Diabetes Flashcards

(71 cards)

1
Q

Define Diabetes Mellitus

A

An absolute or relative deficiency of insulin causing hyperglycaemia

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2
Q

What is the problem of hyperglycaemia?

A

Proteins become glycosylated and lose their function

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3
Q

To diagnose DM, what does the fasting blood glucose have to be above?

A

7

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4
Q

To diagnose DM, what does the random blood glucose level have to be below?

A

11.1

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5
Q

To diagnose DM, what does the HbA1c have to be above?

A

6.5%

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6
Q

Describe DM1

A

Absolute insulin deficience
Childhood diagnosis
Autoimmune islet damage

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7
Q

Describe DM2

A

Genetic and environmental factors

Insulin deficiency and resistance

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8
Q

When is DM1 diagnosed?

A

Childhood

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9
Q

What are the 3 main symptoms of diabetes?

A

Thirst, polyuria, nocturia

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10
Q

What is Gestational diabetes?

A

Occurring for the first time in pregnancy

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11
Q

What are some causes of secondary DM?

A

Pancreatic disease, congenital abnormalities, drugs, endocrine disorders.

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12
Q

What is Insulin stimulated by?

A
High blood glucose
AAs
FAs
GI hormones
Sulphonylureas
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13
Q

What does insulin do? (4)

A

Stops liver releasing glucose
Decreases gluconeogenesis and glycogenolysis in liver
increases glycogenesis
increases muscle and adipose uptake of glucose

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14
Q

What are the two important Glucose transporters in DM?

A

GLUT2 (beta cells) and GLUT4 (insulin sensitive on muscle and adipose)

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15
Q

How does insulin cause extra glucose uptake to muscle and fat?

A

Stimulates GLUT4 to move to the membrane to provide more receptors to which Glucose can bind.

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16
Q

What does insulin promote the synthesis of?

A

lipoproteins, TGs, proteins

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17
Q

Is GH mainly anabolic or catabolic?

A

anabolic

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18
Q

What is Glucagon stimulated by?

A

Low blood glucose, High AAs, and exercise

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19
Q

What inhibits Glucagon?

A

Insulin, KBs

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20
Q

When might Glucose and Insulin work together?

A

To prevent hypoglycaemia when high protein foods are eaten.

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21
Q

Where is GH secreted from?

A

Anterior pituitary

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22
Q

What does GH do?

A

Protein synthesis
Lipolysis
glycogenesis

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23
Q

What is IGF and what does it do?

A

Insulin like growth factor. Growth, cell division, protein synthesis.

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24
Q

What are IGFs stimulated by?

A

Insulin and GH

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25
When is cortisol released?
stress, low glucose
26
What does cortisol do?
Proteolysis gluconeogenesis inhibits glucose use.
27
What are catecholamines stimulated by?
Stress | low glucose
28
What do catecholamines do?
Glycogenolysis Lipolysis Gluconeogenesis
29
How does insulin resistance happen?
Constant xs of glucose in the blood causes constant stimulation of the insulin receptors, causing them to downregulate
30
Why is there decreased insulin secretion in DM2 as well as resistance?
When there first started being hyperglycaemia, the beta cells would overwork to produce enough insulin to combat the raised glucose. Eventually, this wears them out and they stop secreting insulin.
31
What happens during starvation?
Muscles break down and so does fat to allow gluconeogenesis. TGs are hydrolysed into FAs which are used to make KBs. (Glycogenolysis happens in fasted state)
32
What are the risks of DM?
Ketoacidosis (DM1) Dehydration Hypertriglyceridemia Hypoglycaemia
33
What are some of the genetic causes of DM1?
IDD1, IDD2, IDD3 mutations = poor T cell activation regulation
34
How would you dx DM1?
Clinical symptoms and a biochemical test for autoantibodies
35
Explain the Immunology of DM1
Islet cell virus = cytokines released = Dendritic cell activation = DC takes up beta cell antigen = DC presents this to CD4 via MHC2 = CD4 then presents it to B cells which become plasma cells = Plasma cells produce autoantibodies against the beta cells. ---- The DC also presents to CD8 via MHC1 = CD8 becomes cytotoxic and releases granules containing perforin when it finds beta cells
36
What is diabetic ketoacidosis?
Medical emergency | Uncontrolled catabolism in DM1
37
What are the symptoms of DKA?
Polyuria, thirst, weight loss, vomiting, hypotension, confusion, coma, tacchcardia, tacchpnoea, sweet smelling breath
38
What is the metabolic cause of DKA?
Increased catabolic hormones (inc ketogenesis) | KBs are acidic. Depletes bicarb buffering stuff.
39
How does cortisol play a part in DKA?
Its released during dehydration and acidosis which further increases glucose by catabolism.
40
Is glucose high or low during DKA?
HIGH!
41
What happens to respiration during DKA?
Tacchypnoea - compensation for metabolic acidosis
42
Why is there dehydration in DKA?
KBs in urine draws water out. Loss of ion gradients - Na and K depleted.
43
How do you treat DKA?
Insulin, IV fluids, Potassium
44
Waist circumference risk levels?
M - 102cm F - 88cm
45
Is a lower GI index slower absorbed or faster?
Slower
46
What does alcohol do to gluconeogenesis?
Suppresses it - may cause hypo!!!
47
What is a basal bolus?
Insulin 4 times a day. Less fluctuations in base levels of insulin.
48
what is carb counting?
Matching the amount of insulin given to the amount of car consumed. Only with basal bolus.
49
Disadvantages of subcut insulin?
Too much to periphery, not enough to liver No feedback mechanism Carb counting is hard
50
What are the symptoms of hypoglycaemia?
Shaking, sweating, palpitations, headache, confusion, fits, unconscious
51
What might cause a hypo?
Too much insulin given reduced clearance Decreased insulin requirement (alcohol and exercise)
52
How do you treat a hypo?
Glucose, glucagon
53
What are some of the lifestyle advice changes for DM2?
Weight loss, exercise, diet
54
What are the drugs for DM2?
Sulphonylureas - TOLAZIDE Post prandial glucose regulators - REPAGLINIDE Bigilanide (insulin sensitisor) - METFORMIN Thiazolidinedione (insulin sensitiser) - PIOGLITAZONE GLP-1 with DPP4 antagonist (SAXAGLIPTIN) SGLT2 inhibitor - DAPAGLIFLOZIN
55
How do sulphonylureas work?
Close Potassium channels on beta cell, altering membrane potential. This causes calcium channels to open, causing insulin exocytosis.
56
How do postprandial glucose regulators work?
Close Potassium channels on beta cell, altering membrane potential. This causes calcium channels to open, causing insulin exocytosis.
57
How does Metformin work?
Increases muscle and adipose glucose uptake Increases gluconeogenesis Decreases glucose absorption from gut
58
What are the side effects of Metformin?
decreased appetite GI upset lactic acidosis
59
What are the side effects of Sulphonylureas?
Hypoglycaemia and weight gain
60
How often do you take METFORMIN?
3 times a day
61
How do Thiazolidinediones work?
Transcription of insulin sensitive genes | Decrease live glucose output, and increase muscle uptake.
62
What are the side effects of Thiazolidinediones?
Weight gain, cardiac failure. hypos
63
Hot does GLP1 work?
Transmits signals from gut to pancreas to increase insulin and dec glucagon.
64
What is GLP1 broken down by?
DPP4
65
How do SGLT2 inhibitors work?
Blocks glucose reabsorption and increases renal glucose excretion
66
What is common in babies born to diabetic mums?
Macrosomia, hypoglycaemia (due to xs insulin production), RDS. May have low birthweight Long term obesity and diabetes.
67
What are the complications of DM?
``` Glomerulosclerosis Arteriosclerosis causing hypertension Infections Diabetic foot Retinopathy Erectile dysfunction ```
68
What causes diabetic foot?
Damaged nerves causes anaesthesia and compromised blood flow means poor healing = ulcers and necrosis. Charcot foot
69
What is charcot foot?
brittle bones break easily
70
How do you treat diabetic foot?
Antibiotics, immobilise, stents, regular foot review, amputation
71
What types of retinopathy is seen in DM?
``` microaneurysms hard exudates dilated vessels cotton wool spots macula oedema traction from fibrosis causing blindness ```