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Treatment and Prevention of illness > Causes and Complications of Diabetes > Flashcards

Causes and Complications of Diabetes Flashcards

1
Q

What is Diabetes?

A
  • Metabolic disease - raised plasma glucose levels
  • Caused by failure of insulin- regulation of metabolism
  • Hyperglycemia causes microvascular and macrovascular complications
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2
Q

How does hyperglycemia cause diabetic complications?

A
  • Microvascular complications caused by hyperglycemia
  • Damage to endothelial lining of small blood vessels
  • Macrovascular complications increased free fatty acids
  • Plaque deposition in arterial walls
  • Increased FAOx -> oxidative stress?
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3
Q

Macrovascular complications

A
  • Diabetes an independent risk factor for
  • coronary artery disease,
  • cerebrovascular disease,
  • peripheral vascular disease. eg deep vein thrombosis
  • Often comorbid for other risk factors, including:
  • obesity,
  • hypertension,
  • hyperlipidemia,
  • altered platelet function.
  • Type 2 diabetes - macrovascular disease often present at diagnosis.
  • Type 1 diabetes - age and duration of diabetes correlate with degree of macrovascular disease
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4
Q

Implications for treatment

A
  • Most treatments target hyperglycemia
  • Clear benefits of tight glycemic control for microvascular complications
  • DM clear risk-factor for macrovascular disease
  • Macrovascular benefits of glycemic control less clear
  • Important to treat co-morbities
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5
Q

Insulin Dependent Diabetes Mellitus

A
  • Type 1 Diabetes Juvenile-onset diabetes
  • defect: Autoimmune destruction of β-cells
  • age of onset: 1-25 Years
  • physique: lean
  • prevalence - 0.5%
  • treatment: insulin
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6
Q

Non-Insulin Dependent Diabetes Mellitus

A
  • Type 2 Diabetes Late-onset diabetes
  • defect: insulin resistance Defective insulin secretion,
  • age of onset: >40 Years (but getting younger)
  • physique: obese
  • prevalence - >2%
  • treatment: Diet, drugs, insulin
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7
Q

Type I diabetes is an autoimmune disease

A
  • Antibody-mediated immune destruction of beta cells
  • Insulin-secreting cells in islets of Langerhans
  • Progressive loss (months to years)
  • Usually during adolescence
  • Marked hyperglycaemia seen when 80-90% of beta cells lost
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8
Q

Geographic and seasonal variations suggest environmental factors

A
  • Candidates include:
  • Viruses (incl. mumps, Coxsackie B4, retroviruses, rubella)
  • Specific drugs or chemicals (dietary nitrosamines (found in smoked and cured meats) and coffee)
  • Dietary constituents (cow’s milk in infancy)
  • Reduced exposure to microorganisms in early childhood (hygiene hypothesis)
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9
Q

Major complications of Type I diabetes

A
  • Chronic effects of hyperglycemia
  • Hypoglycemia
  • Due to overadministration of insulin
  • Diabetic ketoacidosis
  • generation of ketone bodies exceeds metabolism
  • Latter both potentially fatal
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10
Q

Diabetic Ketoacidosis

A
  • fatty acids are converted to ketone bodies in the liver
    • Uncontrolled lipolysis & β-oxidation -> over- production of ketone bodies
    • Ketone bodies are strong acids -> overwhelms the buffering capacity of the body -> acidosis -> coma & death
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11
Q

What Causes Type II diabetes?

A
  • Inability of insulin to exert effects on liver & adipose
  • Insulin resistance
  • Secondary “islet exhaustion”
  • Hyperglycemia & high FFA
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12
Q

What causes insulin resistance?

A
  • Strong genetic component
  • Identical twins >90% concordant
  • Indigenous populations
  • Environment Important
  • Increased incidence over last century
  • Genotype clearly hasn’t changed!!
  • What’s changed?
  • Lifestyle, exercise, habits,
  • Most commonly associated with obesity (>80% of cases)
  • DIET!
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13
Q

What causes insulin resistance?

A

• Ectopic lipid accumulation
• Liver and muscle triglyceride “ insulin sensitivity
• Accumulation of lipid mediators (diacylglycerol & ceramide) may alter protein phosphorylation
• Cellularstress-responses
• Mitochondrial and protein-production machinery
breaks down
• Alters insulin signaling pathways
• Likely downstream of ectopic lipid accumulation
• Inflammation
• Macrophages in adipose tissue accumulate lipid
• ->secretion of inflammatory cytokines (TNFα)
• Alters insulin signalling pathways in muscle & liver
• Ectopic lipid accumulation underlies Insulin resistance
• Driven by over consumption of nutrients
• Fat-storage capacity of adipose tissue overwhelmed

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14
Q

Complications Due To Diabetes

A
  • Microvascular damage leads to:
  • Retina (diabetic retinopathy): leading, ultimately, to blindness
  • Kidney (niabetic nephropathy): leading to end stage renal failure
  • Nerves (diabetic neuropathy): leading to debilitating neuropathy
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15
Q

Peripheral neuropathies Caused by

A
  • Endothelial damage !wall thickening -> ischemia & neural death
  • Segmental demyelinization & slowing of nerve conduction.
  • The clinical manifestations vary with the location of the lesion.
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16
Q

Diabetic Peripheral Neuropathies

A

Somatic: (sensory and motor nerves
• Paresthesias, including numbness and tingling
• Impaired pain, temperature, light touch, two- point discrimination, and vibratory sensation

Autonomic:
• Vasomotor function - Postural hypotension
• Gastrointestinal function - Gastric atony, postprandial and nocturnal Diarrhoea,
• Genitourinary function - Paralytic bladder/ Incomplete voiding; Impotence
• Cranial nerve - Impaired pupillary responses

17
Q

Diabetic foot ulcers

A

• Foot problems are common
• ulceration and infection, even amputation.
• Impaired pain sensation
• often unaware of poorly fitting shoes, improper weight
bearing or infections.
• Motor neuropathy may result in foot deformities
• -> focal areas of high pressure.
• Common sites of trauma
• back of the heel, plantar metatarsal area, or the great toe

18
Q

Diabetic nephropathy

A
  • Diabetic nephropathy is the leading cause of end-stage renal disease,
  • 40% of new cases.
  • Among the suggested risk factors for diabetic nephropathy are:
  • Genetic and familial predisposition
  • Elevated blood pressure
  • Poor glycemic control
  • Smoking
  • Hyperlipidemia
  • Microalbuminuria
  • Diabetic nephropathy is an independent risk factor for cardiovascular events
  • Hence albumin urea closely monitored in type II diabetic patients
19
Q

Diabetic nephropathy - Pathogenesis

A
  • Hyperglycemia -> Transforming growth factor-beta (TGF-beta) in the glomeruli.
  • cellular hypertrophy and enhanced collagen synthesis
  • Patients with overt diabetic nephropathy (dipstick- positive proteinuria and decreasing GFR) generally develop hypertension.
  • adverse factor in all progressive renal diseases
  • Familial/genetic factors.
  • African Americans, persons of Hispanic origin,and American Indians disposed to diabetic renal complications.
20
Q

Retinopathies

A

• Diabetes -> increased risk of glaucoma and retinopathy
cataracts,
• retinopathy is the most common eye disease.
• Risk factors include
• poor glycemic control,
• elevated blood pressure,
• hyperlipidemia.
• Important that people with diabetes have regular eye examinations.
• Macular edema
• damaged blood vessels leak fluid under the macula, the part of the retina that lets us see detail.
• The fluid makes the macula swell, which blurs vision.

21
Q

Diabetic Retinopathy - Pathogenesis

A
  • Microvascular retinal changes.
  • Endothelial change ! of the vascular walls
  • Microaneurysms
  • Ischemia
  • Microaneurysms ! burst
  • Scarring, damage to cellular environment
  • Macular oedema - fluid under the macula makes it swell -> blurred vision
  • Ischemia !fragile,new,bloodvessels.
  • More prone to aneurysms & bursting
  • grow into the angle of the anterior chamber and cause neovascular glaucoma.
22
Q

Summary

A
  • Diabetic metabolism alters structure and function of vasculature
  • Microvascular changes cause damage to many peripheral tissues increasing morbidity and mortality of diabetic patients
  • Macrovascular damage causes increased risk of cardiovascular disease and mortality
  • Majority of treatments address hyperglycaemia

Treatment and Prevention of illness (32 decks)

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