Session 8 (1) - Diabetes Mellitus Flashcards Preview

Semester 1 - Metabolism > Session 8 (1) - Diabetes Mellitus > Flashcards

Flashcards in Session 8 (1) - Diabetes Mellitus Deck (39):
1

Describe the condition of Diabetes Mellitus

Diabetes Mellitus is a group of metabolic disorders characterised my chronic hyperglycaemia due to insulin deficiency, insulin resistance or both. There are two major types of the disease, clearly distinguished by their epidemiology and probable causation, but not always so easily separated clinically

2

Describe typical presentation of someone with type 1 diabetes

A lean young person with a recent history of viral infection who present a triad of symptoms - Polyuria, Polydispsia and weight loss
Hyperglycaemia
Glycosuria
Keto acidocis

3

What causes B cell destruction in type 1 diabetes?

A genetic predisposition to the type 1 diabetes interacts with an environmental trigger to produce immune activation.

4

What progressively destroys B cells in type 1 diabetes?

killer lymphocytes and macrophages and antibodies.

5

Describe Polyuria, and what causes it?

Excess urine production.

Not all glucose reabsorbed into blood from kidney due to hyperglycemia. Extra glucose in nephron places extra osmotic load on it, so less water reabsorbed in order to maintain osmotic pressure. More wee.

6

What is polydipsia, and what causes it?

thirst and drinking a lot, due to polyuria. Caused by osmotic effects of glucose on thirst centres.

7

What causes weight loss in type 1 diabetes?

Fat and protein are metabolised because insulin is absent.

8

Name three metabolic effects of a lack of insulin

Decreased uptake of glucose into adipose tissue and skeletal muscle
Decreased storage of glucose as glycogen in muscle and liver
Increase gluconeogenesis

9

How can type 1 diabetes be diagnosed?

Via measurement of blood glucose levels, via urine or blood

10

What will happen to an individual with type 1 diabetes if it is not dealt with immediately?

Life threatening keto acidocis

11

In addition to triad of symptoms, what are type 2 diabetics most likely to complain of?

Lack of energy
Persistent infections (thrush, feet)
Slow healing of minor skin damage
Visual problems

12

List the four main differences between type 1 and type 2 diabetes

Type 1 --> Type 2
1) Commonest in young
2) Affects a large number of older individuals

1) Characterised by progressive loss of all or most of pancreatic B cells
2) Characterized by slow progressive loss of B cells, but with disorders of insulin secretion and tissue resistance

1) Rapidly fatal if not treated
2) May be present for a long time before diagnosis

1) Must be treated with insulin
2) May not initially need treatment with insulin, but all do eventually

13

Describe typical pattern of presentation of type 1 diabetes

People may have relevant HLA markers and autoantibodies, but no G or I abnormalities

May then developed impaired glucose tolerance, then diabetes, before becoming totally insulin dependant

14

Describe typical pattern of presentation of type 2 diabetes

Insulin resistance (obesity), then as insulin production fails develop impaired glucose tolerance.

Finally develop diabetes, but can be controlled by diet, then tablets, then insulin.

May eventually lose all insulin production.

15

Give three blood tests with which diabetes can be diagnosed if triad of symptoms present

A random venous plasma glucose concentration > 11.1 mmol/l

A fasting plasma glucose concentration > 7.0 mmol/l (whole blood > 6.1 mmol/l

Plasma glucose concentration > 11.1 mmol/l 2 hours after 75g anhydrous glucose in a oral glucose tolerance test

16

What happens if no symptoms present, but glucose plasma concentration high?

Why is it important to not misdiagnose?

At least one additional glucose test result on another day.

A diagnosis of diabetes has important legal and medical implications for the patient

17

Explain sequence of events leading to diabetic ketoacidocis

High rate of B-oxidation of fats + Low insulin/anti-insulin leads to production of ketone bodies

Ketones acidic, so build up causes ketoacidocis

18

How can high levels of ketones be diagnosed? (2)

Ketones in urine
Acetone on patients breath

19

Give 6 symptoms of ketoacidocis

Prostration, hyperventilation, nausea, vomiting, dehydration`` and abdominal pain

20

How can a diabetic become hypoglycaemic?

From insulin or suphnoylurea treatment, overdose or by missing a meal

21

What are the symptoms of hypoglycaemia?

Sweating, tremor, confusion, drowsiness, coma, death

22

What is hyperglycaemia?

Blood glucose >10mmol/l

23

What do the symptoms of hyerglycaemia include?

polyuria, polydipsia, weight loss, fatigue, poor wound healing.
Glycosylation of plasma proteins, affecting function.

24

How are type 1 diabetes and some cases of type 2 managed?

Insulin injections

25

Why can't insulin be ingested?

Peptide hormone that would be digested

26

Give four ways other than insulin that type 1 diabetes has to be managed

Patients educated to treat themselves at appropriate times and with appropriate doses

Dietary management

Regular exercise

Frequent blood glucose measurement

27

When must treatment of type 1 diabetes change?

When patients has infection or suffered trauma, insulin must be increased or risk ketoacidocis.

DUE TO EFFECTS OF ADRENALINE/CORTISOL WHICH SUPPRESS INSULIN

28

Give two ways that type 2 diabetes can be managed

Diet or oral hypoglycaemic drugs

29

Name two types of hypoglycaemic drugs and their effects

Sulphylonureas increase cell sensitivity to insulin and increase insulin release from remaining B cells.

Metforming reduces gluconeogenesis

30

Why is persistent hyperglycaemia a problem for peripheral nerves, the eye and the kidney?

Because uptake of glucose to these tissues is determined by extracellular glucose concentration. Glucose causes damage via variety of mechanisms.

31

What effect does high glucose have on glucose dependent tissues, and what is the reaction involved? What enzyme catalyses, and what reaction is it similar to?

Glucose + NADPH + H+ --> Sorbitol + NADP+
Catalysed by aldose reductase
Depletes NADPH, leading to increased disulphide bond formation in cellular proteins, altering structure.
Similar to conversion of galactose to galacticol in galactosaemia.
Accumulation of sorbitol also causes osmotic damage.

32

What is glycosylation, and how can it be used in diagnosis?

Glucose reacts with free amino groups in proteins to form stable covalent linkages. Plasma proteins, such as haemoglobin, are glycosylated. This is used in HbA1c test.

33

How does the HbA1c test work?

Glucose in blood reacts with terminal valine of the haemoglobin molecule to produce HbA1c.
% HbA1c good indicator of how effect effective glucose control. Give average blood glucose over past 2-3 months by measuring % haemoglobin glycosylated.

34

What are the three macrovascular complications of chronic hyperglycaemia?

Increased risk of stroke
Increased risk of myocardial infarction
Poor circulation to the periphery - particularly the feet

35

List four microvascular complications of chronic hyperglcaemia

Diabetic eye disease
Diabetic kidney disease
Diabetic neuropathy
Diabetic feet

36

Briefly describe diabetic eye disease cause

damage to blood vessels in the retina, which can lead to blindness

37

Briefly describe diabetic kidney disease

poor blood supply because of change in kidney blood vessels, or damage from infections of the urinary tract

38

Briefly describe diabetic neuropathy

Damage to the peripheral nerves which directly absorb glucose causing changes of or loss of sensation, and changes due to alteration in the function of the autonomic nervous system

39

Briefly describe diabetic feet

Poor blood supply, damage to nerves and increase risk of infection all sum up to make the feet of a diabetic vulnerable