Brainscape's Knowledge GenomeTM

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


See full index

Y2 BRS (Haroop) > Type I Diabetes > Flashcards

Type I Diabetes Flashcards

1
Q

What is Type 1 diabetes?

A

Type I diabetes mellitus is characterised by an autoimmune condition in which pancreatic beta-cells of the Islets of Langerhans are dysfunctional.

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

What is the long-term treatment for partial or complete insulin production in T1DM?

A

Chronic insulin treatment

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

What is LADA?

A

Autoimmune diabetes leading to insulin deficiency can present later in life = latent autoimmune diabetes in adults (LADA).

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

Which metabolic feature is characteristic of T1DM?

A

Diabetic ketoacidosis

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

What is the relationship between pancreatic B-cell function and age in those with a genetic predisposition to T1DM?

A

• The number of pancreatic beta-cells progressively decrease with age, resulting in a decline in insulin output and glucose control.

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

What is the cleavage product of pro-insulin?

A

C-peptide

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

What is C-peptide used for?

A

C-peptide is the cleavage product of pro-insulin  Used as a marker of insulin concentrations and beta-cell function.

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

What is the pathoimmunology underlying T1DM?

A

autoreactive CD4+ T-lymphocyte by antigen-presenting cells.
• CD4+ cells activate CD8+ T lymphocytes.
• CD8+ cells travel to islets and lyse beta cells expressing autoantigen (travel via lymph nodes)
• Release of pro-inflammatory species and reactive oxygen species (Granzyme and perforin are released from cytotoxic granules).

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

Defects in which type of tolerance is evident in T1DM pathoimmunology?

A

Peripheral tolerance (Impaired regulatory T-cells)

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

Which allele identified in GWAS is implicated in T1DM?

A

HLA-DR allele

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

What are the environmental factors implicated in T1DM?

A 
Environmental factors 
Multiple factors implicated  Causality not 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
12
Q

What are the common pancreatic auto-antibodies involved in T1DM?

A
  • Glutamic acid decarboxylase (GADA) – widespread neurotransmitter
  • Insulin antibodies (IAA)
  • 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
13
Q

What is the clinical presentation of type 1 diabetes?

A
  • Polyuria – excessive urination
  • Polydipsia – excessive thirst
  • Blurring of vision – Diabetic nephropathy
  • Recurrent infections e.g thrush
  • Weight loss
  • Fatigue- Catabolic muscle breakdown (proteolysis considering to produce both glucogenic and ketogenic amino acids).
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

What are the clinical signs of type 1 diabetes?

A
  • Dehydration
  • Cachexia – Catabolic catabolism increases to provide alternative substrate including amino acids gluconeogenesis and ketone body formation.
  • Hyperventilation – diabetic ketoacidosis (Respiratory compensation to remove carbon dioxide)
  • Smell of ketones
  • Glycosuria
  • Ketonuria
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Why does hyperventilation occur in T1DM?

A

Diabetic ketoacidosis (Respiratory compensation to remove carbon dioxide)

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

Why does cachexia occur in T1DM?

A

Catabolic catabolism increases to provide alternative substrate including amino acids gluconeogenesis and ketone body formation.

17
Q

What is the fate of non-esterified fatty acids in a hyperglycaemic state?

A

Non-esterified fatty acids undergo beta-oxidation resulting in the production of fatty Acyl-CoA.
• Carnitine shuttle facilitates the transport of fatty acids through the mitochondrial membrane.
• Insulin exerts an inhibitory effect on the shuttle –> Downregulates ketone body formation.
• Glucagon potentiates the rate at which fatty-acyl-CoA undergoes ketogenesis to synthesise ketone bodies.

18
Q

What are the treatment aims for a patient with T1DM?

A

Insulin dependent for life (Patients with T1DM) + dietary support.
Aim:
• Maintain glucose levels without excessive hypoglycaemia
• Restore a close to physiological insulin profile
• Prevent acute metabolic decompensation
• Prevent microvascular and macrovascular complications.

19
Q

What are the three chronic microvascular complications with T1DM?

A
  • Retinopathy
  • Neuropathy
  • Nephropathy
20
Q

What are the three macrovascular complications with T1DM?

A
  • Ischaemic heart disease
  • Cerebrovascular disease
  • Peripheral vascular disease
21
Q

What is first phase insulin release?

A

Prandial peak of significant exocrine release of preformed insulin into circulation

22
Q

How many phases are associated with prandial insulin release?

A

First phase insulin release and second phase (2)

23
Q

What is the second insulin release phase associated with?

A

Second phase is dependent on pancreatic B-cell function

24
Q

What are the two forms of quick acting insulin?

A

Human insulin

insulin analogue

25
Q

What are the two forms of long-acting basal insulin?

A

Bound to zinc or protamine

Insulin analogue

26
Q

What is the typical basal bolus regime?

A

Injected 15 minutes pre-prandially short acting

27
Q

What is 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.
28
Q

What is the available dietary advice for diabetes?

A

Dose adjustment for carbohydrate content of food.
• Patients receive training for carbohydrate counting.
• Substitute refined carbohydrate containing goods (high glycaemic index) with complex carbohydrates (starchy/low glycaemic index).

NICE Guidelines (NG17) for type I diabetes
• Structured Education Programme
• DAFNE
• 5-day course on skills and training in self-management.

29
Q

Why are starch and complex carbohydrates a better substitute than refined carbohydrates?

A

Complex carbohydrates have a low glycemic index

30
Q

What is the aim for simultaneous pancreas and kidney transplant?

A

Aim: Restore physiological insulin production to the extent that administered insulin can stop.
• Incomplete –> Results in better control.

31
Q

What are the limitations with a pancreas and kidney transplant?

A

Limitations: Availability of donors, complications of life-long immunosuppression

32
Q

What is glycated haemoglobin?

A
  • HbA1c represents 3 months of glycaemia (red blood lifespan).
  • Biased to the 30 days preceding measurement
33
Q

Which amino acid terminal is glucose associated with in HbA1C?

A

Glycated not glycosylated (enzymatic)  Glucose is associated with the N-terminal valine residue of the B-chain.
• Linear relationship
• Irreversible reaction

34
Q

What are the four limitations to using HbA1c as a marker?

A
  1. Erythropoiesis

Increased HbA1c: Iron, vitamin B12 deficiency, decreased erythropoiesis
Decreased HbA1c: Administration of erythropoietin, iron, vitamin B12, reticulocytosis, chronic liver disease.

  1. Altered Haemoglobin
    Genetic or chemical alterations in haemoglobin: Haemoglobinopathies, HbF, methaemoglobin, may increase or decrease HbA1c.
  2. Glycation
    Increased HbA1c: Alcoholism, chronic renal failure, decreased intra-electrolyte pH
    Decreased HbA1c: Aspirin, Vitamin C and E, certain haemoglobinopathies, increased intra-erythrocyte pH.

Variable HbA1c: Genetic determinants.

  1. Erythrocyte destruction

Increased HbA1c: Increased erythrocyte lifespan: Splenectomy

Decreased HbA1c: Decreased erythrocyte lifespan: Haemoglobinopathies, splenomegaly, rheumatoid arthritis or drugs such as antiretrovirals, ribavirin and dapsone.

35
Q

What is the diagnosis for diabetic ketoacidosis?

A

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

36
Q

What is the risk of type 1 diabetes?

A

Complications

1) Diabetic ketoacidosis
2) Uncontrolled hyperglycaemia
3) Hypoglycaemia

37
Q

What is the diagnostic parameter for hypoglycaemia?

A

<3.6mmol/L  Hypoglycaemia

38
Q

What are the risks of hypoglycaemia?

A 
Hypoglycaemia problems
•	Excessive frequency
•	Impaired awareness (unable to detect low blood glucose)
•	Nocturnal hypoglycaemia
•	Recurrent severe hypoglycaemia
  • Seizure/coma/death
  • Impacts on emotional well-being
  • Impacts on driving
  • Impacts on day-to-day function
  • Impacts on cognition
39
Q

What are the risk factors for hypoglycaemia?

A 
Risk factors
•	Exercise
•	Missed meals
•	Inappropriate insulin regime
•	Alcohol intake
•	Lower HbA1c
•	Lack of training around dose-adjustment for meals

Y2 BRS (Haroop) (62 decks)

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