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Clinical Nutrition > Intro to Diabetes > Flashcards

Intro to Diabetes Flashcards

1
Q

LADA

A

happens later in life, destruction of beta cells but a a slower rate

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2
Q

Risk factors for diabetes

A

male, age, ethnicity, aboriginal, overweight, low income,

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3
Q

undiagnosed diabetes

A

27.4% living with it or many years - uncontrolled blood glucose levels which can have detrimental effects

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4
Q

Type 1 causes

A

body produces islet cell auto-antibodies
- still not sure why this starts; some gene involved but not sure which one; is it environmentally triggered?- virus, toxins and stress.

steps: genetic predisposition leads to islet cell auto-antibodies if exposed to environmental factors ( virus, toxins, stress), net other causes will cause B cell injury and there will be no insulin

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5
Q

symptoms of diabetes

A

polydipsia, polyuria, polyphasic, weight loss ( T1) or weight gain ( T2)

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6
Q

where are symptoms more severe?

A

T1

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7
Q

clinical lab test results indicating diabetes

A

glycosuria
hyperglycaemia
abnormal glucose tolerence (GTT)

diagnosis criteria:
-A1C
-FPG
for T1 need to measure antibodies

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8
Q

what does insulin do?

A

promote glucose uptake
stimulate glycogenesis (making glycogen) making protein and making TG (lipogenesis)
decrease gluconeogenesis, glycogenolysis, lipolysis and proteolysis

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9
Q

total def in insulin (type 1) leads to what in terms of glucose metabolism? (talk through table)

A

1) in terms of glucose metabolism = less uptake in HAM (GLUT 4)- leads to intracellular glucose def= polyphasic. In contrast there is greater hepatic glucose output ( highest rate of gluconeogenesis from lipids and aa’s)
- these both lead to hyperglycaemia in which some spills into the urine. bc glucose is osmotic ( attracts water) –> polyuria which can lead to dehydration–> polydipsia ( always thirsty). with dehydration we can have cell shrinking and therefore NS malfunction ==> death
there may also be a decrease in blood volume-> increase HR, peripheral circulatory flare and low blood flow and renal failure==> death

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10
Q

describe how polyuria happens in type 1

A

hyperglycaemia leads to glycosuria which attracts water and leads to polyuria

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11
Q

How does total deficiency in insulin (type 1) fat metabolism? (talk through table)

A

Cells fell starved–> increase in gluconeogenesis–> lipolysis and decreases in TG synt, which ultimately leads to increase in blood FFA ( used as an alternate fuel source = ketosis => which may lead to metabolic acidosis –> increased ventilation and diabetic coma and death

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12
Q

why is there increase in ventilation in T1 DM?

A

increase in blood FA leads to ketosis and metabolic acidosis; therefore, to excrete more H+ ( more CO2 and H2O in breath) fall in plasma H2CO3

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13
Q

is ketosis state a big deal in T1?

A

not a big deal, but the issue is when ketosis is prolonged and develops into metabolic acidosis

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14
Q

what is metabolic acidosis

A

ketone bodies 10x higher than in ketosis

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15
Q

why is metabolic acidosis so bad?

A

affects the respiratory system –> increased ventilation to excrete CO2 and decrease in pH and metabolic imbalances that accompany could lead to diabetic coma

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16
Q

when do most ppl find out they have T1

A

administered to hospital with symptoms of diabetic coma ( increased ventilation, decrease in pH )

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17
Q

how does Type 1 affect protein metabolism?

A

less aa uptake in cells and increase protein catabolism –> muscle wasting and weight loss
- more aa in circulation causes more gluconeogenesis, aggravating hyperglycaemia

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18
Q

diabetes fasted state

A

exacerbated fasted state due to lack of insulin

  • lots of gluconeogenesis, proteolysis and lipolysis
  • cause negative nitrogen balance due to non-gluconeogenic AA’s getting catabolized and broken down
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19
Q

what happens when type 1 fed?

A

worsens the situation
- increases the substrates to the liver- more hyperglycaemia as cells can still not uptake glucose(none getting converted to glycogen ) more glucosuria

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20
Q

ER type 1 blood sugar is normally at?

A

above 25mmol/L and mediate insulin infusion, electrolytes and potassium

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21
Q

cause of T2DM?

A

major cause is obesity and inflammation ( which goes hand in hand with obesity)
- obestity caused by genetics, lack of exercise and excess calories
- this leads to IR= hyperglycaemia and the pancreas trying to overcompensate and secreting more insulin.
-

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22
Q

is sugar a cause of diabetes?

A

no

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23
Q

when IR develops is this diabetes?

A

NO, bc the hyperinsulinemia will work to control blood glucose
- officially have diabetes when there is B-cell destruction and the pancreas can no longer compensate with enough insulin

24
Q

what causes the transition from IR to B-cell destruction leading to diabetes?

A

may be genetic component or lipotoxicity

high levels of lipids in the blood that impact cell function and causes inflammation

25
Q

what is IR? why does it happen?

A

less sensitivity to insulin’s actions of stoping gluconeogeneis and up taking glucose
- mostly due to defect in cell signalling, NOT THE RECEPTOR

26
Q

what organs don’t get effected by insulin resistance ( in terms of glucose def)

A

brain, RBC, liver

27
Q

is T1DM genetic?

A

no not atall

28
Q

T2Dm risk factors

A

GDM, low or high BW, PCOS, aboriginal, African, south asian, hispanic, obesity, sedentary, male, age, prediabetes

29
Q

describe the stages and development of type 2 diabetes

A

obesity—> IR –> hyperinsulemia and hyperglycaemia –> impaired glucose tolerance and overnight fasting glucose ( always high) –> beta-cell defect leads to early diabetes ( we can intervene here with diet, medication and lifestyle and reverse the disease BUT if beta- cell failure ( genetic and lipotoxicity) then leads to late diabetes

30
Q

short term complications of DM

A
  • hypoglycaemic episodes
  • diabetic keto acidosis ( more in T1)
  • HHS ( more in type 2) (when BG >33 mol/L)
31
Q

how does hypoglycaemia happen in DM

A

BG < 3.9 mol/L but individual symptoms

  • neurogenic –> sweating, tachycardia, anxiety, sensation of hunger
  • neuroglycopenia ( weakness and dizziness, confusion and poor coordination blurred vision
  • this happens when skip meal, delay meal, reduce CHO intake without med compensation or unplanned exercise
32
Q

long term complications

A

microvascular and microvascular (CVD, CHD, stroke)

33
Q

pathophysiology of the long term consequences of DM

A

ultimately from endothelial damage caused by chronic amounts of glucose in circulation (glucotoxity) and which glycosyalte certain proteins ( glycated hemoglobin- A1C) there will also be lipotoxicity which further increases endothelial damage–> leading to increased acceleration of atherosclerotic plaque –> HPT, thrombosis, ischemic and organ failure

34
Q

what is A1C

A

glycated hemoglobin - one molecule of glucose is bound to hemoglobin
- measured as % of total Hb in circulation - normal is 4.3-6 but when higher indicative of chronic glycemia

35
Q

why is there hyperTG in T1

A

defective removal of CM and VLDL bc LPL is insulin dependent and if no insulin than no LPL activity

36
Q

can hyper TG be cured ?

A

with insulin injections and controlled T1 yes

37
Q

what happen to HDL and LDL in hyperTG in T! vs T@

A

in T! hdl and ldl may be normal but in T@ HDl is usually low bc obesity and Ldl is usually high bc obesity

38
Q

why can hyperTG arise in T2

A

due to elevated de nova synthèses from glucose and from FFA (similar to obesity) - excess substrates

39
Q

diabetes and heart disease, why is there’s such a great risk?

A

2-4x greater risk of CVD - greater risk than smoking, HPT, HyperCH, obesity
- risk due to elevated glucose which has a huge impact on endothelial damage

40
Q

heart disease is the cause of ____ of deaths related to DM

A

65%

41
Q

diabetes screening- who to screen?

A

everyone over 40 every 3 years OR ppl at high risk then screen more regularly with ppl who have additional risk factors for diabetes

42
Q

who doesn’t need to be screened?

A

under 40 and no risks

43
Q

what does screening mean? what is the main screening tool

A

blood test

- fasting plasma glucose (FPG)

44
Q

diagnostic criteria * very important

A

1) FPG - 6.1-6.9 indicates impaired fasting and above 7 indicates diabetes
2) plasma glucose after 2 hours after oral glucose tolerance test ( not often for screening - long test) but 7.8 to 11 indicate impaired fasting glucose and >11 indicate diabetes
3) A1-C % –> 6-6.4% indicate prediabetes and >6.5 indicates diabetes

45
Q

what happens if patients blood work indicates diabetic BUT asymptomatic?

A

redo confirmatory test (FPG, A1C or 2hrPG)

46
Q

if half the tests are in diabetes range than what?

A

tests repeated

47
Q

when is the only case when diabetes can be diagnosed with only one test?

A

random glucose test and symptoms

48
Q

derive the difference between impaired glucose tolerance and T2DM in relation tot he OGTT blood glucose curve

A

T2DM has a higher base line (set point) before administration whereas IGT will have a normal level before oral glucose administered

49
Q

diabetes prevention program effective?

A

YES, prediabetes diagnosis is crucial - DPP study found that diet, exercise or metformin conducted over 4 years with 3234.

metformin = 31% decreases diabetes
lifestyle intervention - decrease by 58%

50
Q

what are ABCDEs of diabetes

A

recommendations fro vascular protection with diabetes:

A1C, BP, CH, Drugs to protect the heart, exercise, smoking

51
Q

what A1C target should aim for?

A

not nessasarily the non-diabetic target, but a healthy safe range–> have to keep in mind intensity of medications and the side effects along with them ( main risk of treating hyperglycaemia is hypoglycaemia)
- target is >7% for MOST patients with T1 tr T2

52
Q

limited life expectancy A1C target

A

7.1-8.5%

53
Q

can 6.5% be a realistic target?

A

for SOME T2 patients but must be carefully balanced with hypoglycemia

54
Q

optimal ranges for DM patients (A1C, FG, 2hrPG)

A

<7%, 4-7, 5-11

55
Q

what is the CANRISK

A

the Canadian diabetes risk questionnaire –> tells you (for adults aged 40-75) if you are at risk

  • age
  • waist circumference
  • sex
  • PA
  • vegtable intake
  • BP, BG and pregnency
  • family history
  • ethnicicty

low risk, moderate risk and high risk

56
Q

if patient has CVD which medications ?

A

statins + ACEi?ARB + ASA

57
Q

if patients is above 40 and has diabetes, should they be on statins?

A

yes, or if have had diabetes for more than 15 years

Clinical Nutrition (25 decks)

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