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Type 1 Diabetes 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
What causes polydipsia?
fluid shifts due to high blood sugar → hyperglycemia ↑ osmotic pressure in ECF shifting water to ICF
26
What can polydipsia result in?
1) cellular dehydration 2) triggers thirst sensation
27
What is polyuria?
Frequent urination
28
How is polyuria related to type 1 DM?
Renal threshold for glucose reabsorption is exceeded
29
Polyuria: What happens when glucose is > 180...
it exceeds the renal threshold, leads to increased glucose excretion & hypovolemia & increased serum osmolality
30
What does polyuria result in?
Glucose remaining in renal tubules
31
Polyuria: What develops to pull water from the tubule cells into the urine?
Osmotic gradient
32
List 2 things polyuria results in
1) excessive glucose in the bloodstream 2) kidneys filter out excess glucose, pulling water with it
33
What is polyphagia?
Increased appetite with weight loss
34
What do we see in polyphagia?
Insulin deficiency → cells not receiving glucose → sets into effect compensatory processes to ↑ blood glucose levels
35
Polyphagia is when the body is unable to properly utilize ____
glucose **High glucose levels, but cells remain energy starved**
36
Liver breaks glycogen into ____
glucose
37
When exhausted fat breakdowns (lipolysis) into: **Hint: 3**
1) fatty acids & glycerol 2) fatty acids converted to ketones in blood stream → ketosis 3) glycerol to liver to make glucose (gluconeogenesis)
38
When fat exhausted muscle breakdown occurs it breaks into ____ ____
Amino acids
39
Where do amino acids go to make glucose (gluconeogenesis)
The liver
40
Blurred vision is accumulation of what?
Glucose in aqueous fluid in cornea; osmolarity change **Alters retraction of light entering the eye**
41
Important things to note about ketones **Hint: 5**
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
DKA is considered what type of emergency?
Hyperglycemic emergency
43
Insulin levels in DKA
Markedly decreased or absent **life-threatening condition due to lack of insulin**
44
Is DKA seen in both type 1 & 2 DM?
Typically seen in type 1, but can occur in type 2
45
What do blood sugar levels look like in someone with DKA?
> 250 mg/dL (often > 500 mg/dL)
46
What age group is DKA commonly seen in?
Younger people, but can occur at any age
47
DKA is characterized by what 4 things
1) hyperglycemia 2) metabolic acidosis 3) dehydration 4) electrolyte loss
48
DKA results from development of ____
ketosis
49
List the 4 main causes of DKA
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
What 4 things help to Dx DKA?
1) serum glucose > 250 mg/dL 2) ketonemia & ketonuria 3) low pH 4) low HCO3
51
What are the 4 presenting Sx of DKA?
1) 3 P's & weight loss 2) abdominal pain 3) severe N/V 4) marked fatigue
52
List 4 other Sx seen in DKA
1) extreme dehydration 2) acetone breath 3) Kussmaul respirations 4) changes in LOC
53
What is commonly seen due to extreme dehydration in DKA? **Hint: 3**
1) poor skin turgor 2) dry mucous membranes/ skin 3) tachycardia & hypotension (shock response)
54
What is acetone breath?
Fruity smelling breath due to ketones
55
What are Kussmaul respirations?
**deep, rapid breathing** the body tries to compensate for metabolic acidosis by blowing off CO2
56
What kind of changes in LOC might we see in DKA?
Confusion to unconsciousness
57
What is first line Tx for DKA & why?
**Fluid replacement** 1) to restore intravascular volume (correct dehydration) 2) to clear ketones 3) to correct electrolyte imbalances
58
How should regular insulin be given for TX of DKA? **Hint: think route**
IV insulin until blood glucose is < 250 then switch to SQ insulin
59
Insulin therapy for DKA should be administered ___
slowly to avoid rapid fluid shifts
60
What is the goal of insulin therapy when Tx DKA?
Gradual blood sugar reduction to avoid hypoglycemia
61
What is important to monitor for when Tx DKA?
Cerebral edema → as fluid shifts back to the cells
62
List the 2 most common electrolyte imbalances seen with DKA
1) hyponatremia 2) hyperkalemia
63
Why are potassium levels especially important to monitor when Tx DKA?
Insulin shifts potassium back into cells, possibly leading to **hypokalemia**
64
Hypoglycemia is defined as
Blood glucose < 70 mg/dL with or w/o Sx
65
What patients does hypoglycemia most commonly occur in?
Patients treated with insulin - but can also occur from some oral antidiabetic agents
66
List 6 factors that can precipitate hypoglycemia in patient on insulin
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
List 15 common Sx of hypoglycemia (box from txt)
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
List 5 Sx of nocturnal hypoglycemia
1) sleep disturbances 2) vivid dreams 3) morning headache 4) chronic fatigue 5) depression
69
Morning hyperglycemia: What is Dawn phenomenon?
Increase in fasting blood glucose &/or insulin requirements during early morning hrs
70
Is dawn phenomenon triggered by a nocturnal hypoglycemic event?
No
71
Cause of dawn phenomenon
Natural (nocturnal) rise of cortisol & growth hormone early in the morning → slows cells use of glucose
72
Morning hyperglycemia: Somogyi effect cause
Nocturnal hypoglycemia followed by rebound hyperglycemia (overcorrection)
73
How does Somogyi effect occur?
Hypoglycemia triggers the release of counter-regulatory hormones: releasing glycogen from liver; epinephrine, cortisol, & growth hormone
74
What occurs at night that leads to Somogyi effect?
Too much or too little insulin at bedtime or skipped nighttime snack
75
Tx of Somogyi effect
Decrease insulin dose or change time of medication
76
What are the key differences between Dawn phenomenon & Somogyi effect
Dawn → blood sugar is normal/ high at 3AM Somogyi → Blood sugar is low at 3 AM then rebounds high
77
Management for morning hyperglycemic episodes
Adjust insulin dose or alter bedtime snack timing

Pharm Final Exam (34 decks)

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