Brainscape's Knowledge GenomeTM

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


See full index

Year 2 Endo > Type 1 diabetes > Flashcards

Type 1 diabetes Flashcards

1
Q

What causes type 1 diabetes?

A

An autoimmune condition in which insulin-producing beta-cells in the pancreas are attacked and destroyed by the immune system

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

What does type 1 diabetes result in?

A

The result is a partial or complete deficiency of insulin production, which results in hyperglycaemia

The resultant hyperglycaemia requires life-long insulin treatment

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

What are the different types of diabetes?

A 
Type 1 Diabetes
Type 2 Diabetes
Hybrid forms
Other
Unclassified
During pregnancy
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

What is LADA?

A

Latent autoimmune diabetes in adults

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

Can T2DM present in childhood?

A

Yes

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

Can diabetic ketoacidosis feature of T2DM?

A

Yes

Although more typical in type 1

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

How can monogenic diabetes present?

A

phenotypically as Type 1 or Type 2 diabetes (eg. MODY, mitochondrial diabetes)

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

What event might diabetes present after?

A

following pancreatic damage or other endocrine disease

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

How does the evidence showing that type 1 diabetes presenting in adulthood challenge clinicians?

A

Clinicians are faced with a challenge, trying to differentiate adult-onset type 1 diabetes from the much large numbers of cases of type 2 diabetes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

What are the stages of development of type 1 diabetes?

A

Genetic predisposition

Potential precipitating event

Overt immunological abnormalities; normal insulin release

Progressive loss if insulin release; glucose normal

Overt diabetes; C-peptide present

No C-peptide present

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

What do we measure when looking at beta cell function?

A

C-peptide cleaved from pro-insulin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Why is T1DM not diagnosed early?

A

Initially maintain normal blood sugar, lots of immune cells crowding around islets

clinically only diagnosed when hyperglycaemia manifests as symptoms

then develops to long duration T1DM, fibrosis of pancreatic tissue

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Why is the immune basis of T1DM important?

A

Increased prevalence of other autoimmune disease

Risk of autoimmunity in relatives

More complete destruction of B-cells

Auto antibodies can be useful clinically

Immune modulation offers the possibility of novel treatments (not there yet)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Summarise immunology of T1DM?

A

Primary step is the presentation of auto-antigen to autoreactive CD4+ T lymphocytes

CD4+ cells activate CD8+ T lymphocytes (cytotoxic)

CD8+ cells travel to islets and lyse beta-cells
expressing auto-antigen

Exacerbated by release of pro-inflammatory cytokines

Underpinned also, by defects in regulatory T-cells that fail to supress autoimmunity

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Are all the beta cells destroyed in T1DM?

A

Not always, some beta cells escape the immune response

Some people with type 1 diabetes continue to produce small amounts of insulin and have C-peptide

Not enough to negate the need for insulin therapy

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

What is HLA?

A

Human Leukocyte antigen

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

What HLA is associated with diabetes?

A

HLA-DR

If you have these polymorphisms you are 6x more likely to develop T1DM

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

What are the environmental factors involved with T1DM?

A

Multiple factors implicated, but causality has not been established

Enteroviral infections
Cow’s milk protein exposure
Seasonal variation
Changes in microbiota

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

When are auto-antibodies detectable?

A

Detectable in the sera of people with Type 1 diabetes at diagnosis

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

Are auto-antibodies needed for diagnosis?

A

Not generally needed for diagnosis in most cases

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

When are pancreatic auto-antibodies made?

A

Made when the beta cells content is exposed

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

What are the different types of pancreatic auto-antibodies ?

A 
Insulin antibodies (IAA)
Glutamic acid decarboxylase (GADA) – widespread neurotransmitter
Insulinoma-associated-2 autoantibodies (IA-2A)-Zinc-transporter 8 (ZnT8)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

What are symptoms of T1DM?

A 
Excessive urination (polyuria) 
Nocturia
Excessive thirst (polydipsia) 
Blurring of vision
Recurrent infections eg thrush
Weight loss
Fatigue
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

Why does T1DM lead to blurry vision?

A

Glucose goes into eyeball

Causes osmotic change in lens

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

What are the signs of T1DM?

A 
dehydration 
cachexia
hyperventilation
smell of ketones
glycosuria 
ketonuria
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

What are the 4 Ts of T1DM?

A

Toilet
Thirsty
Tired
Thinner

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

How is T1DM diagnosed based on clinical features?

A

Ketones

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

What happens with insulin deficiency?

A

Proteinolysis
Hepatic glucose output
Uninhibired lipolysis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

What ketone bodies are produced in T1DM?

A

Acetyl CoA
Acetoacetate
Acetone + 3 OH-B

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

What are the aims of treatment in type 1 diabetes?

A

Maintain glucose levels without excessive hypoglycaemia

Restore a close to physiological insulin profile

Prevent acute metabolic decompensation

Prevent microvascular and macrovascular complications

31
Q

What is the only thing can prevent patients from taking insulin for life?

A

Transplant

32
Q

What are the acute complications of hyperglycaemia?

A

Diabetic ketoacidosis

33
Q

What are the microvascular chronic complications of hyperglycaemia?

A

Retinopathy
Neuropathy
Nephropathy

34
Q

What are the macrovascular chronic complications of hyperglycaemia?

A

Ischaemic heart disease
Cerebrovascular disease
Peripheral vascular disease

35
Q

How is T1DM managed?

A

Insulin Treatment
Dietary support / structured educations
Technology
Transplantation

36
Q

What is really key to note about T1DM as a condition?

A

Type 1 diabetes is a condition that is ‘self-managed’

37
Q

What are the main features of physiological profile of insulin?

A

Basal insulin has a flat profile

Prandial peak has two phases

Insulin is never completely suppressed

38
Q

What are the different types of insulin with meals?

A

(short / quick-acting insulin)

Human insulin – exact molecular replicate of human insulin (actrapid)
Insulin analogue (Lispro, Aspart, Glulisine)
39
Q

What are the different types of long-acting insulin?

A 
Bound to zinc or protamine (Neutral Protamine Hagedorn, NPH)
Insulin analogue (Glargine, Determir, Degludec)
40
Q

What is the typical regime for taking insulin?

A

Typical basal bolus regime

Background and meal times
3x a day but can be more with snacks

41
Q

What are the main features of insulin pump therapy?

A

Continuous delivery of short-acting insulin analogue e.g. novorapid via pump

Delivery of insulin into subcutaneous space

Programme the device to deliver fixed units / hour throughout the day (basal)

Actively bolus for meals

42
Q

What is CSII?

A

Alternative name for pump therapy

Continuous subcutaneous insulin infusion

43
Q

What are the principles of dietary advice for T1DM?

A

Dose adjustment for carbohydrate content of food.

All people with type 1 diabetes should receive training for carbohydrate counting

44
Q

What are the NICE guidelines for diet and T1DM?

A

All people with type 1 diabetes should be offered a Structured Education Programme

e.g. DAFNE but many others

5 day course on skills and training in self-management

45
Q

What substitutes should be made in diet?

A

Where possible, substitute refined carbohydrate containing foods (sugary / high glycaemic index) with complex carbohydrates (starchy / low glycaemic index

46
Q

What is the closed-loop/artificial pancreas?

A

Real-time continuous glucose sensor
Algorithm to use glucose value to calculate insulin requirement
Insulin pump delvers calculated insulin
Change in glucose

47
Q

What are Hybrid closed loop systems?

A

Not quite closed loop

The pump still needs to be told before a meal

Available on NHS

48
Q

What are the two types of transplant?

A

Islet cell transplants

Simultaneous pancreas and kidney transplants

49
Q

What are the main features of islet cell transplants?

A

Isolate human islets from pancreas of deceased donor
Transplant into hepatic portal vein
Requires life-long immunosuppression

50
Q

What are the main features of Simultaneous pancreas and kidney transplants?

A

Better survival of pancreas graft when transplanted with kidneys
Requires life-long immunosuppression

51
Q

Why are transplants not more frequently used?

A

Limited organ availability

Pancreas is not generally viable

Risks of long-term immunosuppressants

52
Q

What are the aims of transplantation?

A

try to restore physiological insulin production to the extent that insulin can be stopped

Even if incomplete, often results in better control

53
Q

How do you measure glucose levels?

A

Capillary (finger prick) blood glucose monitoring

Continuous glucose monitoring (restricted availability, NICE guidelines)

54
Q

What are the main features of HbA1c?

A

Reflect last 3 months (red blood cell lifespan) of glycaemia
Biased to the 30 days preceding measurement
Glycated NOT glycosylated (enzymatic)
Therefore linear relationship
Irreversible reaction

55
Q

What are the limitations of HbA1c?

A

Not perfect

Things affect it

56
Q

What is used to guide insulin doses?

A

Using self-monitoring of blood glucose results at home and HbA1c results every 3-4 months

Based on results, increase or decrease insulin doses

57
Q

What are the main features of diabetic ketoacidosis?

A

Can be a presenting feature of new-onset type 1 diabetes
Occurs in those with established type 1 diabetes
Acute illness
Missed insulin doses
Inadequate insulin doses
Life-threatening complication
Can occur in any type of diabetes

58
Q

How is diabetic ketoacidosis diagnosed?

A

pH <7.3, ketones increased (urine of capillary blood), HCO3- <15 mmol/L and glucose >11 mmol/L

59
Q

What are the main features of hypoglycaemia?

A

To some extent an inevitable feature of the self-management of type 1 diabetes
‘Lost normal physiology and homeostasis’
May become debilitating with increased frequency
Numerical definition (variable) <3.6 mmol/L
Severe hypoglycaemia: any event requiring 3rd party assistance

60
Q

What are the symptoms of a hypo?

A

Adrenergic

  • Tremors
  • Palpitations
  • Sweating
  • Hunger

Neuroglycopaenic

  • Somnolence
  • Confusion
  • Incoordination
  • Seizures, coma
61
Q

What defines low glucose?

A

< 3.5 mmol/L

62
Q

When does hypoglycaemic become a problem?

A

Excessive frequency

Impaired awareness (unable to detect low blood glucose)

Nocturnal hypoglycaemia

Recurrent severe hypoglycaemia

63
Q

What are the risks of hypoglycaemia?

A 
Seizure / coma/ death (dead in bed)
Impacts on emotional well-being
Impacts on driving
Impacts on day to day function
Impacts on cognition
64
Q

What are the risk factors for a hypo?

A 
Exercise
Missed meals
Inappropriate insulin regime
Alcohol intake
Lower HbA1c
Lack of training around dose-adjustment for meals
65
Q

What are the strategies to support problematic hypoglycaemia?

A

Indication for insulin-pump therapy (CSII)
May try different insulin analogues
Revisit carbohydrate counting / structured education
Behavioral psychology support
Transplantation

66
Q

How do you manage acutely manage a hypo when they are alert and orientated?

A

Oral carbohydrates
Rapid acting juice/sweets
Sandwich (longer acting)

67
Q

How do you manage acutely manage a hypo when they are Drowsy / confused but swallow intact?

A

Buccal glucose

e.g. Hypostop / glucogel

Complex carbohydrate

68
Q

How do you manage acutely manage a hypo when they are Unconscious or concerned about swallow?

A

IV access

20% glucose IV

69
Q

What does insulin do to potassium?

A

Drives potassium into cells

70
Q

What does insulin do to potassium?

A

Drives potassium into cells

71
Q

What is the process of DKA?

A 
Hyperglycaemia
Osmotic diuresis
Dehydration
Reduced renal perfusion
Impaired excretion of H+ 
Metabolic acidosis
Hyperventilation
72
Q

What is the treatment for DKA?

A

Give fluids

IV insulin

73
Q

Why do you get abdo pain in DKA?

A

Hyperventilation

Acidic ketones

Year 2 Endo (15 decks)

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