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RB Y2 Endocrine - 1 Diabetes > Microvascular Complications of Diabetes - Neuropathy > Flashcards

Microvascular Complications of Diabetes - Neuropathy Flashcards

1
Q

what are the chronic complications of diabetes

A

macrovascular: IHD and stroke (risk x2)

microvascular

cognitive dysfunction/dementia

erectile dysfunction

psychiatric

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2
Q

traditionally, what did diabetes lead to

A

blindness, amputation and dialysis

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3
Q

what are the most important interventions in the long term care of DM

A

control blood pressure - use an ACE (reduces intraglomerular pressure)

vascular disease is the chief cause of death - use a statin for ALL

adress other risk factors eg diet

renal damage may be preventable with good BP and glycaemic control

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4
Q

pathophysiology

A

non-enzymatic glycolysation (glucose simply sticking to proteins in blood) of proteins leads to accumulation of AGE causing injury and inflammation via stimulation of proinflammatory factors

Poyol pathway

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5
Q

Poyol pathway

A
  • becomes active in raised intracellular glucose (nerves and blood vessels etc are insulin independent so cannot regulate glucose influx) as aldose reductase has a higher KM for glucose.
  • the metabolism of glucose by aldose reducatse leads to the accumulation of sorbitol and fructose
  • this causes disruption in structure and function of eg nerves
  • increase in total body Na which predisposes one to hypertension
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6
Q

neuropathy - pathophysiology

A

occlusion of the vasa nervorum (small arteries that provide blood supply to peripheral nerves)

hyperglycaemia (Poyol pathway) leads to increased formation of sorbitol and fructose in Schwann cells - accumulation of these disrupts function and structure

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7
Q

risk factors for neuropathy

A

increased length of diabetes

poor glycaemic control

type 1 (>type 2)

high cholesterol/lipids

smoking

alcohol

inherited traits

mechanical injury

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8
Q

functional and histological changes in nerves

A

delayed conduction velocity

segmental demyelination caused by damage to Schwann cells (due to accumulation of sorbitol and fructose (Poyol pathway))

  • in the early stages the axons are preserved (recovery?), but at a later stage irreversible axonal degeneration develops
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9
Q

symptoms of neuropathy

A

sensorimotor:

numbness/insensitivity

tingling/burning

sharp pains or cramps

sensitivity to touch

loss of balance and coordination

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10
Q

peripheral neuropathy

A
  • eg pain/loss of feeling in feet and hands
  • Commonly gives plantar ulcers
  • Often not noticed by patient in the early stages, early clinical signs are loss of vibration sense, temperature and pain sensation
  • At later stages patient can lose balance due to loss of proprioception
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11
Q

what can peripheral neuropathy lead to

A

interosseous muscle wasting

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12
Q

autonomic neuropathy

A

affects the nerves that regulate heart rate and blood pressure, as well as control of internal organs eg gastric motility, respiratory function, urination, sexual function and vision

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13
Q

autonomic neuropathy: digestive system

A
  • Gastric slowing/frequency and constipation/diarrhoea often accompanied by urgency and incontinence
  • Oesophagus nerve damage can make swallowing difficult
  • Can lead to weight loss
  • Vagal damage can lead to gastroparesis (slowing of stomach emptying) causes persistent nausea and vomiting, bloating and loss of appetite
    • This can make blood glucose levels fluctuate widely, due to abnormal food digestion
  • Diarrhoea and steatorrhoea may occur owing to small bowel bacterial overgrowth
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14
Q

treatment of gastroparesis

A
  • improved glycaemic control
  • dietary - small portions, low in fat and fibre (can lead to bezoar formation)
  • promotility drugs
  • anti nausea medications
  • botulinum toxin injection
  • gastric pacemaker
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15
Q

promotility drugs used in gastroparesis

A

metoclopramide, domperidone

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16
Q

anti nausea medications used in gastroparesis

A

prochlorperazine and serotonin antagonists (eg ondansetron)

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17
Q

abdominal pain treatment in gastroparesis

A

NSAIDs, low dose tricyclic antidepressants, gabapentin , tramadol

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18
Q

botulinum toxin injection

A

inhibits the release of ACh and causes transient paralysis when injected into gastric smooth muscle

19
Q

autonomic neuropathy: bladder

A
  • loss of tone, incomplete emptying and stasis predisposes one to infections
  • May ultimately result in atonic, painless and distended bladder
20
Q

autonomic neuropathy: sweat glands

A

nerves that control sweating are affected - body cannot regulate its temperature

can get profuse sweating at night and when eating - gustatory sweating

extremes of ani and hyper hidrosis occur

21
Q

treatment of excess sweating due to autonomic neuropathy

A

topical glycopyrrolate (decrease sweating - increase risk of heat related illness)

clonidine (decrease sweating)

botulinum toxin

22
Q

autonomic neuropathy: heart and blood vessels

A
  • Cardiovascular system nerve damage interferes with the body’s ability to adjust blood pressure and heart rate.
  • CV reflexes, e.g. Valsalva manoeuvre, are impaired
  • Blood pressure may drop sharply after sitting or standing, causing a person to feel light-headed or faint (postural hypotension) due to loss of sympathetic tone to peripheral arterioles
  • Vagal neuropathy results in tachycardia at rest and loss of sinus arrhythmia
  • Heart rate may stay high, instead of rising and falling in response to normal body functions and physical activity.
23
Q

proximal neuropathy

A

eg pain in the thighs, hips or buttocks leading to weakness in the legs

amyotrophy - painful wasting of the quadriceps and other pelvifemoral muscles

24
Q

who is proximal neuropathy more common in

A

elderly

25
Q

what is proximal neuropathy often associated with

A

marked weight loss

26
Q

focal neuropathy

A
  • E.g. mononeuritis and mononeuritis multiplex
  • Onset is typically abrupt and sometimes painful
  • Radiculopathy may occur
  • eg carpal tunnel, foot drop, bell’s palsy, cranial nerve palsy
  • eg inability to focus eye, double vision, aching behind eye
  • pain on outside of foot, pain in thigh, chest etc
27
Q

what is a classical sign of CNIII palsy in DM

A
  • A characteristic feature of CNIII palsy is that pupillary reflexes are retained owing to sparing of pupillomotor fibres
28
Q

foot screening tool

A

FRAME - e learning resource that helps to standardise diabetic foot screenings performed by heath care professionals

29
Q

diagnostic tools for neuropathy

A

nerve conduction studies/EMG (can determine type/extent of nerve damage and how well the muscles respond to electrical signals transmitted by nerves)

heart rate variability (show response to deep breathing and changes in BP and posture)

ultra sound (of bladder/UT eg to see if bladder empties completely after urination)

gastric emptying studies

30
Q

what does a foot examination entail

A
  • monofilament testing at 5 sites on each foot
  • palpation of pedal pulses
  • tuning fork
31
Q

charcot foot

A

complication that follows on from severe neuropathy

thought to be initiated by injury to the foot and increased mechanical stress on the foot, which patients with diminished sensation in the foot are prone to

injuries accumulate, and bone density is reduced and joints are destroyed

32
Q

what is found on examination of Charcots foot

A

gross deformity and insensate foot

33
Q

what is found on an X ray of Charcots foot

A

bag of bones appearance

34
Q

foot ulcer

A

typically a painless, punched out ulcer in an area of thick callus ± superadded infection

treatment by nursing, podiatry care, offload of pressure, wound care, debridement

35
Q

what type of trauma often occurs

A

painless

36
Q

what class of medications are used in the treatment of neuropathic pain

A

it is found that medications used to treat depression and epilepsy are far more effective than paracetamol/ibuprofen etc

37
Q

name some medications used to treat neuropathy

A

amitryptline, duloxetine, gabapentin, pregabalin

(combinations are not recommended, titrate up as needed)

38
Q

what is the choice of medications based on

A

patient preference and co-morbidities

39
Q

if there is localised neuropathic pain and the patient wishes to avoid/cannot tolerate oral treatments, what is the management

A

topical Capsaicin cream

40
Q

metoclopramide action

A
  • increases gastric peristalsis and lower oesophageal sphincter tone
  • blocks D2 receptors in CTZ in brain - anti emetic
    • crosses the BBB unlike domperidone
41
Q

erectile dysfunction

A
  • is common - occurs in half of all diabetic men, particuarly those over the age of 60
  • The first sign is incomplete erection which may in time progress to total failure
42
Q

contributing risk factors for erectile dysfunction

A
  • Chronic renal failure
  • Hepatic failure
  • Multiple sclerosis
  • Severe depression
  • Spinal cord injuries
  • Pelvic and urogenital surgery and radiation
  • Substance abuse
  • Alcohol
  • Smoking amplifies other risk factors
  • Medications (25% of all ED)
43
Q

which medications can cause ED

A
  • All capable
  • Commonly, thiazides and ß blockers.
  • Uncommonly, Ca2+ channel blockers, alpha-adrenergic blockers and ACE inhibitors.

RB Y2 Endocrine - 1 Diabetes (16 decks)

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