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GIT physiology > Complications of diabetes > Flashcards

Complications of diabetes Flashcards

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1
Q

Micro vascularisation complications (4)

A
  1. Ophthalmogical
  2. renal
  3. neurological
  4. lower extremity
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2
Q

Macro vascularisation complication

A

Cardiovascular

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3
Q

Acute complications of diabetes mellitus

A

Diabetic keto acidosis (type 1)

Nonketotic hyperosmolar syndrome (NKHS - type 2)

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4
Q

Chronic complications of diabetes mellitus

A

VASCULAR

  • Micro = nephropathy, retinopathy, neuropathy
  • Macro = cardiovascular, cerebrovascular, peripheral vascualr

NON - VASCULAR

  • Sexual dysfunction
  • Skin manifestation
  • Gum infection
  • Cataracts
  • Glaucoma
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5
Q

What are the 3 major mechanisms underlying the hyperglycemic damage in diabetes mellitus

A
  1. Protein glycosylation
  2. Up regulation of polyol pathway
  3. Dyslipidemia
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6
Q

Polyol pathway

A
  • Glucose entry into most cells of body is insulin dependent EXCEPT vascular endothelium in the retina, kidney, nervous system
  • Glucose in tissue can be metabolised to sorbitol
  • normal glucose => little glucose entering polyol pathway (aldose reductase has low affinity for glucose)
  • hyperglycemia => excess glucose enters the polyol pathway (excess sorbitol pathway)
  • Depletion of NADPH & nitric oxide in endothelial cells => increased oxidative stress - cell damage
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7
Q

Compound associated with 30% of Neural Tube Defects

A

Ionositol - diminished in excess sorbitol production

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8
Q

Link between type 2 diabetes mellitus and CVD

A

Increased risk of CVD with type 2 diabetes mellitus

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9
Q

Dyslipidemia - macrovascular disease: what does it cause

A

MACROVASCULAR ATHEROSCLEROSIS

  • Increased coronary, cerebral, peripheral artery diseases
  • Increased LDL and Triglycerides, decreased HDL
  • Reduced fibrinolytic activity

CONSEQUENCES OF ARTERIAL INSUFFICIENCY/OBSTRUCTION

  • MI
  • Stroke
  • Peripheral arterial disease (gangrene)

** SD LDL => upregulation of hepatic lipases - directly related to MIs and peripheral arterial diseases

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10
Q

Physiological consequences of protein glycosylation

A

PROLONGED HYPERGLYCEMIA

  • Covalent binding of glucose to various proteins
  • Advanced glycosylation end products
  • Hb (RBCs are freely permeable to glucose - O2 won’t bind to glycosylated Hb), collagen in BV wall & BVs become leaky

ALTERED PROTEIN FUNCTION

  • Altered charge - highly reactive - oxidative stress
  • Altered structure, resistant to proteolysis
  • Induction of cytokines, trap macromolecules (LDL etc)
  • Diabetic retinopathy, nephropathy, neuropathy
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11
Q

What happens in diabetic retinopathy

A

Vessel basement mebrane deterioration

Ischemia, microhemorrhages

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12
Q

What happens in diabetic nephropathy

A

Basement membrane thickening

Hyperfiltration, increase glomerular pressure

Progress microalbuminuria -> proteinuria, eventually end-stage renal disease

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13
Q

What is sensory neuropathy

A

Loss of sensation

Abnormal sensation

Pain in hands and/or feet

Can progress to partial or complete loss of sensitivity to touch and temp

High risk of injury without pain

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14
Q

Autonomic neuropathy

A

Regulates sweating and perfusion to the limb

Loss of autonomic control inhibits thermoregulatory function and sweating

Results in dry, scaly and stiff skin that is prone to cracking and allows a portal of entry for bacteria

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15
Q

Hyperosmotic Hyperglycemic Non-Ketotic Syndrome (HHNS)

  • Insulin
  • Hyperglycemia
A
  • Enough insulin to prevent ketosis but not enough to prevent hyperglycemia
  • Extreme hyperglycemia without acidosis
  • Poor glucose uptake and increase in hepatic glucose
  • Enough insulin to suppress ketone synthesis
  • Extreme hyperglycemia => severe electrolyte and fluid loss
  • Vascular collapse
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16
Q

Diabetic KetoAcidosis (DKA) of DM

  • Caused by
  • Effect on blood:
  • glucose
  • pH
  • bicarbonate
  • ketone conc
  • electrolytes
A
  • Complete lack of insulin - unrestrained lipolysis and ketone synthesis
  • Blood glucose > 250 mg/dL
  • Blood pH < 7.3
  • Blood bicarbonate < 15mEq/L
  • Ketones present in blood and urine - BETAHYDROXYBUTYRATE => increase in production of ROS and may lead to decreased egg survival (infertility)
  • Electrolyte abnormalities (Na, K, Cl, HCO3-)
17
Q

What happens in beta oxidation

A

Breakdown of FAs to provide energy

Acetyl CoA generated enters Krebs Cycle

18
Q

Impact of excess lipolysis (source of energy for diabetics) on beta oxidation

A

Vast amounts of beta oxidation in liver

  • Liver uses little Acetyl CoA
19
Q

Condensation of 2….

A

Acetyl CoA molecules

=> formation of acetoacetic acid - release of CoA

Exits hepatocytes easily

Enters tissues - reformed into Acetyl CoA

Used for energy

20
Q

What is acetoacetic acid converted to

A

Acetoacetic acid is converted to ketones

  • Beta-hydroxybutyric acid/acetone

Ketone levels in blood increase - tissue use limited // OXALOACETATE (this combines with Acetyl CoA in TCA Cycle but as diabetics can’t metabolise CHOs, limits acetyl CoA entry to krebs cycle)

Ketones build up

Severe acidosis with acetone breath

Decreases blood pH, HCO3-, Hb avidity for O2

Hypoxic coma &/or tachycardia

21
Q

Diagnostic criteria for diabetes and impaired glucose regulation

A
22
Q

Glucose tolerance test

A
23
Q

What is gestational diabetes

A

Form of glucose intolerance diagnosed in some women in pregnancy

(normal for a pregnant woman to become less sensitive to insulin)

Occurs more frequently among obese women and women with a family history of diabetes

Women have increased chance of having/developing type 2 diabetes

24
Q

7 secondary causes of diabetes mellitus

A
  1. Acromegaly
  2. Cushing syndrome
  3. Thyrotoxicosis
  4. Pheochromocytoma
  5. Chronic pancreatitis
  6. Cancer
  7. Drug induced hyperglycemia
25
Q

Beta blockers

A

Inhibit insulin secretion

26
Q

Calcium channel blockers

A

Inhibit secretion of insulin

27
Q

Corticosteroids

A

Cause peripheral insulin resistance and gluconeogenesis

28
Q

Protease inhibitors

A

Inhibit the conversion of proinsulin -> insulin

29
Q

Thiazide diuretics

A

Inhibit insulin secretion due to hypokalemia

Also cause increased insulin resistance due to increase FFA mobilisation

GIT physiology (11 decks)

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