Brainscape's Knowledge GenomeTM


Top Flashcards (Certified)
All Flashcards

chronic > chronic exam 1-diabetes > Flashcards

chronic exam 1-diabetes Flashcards

1
Q

beta cells produce

A

insulin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

alpha cells produce

A

glucagon

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

functions of insulin

A 
lowers blood glucose by:
regulates rate of CHO metabolism
promotes glycogen storage
inhibits fats breakdown
inhibits protein breakdown
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

functions of glucagon

A

raises blood sugar by promoting conversion of glycogen to glucose

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

name of type 1 diabetes

A

IDDM (insulin dependent diabetes mellitus)

previously called juvenile diabetes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

name of type 2 diabetes

A

NIDDM (non-insulin dependent diabetes mellitus)

previously called maturity onset diabetes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

type 1 diabetes is characterized by

A

a total lack of insulin production

suggests an autoimmune process that destroys beta cells

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

type 2 diabetes is characterized by

A

an inadequate production of insulin or increased cellular resistant to the body’s own insulin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

type 1 diabetes onset

A

faster onset
usually before 30yo but can occur at any age
tend to be normal weight

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

type 2 diabetes onset

A

slower onset
usually 35+ years but can occur at any age
tend to be obese

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

% of diabetics that are type 1

A

10-15%

insulin required by all

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

% of diabetics that are type 2

A

85-90%
increased familial predisposition
insulin required for 20-30%

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

clinical manifestations

A
  1. three P’s
  2. weight loss-cant breakdown glucose so it’ll breakdown fat
  3. fatigue/weakness
  4. blurred vision
  5. frequent infections-glucose harbors bacterial growth
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

three P’s

A

polydipsia-excessive thirst
polyphagia-excessive hunger
polyuria-excessive urination

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

fasting blood sugar

A

70-110 mg/dL

Diagnosis= FBS>126 on 2 different occasions

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

glycoslyated hemoglobin

A

Hgb A1C
Hgb molecules combine with glucose to from glycohemoglobin which is stored by red blood cells
the percentage of “glycosylated hemoglobin” can be measured by a blood test (4%-6%)
indicator od an individual’s glucose level for the previous three months

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

6 food groups

A 
Starch/Bread
Protein/Meat
Dairy/Milk
Fruits
Vegetables
Fats
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

distributions of calories

A

50-60% Carbs
20-30% Fats
20% protein

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

dietary considerations

A 
special foods are not necessary
alcohol promotes hypoglycemia
dont skip meals
do strive for regular meal times
do control fat
do use sugar substitutes (equal splenda etc)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

net effect of exercise

A

lower blood sugar by transporting glucose into the muscle cell (must be aerobic exercise)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

controlling type 2 diabetes

A

may be controlled with diet and exercise alone, or in combination with oral hypoglycemics

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

original source of insulin

A

beef and pork pancreas

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

persons using synthetic insulins….

A

have a lower risk of insulin resistance

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

rapid acting types

A

Humalog (lispro)

Novalog (aspart)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Short Acting types
regular
26
Intermediate acting types
NPH (cloudy)
27
Long acting types
Glargine (Lantus) | Detemir (Levemir)
28
onset peak duration of Rapid Acting
Onset: 10-15 min Peak: 1 hr Duration: 2-4 hr
29
onset peak duration of Short Acting
Onset: 1/2 hr-1 hr Peak: 2-4 hr Duration: 5-7 hr
30
onset peak duration of Intermediate Acting
Onset: 2-4 hr Peak: 6-12 hr Duration: 18-24 hr
31
onset peak duration of Long Acting
Onset: 3-4 Peak: none for lantus; 3-14 hr for detemir Duration:24-36 hr
32
insulin preparation
cloudy clear clear cloudy
33
insulin storage
keep vial at room temp refrigerate spare vials protect from extreme heat, freezing
34
injection teaching
more rapid absorption from abdomen, then arms, then legs
35
lipohypertrophy
fat accumulation which occurs at sites of frequent insulin injection
36
injection rotation
rotate within each site, spacing injections 1 inch apart | do not se a site longer than a month
37
sulfonylureas
Glucatrol, Glimepiride | Stimulates beta cells to produce insulin; increase cellular receptivity
38
Meglitinides
Prandin | stimulates beta cells to produce insulin
39
Biguanides
Glucophage | Increase cellular receptivity to insulin; decrease hepatic production of glucose
40
Thiazolidinediones (TZDs)
Avandia, Actos | Decrease insulin resistance by increasing receptor sensitivity
41
Alpha-glucosidase Inhibitors
Precose | Delay digestion of complex carbs
42
Incretin Mimetics
decrease glucagon secretion from pancreas, increase insulin release
43
DDP-4 Inhibitors
Inhibit enzyme that inactivates incretin
44
Diabetic Ketoacidosis
usually occurs in type 1 diabetes As a result of severe insulin deficiency, the body resorts to breakdown of fats and proteins since it cannot utilize glucose
45
DKA pathophysiology
``` ketone production (incomplete fat metabolism) acidosis profound dehydration (due to osmotic diuresis) Hyperkalemia (potassium shifts out of the cells) ```
46
DKA causes
undiagnosed Diabetes omitting insulin especially on sick days not enough insulin in relation to a physical stressor
47
DKA stressors
``` cause a sympathetic response which mobilizes glycogen from the liver resulting in hyperglycemia surgery infection trauma illness ```
48
DKA clinical manifestations
``` 3P's dehydration tachycardia hypotension warm, dry skin n/v fruity breath Kussmaul Respirations ```
49
Kussmaul Respirations
increases rate and depth to blow off CO2 and raise pH
50
DKA diagnostics
pH 350 mg/dL positive serum acetone positive ketonuria potassium >5.0
51
DKA management
IV fluids IV insulin (regular only, continuous low dose) IV K+ prn (as pH improves, K levels drop)
52
DKA complications
hypovolemic shock coma death
53
HHNK
hyperglycemic, hyperosmolar Nonketotic Coma primarily occurs in T2Diabetes insufficient insulin prevents ketoacidosis but not severe hyperglycemia
54
HHNK causes
often the same precipitating factors as for DKA
55
HHNK clinical manifestations
``` severe hyperglycemia (>1000mg/dL) severe dehydration hypotension tachycardia hypovolemic shock leading to coma ```
56
HHNK Management
Rapid IV fluid replacement to correct fluid deficit | continuous low dose infusion of regular IV insulin
57
hypoglycemia (insulin reaction)
Most common type one diabetic's related to insulin therapy with the rapid onset
58
Causes of hypoglycemia (insulin reaction)
Excessive insulin, delayed or skipped a meal, alcohol usage, excessive exercise without calorie supplementation
59
Clinical manifestations of hypoglycemia (insulin reaction)
Shakiness, palpitations, dizziness, anxiety, hunger, headache, confusion, irritable, fatigue, diaphoresis, may appear as if person is drunk
60
management of hypoglycemia (insulin reaction) in conscious
orange juice jam, honey hard candy "regular" soda
61
management of hypoglycemia (insulin reaction) in unconscious
glucagon subQ | dextrose 50% IVP
62
microvascular disease
Disease of the small blood vessels; more common in type one diabetics; includes retinopathy, nephropathy, and neuropathy
63
Retinopathy
Diabetic retinopathy increases the risk of glaucoma (increased intraocular pressure) and cataracts
64
Management of retinopathy
Slow the onset and progression buy near euglycemia (near normal blood glucose levels) photocoagulation (laser therapy) to coagulate bleeding
65
Nephropathy
Damage blood vessels become leaky allowing proteins to form deposits in the vessels deposits decrease oxygenation resulting in death of kidney cells
66
Management of nephropathy
Euglycemia ("normal" blood sugar levels) | dialysis or kidney transplant for end-stage renal disease
67
Neuropathy
Deterioration of nerves due to nerve hypoxia
68
sensorimotor neuropathy
bilateral and distal paresthesias characterized bu numbness, tingling, burning pain, or weakness
69
autonomic neuropathy
can affect CV, GI, Urinary, or other function
70
atherosclerosis
damage to blood vessels due to increased lipid and cholesterol levels with fatty plaque formation, increasing risk of coronary heart disease, HTN, MI
71
home blood glucose monitoring
test 1-4 times a day (before/after meals) keep diary of results stress good control of FBS
72
Sick Day care
``` test BS q4hr sip fluids q1hr if vomiting, take regular soda or easily tolerated foods if BS> 300mg/dL, test urine for ketones DO NOT skip insulin or oral medication ```

chronic (17 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2025 Bold Learning Solutions. Terms and Conditions