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PHAR152 > Diabetes 1 > Flashcards

Diabetes 1 Flashcards

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1
Q

What is the definition of diabetes mellitus?

A

a metabolic disorder characterized by the presence of hyperglycemia due to defective insulin secretion, insulin action, or both

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2
Q

How prevalent is diabetes in Canada?

A

~4 million diagnosed (10% of population)–>about 30% diagnosed, undiagnosed, or prediabetes

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3
Q

How prevalent is diabetes in Saskatchewan?

A

~113,000 (9%); another 220,000 with prediabetes or undiagnosed (26%)

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4
Q

What are the estimated economic impacts of diabetes?

A

$30 billion/yr
-SK: $100 million/yr in direct costs
medical costs are 2-3x higher in those with diabetes

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5
Q

What are some broad complications of diabetes?

A

CVD, kidney disease, neuropathy, amputation
~80% will die from heart disease or stroke

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6
Q

True or false: if properly managed, diabetes may shorten life expectancy by 5-15 years

A

false
if not properly managed, diabetes may shorten life expectancy by 5-15 years

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7
Q

What are the different cells that make up the Islets of Langerhans?

A

delta (10%): somatostatin
alpha (30%): glucagon
beta (60%): insulin

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8
Q

How is euglycemia maintained?

A

insulin, glucagon, and somatostatin working together

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9
Q

Differentiate between alpha and beta cells.

A

beta:
-50% of endocrine mass of pancreas
-produce insulin and amylin
-insulin released in response to elevated blood glucose levels
alpha:
-35% of endocrine mass of pancreas
-produce glucagon
-glucagon released in response to low blood glucose levels

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10
Q

What are normal blood glucose levels?

A

4-6mmol/L

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11
Q

Whats the stimulus for secretion of insulin? What about glucagon?

A

insulin:
-increased glucose, amino acids, ffa
-glucagon
-growth hormone
-cortisol
-GIP
glucagon:
-low glucose, amino acids
-epinephrine, norepinephrine

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12
Q

What is the net effect of insulin? What about glucagon?

A

insulin:
-decreased blood glucose
-increased storage of energy: glycogenesis, lipogenesis, protein
synthesis
glucagon:
-increased serum glucose
-increased energy release: protein breakdown, lipolysis,
gluconeogenesis, glycogenolysis

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13
Q

What is the major site of glucose uptake?

A

skeletal muscle
-with the ingestion of a meal and excess CHO, insulin
stimulates the uptake of glucose in skeletal muscle
-glucose is stored as glycogen in muscle & used in energy
metabolism (glycogenesis)

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14
Q

True or false: insulin stimulates the breakdown of proteins into amino acids

A

false
insulin stimulates production of protein from amino acids

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15
Q

In the fasted state what can the body do with proteins?

A

proteins converted to amino acids, transported to liver, converted to glucose via gluconeogenesis

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16
Q

Describe the liver and its role with glycogen.

A

site where glycogen is made, stored, & broken down
fed state: insulin released and stimulates liver to store glucose as glycogen (glycogenesis)
fasted state: glucagon released and liver provides glucose by glycogenolysis and gluconeogenesis

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17
Q

What happens when the amount of glucose entering the liver is greater than the storage capacity for glycogen?

A

insulin promotes conversion of glucose to fatty acids
stored as TG in adipose tissue

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18
Q

What can the body do with fats in the fasted state or insulin deficiency?

A

lipolysis
-TG split back to glycerol and FAs–>metabolism of FFA–>ketone bodies (ketone bodies can be used as energy source)

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19
Q

Which organ is constantly using glucose and does not depend on insulin?

A

the brain
-very sensitive to reduced glucose levels
-uses 20% of glucose even though its only 2% body weight

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20
Q

What are the different types of diabetes?

A

prediabetes:
-impaired glucose tolerance (IGT)
-impaired fasting glucose (IFG)
Type 1
Type 2
gestational diabetes
others: LADA, MODY, Type 3c

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21
Q

Describe Type 1 diabetes.

A

absolute lack of insulin secretion
primarily due to autoimmune beta-cell destruction
typically see markers of immune destruction present:
-islet cell antibodies, insulin antibodies, GAD antibodies
not uncommon to see with other autoimmune diseases

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22
Q

How does Type 1 diabetes usually present itself?

A

acute metabolic syndrome of relatively short duration in a child, adolescent, or young adult
-most incident cases <25yo; peak age 13-14yo
-can present up to 6th or 7th decade of life

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23
Q

How prevalent is Type 1 diabetes?

A

~10% of all diabetes
in adults: 10%
in children: 95%

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24
Q

When does hyperglycemia present itself in Type 1 diabetes?

Study These Flashcards
A

when 80-90% of B-cells are destroyed

25
What is the honeymoon phase in Type 1 diabetes?
correction of hyperglycemia causes insulin secretion to recover temporarily & insulin requirements may be quite low occurs in the days to weeks following diagnosis and initiation of insulin (can last months) this period is transient: continue to receive insulin, monitor for hypoglycemia
26
What is prediabetes?
intermediate state between normal glucose levels and diabetes includes IFG and IGT strong predictor of T2DM & CVD 30-60% will develop T2DM in the following 8-10yrs
27
How can diabetes be prevented in those with prediabetes?
lifestyle interventions or medications
28
Describe the diagnosis of prediabetes.
fasting plasma glucose: 6.1-6.9=IFG 2h PG in a 75g OGTT: 7.8-11=IGT A1C (%): 6-6.4=prediabetes
29
What is the 5-year incidence of diabetes if your A1C is one of the following: 5.0-5.5 5.5-6.0 6.0-6.5
5.0-5.5: <5-9% 5.5-6.0: 9-25% 6.0-6.5: 25-50%
30
What percentage of diabetes cases are made up by Type 2?
~90%
31
Describe Type 2 diabetes.
impaired insulin secretion and insulin resistance manifests in those who lose the ability to produce sufficient quantities of insulin to maintain normoglycemia in the face of insulin resistance interaction of genetics and environmental factors:
32
What are the many risk factors for Type 2 diabetes?
age >40 first-degree relative with T2DM member of high-risk population (African, Arab, Asian, Hispanic, Indigenous, South Asian, low socioeconomic status) overweight/obesity history of prediabetes history of GDM history of delivery of a macrosomic infant presence of end organ damage associated with diabetes -microvascular (retinopathy, neuropathy, nephropathy) -CV associated diseases vascular risk factors (low HDL, high TG, HTN, overweight, smoking) medications
33
What are some common medications which may increase blood glucose?
beta-blockers corticosteroids statins immunosuppressive agents thiazide or loop diuretics
34
Describe abdominal obesity as a risk factor for Type 2 diabetes.
insulin resistance found in most obese people -WC >102cm in men, >88cm in women=90% chance degree of obesity correlates with degree of insulin resistance visceral adipose tissue: stronger predictor of T2DM than BMI
35
True or false: T2DM patients have a significantly decreased B-cell mass as well as B-cell secretory deficit, this continues to deteriorate with time
true
36
Why is there impaired insulin secretion in response to food in Type 2 diabetes?
impaired B-cell function a reduced stimulus from incretin hormones
37
What are the consequences of defective insulin secretion?
hyperglycemia -first a reduced early phase of insulin secretion-->elevated PPG -then, late phase secretion diminishes-->elevated FPG
38
What is the primary site of insulin resistance?
skeletal muscle
39
What are the effects of insulin resistance on the liver and adipose tissue?
liver: inability to suppress hepatic glucose production adipose: increased lipolysis, leads to elevated FFAs which can stimulate liver glucose production
40
What is the ominous octet of Type 2 diabetes?
decreased insulin secretion from B-cells+increased glucagon secretion from a-cells decreased incretin effect increased lipolysis increased glucose reabsorption decreased glucose uptake neurotransmitter dysfunction increased hepatic glucose production inflammation
41
What is the clinical presentation of Type 1 diabetes?
acute symptoms of short duration: -polyphagia -polydipsia -polyuria -weight loss -fatigue -blurred vision -infections *20-40% present with DKA after several days of above symptoms*
42
What is the clinical presentation of Type 2 diabetes?
commonly discovered incidentally as patients may be asymptomatic: -nonspecific symptoms: polyuria, polydipsia, nocturia -may have complications at diagnosis
43
Differentiate between T1DM and T2DM based on the following: age of onset weight islet auto-antibodies C-peptide onset/symptoms first line treatment microvascular complications DKA
age of onset: -T1DM: most <25 but can occur at any age except <6mo -T2DM: usually >24 weight: -T1DM: usually thin but can be overweight or obese -T2DM: >90% at least overweight islet auto-antibodies: -T1DM: usually present (approx 90%) -T2DM: absent C-peptide: -T1DM: undetectable/low -T2DM: gradual/asymptomatic onset/symptoms: -T1DM: abrupt/symptomatic -T2DM: gradual/asymptomatic first line treatment: -T1DM: insulin -T2DM: antihyperglycemic agents, maybe insulin microvascular complications: -T1DM: absent at diagnosis -T2DM: present at diagnosis DKA: -T1DM: common -T2DM: rare
44
Which form of diabetes has the higher rate of family history?
Type 2 (75-90%)
45
What are the risk factors for T2DM in children?
T2DM in a 1st or 2nd degree relative high risk ethnic or racial group obesity IGT PCOS exposure to diabetes in utero acanthosis nigricans HTN and dyslipidemia NAFLD atypical antipsychotics
46
What is gestational diabetes mellitus?
condition that develops during pregnancy primarily due to insulin resistance increases risk of fetal hyperinsulinemia, heavier birth weight, higher rates of caesarian deliveries, and neonatal hypoglycemia increased risk of developing T2DM in mother and child
47
What are the risk factors for GDM?
previous GDM high-risk population previous delivery of macrosomic infant age >35 obesity PCOS acanthosis nigricans corticosteroid use
48
When should pregnant women be screened for GDM?
weeks 24-28 earlier if risk factors are present
49
True or false: there have been successful intervention methods for T1DM
false
50
What are the methods for prevention of T2DM?
lifestyle modification metformin acarbose piaglitazone rosiglitazone orlistat liraglutide *primarily involves targeting high risk individuals*
51
Describe the screening for diabetes.
T1DM: screening not recommended -low prevalence, no identifiable intervention T2DM: important due to large # of undiagnosed people -use FPG or A1C as initial screening tests
52
True or false: the tests used to screen for diabetes are different from those used to diagnose diabetes
false same tests for both
53
Describe the screening for Type 2 diabetes. (flow chart)
screen every 3yrs in ppl >40yrs or at high risk using calculator screen earlier and/or more frequently q6-12mo in people with additional risk factors or at very high risk using calculator FPG <5.6 and/or A1C <5.5%: -normal, rescreen as recommended FPG 5.6-6.0 and/or A1C 5.5-5.9%*: -at risk, rescreen more often FPG 6.1-6.9 and/or A1C 6.0-6.4%**: -prediabetes, rescreen more often FPG >7 and/or A1C >6.5%: -diabetes *=consider 75g OGTT if 1 risk factor **=consider 75g OGTT
54
What is CANRISK?
validated tool (in those >40) to assess risk available in 13 languages quick and easy stratifies people into low, medium, and high risk of having prediabetes or T2DM helps identify patients who should be referred
55
What is the diagnosis of diabetes for FPG, A1C, 2hPG in a 75g OGTT, and random PG?
FPG: >7.0mmol/L -fasting=no caloric intake for 8hrs A1C: >6.5% 2hPG in a 75g OGTT: >11.1mmol/L random PG: >11.1mmol/L -random=any time of the day *if asymptomatic do a confirmatory test another day, if symptomatic a confirmatory test is not required*
56
What are the advantages of FPG? Disadvantages?
advantages: -established standard -fast and easy disadvantages: -inconvenient -less sensitive than OGTT
57
What are the advantages of A1C? Disadvantages?
advantages: -convenient -better predictor of CVD -no day-to-day variability disadvantages: -cost -not valid for all medical conditions -altered by ethnicity and aging -not to be used for children, GDM, suspected T1DM
58
What are the advantages of 2hrPG 75 OGTT? Disadvantages?
advantages: -established standard disadvantages: -inconvenient -taste -cost

PHAR152 (21 decks)

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