L20 - Long term diabetic complications COPY Flashcards
COMPLICATIONS
i) name three microvascular complications
ii) name three macrovascular complications
i) retinopathy, nephropathy, neuropathy
ii) IHD, CVD and PVD
MICROVASCULAR COMPLICATIONS
i) what is most cells response to high extracellular hyperglycaemia?
ii) name three types of cell that cannot protect themselves from high extracell hypergly (retina, glomerulus and nerve)
iii) how long do these complications take to develop?
iv) in what condition may they be detected at presentation? why?
i) can reduce glucose transport/wont internalise glucose
ii) cells that cant protect themselves from high glucose
- retinal endothelial cells
- mesangial cells of glomerulus
- schwann and peripheral nerve cells
iii) these complications take many years to develop
iv) may be detected at dx of T2DM because it often goes for a long time undiagnosed (5-10yrs)
RETINOPATHY
i) what can it cause?
ii) how many x increase is the risk of blindness for those with diabetes?
iii) name two other eye conditions it also increases the risk of
iv) how dense are retinal capillaries? what does this mean
v) which cells are key to local regulation of blood flow? how do they do this
i) second most common cause of blindness in people of working age
ii) 10-20x increased risk of blindness if have diabetes
iii) glaucoma and cataracts
iv) low density of capillaries in the retina means there is little functional reserve
v) pericytes are key to regulating blood flow
- have contractile function and wrap around capillaries and direct blood flow where needed
PATHOLOGICAL FINDINGS OF DIABETIC RETINOPATHY
i) what cells are lost?
ii) what happens to the basement membrane under the capillaries? what does this impair?
iii) what does capillary collapse cause in the retina?
iv) what does the retina release in response to capillary collapse? what does this then cause
v) what can leak out of vessels and form a hard exudate?(2)
vi) what is seen as ‘cotton wool spots’ on retinography?
i) loss of pericytes
ii) basement membrane thickens which impairs diffusion of molecules to the retina
iii) capillary collapse can cause ischaemia
iv) the retina releases VEGF in response to ischaemia which can increase cap permeability and cause leakage
v) fluid and cholesterol
vi) ischaemia
RETINOPATHY
i) what is seen in A? what may this cause?
ii) what has happened in B? how may this be treated?
iii) what are the white spots on C?
iv) what are the white spots on D?
i) fibrous scar on the back of the retina - may cause detachment of the retina
ii) catastrophic bleed into the vitreous humour
- do a vitrectomy and replace it with salone
iii) ischaemia
iv) exudate
SCREENING FOR RETINOPATHY
i) how may vision be affected with complex disease?
ii) what is used to take a photo of the eye/retina?
iii) how many fields are taken from each eye?
iv) what is shown by the arrow? how advanced is this eye disease? what may it be associated with?
i) can still have normal vision even in very complex disease
ii) use a high resolution digital camera
iii) take two fields from each eye
iv) new vessels are growing over the iris
- advanced eye disease
- can be assoc with glaucoma
CLINICAL STAGES OF RETINOPATHY
i) name three things that may be seen in non proliferative retinopathy
ii) what may changes in proliferative retinopathy be due to? what action should be taken?
iii) name one other consequence of retinopathy
i) dots, haemmorhage, microaneurysms, hard exudate
ii) prolif changes due to ischaemia
- refer to an opthalmologist
iii) macular oedema (can be sight or non sight threatening)
DIABETIC RETINOPATHY
i) what parameter can accelerate disease progression?
ii) name one treatment - which two ways can this be given
iii) what treatment can be injected into the vitreous? how does this work?
i) high blood pressure
ii) laser treatment
- can be pan retinal (everywhere but macula) or focal
iii) intra vitreal anti VEGF antibody
- agents against VEGF (which drives angio and leaky bv)
NEUROPATHY
i) what % of diabetic patients may this affect?
ii) what % have painful neuropathy?
iii) name three types of neuropathy
i) up to 50% of diabetic patients
ii) 15% have painful neuropathy
iii) peripheral, mono and autonomic
PERIPHERAL NEUROPATHY
i) name three symptoms
ii) what is the effect on motor nerves? what is particularly seen in the hands?
iii) what is the common distribution?
iv) which nerves are the most affected?
v) is most damage proximal or distal?
i) tingling, numbness, burn, electric shock
ii) affects motor nerves which causes muscle weakness
- see interossus wasting in the hands
iii) symmetrical stocking and gloves distribution
iv) longest nerves are most affected
v) damage is distal more than proximal
NEUROPATHY FOOT PROBLEMS
i) what single thing do you need to develop a neuropathic ulcer?
ii) name three characterstics of a neuropathic ulcer
iii) how do neuropathic ulcers start of?
iv) what acute foot problems are diabetics also at risk of? what kind of process occurs here? what is the result?
v) how is the above acute problem treated?
i) nerve damage
ii) on a pressure area, callus build up and soft tissue necrosis
iii) ulcers start off as a callus
iv) diabetics also at risk of charcot foot
- inflammatory process due to dense nerve damage
- makes joints and bones vulnerable -> fractures and foot deformity
v) treat charcot foot by putting it into a cast and stop weight bearing on the foot
MONONEUROPATHY
i) what single nerve does this affect?
ii) name two symptoms
iii) how many weeks does it take to reverse?
iv) which two other symptoms may accompany this
i) CN III (oculomotor nerve)
ii) ptosis (eye down and out - can be partial)
- pupil dilation (only if surgical)
iii) always reverses in 12 weeks
iv) can also get foot and wrist drop
AUTONOMIC NEUROPATHY
i) how is stomach emptying affected? what is this called? how does this leave the person feeling?
ii) what type of hypotension may be seen? why?
iii) what type of sweating may be seen?
iv) name two other symptoms
v) can the underlying cause be treated?
i) impaired emptying = gastroparesis
- leaves patient feeling full and bloated
ii) postural hypotension as the ANS cant maintain BP
iii) gustatory sweating (sweat when eating)
iv) dirhoea and erectile dysfunction
v) cant treat nerve damage so have to treat the symptoms
NEPHROPATHY
i) what is the most common cause of end stage renal disease in the western world?
ii) which patients are likely to die earlier if they get nephropathy
iii) name the three components of the filtration barrier in the kidney
i) diabetes
ii) T1DM patients
iii) fenestrated glom capillaries, basement membrane and podocytes
DIABETIC NEPHROPATHY - PATHOL FINDINGS
i) how does the basement membrane change? how is the charge affected and what does this cause?
ii) which type of specialised cells are lost? what does this lead to
iii) name two things that occur that further decrease renal function
iv) what is one of the first things seen in this pathology?
i) thickening of BM
- loss of negative charge which usually helps it repel proteins
- loss of charge allows proteins through
ii) loss of podocytes
- leads to loss of integrity of the filtration barrier
iii) glomerular sclerosis and mesangial expansion further decrease renal function
iv) leaking protein (albumin)