X Diabetes Mellitus - Burke Ch 36 Flashcards
1
Q
Definition of Diabetes Mellitus
A
a group of systemic metabolic disorders characterized by hyperglycemia
2
Q
How much of US population is Diabetic?
A
- 1 mil, 9.3% of population
- 21 mil Dx
- 8.1 mil Un Dx
3
Q
Diabetes interferes w ability to use?
A
Glucose
4
Q
What is Glucose?
A
Simple sugar, monosaccharide
5
Q
What is glucose used for and by
A
Used by cells for energy
6
Q
Does brain need insulin?
A
No, brain only uses glucose. When none available, brain cells die
7
Q
Glucose comes from ?
A
Carbs broken down into sugar.
8
Q
End products of digestion?
A
Protein, fats, carbs
9
Q
Carbs break down to….
A
Glucose, fructose, lactose
10
Q
Fats (lipids) break down to….
A
Fatty acids, glycerol
11
Q
Protein breaks down to…..
A
Amino acids
12
Q
Pathway of glucose from intestines…..
A
Intestines absorb water And nutrients……glucose to blood……from blood to cells……
13
Q
Where is excess glucose stored?
A
Liver and adipose and muscles
14
Q
Explain lock and key method
A
Insulin attached to insulin receptor, opens door, allows glucose in.
15
Q
Stimulus for insulin release?
A
Body senses UP glucose and stimulates pancreas to release insulin
16
Q
Excess glucose converted to ? Stored where?
A
Converted to glycogen and stored in liver
17
Q
Organs involved in BG regulation?
A
Pancreas and liver
18
Q
What is glucagon?
A
Pancreas releases glucagon when senses LO BG, glucagon stimulates liver to break down glycogen into glucose.
19
Q
Glycogen bs Glucagon
A
Glycogen lowers BG
Glucagon raises BG
20
Q
Some fictions of liver
A
- Regulate BG
- Synthesis and storage of amino acids, proteins, vits, fat
- detox
- blood circulation and filtration
- bile drainage
21
Q
What other sources of energy can the body use other than carbs
A
fat
22
Q
what are complications of metabolizing fat for energy?
A
ketones are released. Too many ketones in body give off fruity breath. (acetone)
23
Q
what does buildup of ketones do to body’s pH
A
acidotic
24
Q
3 Ketone bodies?
A
AHH….
Acetone, Acetoacetic Acid, Hydroxybutyric Acid
25
normal body pH
7.35 - 7.45 pH
26
Ketosis
presence of ketone bodies in blood
27
Ketonuria
ketones eliminated in urine
28
common people ketones found in?
starving, fasting, diabetic
29
Glycogen
storage form of glucose. stored in liver
30
Glucagon
Hormone secreated by pancreas in response to LO BG, stimulating liver to breakdown glycogen into glucose
31
Insulin
Hormone secreted by Pancreas to LOWER BL levels
32
DM risk factors
- Diet/Lifestyle (diet hi in fried, carbs and sweets)
- Aging
- Obesity
- Genetic pre-disposition
- virus
- T-lymph/autoimmune
- race
33
Non-Modifiable risk factors for NIDDM
- Family Hx
- Race/Ethnicity
- Age
- Hx of gestational diabetes. chance of devoping later in life.
- Gave birth to large UP 9lb baby.
34
Races at risk of NIDDM
```
Af-Am
Latino
Asian Am
Native Am
Pacific Islanders
```
35
Modifiable risk factors for NIDDM
- overweight/obese (50% men, 70% women w diabetes are obese)
- Physical inactivity
- Hypertension
- UP alchohol consumption
- smoking (18-24 cigs per day)
36
How much of US population is pre-diabetic
86 mil
1/3 adults are pre-diabetic
9/1 adults don't know they are
37
Definition of Pre-Diabetics
BG levels are abnormal (80 - 100mg/dL) but don't meet criteria for being diabetic
11% of PD develop DM within 1 year
38
common Dx tests
- Hb A1C (glycosylated Hemoglobin)
- FBG, Fasting Blood Glucose
- OGTT, Oral Glucose Tolerance Test (drink bottle fast, test BG in 1 hr)
- serum Insulin
- C-Peptide test
- Post Prandial Blood Sugar (2 hr after meal)
39
What does it mean if glucose is in the urine?
Body is not absorbing it, causing build up and spill over
40
Insulin made in what part of Pancreas? by what cells?
Islets of Langerhorn by B cells
41
Types of DM
- Type 1, IDDM (Juvenile)
- Type II, NIDDM
- Gestational
- Other: Meds (long term steroid use, Chemo), Organ Transplant Recipients, Trauma to Pancreas, Cancer of Pancreas)
42
How common is Type I
5-10% of cases
43
IDDM, Pathos, Cause
- Insulin Dependent Diabetes Mellitus
- Progressive destruction of B cell function (lose ability to secrete Insulin)
- Cause unknown
44
How does blood work show Type I?
Islet cell antibodies. Means body is attacking the Islet cells
45
upon Dx, how many B cells are destroyed?
80-90%
| within 5 years, 100% will be destroyed
46
How does Type I lead to Hyperglycemia?
No insulin. Body BG UP, body can't use glucose for energy, blood becomes Hyperglycemic.
47
How are symptoms displayed in IDDM?
Sudden Onset. Usually discover when body goes into DKA. Diabetic Keto Acidosis
48
DKA
Diabetic Keto Acidosis
| when body starts metabolizing fat, creating ketones in the body. Ketones make body acidotic.
49
NIDDM
- Non-Insulin Dependent DM
- Type II
- Gradual onset of symptoms. Body always making some insulin, but insufficient amounts
- Insulin RESISTANT rather than LACK of insulin
50
Insulin Resistance
cells become resistant to effect of Insulin. More insulin needed for same effect.
51
Causes of Insulin Resistance
- Obesity
- Metabolic Syndrome
- Pregnancy
- Infection
- Stress
- Long term steroid use
52
Rx for Type I vs Type II
Insulin vs Diet, exercise, meds
53
Incidence of complications for Type 1 v Type II
both frequent
54
High BG complications for Type 1 v Type II
DKA (metabolize fat) vs Hyperglycemic, hyperosmolar, nonketotic syndrome
55
Usual age onset Type 1 vs Type II
40 and below vs 40 and up
56
Body weight of Type 1 vs Type II
lean vs Obese
57
Onset of SS for Type I vs Type II
sudden vs gradual
58
When do mothers usually find out about Gestational Diabetes
- ~ 28wks at time of OGTT
- 2-10% of US pregnancies
- Rx, Glucose control, diet, excercise
- Risk of dev DM later in life
59
Macrosomomia
Big Baby, over 9lbs. due to uncontrolled insulin production and UP BG in mom and baby during gestation
60
Women w Gestational DM have 30-65% chance of
developing DM in 10-15yrs
61
Glycosuria
glucose in urine
62
Gluycosuria --> Polyuria --> Polydipsia
Hyperclycemia --> Polyphagia
63
Difference between Glycogen and Glucagon?
Glycogen - stored in liver
| Gloucagon - Hormone that breaks down Glycogen to Glucose.
64
3 Ps?
Polyuria - frequent urination
Polydipsia - frequent drinking
Polyphagia - frequent eating
65
Other S/S of DM
- Nausea
- Cold extremities
- blurred vision
- halos (vision)
- Neuropathy (nerve pain)
- LO sensation to pain/temp in feet
- Impotence (ED)
- Slow wound healing
66
Hirsutism
in Type I, male pattern hair growth in women (beard)
67
Dx test for PreDiabetes (only need 1 out of 3 to be diagnosed)
- Fasting BG (100 - 125 mg/dL)
- Elevated Hba1c (5.7 - 6.4)
- 2hr Oral Glucose Tolerance (140-199mg/dL)
68
DM Dx tests (only need 1 out of 4 to be diagnosed)
- Elevated fasting BG on 2 occassions (>126mf/dL)
- Casual BG level (>200mg/dL w 3 classic Ps)
- OGTT w 2hr BG (>200mg/dL)
- Hba1c (>6.5%)
69
Fasting BG test steps
1) Fast for 8 hrs
2) obtain blood sample
3) normal = 99mg/dL or less
70
Normal BG Ranges for Adults
-Preprandial glucose (before meal) =
71
What does OGTT measure and recomendations
this test involves drawing a fasting blood test, followed by having a person drink a 75-gram glucose drink and then drawing another sample two hours after consuming the glucose.
- ability to use glucose
- NPO for 8-12hrs before test
- no smoking, caffeing
- drink glucose drink
- test 2 hrs later (pregnant women only wait 1 hr)
- ptn can drink water during test
72
Normal Insulin levels
5-24mcU/mL
73
Serum Insulin test steps
| used to dx ?
1) NPO for 8 hrs
2) obtain blood sample
diagnose IDDM
abnormal: no insulin present. in NIDDM, level will be normal to High
74
Post Prandial Blood Sugar test steps
- 12hr fasting. BG done before meal
- eat entire meal (75g of CHO)
- rest and no smoking after meal
- Blood sample obtained 2 hrs after meal
if result >200mg/dL = DM
if result 140 - 160 = Pre DM
if result
75
Glocosylated Hemoglobin (HbA1c) test steps
- monitors Rx, Dx DM, How well controlled DM is
- 2-3 mos blood sugar average
- shows Hgb to which glucose is bound
- no fasting required
- results
A1c Level
Normal - or equal 6.5%
76
C-Peptide Test steps
- Determines insulin production. (for every insulin produced, 1 c-peptide made)
- identify's pts who secretly seld administer insulin = Facticious Hypoglycemia
- C-Peptide levels corrolate 1:1
- NPO 8 hrs prior
- obtain blood sample
- Normal fasting level = .78mg/ml
Can distiguish btwn Type I and II. NO insulin produced = no cpeptide produced.
77
Facticious Hypoglycemia
when patients deliberately administer insulin to create hypoglycemia (suicide?)
78
DISEASE
Fasting Sugar >120
OG TT > or equal 200
HbA1c >6.5
PRE-DISEASE
Fasting Sugar 100-125
OGTT 140-199
HbA1c = 5.7-6.4
NORMAL
Fasting Sugar 99 or less
OGTT
.
79
People w Diabetes are at higher risk of developing .....?
heart disease & stroke
80
DM is the ? leading cause of ? in the US
6, death
81
What virus' trigger Type 1 DM?
Mumps/Rubella, Coxsackie 4
82
Lantus is a type of ?
long acting insulin
83
Name of Intermediate acting Insulin?
NPH, NovolinkR, HumalinR
84
Table 36-2 Action of Insulin Preps
see pic in phone
85
Short Term Complications
- DKA
- Hyperglycemic Hyperosmolar Noketotic Syndrome (HHNS)
- Hyperglycemia
- Hypoglycemia
You can NOT live with these conditions chronically. They are acute.
86
Normal body pH?
7.35-7.45
87
How does glucose end up in the urine?
Blood going into nephron is so concentrated that re absorption in the tubules can't remove everything. Excess is excreted in urine.
88
Osmotic diuretic
Substance that attracts water and takes it along into the Urine
Glucose, Na, Asparagus
89
How does body compensate for acidosis?
Kussmal breathing to breath off acetone, a Ketone
90
Ketonuria
Ketones in the urine
91
Metabolism of fat creates ?
Ketones. Acids
92
Ketones excreted in what ways?
Via lungs- fruity breath
| Via urine- acetonuria or Ketonuria
93
What complication does Ketonuria cause ?
Dehydration, E imbalance
94
DKA causes
- Type 1 - no insulin production
| - problem w insulin therapy (missed doses, not enough etc)
95
DKA triggers
```
Infection- UP BG
PNA (pneumonia)
UTI
Stress
ETOH abuse
Drug abuse
MI (myocardial infarction) heart attack
CVA (cerebro vascular accident) stroke
```
96
???learn level
Na, K, creatinine, BUN, hematocrit, platelets etc
.
97
Hyperglycemia leads to ?
Polyuria --> dehydration --> tachycardia--> hypotension-->hypovolemic shock
98
Acidosis leads to ?
K+ leaving cellS and accumulate in blood --> hyperkalemia --> UP K can lead to heart attack
99
Hyperglycemia and Acidosis can both lead to loss of consciousness and ?
Death
100
DKA symptoms
```
3Ps
Glucosuria
Ketonuria
Acetone breath
Kussmaul respirations
Drowsiness
BG 250-800 mg/dL
Loss consciousness
```
101
DKA tests
BG, Ketone levels
Urine glucose , ketone levels
Blood pH (acidosis) - ABG arterial blood gas
102
DKA Treatment
- IV Fluids
- Drip: IV Insulin (REGULAR insulin ONLY)
- Monitor qH BG (finger prick, side less painful than center fingertip)
- Monitor Elecrolytes (E)
- ABG for acidosis
103
DKA patient education
- Teach PREVENTION
- careful SELF/HOME monitoring of BG
- if BG >250 then check for Ketones
- If KETONES present, drink H20 and recheck Ketones again w next urination
- If KETONES present, call MD
- Never stop Insulin w/out MD supervision
104
STEROIDS increase
UP BG levels
105
about HHNS (Hyperosmolar, Hyperglycemic Nonketotic Syndrome)
Occurs Primarily in: Type II, Meds (steroids)
| Cause: Stress, Illness, Infection, MI, CVA
106
DKA vs HHNS
DKA
No insulin
metabolizes fat
HHNK
severe hypoglycemia but no Acidotic state (DKA). No DKA because there is always at least a little insulin present
107
HHNK Pathophisiology. How fast develops?
- Hyperglycemia ---> Polyuria ---> Dehydration --> a hyperosmolar state (concentrated urine) --> E imbalance
- Develops slowly
108
HHNK BG levels?
>600-1500 mg/dL
109
HHNK Symptoms
- Extreme Polydypsia
- Glucosuria
- 3 Ps
- Lethargy
- Confusion
- Shock
- coma
- death
No ketones (no ketonuria)
110
HHNK Treatment
- IV fluids
- DRIP: IV REGULAR insulin
- Monitor: qH BG (finger prick)
- Monitor: E
- Teach prevention
111
All DM patients should have an Endocrinologist
.
112
HHNK Long Term complications
- Cardiovascular Disease
- Neuropathy
- Nephropathy
- Retinopathy
- Foot damage: blisters, cuts
- Osteoporosis
113
Hyperglycemia Definition, Cause
Def: calories in excess of insulin available for glucose used
Cause: over-eating, stress, illness, LO DM meds (need to be adjusted)
Stress = release of counter regulatory hormones (epi, cortisol, GH, Glucagon)
114
S/S Hyperglycemia
- 3Ps
- Fatigue
- Blurred vision
- Headache
- Abdominal Pain
115
Hyperglycemia Rx
- BG meter monitoring
- BG >250 check urine for Ketones
- sliding insulin scale, oral agents
116
Hypoglycemia Def.
- not enough glucose in relations to Insulin
| - BG
117
cause of Hypoglcemia?
- meds
- malnutrition
- fasting
- excercise
118
What's the danger of repeated hypoglycemic episodes
- Diabetic Coma
| - Brain cells deprived of enegy (neuro damage)
119
Hypoglycemic S/S
- hunger
- sweating
- palor
- tremors
- palpitation
- headache (h/a)
- weakness
- blurred vision
120
as Hypoglycemia progresses.....s/s
- irritability
- confusion
- seizures
- coma
121
Hypoclycemia Rx
- if pt AOO (awake, alert, oriented), NON ACUTE
- confirm hypoglycemia w Glucometer
- administer a Fast Sugar, recheck in 15min, if not BG not high enough (~80-120), more fast sugar. End w long acting sugar.
122
Fast Sugar
- 4oz OJ
- 1 Glucose Tab
- 6-8 lifesavers
- 6oz reg soda
123
Long Acting Sugar (complex carb)
- crackers
- milk
- peanut butter
- 1/2 sandwich
124
Hypoglycemia Treatment: If pt not alert or unable to swallow
admin SC, IB, IM
- IVP 50% Dextrose (D50) (admin by RN)
- recheck BG in 15 min
- repeat steps until hypoglycemia subsides
125
If hypoglycemic exhibit neuro S/S, administer STAT?
D50 (IV)
Glucagon (SubQ)
Treat asap because brain cells dying. If it turns out to NOT be hypoglycemia, you can always correct the condition by administering insulin.
126
Fasting BG Levels (8-12hrs NPO)
- 70 to 99 mg/dL - Normal
- 100 to 125 mg/dL - Pre DM
- >126 mg/dL on more than 1 test occasion - DM
127
Long Term Complications of DM
- Macrovascular
- Microvascular
- Nerves
- Infection
- Foot Complications
128
MACROvascular Complications
Involve circulatory system
- Atherosclerosis (plaque/narrowing of arteries)
- Arterioosclerosis (Hardening of arteries)
- HTN (UP press in vessels, risk for heart attack)
- UP LDL/Triglycerides
- Platelet fx - MI/CVA
- Poor circulation in feet/legs
- DM alters clotting ability (clotting when not necessary)
129
MICROvascular Complications
Eyes
- Retinopathy (disease of retina. dmg tiny blood vess that supply eye)
- Cataracts (clouding of lens)
- Glaucoma (UP press in eyes)
Kidneys
-Nephropathy
130
What % of DM develop cataracts? Glaucoma?
60%, Cataracts
| 40%, Glaucoma
131
Leading cause of blindness
Glaucoma
132
Types of Retinopathy
Nonproliferative
| Proliferative
133
Non Proliferative Retinopathy
capillaries in back of eye balloon, form pouches that inhibit passage of substances btwn blood and retina
134
Proliferative Retinopathy
blood vessels so damaged they close off. new weak vessels grow in retina, leak blood
135
Nephropathy
Disease of kidneys. Blood vessels damaged due to hyperglycemia. Result in ESRD - Dialysis. affect filtering ability
136
Leading cause of ESRD?
DM
137
what % of DM px develop nephropathy?
40% develop some degree of kidney problems
138
Neuropathy
nerve damage from Chronic Hyperglycemia
- numbness/pain in extremities
- Gastroparesis
139
Gastroparesis?
delayed gastric emptying (paralyzed stomach)
140
MED: REGLAN, 2 uses?
Nausea and Gastroparesis
| -Increase speed in which contents empty from stomach
141
Complications of INFECTION
DM px prone to infection
- UP BG
- lead to DKA in Type 1
- slow healing, impaired circulation. not enough blood getting to would
- Hyperglycemia -> WBCs sluggish/ineffective. can't fight infection
- ulcers/infections -> gangrene, necrosis, death
- Abx given, but not effective due to poor circulation
- use TOPICAL Abx
142
what 3 factors lead to Foot Complications?
- poor circulation (vascular disease)
- prone to infection (poor would healing)
- neuropathy (limits sensation)
143
leading cause of Amputation?
DM
144
Foot Care Steps
- wash and dry feet DAILY
- Inspect for cracks, sores, foreign objects
- clip toe nails across, not angle, to avoid ingrown
145
Teaching Footcare. What to AVOID?
- pantyhose, garters, tight socks
- crossing legs
- foot soaks/powders
- lotion btwn toes --> fungal infec.
- never barefoot
- hot H2O bottles, heating pads on feet
146
Teaching Footcare. What to DO?
- use alcohol free lotion, NONE btwn toes
- wear proper shoes, wide, sturdy
- see podiatrist
- annual checkups
- notify MD of abnormalities
147
DM Rx
- education w monitoring
- diet
- excercise
- oral agents
- Insulin (last resort)
148
Goals of Diet
1) achieve/maintain BG and Lipids to near normal (CONTROL to avoid complications)
2) weight loss and BP control / Meal planning
149
3 Methods of Meal planning
-Plate method
-carb counting
-glycemic index
(refer pt to nutritionist/dietitian)
150
Benefits/Risk of Excercise
UP Muscular activity -> glucose utilization, insulin receptors become more sensitive to insulin
Risk for HYPOglycemia (supervised exercise recommended)
151
Exercise Concerns
- monitor BG before, during, after (to see how BG affected)
- Gradually UP level of activity
- Avoid extremes -> Hypoglycemia
- Excercise SAME time daily. easier to monitor
- BG 90andUP before exercise (if on oral meds)
- BG 110andUP before exercise (if on insulin)
152
When Exercise make sure to:
- carry Fast Sugars
| - eat carb snacks before and at intervals during strenuous workouts.
153
If on INT acting Insulin, DO NOT exercise during
PEAK hours (when BG is lowest)
154
Type1, if BG is 250andUP, what to do before excercise? why?
-check for Ketones. If present, DON'T excercise because Ketones will increase. Body will start metabolizing fat after all glucose is done.
- Drink H2O, check urine again
- H2O to prevent dehydration because Glucose and Ketones in urine are Osmolor diuretics.
155
Excercise - pre-workout list
- Med alert ID
- Comfy shoes (prevent blisters)
- bring glucometer
- carry fast sugar
- bring emerg glucagon kit
156
If BG is 300andBLO, no ketones present, can you exercise?
yes
157
Exercise if Type II, if BG 400andBLO?
YES
158
Exercise if Type II, if BG 400andUP?
NO
159
BG monitoring
- self monitoring
- take daily log w times, #s
- Tight glucose control - qac and qhs (b4 meals and bedtime)
160
??? Glucosuria when BG is ?
>80 mg/dL
161
Test urine for ketones when ?
>250 mg/dL
Type II don't check for ketones because they always make insulin
162
MEDS: 6 class of Oran HYPOglycemics
1) Sulfonylureas
2) Meglitinides
3) Alpha-glucosidase inhibitors
4) Thiazolidinediones
5) Biguanide
6) DPP-4 Inhibitors
163
Ca and K for?
Ca - relieves contracting Muscles
| K - relaxing muscles (too much, risk for MI)
164
MEDS: Sulfonylureas - how do they work?
| Type II DM
- stimulate pancreas to release more insulin
- NOT dependent on BG
- can --> HYPOglycemia (monitor BG because of this)
- NEVER use on Type 1 (IDDM)
165
MEDS: Sulfonylureas - examples
1st gen:
Diavinese
2nd gen:
Glipizide (Glucotrol)
Glyburide (Diabeta, Micronase, Glynase)
3rd gen:
Glimepiride (Amaryl)
SIDE EFFECTS: Nausea, Diarrhea, Constipation
166
MED: Diavinese
- 1st Gen Sulfonylurea
| - not used often. stress on kidney. Renal function can be altered
167
MED: Glipizide (Glucotrol)
- 2nd gen Sulfonylurea
- given 30 min B4 1st meal, breakfast
SE: Nausea, Diar, Constip
168
MED: Glyburide (Diabeta, Micronase, Glynase)
- 2nd gen Sulfonylurea
- given 1x day w 1st meal
SE: Nausea, Diar, Constip
169
MED: Glimepiride (Amaryl)
- 3rd gen Sulfonylurea
- 1x day w 1st meal
SE: Nausea, Diar, Constip
170
MEDS: Meglitinides - how do they work?
- stim pancreas to release insulin
- Glucose DEPENDENT
- Taken 30min B4 meal
once pt eats, UP BG, then pancreas w stim insulin. absorption happens in sm intestines. Med will already be working
171
MED: Meglitinides - examples
- Prandin (Repaglinide)
- Starlix (Nateglinide)
- stim pancreas to release insulin
- Glucose DEPENDENT
- Taken 30min B4 meal
172
MED: Alpha-glucosidase Inhibitors - how do they work?
- prolong absorption of carbs in stomach & intestines. BLOCKS enzyme needed to digest starch.
- slows post prandial, UP BG
- given w EACH meal on 1st bite, not convenient
173
MED: Alpha-glucosidase Inhibitors - i.e.
Precose (Acarbose)
not convenient because have to remember for each meal.
174
MED: Precose (Acarbose)
w EACH meal on 1st bite.
175
MED: Thiazolidinediones - how do they work? (like Biguanides)
-UP insulin sensitivity at insulin receptors
-LO amount of glucose released by liver
-taken daily w NO regard to meals
-similar to Biguanide's
UP risk/rate of bladder CA. Contraindicated in pts w Hx of Bladder CA
176
MED: Thiazolidinediones - i.e.
Avandia (risk for MI) not used anymore
Actos (Pioglitizone)
- UP insulin sensitivity at insulin receptors
- LO amount of glucose released by liver
- taken daily w NO regard to meals
177
MED: Actos (Pioglitizone) class
Thiazolidinedione
- UP insulin sensitivity at insulin receptors
- LO amount of glucose released by liver
- taken daily w NO regard to meals
178
MED: Biguanide -(2 uses, Bi) how does it work?
- used in combo w Sulfonylureas
- LO hepatic glucose output
- UP insulin sensitivity at cell. so don't need as much
- taken w 1st meal, 1x day
- DOES NOT cause HYPOglycemia because it doesn't raise insulin. only makes insulin already there more effective.
- RISK hepatotoxicity. don't use on pts using contrast mediums because dyes are nephrotoxic. drug already hard on kidneys
179
MED: Metformin (Glucophage) class
Biguanide
- taken w 1st meal, 1x day
- DOES NOT cause HYPOglycemia because it doesn't raise insulin. only makes insulin already there more effective.
- used in combo w Sulfonylureas
- LO hepatic glucose output
- UP insulin sensitivity at cell. so don't need as much
180
MED: DPP-4 Inhibitors aka (Gliptins) - how do they work?
- hormone in GI tract sign pancreas to produce insulin
- glucagon like polypeptide 1 (GLP-1)
- DPP-4 is protein found in blood. it stops breakdown of diff hormones to UP insulin to LOWER BG.
- short acting in blood
- taken w/out regard to food
- Only for Type II, dependent on insulin releasing cells
i.e. Januvia
181
MED: Januvia class
Gliptin (DPP-4 Inhibitor)
| -taken w/out regard to food. anytime
182
MED: Glucagon
- converts Glycogen to Glucose
- Emergency med
- UP BG levels
- Rx for unconsios pt (subQ, IV, IM, parenteral)
- must be constituted STAT before injection
- RISK for bleeding with pts on Cumadin
183
Evidence of internal bleeding?
- urine in blood
- bruising
- bleeding mouth
184
Insulin pump
- CSII - Continuous SubQ Insulin infusion (mimics pancreas)
- Batter powered computer device
- Admin a BASAL rate or a BOLUS rate
GOAL: keep BG steady btwn meals and at night
185
Insulin made of
Human or Pork
| -if you don't know what type of insulin pnt uses, use Human
186
Types of Insulin
Rapid, short, inter, long acting
187
What type of Insulin can you mix?
All but Lantus (Long Acting)
188
Where to store insulin?
in fridge. Avoid Extreme temp and agitation.
| Discard after 1 mos. and if has precipitate, lumpy, frosted.
189
Safe use of pump requires?
- committed to checking BG at lease qID (4x day)
- CHO counting method
- adjust Insulin based on BG levels, CHO and physical activity
190
Pump Advantages
- flexibility in lifestyle
- predictable insulin delivery
- precise insulin deliver
- accurate deliver (up to 1/10th unit) human eye can only see 1u.
- LO episodes of HYPOglycemia
- LO fluctuations in BG
- helps manage Dawn Phenomenon
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Pump Disadvantages
- risk of skin infections
- risk of DKA from pump malfunction
- cost
- lets other know you have DM (?)
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Good sites for Insulin inj.
fleshy parts
- Abdomen
- back of arm where you can bunch skin
- 45* subq, if can bunch more than 1", 90*
- needle bevel up
- only RN can administer
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Somogyi effect
rebounding high blood sugar that is a response to low blood sugar.
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Dawn Phenomenon/Dawn Effect,
abnormal early-morning increase in blood sugar (glucose) — usually between 2 and 8 a.m. — in people with diabetes.
