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1 - Metabolism > Diabetes Mellitus > Flashcards

Diabetes Mellitus Flashcards

1
Q

Describe the condition of Diabetes Mellitus

A

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

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2
Q

Describe typical presentation of someone with type 1 diabetes

A

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

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3
Q

What causes B cell destruction in type 1 diabetes?

A

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

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4
Q

What progressively destroys B cells in type 1 diabetes?

A

killer lymphocytes and macrophages and antibodies.

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5
Q

Describe Polyuria, and what causes it?

A

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.

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6
Q

What is polydipsia, and what causes it?

A

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

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7
Q

What causes weight loss in type 1 diabetes?

A

Fat and protein are metabolised because insulin is absent.

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8
Q

Name three metabolic effects of a lack of insulin

A

Decreased uptake of glucose into adipose tissue and skeletal muscleDecreased storage of glucose as glycogen in muscle and liverIncrease gluconeogenesis

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9
Q

How can type 1 diabetes be diagnosed?

A

Via measurement of blood glucose levels, via urine or blood

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10
Q

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

A

Life threatening keto acidocis

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11
Q

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

A

Lack of energyPersistent infections (thrush, feet)Slow healing of minor skin damageVisual problems

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12
Q

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

A

Type 1 –> Type 21) Commonest in young 2) Affects a large number of older individuals1) 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 resistance1) Rapidly fatal if not treated 2) May be present for a long time before diagnosis1) Must be treated with insulin 2) May not initially need treatment with insulin, but all do eventually

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13
Q

Describe typical pattern of presentation of type 1 diabetes

A

People may have relevant HLA markers and autoantibodies, but no G or I abnormalitiesMay then developed impaired glucose tolerance, then diabetes, before becoming totally insulin dependant

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14
Q

Describe typical pattern of presentation of type 2 diabetes

A

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.

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15
Q

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

A

A random venous plasma glucose concentration > 11.1 mmol/lA fasting plasma glucose concentration > 7.0 mmol/l (whole blood > 6.1 mmol/lPlasma glucose concentration > 11.1 mmol/l 2 hours after 75g anhydrous glucose in a oral glucose tolerance test

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16
Q

What happens if no symptoms present, but glucose plasma concentration high? Why is it important to not misdiagnose?

A

At least one additional glucose test result on another day.A diagnosis of diabetes has important legal and medical implications for the patient

17
Q

Explain sequence of events leading to diabetic ketoacidocis

A

High rate of B-oxidation of fats + Low insulin/anti-insulin leads to production of ketone bodiesKetones acidic, so build up causes ketoacidocis

18
Q

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

A

Ketones in urineAcetone on patients breath

19
Q

Give 6 symptoms of ketoacidocis

A

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

20
Q

How can a diabetic become hypoglycaemic?

A

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

21
Q

What are the symptoms of hypoglycaemia?

A

Sweating, tremor, confusion, drowsiness, coma, death

22
Q

What is hyperglycaemia?

A

Blood glucose >10mmol/l

23
Q

What do the symptoms of hyerglycaemia include?

A

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

24
Q

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

A

Insulin injections

25
Q

Why can’t insulin be ingested?

A

Peptide hormone that would be digested

26
Q

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

A

Patients educated to treat themselves at appropriate times and with appropriate dosesDietary managementRegular exerciseFrequent blood glucose measurement

27
Q

When must treatment of type 1 diabetes change?

A

When patients has infection or suffered trauma, insulin must be increased or risk ketoacidocis.DUE TO EFFECTS OF ADRENALINE/CORTISOL WHICH SUPPRESS INSULIN

28
Q

Give two ways that type 2 diabetes can be managed

A

Diet or oral hypoglycaemic drugs

29
Q

Name two types of hypoglycaemic drugs and their effects

A

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

30
Q

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

A

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

31
Q

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?

A

Glucose + NADPH + H+ –> Sorbitol + NADP+Catalysed by aldose reductaseDepletes 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
Q

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

A

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
Q

How does the HbA1c test work?

A

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
Q

What are the three macrovascular complications of chronic hyperglycaemia?

A

Increased risk of strokeIncreased risk of myocardial infarctionPoor circulation to the periphery - particularly the feet

35
Q

List four microvascular complications of chronic hyperglcaemia

A

Diabetic eye diseaseDiabetic kidney diseaseDiabetic neuropathyDiabetic feet

36
Q

Briefly describe diabetic eye disease cause

A

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

37
Q

Briefly describe diabetic kidney disease

A

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

38
Q

Briefly describe diabetic neuropathy

A

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
Q

Briefly describe diabetic feet

A

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

1 - Metabolism (17 decks)

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