Diabetes Flashcards

0
Q

Fatigue, micro & macro vascular complications and autonomic neuropathy are indications of?

A

Hyper-glycaemia

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1
Q

What is the fuel for CNS?

A

Glucose

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2
Q

What is the prevalence rate of diabetes mellitus?

A

7.4%

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3
Q

High blood sugar’s affect on the pancreas

A

Release of beta cells (insulin)

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4
Q

Three cardinal signs of diabetes mellitus

A

Polyuria
Polydipsia
Polyphagia

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5
Q

Gold standard in measuring insulin sensitivity and glucose metabolisation

A

Euglycemic clamp

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6
Q

Two types of euglycemic clamps

A

Hyperglycemic clamp

Hyperinsulinemic clamp

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7
Q

HOMA-IR

A

Homeostatic model assessment-insulin resistance

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8
Q

Diabetes mellitus has a fasting plasma glucose concentration of

A

Greater than 7

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9
Q

A 2h post glucose load plasma glucose concentration of someone with pre-diabetes

A

> 7.8-<11.1

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10
Q

IGT

A

Impaired glucose tolerance

7.8-11.1 PGC

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11
Q

IFG

A

Impaired fasting glycaemia

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12
Q

Impaired fasting glycaemia plasma glucose concentration

A

> 6.1-<7

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13
Q

Diabetic autonomic neuropathy

A
Stealthy complication (maybe 100%)
Decreased sensation and decrease functions
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14
Q

Upstroke represents diastole or systole?

A

Systole

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15
Q

Polydipsia

A

Excessive Thirst

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16
Q

Polyuria

A

Excessive urination

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17
Q

Sudomotor dysfunction

A

Affects the activity of the sweat glands & often manifests as anhidrosis of the extremities

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18
Q

‘Head rush’ due to blood pressure falls suddenly as a result of standing up quickly

A

Orthostatic hypotension

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19
Q

Mechanism of atherosclerosis

A
LDL build up
Plaque
Decreased BF
Rupture
Thrombus
Blocked flow
Tissue ischemia
Myocardial infarction
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20
Q

Intimal thickening is caused by

A

Smooth muscle cell proliferation

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21
Q

At herons or plaque formation

A

Intimal thickening & lipid accumulation

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22
Q

Fatty streak

A

Excess LDL accumulates between the endothelium and connective tissue.
There it is oxidised and phagocytosed.
Macrophages produce paracrines that attract smooth muscle cells.

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23
Q

Normal cell wall consists of

A

Smooth muscle and connective tissue with an endothelial cell lining

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24
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.
25
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
26
Atherosclerosis Stage I
Monocytes adhesion/migration
27
Atherosclerosis mechanism Stage II
Foam cells in intima
28
Foam cells
Lipid containing macrophages
29
Atherosclerosis stage III
Appearance of extra cellular lipid
30
Atherosclerosis stage IV
Core formation
31
Atherosclerosis stage VI
Thrombosis
32
Atherosclerosis stage V
Fibrous cap and core formation
33
Extra cellular lipid coalescing into the centre of the plaque
Core formation in stage IV of the development of atherosclerosis
34
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
35
Glycosylation of the plantar fascia
Stiffer tissues = reduced shock absorption | Hypothesis to cause pes cavus foot type
36
Pes cavus foot type
Increased forefoot & rearfoot plantar pressures
37
Unperceived injury, breakdown & infection --> ulceration can result from
Sensory neuropathy
38
Key diabetic changes to gait
Reduced heel contact phase
39
Preventing complications
Prevent hyperglycaemia Prevent neuropathy & PAD Prophylactic Intervention
40
Prophylactic intervention
- diabetes education - footwear - podiatrist assessments - plantar pressure reduction
41
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
42
What happens to the proteins in non enzymatic glucosylation
They combine with free glucose and form ketoamines
43
What are AGEs
Advanced glycated end products | Byproduct of the ketoamines formed when the proteins and free glucose combine
44
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
45
The biomechanics of the diabetic foot have one common denominator which is
Increased plantar pressure
46
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 ```
47
Limited joint mobility affects gait?
Reducedpnility of joints reduces shock absorbing capacity and so increases plantar pressures
48
Aldose reductase
Converts glucose into sorbitol
49
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
50
Thickening of the basement membrane
Result of osmotic stress due to sorbitol accumulation in cells
51
Highest plantar pressure areas in a diabetic foot
Lateral forefoot
52
Diabetes mellitus
Is a metabolic disease in which there is chronic hyperglycaemia
53
T2DM
Pancreas can't make enough insulin OR insulin is not affective
54
T1DM
Pancreas does not make insulin
55
Charcot neuropathy
Neurogenic athroropathy aka neuroarthropathy Rapidly progressive non infectious degenerative arthritis affecting single/multiple joints
56
CN
Charcot neuroarthropathy
57
Four probable pathogenesis of CN
Peripheral neuropathy Unrecognised injury Continued repetitive stress on injured structures Increased local BF
67
DDx Charcot foot
DVT | Osteomyelitis
68
How do you differentiate DVT from Charcot?
Doppler
69
How do you differentiate osteomyelitis from Charcot?
Bone probe
84
What is the BMI of an obese individual
> 30.0
85
What is the BMI of a overweight individual?
25.0- 30.0
86
What grade is the diabetic risk category assessment for a minimal pathology?
Grade 1
87
What grade is the diabetic foot risk category assessment for insensate with deformity?
Grade 2
88
What grade is the diabetic foot risk category assessment for - demonstrated pathology
Grade 3
89
What grade is the diabetic foot risk category assessment for - neuropathic ulceration
Grade 4a
90
What grade is the diabetic foot risk category assessment for - acute chariot joint deformity
Grade 4b
91
What grade is the diabetic foot risk category assessment for - infected diabetic foot?
Grade 5
92
What grade is the diabetic foot risk category assessment for - days vascular foot
Grade 6
93
Chelation therapy
Mobilisation of calcium within atherosclerotic lesion (?lesion regression) Side effects hypoglycaemia & renal failure
94
CN 4 factors
Peripheral neuropathy Increased trauma Increased bf Unrecognised injury
95
Ineffective agents in IC treatment
Purely vasodilators
96
Treatment for osteomyelitis
Long course of antibiotics | 8 weeks of ciprocloxacin
97
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
98
What nutritional components are necessary for wound healing
Carbs, vitamins and proteins
99
Nitric oxide is a vasodilator or vasoconstrictor?
Potent vasodilator
100
Tulle e.g
Shallow flat wound Jelonet Paranet
101
Semipermeable film
shallow wound with low/minimum exudate | Onsite tegaderm
102
Hydrocolloids
Light to heavy exudate, sloughing or granulating wounds | DuoDERM, tegasorb
103
Hydrogel a
Necrotic or sloughy wound beds | Regardless, intrasite
104
Alginates
Exudating & sloughy wounds | E.g kaltostat, sorbsan
105
Foam
Absorb and protect (do not out on dry wound) | Allevyn, lyofoam, biatain
106
Hydro fibre
Deep wound with heavy level of drainage
107
Antimicrobial
Reduce bacterial load to improve healing | Silver, iodine