type 1 diabetes Flashcards

1
Q

What is happening in type 1 DM?

A

total destruction of the pancreatic beta cells

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2
Q

What is type 1 DM considered?

A

an autoimmune disorder

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3
Q

What are the two types of type 1 DM?

A

type 1A (90-95%)
Type B (idopathic, no autoimmune)

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4
Q

What is the prevalence of type 1 DM?

A

accounts for 5-10% of all diabetes

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5
Q

What are the sx of short-term acute complications of T1D?

A

three Ps
- polyuria
- polydipsia
- polyphagia
- may have visual disturbances, fatigue, weakness
- DKA is often the presenting sign

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6
Q

What is required for short-term acute complications of T1D?

A

requires exogenous insulin to stop the catabolic process, lower the blood sugar, & prevent ketosis

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7
Q

What is ketosis?

A

a metabolic state where the body uses free fatty acids for energy instead of glucose

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8
Q

What causes T1D?

A

genetic predisposition
- mutation on human leukocyte antibodies on chromosome 6

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9
Q

What triggers T1D?

A

triggered by illness, viral infection or autoimmune disease

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10
Q

T1D is __ - ______________ mediated hypersensitivity to _____ - _____ antibodies

A

T- lymphocyte; beta-cell

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11
Q

What are those with T1D at increased risk for?

A

increased risk for other diseases, such as celiac disease, rheumatoid arthritis & hypothyroidism

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12
Q

What are the clinical manifestations of T1D?

A
  • polydipsia
  • polyuria
  • polyphagia
  • weight loss
  • abd pain
  • blurred vision (accumulation of aqueous humor in the eye)
  • frequent candida infections
  • extremely elevated glucose
  • ketones in urine
  • metabolic acidosis
  • often presents in DKA
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13
Q

What causes polydipsia in T1D?

A
  • hyperglycemia increases osmotic pressure in extracellular compartments
  • results in water shifting out of intracellular space
  • cellular dehydration creates sense of thirst
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14
Q

What is polyuria?

A

increased amount & frequency of urination

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15
Q

What causes polyuria?

A
  • renal threshold for glucose reabsoprtion is exceeded
  • results in glucose remaining in renal tubule
  • osmotic gradient develops which pulls water from the tubule cells into urine
  • “spilling” glucose in urine = renal threshold is exceeded
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16
Q

What is polyphagia?

A

increased hunger (w/ weightloss in T1D)

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17
Q

What causes polyphagia?

A

insulin deficiency; cells are not recieving glucose which sets compensatory processes into place to incrrease blood glucose levels

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18
Q

polyphagia:
What does the liver break glycogen into?

A

glucose

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19
Q

What is the process of fat breakdown called?

A

lypolysis

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20
Q

What does fat breakdown into?

A

fatty acids and glycerol

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21
Q

What are fatty acids converted to in T1D?

A

converted to ketones in the blood stream

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22
Q

What is the process of fatty acids being converted into ketones called?

A

ketosis

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23
Q

Where does glycerol go and what does it make?

A

glycerol goes to the liver to make glucose

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24
Q

What is the process of glycerol being converted to glucose called?

A

gluconeogenesis

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25
When fat has been exhausted what occurs?
muscle breakdown occurs
26
What is muscle brokendown into?
amino acids
27
Where do amino acids go to be converted to glucose?
the liver
28
Why does blurred vision occur T1D?
accumulation of glucose in aqueous fluid in cornea; causes osmolarity change
29
What does the osmolarity change in the eye do?
alters refraction of light entering the eye
30
What is a result of the altered process of aerobic and anaerobic metabolism?
ketones
31
What are ketones a result of?
breakdown of fat into free fatty acids & glycerol for energy
32
What organ converts fatty acids and glycerol into ketones?
the liver
33
What are strong acids that accumulate in the blood and can lead to metabolic acidosis?
ketones
34
__________________ occurs instead of ________ or citric acid cycle when ketones are made
gluconeogenesis; krebs
35
What is considered a hyperglycemic emergency?
diabetic ketoacidosis
36
What causes diabetic ketoacidosis?
markedly decreased or absence in the amount of insulin
37
diabetic ketoacidosis is typically seen in _______ but can occur in ______
T1D; T2D
38
___________ _____________ may be the initial presentation of type 1
diabetic ketoacidosis
39
In what age group does diabetic ketoacidosis usually occur?
occurs most often in younger people but can happen at any age
40
What is diabetic ketoacidosis characterized by? (hint:4)
1. hyperglycemia 2. metabolic acidosis 3. dehydration 4. electrolyte loss
41
diabetic ketoacidosis results from development of ________
ketosis
42
How is diabetic ketoacidosis diagnosed?
- serum glucose >250mg/dl - ketonemia and urine - low pH - low HCO3
43
What are the three main causes of diabetic ketoacidosis?
- infection or illness - lack of insulin - undiagnosed or undertreated diabetes - poor compliance (teens)
44
What are the sx of DKA?
- 3 Ps - weight loss - severe N/V - marked fatigue - extreme dehydration - poor skin turgor - dry mucous membranes - tachycardia - hypotension - acetone breath - kussmaul resp - changes in LOC
45
What is the first step to treat DKA?
fluid replacement!
46
Why do we want to begin with fluid replacement when treating DKA?
- to restore intravascular volume - to clear ketones - to correct electrolyte imbalances
47
What kind of insulin should you give to treat DKA?
regular; IV insulin BG is <250. Then switch to SQ insulin
48
What should you monitor when treating DKA?
- need to monitor for cerebral edema as fluid shifts back to the cells - need to monitor for hypokalemia as insulin shifts potassium back into cells
49
What are the most common electrolyte imbalances seen in DKA?
hyponatremia & hyperkalemia
50
What is the final part of treating DKA after immediate issues are solved?
treating the underlying cause
51
What is hypoglycemia defined as?
defined as BG <70 mg/dl with or w/o sx
52
In what group does hypoglycemia usually occur?
occurs most commonly in patients treated with insulin but can occur from some oral antidiabetic agents
53
What factors can precipitate hypoglycemia in patients on insulin?
- errors in insulin dosing - failure to eat - increased exercise - decreased insulin need after removal of stressful situation - medication changes - alcohol ingestion (decreases liver gluconeogenesis)
54
What are the sx of hypoglycemia?
- sweating - hunger - dizziness - nervousness - tremulousness - irritability - headache - heart palpitations - confusion - disorientation - inability to concentrate - seizures - stupor or LOC - unexplained night sweats cloudy mental state upon arising
55
What are sx of nocturnal hypoglycemia?
- sleep disturbances - vivid dreams - morning headache - chronic fatigue - depression
56
What is the dawn phenonmenon?
increase in fasting blood glucose and/or insulin requirements during the early morning hours
57
What is not triggered by a nocturnal hypoglycemia event?
the dawn phenomenon
58
What causes the dawn phenonmenon?
due to nocturnal elevation of growth hormone which raises BG - slows cells use of glucose
59
What is the somogyi effect?
nocturnal hypoglycemia followed by rebound hyperglycemia
60
What does hypoglycemia trigger during the somogyi effect?
hypoglycemia triggers the release of counter-regulatory hormones: releasing glycogen from the liver; epinephrine, cortisol & growth hormone
61
What does the somogyi effect occur?
occurs due to too much or too little insulin at bedtime or skipped nighttime snack
62
How do you treat the somogyi effect?
decrease insulin dose or changing the time of medication
63
How do you tell the difference between dawn phenomenon and somogyi effect?
check the glucose level in the middle of the night
64
What are the glucose levels at 3am in the dawn phenomenon and somogyi effect?
dawn - normal/ high glucose somogyi - low glucose