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MVC 3/22 EA > Med Surg - Exam3- Mandy- ch49 lecture > Flashcards

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
Q

Excessive LDL

A

LDL builds up on arterial walls and hardens to create plaque, constricting flow and contributing to heart disease.

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26
Q

Triglyceride

A

storage of fat for energy use

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27
Q

Cholesterol

A

for construction of cell and hormone

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28
Q

HDL for

A

transportation

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29
Q

Hyperglycemia causes a diabetic to produce

A

a high volume of glucose containing urine

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30
Q

other types of DM

A

prediabetes
gestational
secondary

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31
Q

prediabetes

A

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

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32
Q

Impaired fasting glucose (IFG)

A

between 100 -125 mg/dl

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33
Q

to diagnose diabetes, fasting glucose needs

A

tested twice at more than 126 mg/dl

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34
Q

Impaired glucose tolerance (IGT)

A

2 hour oral glucose tolerance test (OGTT) level between

140 -199mg/dl

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35
Q

Diagnostics for DIABETES

A
  • 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
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36
Q

normal HBA1c

A

glycosylated hemoglobin. 4-6%

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37
Q

prediabetes HbA1C

A

5.7-6.4%

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38
Q

Oral contraceptives

A

could elevate OGTT

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39
Q

prediabetes FG

A

100-125 mg/dl

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40
Q

prediabetes OGTT

A

140-199 mg/dl

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41
Q

collaborative care of diabetes

A

medication
Nutritional therapy
Self-monitoring blood glucose
Exercise

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42
Q

Insulin Bolus

A

given before meals

Rapid acting or short acting

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43
Q

Rapid Acting Insulin

A 
Lispro (Humalog), 
aspart (NovoLog), 
glulisine (Apidra)
Injected 0 to 15 minutes before meal
Onset of action 15 minutes
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44
Q

Short Acting Insulin

A

ie REGULAR insulin
Regular (Humulin R, Novolin R)
Injected 30 to 45 minutes before meal
Onset of action 30 to 60 minutes

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45
Q

BASAL Insulin

A

Basal – control glucose level between meals and overnights

Intermediate or long acting

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46
Q

Basal insulins

A

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

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47
Q

Intermediate acting insulin

A

NPH (Humulin N, Novolin N)

Has a peak which can result in hypoglycemia

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48
Q

Long-acting insulin

A

Glargine (Lantus) and Detemir (Levemir

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49
Q

Long acting insulins

Lantus and Levemir for Basal

A

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

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50
Q

NPH appearance

A

is cloudy

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51
Q

Rapid Acting times

A

onset: 10-30min
peak: 30min-3 hrs
duration: 3-5hr

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52
Q

Rapid Acting names

A

lispro Humalog
aspart NovoLog
gluslisine Apidra

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53
Q

Short Acting times

A

onset: 30-60min
peak: 2-5 hr
duration: 5-8 hr

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54
Q

Short Acting names

A

Regular: Humulin R

Novolin R

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55
Q

Intermediate acting times

A

onset: 1.5-4hr
peak 4-12 hr
duration 12-18 hr

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56
Q

Intermediate names

A

NPH: Humulin N, Novolin N

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57
Q

Long acting names

A

glargine Lantus

detemir Levemir

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58
Q

Long acting times

A

onset: .8 -4hr
peak: no pronounced peak
duration: 24 plus hours

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59
Q

mixing insulins

A

Mixing insulins: always withdraw Regular insulin first then NPH

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60
Q

combination insulin therapy

A

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

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61
Q

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?

A

1 am, while sleeping

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62
Q

Insulin storage (4 points)

A
  • 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
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63
Q

what size syringe to use for insulin?

A

0.3 or 0.5 ml syringe

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64
Q

How long to leave syringe in place after injection?

A

5 seconds

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65
Q

Administration of insulin:

what site has fastest absorbtion?

A

Abdomen, followed by arm, thigh, butt

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66
Q

Do not inject insulin into site..

A

that is to be exercised

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67
Q

Insulin & alcohol wiping

A

At home, by patient: not recommended.

In the hospital, by nurse: absolutely…to prevent HAIs

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68
Q

Insulin concentrations

A

usually 100 units/ml

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69
Q

Insulin injections should be

A

rotated within one particular site…this decreases variablility of absorption

70
Q

only IV insulin

A

Regular insulin only

71
Q

Both Somogyi and Dawn phenomenon

A

characterized by hyperglycemia in the morning

72
Q

Is AM hyperglycemia because insulin dosage is too high or too low?

A

check blood glucose at 2-4am

73
Q

Somogyi effect

A

Somogyi caused by hypoglycemia rebounded by counterreulatory hormone

74
Q

Dawn phenomenon

A

Down phenonmenon due to counterregulatory hormone

75
Q

Insulin pump

A
  • 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
Q

Oral agents that increase insulin production from the pancreas

A

SULFONYLUREAS (Glipizide (Glucotrol), Glyburide (Micronase), Glimepiride (Amaryl)
*MEGLITINIDES (Repaglinide (Prandin), Nateglinide (Starlix)

SIDE EFFECT: hypoglycemia

77
Q

Meglinides

A

Oral agent, increases insulin production, short acting

*take 30 minutes before each meal

78
Q

Sulfonylureas: Glucotrol, Micronase, Amaryl

A

Oral agent that increases insulin production and release from pancreas

79
Q

Megliniede

A

like regular insulin, comes & goes fast

80
Q

postprandial

A

post meal

81
Q

Oral agent that reduces glucose production by liver

A

Biguanides: Metformin (Glucophage)

82
Q

Metformin (Glucophage)

A

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
Q

Oral agents that delay the absorption of glucose from intestines

A

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
Q

Acarbose (Precose)

A

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
Q

Biguanides do not

A

promote weight gain, beneficial to people with prediabetes

86
Q

Metformine

A

increases lactic acidosis…kidney problem

87
Q

oral agents that improve insulin sensitivity

A

Thiazolidiediones

88
Q

Thiazolidiediones

A

IMPROVES INSULIN SENSITIVITY. does not increase insulin production, thus will not cause hypoglycemia

89
Q

Thiazolidinediones: drug names

A

IMPROVES INSULIN SENSITIVITY.

Pioglitazone (Actos), Rosiglitazone (Avandia)

90
Q

Thiazolidinediones

A

impair liver function, do not use in pt with MI, stroke or heart failure

91
Q

DDP-4 inhibitor

A

Oral agent: blocks dipeptidyl peptidase-4, which decreases insulin production.

92
Q

DDP-4 inhibitors do not cause

A

weight gain or hypoglycemia

93
Q

DDP-4 inhibitor names

A

Sitagliptin (Januvia)

94
Q

Byetta

A

3rd category of DM med. from Gila monster saliva. stimulates insulin production and decreases liver sugar production. causes weight loss.

95
Q

Non insulin Injectable Agents. Names

A

Exenatide (Byetta)

Praminitide (Symlin)

96
Q

Noninsulin Injectable Agents

A

Increase insulin sysnthesis and release from the pancrease. Inhibit glucagon secretion, & Delays gastric emptying. watch for hypoglycemia.

97
Q

Exenatide (Byetta)

A

Noninsulin injectable: Glucagon like peptide 1 (GLP1) Receptor Agonist.
Need to take oral medication >1 hour before injecting Byetta.

98
Q

What to teach pt about glyburide (Micronase, DiaBeta, Glynase)?

A

Glyburide stimulates insulin production and release from the pancreas.

99
Q

Glyburide is a sulfonylurea it

A

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
Q

Metformin should be held…

A

held for 48 hours after administration of IV contrast media, but this is not necessary for glyburide.

101
Q

Glucagon secretion & glyburide

A

Glucagon secretion is not affected by glyburide.

102
Q

nutritional therapy: Carbohydrates, 7pts

A
  • 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
Q

Nutritional therapy - protein

A

15-20% of calories

high protein diets for wt loss, not recommended

104
Q

Nutritional therapy - fat

A

low fat: 20-30% total calories

saturated fat <200 mg/day

105
Q

Alcohol & diabetes

A

Alcohol consumption : can cause severe hypoglycemia, should be consumed with food

106
Q

Glycemic index (GI):

A

Glycemic index (GI): rises in blood glucose level after consuming carbohydrate-containing food.

107
Q

a slice of bread is

A

Simple complex carbohydrate

1 slice of bread – 15 g one serving

108
Q

Alcohol inhibits liver to

A

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
Q

SMBG

A

Self Monitoring Blood Glucose

ie AccuCheck

110
Q

When NOT to exercise?

A

Hold exercise if glucose ≤ 100 mg/dl or ≥ 250 mg/dl, or if ketones are present in the urine.

111
Q

When TO exercise?

A

Exercise daily same time same amount

Best to excise 1-2 hours after meals

112
Q

Small CHO snack..

A

can be taken during exercise to prevent hypoglycemia

113
Q

Exercise & SMBG

A

Monitor blood glucose levels before, during, and after exercise

114
Q

Diabetics need ___ B4 exercise

A

Need medical clearance before exercise

115
Q

When patient is ill,

A

When patient is ill, blood glucose should be tested at least every 4 hours

116
Q 
Nursing Management of DM:
Overall Goals (5)
A
  • 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
Q

Nursing Management of DM

Acute interventions:

A

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
Q

Nursing Management:
Ambulatory & home care
Tables 49-13–15
6 points

A
  • 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
Q

A client with type 1 diabetes calls the clinic with complaints of nausea, vomiting, and diarrhea. The nurse should advise the client to

A

Check the blood glucose level every 2 to 4 hours

120
Q

Acute Complications

A

see table 49-16 pg 1175

121
Q 
Diabetic ketoacidosis (DKA)
caused by
A

profound deficiency of insulin

122
Q

DKA characterized by….

6 points

A
  • 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
Q

DKA is common in

A

Common in type 1 or poor self management

124
Q

ketone

A

by product of fat metabolism

125
Q

fruity odor

A

is acetone, simplest ketone

126
Q

pH range: normal

A

7.35-7.45

127
Q

Bicarbonate range: normal

A

21-28

128
Q

DKA interventions table 49-18

Emergency Management

A

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
Q

HHS

A

Hyperosmolar Hyperglycemic Syndrome

130
Q

HHS 5 points

A
  • 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
Q

glucose level in HHS

A

more than 600

132
Q

HHS vs DKA in terms of fluids

A

HHS requires greater fluid replacement

133
Q

Hypoglycemia

A

Low blood glucose < 70 mg/dl

134
Q

hypoglycemia caused by

A

mismatch in timing of food intake and peak action of insulin or oral hypoglycemic agents

135
Q

common manifestations of hypoglycemia

A

Common manifestations: confusion, irritability, diaphoresis, tremors, hunger, weakness, visual disturbances, can mimic alcohol intoxication

136
Q

untreated hypoglycemia

A

Untreated can progress to loss of consciousness, seizures, coma, and death

137
Q

Nursing management of DKA/HHS: Patient closely monitored. Administer:

A

IV fluids
Insulin therapy
Electrolytes

138
Q

Nursing management of DKA/HHS: Patient closely monitored. Assess:

A

Cardiac monitoring - EKG
Renal status
Cardiopulmonary status
Level of consciousness

139
Q

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

A

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
Q

AT first sign of Hypoglycemia:

A

Check blood glucose

If 70 mg/dl, investigate further for causes

141
Q

If having hypoglycemic symptoms, and monitoring equipment is not available:

A

treatment should be initiated

If alert enough to swallow, 15 to 20 g of a simple carbohydrate, avoid foods with fat

142
Q

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.

A

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
Q

Intramuscular Glucagon stimulates

A

the liver to produce glycogen to supply glucose

144
Q

Which action should the nurse take after a 36-year-old patient treated with intramuscular glucagon for hypoglycemia regains consciousness?

A

Give the patient a snack of peanut butter and crackers

145
Q

After Glucagon administration what can happen? what could prevent?

A

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
Q

Acute complications of DM

A

HHS
DKA
hypoglycemia

147
Q

Chronic Complications of DM:

A 
Angiopathy (micro &amp; macrovascular)
Retinopathy
Nephropathy
Neuropathy
feet &amp; lower extremities
skin
infections
psychologic considerations
148
Q

Angiopathy

A

Blood vessel damage secondary to chronic hyperglycemia resulting in organ disease

149
Q

Macrovascular angiopathy

A
  • 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
Q

Risk factors for Macrovascular angiopathy in DM pts

A

Obesity, Smoking, Hypertension, High-fat intake, Sedentary lifestyle

151
Q

Key to prevent CVD in DM pts

A

Control of blood pressure and lipid panel is the key to prevent cardiovascular diseases

152
Q

Microvascular angiopathy specific to DM

A

Result from thickening of vessel membranes in capillaries and arterioles in response to chronic hyperglycemia
*Affect eyes, kidneys, skin

153
Q

Lab value:

Cholestrol

A

<200 mg/dL

154
Q

Lab value:

LDL

A

<130 mg/dL

155
Q

Lab value:
HDL
male & female

A

Male: >45
Female: >55 mg/dL

156
Q

Lab value:

triglycerides

A

< 150

157
Q

Diabetic retinopathy

A

Microvascular damage to retina

Early detection: patient should have annual eye examination

158
Q

diabetic nephropathy:
associated with:
leading cause of:
prevent by:

A

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
Q

nonproliferative retinopathy

A

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
Q

proliferative retinopathy

A

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
Q

Paresthesia

A

an abnormal sensation, typically tingling or pricking (“pins and needles”), caused chiefly by pressure on or damage to peripheral nerves.

162
Q

% of DM pts with some degree of neuropathy

A

60-70%

163
Q

Diabetic neuropathy

A

nerve damage due to metabolic derangements associated w/ DM.

164
Q

most common neuropathy

A

sensory neuropathy

165
Q

2 categories of diabetic neuropathy

A

sensory - affects peripheral nervous system

autonomic- affects all body systems

166
Q

Sensory neuropathy

A

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
Q

Autonomic neuropathy : complications

A

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
Q

Most common cause of hospitalization for DM pts

A

Foot complications

169
Q

Risk factors for foot complications

A

Sensory neuropathy
Peripheral arterial disease
Others: smoking, clotting abnormalities, impaired immune function, autonomic neuropathy

170
Q

monofilament screening

A

screen annually for sensation on plantar surface of foot.

apply thin, flexible filament to several spots on plantar foot surface..does pt feel?

171
Q

Annual testing for pt with DM 2

A

Blood pressure
serum creatinine
urine: for microalbuminuria
monofilament test of foot

MVC 3/22 EA (28 decks)

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