Brainscape's Knowledge GenomeTM

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


See full index

Endocrinology, life cycle and RCR2 > Diabetes > Flashcards

Diabetes Flashcards

1
Q

Define Diabetes Mellitus

A

An absolute or relative deficiency of insulin causing hyperglycaemia

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

What is the problem of hyperglycaemia?

A

Proteins become glycosylated and lose their function

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

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

A

7

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

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

A

11.1

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

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

A

6.5%

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

Describe DM1

A

Absolute insulin deficience
Childhood diagnosis
Autoimmune islet damage

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

Describe DM2

A

Genetic and environmental factors

Insulin deficiency and resistance

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

When is DM1 diagnosed?

A

Childhood

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

What are the 3 main symptoms of diabetes?

A

Thirst, polyuria, nocturia

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

What is Gestational diabetes?

A

Occurring for the first time in pregnancy

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

What are some causes of secondary DM?

A

Pancreatic disease, congenital abnormalities, drugs, endocrine disorders.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

What is Insulin stimulated by?

A 
High blood glucose
AAs
FAs
GI hormones
Sulphonylureas
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

What are the two important Glucose transporters in DM?

A

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

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

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

What does insulin promote the synthesis of?

A

lipoproteins, TGs, proteins

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Is GH mainly anabolic or catabolic?

A

anabolic

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

What is Glucagon stimulated by?

A

Low blood glucose, High AAs, and exercise

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

What inhibits Glucagon?

A

Insulin, KBs

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

When might Glucose and Insulin work together?

A

To prevent hypoglycaemia when high protein foods are eaten.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

Where is GH secreted from?

A

Anterior pituitary

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

What does GH do?

A

Protein synthesis
Lipolysis
glycogenesis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

What is IGF and what does it do?

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

What are IGFs stimulated by?

A

Insulin and GH

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

When is cortisol released?

A

stress, low glucose

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

What does cortisol do?

A

Proteolysis
gluconeogenesis
inhibits glucose use.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

What are catecholamines stimulated by?

A

Stress

low glucose

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

What do catecholamines do?

A

Glycogenolysis
Lipolysis
Gluconeogenesis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

How does insulin resistance happen?

A

Constant xs of glucose in the blood causes constant stimulation of the insulin receptors, causing them to downregulate

30
Q

Why is there decreased insulin secretion in DM2 as well as resistance?

A

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
Q

What happens during starvation?

A

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
Q

What are the risks of DM?

A

Ketoacidosis (DM1)
Dehydration
Hypertriglyceridemia
Hypoglycaemia

33
Q

What are some of the genetic causes of DM1?

A

IDD1, IDD2, IDD3 mutations = poor T cell activation regulation

34
Q

How would you dx DM1?

A

Clinical symptoms and a biochemical test for autoantibodies

35
Q

Explain the Immunology of DM1

A

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
Q

What is diabetic ketoacidosis?

A

Medical emergency

Uncontrolled catabolism in DM1

37
Q

What are the symptoms of DKA?

A

Polyuria, thirst, weight loss, vomiting, hypotension, confusion, coma, tacchcardia, tacchpnoea, sweet smelling breath

38
Q

What is the metabolic cause of DKA?

A

Increased catabolic hormones (inc ketogenesis)

KBs are acidic. Depletes bicarb buffering stuff.

39
Q

How does cortisol play a part in DKA?

A

Its released during dehydration and acidosis which further increases glucose by catabolism.

40
Q

Is glucose high or low during DKA?

A

HIGH!

41
Q

What happens to respiration during DKA?

A

Tacchypnoea - compensation for metabolic acidosis

42
Q

Why is there dehydration in DKA?

A

KBs in urine draws water out. Loss of ion gradients - Na and K depleted.

43
Q

How do you treat DKA?

A

Insulin, IV fluids, Potassium

44
Q

Waist circumference risk levels?

A

M - 102cm F - 88cm

45
Q

Is a lower GI index slower absorbed or faster?

A

Slower

46
Q

What does alcohol do to gluconeogenesis?

A

Suppresses it - may cause hypo!!!

47
Q

What is a basal bolus?

A

Insulin 4 times a day. Less fluctuations in base levels of insulin.

48
Q

what is carb counting?

A

Matching the amount of insulin given to the amount of car consumed. Only with basal bolus.

49
Q

Disadvantages of subcut insulin?

A

Too much to periphery, not enough to liver
No feedback mechanism
Carb counting is hard

50
Q

What are the symptoms of hypoglycaemia?

A

Shaking, sweating, palpitations, headache, confusion, fits, unconscious

51
Q

What might cause a hypo?

A

Too much insulin given
reduced clearance
Decreased insulin requirement (alcohol and exercise)

52
Q

How do you treat a hypo?

A

Glucose, glucagon

53
Q

What are some of the lifestyle advice changes for DM2?

A

Weight loss, exercise, diet

54
Q

What are the drugs for DM2?

A

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
Q

How do sulphonylureas work?

A

Close Potassium channels on beta cell, altering membrane potential. This causes calcium channels to open, causing insulin exocytosis.

56
Q

How do postprandial glucose regulators work?

A

Close Potassium channels on beta cell, altering membrane potential. This causes calcium channels to open, causing insulin exocytosis.

57
Q

How does Metformin work?

A

Increases muscle and adipose glucose uptake
Increases gluconeogenesis
Decreases glucose absorption from gut

58
Q

What are the side effects of Metformin?

A

decreased appetite
GI upset
lactic acidosis

59
Q

What are the side effects of Sulphonylureas?

A

Hypoglycaemia and weight gain

60
Q

How often do you take METFORMIN?

A

3 times a day

61
Q

How do Thiazolidinediones work?

A

Transcription of insulin sensitive genes

Decrease live glucose output, and increase muscle uptake.

62
Q

What are the side effects of Thiazolidinediones?

A

Weight gain, cardiac failure. hypos

63
Q

Hot does GLP1 work?

A

Transmits signals from gut to pancreas to increase insulin and dec glucagon.

64
Q

What is GLP1 broken down by?

A

DPP4

65
Q

How do SGLT2 inhibitors work?

A

Blocks glucose reabsorption and increases renal glucose excretion

66
Q

What is common in babies born to diabetic mums?

A

Macrosomia, hypoglycaemia (due to xs insulin production), RDS. May have low birthweight
Long term obesity and diabetes.

67
Q

What are the complications of DM?

A 
Glomerulosclerosis
Arteriosclerosis causing hypertension
Infections
Diabetic foot
Retinopathy
Erectile dysfunction
68
Q

What causes diabetic foot?

A

Damaged nerves causes anaesthesia and compromised blood flow means poor healing = ulcers and necrosis.
Charcot foot

69
Q

What is charcot foot?

A

brittle bones break easily

70
Q

How do you treat diabetic foot?

A

Antibiotics, immobilise, stents, regular foot review, amputation

71
Q

What types of retinopathy is seen in DM?

A 
microaneurysms
hard exudates
dilated vessels
cotton wool spots
macula oedema
traction from fibrosis causing blindness

Endocrinology, life cycle and RCR2 (4 decks)

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