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pathophysiology 4802 > Diabetes Mellitus > Flashcards

Diabetes Mellitus Flashcards

1
Q

this defines a group of metabolic disorders that share the phenotype of hyperglycaemia that affects multiple organ systems.

A

diabetes mellitus

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2
Q

what are the 3 factors that contribute to hyperglycaemia

A
  • reduced insulin secretion
  • decreased glucose utilization
  • increased glucose production
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3
Q

what are some consequences of DM

A
  • end stage renal disease
  • non traumatic lower extremity amputations
  • adult blindness
  • CVD
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4
Q

what are the two types of DM

A

Type 1 -> autoimmune
type 2 -> insulin resistant/insulin secretion impaired

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5
Q

true or false: type 1 DM is “reversible”

A

false

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6
Q

true or false: type 2 DM is “reversible”

A

true

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7
Q

true or false: gestational DM is “reversible”

A

true

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8
Q

what is a normal fasting plasma glucose level

A

<5.6 mmol/L

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9
Q

what is a fasting plasma glucose level in someone who has DM

A

> 7.0 mol/L

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10
Q

what is considered an impaired plasma glucose level

A

6.1-6.9mmol/L

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11
Q

what is a normal hemoglobin A1C

A

<5.7%

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12
Q

what is an impaired hemoglobin A1C

A

5.7-6.4%

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13
Q

what is a hemoglobin A1C in someone with DM

A

> 6.5%

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14
Q

widespread use of FPG or HbA1c is recommended due to asymptomatic cases, complications etc. what characteristics of an individual would lead to testing

A

recommended for all individuals age > 45 every three years or earlier if a BMI >25 or ethnically relevant definition for overweight

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15
Q

what is the function of the LIVER in glucose homeostasis

A

glucose production and storage

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16
Q

what is the function of the MUSCLE and FAT tissue in glucose homeostasis

A

glucose utilization

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17
Q

what is the function of the PANCREATIC ISLET in glucose homeostasis

A

releases hormones that helps with utilization and production of glucose

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18
Q

ingestion of nutrients stimulates cells in the gut to release these two incretins

A

glucose-dependant insulinotropic peptide (GIP) and glucagon-like peptide (GLP-1)

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19
Q

what are the functions of GIP and GLP-1

A
  • stimulate the production of insulin and inhibit glucagon
  • promote proliferation of beta-cells and inhibit apoptosis
  • GLP-1 delays gastric emptying and increases satiety
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20
Q

what happens when the pancreas becomes aware that blood glucose levels are decreased

A
  • pancreas decreases insulin and increases glucagon
  • the liver and the kidney contribute to increased glucose production
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21
Q

what happens when the brain becomes aware that blood glucose levels are decreased

A
  • increased sympathoadrenal outflow which increases release of catecholamines (epi, NE, acetylcholine)
  • this can either cause symptoms which in turn results in ingestion or
  • signals to the kidneys and liver to make more glucose
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22
Q

what are some clinical manifestations of hyPOglycemia

A
  • confusion, fatigue, loss of conciousness
  • palpitations, tremor
  • sweating, hunger, pallor
  • BP usually elevated
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23
Q

this activates pro-inflammatory, pro-coagulant and pro-atherothrombotic responses in T1DM, T2DM and non-diabetic individuals. results in:
- increased platelet aggregation
- increased intravascular coagulation
- decreases arterial vasodilator mechanisms

A

hypoglycaemia

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24
Q

this has an attenuated sympathoadrenal response, impaired counter regulatory effect, six times the risk of severe iatrogenic hypoglycaemia and it is reversible

A

hypoglycaemia unawareness HAAF (hypoglycaemia associated autonomic failure)

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25
Q

____ is secreted in the pancreas by the beta cells of the islets of langerhans

A

insulin

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26
Q

the two insulin chains are synthesized as a single high moclular weight precursor called _________

A

preproinsulin

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27
Q

proinsulin is cleaved to form _______ and _______ in the secretory granule cells of there beta-cell

A

insulin and C-peptide

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28
Q

how is insulin secreted from the beta cells

A

glucose enters the beta cells by GLUT -> glucose in transformed into glucose-6-phospohate but glucokinase and then into pyruvate -> ATP/ADP is produced from the mitochondria -> ATP sensitive K+ channel is activated and K+ is released -> depolarization occurs and Ca2+ enters the beta cell -> increase cAMP levels -> stimulates exocytosis of secretory granules from the beta cell -> insulin is released

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29
Q

mutations in what proteins may cause monogenic forms of diabetes (e.g. neonatal DM, maturity-onset diabetes of the young)

A
  • GLUT
  • Mitochondria
  • ATP sensitive K+ channel
  • Islet transcription factors
  • Glucokinase
30
Q

explain the insulin receptor and its action

A
  • alpha subunit (hormone binding domains) are located extracellular
  • beta subunit is intracellular
  • when insulin binds to the receptor it stimulates intrinsic tyrosine kinase activity
  • receptor autophosphorylation occurs
  • activation of PI-3 kinase
  • translocation of GLUT-4 to the cell surface
  • glucose uptake ip skeletal muscle and fat
31
Q

true or false: insulin promotes catabolic effects

A

false - anabolic

32
Q

what effects does insulin have regarding carbohydrates (in muscles, adipose tissue and liver)

A
  • increases glucose uptake, oxidation and storage (increased glycogen synthesis, decreased glycogenolysis)
  • decreased gluconeogenesis
33
Q

what effects does insulin have regarding AAs and proteins (in muscles)

A
  • increase amino acid uptake and protein synthesis
  • decrease amino acid release
34
Q

what effects does insulin have regarding lipids (adipose tissue and liver)

A
  • increased triglyceride synthesis
  • decreased free fatty acids and glycerol
  • decreased oxidation of FFA to ketoacids (liver)
35
Q

this is the result of autoimmunity against the pancreatic beta cells; consequence is complete or near-total insulin deficiency

A

type 1 DM

36
Q

are islet cell autoantibodies more present in type 1 or type 2 DM

A

type 1

37
Q

what are some causes of type 1 DM

A
  • genetics: class II MHC genes involved (e.g. DQA10301, DWB10302 and DQB1*0201 have a strong risk)
  • environmental: molecular mimicry, vitamin D def., microbiome
38
Q

interactions of genetic, environmental and immunologic factors lead to immune-mediated destruction of the pancreatic beta cells and insulin ________

A

deficiency

39
Q

type 1 DM can develop at any age but most commonly before the ago of __

A

20

40
Q

there are 3 stages to developing type 1 DM. this stage is characterized by the development of two or more islet cell autoantibodies but the maintenance of normoglycemia

A

stage 1

41
Q

there are 3 stages to developing type 1 DM. this stage is defined by continued autoimmunity and the development of dysglycemia

A

stage 2

42
Q

there are 3 stages to developing type 1 DM. this stage is defined by the development of hyperglycaemia that exceeds the diagnostic criteria for the diagnosis of diabetes

A

stage 3

43
Q

type 1 DM is _________ (selective/nonselective) autoimmune destruction of beta cells

A

selective

44
Q

_________, which is inflammation of the islets of langerhans occurs after beta cells are destroyed in type 1 DM

A

insulitis

45
Q

what is the current theory regarding the mechanism of beta cell destruction

A
  • begins with one beta cell molecule then spreads to other islet molecules
  • neoantigens (foreign proteins absent in normal tissues) occur which is a result go excessive cells killed
46
Q

why does an individual with diabetes have hyperglycaemia?

A
  • no beta cells
  • no insulin available to cells
  • no glucose entering cells, therefore it accumulates in the blood causing hyperglycaemia
  • cells starve (decreased ATP production, decreased energy = tired)
47
Q

what are some of the compensatory mechanisms of hyperglycaemia (no glucose going into cells - all accumulating in blood)

A
  • catecholamines released (episode/NE): this increases glycogenolysis in the liver
  • cortisol is released: promotes gluconeogenesis
  • patient tends to eat more because cells are starving (still rapid weight loss)
  • ketones from lipolysis produces halitosis
48
Q

when an individual has hyperglycaemia, it causes an increase in intravascular osmotic pressure which causes ___________ (fluid retention/dehydration)

A

dehydration

49
Q

what happens to the kidney in hyperglycaemia

A

kidney increases (GFR)
- polyuria (urinate more frequently)
- glucosuria (sweet tasting urine)

50
Q

what happens to the thirst centre in hyperglycaemia

A

polydipsia (excessive thirst)

51
Q

this is a complication of hyperglycaemia; commonly caused by alterations in nutrition, inactivity, or inadequate use of antidiabteic meds; more prone to infections

A

acute hyperglycaemia

52
Q

this is a complication of hyperglycaemia; includes hypertension, CVD, ESRD, and stroke risk

A

chronic hyperglycaemia

53
Q

what are some macrovascular complications of hyperglycaemia

A

CVD and stroke

54
Q

what are some mcirovascular complications of hyperglycaemia

A
  • retinopathy (damage to the blood vessels of the light sensitive tissue at the back of the eye (retina)
  • neuropathy (deterioration of kidney function)
55
Q

true or false: DM is an independant risk factor for coronary artery disease (CAD). CAD risk factors (dyslipidemia, hypertension) are present in uncontrolled DM and can improve with adequate blood glucose control

A

true

56
Q

hyperglycaemia disrupts platelet function and growth of the basement membrane. __________ (thinning/thickening) of the basement membrane may improve with glycemic control

A

thickening

57
Q

what are some automonomic disturbances in diabetic neuropathy

A
  • GI disturbances
  • bladder dysfunction
  • tachycardia
  • postural hypotension
  • sexual dysfunction
58
Q

what are some sensory disturbances of diabetic neuropathy

A
  • carpal tunnel syndrome
  • paresthesia (burning or prickling sensation in hands, feet, etc)
  • dysesthesias (symptoms that disrupt how you experience touch-based sensations)
59
Q

this occurs when your body doesn’t have enough insulin to allow blood sugar into your cells for energy. therefore the liver breaks down fat for fuel, a process that produces acids called ketones. when too many ketones are produced quickly they can build up to a dangerous amount in your body

A

diabetic ketoacidosis

60
Q

describe the steps of DKA

A

insulin deficiency -> altered fat metabolism -> increased lipolysis -> increased conc. of FFF -> FFA oxidation -> increased ketoacids -> ketosis (can lead to vomiting and dehydration then shock) -> ketoacidosis -> shock

61
Q

are K+ levels normal in someone with ketoacidosis?

A

serum levels are normal but intracellular levels are decreased

62
Q

this is a polygenetic multifactorial disease with a strong genetic component; it is the most common form of DM

A

type 2 DM

63
Q

what is the main contributing environmental factor to type 2 DM

A

obesity

64
Q

true or false: type 2 DM is defined as decreased insulin secretion

A

false: change in number or sensitivity of insulin receptors

65
Q

this can be characterized by
- impaired insulin secretion and resistance
- excessive hepatic glucose production
- abnormal fat metabolism
- systemic low-grade inflammation

A

type 2 DM

66
Q

true or false: 5-10% of weight loss can terminate type 2 DM

A

true

67
Q

obesity (increased FFA) effects: ____________: decreases muscle responsiveness by interfering with IRS signalling, decreases adiponectin and leptin levels

A

lipotoxcity

68
Q

obesity (increased FFA) effects __________: inhibition of PPAR gamma by TNF from hypertrophic adipocytes and macrophages

A

inflammation

69
Q

obesity (increased FFA) effects _________ deposition from cell apoptosis combined with hyperglycaemia and FFA may cause impaired insulin secretion

A

amylin

70
Q

what is the relationship between insulin secretion and insulin resistance in a normal individual

A

when an individual becomes more insulin resistant, insulin secretion increases

71
Q

what is the relationship between insulin secretion and insulin resistance in an individual with impaired glucose tolerance

A

if insulin secretion increases and there is not more resistance

pathophysiology 4802 (16 decks)

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