Med Sheet For Exam 2

Front 1

ACS- Signs and Symptoms

Back 1

Signs and Symptoms
Acute Compartment Syndrome
• Cyanosis (if venous insufficiency present)
• Pallor (if arterial insufficiency)
• Numbness and tingling
• Paresis
• Severe pain
If not treated within 4-6 hours of onset of ACS, neuromuscular damage is irreversible. The limb can become useless in 24-48 hours.

Front 2

ACS- what happens if left untreated?

Back 2

If not treated within 4-6 hours of onset of ACS, neuromuscular damage is irreversible. The limb can become useless in 24-48 hours.

Front 3

ACS treatment?

Back 3

• Elevation of extremity
• Splitting of cast or removal of cast
• Fasciotomy--incision is made through the skin and subcutaneous tissues into the fascia of the affected compartment. Relieves pressure and restores circulation to the affected area.

Front 4

Fat Embolism- s/sx

Back 4

• Appears 12-72 hours after injury
• respiratory distress
• confusion from hypoxia
• tachycardia, tachypnea
• hypertension, fever
• petechiae--characteristic of fat embolism--possibly due to capillary occlusion.

Front 5

Fat Embolism-treatment

Back 5

•bedrest, gentle handling, O2, steroids
• If left untreated, can lead to ARDS which has a mortality rate of up to 50%

Front 6

Nursing care prior to cast application:

Back 6

Explain purpose and procedure for application.
 For plaster cast--warn pt about heat that will be felt immediately after wet cast applied.
New cast, sometimes called green cast, is not covered to facilitate drying.

Front 7

Post nursing care to cast:

Back 7

 Monitor neurovascular status of casted extremity Q1h for 24 hours, then Q4H.
 Teach ROM exercises of unaffected extremities
 Ask pt if cast feels too tight
 Have cast cutter available Maintenance of skin care and proper hygiene:

Front 8

Pre-op intervention for Clients with Fractured Joints

Back 8

– C and DB exercises, IS
– Calf exercises to prevent DVT
– Use of AES, SCD
– Early ambulation and PT routines
– Discharge planning

Front 9

Post-op Interventions for Clients with Fractured Joints

Back 9

– pain control
– early mobility
– prevent skin breakdown

Front 10

Laminectomy Post-Op Care

Back 10

• VS and neuro check q4H
• Check for voiding. Inability to void may indicate damage to the sacral spinal nerves which control the detrusor muscle in the bladder.
• Pain control.
• Check dressing for blood or CSF leak. Bulging at incision site may be due to CSF leak or a hematoma. CSF leak may cause spinal headache.Call MD ASAP if dressing with clear fluid. Bedrest--HOB flat for 24-48 hrs
• Logroll Q2H
• OOB typically on the evening of surgery. Spinal fusion pt. Stays in bed for 24-48 hours longer. Assist to straight back chair.
• C and DB, IS Q1-2H while awake.
• AES, SCD
• Use lumbosacral brace when getting OOB.

Front 11

Pre-operative care- amputation

Back 11

- when the pt has PVD, nurses primary goal is to access circulation in other parts of the body. Assess skin color, temp, sensation, and pulses in both affected and unaffected extremities. Cap. Refill also, although this isn’t a reliable indicators.
-psyschosocial assessmentassess family’s or significant other’s reaction to surgery.
- people may go through grieving process. Ask about their coping mechanism.
-preoperative x ray,
-segmented limb blood pressure- ankle systolic divided by brachial systolic pressure. A normal ABI is greater or equal to one.
-doppler flowmetry, transcutaneous oxygen pressure-predicts healing of amputation, angiography-not a reliable predictor of healing,

Front 12

Post-operative care-amputation

Back 12

Phantom limb must be treated seriously. Opioids does not work as well for phantom limb as it does for residual limb. Other drugs include intravenous infusion calcitonin, beta blockers, anticonvulsants, and antispasmodics.
- ROM to prevent flexion contractures, particularly of the hip and knee
-Trapeze and overhead frame
-Firm mattress
-Prone position every 3 to 4 hours
-Elevation of lower-leg residual limb controversial
-teach how to use protheses and how to clean it.
-help with coping.

Front 13

Total WBCs-
normal range and indication if it's not normal

Back 13

5,000 to 10,000 mm3
# of WBCs in 1 mm3 blood
• Increased in acute infection,
• Decreased in certain viral infections, bone marrow depression

Front 14

Differential Neutrophils- normal range and indication if it's not normal

Back 14

Most common circulating WBC, and responds more rapidly to the inflammatory process and tissue injury sites. During acute infection, these are the body’s first line of defense

• Increased in acute supportive infections
• Decreased in overwhelming bacterial infections (elderly)

Front 15

Lymphocytes- normal range and indication if it's not normal

Back 15

Play a major role in immune response (T and B).
• Decrease number during excess adrenocortical hormone secretion/therapy
• Increase in chronic bacterial and viral infections
• Decrease during sepsis

Front 16

Active transport –

Back 16

Example is the sodium-potassium pump, ATPase pump. Sodium is pumped out of the cell and potassium is pumped in, against the concentration gradient. This process keeps a higher concentration of potassium in the ICF and a higher concentration of sodium in the ECF.

Front 17

Hypertonic solution -

Back 17

such as 3% sodium chloride, pulls fluid from cells, causing them to shrink.

Front 18

Hypotonic solution

Back 18

(a solution of lower osmotic pressure), such as 0.45% sodium chloride, moves fluid into the cells, causing them to enlarge

Front 19

Isotonic solution

Back 19

0.9% sodium chloride, expand the body's fluid volume without causing a fluid shift from one compartment to another.

Front 20

Normal Saline Osmolarity

Back 20

A solution with the same osmolarity as blood plasma such as normal saline, 0.9% sodium chloride, expand the body's fluid volume without causing a fluid shift from one compartment to another.

Front 21

Osmotic pressure

Back 21

The osmotic pressure of a solution is its osmolality, which is expressed in osmols, or milliosmols per kilogram (mOsm/kg) of the solution. The normal serum osmolality is 275 to 295 mOsm/kg.
A solution with a high solute concentration has a high osmotic pressure and draws water toward itself.

Front 22

normal blood plasma

Back 22

Normal plasma osmolarity is about 290 mOsm/L.

Front 23

fluids

Back 23

The ECF space contains about one third (15 L) of total body water.
. ICF contains the remaining two thirds (25 L) of total body water.

Front 24

Comparison of total body weight/water:

Back 24

Newborn infant – 75-80% water
Adult – 60% water
Adult over age 65 – 45-50% water

Front 25

Calcium

Back 25

normal 9.0 -10.5
Critical values: <6 or >13

Front 26

Carbon dioxide:

Back 26

Carbon dioxide: 23-30 mEq/L Critical values: <6 mEq/L

Front 27

Chloride:

Back 27

Chloride: 98-106 mEq/L Critical values: <80 or >115

Front 28

Creatinine:

Back 28

Creatinine: 0.5-1.2 mg/dL critical values: >4 mg/dL

Front 29

Glucose

Back 29

Glucose: <110 mg/dL Critical values: <40 and >400 mg/dL

Front 30

Potassium:

Back 30

Potassium: 3.5 -5.0 mEq/L Critical values: <2.5 or >6.5 mEq/L

Front 31

Sodium:

Back 31

Sodium: 136-145 mEg/L Critical values: <120 or >160 mEq/L

Front 32

Urea Nitrogen, Blood (BUN)

Back 32

Urea Nitrogen, Blood (BUN): 10-20 mg/dL Critical: 100 mg/dL

Front 33

• Fluids are given for maintenance - normal daily need for fluids/electrolytes –

Back 33

usually 3,000 over 24 hrs for an adult – 125 mL/hr.

Front 34

parenteral therapy

Back 34

Anything going through IV route or venous route is parenteral. Enteral is anything going through GI tract.

Front 35

Indications for Intravenous Therapy:

Back 35

1. To achieve normal fluid and electrolyte balance
2. Administer continuous or intermittent medication
3. Maintain or correct a patient's nutritional state
4. Administer blood or blood components
5. Administer diagnostic reagents
6. Some elderly will have IV fluids to restore hydration as they have a diminished thirst mechanism.
7. Monitor cardiac functions – can measure cardiac functions thru IV lines. (We will learn this later.)

Front 36

TPN

Back 36

can never be given through a peripheral line, needs to be given through a central line (it always end at the superior vena cava). Peripheral line only goes one to two inches inside body and does not end in the superior vena cava.
There are central lines through different places, different from PICC line.

Front 37

PPN

Back 37

debate over whether this means partial or peripheral parenteral nutrition.
Any RN can start a peripheral line.

Front 38

PICC lines

Back 38

only specially trained nurses (one or two per hospital) can insert, always ultra sound guided, could do at bedside or not, completely sterile procedure

Front 39

Central lines

Back 39

through jugular or subclavians – only MDs can do this. First choice is basilic route, then median and cephalic veins.

Front 40

PICC lines

Back 40

PICC line is a type of central line, but it starts peripherally.

Front 41

Plasma osmolality

Back 41

Plasma osmolality is normally about 290 mOsm/KG

Front 42

Insulin Resistance

Back 42

is a cause of type 2 diabetes mellitus characterized by a need for an increased amount of insulin per day to control hyperglycemia and ketosis. The cause is associated with decreased or ineffective glucose transporter proteins with
insulin-sensitive cells or insulin-binding by high levels of antibody
B-cell dysfunction, which in combination with insulin resistance leads to type 2 diabetes.

Front 43

Definition of insulin resistance:

Back 43

• Also known as Metabolic Syndrome
• High fasting blood glucose (110 mg/dL or higher
• Abdominal fat is especially active hormonally, secreting a group of hormones called adipokines that may possibly impair glucose tolerance

Front 44

Precursor to TYPE 2

Back 44

Studies have shown that most people with insulin resistance go on to develop type 2 diabetes within 10 years.

Front 45

Insulin Resistance: Labs

Back 45

• High LDL
– (bad) blood cholesterol levels
– (above 180 mg/dl)
• Low HDL
– (good) cholesterol levels
– (below 40 mg/dL for men and below 50 mg/dL for women)
• High levels of triglycerides
– (150 mg/dL or higher)
• Hypertension
– (130/85 mm Hg or higher)

Front 46

Insulin Resistance symptoms:

Back 46

• Acanthosis nigricans
– Dark patches of skin
• On the back of the neck
• Dark ring around their neck
• elbows, knees, knuckles, and armpits

Front 47

Describe how an individual can restore their body to a normal insulin sensitivity state.

Back 47

To avoid IR turning into DM
– Control intake of carbohydrates
– Physical exercise
– Weight loss
• Drugs, normoglycemia, and salicylates can affect insulin resistance and improve glucose tolerance. There is a lot of ongoing research at the National Institutes of Health looking at role of salicylates as a potential treatment for insulin resistance.

Front 48

•
State the normal blood glucose level

Back 48

• Normal
– 70 mg/dl and 110 mg/dl (fasting)
• Hypoglycemia
– Below 70 mg/dl
• Hyperglycemia
Above 180 mg/dl

Front 49

Throughout the 24 hour cycles of eating, digestion, and fasting, blood plasma glucose levels are ?

Back 49

generally maintained within a range of 70-150 mg/dL

Front 50

fasting blood glucose is diagnostic...it should be between ?

Back 50

70 and 110. Even after eating, however, the glucose should be below 180.

Front 51

After fasting for 12 hours

Back 51

you go into lab and glucose should be within 70-110 levels.

Front 52

Breakfast and labs right after probably should be ?

Back 52

a little high, but should not be above 140.

Front 53

HYPOGLYCEMIA
Symptoms

Back 53

Symptoms
Brain is dependent on a continual supply of glucose
If the amount of glucose supplied by the blood falls, the brain is one of the first organs affected
a. Impairment of action and judgment
b. Seizures
c. Coma
Prolonged, severe hypoglycemia can produce lasting brain damage!
• Other Sx
– Cool, clammy skin
– Profuse perspiration*
– Anxious, nervous*, disoriented*
– Behavior change!
– Double vision, blurred vision, hunger, tremors
– Tachycardia, palpitations

Front 54

HYPOGLYCEMIA
• Adaptive response

Back 54

– Glycogenolysis – the breakdown of glycogen to glucose
– Gluconeogenesis – formation of glucose from glycerol & proteins rather than from carbohydrates
– Liver converts a storage of glycogen into glucose and releases it into the bloodstream

Front 55

Treatment: HYPOGLYCEMIA

Back 55

For mild hypoglycemic manifestations, if the symptoms do not resolve immediately, repeat the PO treatment.
Glucagon administration often induces vomiting, increasing the client's risk for aspiration.
• Follow Hosp. Protocol
• Suspect hypoglycemia in any pt. with sudden change in mental status
• Can do a FSBS prn to determine
• Sudden change in mental status might be first indicator of hypoglycemia in ANY patient.
• FSBS done before they eat. We can do FSBS at anytime and use critical thinking to find out what we need to do then.

Front 56

things you could do for hypoglycemia

Back 56

• Blood glucose can be raised to normal within minutes by taking (or receiving) 10-20 grams of carbohydrate
• PO—juice, icing, candy, coke
• IM—Glucagon---1 to 2 milligrams
• IV---Dextrose---50% (adult) push

Front 57

HYPERGLYCEMIA

Back 57

• Polyuria – body is trying to get out excess glucose. Formerly, urine was tested with dipstick, urine is very sweet. Can lead to dehydration. Dehydration then leads to hemoconcentration (fluid is gone, now it’s all cells).
• Hypovolemia – now volume is less.
• Hyperviscosity – now blood that’s left has a high concentration of glucose, very thick and sticky.
• Hyperfusion – reduced circulation, now blood is not getting out to the periphery, too thick/sticky and can’t get thru capillaries. Some lose toes.
• Hypoperfusion – decreased circulation.
• Hypoxia – poor tissue oxygenation.
• Hyperketonemia – now body is trying to convert fats to glucose, body is giving off ketones also.

Front 58

HYPERGLYCEMIA

Back 58

• When the pancreas does not make enough insulin
• Or the body is unable to use the insulin that is present
• The cells cannot take up & use glucose
• Excess glucose builds up in the bloodstream

Front 59

Insulin normally stimulates

Back 59

lipogenesis and inhibits lipolysis, thus preventing fat catabolism. With insulin deficiency, lypolysis is enhanced and there is an increase in the amount of nonesterified fatty acids delivered to the liver. The consequence is increased glyconeogenesis contributing to hyperglycemia and production of ketone bodies (acetoacetate, hydroxybutyrate, and acetone) by the mitochondria of the liver at a rate that exceeds peripheral use.

Front 60

hyperglycemia-Adaptive Response

Back 60

– Polydipsia - they are thirsty because they are peeing too much and getting dehydrated.
– Polyuria - they are peeing too much.
– Polyphagia - they are hungry because cells are hungry. Even though glucose levels are high, but they don’t’ have insulin to get glucose into cells.

Front 61

Hyperglycemia symptoms:

Back 61

• Hot, dry*
• Rapid, deep, Kussmaul type resp; acetone odor (only if ketones present) – may be in a coma at this point; body is blowing off the extra glucose
• Acidosis s/sx
• Dehydration s/sx
•

Front 62

Nursing interventions:
Hyperglycemia: Tx

Back 62

• VS q 15 min
• Urine output & mental status q hour
• Insulin SQ or IV (bolus plus cont. infusion)
• Treat for DKA (we will learn about DKA in 305)
If we see anyone in this stage, take VS. Doesn’t matter if they are up or down. VS are very important to give us info.
• Person will probably be in ICU.
• FSBS – doctor will probably want done every hour. Person is in a bad situation.

Front 63

Relate the statistical impact of Diabetes Mellitus as a cross cultural disease.

Back 63

DM is especially prevalent in elderly.
Higher rates in black, Hispanic and asian groups than whites.
Some American Indian tribes have the highest known rate of diabetes.
In the world, 20-50% of adults have diabetes.
40% of the diabetic population is 65 or older.
Women are 50% more likely to have diabetes than men.
DM is the third leading cause of death by disease. It reduces lifespan by 1/3.

Front 64

Dyslipidemia

Back 64

– a lot of fat in the bloodstream, a lot coming from liver.
Muscle is eating itself.
With our diabetic pts, we are fighting this every single day. These are the first symptoms we see in an undiagnosed diabetic.

Front 65

Type I: Etiology

Back 65

• Genetic Predisposition
• Environmental Trigger
• Active autoimmunity
• Progressive beta cell dysfunction

Front 66

Type I-• Increase risk

Back 66

• Tissue types HLA-DR3 or HLA-DR4
• Bacterial/viral infections; mumps, congenital rubella, coxsackievirus, etc
• May have circulating ICA (islet cell antibodies) and IAA (insulin autoantibodies) PRIOR to manifestation of type 1 DM

Front 67

type 1 treatment

Back 67

insulin, diet and exercise

Front 68

type 1
Characteristic
Insulin Status
Age
Clinical Presentation
Body Build
Family History
Genetics

Back 68

Insulin secretion decreases
Usually under 30 but may occur at any age
Rapid onset
Lean or normal usually
Weak
Islet Cell Antibodies
Present at onset in 85-90%
Human Leukocyte Antigen association
(HLA – usually positive)

Front 69

Type II

Back 69

• Progressive disorder in which the pancreas makes less insulin over time.
– Reduced ability of most cells to respond to insulin (insulin resistance)
– Poor control of liver glucose output
– Decreased beta cell function = beta cell failure
-Obese –Heredity

Front 70

type 2 • Treatment

Back 70

diet, exercise, oral agents, insulin.

Front 71

type2

Back 71

• May also see patients with ESRD before they are diagnosed with DM Type II.