Diabetes Flashcards
Fatigue, micro & macro vascular complications and autonomic neuropathy are indications of?
Hyper-glycaemia
What is the fuel for CNS?
Glucose
What is the prevalence rate of diabetes mellitus?
7.4%
High blood sugar’s affect on the pancreas
Release of beta cells (insulin)
Three cardinal signs of diabetes mellitus
Polyuria
Polydipsia
Polyphagia
Gold standard in measuring insulin sensitivity and glucose metabolisation
Euglycemic clamp
Two types of euglycemic clamps
Hyperglycemic clamp
Hyperinsulinemic clamp
HOMA-IR
Homeostatic model assessment-insulin resistance
Diabetes mellitus has a fasting plasma glucose concentration of
Greater than 7
A 2h post glucose load plasma glucose concentration of someone with pre-diabetes
> 7.8-<11.1
IGT
Impaired glucose tolerance
7.8-11.1 PGC
IFG
Impaired fasting glycaemia
Impaired fasting glycaemia plasma glucose concentration
> 6.1-<7
Diabetic autonomic neuropathy
Stealthy complication (maybe 100%) Decreased sensation and decrease functions
Upstroke represents diastole or systole?
Systole
Polydipsia
Excessive Thirst
Polyuria
Excessive urination
Sudomotor dysfunction
Affects the activity of the sweat glands & often manifests as anhidrosis of the extremities
‘Head rush’ due to blood pressure falls suddenly as a result of standing up quickly
Orthostatic hypotension
Mechanism of atherosclerosis
LDL build up Plaque Decreased BF Rupture Thrombus Blocked flow Tissue ischemia Myocardial infarction
Intimal thickening is caused by
Smooth muscle cell proliferation
At herons or plaque formation
Intimal thickening & lipid accumulation
Fatty streak
Excess LDL accumulates between the endothelium and connective tissue.
There it is oxidised and phagocytosed.
Macrophages produce paracrines that attract smooth muscle cells.
Normal cell wall consists of
Smooth muscle and connective tissue with an endothelial cell lining
Stable plaque/ fibrous plaque
A fibrous scar forms around the cholesterol build up, migrating smooth muscle cells divide, thickening the arterial wall and narrowing the lumen of the artery.
Vulnerable plaque/thrombus
Calcified scar tissue will form, if the endothelium is damaged and collagen is exposed, platelets stick to the damaged area and a thrombus forms
Atherosclerosis Stage I
Monocytes adhesion/migration
Atherosclerosis mechanism Stage II
Foam cells in intima
Foam cells
Lipid containing macrophages
Atherosclerosis stage III
Appearance of extra cellular lipid
Atherosclerosis stage IV
Core formation
Atherosclerosis stage VI
Thrombosis
Atherosclerosis stage V
Fibrous cap and core formation
Extra cellular lipid coalescing into the centre of the plaque
Core formation in stage IV of the development of atherosclerosis
Fully formed lipid core and and well developed cap of fibrous tissue separating the core from the lumen
Stage V of the atherosclerosis development of a fibrous cap and core
Glycosylation of the plantar fascia
Stiffer tissues = reduced shock absorption
Hypothesis to cause pes cavus foot type
Pes cavus foot type
Increased forefoot & rearfoot plantar pressures
Unperceived injury, breakdown & infection –> ulceration can result from
Sensory neuropathy
Key diabetic changes to gait
Reduced heel contact phase
Preventing complications
Prevent hyperglycaemia
Prevent neuropathy & PAD
Prophylactic Intervention
Prophylactic intervention
- diabetes education
- footwear
- podiatrist assessments
- plantar pressure reduction
Non enzymatic glucosylation
Proteins combine with free glucose & form ketoamines
Ketoamines form AGES - haphazard process that impairs the function of biomolecules
Causes a decrease on nerve function as atonal transport is disrupted and myelin sheaths damaged - changes to the collagen fibres
What happens to the proteins in non enzymatic glucosylation
They combine with free glucose and form ketoamines
What are AGEs
Advanced glycated end products
Byproduct of the ketoamines formed when the proteins and free glucose combine
Changes in the cross linkage of the collagen fibres has what effect of the nerve
Disrupted axonal transport and damaged myelin sheaths
- decrease in nerve function
The biomechanics of the diabetic foot have one common denominator which is
Increased plantar pressure
Soft tissue alterations
Glucosylation of tissues Limited joint mobility Changes to foot architecture Changes to skin and soft tissue (Distal) migration of tissue This tissue
Limited joint mobility affects gait?
Reducedpnility of joints reduces shock absorbing capacity and so increases plantar pressures
Aldose reductase
Converts glucose into sorbitol
Poly sorbitol pathway
Sorbitol is accumulated in neurons and supporting tissue
Osmotic effect -> H2O moves into the neural tissue
Neural and peri neural oedema
Demyelination of the Schwann cell
Thickening of the basement membrane
Result of osmotic stress due to sorbitol accumulation in cells
Highest plantar pressure areas in a diabetic foot
Lateral forefoot
Diabetes mellitus
Is a metabolic disease in which there is chronic hyperglycaemia
T2DM
Pancreas can’t make enough insulin OR insulin is not affective
T1DM
Pancreas does not make insulin
Charcot neuropathy
Neurogenic athroropathy aka neuroarthropathy
Rapidly progressive non infectious degenerative arthritis affecting single/multiple joints
CN
Charcot neuroarthropathy
Four probable pathogenesis of CN
Peripheral neuropathy
Unrecognised injury
Continued repetitive stress on injured structures
Increased local BF
DDx Charcot foot
DVT
Osteomyelitis
How do you differentiate DVT from Charcot?
Doppler
How do you differentiate osteomyelitis from Charcot?
Bone probe
What is the BMI of an obese individual
> 30.0
What is the BMI of a overweight individual?
25.0- 30.0
What grade is the diabetic risk category assessment for a minimal pathology?
Grade 1
What grade is the diabetic foot risk category assessment for insensate with deformity?
Grade 2
What grade is the diabetic foot risk category assessment for - demonstrated pathology
Grade 3
What grade is the diabetic foot risk category assessment for - neuropathic ulceration
Grade 4a
What grade is the diabetic foot risk category assessment for - acute chariot joint deformity
Grade 4b
What grade is the diabetic foot risk category assessment for - infected diabetic foot?
Grade 5
What grade is the diabetic foot risk category assessment for - days vascular foot
Grade 6
Chelation therapy
Mobilisation of calcium within atherosclerotic lesion (?lesion regression)
Side effects hypoglycaemia & renal failure
CN 4 factors
Peripheral neuropathy
Increased trauma
Increased bf
Unrecognised injury
Ineffective agents in IC treatment
Purely vasodilators
Treatment for osteomyelitis
Long course of antibiotics
8 weeks of ciprocloxacin
What is Slough
Glutinous yellow covering comprised of fibrin, deoxyribonucleo-protein, serous exudate, leukocytes and bacteria. It may build up rapidly on the surface of a previously clean wound and predispose a wound to infection
What nutritional components are necessary for wound healing
Carbs, vitamins and proteins
Nitric oxide is a vasodilator or vasoconstrictor?
Potent vasodilator
Tulle e.g
Shallow flat wound
Jelonet
Paranet
Semipermeable film
shallow wound with low/minimum exudate
Onsite tegaderm
Hydrocolloids
Light to heavy exudate, sloughing or granulating wounds
DuoDERM, tegasorb
Hydrogel a
Necrotic or sloughy wound beds
Regardless, intrasite
Alginates
Exudating & sloughy wounds
E.g kaltostat, sorbsan
Foam
Absorb and protect (do not out on dry wound)
Allevyn, lyofoam, biatain
Hydro fibre
Deep wound with heavy level of drainage
Antimicrobial
Reduce bacterial load to improve healing
Silver, iodine
