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Diabetes Mellitus - Coggle Diagram
Diabetes Mellitus
Type 2 DM
85% of diabetic pt
- lifestyle/environment
- deficient/defective insulin
- preventable
- Insulin resistance &/or insulin deficiency
- lifestyle/environment combined with genetics
- not autoimmune
Genetic factors - not linked to same markers as type 1 DMGlucose cannot enter if cells are not responding to insulin
Insulin resistance:
decreased ability of peripheral tissues to respond to insulin
- loss of insulin post-receptor signalling
- down regulation of insulin receptors
obesity inhibits insulin signalling
- free fatty acids
- cytokines from fat cells
Insulin deficiency:
- b cell dysfunction
- inadequate insulin secretion
- inadequate glucose uptake into cells
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TREATMENT:
- diet/ exercise
- oral hypoglycaemic agents:
- stimulate insulin release/decrease insulin resistance
- alter carbs absorption &in reduce glucose load
Glucose uptake
- After eating = increased BGLs trigger B cells to release insulin
1st phase (within 2mins - lasts 10-15mins)
2nd phase (lasts until BGL's back to normal)
Insulin binds to insulin receptors on target cells
- causes glucose transport units (GLUTs) to move to cell membrane from inside target cells
- liver (GLUT 2), muscle (GLUT 4) and fat (GLUT 4) cells
- neural cells (GLUT 3) - don't require insulin
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If not enough glucose/insulin receptor/insulin signal pathway does not work we don't get glucose entering the cell
Type 1 DM
- 15% of pts
- autoimmune disease (destruction of pancreatic b cells) - spontaneous or triggered, T cells destroy B cells
- absolute lack of insulin - immune mediated or idiopathic
- not preventable
- genetic susceptibility - protein markers ob B cells
- glucose cannot enter cell
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TREATMENT: INSULIN
- Increases glucose uptake by body cells (decreased BGL)
- decreases blood amino acids, free fatty acids and ketones
- different formulations (ultra short, short, long-acting)
Amputation/Diabetes
PVD is the most cpmmon cause of lower extremity amputation - where re-vascularisation is no longer possible
atherosclerosis & DM are leading causes of PVD:
- leads to impaired circulation, (particularly in the lower extremities)
- healing impaired > persistent infections > gangrene
The area/extent of irreparable tissue damage, necrosis, infection, tumor/trauma will determine the level of amputation
A soft tissue envelope provides an interface between the remaining limb & prothesis & is required to effectively transfer weightkeeping the knee joint intact improves a person ability to balance and move up & down while wearing prothesis -BGL's are controlled by:
- insulin - released from pancreatic b cells: decreased BGL
- glucagon - released from pancreatic a cells: increase BGL
Consequences of DM
Clinical manifestations:
- increased thirst (polydipsia), urination (polyuria), hunger, (polyhagia)
Uncontrolled hyperglycaemia
- acute:
- diabetic ketoacidosis (Type 1DM)
- non-ketotic hyperosmolar coma (Type 2 DM)
- Chronic
- vascular complications
- neuropathies
Chronic hyperglycaemia:
- long term poor glucose control
- Macrovascular
- damage to large blood vessels of brain, heart, extremities
- CVD and stroke
- Peripheral vascular disease
- Microvascular
- abnormal thickening of basement membrane of capillaries
- retinopathy (eyes)
- nephropathy (kidneys)
- neuropathy
- Diabetic neuropathy
Diabetic neuropathy
Peripheral neuropathy:
- damage to peripheral nerves due to long term hyperglycaemia
- loss of feeling in hands and feet
- decrease pain signalling & awareness
- Largely responsible for serious foot problems - loss of sensation in feet
- Usually seen with concomitant peripheral vascular disease:
- decrease blood flow
- poor healing
- decrease immune response
Diabetic foot: umbrella term for foot problems in diabetics
Peripheral vascular disease/diabetic neuropathy
- loss of sensation
- impaired wound healing in extremities
- infection and gangrene
Diabetic foot ulcers: 10-15% of diabetic pts develop foot ulcers
- Foot related problems responsible for 50% of diabetes related hospital admissions
- almost half of all amputations caused by neuropathy and circulatory problems could be prevented.
Causes: peripheral neuropathy, deformity, callus, shoes, trauma, pressure
Risk factors of Ulceration:
- uncontrolled hyperglycemia
- duration of diabetes
- peripheral vascular disease
- blindness/visual loss
- chronic renal disease
- age
Local issues:
- peripheral neuropathy
- structural foot deformity
- trauma/improperly fitted shoes
- callus
- history of prior ulcer amputation
- prolonged elevated pressures
- limited joint mobility
Insulin
A hormone that allows the transport of glucose into cells, thus lowering the blood glucose level
synthesis: b cells of the islets of langerhans in pancreas
storage and release:
- packaged into granules within b cells
- released triggered by increased BGLs
- biphasic release > 1st and 2nd phase release (10/15mins after 1st phase) and continues to BGLs returns to noraml
Is released from the pancreases.
Exocrine (99%) and endocrine (1%) functions
- b cells synthesis & secrete insulin = decrease in BGL
- a cells synthesis & secrete glucagon = increase BGL
Gestational diabetes
- glucose intolerance - appears in pregnancy
- 1-14% of pregnant women
- resembles type 2 DM
- hormones/weight gain
- usually resolves after birth
Other specific types:
- Pre-diabetes
- metabolic syndrome
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- 381 million worldwide
- prevalence expected to double by 2030
- Indigenous 4 x greater prevalence
- close to 10% of adult pop world-wide
- 5.4% of all deaths in Aus
- blindness, kidney failure, amputation
- 5-=80 % deaths due to CVD related to DM
- Type 2 DM more common (9-% of cases worldwide
- many cases of type 2 DM can be prevented
- 8th leading cause of death
- chronic disorder of carbs, fat and protein metabolism due to defective/deficient insulin.
- Glucose - carb used to make ATP
- Hyperglycaemia
- high blood glucose level
- inability of cells to take to take in glucose from the blood due to a lack of or defect in the hormone of insulin
- normal blood glucose levels (fasting) > 4-6 mmol/L
- Fasting blood glucose > 7.8mmol/L
- 2h post glucose ingestion > 11.1 mmol/L
Regulation of glucose metabolism
- we eat food > carbs (glucose), fat, protein
- glucose supplied to bloodstream
- glucose transported from blood to cells using INSULIN
- Glucose used by cells to make ATP (glycolysis)
Leading cause of lower extremity amputation:
- can damage nerves/cause neuropathy, impair circulation due to high blood glucose levels
- loss of sensation, impaired wound healing, infection = amputation
- maintain normal blood glucose levels/regular check-up & maintain the condition of the extremities, especially feet