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Clinical nutrition 1 > Diabetes > Flashcards

Diabetes Flashcards

1
Q

can we get diabetes because of eating too much sugar or too much fat?

A

its not so much the sugar or fat that causes diabetes, but the excess energy from eating these in excess leading to to excess weight and fat deposition

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2
Q

diabetes mellitus definition

A

a metabolic disorder characterized by elevated blood glucose concentrations and disturbances of carbohydrates, lipids, and protein due to defective insulin secretion and/or action

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3
Q

characteristics of type 1 DM

A
  • insulin dependent (IDDM)
  • juvenile or growth onset
  • ketosis prone [lack of insulin secretion]
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4
Q

characteristics of type 2 DM

A
  • non-insulin dependent mostly
  • maturity onset mostly
  • not prone to ketoses
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5
Q

characteristics of gestational diabetes

A

diagnosed during pregnancy, resolved at delivery

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6
Q

what causes type 1 diabetes

A

caused by an autoimmune or idiopathic destruction of pancreatic beta-cells due to islet cell auto-antibodies (ICA) causing absolute deficiency in insulin production
- predisposition, viruses, toxins can trigger development of ICA

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7
Q

what causes type 2 diabetes

A

excessive food intake, lack of exercise, genetic predisposition -> obesity -> inflammation

  • > cells do not respond normally to insulin (resistance)
  • cells do not take up and utilize glucose efficiently -> hyperglycemia
  • pancreas may compensate or not with insulin production -> hyperinsulinemia or normal levels followed by beta-cell insufficiency [decreased production fo insulin]
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8
Q

how do you treat type 1 diabetes

A

insulin injection

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9
Q

how do you treat type 2 diabetics prone to ketosis

A

insulin injection

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10
Q

how do you treat type 2 diabetics resistant to ketosis

A
  • diet treatment
  • oral medication
  • insulin injection when prolonged duration
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11
Q

what are some risk factors associated with diabetes

A

age and obesity

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12
Q

which populations are more at risk of diabetes?

A
  • south asian, Asia, African, hispanic descent
  • aboriginal, First Nations: 2-5 times more diabetes
  • overweight, older, low income
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13
Q

what are the symptoms of type 1 diabetes

A
  • increased thirst
  • increased urination
  • increased hunger
  • weight loss or obesity
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14
Q

which clinical laboratory tests reveal T1 diabetes?

A
  • glycosuria
  • hyperglycemia
  • abnormal glucose tolerance GTT
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15
Q

what are the various actions of insulin

A
  • increased glucose uptake ans storage
  • decreased glycogenolysis and gluconeogenesis = decreased endogenous glucose production
  • increased lipogenesis
  • decreased lipolysis
  • increased protein synthesis
  • decreased proteolysis
  • growth/mitogenesis
  • reproduction
  • lifespan
  • cognition
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16
Q

what are the general effects on insulin deficiency

A

There is a decrease in glucose uptake by cells, causing polyphagia, and an increase in hepatic glucose production both causing hyperglycemia -> glycosuria -> polyuria -> dehydration -> peripheral circulatory failure -> renal failure and low cerebral blood flow.
There is also decreased TG synthesis and increased lipolysis -> increased blood fatty acids -> ketosis -> metabolic acidosis > diabetic coma.
+ decreased amino acid uptake by cells [increased blood AA -> gluconeogenesis] and increased protein degradation -> muscle wasting -> weight loss

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17
Q

what happens metabolically in the fasted state in a diabetic patient

A

high lipolysis -> a lot of FA substrate for kept acids
+ high rates fo proteolysis releasing AA in circulation -> gluconeogenesis in liver -> glucose in the circulation + kept acids -> excess excreted in urine

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18
Q

what happens metabolically in the fed state in a diabetic patient

A

same as fasted start but worse: high lipolysis -> a lot of FA substrate for kept acids
+ high rates fo proteolysis releasing AA in circulation -> gluconeogenesis in liver -> glucose in the circulation + kept acids -> excess excreted in urine
++++ glucose and AA from food

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19
Q

what is insulin resistance

A

defines as a lesser sensitivity to insulin’s action in suppressing hepatic glucose production and stimulating glucose uptake. Mostly due to defective insulin signaling within cells

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20
Q

what are the steps involved in insulin-induced glucose uptake

A
  1. in response to a rise in blood glucose, the pancreas releases more insulin into the blood
  2. insulin bond to a membrane-bound receipt
  3. the binding of insulin to its receptor signals glucose transporters to move from the cytoplasm to the cell membrane
  4. glucose transporters enable glucose to move from the extracellular space into the cytoplasm
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21
Q

what are the mechanisms that can cause insulin resistance

A
  • receptor defects: decreased number and affinity [rare cases of genetic mutations of INSR gene]
  • post-receptor second messenger signaling [most cases of IR]
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22
Q

what are the risk factors of type 2 diabetes

A
  • age
  • family history
  • high-risk population
  • prediabetes: impaired fasting glucose or impaired glucose tolerance
  • history of GDM/delivery of macrosomic infant
  • cardiovascular risk factors
  • presence of end-organ damage associated: CV ad microvascular
  • Low birth weight (<2.5kg) and high birth weight (>4.0kg)
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23
Q

which are the cardiovascular risk factors for T2D?

A

dyslipidemia, abdominal obesity, HTN, smoking, sedentary lifestyle

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24
Q

what are the metabolic stages of type 2 diabetes?

A
  • pre-diabetes: obesity -> insulin resistance and impaired fasting glucose and glucose tolerance + beta-cell defect -> decreased insulin secretion
  • late diabetes: beta-cell failure, non-reversible
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25
Q

how can pre-diabetes be reversed

A

with weight loss, exercise, and medication

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26
Q

what is the first sign of type 2 diabetes?

A

high fasting glucose on routine blood test

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27
Q

what are the common symptoms of T1D

A

very pronounced symptoms; wasted appearance; polyphagia, polydipsia, polyuria, HLA and islet cell antibodies present

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28
Q

what are the common symptoms of T2D

A

often not evident; usually obese; fatigue, vision changes, recent weight loss, HLA and islet cell Ab ABSENT

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29
Q

what has to be done to manage/stabilize type 1 diabetes

A

there has to be a tight matching of insulin dose and food intake

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30
Q

why is ketoacidosis rare in type 2 diabetes

A

because there is always some insulin being secreted unlike in T1D where there’s no insulin secretion/deficiency

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31
Q

in which case are oral antihyperglycemic agents used

A

in type 2 diabetes

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32
Q

what are some complications observed with T2D

A

vascular complications become evident after 5 years from diagnosis

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33
Q

what are some complications that can be observed with diabetes in the short term

A
  • hypoglycaemic episodes (if treated with insulin)
  • diabetic ketoacidosis (when insulin injection is forgotten - more in T1D)
  • hyperglycemic hyperosmolar syndrome (more in T2D - BG>33mmol/L)
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34
Q

what are the early signs of hypoglycemia? and late signs?

A

BG<3.9mmol/L

early: neurogenic (sweating, shakiness, anxiety, sensation of hunger) and neuroglycopenic (weakness, dizziness)
late: (develop over hours) neuroglycopenic (confusion, poor coordination, blurred vision, loss of consciousness, coma

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35
Q

what are the common etiologies of hypoglycemia?

A

skipping or delaying meals, reduced CHO intake without med compensation, misdosage of insulin, unplanned exercise

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36
Q

why is unplanned exercise a risk factor for hypoglycemia?

A

exercise stimulates glucose uptake, therefore if meals are not adjusted aka high CHO intake, it can cause hypoglycemia

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37
Q

what is the treatment for hypoglycemia

A

15-15 rule
give 15g of fast absorbed CHO [fruit juice, soft drinks, glucose tablets], check blood glucose 15min later, repeat if BG is still low

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38
Q

if there is severe hypoglycemia, the care provider can inject _____

A

glucagon which stimulate endogenous glucose production, or glucose

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39
Q

what are some complications that can be observed with diabetes in the long term

A

microvascular complications:

  • retinopathy: cataracts, glaucome -> blindness
  • nephropathy: chronic kidney disease/failure -> dialysis, transplantation
  • neuropathy: impaired sensation of pain in extremeties -> amputations

macrovascular: CVD, CHD, stroke

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40
Q

what causes the long term complications with diabetes

A

due to poorly controlled diabetes, there is a high chronic glucose level which causes protein glycation [A1c] and high lipolysis [lipotoxicity] all of which causes endothelial damage, acceleration of plaque formation and atherosclerosis => hypertension, thrombosis, ischemic end-organ damage

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41
Q

what is A1c

A

glycated hemoglobin measured as % of Hb

-> A1c is an indicator of long-term glycemic control because Hb half-life is about 3 months

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42
Q

what is the normal range of A1c?

A

4.3-6.0%

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43
Q

what is the effect of diabetes on dyslipidemia in type 1 diabetes?

A
  • hypertriglyceridemia due to defective removal of chylomicrons and VLDL resulting from impaired LDL activity as LDL is insulin dependent
  • HDL and LDL-c may be normal
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44
Q

what is the effect of diabetes on dyslipidemia in type 2 diabetes?

A
  • hypertriglyceridemia due to elevated de novo synthesis from glucose and from FFA
  • low HDL-c due to obesity
  • LDL-c often elevated but may be normal
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45
Q

what is the effect of diabetes on heart disease

A

diabetic patients have 2-4x risk of developing CVD [greater independent risk than smoking, HTN, hypercholesterolemia, obesity]

  • > heart disease is the major cause of death in DM
  • ABCDES for cardiovascular protection
46
Q

who should be screened for type 2 diabetes in adults?

A
  1. assess risk factors for type 2 diabetes annually, if:
    - no risk factors: age<40 years [no screen], age>40 or high risk [screen every 3 years]
    - presence of risk factors or very high risk (50% chance of developing T2D within 10 years) [screen every 6 to 12 months]
47
Q

how do you screen for T2D

A
  • FPG (fasting plasma glucose): 6.1-6.9mmol/L [impaired fasting glucose] or >7 [diabetes]
  • A1C: 6-6.4% [prediabetes] or >6.5 [diabetes]
48
Q

impaired glucose tolerance has high fasting glucose. true or false

A

false, it has normal fasting glucose as there was enough insulin secretion to keep regular glucose levels during fasting

49
Q

both T2D and Impaired glucose tolerance have a ______ when challenged with 75g of glucose. why?

A

higher response due to decreased glucose uptake - insulin resistance

50
Q

how do you diagnose prediabetes

A

Impaired Fasting Glucose IFG, Impaired Glucose Tolerance IGT, A1C 6-6.4%

51
Q

what was observed during the diabetes prevention program DPP

A

diet and exercise (lifestyle) changes or Metformin prevented diabetes development.
the lifestyle approach was the most efficient preventative method

52
Q

what is the target A1c for adults with T2D but at low risk of hypoglycemia

A

<6.5%

53
Q

what is the target A1c for most adults with T1 or T2D

A

<7%

54
Q

what is the target A1c for adults with T2D but at risk of hypoglycemia

A

7.1-8.5%

55
Q

targets of A1c aim to reach normal levels of glucose or A1c. true or false?

A

false

56
Q

what are the ABCDES of diabetes care

A
  • A1c targets (<7.0%)
  • BP targets (<130/80)
  • Cholesterol targets (LDL <2.0mmol/L or 50% reduction from baseline)
  • Drugs for CV and/or cardiorenal protection
  • Exercise goals and healthy eating (150min of mod/vig aerobic activity/week + meditation diet)
  • Screening for complications
  • Smoking cessation
  • Self-management, stress, other barriers
57
Q

what is the optimal DM target for fasting glucose

A

4.0-7.0 mmol/L

58
Q

what can be monitored to see if diabetes is under control

A
  • Self-monitoring blood glucose SMBG
  • blood glucose
  • urine glucose
  • urine ketones
  • blood ketones
  • glycated proteins
59
Q

about SMBG

A
  • three times in a day for type 1 diabetes
  • important for people on antihyperglycemic agents or insulin to prevent hypoglycemia
  • may not be necessary for those only on diet treatment
60
Q

what kind of receptors are insulin receptors?

A

tyrosine kinases

61
Q

which intracellular pathways are activated once insulin binds to its receptors [insulin signaling]

A
  • PI3K pathway -> AKT2 activation causing:
    > GLUT4 translocation to membrane for glucose uptake
    > inactivation of GSK3 and GS -> glycogen synthesis
    > cAMP - PKA -> lipolysis and fatty acid synthesis
    > inhibits gluconeogenesis and apoptosis through FOXO
    > activation of mTORC1 which promotes protein synthesis
  • MEK and ERK pathway -> transcription and DNA synthesis - cell growth
62
Q

which intracellular pathways are affected due to insulin resistance induced by FFA

A
  • accumulation of FFA in cytoplasm causing increased reactive oxygen species in mitochondria, accumulation of DAG which inhibits PI3K pathway and causes inflammatory genre expression
  • PKB/AKT inhibited by CERAMIDE
    => resistance [not complete inhibition]
63
Q

definition of metabolic syndrome

A

a cluster of closely related metabolic disorders increasing the risk of development of T2DM and CVD

64
Q

what is the difference between a syndrome and a disease

A

a syndrome is a cluster of different conditions put together that do not make a disease => you diagnose a disease with a diagnostic criteria [diabetes with fasting elevated BG and A1c] but there is no diagnostic criteria for a syndrome

65
Q

what is the required criteria for metabolic syndrome

A

abdominal obesity = central obesity = waist circumference >102cm for men and >88cm for women

66
Q

what other constituents associated with abdominal obesity could make up a syndrome

A
  • insulin resistance and high fasting BG >5.6mmol/L
  • dyslipidemia [HDL-c <1.0 in men or <1.3mmol/L in women; TG>1.7mmol/L]
  • hypertension >130 systolic or >85 diastolic
67
Q

due to insulin resistance, there is increased ____ in adipocytes causing elevated _____ in circulation

A

increased lipolysis

elevated free fatty acids

68
Q

high free fatty acid in circulation causes ______ and in turn hyperglycemia and hyperinsulinemia

A

insulin insensitivity

69
Q

what causes inflammation in conjunction with insulin resistance

A

hypertrophy of adipocytes causes release of macrophages and positive acute phase protein release such as C-reactive protein and fibrinogen

70
Q

metabolic syndrome usually starts with a _______

A

positive energy balance

71
Q

what makes up the metabolic syndrome and what causes this

A
  • systemic glucotoxicity [hepatic glucose output]
  • fatty liver disease [glucose uptake and conversion into lipids + FA uptake]
  • heart disease
  • pre-diabetes, followed by overt diabetes [pancreatic islet mass followed by exhaustion]
  • systemic low-grade inflmmation
  • systemic lipotoxicity [increase lipolysis]
72
Q

what is the proposed mechanism for developing metabolic syndrome

A
  • insulin resistance + direct venous drainage of visceral fat and hepatic portal vein -> increase hepatic FFA delivery
  • adipose tissue macrophage content linked with IR - release inflammatory cytokines impairing insulin action and promoting release of FFA
73
Q

with adipocyte hypertrophy, leptin secretion ____ and adiponectin secretion _____

A

leptin secretion increases and adiponectin secretion decreases

74
Q

what is the “overflow hypothesis” in terms of excess fat

A

with excessive energy intake there is lipid accumulation in hepatocytes, skeletal muscles, visceral adipocytes and heart instead of subcutaneous adipose tissue

75
Q

what are the consequences of lipid accumulation in hepatocytes

A
  • hepatosteatosis (fatty liver or NAFLD)

- drive formation of VLDL

76
Q

what are the consequences of lipid accumulation in muscle

A
  • myosteatosis (fat infiltration in muscle)

- cause insulin resistance - reduced glucose uptake

77
Q

do the factors involved in metabolic syndrome increase the risk additively or synergistically?

A

probably additively

78
Q

what are the goals of the diet therapy for diabetes

A
  • encourage the attainment or maintenance of a healthy body weight
  • achieve the best possible metabolic control with seriously compromising quality of life
  • to delay or prevent complications associated with diabetes
79
Q

what are the lab targets of the diet therapy for diabetes

A
  • glycemic control: near normal or targets
  • lipid profile: primary target LDL-C <2.0mmol/L
  • BP: <130/80
80
Q

what is the first approach to treating T2D

A

initiate intensive healthy behaviour interventions or energy restriction and increased PA to achieve/maintain a healthy body weight

81
Q

what are the health benefits of weight loss of 5-10% of initial body weight

A

improved insulin sensitivity, glycemic control BP control, lipid levels

82
Q

what are the macronutrient distributions for T2D

A
  • CHO: 45-60% [low GI]
  • PRO: 15-20% [1-1.5g/kg]
  • FAT: 20-35%
83
Q

what should the protein ink bee for weight stable diet? weight reduction program?

A
  • weight stable: 20%

- weight reduction w/ energy deficit 1.0-1.5g/kg (25%)

84
Q

specificities on CHO intake when dealing with diabetes

A
  • minimum intake of 130g/d to void ketosis
  • > 45% to prevent high intake of saturated fats and higher risk fo CVD
  • include low GI and high fiber
  • <10% of added sugar (sucrose)
85
Q

what is the difference of glycemic index vs. load

A
  • GI: area under the curve in BG response of a given food compared to standard (glucose or white bread) for he SAME CONTENT IN g CHO [GI= AUC pasta/AUC glucose x 100
  • GL= g CHO in normal serving x GI /100
86
Q

what is considered a low GI? low GL?

A

low GI < 55

low GL <10

87
Q

are CHO recommendations based on GI or GL?

A

GI

88
Q

what are the benefits of replacing high GI with low GI

A
  • improvement fo glycemic control in type 1 and type 2 diabetes
  • increased HDL-c, decreased CRP, hypoglycaemic events in T1D and medications
89
Q

what are the recommendations of dietary fiber and diabetes

A

higher total intake of soluble fibres recommended in diabetes: 30-50g/d or 15-25g/1000kcal

90
Q

what are the benefits associated with higher intake of soluble fibers

A
  • slows gastric emptying and glucose absorption

- improvement in A1c, fasting BG and lipid profile

91
Q

specificities on fat intake when dealing with diabetes

A
  • avoid trans fats acids
  • saturated <9% of energy
  • replace saturated fats from processed meat and baked goods with PUFA [w-3 and 6], MUFA [plants]
  • linoleic acid: w 12g, m 17g/day
  • linolenic acid: w 1.1g, m 1.6g/day
92
Q

supplements of omega-3 FA are recommended for diabetes. true or false

A

false, not recommended except for severe hyperTG
however it is recommended to have a higher intake of fish to reduce CAD and kidney sides in T2D and less albuminuria in T1D (2-3 servings of fish/week)

93
Q

what are the protein recommendations for diabetics with chronic kidney disease

A

no more than 0.8 g/kg/d
monitor protein status in patients with DM and CKD to avoid malnutrition
plant sources of protein rich in potassium

94
Q

what are the benefits of replacing animal with plant protein sources

A

improved A1c, fasting BG and insulin

95
Q

what are the macronutrient substitutions that have shows to have cardiometabolic benefits in T2D

A

replacement of:

  • high GI CHO with MUFA
  • fat with low GI CHO
  • high GI CHO with high protein diet during weight loss
96
Q

which dietary patterns are recommended for diabetes

A
  • mediterranean diet
  • vegetarian diet
  • portfolio diet
  • DASH diet
97
Q

what are the limitations of non-nutritive sweetness

A
  • Gi symptoms because attract water (diarrhea and bloating)

- alteration of gut microbiome

98
Q

what are the consequences fo alcohol intake

A

it can mask symptoms of hypoglycemia and increase ketones + delayed hypoglycemia

99
Q

bed-time snacks containing ____ may help avoiding nocturnal hypoglycemia

A

protein

100
Q

persons with T1D tend to consume diets low in fiber, high in fat and protein -> may require additional ____

A

insulin

101
Q

what are the recommendations during illness for patient with diabetes

A
  • take DM medications as prescribed
  • self-monitoring BG >4/d
  • replace CHO with liquid CHO is N/V
  • hydrate 300mL/hr
102
Q

decrease calories in T1 and T2?

A
  • T1: no

- T2: yes

103
Q

strategy to improve insulin action (sensitivity) in T1 and T2?

A
  • T1: seldom important, beta cells are inactive and no IR

- T2: very urgent

104
Q

increase frequency of feedings in T1 and T2?

A
  • T1: yes for conventional treatment, no for intensive treatment
  • T2: not usually
105
Q

consistent intake of kcal, CHO, pro, fat in T1 and T2?

A
  • T1: important for conventional treatment and not critical for intensive treatment
  • T2: better but not critical
106
Q

consistent ratio of CHO, pro, fat/meal in T1 and T2?

A
  • T1: very important for conventional treatment, not critical for intensive treatment
  • T2: not crucial
107
Q

consistent timing of meals in T1 and T2?

A
  • T1: important

- T2: not crucial

108
Q

extra food for unusual exercise in T1 and T2?

A
  • T1: conventional treatment yes, variable for intensive treatment
  • T2: not usually
109
Q

during illness, provide CHO (w/ ends and close monitoring) in T1 and T2

A
  • T1: to prevent ketosis [insulin needs to be higher than usual]
  • T2: to prevent HHS
110
Q

use of food to treat, prevent hypoglycemia in T1 and T2

A
  • T1: importnat

- T2: less important (yes to treat)

Clinical nutrition 1 (7 decks)

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