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Pathophysiology Final > Type 2 Diabetes > Flashcards

Type 2 Diabetes Flashcards

1
Q

maintaining balance of insulin and glucagon

A
  • always have each - depending on which is predominate will dictate what happens
  • trying to prevent glucotoxicity (damage to arteries, Beta cells, eyes, nerves and kidneys)
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2
Q

insulin/ key analogy

A

-dominates in fed state and opens up storage organs for glucose

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3
Q

when does glucagon start to predominate?

A

-in fasting state, about 8 hours after you eat

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4
Q

fed state

A
  • insulin is predominate
  • insulin is like a key that unlocks the storage organs
  • insulin promotes the storage organs
  • insulin promotes storage of glucose
  • liver and muscle tissue: glucose-> glycogen: glycogenesis
  • adipose tissue: glucose-> glycerol (+ FFA)-> TGA: fat synthesis
  • net effect: decrease blood glucose
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5
Q

fasting state

A
  • glucagon is predominant
  • liver and muscle: glycogenolysis (glycogen-> glucose)
  • after 8 to 12 hours: muscle breakdown releases aa and glycogen
  • fat tissue breaks down FFA and glycerol-> glucose
    liver: gluconeogeneis (fats and proteins-> glucose)
  • net effect: increase blood glucose
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6
Q

bolus insulin

A

-the additional insulin that has been secreted to deal with the carb load that has come form your meal

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7
Q

incretin effect

A

-once in the small intestine, the GLP-1 causes an increase in the release of insulin; this is why there is a little jump of insulin right after the decrease of insulin after bolus insulin

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8
Q

what is the purpose of maintaining the balance between insulin and glucagon

A

-prevent glucotoxicity

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9
Q

24 hour blood sugar regulation

A

-the increase in insulin level will differ depending how large the meal and how many carbs

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10
Q

DAWN phenomenon

A
  • surge of growth hormone and cortisol (aka counter regulatory hormones) in the early hours of the morning to presumably prepare the body for daytime activities after a period of fasting.
  • this is accomplished by the brain to prepare for the beginning of your day-> gives you energy when you wake up
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11
Q

diagrams on slide 11
common effects of insulin and amylin and GLP1;
common effects of glucagon

A
  • insulin and amylin effects
  • glucagon effect
  • -> insulin, amylin, GLP1 lower blood sugar (fat tissue increases uptake of excess glc; fat synthesis, muscle tissue increases uptake of glc; protein synthesis, liver begins glycogenesis); then glucagon is stimulated to be released and this increases blood sugar (fat tissue decreases uptake of glc; fat is broken down (FA + glycerol), muscle tissue decreases uptake of glc: protein breakdown (aa + glycogen), liver begins glycogenolysis, gluconeogenesis, and increases hepatic output of glc) … and so on…
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12
Q

type 1 diabetes

A
  • beta cell destruction with absolute insulin deficiency
  • autoimmune
  • iodopathic
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13
Q

type 2 diabetes

A

-insulin resistance or relative insulin deficieny or combo; metabolic syndrome

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14
Q

other specific types of diabetes

A
  • genetic defects in beta cel auction (mature onset diabetes in the young)
  • genetic defects in insulin sensitivity
  • diseases of the exocrine pancreas
  • endocrinopathies
  • drug or chemical induced
  • infections
  • uncommon forms of immune mediated
  • other genetic syndromes associated with diabetes
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15
Q

what kind of diabetes may occur with pregnancy

A

gestational diabetes

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16
Q

etiology of T2D

A
  • beta cell destruction/ dysfunction with relative insulin deficiency and insulin resistance (IR)
  • beta cell destruction: 5 to 8 years prior to symptoms: CANRISK assessment tool
  • lack of insulin sensitivity (IR) linked to: hyperglycaemia (over 7mmol/L), central obesity, hereditary, ?aging, ?inactivity, ?high fate diet, and physiological state
  • pre-diabetes
  • metabolic syndrome
  • gestational diabetes
  • others
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17
Q

what are the risk factors to develop T2D

A
  • medical and family history (i.e. first degree relative with T2D, presence of vascular risk factors, presence of other diseases) - slide 16 fore more
  • however history of pre-diabetes is a strong indicator because if they do not live a healthier lifestyle to keep blood sugars low they could keep destroying beta cells
  • chronic medications (drugs from some of the related diseases: HIV-> HAART, psych disorder-> atypical antipychotics)
  • other secondary causes (down syndrome, huntingtons)
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18
Q

diagnostic criteria for T2D

A

classic clinical features (overweight, 40+, polydipsia, polyuria, blurred vision, fatigue)

  • family, medical, and medication history
  • diagnostic testing (same as type 1- FPG, A1C, ZhPG in 75g OGTT, random PG)
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19
Q

what did T1D and T2D use to be referred to

A

1- IDDM (insulin dependent diabetes mellitus)
2- NIDDM
-but now we know that patients can be allow the entire spectrum regardless- therefore we treat them based on their symptoms

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20
Q

which of the diagnostic tests are more common for T2D over type 1

A
  • A1C (because it looks over past 3 months, whereas in type 1 we need to look at right now)
  • A1C just got validation to be diagnostic (and not confirmation)
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21
Q

ZhPH test

A

give patient CHO load- test-> this is more of a confirmation test (if not 100% sure from another test)

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22
Q

true or false: pre-diabetes is reversible

A

true

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23
Q

pre-diabetes

A
  • increased risk of developing T2D and complications
  • impaired fasting glucose but normal post-prandial OR impaired glucose tolerance 2 hours after 75g OGTT OR BUT BUT NOT diagnostic for diabetes OR HbA1c 6-6.4%
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24
Q

classic presentation of pre-diabetes

A

1) postprandial glucose levels deteriorate first- B cell dysfunction (this deteriorates first because of the beta cell dysfunction)
2) then pre- and post breakfast levels- IR and B cell dysfunction
3) Followed by nocturnal hyperglycaemia and increased fasting glucose

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25
Q

nocturnal hyperglycemia

A

-high bp glucose after a person wakes up- no longer a balance in the insulin and glucagon

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26
Q

How can you reduce the progression of pre-diabetes by 58%

A

-5-10% weight loss and frequent moderate intensity physical activity (i.e. walking)

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27
Q

metabolic syndrome

A

-metabolic disorder linked to T2D, HTN, Dyslipidemia, Atherosclerosis, Obesity, certain Cancers

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28
Q

what is the main feature of metabolic syndrome?

A

insulin resistance

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29
Q

true or false: there is now a harmonized definition of metabolic syndrome

A

true- different organizations through the world that uses slightly different definitions -> therefore have taken all the info and combined into one

30
Q

what are some of the measures of metabolic syndrome? (need 3 or more)

A
  • waist circumference- measure with tape measure around where hip bone is (different criterion numbers because people around the world have genetically different body types
  • elevated TGA (because excess glucose is stored as TGA
  • reduced HDL
  • elevated BP
  • elevated FPG
  • the physiological blood sugar level (5.6) plus 2 other factors= metabolic syndrome
31
Q

which body type leads to more of a problem: apple or pear?

A

apple

32
Q

true or false: waist circumference is related to many medical problems

A

true-> lots of inflammation (high was it circumference causes more mediators of inflammation to be released (TNF-a, IL-6)
-leptin, FFA, angiotensin, PAI-1, Resistin, Visfatin, Glucocorticoids, Adiponectin, and sex steroids are all also released

33
Q

Gestational diabetes

A
  • physiological state of insulin resistance requiring a higher level of insulin (because of the fetus)
  • usually detected week 24 to 28 of gestation
  • often asymptomatic
  • resolves after pregnancy termination
  • significant risk of developing T2D later (30-60% over 10 year)
  • different diagnostic criteria
  • incidence varies among populations: Aboriginal populations 8-18%
34
Q

true or false: gestational diabetes leads to a smaller baby

A

false- since the mom has excess sugar lots goes to the baby causing it to be bigger

35
Q

pathophysiology diagram of ketoacidosis- what type of diabetes does this refer to?

A

type 1

  • slide 25
  • brain communicates with the adrenal glands to secrete the counter-regulatory hormones/ pancreas for insulin
  • kidney function will eventually suffer because you need to have volume for proper function
36
Q

pathophysiology diagram of hyperglycaemic hyperosmolar state

A

-same process occurs but there is no lipolysis in T2 therefore no ketoacidois
slide 26

37
Q

main features of T2D

A
  • cellular energy starvation
  • insulin resistance
  • hyperinsulinemia (cells are still starving, but insulin stays in the blood and is unable to do anything= hyperinsulemic)
  • hyperglycemic hyperosmolar state (= glycosuria and dehydration)
38
Q

what does HHS lead to in T2D

A
  • polyuria
  • polydipsia
  • blurred vision
  • muscle cramps
  • headache
  • anxiety and irritability
  • confusion
  • slow healing wounds
  • prone to fungal and and bacterial infections
39
Q

what does energy starvation lead to in T2D

A
  • fatigue

- weight loss

40
Q

what are some chronic complications of T2D

A
  • retinopathy
  • nephropathy
  • neuropathy
  • loss of functionality and QoL
41
Q

true or false: when diagnosing diabetes, you need to look at all diagnostic numbers (no just those related to DM, but also bp, BMI, etc)

A

true

42
Q

true or false: if you are hyperinsulemic you cannot also be hyperglycemic

A

false, it is possible to be both (i.e. in type2, it is insulin doesn’t work therefore could have high levels of sugar and insulin at the same time)

43
Q

what are some good treatment suggestions of people with type 2 diabetes

A
  • nutrition therapy (diet, reduce CHO load-> can reduce A1C by 2%- this is more than any drug)
  • drugs also important to-> to try to reduce insulin sensitivity, work on gut (on GLP-1), try to utilize kidney (block some of the transporters that block glucose)
44
Q

pathogenesis: T1 vs T2

A

1- genetic, enviro, autoimmune, idiopathic

2- genetic, lifestyle, secondary causes, med induced, idiopathic

45
Q

insulin production: T1 vs T2

A

1- absent or relative
2- relative insulin deficiency (most puts have lost 50% beta cell function by time of diagnosis
-hyperinsulemia and HHS

46
Q

age of onset: T1 vs T2

A

1- usually younger than 20, insidious up to 8th decade

2- usually after 45, but increasing incidence amongst younger people

47
Q

symptoms T1 vs T2

A 
1- quick onset and classic criteria; 3 poly's
-minimal or gradual in adults
-slow healing wounds
-prone to fungal infections
2- absent or mild- asymptomatic for 5-8 years
-slow onset
-slow healing wounds
-prone to fungal infections
(2 poly's)
48
Q

body type: T1 vs T2

A

1-usually lean

2- 70-80% are obese

49
Q

family history: T1 vs T2

A

1- some genetic markers

2- marked but not fully understood

50
Q

DKA/HHS

A

1- DKA is hallmark feature in patients with absolute insulin deficiency
2- seldom DKA except with major stress/ illness
-HHA is hallmark feature

51
Q

chronic complications T1 vs T2

A

1- microvascular
-macrovascuar
-depends on degree of hyperglycaemia
2- same as type 1; 50% have 1 complication at time of diagnosis

52
Q

good video on slide 35

A

watch if confused on anything

53
Q

what percentage of CHO are broken down?

A

90%

54
Q

which CHO cannot be broken down?

A

Fibre

55
Q

can proteins and fats raise blood sugar level right after a meal?

A

no

56
Q

3 types of secreting cells in pancreas

A

alpha, beta, delta

57
Q

what do delta cells secrete

A

somatostatin

58
Q

net effect of glucagon

A

blood glucose increases

59
Q

what is it called wen glucose-> glycogen

A

glycogenesis

60
Q

what process forms glucose from other sources?

A

gluconeogenesis

61
Q

what is the form in which glucose is stored in fat tissue

A

TGA

62
Q

where is glucagon like peptide 1 secreted

A

small intestine

63
Q

what is the level of sugar that we describe glucotoxicity (aka hyperglycemia)

A

equal or greater than 7

64
Q

what initiates the DAWN effect

A

brain

65
Q

is the DAWN effect related to the level of sugar on the body

A

no

66
Q

what is the threshold for blood sugar absorption

A

10mmol/L

67
Q

what is never in the urine if kidneys are working well

A

glucose and aa

68
Q

what are the clinical features in type 1 that start with P and which is not found in T2

A

polydipsia, polyuria, polyphagia (polyphagia not found in T2)

69
Q

what is the physiological blood glucose level

A

5.6mmol/L

70
Q

complications from T2D

A
  • nerve damage
  • kidney damage
  • eye damage
  • blood vessel damage
  • heart disease
  • foot damage
71
Q

hypoglycemia

A
  • blood sugar under 4mmol
  • tremor
  • tachycardia
  • sweaty palms
  • hungry
  • nausea
  • headache
  • irritable
  • confusion

Pathophysiology Final (10 decks)

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