DISORDERS OF THE PANCREAS - Avoid alcohol, coffee, and smoking for 36 hours

before the test.

DIABETES MELLITUS - NPO for 10 to 16 hours
- Initial blood and urine specimen are collected
➔ is a chronic disorder of carbohydrate, fat and
- 150 to 300g of glucose per orem or IV is given
protein metabolism.
- series of blood specimen is collected after
● It is due to inadequate insulin and production
administration of glucose ( 30 mins, 1 hour, 2 hours,
or increased resistance to insulin
if required 3 hours , 4 hours, and 5 hours after)
● The cause of DM is unknown
- If glucose level peak at higher than normal at 1 to 2
● The predisposing factor to DM are as
hours after ingestion or injection of glucose and
follows:
slower than normal to return to fasting levels, the DM
a. STRESS: It stimulates secretion of
is confirmed.
epinephrine, norepinephrine and
- Done when results of FBS and 2 PPBS are
glycogenolysis and gluconeogenesis.
borderlined ( high normal)
b. HEREDITY: It is strongly associated
with Type II DM
4. HGT- No NPO ( Blood) Hemoglucotest/ Capillary
c. OBESITY: Adipose tissues are
Blood Glucose Test
resistant to insulin. Therefore, glucose
uptake by the cells is poor.
4. Glycosylated Hemoglobin ( HbA1c)
d. VIRAL INFECTIONS: Increase risk to
- most accurate indicator of DM ( Diabetes Mellitus)
autoimmune disorders that may affect
- reflects serum glucose levels for past 3 to 4 mos
the pancreas.
- evaluate amount of glucose attached to the
e. AUTOIMMUNE DISORDERS: It is
hemoglobin of your blood for previous 120 days,
more associated with Type I DM. This
- NV: 4% to 6% ( up to 7%) for non diabetics
is because it is the children who are
-the goal for client with DM is 7.5% or less
more prone to viramol infections
f. WOMEN: who are multigravida with
5. Acetest- evualate Ketunuria : fats
large babies.
- Get acetest tablet( offwhite, creamy, white color)
➔ During pregnancy, human placental
- 1-2 drops of urine.
lactogen (HPL) is produced HPL
- if color is LAVANDER (+) Ketonuria
antagonizes insulin thus,
- No change (-)
hyperglycemia occurs during
pregnancy.
6. Clinitest ( Glycosuria)
DIAGNOSTIC TEST: - 2nd voided/double voieded Procedure:
1. Fasting Blood Sugar( FBS) - Clinitest tablet- Do not hold with barehand, its
Normal: 70- 110mg/dl corrosive.
DM : Increase 140mg/dl for 2 readings - Test tube- 10 gtts water, 5gtts of urine, put tablet
and SIZZLE sound is present.
2. 2hours Post Prandial Blood Sugar(2PPBS) - Result:
- initial blood specimen is withdrawn 0- 0% - blue
- 100g of carbohydrates in diet is taken by the client trace- ¼ %- blue geen
- 2 hours after meal, blood specimen is withdrawn- + - ½% - green
blood sugar returns to normal level. ++ - 3/4%- yellow green
+++ - 1% - yellow green
3. OGTT/GTT ( Oral Glucose Tolerance Test) ++++ - 2% - orange
- Take high carbohydrate diet (200 to 300g)
for 3 days
7. Benedicts Test
Procedure:
i. Take 5 ml ( one teaspoon) of Benedicts solution
in the test tube.
ii. Holding the test tube with holder, heat it over the
alcohol lamp, till the Benedicts solution boils
without overflowing.
iii. Drop 8-10 drops of urine into the boiling
Benedicts solution.
iv. After again boiling the mixture, let it cool down
v. While cooling, the mixture changes color
vi. Result
(-) blue
(+)0.5%- green
(++)1% - yellow
(+++)1.5% - orange
(+++++)2%- brick- red
Note: It is essential that the above test be performed
two hours after a meal.
TYPE I DIABETES MELLITUS
➔ Also called Insulin Dependent Diabetes
Mellitus (IDDM), Juvenile onset, brittle or
unstable DM
➔ Onset is before 30 years of age
➔ Absolute deficiency of insulin due to absence
of islet of langerhans in the pancreas
➔ The client is thin. This is due to inability of the
body to obtain glucose from carbohydrates.
Therefore the body breaks down fats, and
protein for glucose supply
➔ The client is prone to Diabetic Ketoacidosis
(DKA) in the absence of insulin, fats are
metabolized. There is increased production of
acetone ketones resulting in ketoacidosis.
➔ The collaborative management for IDDM
include:
● Diet
● Activity and exercise
● Insulin (always a component of
management for IDDM)
TYPE II DIABETES MELLITUS
➔ Also called Non-Insulin Dependent
Diabetes Mellitus (NIDDM), maturity onset,
ketosis -resistant DM
➔ Onset is after aged 30 years
➔ With relative lack of insulin or resistance to
the actions of insulin, usually insulin is
sufficient to stabilize fat and protein
metabolism but not to deal with carbohydrate
metabolism
➔ The client is obese
➔ The client is prone to Hyperglycemic,
Hyperosmolar, Nonketotic Coma (HHNC).
This is extreme hypoglycemia without
acidosis. It may result in dehydration and
vascular collapse
➔ The collaborative management for NIDDM
include:
● Diet
● Activity and exercise
● Oral Hypoglycemic Agents (OHA) or
Injectable Hypoglycemic Agents
(IHA). If hypoglycemia is uncontrolled
● Insulin in case of stress, surgery,
infections and pregnancy. These
conditions trigger stress responses
and stimulate secretion of
epinephrine, norepinephrine and
glucocorticoids. These hormones
cause hyperglycemia
➔ A deficiency in insulin results in
Hyperglycemia
The Clinical Manifestations of DM are as follows:
a. Polyuria, Polydipsia, Polyphagia (3P’s)
more common in Type I DM
b. Weight loss more common in Type I DM
c. Blurred vision
d. Slow wound healing
e. Infections: pyorrhea (periorbital infections),
urinary tract infection, vasculitis, cellulitis,
furuncles, carbuncles, vaginal infections
f. Weakness and paresthesia
g. Signs if inadequate circulation to the feet
h. Signs of accelerated atherosclerosis
(renal, cerebral, cardiac, peripheral)
● MACROVASCULAR COMPLICATIONS:
Coronary artery disease, Cardiomyopathy,
 Hypertension, Cerebrovascular disease,
Peripheral vascular disease and Infections
● MICROVASCULAR COMPLICATIONS:
Retinopathy, Nephropathy and
Neuropathy
The collaborative management for DM are as
follows:
1. DIET
➔ Low calorie diet, especially if the
client is obese
➔ The diet should consists of 20%
protein, 30% fats and 50%
carbohydrates
➔ High fiber diet, especially
vegetables. Fiber inhibits glucose
absorption in the intestines and
prevents hyperglycemia. Fruit
exchanges may be eaten , according
to the dietary exchange list. The
Diabetic client should not eat as much
as fruit as he wants, fruits contain
fructose that is converted into
glucose. Therefore, eating too much
fruit may cause hyperglycemia.
➔ Complex carbohydrates like rice,
bread, pasta, and root crops are
preferred. Simplex Carbohydrates
like cakes, pastries are more likely
to cause hyperglycemia.
2. ACTIVITY AND EXERCISE
➔ The benefits of regular exercise are
as follows:
● Exercise increases glucose
uptake by the cells. Therefore
it lowers blood glucose levels
● Exercise lower insulin
requirements
● Exercise help achieve
desirable body weight
● Exercise helps maintain
normal serum lipids. This
reduces vascular risks
➔ Instruct client on dietary adjustment
when exercising
➔ Instruct client to monitor blood
glucose before, during and after the
exercise period
➔ Initially, the client who requires insulin
should be instructed to eat 15g
carbohydrate snack (a fruit exchange
or a snack of complex carbohydrate
with a protein) before engaging in
moderate exercise to prevent
hypoglycemia
➔ If blood glucose level is greater than
250 mg/dl and urinary ketones are
presentsDM Type 1 the client is
instructed not to exercise until blood
glucose is normal and urinary ketones
are absent
3. MEDICATIONS
❖ ORAL HYPOGLYCEMIC AGENTS
➢ Stimulate islet of langerhans to
secrete insulin, increase sensitivity of
peripheral receptors to insulin
decreases hepatic glucose output or
delay intestinal absorption of glucose,
thus decreasing serum glucose levels
➢ Indicated only in Type 2 DM
➢ Drug Interactions and
contraindications of OHA
1. Aspirin, alcohol, sulfonamides,
contraceptives and
monoamine oxidase inhibitor
(MAOI’s) increase the
hypoglycemic effect, causing a
decrease in blood glucose
levels (hypoglycemia)
2. Glucocorticoids, thiazide
diuretics, and estrogen
increase blood glucose levels
(hyperglycemia)
3. Sulfonylureas should not be
taken with alcohol. To prevent
disulfiram -like reactions
4. Inderal (Propranolol) and other
beta- adrenergic blockers may
cause hypoglycemia
5. Sulfonylureas may cause GI
symptoms, Hypoglycemia may
occur
❖ SULFONYLUREAS
● Dymelor (Acetohexamide)
● Diabinese (Chlorpropamide)
● Amaryl (Glimepiride)
● Glucotrol (Glipizide)
● Diabeta, Micronase (Glyburide)
● Tolinase (Tolazamide)
● Orinase (Tolbutamide)
● Non- sulfonylureas

❖ NON- SULFONYLUREAS
● Alpha Glucosidase Inhibitors: Precose
(Acarbose) Glyset (Miglitol)
● Biguanide: Metformin (Glucophage)
● Meglitinide: Starlix (Nateglinide)
Prandin (Repaglinide)
● Thiazolidinediones: Actos
(Pioglitazone) Avandia (Rosiglitazone)

*ADVICE THE CLIENT TO WEAR A MEDIC-

ALERT BRACELET*

❖ INSULIN
➢ Indicated in Type 1 DM
➢ Indicated in Type 2 DM when diet and
weight control are ineffective to maintain
blood glucose levels.
➢ Regular insulin is the only insulin that can
be administered intravenously in the
emergency treatment of diabetic
ketoacidosis
➢ Aspirin, alcohol, oral anticoagulant, oral
hypoglycemic drugs, tetracycline, and
MAOI’s increase hypoglycemic effects of
insulin, causing hypoglycemia
➢ Glucocorticoids,thiazide diuretics, thyroid
agents. oral contraceptives, and estrogen
may cause hyperglycemia
➢ Illness, infection, and stress can elevate
blood glucose levels and the need for
insulin. Insulin should not be withheld
during illness, infections and stress
because hyperglycemia and ketoacidosis
can result
➢ The peak of action time of insulin is
important because of the possibility of
hypoglycemic reactions of hearing that
time
The common types of insulin are as follows:

1. VERY RAPID - ACTING or RAPID - ACTING INSULIN

ONSET PEAK DURATION

HUMALOG (Lispro) 15 mins ½ - 1 ½ hrs 4 - 5 hrs

NOVOLOG (Insulin Aspart) 5 - 10 mins 1 - 3 hrs 3- 5 hrs

2. SHORT - ACTING INSULIN

ONSET PEAK DURATION

REGULAR: Humulin R; Novolin R ½ - 1 hr 2 -4 hrs 5 -7 hrs

3. INTERMEDIATE - ACTING INSULIN

ONSET PEAK DURATION

NPH (Humulin N; Novolin N 1 - 2 hrs 6 - 14 hrs 24 hrs

LENTE (Humulin L; Novolin L) 1 - 2 hrs 6 - 14 hrs 24 hrs

4. LONG - ACTING INSULIN

ONSET PEAK DURATION

ULTRALENTE (Humulin U) 6 hrs 18- 24 hrs 24 hrs

INSULIN GLARGINE (Lantus) - - 24 hrs

5. PREMIXED INSULIN

ONSET PEAK DURATION

HUMULIN 70/30 (70% NPH/ 30% ½ - 1 hr 2 - 12 hrs 18 -24 hrs

Regular)

HUMULIN 50/50 (50% NPH/ 50% ½ hr 3 -5 hrs 24 hrs

Regular)

LISPRO / PROTAMINE 75/25 (75% 10 - 15 mins 5 24 hrs

Lispro/ 25% Protamine)
NURSING INTERVENTION IN INSULIN THERAPY:
1. The main route of insulin injection is
SUBCUTANEOUS. This promotes lower
absorption and is less painful. There are
lesser blood vessels and nerves in the
subcutaneous areas
2. The main areas for insulin injections are the
ABDOMEN, ARMS (Posterior surface),
THIGHS (Anterior surface), and
BUTTOCKS
3. Administer insulin at 90 degrees Left. Most
insulin syringes have needle gauge 27 to 29,
that is about ½ inch long
4. Do not massage injection sites to prevent
rapid absorption. Rapid absorption of insulin
may cause hypoglycemia
5. Injections should be ½ inch apart within the
anatomical area. Finish all sites in one
anatomical area before going to another area
6. To prevent Lipodystrophy (hard fatty
masses and the subcutaneous layers)
a. Systematic rotation of the site of
injection . use one site after at least
two to three weeks
b. Administer at room temperature. Cold
insulin causes lipodystrophy which is
inhibit insulin absorption
7. Gently roll vial in between the palms to
redistribute insulin particles. Do not shake the
vial bubbles make it difficult to aspirate exact
amount
8. Storing insulin
a. Prefilled insulin syringes should be
kept in the refrigerator. These will be
potent for 7 days (1 weeks). The
syringes should be kept flat or with the
needle in an upright position to
prevent clogging of the needle.
b. If a vial of insulin will be used up in 30
days or 1 month it may be kept at
room temperature . otherwise the vial
should be refrigerated
c. Avoid exposing insulin to extremes of
temperature
d. Insulin should not be frozen or kept in
direct sunlight or a hot car
9. Regular insulin may be mixed with another
type of insulin
10. Insulin zinc suspensions (intermediate -
acting) may be mixed only with each other
and regular insulin; not with other types of
insulin
11. To mix insulin, the following nursing actions
are done :
a. Introduced air into the vial of
intermediate-acting insulin (e.g NPH)
Do not aspirate/draw at the insulin, yet
b. Introduced air into the vial of regular
insulin, and draw up the insulin
c. Draw at the intermediate-acting insulin
(NPH)
REMEMBER: DRAW UP THE REGULAR
INSULIN FIRST
12. Administer a mixed dose of insulin within 5 to
15 minutes of preparation; after this time the
regular insulin binds with the NPH insulin and
its action is reduced
13. Avoid exposing insulin to extremes in
temperature. Insulin should not be frozen or
kept in direct sunlight or a hot car. If it
becomes frozen, discard it.
14. Monitor clients for complications of insulin
therapy:
a. LOCAL ALLERGIC REACTIONS
➔ redness, swelling, tenderness and
induration or a wheal at the site of
injection may occur 1-2 hours after
administration
➔ Instruct the client to avoid the use of
alcohol to clean that can before
injection
➔ admin administered 1 hour before
injection as prescribed to by the
physician
b. INSULIN LIPODYSTROPHY
➔ is Loss of subcutaneous fat and
appears as light dumpling or more
serious fitting of subcutaneous fat; the
use of human insulin helps to prevent
this complication
➔ Is the development of fibrous fatty
masses at the injection site amd is
caused by repeated use of an
injection site
➔ Instruct the client to avoid injecting
Insulin into affected side
➔ Instruct the client about the
importance of rotating injection sites
 ➔ Instruct the client to inject insulin at ACUTE COMPLICATIONS OF DIABETES
room temperature; not at room MELLITUS:
temperature
c. INSULIN RESISTANCE A. HYPOGLYCEMIA
➔ Lack of tissue sensitivity to the ➔ Occurs when blood glucose level falls
instrument from the body which is below 60 mg/dL
result in hyperglycemia ➔ Causes of hypoglycemia are as
➔ the client receiving insulin develops follows :
immune antibodies that bind with the 1. Overdose of insulin or oral
insulin thereby decreasing the insulin hypoglycemic agents
available for use in the body 2. Commission of meals are too
➔ This condition may be managed by little food
administering a purer insulin 3. Strenuous exercise or
preparation excessive activity
d. DAWN PHENOMENON 4. Gastro gastrointestinal (e.g.
➔ Results from the reduced tissue nausea and vomiting,
sensitivity to insulin that develops diarrhea)
between 5 and 8 AM (prebreakfast ➔ The client should be instructed to
hyperglycemia). this may be always Carry some form of fast acting
associated with nocturnal release of simple carbohydrates
growth hormone
➔ Treatment is administering CLINICAL MANIFESTATIONS OF
intermediate-acting insulin (NPH) at HYPOGLYCEMIA:
10 PM to control early morning 1. MILD HYPOGLYCEMIA BLOOD GLUCOSE
hyperglycemia LEVEL LESS THAN 60 mg/dL
e. SOMOGYI PHENOMENON ● Hunger
➔ Normal or elevated blood glucose ● Nervousness
levels are present at bedtime, ● Palpitations
Hypoglycemia occur at 2-3 AM which ● Sweating
triggers production of ● Tachycardia
counterregulatory hormones ● Tremors
(epinephrine, norepinephrine,
glucocorticoid) 2. MODERATE HYPOGLYCEMIA BLOOD
➔ By 7 AM In response to the country GLUCOSE LEVEL LESS THAN 40 mg/dL
regulatory herman's glucose wants to ● Confusion
hyperglycemic range rebound ● Double vision
hyperglycemia ● Drowsiness
➔ Treatment for sumo a phenomenon ● Emotional changes
includes decreasing the evening ● Headache
(predinner or bedtime) dose of ● Impaired coordination
intermediate-acting insulin or ● Inability to concentrate
increasing the bedtime snack ● Irrational or combative behavior
f. INSULIN WANING ● Light- headedness
➔ Is a progressive use in the blood ● Memory lapses
glucose level from the time to morning ● Numbness of the lips and tongue
➔ treatment includes increasing the ● Slurred speech
evening (predinner or bedtime) those
of intermediate long-acting insulin 3. SEVERE HYPOGLYCEMIA BLOOD
before the evening meal if one is not GLUCOSE LEVEL LESS THAN 20 mg/dL
already prescribed ● Inability to swallow
● Loss of consciousness
● Seizures
THE COLLABORATIVE MANAGEMENT FOR
HYPOGLYCEMIA ARE AS FOLLOWS:
1. MILD HYPOGLYCEMIA
❖ Give 10-15 grams of fast acting -acting
simple carbohydrates
➢ Commercially prepared glucose
tablets
➢ 5-10 life savers of hard candy
➢ 4 tsp of sugar
➢ 4 sugar cubes
➢ 1 Tbs of honey or syrup
➢ ½ cup of fruit juice or regular softdrink
(soda)
➢ 8 oz low-fat milk
➢ 6 satline crackers
➢ 3 graham crackers
❖ Retest the blood glucose level in 15 minutes
repeat the treatment if symptoms do not
resolve
❖ Once symptoms resolve give 2 slices of white
read (sandwich) or crackers, then a cup of
skim milk or cheese or provide a regular meal
within 50 minutes
2. MODERATE HYPOGLYCEMIA
❖ Give 15-30 g of fast acting-acting
simple carbohydrates
❖ Give additional food such as low-fat
milk or cheese after 10-15 minutes
3. SEVERE HYPOGLYCEMIA
❖ If unconscious or unable to swallow,
an injection of glucagon is
administered subcutaneously or
intramuscularly, or intravenously
❖ Administer a second dose of client
remains unconscious
❖ A small meal is given to the client
when he awakens as long ashe is not
nauseated
❖ Notify the physician if severe
hypoglycemic reaction occurs
❖ Administer 50% dextrose in water 25
to 50 ml per IV as prescribed
❖ Glucagon is used to treat insulin
induced hypoglycemia when the client
is semi-conscious or unconscious and
is unable to digest liquids
B. DIABETIC KETOACIDOSIS (DKA)
➔ Is a life-threatening complication of Type 1
DM. This is due to severe insulin deficiency
➔ Causes of DKA are as follows:
1. Underdose or missed dose of
insulin
2. Illness or infection
3. Overeating
4. Stress, surgery
5. Undiagnosed and untreated type 1
DM
➔ The clinical manifestations of DKA are
based on the following concepts:
1. HYPERGLYCEMIA
2. DEHYDRATION AND
ELECTROLYTE LOSS
3. ACIDOSIS
Blood glucose level range from 300-800
mg/dL
Low serum bicarbonate and a low pH are
present
➔ The Clinical Manifestations of Diabetic
ketoacidosis are as follows:
1. Acetone breath (fruity odor)
2. Anorexia, nausea, vomiting,
abdominal pain
3. Blurred vision
4. Headache
5. Hypotension
6. Kussmaul’s respirations
7. Mental status changes
8. Polydipsia
9. Polyuria
10. Weak, rapid pulse
11. Weakness
THE COLLABORATIVE MANAGEMENT FOR
DIABETIC KETOACIDOSIS ARE AS FOLLOWS:
1. Maintain patent airway
2. Administer oxygen therapy as prescribes
3. Treat dehydration with Normal Saline 0.9% or
0.45% rapid IV as prescribed
4. D5NS or 5% dextrose in 0.45% saline when
the blood glucose level reaches 250-300
mg/dL
5. Treat hyperglycemia with regular insulin IV as
prescribed. A dose of 5-10 units of regular
insulin by IV bolus may be prescribed,
followed by a continuous infusion
6. Mix prescribed IV dose of regular insulin for
continuous infusion in 0.9% or 0.455 saline or
prescribed
7. Small dose of albumin may be mixed with the
insulin and the saline solution to prevent
adherence of insulin molecules to the plastic
IV infusion set
8. Always use infusion pump for insulin infusion
9. Monitor potassium levels, gluco, and urinary
output, And for signs of increased intracranial
pressure (ICP) . If blood glucose severely
drops too fast before the brain can
equilibrate, Water is pulled from the blood to
 the cerebrospinal fluid in the brain. This
causes cerebral edema and increased ICP
❖ Correct electrolyte imbalances (Potassium
level may be elevated as a result of acidosis
and dehydration)
❖ Serum potassium level will fall rapidly as
dehydration and acidosis are treated
❖ Potassium replacement (e.g. KCI, K- Rider)
may be required. Ensure adequate renal
function (e.g. urine output of 30-60 ml/hour)
before administering potassium (if there’s no
adequate urine output, don’t administer
potassium supplement. (To prevent renal
damage)
CRITICAL TO REMEMBER: “NO
PEE, NO K”
❖ The maximum amount of Potassium Chloride
(KCI) that may be mixed with 1 liter of IV
fluids is 40mEq
❖ The maximum amount of potassium
supplement that may be given per iv infusion
is 10mEq/hour
❖ Always use iv infusion pump for potassium
infusion
CRITICAL TO REMEMBER: NEVER
ADMINISTER POTASSIUM AS
BOLUS OR IV PUSH! (Cardiac
arrest and death may occur if
potassium is given as bolus or IV
push)
C. HYPERGLYCEMIC HYPEROSMOLAR
NONKETOTIC SYNDROME
➔ Is severe hyperglycemia that occurs without
ketosis and acidosis
➔ The syndrome occurs in Type 2 diabetics
➔ The clinical manifestations of HHNS are as
follows:
1. Blood glucose level from 600-2,000
mg/dL
2. Hypotension
3. Dehydration
4. Tachycardia
5. Mental status changes
6. Neurologic changes
7. Neurologic deficits
8. Seizures
➔ The collaborative management for HHNS
are as follows:
1. Treatment is similar to DKA
● Fluid replacement
● Correction of electrolyte imbalances
● Insulin administration (although insulin
plays a less critical role in the
treatment of HHNS than it does for the
treatment of DKA, because insulin is
not needed for reversal of acidosis in
HHNS)
CHRONIC COMPLICATIONS OF DIABETES
MELLITUS:
1. DIABETIC RETINOPATHY
➔ Is a chronic and progressive
impairment of the retinal circulation
that eventually causes hemorrhage
➔ Permanent blindness can occur
➔ The clinical manifestation of
diabetic retinopathy are as follows:
1. Rupture microaneurysms in
retinal blood vessels causes
change in visions
2. Blurred vision to macular
damage
3. Sudden loss of vision due to
retinal detachment
4. Cataract from lens opacity
➔ The collaborative management for
diabetic retinopathy are as follows:
● Maintain safety
● Control hypertension and
blood glucose levels
● Laser therapy to remove
hemorrhagic tissue to
decrease scarring
● Vitrectomy to remove vitreous
hemorrhage and prevent
retinal detachment
● Cataract removal
2. DIABETIC NEPHROPATHY
➔ Is a progressive loss of kidney
function
➔ The clinical manifestation of
diabetic nephropathy are as
follows:
1. Microalbuminuria
2. Thirst
3. Fatigue
4. Anemia
5. Weight loss, malnutrition
6. Frequent urinary tract infection
(UTI)
7. Signs of neurogenic bladder
➔ The collaborative management for
diabetic nephropathy are as
follows:
● Control of hypertension and
blood glucose level
● Monitor VS, intake and output,
serum BUN and creatinine,
urine albumin levels
 ● Restrict dietary protein,
sodium and potassium intake
as needed
● Prepare the client for dialysis
kidney transplant or pancreas
transplant as prescribed
3. DIABETIC NEUROPATHY
➔ Is general deterioration of nervous system
throughout the body
➔ Complications include non-healing ulcers of
the feet, gastroparesis, erectile
dysfunction
➔ The clinical manifestation of diabetic
nephropathy are as follows:
1. Paresthesia
2. Decreased or absent reflexes
3. Diminished sensation
4. Pain, aching and burning in the lower
extremities
5. Diminished peripheral pulses
6. Skin breakdown and signs of infection
7. Dizziness, postural hypotension
8. Nausea and vomiting
9. Diarrhea or constipation
10. Incontinence
11. Dyspareunia (painful intercourse)
12. Impotence
13. Hypoglycemia unawareness
➔ The collaborative management for
diabetic nephropathy are as follows:
● Control of hypertension and blood
glucose level
● Administer pain medication as
prescribed
● Initiate bladder training program ( for
neurogenic bladder)
● Use estrogen containing lubricant for
dyspareunia
● Penile injection or implantable devices
as prescribed (Consider religious and
cultural beliefs. May not be acceptable
in some religions and cultures)
● Foot care to prevent trauma and
prevent gangrene formation
○ Inspect the feet daily
○ Wash feet with warm water
and mild soap. Pat dry the
feet. avoid foot soak
○ Wear a comfortable, properly-
fitted pair of shoes (leather or
canvass; although leather is
more preferred). These
materials follow the contour of
the feet and prevent trauma
○ Do not wear open toed shoes
shoes with strap that goes
between the toes
○ do not wear the same pair of
shoes two days in a row
○ check shoes for cracks or
tears in the lining and for
foreign objects before putting
them on
○ Break- in new pairs of shoes
for 1 to 2 hours only until it
becomes comfortable
○ Do not go barefooted
○ Wear clean cotton socks daily.
Cotton absorbs moisture and
prevents impairment of skin
integrity in the feet
○ Trim toenails straight across or
follow the curve/contour of the
toe. Do not cut at lateral ages
to prevent development of
ingrowns. Ingrowns may cause
trauma to the lateral edges of
the toe. Smoothen nails with
emery board
○ Apply lotion to the feet but not
between the toes. Lotion
impairment of the skin integrity
and infection
○ Do not cross legs or wear tight
garments that may abstract
blood flow (due to viscosity of
legs)
○ For any signs and symptoms
of injury to the feet, notify
physician
○ Avoid use of hot water heating
pads. There is diminished
sensation in the lower
extremities. Burns may occur
unnoticed by the client
○ Exercise and massage the
feet. To improve circulation
○ Do not smoke. To prevent
vasoconstriction
○ Avoid self-treatment of corns
blisters or ingrowns toenails.
Consult the podiatrist.