Lecture 11: Diabetes Flashcards

1
Q

pancreatic alpha cells

A

produce glucagon (hormone) = increases blood sugar levels

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2
Q

pancreatic beta cells

A

produces insulin = lower blood sugar levels by allowing cells to absorb glucose from blood

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3
Q

rise of glucose triggers what when you eat

A

insulin

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4
Q

what spikes after every meal to make levels go back to normal

A

insulin

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5
Q

what is insulin

A

key hormone that promotes uptake of glucose

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6
Q

what are counter-regulatory hormones

A
  • oppose effect of insulin
  • stim glucose production and output by liver
  • decrease movement of glucose into the cells
  • ex: glucagon, epinephrine, growth hormone, and cortisol
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7
Q

what is prediabetes

A
  • ppl at risk for diabetes
  • blood glucose high but not high enough to have diabetes
  • long term damage alr occuring
  • impaired fasting glucose (6.1-6.9 mmol/L)
  • impaired glucose tolerance (2 hour plasma glucose levels between 7.1 and 11 mmol/L)
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8
Q

prediabetes symptoms

A
  • polyuria (increased urine)
  • polyphagia (increased eating)
  • polydipsia (excessive thirst)
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9
Q

diagnosis of diabetes

A
  • fasting glucose greater or equal to 7 mmol/L
  • A1C greater or equal 6.5%
  • 2 hr plasma glucose in a 75g oral glucose
  • random PG greater or equal to 11.1 mmol/L + sympt
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10
Q

types of diabetes

A

type 1, and type 2
also gestational and prediabetes

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11
Q

type 1 diabetes

A

“insulin dependent diabetes”
- progression destruction of beta cells
- antibodies present for months to years before sympt occur
- sympt come when ur pancreas can no longer produce insulin

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12
Q

when you have dangerously high blood glucose levels at the ER what do you show up with

A

ketoacidosis
- also weight loss, polydipsia, polyuria, polyphagia

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13
Q

type 2 diabetes

A
  • most prevalent type
  • overweight
  • genetic basis
  • pancreas continues to produce some endogenous insulin. insulin produced is insufficient or is poorly utilized by tissues
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14
Q

type 2 diabetes abnormalities

A
  • insulin resistance: body tissues don’t respond to insulin
  • pancreas decreases ability to produce insulin
  • inappropriate glucose production from liver
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15
Q

clinical manifestations of type 1 diabetes

A
  • usually acute onset
  • polyuria, polyphagia, polydipsia
  • weight loss
  • weakness, fatigue
  • visual changes
  • women-yeast infections
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16
Q

type 2 diabetes clinical manifestations

A
  • non-specific
  • gradual onset
  • fatigue
  • poor wound healing
  • recurrent infections
  • visual acuity changes
  • painful peripheral neuropathy in the feet
17
Q

type 1 diabetes diet

A
  • balance meal plan
  • insulin + exercise balance = good
18
Q

type 2 diabetes diet

A
  • emphasis on achieving glucose, lipid, and bp goals
  • calorie reduction and weight loss
19
Q

why is exercise important for diabetes

A
  • increases insulin receptor sites
  • lowers blood glucose levels
  • contributes to weight loss
20
Q

administration of insulin

A
  • SC injection for self-admin
  • IV admin in care setting
21
Q

where is the fastest absorption for insulin therapy

A

abdomen, followed by arm, thigh, and buttock

rotate injections within one particular site

do not inject in site to be exercised

22
Q

no diabetes level

A

HbA1C : <5.7%

23
Q

hypoglycemia level

A

< 4 mmol/L

24
Q

insulin therapy problems

A
  • hypoglycemia
  • allergic reactions
  • lipodystrophy
  • somogyi effect
  • dawn effect
25
Q

biguanides

A

(1st line for most type 2 diabetes)
- antihyperglycemics
ex: metformin

26
Q

sulphonylureas

A

-increase insulin production from pancreas
-increase risk of hypoglycemia
ex:Gliclazide and glyburide

27
Q

Non-sulfonylureas

A

-increase insulin production from pancreas
-takes 30 mins before meal
ex: Repaglinide

28
Q

Dipeptidyl peptidase-4 (DDP-4) Inhibitors

A
  • increase and prolong incretin levels
  • glucose dependent
  • antihyperglycemics
    ex: sitagliptin