Med Surg - Exam3- Mandy- ch49 lecture Flashcards

KNOW EVERYTHING!!!

1
Q

Islets of Langerhans

A

hormone secreting portion of pancreas

alpha & beta cells

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2
Q

alpha cells

A

Alpha cells: produce Glucagon in response to low blood glucose levels

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3
Q

beta cells

A

Beta cells: produce Insulin in response to high blood glucose-

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4
Q

insulin facilitates

A

glucose metabolism, glucose transport across cell membranes, and synthesis and storage of glucose, fats, and proteins

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5
Q

Glucagon

A

Glukegone hormone to increase blood sugar level. When low sugar, protein ingestion, and exercise

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6
Q

Glycogen

A

storage of glucose in liver

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7
Q

Insulin function

A

transport glucose into cell and incorporate into protein in muscle, glycogen in liver, and fat trigliceride to adipose tissue.
Fat(/adipose /’edapous/ tissue), glycogen, and protein are the three format of energy storage in human body.

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8
Q

counter regulatory hormones to insulin

A

: glucagon, epinephrine, growth hormone, and cortisol…raise blood glucose levels

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9
Q

counter regulatory hormones (of insulin)

A
  • Respond to a decline in blood glucose level during fasting or overnight
  • Stimulate lipolysis, gluconeogenesis, and glycogenolysis processes
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10
Q

Gluconeogenesis

A

Gluconeogenesis is the process of synthesizing glucose in the body from non-carbohydrate sources such as protein and fat.

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11
Q

Blycogenolysis

A

Blycogenolysis - is the breakdown of glycogen to glucose.

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12
Q

Lypolysis

A

Lipolysis: break down of lipid (fatty tissues) to fatty acid and glycerol.

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13
Q

Diabetes Mellitus (DM)

A

A chronic multisystem disease related to
Abnormal insulin production
Impaired insulin utilization
Or both

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14
Q

abnormal insulin production in

A

D1 and D2; insulin resistance due to fatigue/B cell defect

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15
Q

Pancreas of DM type 1

A

Autoimmune destruction of B cells
Autoantibodies present for months/years before clinical symptoms
No production of insulin

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16
Q

Pancreas of DM type 2

A

Defective B cell insulin secretion
Insulin resistance stimulates insulin secretion
Eventually exhausting B cells

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17
Q

Liver of DM type 2

A

Excess glucose production.

Inapprpriate regulation of glucose production

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18
Q

Adipose tissue of DM type 2

A

Decrease in Adiponectin and Increase in Leptin: results in altered glucose and fat metabolism

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19
Q

Muscle tissue of DM type 2

A

Defective insulin receptors
Insulin resistant
Decreased uptake of glucose results in hyperglycemia

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20
Q

all you really need to know is that DM2 involves…

A

metabolic problems in muscle, liver (glucose higher), and adipose tissue (high cholesterol)

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21
Q

TYPE 1 DM

A

Autoimmune disease, peak onset by 20 years old
Insulin dependent
Rapid & Acute
Classic symptoms: Polyuria, Polydipsia, Polyphagia
Others: weight loss, weakness, fatigue

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22
Q

TYPE 2 DM

A
  • Major contributor for heart, renal disease, and stroke
  • Associated with metabolic syndrom
  • Asymptomatic in the early stage
  • May have classic symptoms of type 1
  • Nonspecific symptoms are common: fatigue, prolonged wound healing, visual changes
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23
Q

metabolic syndrome characterized by

A
  • Insulin resistance, elevated insulin levels
  • ↑ triglycerides & Low-density lipoproteins, ↓High-density lipoproteins
  • Hypertension
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24
Q

HDL

A

removes excess cholesterol from the body

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25
Excessive LDL
LDL builds up on arterial walls and hardens to create plaque, constricting flow and contributing to heart disease.
26
Triglyceride
storage of fat for energy use
27
Cholesterol
for construction of cell and hormone
28
HDL for
transportation
29
Hyperglycemia causes a diabetic to produce
a high volume of glucose containing urine
30
other types of DM
prediabetes gestational secondary
31
prediabetes
Blood glucose levels are at borderlines No symptom but damages may already occurred Healthy eating, healthy weight, regular exercise, and monitoring blood glucose and symptoms can reduce the risk of DM
32
Impaired fasting glucose (IFG)
between 100 -125 mg/dl
33
to diagnose diabetes, fasting glucose needs
tested twice at more than 126 mg/dl
34
Impaired glucose tolerance (IGT)
2 hour oral glucose tolerance test (OGTT) level between | 140 -199mg/dl
35
Diagnostics for DIABETES
* HbA1C ≥ 6.5% * FG level ≥126 mg/dl * OGTT: Two-hour plasma glucose level ≥ 200 mg/dl * Random plasma glucose ≥ 200 mg/dl plus symptoms
36
normal HBA1c
glycosylated hemoglobin. 4-6%
37
prediabetes HbA1C
5.7-6.4%
38
Oral contraceptives
could elevate OGTT
39
prediabetes FG
100-125 mg/dl
40
prediabetes OGTT
140-199 mg/dl
41
collaborative care of diabetes
medication Nutritional therapy Self-monitoring blood glucose Exercise
42
Insulin Bolus
given before meals | Rapid acting or short acting
43
Rapid Acting Insulin
``` Lispro (Humalog), aspart (NovoLog), glulisine (Apidra) Injected 0 to 15 minutes before meal Onset of action 15 minutes ```
44
Short Acting Insulin
ie REGULAR insulin Regular (Humulin R, Novolin R) Injected 30 to 45 minutes before meal Onset of action 30 to 60 minutes
45
BASAL Insulin
Basal – control glucose level between meals and overnights | Intermediate or long acting
46
Basal insulins
Basal – control glucose level between meals and overnights Intermediate-acting: NPH (Humulin N, Novolin N) Has a peak which can result in hypoglycemia Long-acting: Glargine (Lantus) and Detemir (Levemir) Injected once a day at bedtime or in the morning Released steadily and continuously Has no peak action thus decrease risk of hypoglycemia Do not physically mixed with any other insulin or solution
47
Intermediate acting insulin
NPH (Humulin N, Novolin N) | Has a peak which can result in hypoglycemia
48
Long-acting insulin
Glargine (Lantus) and Detemir (Levemir
49
Long acting insulins | Lantus and Levemir for Basal
Injected once a day at bedtime or in the morning Released steadily and continuously Has no peak action thus decrease risk of hypoglycemia Do not physically mixed with any other insulin or solution
50
NPH appearance
is cloudy
51
Rapid Acting times
onset: 10-30min peak: 30min-3 hrs duration: 3-5hr
52
Rapid Acting names
lispro Humalog aspart NovoLog gluslisine Apidra
53
Short Acting times
onset: 30-60min peak: 2-5 hr duration: 5-8 hr
54
Short Acting names
Regular: Humulin R | Novolin R
55
Intermediate acting times
onset: 1.5-4hr peak 4-12 hr duration 12-18 hr
56
Intermediate names
NPH: Humulin N, Novolin N
57
Long acting names
glargine Lantus | detemir Levemir
58
Long acting times
onset: .8 -4hr peak: no pronounced peak duration: 24 plus hours
59
mixing insulins
Mixing insulins: always withdraw Regular insulin first then NPH
60
combination insulin therapy
Short- or rapid-acting combined with intermediate-acting or long-acting insulin to provide basal-bolus coverage There are commercially premixed formula available: 70/30, 75/25, 50/50
61
The client with type I diabetes mellitus is taught to take NPH (Humulin N) at 5 pm. each day. The client should be instructed that the greatest risk of hypoglycemia will occur at about what time?
1 am, while sleeping
62
Insulin storage (4 points)
- Do not heat/freeze, extra insulin should be refrigerated - In-use vials may be left at room temperature up to 4 weeks - Avoid exposure to direct sunlight - Vials or prefilled syringes should be generally rolled between the palms before injection
63
what size syringe to use for insulin?
0.3 or 0.5 ml syringe
64
How long to leave syringe in place after injection?
5 seconds
65
Administration of insulin: | what site has fastest absorbtion?
Abdomen, followed by arm, thigh, butt
66
Do not inject insulin into site..
that is to be exercised
67
Insulin & alcohol wiping
At home, by patient: not recommended. | In the hospital, by nurse: absolutely...to prevent HAIs
68
Insulin concentrations
usually 100 units/ml
69
Insulin injections should be
rotated within one particular site...this decreases variablility of absorption
70
only IV insulin
Regular insulin only
71
Both Somogyi and Dawn phenomenon
characterized by hyperglycemia in the morning
72
Is AM hyperglycemia because insulin dosage is too high or too low?
check blood glucose at 2-4am
73
Somogyi effect
Somogyi caused by hypoglycemia rebounded by counterreulatory hormone
74
Dawn phenomenon
Down phenonmenon due to counterregulatory hormone
75
Insulin pump
- Continuous infusion of a rapid-acting insulin - Dosage can be temporarily increased and decreased by programming - 2-3 days rotate sites and change synringe. - Plunzher.
76
Oral agents that increase insulin production from the pancreas
SULFONYLUREAS (Glipizide (Glucotrol), Glyburide (Micronase), Glimepiride (Amaryl) *MEGLITINIDES (Repaglinide (Prandin), Nateglinide (Starlix) SIDE EFFECT: hypoglycemia
77
Meglinides
Oral agent, increases insulin production, short acting | *take 30 minutes before each meal
78
Sulfonylureas: Glucotrol, Micronase, Amaryl
Oral agent that increases insulin production and release from pancreas
79
Megliniede
like regular insulin, comes & goes fast
80
postprandial
post meal
81
Oral agent that reduces glucose production by liver
Biguanides: Metformin (Glucophage)
82
Metformin (Glucophage)
Do not use in pt with kidney or liver disease, or heart failure. Hold B4 & 48 hrs after contrast procedures or till kidney function is normal
83
Oral agents that delay the absorption of glucose from intestines
α – Glucosidase Inhibitors take with the first bite of the meal, effective on controlling post-meal blood glucose, effectiveness to be measured 2 hours after the meal. Acarbose (Precose)
84
Acarbose (Precose)
α – Glucosidase Inhibitors take with the first bite of the meal, effective on controlling post-meal blood glucose, effectiveness to be measured 2 hours after the meal.
85
Biguanides do not
promote weight gain, beneficial to people with prediabetes
86
Metformine
increases lactic acidosis...kidney problem
87
oral agents that improve insulin sensitivity
Thiazolidiediones
88
Thiazolidiediones
IMPROVES INSULIN SENSITIVITY. does not increase insulin production, thus will not cause hypoglycemia
89
Thiazolidinediones: drug names
IMPROVES INSULIN SENSITIVITY. | Pioglitazone (Actos), Rosiglitazone (Avandia)
90
Thiazolidinediones
impair liver function, do not use in pt with MI, stroke or heart failure
91
DDP-4 inhibitor
Oral agent: blocks dipeptidyl peptidase-4, which decreases insulin production.
92
DDP-4 inhibitors do not cause
weight gain or hypoglycemia
93
DDP-4 inhibitor names
Sitagliptin (Januvia)
94
Byetta
3rd category of DM med. from Gila monster saliva. stimulates insulin production and decreases liver sugar production. causes weight loss.
95
Non insulin Injectable Agents. Names
Exenatide (Byetta) | Praminitide (Symlin)
96
Noninsulin Injectable Agents
Increase insulin sysnthesis and release from the pancrease. Inhibit glucagon secretion, & Delays gastric emptying. watch for hypoglycemia.
97
Exenatide (Byetta)
Noninsulin injectable: Glucagon like peptide 1 (GLP1) Receptor Agonist. Need to take oral medication >1 hour before injecting Byetta.
98
What to teach pt about glyburide (Micronase, DiaBeta, Glynase)?
Glyburide stimulates insulin production and release from the pancreas.
99
Glyburide is a sulfonylurea it
sulfonylureas stimulate the production and release of insulin from the pancreas. If the glucose level is low, the patient should contact the health care provider before taking the glyburide, because hypoglycemia can occur with this class of medication.
100
Metformin should be held...
held for 48 hours after administration of IV contrast media, but this is not necessary for glyburide.
101
Glucagon secretion & glyburide
Glucagon secretion is not affected by glyburide.
102
nutritional therapy: Carbohydrates, 7pts
* miniumum of 130g/day * CHOs from fruits, veggies, grains legumes, milk * use a method: carb counting, exchange lists, portion control * use Glycemic index * sucrose containing food subbed for other CHOs * Fiber:25-30g/day * Nonnutritive sweetners ok.
103
Nutritional therapy - protein
15-20% of calories | high protein diets for wt loss, not recommended
104
Nutritional therapy - fat
low fat: 20-30% total calories | saturated fat <200 mg/day
105
Alcohol & diabetes
Alcohol consumption : can cause severe hypoglycemia, should be consumed with food
106
Glycemic index (GI):
Glycemic index (GI): rises in blood glucose level after consuming carbohydrate-containing food.
107
a slice of bread is
Simple complex carbohydrate | 1 slice of bread – 15 g one serving
108
Alcohol inhibits liver to
break down glycogen to glucose thus cause hypoglycemia. Liver busy with detoxicating alcohol Normally, the liver releases glucose to maintain blood sugar levels. But when you drink alcohol, the liver is busy breaking the alcohol down, so it does a poor job of releasing glucose into the bloodstream.
109
SMBG
Self Monitoring Blood Glucose | ie AccuCheck
110
When NOT to exercise?
Hold exercise if glucose ≤ 100 mg/dl or ≥ 250 mg/dl, or if ketones are present in the urine.
111
When TO exercise?
Exercise daily same time same amount | Best to excise 1-2 hours after meals
112
Small CHO snack..
can be taken during exercise to prevent hypoglycemia
113
Exercise & SMBG
Monitor blood glucose levels before, during, and after exercise
114
Diabetics need ___ B4 exercise
Need medical clearance before exercise
115
When patient is ill,
When patient is ill, blood glucose should be tested at least every 4 hours
116
``` Nursing Management of DM: Overall Goals (5) ```
* Active pt participation * fewer/no episodes of acute hyper/hypoglycemic emergencies * maintain normal blood glucose levels * prevent/delay chronic complications * lifestyle adjustments w/ minimal stress
117
Nursing Management of DM | Acute interventions:
Under stress of illness and surgery: *Blood glucose level could be high * Continue regular meal plan, increase intake of noncaloric fluids * Continue taking oral agents and insulin * Closely monitor blood glucose
118
Nursing Management: Ambulatory & home care Tables 49-13--15 6 points
* Reach an optimal level of independence * Insulin therapy and oral agent * Personal hygiene with emphasis on foot care * Medical identification and travel card * Patient and family teaching * Learn early symptoms of hyperglycemia and hypoglycemia
119
A client with type 1 diabetes calls the clinic with complaints of nausea, vomiting, and diarrhea. The nurse should advise the client to
Check the blood glucose level every 2 to 4 hours
120
Acute Complications
see table 49-16 pg 1175
121
``` Diabetic ketoacidosis (DKA) caused by ```
profound deficiency of insulin
122
DKA characterized by.... | 6 points
* Hyperglycemia (glucose > 250 mg/dl) * Ketosis (ketones in blood and urine) * Acidosis (blood PH < 7.3, bicarbonate < 15 mEq/L) * Dehydration (poor skin turgor, dry mucous membranes, tachycardia, orthostatic hypotension) * Kumaul respirations: rapid deep breathing to attempt to reverse metabolic acidosis * Sweet fruity odor, abdominal pain, nausea/vomiting
123
DKA is common in
Common in type 1 or poor self management
124
ketone
by product of fat metabolism
125
fruity odor
is acetone, simplest ketone
126
pH range: normal
7.35-7.45
127
Bicarbonate range: normal
21-28
128
DKA interventions table 49-18 | Emergency Management
Airway patency, O2 administration *Correct fluid/electrolyte imbalance IV infusion 0.45% or 0.9% NaCl to restore urine output and raise blood pressure *Early potassium replacement – insulin drives potassium into the cells and lead to hypokalemia *Insulin therapy start when fluid resuscitation begins and potassium is normal *When blood glucose levels approach 250 mg/dl, 5% dextrose added to regimen to prevent hypoglycemia
129
HHS
Hyperosmolar Hyperglycemic Syndrome
130
HHS 5 points
* Common in patients over 60 years with type 2 * Caused by dehydration – require greater fluid replacement * Patient has enough circulating insulin so ketoacidosis does not occur (Absent/minimal ketone bodies in blood or urine) * Produces fewer symptoms in earlier stages * Neurologic manifestations occur
131
glucose level in HHS
more than 600
132
HHS vs DKA in terms of fluids
HHS requires greater fluid replacement
133
Hypoglycemia
Low blood glucose < 70 mg/dl
134
hypoglycemia caused by
mismatch in timing of food intake and peak action of insulin or oral hypoglycemic agents
135
common manifestations of hypoglycemia
Common manifestations: confusion, irritability, diaphoresis, tremors, hunger, weakness, visual disturbances, can mimic alcohol intoxication
136
untreated hypoglycemia
Untreated can progress to loss of consciousness, seizures, coma, and death
137
Nursing management of DKA/HHS: Patient closely monitored. Administer:
IV fluids Insulin therapy Electrolytes
138
Nursing management of DKA/HHS: Patient closely monitored. Assess:
Cardiac monitoring - EKG Renal status Cardiopulmonary status Level of consciousness
139
An unresponsive client with type 2 diabetes is brought to the emergency department and diagnosed with hyperosmolar hyperglycemic syndrome (HHS). The nurse will anticipate the need to
insert a large-bore IV catheter. HHS is initially treated with large volumes of IV fluids to correct hypovolemia. Regular insulin is administered, not a long-acting insulin. There is no indication that the patient requires oxygen. Dextrose solutions will increase the patient’s blood glucose and would be contraindicated.
140
AT first sign of Hypoglycemia:
Check blood glucose | If 70 mg/dl, investigate further for causes
141
If having hypoglycemic symptoms, and monitoring equipment is not available:
treatment should be initiated | If alert enough to swallow, 15 to 20 g of a simple carbohydrate, avoid foods with fat
142
Hypoglyemia: Hypoglycemia (cont’d) Avoid____ and overtreatment by __________. Recheck blood sugar _______ after treatment. Repeat until blood sugar ________. Patient should eat regularly scheduled meal/snack (complex carbohydrate) to prevent rebound _________. Check blood sugar again ________ after treatment. If no improvement after _____ or patient not alert enough to swallow, then: Administer ___________. In acute care settings: give ________ IV push.
Hypoglycemia: Avoid fat and overtreatment by simple carbohydrate Recheck blood sugar 15 minutes after treatment Repeat until blood sugar >70 mg/dl Patient should eat regularly scheduled meal/snack (complex carbohydrate) to prevent rebound hypoglycemia Check blood sugar again 45 minutes after treatment If no improvement after 2 or 3 doses of simple carbohydrate or patient not alert enough to swallow, then: Administer 1 mg of glucagon IM or subcutaneously In acute care settings: 20 to 50 ml of 50% dextrose IV push
143
Intramuscular Glucagon stimulates
the liver to produce glycogen to supply glucose
144
Which action should the nurse take after a 36-year-old patient treated with intramuscular glucagon for hypoglycemia regains consciousness?
Give the patient a snack of peanut butter and crackers
145
After Glucagon administration what can happen? what could prevent?
Rebound hypoglycemia can occur after glucagon administration, but having a meal containing complex carbohydrates plus protein and fat will help prevent hypoglycemia...cheese and crackers will stabilize blood glucose...The patient should be assessed for symptoms of hypoglycemia after glucagon administration.
146
Acute complications of DM
HHS DKA hypoglycemia
147
Chronic Complications of DM:
``` Angiopathy (micro & macrovascular) Retinopathy Nephropathy Neuropathy feet & lower extremities skin infections psychologic considerations ```
148
Angiopathy
Blood vessel damage secondary to chronic hyperglycemia resulting in organ disease
149
Macrovascular angiopathy
* Diseases of large and medium-sized blood vessels, caused by altered lipid metabolism * Risk factors: Obesity, Smoking, Hypertension, High-fat intake, Sedentary lifestyle * Control of blood pressure and lipid panel is the key to prevent cardiovascular diseases
150
Risk factors for Macrovascular angiopathy in DM pts
Obesity, Smoking, Hypertension, High-fat intake, Sedentary lifestyle
151
Key to prevent CVD in DM pts
Control of blood pressure and lipid panel is the key to prevent cardiovascular diseases
152
Microvascular angiopathy specific to DM
Result from thickening of vessel membranes in capillaries and arterioles in response to chronic hyperglycemia *Affect eyes, kidneys, skin
153
Lab value: | Cholestrol
<200 mg/dL
154
Lab value: | LDL
<130 mg/dL
155
Lab value: HDL male & female
Male: >45 Female: >55 mg/dL
156
Lab value: | triglycerides
< 150
157
Diabetic retinopathy
Microvascular damage to retina | Early detection: patient should have annual eye examination
158
diabetic nephropathy: associated with: leading cause of: prevent by:
Associated with damage to small blood vessels that supply the glomeruli of the kidney Leading cause of end-stage renal disease Prevention/delay: glucose and hypertension control, annual screening of kidney function
159
nonproliferative retinopathy
most common form. partial occlusion of the small blood vessels in the retina causes microaneurysms in capillary walls that leak causing retinal edema & hard exudates or intraretinal hemorrhages.
160
proliferative retinopathy
most severe form involves retina & vitreous. capillaries become occluded, body compensates by neovascularization to supply retina w/ blood. the new vessels are fragile & hemorrhage easily, producing vitreous contraction. pt sees black & red spots
161
Paresthesia
an abnormal sensation, typically tingling or pricking (“pins and needles”), caused chiefly by pressure on or damage to peripheral nerves.
162
% of DM pts with some degree of neuropathy
60-70%
163
Diabetic neuropathy
nerve damage due to metabolic derangements associated w/ DM.
164
most common neuropathy
sensory neuropathy
165
2 categories of diabetic neuropathy
sensory - affects peripheral nervous system | autonomic- affects all body systems
166
Sensory neuropathy
affects hands and/or feet bilaterally Characteristics include Loss of sensation, abnormal sensations, and pain Foot injury and ulcerations can occur without feeling pain
167
Autonomic neuropathy : complications
Autonomic neuropathy: can affect nearly all body systems Complications: delayed gastric emptying, orthostatic hypotension, tachycardia, painless myocardial infarction, sexual dysfunction, neurogenic bladder – urine retention
168
Most common cause of hospitalization for DM pts
Foot complications
169
Risk factors for foot complications
Sensory neuropathy Peripheral arterial disease Others: smoking, clotting abnormalities, impaired immune function, autonomic neuropathy
170
monofilament screening
screen annually for sensation on plantar surface of foot. | apply thin, flexible filament to several spots on plantar foot surface..does pt feel?
171
Annual testing for pt with DM 2
Blood pressure serum creatinine urine: for microalbuminuria monofilament test of foot