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Nurse Licensure Examination

Review

Diabetes Mellitus
Diabetes Mellitus
 A group of metabolic diseases
characterized by elevated levels
of glucose in the blood resulting
from defects in insulin secretion,
insulin action, insulin receptors
or any combination of conditions.
Diabetes Mellitus

 A chronic disorder of impaired
glucose metabolism, protein
and fat metabolism
Diabetes Mellitus
 BASIC PATHOLOGY :
Insulin problem
(deficiency or impaired
action)
Diabetes Mellitus
 Insulin is a hormone
secreted by the BETA cells
of the pancreas
 Stimulus of insulin-
HYPERGLYCEMIA
Diabetes Mellitus
 Action of insulin: it
promotes entry of Glucose
into the body cells by
binding to the insulin
receptor in the cell
membrane
INSULIN : Physiology
Insulin Metabolic Functions:
 1. Transports and metabolizes GLUCOSE
 2. Promotes GLYCOGENESIS
 3. Promotes GLYCOLYSIS
 4. Enhances LIPOGENESIS
 5. Accelerates PROTEIN SYNTHESIS
Diabetes Mellitus
RISK FACTORS for Diabetes
Mellitus
 1. Family History of diabetes
 2. Obesity
 3. Race/Ethnicity
Diabetes Mellitus
RISK FACTORS for Diabetes
Mellitus
 4. Age of more than 45
 5. Previously unidentified
IFG/IGT
 6. Hypertension
Diabetes Mellitus
RISK FACTORS for
Diabetes Mellitus
 7. Hyperlipidemia
 8. History of Gestational
Diabetes Mellitus
Diabetes Mellitus
CLASSIFICATION OF DM
1. Type 1 DM
 Insulin dependent Diabetes Mellitus
2. Type 2 DM
 Non-insulin dependent Diabetes Mellitus
3. Gestational DM
 Diabetes Mellitus diagnosed during pregnancy
4. DM associated with other conditions or
syndromes
Diabetes Mellitus
CLASSIFICATION OF DM
1. Type 1 DM
 Insulin dependent Diabetes
Mellitus
Diabetes Mellitus
CLASSIFICATION OF DM
2. Type 2 DM
 Non-insulin dependent
Diabetes Mellitus
Diabetes Mellitus
CLASSIFICATION OF DM
3. Gestational DM
 Diabetes Mellitus diagnosed
during pregnancy
Diabetes Mellitus
CLASSIFICATION OF DM
4. DM associated with other
conditions or syndromes
Diabetes Mellitus
Other types of DM
 1. Impaired Glucose
Tolerance
 2. Impaired Fasting Glucose
 3. Pre-diabetes
TYPE 1- Diabetes Mellitus
This type of DM is
characterized by the
destruction of the
pancreatic beta cells
TYPE 1- Diabetes Mellitus
Etiology:
1. Genetic susceptibility- HLA DR3
and DR4
2. Autoimmune response
3. Toxins, unidentified viruses and
environmental factors
TYPE 1- Diabetes Mellitus
PATHOPHYSIOLOGY
 Destruction of BETA cells
decreased insulin production 
uncontrolled glucose production
by the liver hyperglycemia 
signs and symptoms
TYPE 1- Diabetes Mellitus
PATHOPHYSIOLOGY
CLASSIC P’s
 Polyuria
 Polydipsia
 Polyphagia
TYPE 2- Diabetes Mellitus
 A type of DM characterized
by insulin resistance and
impaired insulin production
TYPE 2- Diabetes Mellitus
Etiology:
1. Unknown
2. Probably genetic and
obesity
TYPE 2- Diabetes Mellitus
PATHOPHYSIOLOGY
 Decreased sensitivity of insulin
receptor to insulin  less
uptake of glucose 
HYPERGLYCEMIA
TYPE 2- Diabetes Mellitus
PATHOPHYSIOLOGY
 Decreased insulin production 
diminished insulin action 
hyperglycemia  signs and
symptoms
TYPE 2- Diabetes Mellitus
PATHOPHYSIOLOGY
 BUT (+) insulin in small
amount  prevent
breakdown of fats  DKA is
unusual
GESTATIONAL Diabetes Mellitus
 Any degree of glucose
intolerance with its onset
during pregnancy
 Usually detected between 24-
28 week gestation
th
GESTATIONAL Diabetes Mellitus
 Blood glucose returns to normal
after delivery of the infant
 NEVER administer ORAL
HYPOGLYCEMIC AGENTS to
PREGNANT MOTHERS!
Diabetes Mellitus
ASSESSMENT FINDINGS
 1. Classic 3 P’s
 2. Fatigue
 3. Body weakness
Diabetes Mellitus
ASSESSMENT FINDINGS
 4. Visual changes
 5. Slow wound healing
 6. Recurrent skin and mucus
membrane infections
Diabetes Mellitus
DIAGNOSTIC TESTS
 1. FBS- > 126
 2. RBS- >200
 3. OGTT- > 200
Diabetes Mellitus
DIAGNOSTIC TESTS
 4. HgbA1- for monitoring!!
 5. Urine glucose
 6. Urine ketones
Diabetes Mellitus
DIAGNOSTIC CRITERIA
 1. FBS equal to or greater
than 126 mg/dL (7.0mmol/L)
 (Normal 8 hour FBS- 80-
109 mg/dL)
Diabetes Mellitus
DIAGNOSTIC CRITERIA
 2. OGTT value 1 and 2 hours
post-prandial equal to or
greater than 200 mg/dL
 Normal OGTT 1 and 2 hours
post-prandial- is
 140 mg/dL
Diabetes Mellitus
DIAGNOSTIC CRITERIA
 3.RBS of equal to or
greater than 200 mg/dL
PLUS the 3 P’s
Diabetes Mellitus
NURSING MANAGEMENT OF
DM
 The main goal is to
NORMALIZE insulin activity
and blood glucose level by:
Diabetes Mellitus
NURSING MANAGEMENT OF DM
1. Nutritional modification
2. Regular Exercise
3. Regular Glucose Monitoring
4. Drug therapy
5. Client Education
Diabetes Mellitus
The Patient with DM
 HISTORY
 Symptoms and characteristics
 PHYSICAL EXAMINATION
 VS, BMI, Fundoscopy, Neuro
 LABORATORY EXAMINATION
 FBS, RBS, HgbA1c, lipid profile, ECG, UA
 REFERRALS
 Ophthalmologist, Podiatrist, Dietician, etc..
Diabetes Mellitus
The Patient with DM
 HISTORY
 Symptoms and characteristics
 PHYSICAL EXAMINATION
 VS, BMI, Fundoscopy, and
Neuro assessment
Diabetes Mellitus
The Patient with DM
 LABORATORY EXAMINATION
 FBS, RBS, HgbA1c, lipid profile,
ECG, and Urinalysis
 REFERRALS
 Ophthalmologist, Podiatrist,
Dietician, etc..
DM Nutritional management
Diabetes Mellitus
NUTRITIONAL MANAGEMENT
 1.Review the patient’s diet history
to identify eating habits and
lifestyle
 2. Coordinate with the dietician in
meal planning for weight loss
Diabetes Mellitus
NUTRITIONAL MANAGEMENT
 3. Plan for the caloric intake
distributed as follows- CHO 50-60%;
Fats 20-30%; and Proteins 10-20%
 4. Advise moderation in alcohol
intake
 5. Using artificial sweeteners is
acceptable
DM Exercise management
Diabetes Mellitus
EXERCISE Management
 1. Teach that exercise can lower
the blood glucose level
 2. Diabetics must first control
the glucose level before initiating
exercise programs.
Diabetes Mellitus
EXERCISE Management
 3. Offer extra food /calories
before engaging in exercise
 4. Offer snacks at the end of the
exercise period if patient is on
insulin treatment.
Diabetes Mellitus
EXERCISE Management
 5. Advise that exercise should be
done at the same time every day,
preferably when blood glucose
levels are at their peak
Diabetes Mellitus
EXERCISE Management
 6. Regular exercise, not sporadic
exercise, should be encouraged.
 7. For most patient, WALKING
is the safe and beneficial form of
exercise
Glucose Self Monitoring
Diabetes Mellitus
GLUCOSE MONITORING
 Self-monitoring of blood glucose
(SMBG) enables the patient to
adjust the treatment regimen to
obtain optimal glucose control
Diabetes Mellitus
GLUCOSE MONITORING
 Most common method involves
obtaining a drop of capillary
blood applied to a test strip.
 The usual recommended
frequency is TWO-FOUR times
a day.
Diabetes Mellitus
When is it done?
 At the peak action time of the
medication to evaluate the need
for adjustments.
 To evaluate BASAL insulin 
test before meals
Diabetes Mellitus
When is it done?
 To titrate bolus or regular and
lispro test 2 hours after meals.
 To evaluate the glucose level of
those taking ORAL hypoglycemics
 test before and two hours after
meals.
Diabetes Mellitus Monitoring therapy
 Testing the glycosylated
hemoglobin (HbA1c)
 This glycosylated hemoglobin
refers to the blood test that
reflects the average blood glucose
over a period of TWO to THREE
months.
Diabetes Mellitus Monitoring therapy
 Normal value is 4 to 6 %
 No patient preparation is
needed for this testing
 Done to monitor therapy
Diabetes Mellitus
 Urine testing for glucose
 Benedict’s test
Diabetes Mellitus
 Urine testing for ketones
 Ketones are by-products
of fat breakdown
Diabetes Mellitus
 Urine testing for ketones
 This is performed whenever
TYPE 1 DM have glucosuria or
persistent elevation of blood
glucose, during illness, and in
gestational diabetes
DM Drug therapy
Diabetes Mellitus
DRUG THERAPY and
MANAGEMENT
 Usually, this type of management is
employed if diet modification and
exercise cannot control the blood
glucose level.
Diabetes Mellitus
DRUG THERAPY and
MANAGEMENT
 Because the patient with TYPE
1 DM cannot produce insulin,
exogenous insulin must be
administered for life.
Diabetes Mellitus
DRUG THERAPY and
MANAGEMENT
 TYPE 2 DM may have
decreased insulin production,
ORAL agents that stimulate
insulin production are usually
employed.
Diabetes Mellitus
PHARMACOLOGIC INSULIN
 This may be grouped into several
categories according to:
1. Source- Human, pig, or cow
2. Onset of action- Rapid-acting,
short-acting, intermediate-acting,
long-acting and very long acting
Diabetes Mellitus
PHARMACOLOGIC INSULIN
 This may be grouped into several
categories according to:
3. Pure or mixed concentration
4. Manufacturer of drug
Diabetes Mellitus
GENERALITIES
 1. Human insulin preparations
have a shorter duration of action
than animal source
Diabetes Mellitus
GENERALITIES
 2. Animal sources of insulin have
animal proteins that may trigger
allergic reaction and they may
stimulate antibody production
that may bind the insulin, slowing
the action
Diabetes Mellitus
 3.
ONLY Regular insulin
can be used
INTRAVENOUSLY!
Diabetes Mellitus
 4. Insulin are measured in
INTERNATIONAL UNITS or
“iu”
 5. There is a specified insulin
injection calibrated in units
Diabetes Mellitus
RAPID ACTING INSULIN
 Lispro (Humalog) and Insulin
Aspart (Novolog)
 Produces a more rapid effect
and with a shorter duration than
any other insulin preparation
Diabetes Mellitus
RAPID ACTING INSULIN
 ONSET- 5-15 minutes
 PEAK- 1 hour
 DURATION- 3 hours
 Instruct patient to eat within 5 to 15
minutes after injection
Diabetes Mellitus
REGULAR INSULIN
 Also called Short-acting insulin
 “R”
 Usually Clear solution
administered 30 minutes before
a meal
Diabetes Mellitus
REGULAR INSULIN
 ONSET- 30 minutes to 1 hour
 PEAK- 2 to 3 hours
 DURATION- 4 to 6 hours
Diabetes Mellitus
INTERMEDIATE ACTING
INSULIN
 Called “NPH” or
“LENTE”
 Appears white and cloudy
Diabetes Mellitus
INTERMEDIATE ACTING
INSULIN
 ONSET- 2-4 hours
 PEAK- 4 to 6-12 hours
 DURATION- 16-20 hours
Diabetes Mellitus
LONG- ACTING INSULIN
 “UltraLENTE”
 Referred to as “peakless”
insulin
Diabetes Mellitus
LONG- ACTING INSULIN
 ONSET- 6-8 hours
 PEAK- 12-16 hours
 DURATION- 20-30 hours
Diabetes Mellitus
HEALTH TEACHING
Regarding Insulin SELF-
Administration
 1. Insulin is administered at
home subcutaneously
Diabetes Mellitus
HEALTH TEACHING Regarding
Insulin SELF- Administration
 2. Cloudy insulin should be
thoroughly mixed by gently
inverting the vial or ROLLING
between the hands
Diabetes Mellitus
HEALTH TEACHING Regarding
Insulin SELF- Administration
 3. Insulin NOT IN USE should be
stored in the refrigerator, BUT
avoid freezing/extreme
temperature
Diabetes Mellitus
 4. Insulin IN USE should be
kept at room temperature to
reduce local irritation at the
injection site
Diabetes Mellitus

 5. INSULIN may be kept at
room temperature up to 1
month
Diabetes Mellitus
 6. Select syringes that match
the insulin concentration.
 U-100 means 100 units per
mL
Diabetes Mellitus
 7.
Instruct the client to draw
up the REGULAR (clear)
Insulin FIRST before
drawing the intermediate
acting (cloudy) insulin
Diabetes Mellitus
 8. Pre-filled syringes can be
prepared and should be kept
in the refrigerator with the
needle in the UPRIGHT
position to avoid clogging the
needle
Diabetes Mellitus
 9. The four main areas for
insulin injection are-
ABDOMEN, UPPER ARMS,
THIGHS and HIPS
Diabetes Mellitus
 Insulin is absorbed fastest in the
abdomen and slowest in the hips
 Instruct the client to rotate the areas
of injection, but exhaust all available
sites in one area first before moving
into another area.
Diabetes Mellitus
 10. Alcohol may not be used to
cleanse the skin
 11. Utilize the subcutaneous
injection technique-
commonly, a 45-90 degree
angle.
Diabetes Mellitus
 12. No need to instruct for
aspirating the needle
 13. Properly discard the
syringe after use.
Diabetes Mellitus
T-I-E
Test blood Inject insulin  Eat
food
Diabetes Mellitus
COMPLICATIONS OF INSULIN
THERAPY
1. Local allergic reactions
 Redness, swelling, tenderness and
induration appearing 1-2 hours
after injection
 Usually occurs in the beginning
stage of therapy
Diabetes Mellitus
COMPLICATIONS OF INSULIN THERAPY
1. Local allergic reactions
 Disappears with continued use
 Antihistamine can be given 1 hour
before injection time
 Porcine and bovine insulin
preparations have a higher
tendency to produce this reaction.
Diabetes Mellitus
2. SYSTEMIC ALLERGIC
REACTIONS
 Very rare
 Generalized urticaria is the
manifestation
 Treatment is desensitization
Diabetes Mellitus

COMPLICATIONS OF INSULIN
THERAPY
3. INSULIN DYSTROPHY
 A localized reaction in the form
of lipoatrophy or lipohypertrophy
Diabetes Mellitus

 Lipoatrophy- loss of
subcutaneous fat usually
caused by the utilization of
animal insulin
Diabetes Mellitus
 Lipohypertrophy-
development of fibrofatty
masses, usually caused by
repeated use of injection site
Diabetes Mellitus
4. INSULIN RESISTANCE
 Most commonly caused by
OBESITY
 Defined as daily insulin requirement
of more than 200 units
 Management- Steroids and use of
more concentrated insulin
Diabetes Mellitus
5. MORNING HYPERGLYCEMIA
 Elevated blood sugar upon arising in
the morning
 Caused by insufficient level of insulin
 DAWN phenomenon
 SOMOGYI effect
 INSULIN WANING
Diabetes Mellitus
DAWN PHENOMENON
 Relatively normal blood glucose until
about 3 am, when the glucose level
begins to RISE
 Results from the nightly surges of
GROWTH HORMONE secretion
 Management: Bedtime injection of
NPH
Diabetes Mellitus
SOMOGYI EFFECT
 Normal or elevated blood
glucose at bedtime, decrease
blood glucose at 2-3 am due to
hypoglycemic levels and a
subsequent increase in blood
glucose (rebound hypergycemia)
Diabetes Mellitus
SOMOGYI EFFECT
 Nocturnal hypoglycemia
followed by rebound
hyperglycemia
Diabetes Mellitus
SOMOGYI EFFECT
 Due to the production of
counter regulatory
hormones- glucagon. cortisol
and epinephrine
 Management- decrease
evening dose of NPH or
increase bedtime snack
Diabetes Mellitus
INSULIN WANING
 Progressive rise in blood glucose
from bedtime to morning
 Seen when the NPH evening dose
is administered before dinner
 Management: Move the insulin
injection to bedtime
Diabetes Mellitus
ORAL HYPOGLYCEMIC
AGENTS
 These may be effective when
used in TYPE 2 DM that cannot
be treated with diet and exercise
 These are NEVER used in
pregnancy!
Diabetes Mellitus
ORAL HYPOGLYCEMIC AGENTS
 There are several agents:
 Sulfonylureas
 Biguanides
 Alpha-glucosidase inhibitors
 Thiazolidinediones
 Meglitinides
Diabetes Mellitus
SULFONYLUREAS
 MOA- stimulates the beta
cells of the pancreas to
secrete insulin
 Classified as to generations-
first and second generations
Diabetes Mellitus
SULFONYLUREAS
 FIRST GENERATION-
Acetoheximide, Chlorpropamide,
Tolazamide and Tolbutamide
 SECOND GENERATION- Glipizide,
Glyburide, Glibenclamide,
Glimepiride
Diabetes Mellitus: Sulfonylureas
 The most common side –effects
of these medications are Gastro-
intestinal upset and
dermatologic reactions.
 HYPOGLYCEMIA is also a
very important side-effect
Diabetes Mellitus: Sulfonylureas
 Chlorpropamide has a very long
duration of action. This also
produces a disulfiram-like reaction
when taken with alcohol
 Second generation drugs have
shorter duration with metabolism in
the kidney and liver and are the
choice for elderly patients
Diabetes Mellitus
BIGUANIDES
 MOA- Facilitate the action of
insulin on the peripheral
receptors
 These can only be used in the
presence of insulin
Diabetes Mellitus
BIGUANIDES= “formin”
 They have no effect on the
beta cells of the pancreas
 Metformin (Glucophage) and
Phenformin are examples
Diabetes Mellitus: Biguanides
 The most important side effect
is LACTIC ACIDOSIS!
 These are not given to patient
with renal impairment
Diabetes Mellitus: Biguanides

 These drugs are usually given
with a sulfonylurea to enhance
the glucose-lowering effect
more than the use of each drug
individually
Diabetes Mellitus
ALPHA-GLUCOSIDASE INHIBITORS
 MOA- Delay the absorption of glucose in the
GIT
 Result is a lower post-prandial blood glucose
level
 They do not affect insulin secretion or
action!
 Side-effect: DIARRHEA and
FLATULENCE
Diabetes Mellitus
 Examples of AGI are Acarbose
and Miglitol
 They are not absorbed
systemically and are very safe
 They can be used alone or in
combination with other OHA
Diabetes Mellitus
 Side-effect if used with other
drug is HYPOGLYCEMIA
 Note that sucrose absorption is
impaired and IV glucose is the
therapy for the hypoglycemia
Diabetes Mellitus
THIAZOLIDINEDIONES
 MOA- Enhance insulin
action at the receptor site
 They do not stimulate insulin
secretion
Diabetes Mellitus
THIAZOLIDINEDIONES
 Examples- Rosiglitazone, Pioglitazone
 These drugs affect LIVER
FUNCTION
 Can cause resumption of
OVULATION in peri-menopausal
anovulatory women
Diabetes Mellitus
MEGLITINIDES
 MOA- Stimulate the
secretion of insulin by the
beta cells
 Examples- Repaglinide and
Nateglinide
Diabetes Mellitus
MEGLITINIDES
 They have a shorter duration
and fast action
 Should be taken BEFORE meals
to stimulate the release of insulin
from the pancreas
Diabetes Mellitus
MEGLITINIDES
 Principal side-effect of
meglitinides- hypoglycemia
 Can be used alone or in
combination
Diabetes Mellitus
ACUTE COMPLICATIONS OF DM
 Hypoglycemia
 Diabetic ketoacidosis
 Hyperglycemic hyperosmolar non-
ketotic syndrome (HHNS)
Diabetes Mellitus
CHRONIC COMPLICATIONS OF DM
 Macrovascular complications- MI,
Stroke, Atherosclerosis, CAD, and
Peripheral vascular disease
 Microvascular complications- micro-
angiopathy, retinopathy, nephropathy
 Peripheral neuropathy
Diabetes Mellitus
HYPOGLYCEMIA
 Blood glucose level less than 50 to 60
mg/dL
 Causes: Too much insulin/OHA, too
little food and excessive physical
activity
 Mild- 40-60
 Moderate- 20-40
 Severe- less than 20
HYPOGLYCEMIA
ASSESSMENT FINDINGS
 1. Sympathetic manifestations-
sweating, tremors, palpitations,
nervousness, tachycardia and
hunger
HYPOGLYCEMIA
ASSESSMENT FINDINGS
 2. CNS manifestations- inability to
concentrate, headache,
lightheadedness, confusion, memory
lapses, slurred speech, impaired
coordination, behavioral changes,
double vision and drowsiness
HYPERGLYCEMIA
HYPOGLYCEMIA
 DIAGNOSTIC FINDINGS
 RBS- less than 50-60 mg/dL
level
HYPOGLYCEMIA
Nursing Interventions
 1. Immediate treatment with the
use of foods with simple sugar-
glucose tablets, fruit juice, table
sugar, honey or hard candies
HYPOGLYCEMIA
Nursing Interventions
 2. For uncons cio us
patient s- glucagon injection 1
mg IM/SQ; or IV 25 to 50 mL of
D50/50
HYPOGLYCEMIA
Nursing Interventions
 3. re-test glucose level in 15
minutes and re-treat if less than
75 mg/dL
 4. Teach patient to refrain from
eating high-calorie, high-fat
desserts
HYPOGLYCEMIA
Nursing Interventions
 5. Advise in-between snacks,
especially when physical activity
is increased
 6. Teach the importance of
compliance to medications
Diabetic Ketoacidosis
 This is cause by the absence of insulin
leading to fat breakdown and production
of ketone bodies
 Three main clinical features:
 1. HYPERGLYCEMIA
 2. DEHYDRATION & electrolyte loss
 3. ACIDOSIS
DKA
PATHOPHYSIOLOGY
 No insulin reduced glucose
breakdown and increased liver
glucose production 
Hyperglycemia
DKA
PATHOPHYSIOLOGY
 Hyperglycemia kidney
attempts to excrete glucose 
increased osmotic load 
diuresis  Dehydration
DKA
PATHOPHYSIOLOGY
 No glucose in the cell fat is
broken down for energy 
ketone bodies are produced
Ketoacidosis
DKA
Risk factors
 1. infection or illness- common
 2. stress
 3. undiagnosed DM
 4. inadequate insulin, missed dose
of insulin
DKA
ASSESSMENT FINDINGS
 1. 3 P’s
 2. Headache, blurred vision and
weakness
 3. Orthostatic hypotension
DKA
ASSESSMENT FINDINGS
 4. Nausea, vomiting and
abdominal pain
 5. Acetone (fruity) breath
 6. Hyperventilation or
KUSSMAUL’s breathing
HYPERGLYCEMIA
Hyperglycemia
DKA
LABORATORY FINDINGS
 1. Blood glucose level of 300-
800 mg/dL
 2. Urinary ketones
DKA
LABORATORY FINDINGS
 3. ABG result of metabolic acidosis-
LOW pH, LOW pCO2 as a
compensation, LOW bicarbonate
 4. Electrolyte imbalances- potassium
levels may be HIGH due to acidosis
and dehydration
DKA
NURSING INTERVENTIONS
 1. Assist in the correction of
dehydration
 Up to 6 liters of fluid may be ordered
for infusion, initially NSS then D5W
 Monitor hydration status
 Monitor I and O
 Monitor for volume overload
DKA
NURSING INTERVENTIONS
 2. Assist in restoring Electrolytes
 Kidney function is FIRST
determined before giving
potassium supplements!
DKA
NURSING INTERVENTIONS
 3. Reverse the Acidosis
 REGULAR insulin injection is
ordered IV bolus 5-10 units
 The insulin is followed by drip
infusion in units per hour
 BICARBONATE is not used!
HHNS
 A serious condition in which
hyperosmolarity and extreme
hyperglycemia predominate
 Ketosis is minimal
 Onset is slow and takes hours to
days to develop
HHNS
PATHOPHYSIOLOGY
 Lack of insulin action or Insulin
resistance  hyperglycemia
 Hyperglycemia osmotic
diuresis  loss of water and
electrolytes
HHNS
PATHOPHYSIOLOGY
 Insulin is too low to prevent
hyperglycemia but enough to
prevent fat breakdown
 Occurs most commonly in type 2
DM, ages 50-70
HHNS
Precipitating factors
 1. Infection
 2. Stress
 3. Surgery
 4. Medication like thiazides
 5. Treatment like dialysis
HHNS
ASSESSMENT FINDINGS
 1. Profound dehydration
 2. Hypotension
 3. Tachycardia
 4. Altered sensorium
 5. Seizures and hemiparesis
HHNS
DIAGNOSTIC TESTS
 1. Blood glucose- 600 to 1,200
mg/dL
 2. Blood osmolality- 350
mOsm/L
 3. Electrolyte abnormalities
HHNS
NURSING INTERVENTIONS
 Approach is similar to the DKA
 1. Correction of Dehydration by
IVF
 2. Correction of electrolyte
imbalance by replacement
therapy
HHNS
NURSING INTERVENTIONS
 3. Administration of insulin
injection and drips
 4. Continuous monitoring of
urine output
MACROVASCULAR CX
Nursing management
 1. Diet modification
 2. Exercise
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Nursing management
 3. Prevention and treatment of
underlying conditions such as
MI, CAD and stroke
 4. Administration of prescribed
medications for hypertension,
hyperlipidemia and obesity
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 Retinopathy- a painless deterioration
of the small blood vessels in the retina,
may be classified as to background
retinopathy, pre-proliferative and
proliferative retinopathy
 Permanent vision changes and
blindness can occur
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Retinopathy-ASSESSMENT
FINDINGS
 Blurry vision
 Spotty vision
 Asymptomatic
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Retinopathy: Diagnostic findings
 1. Fundoscopy
 2. Fluorescein angiography
 Painless procedure
 Side-effects- discoloration of the skin
and urine for 12 hours, some allergic
reactions, nausea
 Flash of camera may be slightly
uncomfortable
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NURSING INTERVENTIONS
 1. Assist in diagnostic procedure
 2. Assist in the preparation for
surgery- laser photocoagulation
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NURSING INTERVENTIONS
 3. Health teaching regarding
prevention of retinopathy by
regular ophthalmic examinations,
good glucose control and self-
management of eye care regimens
 4. Maintain client safety
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DIABETIC NEPHROPATHY
 Progressive deterioration of
kidney function
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DIABETIC NEPHROPATHY
 HYPERGLYCEMIA causes the
kidney filtration mechanism to be
stressed  blood proteins leak into
the urine
 Pressure in the kidney blood vessels
increases stimulate the development
of nephropathy
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ASSESSMENT findings for diabetic
nephropathy
 1. Albuminuria
 2. Anemia
 3. Acidosis
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ASSESSMENT findings for diabetic
nephropathy
 4. Fluid volume overload
 5. Oliguria
 6. Hypertension
 7. UTI
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NURSING MANAGEMENT
1. Assist in the control of
hypertension- use of ACE inhibitor
2. Provide a low sodium and low
protein diet
3. Administer prescribed medication
for UTI
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 NURSING MANAGEMENT
4. Assist in dialysis
5. Prepare patient for renal
transplantation, if indicated
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Diabetic Neuropathy
 A group of disorders that affect
all type of nerves including the
peripheral, autonomic and
spinal nerves
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Diabetic Neuropathy
 Two most common types of
Diabetic Neuropathy are
sensori-motor polyneuropathy
and autonomic neuropathy
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Peripheral neuropathy-
ASSESSMENT findings
 1. paresthesias- prickling, tingling
or heightened sensation
 2. decreased proprioception
 3. decreased sensation of light touch
 4. unsteady gait
 5. decreased tendon reflexes
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Peripheral neuropathy- Nursing
Management
 1. Provide teaching that good glucose
control is very important to prevent
its development
 2. Manage the pain by analgesics,
antidepressants and nerve
stimulation
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Autonomic Neuropathy- ASSESSMENT
findings
 1. Silent, painless ischemia
 2. delayed gastric emptying
 3. orthostatic hypotension
 4. N/V and bloating sensation
 5. urinary retention
 6. sexual dysfunction
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Autonomic Neuropathy-Nursing
management
 1. Educate about the avoidance of
strenuous physical activity
 2. Stress the importance of good
glucose control to delay the
development
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Autonomic Neuropathy-Nursing
management
 3. Provide LOW-fat, small frequent
feedings
 4. Administer bulk-forming
laxatives for diabetic diarrhea
 5. Provide HIGH-fiber diet for
diabetic constipation
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MANAGEMENT OF FOOT AND LEG
PROBLEMS

 Soft tissue injury in the foot/leg
formation of fissures and callus 
poor wound healing  foot/leg ulcer
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RISK FACTORS for the development of
foot and leg ulcers
 1. More than 10 years diabetic
 2. Age of more than 40
 3. Smoking
 4. Anatomic deformities
 5. History of previous leg ulcers or
amputation
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MANAGEMENT of Foot Ulcers
 Teach patient proper care of the
foot
 Daily assessment of the foot
 Use of mirror to inspect the
bottom
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MANAGEMENT of Foot Ulcers
 Inspect the surface of shoes for
any rough spots or foreign objects
 Properly dry the feet
 Instruct to wear closed-toe shoes
that fit well, recommend use of
low-heeled shoes
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MANAGEMENT
 Instruct patient NEVER to walk
barefoot, never to use heating pads,
open-toed shoes and soaking feet
 Trim toenails STRAIGHT ACROSS and
file sharp corners
 Instruct to avoid smoking and over-the
counter medications and home remedies
for foot problems