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Semester 4 (NME) > Diabetes Pathology > Flashcards

Diabetes Pathology Flashcards

1
Q

What % of diabetic patients have T1DM?

A

15%

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2
Q

What is the most common ethnicity of patients with T1DM?

A

Caucasion

North European

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3
Q

What is the most common age of presentation of T1DM patients?

A

Puberty

But can be any age

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4
Q

What is the pathophysiology of T1DM?

A

Gradual destruction of Bcells due to autoimmunity

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5
Q

What is the most common subtype of T1DM?

A

Type 1A
Immune regulated form
90% have mutations in HLA genes on chromosome 6

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6
Q

Name a non genetic risk factor for T1DM?

A

Clean environment during childhood with little exposure to pathogens

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7
Q

Name 5 common symptoms of T1DM at presentation?

A

Polydipsia (increased thirst)
Increased urination (especially at night)
Weight loss/ fatigue
Itching around genitals/ bouts of thrush

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8
Q

Name 3 signs of diabetic patients seen at presentation?

A

Hyperglycemia
Glucosuria
Ketoneuria?

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9
Q

Name 6 emergency signs in a presentation of T1DM?

A

Loss of appetite/ N+V
Fever/ drowsy/ confused
Stomach pain
Fruity (pear drop) breath - ketoacidosis

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10
Q

What glucose levels (fasting and random) indicate possible diabetes?

A

Random glucose >11.1mmol/L

Fasting glucose >7mmol/L

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11
Q

What are the diagnostic criteria for T1DM when doing glucose tests?

A

ONE random/ fasting glucose out of range if symptomatic

TWO randon/fasting glucose out of range if asymptomatic

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12
Q

What HbA1c level is diagnostic of diabetes?

A

> 48mmol/L (6.5%)

Although result lower than this does not exclude diagnosis if glucose test disagrees

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13
Q

What is the treatment for T1DM?

A

Always need insulin!

Education/ healthy diet/ weight loss/ smoking cessation

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14
Q

What are the two different methods of insulin dosing?

A

Twice Daily: Intermediate insulin (isophane)
- Works within 2hrs, lasts 18-24hrs
Multiple Dose: Rapid acting insulin
- Best for Px with good understanding/ control

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15
Q

Px taking insulin on a multiple dose regimen should take their insulin when?

A

Before/ with a meal

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16
Q

What is the main type of twice daily insulin?

A

Hypurin isophane (either bovine or porcrine)

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17
Q

Name the two most common rapid acting insulins?

A

Novorapid
Humalog (works in 15mins)
Lasts 3-5hrs

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18
Q

What is analouge insulin?

A

Similar to human but with recominant DNA

Where AA’s have been changed to change insulin properties

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19
Q

What is HbA1c?

A

A reliable indicator of mean glucose levels over the last 120 days

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20
Q

Why can HbA1c be used to give estimates of glucose?

A

As glycation (adding of sugar) to the Hb occurs at a variable rate over an RBC’s 120 day lifespan, so proportions of glycated reflect how much sugar has been in the blood

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21
Q

What is the normal level of HbA1c?

A

4-6% (20-43mmol/L)

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22
Q

Name 8 symptoms of hypoglycemia?

A

Shaking/ sweating
Weakness/ confusion
Hunger/ tingling lips
Slurred speech/ unconciousness/ transient hemipariesis

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23
Q

How would you treat a hypoglycemic patient when in a hospital?

A

If mild treat sugary drinks/ food

Give 80ml of 20% glucose IV

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24
Q

How would you treat a hypoglycemic patient when not in a hospital?

A

If mild give sugary drinks/ food

1mg (1unit) glucagon intramuscular

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25
Q

Name 4 risk factors than can predispose a diabetic patient to have a ‘hypo’:

A

Exercise
Taking too much insulin
Drinking alcohol on an empty stomach
Skipping meals

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26
Q

What is the clinical definition of hyperglycemia?

A

Blood glucose >11.1mmol/L

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27
Q

What is the classic triad of symptoms of hyperglycemic Px?

A

Polyphagia (hunger)
Polydipsia (thirst)
Polyuria (frequent urination)
(Add diabetic symptoms/ dry mouth/ drowsiness)

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28
Q

Prolonged hyperglycemia can lead to (5)?

A

Diabetic ketoacidosis

Renal/ cardiovascular/ neural/ retina damage

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29
Q

What is the pathophysiology of T2DM?

A

Disorder of receptors (increased triglyceride levels can cause release of inflam proteins/cytokines which damage 2nd messengers). Hyperinsulinaemia initially compensates but this eventually leads to Bcell damage

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30
Q

What % of patients with DM have T2DM?

A

90%

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31
Q

What ethnicity is most subceptible to T2DM?

A

Afrocarribean

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32
Q

Name 7 RF’s for developing T2DM:

A

‘Central’ obesity/ lack of physical activity
Low fibre, high sugar diet/ metabolic syndrome
Family history/ Polycystic ovary syndrome
Low birth weight/ gestational diabetes

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33
Q

How does presentation of T2DM differ to those with T1DM?

A

Longer onset of symptoms

Px with T2 often present much later in life

34
Q

Name 6 presenting complaints for Px with T2DM:

A 
Polyuria/ polydipsia/ lethargy
Boils/ prolonged infections
Pruritus vulvae (itchy genitals)
35
Q

What is the NICE recommended treatment pathway for Px with T2DM?

A

Diet control > metformin >
Metformin + sulfonylurea (or DPP-4 inhib if hypo risk)
> add thiazolidinedione or insulin

36
Q

What is metformin, how does it act, when is it given and what is a possible SE?

A 
Activates AMPK (AMP activated protein kinase) in the liver and muscle to upregulate GLUT-4 receptors 
Take orally w meals
SE: Lactic acidosis
37
Q

How do sulfonylurea drugs work?

A

Bind to ATP sensative K+ channels on B cells, this depolarises the cell and opens Ca2+ channels which increases insulin release

38
Q

Name three sulfonylurea drugs:

A

Glimepiride / Glipizide / Tolbutamide

39
Q

How do DPP-4 inhibitor drugs work?

A

Inactivates the enzyme which inactivates GLP-1 (an incretin)

- This increases levels of GLP-1 which along with GIP causes the incretin effect

40
Q

Name 2 DPP-4 inhibitor drugs:

A

Linagliptin/ Saxagliptin

41
Q

How do thiazolidinediones act? Give an example drug

A

Act on intracellular receptor PPAR-Y to decreases hepatic glucose production and increase uptake and use in muscle
E.g Pioglitazone

42
Q

What is the common presentation of diabetic ketoacidosis?

A

Diabetic symptoms (+ dehydration )
Drowsy/ confused/ fruity breath
Tachycardia/ hyperventilation/ hypotension

43
Q

How common is gestational diabetes, what care should be taken to ensure women are protected?

A

Roughly 1in35 pregnancies- commonly in 2nd trimester
Ensure all high risk women are screened
Monitor and advise on diet, treat if needed (insulin)

44
Q

What is the pathophysiology of diabetic retinopathy?

A 
Usually in 2nd decade of disease
Vascular microaneurysms (permeability changes etc lead to blood flow changes and ischemia)
45
Q

What is the most common presentation of diabetic neuropathy?

A

Distal symmetrical polyneuropathy, starting with distal sensory loss

46
Q

What is the pathophysiology of diabetic foot ulcers?

A

Loss of sensation = more trauma
Anhidrosis = drying and skin damage
Disordered proprioception = abnormal weight bearing

47
Q

What are common diabetic dermatological problems?

A

The most common skin manifestations of DM are protracted wound healing and skin ulcerations

48
Q

Where is acetyl-coA converted into ketone bodies in diabetic ketoacidosis?

A

Mitochondria

49
Q

Soluble insulin produces what effect?

A

Rapid acting and short lasting

50
Q

How are insulin preperations made to act over longer time periods?

A

Precipitating insulin with protamine or zinc

51
Q

What % of T2DM will ultimately take insulin as part of the treatment?

A

33%

52
Q

Which brain area links the osmoreceptors in the ant hypothalamus with the ADH releasing cells in the post pituitary?

A

Supraoptic nuclei

53
Q

Which two area’s of the brain regulate hunger?

A

Lateral nuclei of hypothalamus = feeding centre (stimulation = hunger)
Ventromedial nuclei of hypothalamus = satiety centre (stimulation = feel full)

54
Q

Multiple hormones released from the gastrointestinal tract and adipose tissue converge to regulate food intake as well as energy expenditure- where is this?

A

Arcuate nuclei

55
Q

Which of the ketone bodies can’t be used by the cells and converted back to acetyl-coA, what happens to it?

A

Acetone

Instead it is expired via the lungs

56
Q

What is the pathophysiology of diabetic nephropathy?

A

Renal hypertrophy associated with incr GFR (as afferent arteriole becomes more dilated), this raises intraglomerular pressure and damages cappilaries causing glomerular sclerosis

57
Q

What are some common signs of diabetic nephropathy? (3)

A

Microalbuminuria (1st) > intermittenent albuminuria (2nd) > proteinuria (3rd)
Hyperlipidemia/ generalised oedema

58
Q

How should diabetic nephropathy be treated?

A

ACEI

Aim below 130/80mmHg

59
Q

What is the pathophysiology of diabetic neuropathy?

A

Hyperglycemia can lead to build up of ‘sorbitol’ and fructose in schwann cells- this leads to demyelination

60
Q

How does diabetic neuropathy usually present?

A

Loss of vibration/ pain/ temp (usually feet before hands)
Feeling of walking on cotton wool
Balance impaired in the dark (less proprioception)

61
Q

What is the pathophysiology of diabetic foot and how common is it?

A

10-15% of diabetic patients
Due to combination of ischemia (macrovascular), infection and neuropathy
(Black feet = vascular problem)

62
Q

How should you treat diabetic foot?

A

Keep weight off ulcers

Treat with AB’s if needed

63
Q

How common is diabetic eye disease?

A

90% of T1DM Px go on to develop

64
Q

What is diabetic retinopathy?

A

Nerve damage to retina/ iris damage

Due to intramural pericytes death and basement membrane thickening (so less blood supply to nerves)

65
Q

What are cateracts?

A

Denaturing of proteins in the lens render it opaque

increased risk in diabetes and ketosis

66
Q

What is the recommendation for all patients with diabetes in regards to observing for opthalmic changes?

A

All diabetic Px should have yearly eye screening

67
Q

How does blood glucose testing equipment work?

A

Has ‘glucose oxidase’ which catalyses the reaction of glucose to gluconic acid. Gluconic acid is measured and then the equipment converts this into a glucose level

68
Q

Where should the Px prick when doing a glucose test?

A

Side of finger

69
Q

How often should Px with T2DM which is controlled by diet/ oral agents measure their glucose?

A

Once/twice per week

70
Q

How often should Px on insulin treatment check their glucose levels?

A

~12 hours after long acting insulin dose or
~ 90mins-2hrs after short acting insulin dose
2-4x per day

71
Q

What % of patients on insulin therapy die due to their diabetes?

A

86%

72
Q

What are the three main causes of death in diabetic patients?

A

CVD- 70%
Renal- 10%
Infection- 6%

73
Q

Name 4 macrovascular complication of diabetes?

A

Stroke
MI
Foot gangrene
Atherosclerosis

74
Q

Name 3 BV area’s commonly affected by microvascular disease in diabetes?

A

Retina
Kidney
Nerve sheaths
(often ~10-20 years post diagnosis)

75
Q

Why do alcohol binges predispose to hypoglycemic attacks?

A

Alcohol reduces the livers ability to cope with change to glucose levels in plasma so there’s reduced release of glucose into the blood when your drunk.

76
Q

What is the best test to determine a Px’s glucose control over the last 2-3hours?

A

Glucosuria test

77
Q

Which test would best establish a patient’s current level of glycaemic control?

A

Blood glucose test

78
Q

Which test would best establish a Px’s long term level of glycaemic control?

A

Haemoglobin A1c test

79
Q

What is the most common SE of metformin?

A

GI disturbance

80
Q

What is the most common SE of sulfonylurea’s?

A

Hypoglycemia

81
Q

Px w T1DM should aim for what blood glucose levels (pre and post prandial)?

A

Pre: 4-7mmol/L
Post: Under 9mmol/L

82
Q

What is the clinical definition for hypoglycemia?

A

Glucose levels under 3mmol/L

Semester 4 (NME) (24 decks)

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