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Year 2 RE > Long Term Complication of Diabetes > Flashcards

Long Term Complication of Diabetes Flashcards

1
Q

What are the 3 main microvascular complications that occur in diabetes?

A

1 - Retinopathy
2 - Nephropathy
3 - Neuropathy

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2
Q

What are the 3 main macrovascular complications that occur in diabetes?

A

1 - Ischaemic Heart Disease
2 - Cerebral Vascular Disease
3 - Peripheral Vascular Disease

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3
Q

What are the 3 main microvascular complications that occur in diabetes are

1 - Retinopathy
2 - Nephropathy
3 - Neuropathy

What cells are affected in each of these?

A
  • retinal endothelial cells
  • mesangial cells of glomerulus
  • schwann cells and peripheral nerve cells
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4
Q

What is the leading cause of blindness in the UK working population?

1 - diabetic retinopathy
2 - presbyopia
3 - cataract
4 - glaucoma

A

1 - diabetic retinopathy

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5
Q

Following diagnosis, how long is it before T1DM patients have diabetic retinopathy?

1 - immediately
2 - 3-5 years following diagnosis
3 - 5-10 years
4 - >10 years

A

2 - 3-5 years following diagnosis

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6
Q

What % of patients with T2DM have diabetic retinopathy and how long are they likely to have had it for?

1 - 50-80% of patients for 20 years
2 - 10-20% of patients for 20 years
3 - 50-80% of patients for 10 years
4 - 10-20% of patients for 10 years

A

1 - 50-80% of patients for 20 years

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7
Q

When there is hyperglycaemia the sugar in the blood is able to bind with other molecules in the blood, with no enzymatic activity. What is this process called?

1 - enzymatic glycation
2 - non-enzymatic glycation
3 - glycoselation
4 - glucosurinaemia

A

2 - non-enzymatic glycation

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8
Q

When there is hyperglycaemia the sugar in the blood is able to bind with other molecules in the blood, with no enzymatic activity called non-enzymatic glycation. What 2 molecules do they bind with?

1 - carbohydrates and lipids
2 - lipids and albumin
3 - proteins and lipids
4 - proteins and carbohydrates

A

3 - proteins and lipids

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9
Q

When there is hyperglycaemia the sugar in the blood is able to bind with other molecules in the blood, with no enzymatic activity called non-enzymatic glycation, binding with lipids and proteins. Why is this important?

A
  • creates very pro-inflammatory molecules
  • increases LDL in blood causing atherosclerosis
  • hyaline atherosclerosis causing a thickening of the basement membrane
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10
Q

When there is hyperglycaemia the sugar in the blood is able to bind with other molecules in the blood, with no enzymatic activity called non-enzymatic glycation, binding with lipids and proteins creating very pro-inflammatory molecules. This can then lead to:

  • increases LDL in blood causing atherosclerosis and narrowing of blood flow
  • hyaline atherosclerosis causing a thickening of the basement membrane

At a blood vessel and membrane basis what 2 effects can the 2 above disease processes then cause?

A
  • decreased blood flow

- decreased gas exchange due to basement membrane thickening

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11
Q

What are pericytes?

A
  • specialist cells that are embedded in the basement membrane of blood capillaries
  • pericytes wrap around endothelial cells of capillaries and have a close relationship between endothelial cells, astrocytes and neurons
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12
Q

Pericytes are specialist cells that are embedded in the basement membrane of blood capillaries that wrap around endothelial cells of capillaries and have a close relationship between endothelial cells, astrocytes and neurons. What are the 3 main functions of pericytes?

A

1 - regulate blood vessel formation (angiogenesis)
2 - regulate blood flow
3 - regulates immune cells flow

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13
Q

In diabetic retinopathy, how does the glycation of glucose with lipids and proteins that creates very pro-inflammatory molecules, leading to increases LDL in blood causing atherosclerosis and hyaline atherosclerosis causing a thickening of the basement membrane affect the number of pericytes surrounding the endothelial of the capillaries of the retina?

A
  • pericytes number decreases alongside endothelial damage
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14
Q

In diabetic retinopathy, glycation of glucose with lipids and proteins that creates very pro-inflammatory molecules, leading to increases LDL in blood causing atherosclerosis (narrowing of blood vessels due to plaque build up) and hyaline atherosclerosis causing a thickening of the basement membrane. This then reduces the number of pericytes alongside endothelial damage. What can this then cause in the capillaires of the retina?

A
  • microaneurysm = bulge in blood vessels due to weak blood vessel wall
  • weakness of blood vessel walls increases risk of rupture
  • rupture can lead to blood loss into the eye
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15
Q

In diabetic retinopathy, glycation of glucose with lipids and proteins that creates very pro-inflammatory molecules, leading to increases LDL in blood causing atherosclerosis (narrowing of blood vessels due to plaque build up) and hyaline atherosclerosis causing a thickening of the basement membrane. This thickening of the basement membrane and reduced number of pericytes leads to dysfunction and increased permeability. What can therefore happen in the retina?

A
  • leakage of lipids and proteins causing formation of hard exudate (blood vessel content leakage)
  • appear as thick yellow patches on the retina on fundoscopy
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16
Q

In diabetic retinopathy, there is a thickening of the basement membrane, leading to dysfunction and increased permeability. This can cause leakage of lipids and proteins causing formation of hard exudate (blood vessel content leakage). In addition, what else can happen to the capillaries and blood flow in the retina?

A
  • intraretinal haemorrhage occurs

- blood loss into the retina

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17
Q

In diabetic retinopathy patients can also damage the nerves in the eye, what is this called and how does this appear on a fundascope?

A
  • microinfarcts

- appears as lighter areas, referred to as cotton wool spots

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18
Q

In diabetic retinopathy ischamia occurs due to damage to the blood capillaires in the retina. What can this then lead to in the retina?

A
  • vascular endothelial growth factors are released

- angiogenesis begins (neovascularisation called proliferative retinopathy)

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19
Q

In diabetic retinopathy ischamia occurs due to damage to the blood capillaires in the retina, leading to vascular endothelial growth factors release that then stimulates angiogenesis (neovascularisation called proliferative retinopathy). Although this in principle is a good thing as the vessels aim to increase blood flow to the eye, why can this be bad?

A
  • newly formed blood vessels are weak, which then rupture

- haemorrhaging then occurs leading to further blood in the retina

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20
Q

In diabetic retinopathy there is too much glucose, called hyperglycaemia. As the glucose cannot be effectively absorbed it is converted into something else, what is that?

A
  • sorbital another form of sugar

- converted by aldose reductase

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21
Q

In diabetic retinopathy there is too much glucose, called hyperglycaemia. As the glucose cannot be effectively absorbed it is converted into sorbital, another form of sugar by aldose reductase. Although in principle these may be good, what can excessive levels of sorbitol cause?

A
  • oxidative stress
  • leads to hypoxia and endothelial dysfunction
  • osmotically active so draws H2O into cells
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22
Q

In addition to creating oxidative stress in diabetic retinopathy, what else can excessive levels of sorbitol in the retina cause?

A
  • oedema
  • sorbitol is osmotically active so draws in water
  • leads to macula oedema
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23
Q

What 4 main affects can diabetic retinopathy have on the eye?

A

1 - floaters (changes in vitreous composition)
2 - blurred vision
3 - reduced visual acuity
4 - loss of vision

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24
Q

What are the 2 methods to assess a diabetic patients eye?

A
  • fundoscopy

- visual acuity chart called snellen chart

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25
Q

Label the image below of diabetic retiopathic eye using the labels:

  • neovascularisation
  • haemorrhage
  • cotton wool spots (infarcts)
  • hard exudate
  • microaneurysms
A 
1 - haemorrhage
2 - microaneurysms
3 - hard exudate 
4 - cotton wool spots (infarcts)
5 - neovascularisation
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26
Q

In the UK we use a screening score to assess the severity or risk of a patients diabetic retinopathy. What are the 2 scoring categories?

A

1 - R = proliferative retinopathy (scored 0-3)

2 - M = macular oedema (scored 0-1, and P means previous photocoagulation)

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27
Q

The scoring system for diabetic retinopathy uses the following:

1 - R = proliferative retinopathy (scored 0-3)
2 - M = macular oedema (scored 0-1, and P means previous photocoagulation)

What would happen for the patient with the following scores:

  • R0 and R1
  • R2 and M1
  • R3
A
  • R0 and R1 = annual screening
  • R2 and M1 = seen within 4 weeks
  • R3 = immediate referral to ophthalmologist
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28
Q

Photocoagulation is a laser used to treat diabetic retinopathy. What is the purpose of photocoagulation?

A
  • laser used to shrink or burn new vessel formation
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29
Q

In addition to photocoagulation to remove new blood vessels in diabetic retinopathy, what are the 3 other treatment options?

A

1 - intravitreal steroids (reduces macular oedema)
2 - vitrectomy (removal of opaque vitreous humour)
3 - growth factor inhibitors

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30
Q

What is rubeosis Iridis?

A
  • neovascularization of the iris

- blood vessels develop on the anterior surface of the iris in response to retinal ischemia

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31
Q

The national diabetic screening process ensures which diabetic patients are seen?

A
  • all patients with T1DM and T2DM

- patients aged >12 years old

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32
Q

What is diabetic nephropathy?

A
  • damage to the nephrons caused in T1DM and T2DM
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33
Q

What is the leading cause of chronic kidney disease in most developed countries?

A
  • diabetic nephropathy
34
Q

Label the 3 layers of the filtering system in the glomerulus?

A

1 - endothelium
2 - basement membrane
3 - epithelium (podocytes foot process)

35
Q

When there is hyperglycaemia the sugar in the blood is able to bind with other molecules in the blood, with no enzymatic activity. What is this process called?

A
  • non-enzymatic glycation
36
Q

When there is hyperglycaemia the sugar in the blood is able to bind with other molecules in the blood, with no enzymatic activity called non-enzymatic glycation. What 2 molecules do they bind with?

A
  • lipids

- proteins

37
Q

In diabetic nephropathy, damage is caused by the pro-inflammatory glycalated molecules of glucose with lipids and proteins, means that these glycated molecules can then move through the capillary endothelium of the blood vessels of the nephron. This can lead to thickening and narrowing of the blood vessels. What is this process called?

A
  • hyaline arteriosclerosis (deposits of hyaline on basement membrane)
  • occurs in glomerulus and efferent (leaving nephron) nephrons
38
Q

In diabetic nephropathy, there is damage to the glycation of glucose with lipids and proteins, means that these glycated molecules can then move through the capillary endothelium of the blood vessels of the nephron. This can lead to thickening and narrowing of the blood vessels. called hyaline arteriosclerosis. Which blood vessels are specifically affected in the glomerulus?

A
  • efferent arterioles

- causes vasoconstriction

39
Q

In diabetic nephropathy, there is damage to the glycation of glucose with lipids and proteins, means that these glycated molecules can then move through the capillary endothelium of the blood vessels of the nephron. This can lead to thickening and narrowing of the blood vessels. called hyaline arteriosclerosis, specifically affecting in the efferent (exiting blood vessels) blood vessels of the glomerulus. What affect does this have on afferent blood vessels and the eGFR in the golmerulus?

A
  • afferent arterioles dilate and increase blood flow

- increased blood flow increases filtration, called hyperfiltration

40
Q

What are mesangial cells?

A
  • specialised cells in the kidney that make up the mesangium of the glomerulus
  • role is to remove trapped residues and aggregated protein from the basement membrane thus keeping the filter free of debris
41
Q

In diabetic nephropathy, in response to thickening and narrowing of the blood vessels (hyaline arteriosclerosis) that causes the following:

1st - narrowing of efferent arterioles
2nd - dilation of afferent arterioles and increased eGFR (hyperfiltration)

What affect does this have on the glomerulus?

A
  • mesangial cells are stimulated and secrete matrix

- aim is to increase the size of the glomerulus to assist with filtration

42
Q

In diabetic nephropathy mesangial cells are stimulated and secrete matrix, which increases the size of the glomerulus, which aims is to increase the size of the glomerulus to assist with filtration. Does the matrix secreted by mesangial cells secrete uniformly?

A
  • can be even and uniformly

- can also form kimmelstiel wilson nodules

43
Q

In diabetic nephropathy mesangial cells are stimulated and secrete matrix, which increases the size of the glomerulus, which aims is to increase the size of the glomerulus to assist with filtration. Instead of assisting with filtration, what can this process do to the basement membrane?

A
  • thickens basement membrane and podocyte foot processes spread-out
  • increases permeability to proteins and glucose
44
Q

In diabetic nephropathy, the damage to the glomerulus ultimately does what to the eGFR?

A
  • reduces it
45
Q

In diabetic nephropathy, the damage to the glomerulus ultimately leads to reduces eGFR. How can this present clinically?

A
  • dramatic decline in eGFR

- micro (30-60mg/day) and macroalbuminaemia (>300mg/day)

46
Q

How common is diabetic nephropathy in T1DM and T2DM following 10 years since diagnosis?

A
  • T1DM = 20-30% will have microalbuminuria and 1% renal failure
  • T2DM = 25% will have microalbuminuria
47
Q

In T2DM diabetic nephropathy patients, which ethnicities are at a greater risk of developing diabetic neuropathy?

A
  • African-Caribbean, Mexican and Pima Indians
48
Q

What is the diagnosis of micro and macroalbuminuria?

A
  • microalbuminuria = 30-300mg/day

- macroalbuminuria (also called proteinuria) = >300mg/day

49
Q

What are the 5 main risk factors for developing diabetic nephropathy?

A
  • baseline albumin excretion
  • age of diabetes diagnosis
  • glycemic control – ‘legacy affect’
  • blood pressure
  • lipid profile
50
Q

We cannot reverse diabetic nephropathy, but we can slow it down. What are some of the key treatment options that essentially all aim to reduce the pressure on the kidneys?

A
  • angiotensin-converting enzyme inhibitors (ACEi)
  • angiotensin receptor blockers (ARBs)
  • blood pressure control
  • glycaemic control
  • lipid management
  • protein restricted diet
51
Q

What is diabetic neuropathy is damage to nerve fibres. Are myelinated and non-myelinated both affected?

A
  • yes
52
Q

Diabetic neuropathy is damage to nerves caused by diabetes. What is the incidence of this?

A
  • 6%
53
Q

Diabetic neuropathy is damage to nerves caused by diabetes. What is the prevalence of this in T1DM and T2DM?

A
  • T1DM = 34%

- T2DM = 26%

54
Q

Why are advanced glycosylated end products a risk factor for developing diabetic neuropathy?

A
  • can lead to reactive oxygen species and inflammation
  • macrophages, chemokines and cytokines can signal further inflammation
  • leads to damage to schwann cells
55
Q

Excessive levels of glucose in the body mean that in some tissues this can be converted into sorbitol. Sorbitol has been shown to slow the nerve conduction. How does this occur?

A
  • reduces Na+/K+ ATPase

- less Na+ released at nodes of ranvier meaning less depolarisation

56
Q

What are 2 vascular risk factors for developing diabetic neuropathy?

A

1 - morphological abnormalities and vasa nervorum (blood supply to nerves)
2 - thrombomodulin and plasminogen tissue levels are reduced (both reduce blood clots)

57
Q

Peripherally poor production of growth stimulating factors can be a risk factors for developing diabetic neuropathy. Why is this?

A
  • growth factors are required for nerve growth and repair
58
Q

There are different patterns of nerve injury in diabetic neuropathy. What is distal symmetrical polyneuropathy, also referred to as glove and stockings?

A
  • loss of nerve stimulation where gloves and stockings would be worn
59
Q

There are different patterns of nerve injury in diabetic neuropathy. Distal symmetrical polyneuropathy, also referred to as glove and stockings is damage to multiple nerves in the hands and feet. What sensations are lost?

A
  • pinprick
  • temperature
  • vibration
  • proprioception
  • reduced reflexes
60
Q

There are different patterns of nerve injury in diabetic neuropathy. What is polyradiculopathy?

A
  • damage to multiple nerve roots causing severe pain
  • self limiting and resolves over 6-12 months
  • caused by glucose inflammation of nerve roots
61
Q

There are different patterns of nerve injury in diabetic neuropathy. What is mononeuropathy?

A
  • damage to a single nerve
62
Q

What is autonomic neuropathy?

A
  • nerves controlling involuntary bodily functions are damaged
63
Q

Autonomic neuropathy is where nerves controlling involuntary bodily functions are damaged. What are the most common presentations of this?

A

1 - cardiovascular – resting tachycardia, postural hypotension
2 - gastrointestinal – delayed gastric emptying
3 - genitourinary – bladder dysfunction
4 - hypoglycaemia unawareness
5 - hyperhidrosis (excessive sweating)

64
Q

Although diabetic neuropathy is common in diabetes patients, there are also other differentials that may cause the same symptoms in diabetes. What are the 3 main differentials that it could be instead of diabetic neuropathy?

A
  • B12 deficiency (important for myelin production)
  • hypothyroidism (increased fluid retention that compresses nerves)
  • inflammatory conditions
65
Q

In addition to the standard treatment options for diabetes that will in turn treat diabetic neuropathy, such as:

  • weight loss
  • hypertension
  • alcohol reduction
  • glycemic control
  • smoking
  • blood lipids

There are 3 analgesics as well that can be used to treat pain, which 3 are commonly used to treat diabetic neuropathy?

A

1 - Duloxetine (anti-depressant)
2 - Tricyclic antidepressants
3 - Gabapentin (epilepsy medication)

66
Q

Patients with diabetes can have macro-vascular complications. What are the key 3 we need to know?

A

1 - peripheral vascular disease
2 - ischaemic heart disease
3 - cerebral vascular disease

67
Q

Peripheral vascular disease is a common macro-vascular complication in diabetes. How is this caused?

A
  • increased glucose leads ROS and inflammation that can activate arteriosclerosis pathways
  • elevated lipids can also increase artheroma formation

BOTH LEAD TO NARROWING OF BLOOD VESSELS

68
Q

Peripheral vascular disease (PVD) is a common macro-vascular complication in diabetes that causes narrowing of the blood vessels. What % of diabetic patients >50 years old have PVD?

A
  • 1/3rd or 33%
69
Q

Peripheral vascular disease (PVD) is a common macro-vascular complication in diabetes that causes narrowing of the blood vessels. What 2 other macrovascular complications can this increase the risk of?

A

1 - ischaemic Heart Disease

2 - cerebral Vascular Disease (strokes)

70
Q

What are the 5 main risk factors for developing peripheral vascular disease?

A 
1 - diabetes control
2 - smoking
3 - hypertension
4 - hyperlipidaemia
5 - obesity
71
Q

How can peripheral vascular disease present clinically?

A
  • can be asymptomatic
  • cramp (on exertion)
  • reduced circulation - cold
  • discolouration of legs
  • ulcers
  • hair loss to extremity
72
Q

How can we detect peripheral vascular disease (PVD) in a clinical setting?

A
  • ankle brachial pressure index (ABPI)
  • measure BP at arm and compare to ankle
  • normal ABPI = ratio 1 - 1.3
  • ABPI <0.9 = PVD
  • ABPI >1.3 = calcification of blood vessels
73
Q

What is osteomyelitis?

A
  • infection in the bone

- can be caused by an ulcer

74
Q

Osteomyelitis is an infection in the bone, that can be caused by an ulcer. What are the main treatment options for ulcers

A

1 - mechanical offloading
2 - debridement (surgically remove dead tissue)
3 - antibiotics
4 - amputation

75
Q

What is charcot anthropathy?

A
  • mild trauma causing inflammation

- deformation of the bones of the foot

76
Q

When assessing a diabetic patients risk for developing cardiovascular disease, what blood marker can be a good marker?

A
  • HbA1c
  • <6% HbA1c means low blood glucose, cardiac arrhythmia and increased CVD mortality
  • high HbA1c increases CVD mortality due to damage to blood vessels

SAME PRINCIPLE FOR CEREBRAL VASCULAR DISEASE

77
Q

What does acanthosis nigricans mean?

A
  • acanthus = latin for spine
  • osis = diseased condition
  • nigricans = black fish
78
Q

Acanthosis nigricans translates to:

  • acanthus = latin for spine
  • osis = diseased condition
  • nigricans = black fish

What is this as a dermatological skin condition in diabetes?

A
  • dark brown/reddish colour deformation of the skin
  • typically occurs on back of neck or elbows
  • linked with insulin resistance
79
Q

What is diabetic dermopathy?

A
  • skin condition in diabetes

- characterised by red lesions which are the bursting of small blood vessels under the skin

80
Q

What is necrobiosis lipoidica diabeticorum?

A
  • changes in fat tissue in hypoglycaemia

- results in elevated pink skin, generally on the shins

Year 2 RE (53 decks)

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