Brainscape's Knowledge GenomeTM


Top Flashcards (Certified)
All Flashcards

Yr 2 LCRS - Endo > 15 - Type I Diabetes Mellitus > Flashcards

15 - Type I Diabetes Mellitus Flashcards

(47 cards)

Start Studying
1
Q

What are the two overall categories of classification for diabetes mellitus?

A

Type I

  • typically insulin deficient

Type II

  • typically insulin resistant

However, there is some ambiguity

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

Why can Type I diabetes not just be considered diabetes of the young?

A

Forms of T1DM can present in older people for the first time

Also, some patients with T2DM are now presenting in childhood (mainly due to obesity)

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

What is LADA?

A

Latent Autoimmune Diabetes in Adults (LADA)

  • autoimmune ‘type 1’ diabetes
  • leading to insulin deficiency
  • presents many decades into life
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Where does ambiguity lie in classification of T1DM and T2DM?

A
  • Forms of T1DM can present in older people for the first time
  • Also, some patients with T2DM are now presenting in childhood (mainly due to obesity)
  • Monogenic diabetes can present phenotypically as T1DM or T2DM e.g. MODY, mitochrondial diabetes etc.
  • Diabetic ketoacidosis is a feature of T2DM
  • Diabetes may present following pancreatic damage or other endocrine disease
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

What form of diabetes do the majority of diabetic patients have?

A

T2DM

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

In what form of diabetes does genetics play a more prominent role?

A

Type II Diabetes Mellitus

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

How is Type I Diabetes Mellitus precipitated?

A

Environmental Trigger and/or Genetics

  • Autoimmune destruction of islet cells (β cells)
  • β cells produce insulin
  • Therefore, person becomes insulin deficient
  • Hyperglycaemia
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

How is Type II Diabetes Mellitus precipitated?

A

Genetics and/or Obesity

  • Insulin resistance
  • Hyperglycaemia

After 20-30 years of T2DM, β cell failure typically occurs. Therefore, patients may then need insulin therapy

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

What is the pathogenesis of Type I Diabetes Mellitus?

A

No-one knows completely what causes it:

  • Postulated that there is a relapsing-remitting phase due to an imbalance in between good and bad T-cells
  • Bad T-cells cause more destruction over time

Honeymoon Phase:

  • Not all β cells have been completely destroyed
  • Still some β cell function after acute precipitant
  • Normally only lasts a couple of months

Facts:

  • Destruction of β cells occurs quickly if it occurs at a young age
  • Destruction occurs over time

Combination of events that causes β cell failure:

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

How are insulin levels measured?

A

Typically measure C-peptide levels

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

Why is the immune basis of T1DM important?

A

Increased prevalence of other autoimmune disease, particularly:

  • Coealic Disease
  • B12 Deficiency
  • Hypothyroidism (Hashimoto’s)
  • Addison’s (Occasionally)

Risk of autoimmunity in relatives

More complete destruction of β cells

Auto-antibodies can be useful clinically (i.e. they can be measured)

Immune modulation offers the possibility of novel treatments

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

What can increase your risk of developing autoimmune diseases?

A

Certain genetic markers

  • especially the HLA allele
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

What environmental factors influence T1DM precipitation?

A

Infection

  • certain weather can allow for greater susceptibility to infection
  • infection may precipitate the destruction of β cells
  • more diabetic ketoacidosis seen in winter

Area

  • area in Sardinia with high levels of T1DM
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

When are markers typically utilised clinically for diabetes?

A

Not often needed for most patients

When trying to distinguish where T1 or T2, markers measured may be:

  • Islet Cell Antibodies (ICA) - group O human antibodies
  • Insulin Antibodies (IAA)
  • Glutamic Acid Decarboxylase (GADA) - widespread neurotransmitter
  • Insulinoma-Associated-2-Autoantibodies (IA-2A-) - receptor like family

Having more antibodies doesn’t affect the amount of insulin therapy needed in patients

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

What are the signs and symptoms of T1DM?

A

Symptoms

  • polyuria
  • nocturia
  • polydipsia
  • blurring of vision due to hyperglycaemia
  • increased risk of thrush in females
  • weight loss as insulin normally stores fat in adipose tissue
  • fatigue

Signs

  • dehydrated
  • hypotensive
  • cachexia
  • hyperventilation due to metabolic acidosis as the body’s mechanism to remove CO2
  • smell of ketones on breath due to ketoacidosis
  • glycosuria
  • ketonuria
  • ketones in serum
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Between which three parts of the body are glucose levels balanced?

A

Liver

Muscle

Adipocytes

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

How are excess glucose levels (hyperglycaemia) normally prevented in the body via insulin and what is different in T1DM?

A

Liver

Insulin tries to prevent glucose from leaving the liver

T1DM:

  • insulin deficient
  • lots of glucose released into circulation

Muscle

Insulin causes glucose uptake by muscle

T1DM:

  • insulin deficient
  • excess glucose in circulation not taken up by muscle

Adipocytes

Insulin prevents break up of fatty-cells (adipocytes)

This prevents glycerol release from triglyceride breakdown which can be used to make glucose and increase glucose levels

T1DM:

  • insulin deficient
  • weight loss as adipocytes break up
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

What hormones oppose the actions of insulin?

A
  • Cortisol
  • Growth Hormones
  • Catecholamines
  • Glucagon

Release lots of glucose into the circulation

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

What occurs in the breakdown of adipose tissue as a result of T1DM?

Study These Flashcards
A

Triglycerides in adipose tissue

Break down into glycerol and fatty acids

Glycerol

  • Can be used to form glucose
  • Increase plasma glucose levels

Fatty Acids

  • Released into circulation
  • Taken up by liver
  • Produces ketone bodies
  • These cause metabolic acidosis
20
Q

What are the aims of treatment of T1DM?

Study These Flashcards
A

Reduces early mortality

Avoid acute metabolic decompensation

21
Q

What do T1DM patients need at a basic level?

Study These Flashcards
A

They need exogenous insulin to preserve life

22
Q

What defines insulin deficiency?

Study These Flashcards
A

Presence of ketones (as long as there is no other reason for ketones in the patient)

23
Q

What are 4 main long term complications associated with T1DM?

Study These Flashcards
A
  • Retinopathy - micro
  • Nephropathy -micro
  • Neuropathy - micro
  • Vascular Disease - macro
24
Q

What is the ideal diet to adopt in T1DM?

Study These Flashcards
A

Reduce calories from:

  • fat
  • refine carbohydrates

Increase:

  • calories from complex carbohydrates
  • soluble fibre

Balanced distribution of food over the course of the day with regular food and snacks

25
In a healthy person, how do insulin levels change throughout the course of the day?
Insulin levels rise everytime the person eats Also, basal insulin in constantly being produced. This accounts for 50% of a person's insulin requirement
26
How is insulin treatment administered in T1DM?
_With Food_ * Short-acting (4-6 hours) * Mimic normal release of insulin after eating in healthy people * Human Insulin or Insulin analogue AND _Background (Basal)_ * Long-acting (12-14 hours) * Mimics basal insulin production as in healthy people * Non-c bound to zinc or protamine * Insulin analogue No longer rely on animal insulin. These analogues are all genetically engineered to alter absoprtion, distribution, metabolism and excretion You can alter the types/amounts/timings of insulin administration depending on how many times the patient eats per day and how much they eat each time
27
What insulin analogues are used as short-acting?
Lispro Aspart Glulisine
28
What insulin analogues are used as long-acting?
Glargine (24 hour insulin profile) Determir Degludec
29
Which patients receive an insulin pump?
For T1DM patients who don't have a good insulin profile despite having insulin analogue administration Suffer from severe hypoglycaemic episodes Insulin Pump: * continuous insulin delivery * preprogrammed basal rates and bolus for meals * does not measure glucose, no completion of feedback loop
30
Which T1DM patients receive islet cell transplants?
Patients who still have severe hypoglycaemic episodes despite having an insulin pump
31
What occurs in islet cell transplants?
Islet cells harvested from a deceased donor Placed into patient via the portal system Transplanted cells produce insulin NOT A COMMON PROCEDURE AT ALL
32
How are patients with T1DM monitored short-term?
CAPILLARY MONITORING * Get patients to measure their own blood glucose on a regular basis * Sample from their finger * Encourage them to do it before meals CONTINUOUS MONITOR * Measures glucose at all times (24hours) * Sits on the abdomen * Small needle into the abdomen * See results in real time
33
What is the clinical benefit of having 24 hour glucose monitoring results from a T1DM patient?
Doctor can adjust insulin doses/type depending on rises and falls in blood glucose level across a day
34
How are patients with T1DM monitored long-term?
Using HbA1c * marker of glucose levels over a longer period of time * HbA1c red cells react with glucose as it does will all proteins * Glucose is attached to haemoglobin * Forms irreversible, non-covalent bond This bond depends on: * life-span of red blood cell (approx. 120 days) * rate of glycation (faster in some individuals) * Haemoglobinopathy, renal failure etc. (e.g. HbA1c would not be useful in someone who has sickle cell anaemia) MEASURE GLUCOSE OVER A 3 MONTH PERIOD
35
What does a low HbA1c refer to?
A red cell with not many glucose molecules attached to it
36
What is a benefit to patients with regard to measuring their HbA1c level?
Can show them that lowering HbA1c is associated with a lower risk of complications (particularly microvascular complications)
37
What occurs in ketoacidosis?
Rapid decompensation of T1DM Hyperglycaemia * tissues stop using glucose * reduce tissue glucose utilisation * increased hepatic glucose production Metabolic Acidosis * due to ketone bodies * circulating acetoacetate and hydroxybutyrate * osmotic dehydration * poor tissue perfusion * hypotension
38
What people suffer diabetic ketoacidosis most?
Typically T1DM patients However, Afro-Carribbean, Hispanic and Asian patients are more prone than caucasians to suffer diabetic ketoacidosis with T2DM
39
What defines hypoglycaemia?
Plasma glucose \<3.6mmol/l
40
What defines severe hypoglycaemia?
Any patient experiencing hypoglycaemia that requires help of another person to treat them
41
What can occur in a period of hypoglycaemia?
Normally just dizziness during non-severe hypoglycaemia \<3mmol/l = most mental processes impaired \<2mmol/l = consciousness impaired Severe hypoglycaemia can cause arrythmia and sudden death May have long-term effects on the brain MOST PATIENTS KNOW THEIR HYPO WARNING SIGNS HOWEVER, RECURRENT HYPOS CAN RESULT IN LOSS OF WARNING SIGNS
42
Who is most at risk to recurrent hypoglycaemia/hypoglycaemia unawareness?
Main risk factor is quality of glycaemic control Therefore, patients with low HbA1c are most at risk
43
When does hypoglycaemia occur?
Can occur at any time But often a clear pattern Pre-lunch is most common because a lot of people skip breakfast Nocturnal-hypoglycaemia is very worrying
44
What is the tell sign of nocturnal hypoglycaemia?
Catecholamine production increases during hypoglycaemia periods Therefore, when patients that are experiencing nocturnal hypoglycaemia wake up and measure their glucose level, it is very high first thing in the morning
45
Why does hypoglycaemia occur?
* Unaccustomed exericise with lack of compensation food * Missed meals * Inadequate snacks * Alcohol * Inappropriate insulin regime/dose
46
What are the signs and symptoms of hypoglycaemia?
Due to increased autonomic activation * palpitations (tachycardia) * tremor * sweating * pallor/cold extremities * anxiety Due to impaired CNS function * drowsiness * confusion * altered behaviour * focal neurology * coma
47
How is hypoglycaemia treated?
ORAL (feed the patient if possible!!!) * glucose (rapidly absorbed as solution or tablets) * complex carbs (to maintain blood glucose after initial treatment) PARENTERAL (give if consciouness is impaired) * IV dextrose (e.g. 10% glucose infusion) * 1mg Glucagon I.M. (relies on liver having glucose store) * Avoid concentrated solutions if possible

Yr 2 LCRS - Endo (28 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2025 Bold Learning Solutions. Terms and Conditions