Diabetes Flashcards

1
Q

def’n of diabetes

A

disorder of carb, protein and fat metabolism resulting from an imbalance b/w insulin availability and insulin need resulting in hyperglycemia – multi-system disease

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2
Q

diabetes prevalence

A

6.6% for over 12 years old

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3
Q

type 1 diabetes rate

A

10%; aka juvenile diabetes, IDDM

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4
Q

type 2 diabetes

A

90-95%; NIDDM

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5
Q

gestational diabetes

A

glucose intolerance that is first detected during pregnancy

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6
Q

type 1 def’n

A

pancreatic beta cells are progressively destroyed resulting in an absolute insulin deficiency (10%); onset usually rapid; more common in young people; catabolic disorder

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7
Q

type 1 causes

A
  1. type 1A autoimmune destruction (95%)

2. type 1B ideopathic diabetes (5%). inherited, non evidence of autoimmunity.

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8
Q

with an insulin deficiency…

A

stored fat is broken down to provide energy resulting in production of ketone bodies (which can lead to ketosis)

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9
Q

clinical manis of hyperglycemia

A
polyuria (glucose in urine)
polydipsia (increased thirst)
polyphagia (increased appetite)
wt loss (d/t mm wasting)
blurred vision 
weakness, fatigue
skin infection (too much glucose helps bacteria multiply)
ketoacidosis
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10
Q

type 2 diabetes def’n

A

pancreas usually continues to produce insulin but it is either insufficient for the needs of the body or is poorly utilized by the tissues or both; 95%; a/w obesity; risk increased after 35 years; genetic (runs in fams); aboriginals 3-5x more likely

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11
Q

hyperinsulinemia (a/w diabesity)

A

increased resistance to the action of insulin

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12
Q

(3) major metabolic anomalies have a role in development of type 2:

A
  1. insulin resistance (body tissues do not respond to insulin)
  2. marked decrease in ability to produce insulin (cells become fatigued from overproduction of insulin)
  3. inappropriate glucose production by the liver
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13
Q

insulin resistance

A
  • Insulin resistance stimulates an increase in insulin secretion (hyperinsulinemia), beta cells are trying to maintain a normal blood glucose level. In time, the increased demand for insulin secretion leads to beta cell exhaustion and failure. This results in elevated postprandial blood glucose levels and an eventual increase in glucose production by the liver.
  • Increased insulin resistance at the receptor sites of muscle tissue
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14
Q

what type of DM is LESS prone to ketoacidosis?

A

type 2

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15
Q

type 2 clinical manis

A

-develops gradually (S&S may take years)
-symptoms are non-specific (fatigue, irritability, polyuria, polydipsia)
the following cause ppl to seek med attention:
–Pruritis (hyperglycemia and glucosuria favour fungal growth)
–recurrent infections (increased gluc levels stimulates growth of microorganisms and impaired blood supply hinders healing)
–parasthesias (tingling/numbness)

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16
Q

type 2 DM – insulin resistance & metabolic syndrome CRITERIA

A

THREE OR MORE OF:

  • abdominal obesity: waist >35” women, 40” men
  • triglycerides >1.7 mmol/L
  • HDL 130/85 mm Hg
  • FBS > 6.1 mmol/L
17
Q

dx tests: FBS

A

value = or > 7 mmol/L suggests DM

capillary blood glucose (10-15% higher than serum)

18
Q

dx tests: random BS

A

= or > 11.1 mmol/L plus classic DM S&S

19
Q

dx tests: 2 hr PC blood sugar (postprandial serum glucose)

A

postload blood glucose level

normal <7.8 mmol/L

20
Q

oral glucose tolerance test (OGTT)

A
measures body's ability to store glucose by removing it from the blood; 75g concentrated glucose PO; serum and urine samples taken at test, 30 mins, 1 hr, 2 hr, 3 hrs. 
Normals:
-- fasting < 6.1 mmol/L
-- 30 mins < 11.1 mmol/L
-- 1 hr < 11.1 mmol/L
-- 2 hr < 7.8 mmol/L
ABNORMAL: = or > 11.1 mmol/L
3&4 hrs: <6.4 mmol/L