Type 1 Diabetes Mellitus Flashcards

1
Q

What is the definition of type 1 diabetes mellitus?

A

Total destruction of beta cells in the pancreas
People are not making their own insulin

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2
Q

Onset of Type 1 DM

A

Typically diagnosed before age 30, often in children or teenagers

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3
Q

Prevalence of type 1 DM

A

Accounts for 5-10% of all diabetes cases

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4
Q

What is type 1 DM autoimmune response?

A

The body mistakenly attacks its own beta cells

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5
Q

Type 1 DM often follows what?

A

An infection (viral, bacterial, or fungal)

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6
Q

What should be done if one sibling/ child has type 1 DM?

A

If one sibling has it, others should be tested

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7
Q

Why is type 1 DM considered the most severe form of diabetes?

A

Because of the absolute lack of insulin

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8
Q

List the 2 types of type 1 DM

A

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

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9
Q

How does type 1 DM differ in children and adults?

A

rapid destruction to kids can be slower in adults

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10
Q

What are the three “Ps” known to be classic Sx of type 1 DM?

A

1) Polyuria
2) Polydipsia
3) Polyphagia

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11
Q

What other classic Sx are seen with type 1 DM?

A

1) visual disturbances
2) fatigue
3) weakness

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12
Q

What is often the presenting sign of type 1 DM?

A

Diabetic ketoacidosis (DKA)

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13
Q

What kind of insulin does type 1 DM require?

A

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

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14
Q

Define ketosis

A

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

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15
Q

Genetic predisposition of type 1 DM

A

Mutation on human leukocyte antibodies on chromosome 6

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16
Q

Type 1 DM increases risk of other autoimmune diseases such as… Hint: 3

A

1) celiac disease (gluten intolerance)
2) rheumatoid arthritis
3) hypothyroidism (Hashimoto’s disease)

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17
Q

How do T-lymphocytes play a role in Type 1 DM?

A

T-lymphocytes mediate hypersensitivity to beta-cell antibodies

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18
Q

List 8 clinical manifestations of type 1 DM

A

1) weight loss despite increased appetite
2) abdominal pain
3) neuro Sx
4) extremely elevated glucose
5) ketones in urine
6) Metabolic acidosis
7) often presents in DKA
8) mood changes

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19
Q

Neuro Sx of type 1 DM

A

Blurred vision due to glucose affecting the lens of the eye

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20
Q

What can blurred vision lead to in type 1 DM?

A

Diabetic retinopathy & blindness

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21
Q

What kind of mood changes might we see associated with type 1 DM?

A

1) irritability
2) mood swings
3) cognitive changes
4) confused with personality disorders

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22
Q

What is ketosis & DKA caused by?

A

The body breaking down fatty acids for energy. leads to ketone buildup, metabolic acidosis, & severe dehydration

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23
Q

Frequent ____ infections can also be a clinical manifestation of type 1 DM

A

frequent candida infections

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24
Q

What is polydipsia?

A

Excessive thirst

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25
Q

What causes polydipsia?

A

fluid shifts due to high blood sugar → hyperglycemia ↑ osmotic pressure in ECF shifting water to ICF

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26
Q

What can polydipsia result in?

A

1) cellular dehydration
2) triggers thirst sensation

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27
Q

What is polyuria?

A

Frequent urination

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28
Q

How is polyuria related to type 1 DM?

A

Renal threshold for glucose reabsorption is exceeded

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29
Q

Polyuria:

What happens when glucose is > 180…

A

it exceeds the renal threshold, leads to increased glucose excretion & hypovolemia & increased serum osmolality

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30
Q

What does polyuria result in?

A

Glucose remaining in renal tubules

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31
Q

Polyuria:

What develops to pull water from the tubule cells into the urine?

A

Osmotic gradient

32
Q

List 2 things polyuria results in

A

1) excessive glucose in the bloodstream
2) kidneys filter out excess glucose, pulling water with it

33
Q

What is polyphagia?

A

Increased appetite with weight loss

34
Q

What do we see in polyphagia?

A

Insulin deficiency → cells not receiving glucose → sets into effect compensatory processes to ↑ blood glucose levels

35
Q

Polyphagia is when the body is unable to properly utilize ____

A

glucose
High glucose levels, but cells remain energy starved

36
Q

Liver breaks glycogen into ____

37
Q

When exhausted fat breakdowns (lipolysis) into: Hint: 3

A

1) fatty acids & glycerol
2) fatty acids converted to ketones in blood stream → ketosis
3) glycerol to liver to make glucose (gluconeogenesis)

38
Q

When fat exhausted muscle breakdown occurs it breaks into ____ ____

A

Amino acids

39
Q

Where do amino acids go to make glucose (gluconeogenesis)

40
Q

Blurred vision is accumulation of what?

A

Glucose in aqueous fluid in cornea; osmolarity change
Alters retraction of light entering the eye

41
Q

Important things to note about ketones Hint: 5

A

1) altered process of aerobic & anaerobic metabolism
2) breakdown of fat into free fatty acids & glycerol for energy
3) converted into ketones by liver
4) strong acids that accumulate in the blood & can lead to metabolic acidosis
5) gluconeogenesis occurs instead of Krebs or citric acid cycle

42
Q

DKA is considered what type of emergency?

A

Hyperglycemic emergency

43
Q

Insulin levels in DKA

A

Markedly decreased or absent
life-threatening condition due to lack of insulin

44
Q

Is DKA seen in both type 1 & 2 DM?

A

Typically seen in type 1, but can occur in type 2

45
Q

What do blood sugar levels look like in someone with DKA?

A

> 250 mg/dL (often > 500 mg/dL)

46
Q

What age group is DKA commonly seen in?

A

Younger people, but can occur at any age

47
Q

DKA is characterized by what 4 things

A

1) hyperglycemia
2) metabolic acidosis
3) dehydration
4) electrolyte loss

48
Q

DKA results from development of ____

49
Q

List the 4 main causes of DKA

A

1) infection/ illness (i.e. UTIs, pneumonia)
2) lack of insulin (missed doses)
3) undiagnosed/ under treated diabetes
4) poor compliance (common in teens)

50
Q

What 4 things help to Dx DKA?

A

1) serum glucose > 250 mg/dL
2) ketonemia & ketonuria
3) low pH
4) low HCO3

51
Q

What are the 4 presenting Sx of DKA?

A

1) 3 P’s & weight loss
2) abdominal pain
3) severe N/V
4) marked fatigue

52
Q

List 4 other Sx seen in DKA

A

1) extreme dehydration
2) acetone breath
3) Kussmaul respirations
4) changes in LOC

53
Q

What is commonly seen due to extreme dehydration in DKA? Hint: 3

A

1) poor skin turgor
2) dry mucous membranes/ skin
3) tachycardia & hypotension (shock response)

54
Q

What is acetone breath?

A

Fruity smelling breath due to ketones

55
Q

What are Kussmaul respirations?

A

deep, rapid breathing
the body tries to compensate for metabolic acidosis by blowing off CO2

56
Q

What kind of changes in LOC might we see in DKA?

A

Confusion to unconsciousness

57
Q

What is first line Tx for DKA & why?

A

Fluid replacement
1) to restore intravascular volume (correct dehydration)
2) to clear ketones
3) to correct electrolyte imbalances

58
Q

How should regular insulin be given for TX of DKA? Hint: think route

A

IV insulin until blood glucose is < 250 then switch to SQ insulin

59
Q

Insulin therapy for DKA should be administered ___

A

slowly to avoid rapid fluid shifts

60
Q

What is the goal of insulin therapy when Tx DKA?

A

Gradual blood sugar reduction to avoid hypoglycemia

61
Q

What is important to monitor for when Tx DKA?

A

Cerebral edema → as fluid shifts back to the cells

62
Q

List the 2 most common electrolyte imbalances seen with DKA

A

1) hyponatremia
2) hyperkalemia

63
Q

Why are potassium levels especially important to monitor when Tx DKA?

A

Insulin shifts potassium back into cells, possibly leading to hypokalemia

64
Q

Hypoglycemia is defined as

A

Blood glucose < 70 mg/dL with or w/o Sx

65
Q

What patients does hypoglycemia most commonly occur in?

A

Patients treated with insulin
- but can also occur from some oral antidiabetic agents

66
Q

List 6 factors that can precipitate hypoglycemia in patient on insulin

A

1) error in insulin dose
2) failure to eat
3) increased exercise
4) decreased insulin need after removal of stressful situation
5) medication changes
6) alcohol ingestion (↓ liver gluconeogenesis)

67
Q

List 15 common Sx of hypoglycemia (box from txt)

A

1) sweating
2) hunger
3) dizziness
4) nervousness
5) tremulousness
6) irritability
7) headache
8) heart palpitations
9) confusion
10) disorientation
11) inability to concentrate
12) seizures
13) stupor or loss of consciousness
14) unexplained night sweats
15) cloudy mental state upon arising

68
Q

List 5 Sx of nocturnal hypoglycemia

A

1) sleep disturbances
2) vivid dreams
3) morning headache
4) chronic fatigue
5) depression

69
Q

Morning hyperglycemia:

What is Dawn phenomenon?

A

Increase in fasting blood glucose &/or insulin requirements during early morning hrs

70
Q

Is dawn phenomenon triggered by a nocturnal hypoglycemic event?

71
Q

Cause of dawn phenomenon

A

Natural (nocturnal) rise of cortisol & growth hormone early in the morning → slows cells use of glucose

72
Q

Morning hyperglycemia:

Somogyi effect cause

A

Nocturnal hypoglycemia followed by rebound hyperglycemia (overcorrection)

73
Q

How does Somogyi effect occur?

A

Hypoglycemia triggers the release of counter-regulatory hormones: releasing glycogen from liver; epinephrine, cortisol, & growth hormone

74
Q

What occurs at night that leads to Somogyi effect?

A

Too much or too little insulin at bedtime or skipped nighttime snack

75
Q

Tx of Somogyi effect

A

Decrease insulin dose or change time of medication

76
Q

What are the key differences between Dawn phenomenon & Somogyi effect

A

Dawn → blood sugar is normal/ high at 3AM
Somogyi → Blood sugar is low at 3 AM then rebounds high

77
Q

Management for morning hyperglycemic episodes

A

Adjust insulin dose or alter bedtime snack timing