Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

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

A

15% lifetime risk of amputation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

How is the life expectancy affected by diabetes?

A

Reduced by 5-10 years

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

What is the normal plasma glucose concentration?

A

4-6 mmol/l

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

How do you define diabetes?

A

Abnormally elevated plasma glucose concentration

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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%

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

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

A

1 week

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

What is the classic triad of symptoms for diabetes

A

polyuria, polydipsia and weight loss

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

What other diseases is T1DM associated with?

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

How is T2DM managed?

A 
Lifestyle 
Anti-obesity drugs 
Oral hypoglycaemic drugs 
GLP 1 agonists 
Insulins 
SGLT2s
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

What are contraindications of metformin?

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

How does metformin work?

A

Decrease hepatic glucose production by inhibiting gluconeogenesis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

What are the ADRs of metformin?

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

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

A

modified release preparations or temporarily decrease the dose.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

How do sulphonylureas work?

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

What are the side effects of sulphonylureas?

A

Weight gai, mild GI upset, hypoglycaemia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

What is GLP-1?

A

incretin hormone

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

What are the effects of GLP-1

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

When is GLP-1 release?

A

From the intestinal L cells, during meals

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

When do you use GLP-1 agonists?

A

NICE suggest add-on if triple therapy is ineffective, but evidence for their use is vey strong

29
Q

What are the benefits of GLP-1 agonists?

A

Weight loss

30
Q

When is using GLP-1 agonists contraindicated?

A

Renal impairment

31
Q

When do you use sulphonyureas in diabetes management?

A

Used less now, but often used if patient with T2DM has low weight, to increase their weight.

32
Q

What are DPP-4 inhibitors?

A

They inhibit DPP-4 activity which increases GLP-1 concentrations

33
Q

What are the side effects of DPP-4 inhibitors?

A

GI symptoms, but quite well tolerated
Acute pancreatitis
Hypoglycaemia when prescribed with other hypoglycaemic drugs - SU, insulin

34
Q

When are SGLT-2 inhibitors used?

A

In diabetes but also people who have comorbities such as congestive cardiac failure and CKD

35
Q

What are the acute complications of type 1 DM?

A

DKA

36
Q

How is DKA defined?

A

Hyperglycaemia, ketonaemia and acidosis

37
Q

How is DKA diagnosed ?

A 
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
Q

What are the key issues in DKA?

A 
Hyperglycaemia 
Acidosis 
Dehydration due to osmotic diuresis and vomitting 
Electrolyte loss 
Cerebral oedema 
Hyperkalaemia
39
Q

How do you manage DKA?

A

Rapid fluid administration 0.9% NaCl and insulin
Restoration of circulatory volume
Clearance of ketones
Correct any electrolyte imbalance using crystalloids

40
Q

What insulin therapy do you use for DKA?

A

Fixed rate IV infusion 0.1 units per kilo body weight per hour

41
Q

What are your metabolic treatment targets for DKA?

A

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
Q

What do you measure hourly in patients admitted with DKA?

A

Blood glucose

Hourly ketones

43
Q

What initial investigations should you do for a patient with DKA?

A 
Blood ketones 
Cap blood glucose 
Venous plasma glucose 
Urea and electrolytes 
VBG 
FBC 
Blood cultures 
ECG 
continuous cardiac monitoring 
Urianalysis and culture
44
Q

How many mmol/L in the blood do you start potassium therapy in patients with DKA?

A

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
Q

What must be done/considered in the first 6 hours of DKA treatment?

A 
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
Q

When can you stop the fixed rate insulin infusion (FRII) and convert back to subcut insulin in a patient with DKA?

A

Ketones <0.6mmol/L and ready to eat

No evidence of acidosis

47
Q

What is hyperosmolar hyperglycaemic syndrome?

A

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
Q

How do you diagnose HHS?

A

Hypovolaemia
Marked hyperglycaemia (30mmol/L or more) with significant hyperkenonaemia (<3mmol/L) or without acidosis
Osmolality usually 320 mosmol/kg or more

49
Q

Who is most affected by HHS?

A

Elderly and frail people

50
Q

What can trigger HHS?

A

Usually precipitated by something e.g. infection

51
Q

How can you calculate plasma osmolality?

A

2Na + glucose +urea

52
Q

What are the treatment goals for HHS?

A

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
Q

How do you treat HHS?

A 
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
Q

Name 5 RF for hypoglycaemia?

A
  • 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
Q

What are the causes of inpatient hypoglycaemia?

A

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
Q

How do you treat hypoglycaemia in an adult who is conscious, orientated and able to swallow?

A

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
Q

How do you treat hypoglycaemia in a patient who is confused but able to swallow?

A

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
Q

What are the chronic complications of diabetes?

A

neuropathy
nephropathy
retinopathy
CVS

59
Q

What 3 groups can the symptoms of hypoglycaemia be divided into?

A

Autonomic
Neuroglycopenic
General malaise

60
Q

What are some autonomic symptoms of hypoglycaemia?

A

Sweating
palpitations
shaking
hunger

61
Q

What are some neuroglycopenic symptoms of hypoglycaemia?

A

Confusion
Drowsiness
Odd behaviour
Speech difficulty

62
Q

What are some general malaise symptoms related to hypoglycaemia?

A

Headache and nausea

63
Q

What is charcots foot?

A

Osteoarthropathy associated with neuropathy

64
Q

A patient with T2DM has a dusky and painful foot, what are you thinking?

A

Peripheral vascular disease associated with diabetes- not neuropathic but ischaemic, referral to the vascular surgeons

65
Q

What is a known medication that can worsen blood sugar levels?

A

Bendroflumethiazide

66
Q

What is the pathological mechanism that leads to peripheral neuropathy in diabetes?

A

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
Q

What are the risk factors of osteomyelitis?

A 
DM
Peripheral vascular disease 
Malnutrition 
Immunosuppression 
Malignancy
68
Q

Target HbA1c for patients on a drug the causes hypoglycaemia?

A

The Hba1c target for patients on a drug which may cause hypoglycaemia (eg sulfonylurea) is 53 mmol/mol

69
Q

Causes of hypoglycaemia?

A

Insulinoma
Self-Administered insulin/sulfonyureas
Addisons disease
alcohol

Year 3 Medicine Block (56 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions