ENDO; Lecture 15, 16, 17 and 18 - Type 1 DM, Type 2 DM, Microvascular complications and Macrovascular complications and the Diabetic Foot Flashcards Preview

Y2 LCRS 1 - Pharm, Endo, Reproduction > ENDO; Lecture 15, 16, 17 and 18 - Type 1 DM, Type 2 DM, Microvascular complications and Macrovascular complications and the Diabetic Foot > Flashcards

Flashcards in ENDO; Lecture 15, 16, 17 and 18 - Type 1 DM, Type 2 DM, Microvascular complications and Macrovascular complications and the Diabetic Foot Deck (166)
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1

What are the different types of diabetes?

Type 1 and T2, MODY, Latent autoimmune diabetes in adults (LADA)

2

What is the WHO classification of obesity?

 

3

What is the pathogenesis of T1DM?

4

How is T1DM a relapsing-remitting disease?

The immunological response to T1D is cyclic. An increase in the numbers of autoreactive effector T cells is controlled by an increase in the number of regulatory T cells. However, over time, a gradual disequilibrium of the cyclical behavior could occur, leading to the number of autoreactive effector T cells surpassing the number of regulatory T cells, which would no longer be capable of containing autoreactive effector T-cell responses and thereby lead to a decline in pancreatic islet function

5

What happens in T1DM?

Beta-cells are destroyed so increased number of immune cells and inflammatory factors present

6

Which HLA genes do you need to have genetic susceptibility to T1DM?

NB: DR3, DR4 are important

7

What are the environmental factors that affect T1DM?

Though to have infection type of onset as it is more common in winter months

8

Which blood markers should you test in T1DM patients?

 

9

What is the presentation of diabetes?

 

10

What happens if there is a lack of insulin?

If you lack insulin, then protein breakdown isn't stopped, glucose isn't taken up by the muscles, fats get broken down to make more glucose

11

What happens if there is no insulin acting on adipocytes?

Can also produce a lot of ketones in the body, which are the ones that produce ketoacidosis

12

How is T1DM treated?

Reduce early mortality, avoid acute metabolic decompensation -> need exogenous insulin to preserve life with ketones defining insulin deficiency; preventing long term complications like retinopathy, neuropathy, nephropathy, vascular disease

13

What diet should T1DM patients have?

Reduce calories as fat and refined carbs, increase calories as complex carbs and soluble fibre; balanced distribution of food over course of day with regular meals and snacks

14

How does insulin treatment work?

Short acting insulin given with meals, made from human insulin or insulin analogue (lispro, aspart, glulisine); Long acting for background levels given non-c bound to zinc or protamine OR insulin analogue (Glargine, Determir, Degludec)

15

How long does Short/long acting insulin last?

SAI 4-6, LAI 12h

16

How have insulin analogues been modified?

Genetically engineered to alter absorption, distribution, metabolism and excretion

17

What is an insulin pump?

Continuous insulin delivery, preprogrammed basal rates and bolus for meals; doesn't measure glucose, no completion of feedback loop -> no new needle every time

18

What are islet cell transplants?

Much better glucose control

19

How do we check glucose levels?

Capillary monitoring -> pricking the finger; MiniLink transmitter -> on the abdomen but not as reliable; measure HbA1c

20

What is HbA1c?

In red cells and reacts with glucose irreversibly; lifespan of RBC is 120d so it can be measured for around 4 months -> determine the rate of glycation, faster in some individuals -> however can be unreliable in Hbopathy and renal failure; forms ideal measure of long term glycaemic control and has been shown to be related to risk of complications, also lowering HbA1c associated lower risk of complication particularly microvascular complication

21

What is ketoacidosis?

Rapid decompensation of t1DM causing hyperglycaemia, metabolic acidosis

22

Why is hyperglycaemia caused in ketoacidosis?

Reduced tissue glucose utilisation, increased hepatic glucose production

23

Why is metabolic acidosis caused in ketoacidosis?

Circulating acetoacetate and hydroxybutyrate, osmotic dehydration and poor tissue perfusion

24

What are the causes of ketoacidosis?

Now presentation, insulin omission, infection/other illness

25

What is hypoglycaemia?

Plasma glucose of <3.6 mmol/L, severe hypo = any hypo needing help of another person to treat

26

How can hypo's affect the patient?

Most mental process impaired at <3mmol/L, consciousness impaired at <2mmol/L, severe hypo may contribute to arrhythmia and sudden death; may have long-term effects on the brain, recurrent hypos result in loss of warnings

27

Who do hypos affect?

Main risk factor is quality of glycaemic control, more frequent in patients with low HbA1c

28

When do hypos occur?

Anytime but often a clear pattern, pre-lunch hypos common, nocturnal hypos very common but not recognised

29

Why do hypos occur?

Unaccustomed exercise, missed meals, inadequate snacks, alcohol, inappropriate insulin regime

30

what are the symptoms and signs of hypoglycaemia?

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