycaemia?
Confusion Drowsiness Odd behaviour Speech difficulty
62
What are some general malaise symptoms related to hypoglycaemia?
Headache and nausea
63
What is charcots foot?
Osteoarthropathy associated with neuropathy
64
A patient with T2DM has a dusky and painful foot, what are you thinking?
Peripheral vascular disease associated with diabetes- not neuropathic but ischaemic, referral to the vascular surgeons
65
What is a known medication that can worsen blood sugar levels?
Bendroflumethiazide
66
What is the pathological mechanism that leads to peripheral neuropathy in diabetes?
Hyperglycaemia leads to advanced glycation end products- these act on specific cells such as endothelial cells and monocytes, this leads to increased production of cytokines and adhesion molecules. This has been shown to have an effect on matrix metalloproteinases, which damaged nerve fibres
67
What are the risk factors of osteomyelitis?
``` DM Peripheral vascular disease Malnutrition Immunosuppression Malignancy ```
68
Target HbA1c for patients on a drug the causes hypoglycaemia?
The Hba1c target for patients on a drug which may cause hypoglycaemia (eg sulfonylurea) is 53 mmol/mol
69
Causes of hypoglycaemia?
Insulinoma Self-Administered insulin/sulfonyureas Addisons disease alcohol

Year 3 Medicine Block (56 decks)

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