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Patho Exam 4 > Diabetes > Flashcards

Diabetes Flashcards

1
Q

what is DM?

A

it is a disorder of the carbohydrate (protein and fat) metabolism characterized by high level of blood glucose secondary to inability to produce or utilize insulin

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2
Q

the chronic elevated BG level eventually results in what 4 problems?

A
  1. cardiovascular disease
  2. renal problems
  3. PVDs
  4. disorders of the eyes
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3
Q

what are the 3 types of DM

A
  1. type 1
  2. type 2
  3. gestational
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4
Q

what are the 3 types of testing for DM (diagnostics)

A
  1. Fasting BG/sugar (FBS) - fasted for 12 hours
  2. A1c (HgA1c is the same thing) - avg of the blood sugar over the past 3 months, looking for compliance with managing your DM
  3. others: OGTT (oral glucose tolerance test) and random plasma glucose
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5
Q

what are the ranges for diagnostics with FBS?

A
  • Prediabetes: 100- 125 mg/dl
  • Diabetes: 126 mg/dl or greater
  • Normal: 99 mg/dl (equal or less)
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6
Q

what are the ranges for diagnostics with A1c?

A
  • Prediabetes: 5.7% - 6.4 %
  • Diabetes: 6.5 % or greater
  • Normal: < 5.7%
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7
Q

what 2 diagnostic tests can be paired on the same day?

A

FBS and A1c can be paired on the same day-

  • if both are on diabetes range, diagnosis is confirmed
  • for FBS- must be repeated on 2 different days.
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8
Q

what is the cause of type 1 DM?

A
  • unknown
  • they do NOT produce insulin
    = absolute insulin deficiency, affects the metabolism of carbs, fats, and proteins
  • destruction of pancreatic beta cells
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9
Q

type 1 DM complications from not having insulin (2)

A
  1. glucose can NOT enter muscle tissues
  2. glucose stays in the blood (hyperglycemia)
    = cells are starved = increased hunger sensation (polyphagia)
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10
Q

type 1 DM: high BG causes what effect to the cells?

A

high BG causes osmotic fluid loss from cells
1. intracellular dehydration
2. dehydration stimulates the hypothalamus to feel thirsty
= polydipsia

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11
Q

high BG is filtered where?

A

in the glomeruli within the kidney

- renal threshold for glucose is 160-190 mg

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12
Q

what occurs when high BG exceeds 160-190mg in the glomeruli?

A

glucose spills into the urine = glycosursia

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13
Q

if carbs cannot be metabolized, what happens to energy and the body?

A

if carbs cannot be metabolized = fats and proteins are used for energy
= body tissue loss

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14
Q

pathway of acute DM Pt’s with increased and uncontrolled metabolism of fats and proteins

A
  1. increased formation of ketones
  2. decreases blood pH (becomes acidic!)
  3. compensation: lungs blow off = Kussmaul’s respiration (deep and rapid breathing)
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15
Q

if acute DM Pt’s have increased ketones what happens?

A 
increased ketones = metabolic acidosis
= DKA:
1. hypovolemia
2. hypokalemia
3. increased serum osmolality (person is dehydrated from the polydipsia)
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16
Q

when does type 2 DM start

A

starts as insulin resistance - disorder in which body’s cells do NOT use insulin properly

17
Q

what 2 factors increase insulin resistance

A
  1. obesity

2. inactivity

18
Q

pathway (4) of type 2 DM

A
  1. The insensitivity of body cells to insulin causes the pancreas to secrete more insulin as compensatory mechanism
  2. pancreas eventually become overwork
  3. become exhausted and unable to secrete the needed amount of insulin
  4. = hyperglycemia
19
Q

type 2 DM is associated with (affecting factors)

A
  1. advancing age
  2. obesity
  3. family history
  4. history of gestational DM
  5. physical inactivity
20
Q

race/ethnicity’s that have a higher chance of type 2 DM

A
  • African-American
  • Hispanics
  • Native Americans
  • Asians
  • Native Hawaiians
  • other Pacific Islanders

it is rare but children of these ethnic groups have been getting diagnosed w/ type 2

21
Q

race/ethnicity’s that have a higher chance of type 1 DM

A

caucasians

22
Q

some s/s of DM

A
  • Pruritus
  • Paresthesia
  • 60-80% are obese (just type2)
23
Q

DKA is NOT typically a feature of type 2 because of the presence of some insulin =

A

allows some glucose uptake preventing massive fat breakdown which causes an acute complication of HHS, HHNKS, HHNKC

24
Q

complications of DM (6)

A
  1. hypoglycemia
  2. Somogyi Effect
  3. Dawn Phenomenon
  4. Type 1- DKA, positive for ketones
  5. Type 2- HHS/ HHNKS, negative for ketones
  6. Both DKA and HHS are massively dehydrated so we give them a huge amount of fluids
25
Q

describe hypoglycemia

A

b/c of the insulin, more dangerous than hyperglycemia = can lead to irreversible brain damage
• Lower than 70 the hypothalamus activates = sweating (unexplained night sweats), hungry, dizziness, nervousness, irritability, palpitation
• If left untreated = confusion, disorientation, loss of consciousness

26
Q

treatment of hypoglycemia

A

fast acting carbohydrate like juice, soda (no diet)

27
Q

describe dawn phenomenon

A

characterized by relatively normal BG level until ~3AM it begins to rise = usually due to a nocturnal surge of growth hormone SO a greater need for sugar in the morning
= insulin waning, progressive increase in BG from bedtime to morning

28
Q

treatment of dawn phenomenon

A

moving the evening dose to bedtime

29
Q

describe somogyi effect

A

nocturnal hypoglycemia followed by rebound hyperglycemia, at bedtime it is normal, between 2-3AM BG low and then slowly goes up after 3AM

30
Q

treatment of somogyi effect

A

lower the evening dose of the intermediate acting insulin or increase the bedtime snack

31
Q

long term complications of DM

A
  • Atherosclerosis
  • CAD
  • Poor wound healing
  • Stroke
  • Candidiasis
  • Peripheral arterial diseases = BKA/AKA (below or above the knee amputation)
  • Retinopathy – regular eye exams
  • Autonomic neuropathy
  • Nephropathy
  • peripheral neuropathy – less pain sensation

Patho Exam 4 (6 decks)

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