INTRODUCTION

The term glaucoma is used to refer to a group of ocular conditions characterized by

optic nerve damage. In the past, glaucoma was seen more as a condition of elevated IOP
than of optic neuropathy. Increasingly, that is no longer the case. There is no doubt that
increased IOP damages the optic nerve and nerve fiber layer, but the degree of harm is
highly variable (McKinnon, Goldberg, Peeples, et al., 2008). The optic nerve damage is
related to the IOP caused by congestion of aqueous humor in the eye. A range of IOPs are
considered “normal,” but these may be associated with vision loss in some patients.
Glaucoma is the second leading cause of blindness in adults in the United States. It is
estimated that at least 2.2 million Americans have glaucoma and that 3 to 6 million more
are at risk for the disease (Bressler, et al., 2008). Glaucoma is more prevalent in people
older than 40 years of age, and it is the third most common age-related eye disease in the
United States. It also occurs more frequently in African Americans than Caucasians. There
is no cure for glaucoma, but the disease can be controlled (Sharts Hopko & Glynn-Milley,
2009).

Classification of Glaucoma

There are several types of glaucoma. Although glaucoma classification is changing as

knowledge increases, current clinical forms of glaucoma are identified as open-angle
glaucoma, angle-closure glaucoma (also called pupillary block), congenital glaucoma, and
glaucoma associated with other conditions, such as developmental anomalies or
corticosteroid use. Glaucoma can be primary or secondary, depending on whether
associated factors contribute to the rise in IOP. The two common clinical forms of glaucoma
encountered in adults are primary open-angle glaucoma (POAG) and angle-closure
glaucoma, which are differentiated by the mechanisms that cause impaired aqueous
outflow.

Table 1. GLAUCOMA TYPES, CLINICAL MANIFESTATION, AND TREATMENT

Significant of Study??

 Client will be able to understand the relationship between glaucoma and DM type 2
 Client will be able to identify interventions that help with her disease condition
 The client’s family will have an idea how they can help support the client in
managing her disease condition.

Definition of terms??
ANATOMY AND PHYSIOLOGY

The eye has 3 chambers, the anterior chamber in front of the iris, the posterior
chamber between the iris and the lens, and the vitreous chamber behind the lens.

Intraocular pressure is maintained by a balance between inflow and outflow of the

aqueous humour, the fluid which nourishes the transparent structures of the eye. Aqueous
humour is produced and secreted by the ciliary body, a gland behind the iris of the eye.
Aqueous humour enters the anterior chamber of the eye through the pupil, and leaves by
passing through the trabecular meshwork in the iridocorneal angle of the anterior chamber
and back into venous circulation through the canal of Schlemm.

A number of classification schemes for the glaucoma’s have been proposed. They are
based on the age of the person (infantile, juvenile, adult), the site of obstruction to aqueous
outflow (pre-trabecular, trabecular, post-trabecular), the tissue principally involved (e.g.
glaucoma caused by diseases of the lens), and etiology. Although each of these systems has
value, the classification scheme that separates angle closure from open angle glaucoma has
been used most widely, because it focuses on pathophysiology and points to proper clinical
management.

Figure 2. Anatomy of the Eye

Related Literature
According to Wong VH, Bui BV, Vingrys AJ (2011) Glaucoma represents the leading
cause of worldwide irreversible blindness, as defined by best-corrected central visual
acuity of less than 3/60 or a visual field of less than 10° in the better seeing eye. It is
characterized by pathognomonic optic nerve changes which result in progressive visual
field loss over time. Primary open angle glaucoma (POAG) is the most common form of
glaucoma and is associated with a number of risk factors such as family history, African
ancestry, and elevated intraocular pressure (IOP). Of these, IOP is the only modifiable and
effective target of therapy, and as a result, the mainstay of current glaucoma treatment is
IOP reduction through the use of medications, laser, or surgery. Other pathways by which
investigators have linked diabetes and glaucoma include glial cell dysfunction and
impairment of retrograde axonal transport. Glial cells, such as astrocytes, are non-neuronal
cells that support and protect neurons in the central nervous system, including the retina
and optic nerve. Dysfunction of these cells has been demonstrated in animal models of
diabetes and glaucoma and is believed to contribute to neuroinflammatory pathways of
apoptosis. In addition, it has been postulated that alterations in connective tissue
remodeling due to diabetes may affect both the lamina cribrosa and the trabecular
meshwork, thereby potentially increasing susceptibility to glaucoma through
biomechanical changes at the optic nerve and impairment of aqueous humor outflow
affecting IOP homeostasis
In addition, several common mechanisms have been postulated to contribute to the
possible link between glaucoma and diabetic retinopathy. Diabetes and hyperglycemia are
associated with glycation of lipids and abnormalities of lipid metabolism which may
increase oxidative stress and promote cellular apoptosis, the same mechanism by which
RGC loss occurs in glaucoma. Vascular dysregulation has been described in both diabetic
eye disease and glaucoma, and upregulation of nitric oxide, a potent vasodilator, has been
reported in both conditions. Nitric oxide is a known regulator of not only vascular tone, but
also apoptosis. In addition, reactive nitrogen species have been shown to contribute to
inflammatory responses via oxidative stress and optic nerve degeneration as well (Cavet
ME et, al 2014).
Moreover, Diminished neurotrophic factor delivery secondary to abnormalities in
axonal transport has been demonstrated in both diabetic peripheral neuropathy and the
optic nerve in glaucoma ( ) Alterations in neurotrophic factor expression, such as insulin-
like growth factor and neurotrophin-3, are also seen in the presence of elevated intraocular
pressure, the primary risk factor for glaucomatous optic neuropathy ( ). In particular,
insulin-like growth factor is necessary for proper glucose metabolism in the central
nervous system and resistance to insulin may be a contributor to neurodegenerative
processes as a result [ ]. With regard to the eye and glaucoma, insulin and insulin-like
growth factor have been shown to play a role in RGC survival [ ]. In addition, insulin has
been reported to affect IOP with lower IOP being associated with insulin-induced
hypoglycemia while increased IOP has been associated with insulin resistance [ ].
Clinically, a large retrospective cohort of diabetic patients with open angle glaucoma
reported that metformin, a first-line agent used to treat insulin-resistance in type 2
diabetes, is associated with a decreased risk of developing open angle glaucoma even after
accounting for variations in glycemic control [ ]. In addition, genetic polymorphisms
related to pancreatic beta-cell function in type 2 diabetes mellitus were associated with
increased risk of POAG and provide further support for these findings [ ].

Diabetic Retinopathy

Of all of the medical disorders that the nurse encounters, diabetes mellitus is one of
the most common. One of the most serious complications of diabetes is retinopathy. In the
United States today, diabetes is the leading cause of new cases of blindness in people
between 20 and 74 years of age (Prevent Blindness America, 2008). Before the discovery of
insulin in the 1920s, diabetic retinopathy was relatively rare because most people with
diabetes did not survive for more than 1 or 2 years. However, with the many advancements
in the treatment of diabetes, more and more patients are able to survive and enjoy
relatively normal lifespans, but they are also confronted with the complications of long-
term diabetes. With the rate of obesity in the United States rising, type 2 diabetes has
become epidemic, and the incidence of diabetic retinopathy may be expected to increase.

Pathophysiology

There are two accepted theories regarding how increased IOP damages the optic
nerve in glaucoma. The direct mechanical theory suggests that high IOP damages the
retinal layer as it passes through the optic nerve head. The indirect ischemic theory
suggests that high IOP compresses the microcirculation in the optic nerve head, resulting in
cell injury and death. Some glaucoma’s appear as exclusively mechanical, and some are
exclusively ischemic types. Typically, most cases are a combination of both. Regardless of
the cause of damage, glaucomatous changes typically evolve through clearly discernible
stages
 Figure 1. Glaucoma

Clinical Manifestations

Glaucoma is often called the “silent thief of sight” because most patients are
unaware that they have the disease until they have experienced visual changes and vision
loss. The patient may not seek health care until he or she experiences blurred vision or
“halos” around lights, difficulty focusing, difficulty adjusting eyes in low lighting, loss of
peripheral vision, aching or discomfort around the eyes, and headache.

Medical Management

The aim of all glaucoma treatment is prevention of optic nerve damage. Lifelong
therapy is almost always necessary because glaucoma cannot be cured. Treatment focuses
on pharmacologic therapy, laser procedures, surgery, or a combination of these
approaches, all of which have potential complications and side effects. The object is to
achieve the greatest benefit at the least risk, cost, and inconvenience to the patient.
Although treatment cannot reverse optic nerve damage, further damage can be controlled.
The goal is to maintain an IOP within a range unlikely to cause further damage. The initial
target for IOP among patients with elevated IOP and those with low-tension glaucoma with
progressive visual field loss is typically set at 30% lower than the current pressure. The
patient is monitored for changes in the appearance of the optic nerve. If there is evidence of
progressive damage, the target IOP is again lowered until the optic nerve shows stability.

Pharmacologic Therapy

Medical management of glaucoma relies on systemic and topical ocular medications

that lower IOP. Periodic follow up examinations are essential to monitor IOP, the
appearance of the optic nerve, the visual fields, and side effects of medications. Therapy
takes into account the patient’s health and stage of glaucoma. Comfort, affordability,
convenience, lifestyle, and personality are factors to consider in the patient’s adherence to
the medical regimen. The patient is usually started on the lowest dose of topical medication
and then advanced to increased concentrations until the desired IOP level is reached and
maintained. Because of their efficacy, minimal dosing (can be used once each day), and low
cost, beta-blockers are the preferred initial topical medications. One eye is treated first,
with the other eye used as a control in determining the efficacy of the medication; once
efficacy has been established, treatment of the other eye is started. If the IOP is elevated in
both eyes, both are treated. When results are not satisfactory, a new medication is
substituted. The main markers of the efficacy of the medication in glaucoma control are
lowering of the IOP to the target pressure, appearance of the optic nerve head, and the
visual field. Several types of ocular medications are used to treat glaucoma, including
miotics (medications that cause pupillary constriction), adrenergic agonists (ie,
sympathomimetic agents), beta-blockers, alpha2-agonists (ie, adrenergic agents), carbonic
anhydrase inhibitors, and prostaglandins. Cholinergics (ie, miotics) increase the outflow of
the aqueous humor by affecting ciliary muscle contraction and pupil constriction, allowing
flow through a larger opening between the iris and the trabecular meshwork. Adrenergic

agonists increase aqueous outflow but primarily decrease aqueous production with an
action similar to beta blockers and carbonic anhydrase inhibitors. Prostaglandin analogues
reduce IOP by increasing aqueous humor outflow. They can be used once daily and do not
affect pupil size.

Table 2. MEDICATIONS USED IN THE MANAGEMENT OF GLAUCOMA

Surgical Management

In laser trabeculoplasty for glaucoma, laser burns are applied to the inner surface
of the trabecular meshwork to open the intertrabecular spaces and widen the canal of
Schlemm, thereby promoting outflow of aqueous humor and decreasing IOP. The
procedure is indicated when IOP is inadequately controlled by medications, and it is
contraindicated, when the trabecular meshwork cannot be fully visualized because of
narrow angles. A serious complication of this procedure is a transient increase in IOP
(usually 2 hours after surgery) that may become persistent. IOP assessment in the
immediate postoperative period is essential.
 In laser iridotomy for pupillary block glaucoma, an opening is made in the iris to
eliminate the pupillary block. Laser iridotomy is contraindicated in patients with corneal
edema, which interferes with laser targeting and strength. Potential complications are
burns to the cornea, lens, or retina; transient elevated IOP; closure of the iridotomy; uveitis;
and blurring. Pilocarpine (Pilocar) is usually prescribed to prevent closure of the
iridotomy.

Filtering procedures for chronic glaucoma are used to create an opening or fistula
in the trabecular meshwork to drain aqueous humor from the anterior chamber to the
subconjunctival space into a bleb (fluid collection on the outside of the eye), thereby
bypassing the usual drainage structures. This allows the aqueous humor to flow and exit by
different routes (ie, absorption by the conjunctival vessels or mixing with tears).

Trabeculectomy is the standard filtering technique used to remove part of the

trabecular meshwork. Complications include hemorrhage, an extremely low (hypotony) or
extremely elevated IOP, uveitis, cataracts, bleb failure, bleb leak, and endophthalmitis.
Unlike other surgical procedures, the goal of the filtering procedure is to achieve
incomplete healing of the surgical wound. The outflow of aqueous humor in a newly
created drainage fistula is circumvented by the granulation of fibrovascular tissue or scar
tissue formation on the surgical site. Scarring is inhibited by using antifibrosis agents such
as the antimetabolites fluorouracil (Efudex) and mitomycin (Mutamycin). Like all
antineoplastic agents, they require special handling procedures before, during, and after
the procedure. Fluorouracil can be administered intraoperatively and by subconjunctival
injection during follow-up; mitomycin is much more potent and is administered only
intraoperatively.

Drainage implants or shunts are open tubes implanted in the anterior chamber to
shunt aqueous humor to the episcleral plate in the conjunctival space. These implants are
used when failure has occurred with one or more trabeculectomies in which antifibrotic
agents were used. A fibrous capsule develops around the episcleral plate and filters the
aqueous humor, thereby regulating the outflow and controlling IOP.

Trabectome surgery is reserved for patients in whom pharmacologic treatment

and/or laser trabeculoplasty do not control the IOP sufficiently (Filippopoulos & Rhee,
2008). This minimally invasive procedure is specifically designed to improve fluid drainage
from the eye to balance IOP. By restoring the eye’s natural fluid balance, trabectome
surgery stabilizes the optic nerve and minimizes further visual field damage. The surgery is
performed through a small incision and does not require creation of a permanent hole in
the eye wall or an external filtering bleb or an implant.

Nursing Management
Promoting Home and Community-Based Care
Teaching Patients Self-Care
 The medical and surgical management of glaucoma slows the progression of
glaucoma but does not cure it. The lifelong therapeutic regimen mandates patient
education. The nature of the disease and the importance of strict adherence to the
medication regimen must be included in a teaching plan to help ensure compliance. A
thorough discussion of the medication program, particularly the interactions of glaucoma-
control medications with other medications, is essential. For example, the diuretic effect of
acetazolamide (Diamox) has an additive effect on the diuretic effects of other
antihypertensive medications and can result in hypokalemia. The effects of glaucoma-
control medications on vision must also be explained.

Miotics and sympathomimetics result in altered focus; therefore, patients need to be

cautious in navigating their surroundings. Information about instilling ocular medication
and preventing systemic absorption with punctual occlusion is given in the section of this
chapter on ophthalmic medications. Nurses in all settings encounter patients with
glaucoma. Even patients with long-standing disease and those with glaucoma as a
secondary diagnosis should be assessed for knowledge level and compliance with the

therapeutic regimen.

Table 3. MYDRIATICS AND CYCLOPLEGICS

 Patient Profile III

Name: Mrs. S.G

Age: 47
Sex: Female
Religion: Roman Catholic
Civil Status: Married
Educational Attainment: College Degree
Occupation: Accountant
Health History: Community Acquired Pneumonia
Surgical History: Underwent appendectomy

ADMISSION
Admitting Date: 05/06/21
Admitting Diagnosis: Acute Angle-closure glaucoma of the right eye, DM Type 2
Procedure: LASER Iridotomy
Admitting Physician: ER Doctor

Chief complain: Patient reason why she was admitted in the hospital are due to right
ocular pain, headache accompanied by vomiting, blurring of vision, glare and dizziness and
constipation.
Gordons????

Gordon’s Functional Health Pattern (wafa 😊)

Not final kase di ko pa nakita yung ginawa ni Jen. Draft muna kase i narrative ko pa sya.

1.Health Perception – Health Management Pattern

 had history of Community Acquired Pneumonia 2
 years ago and was hospitalized with “some antibiotics and oxygen” prescribed
 Diagnosed with DM Type 2 last year: metformin (Glucophage) 850 mg PO once daily
as maintenance.
 On the day of the admission, she was in her office doing some paper works. She
called her husband to take her home but the husband insisted to bring her to the
hospital. She was brought to the hospital via their private car. She claims she did not
eat anything since this morning. ?????

2. Nutritional – Metabolic Pattern

 Eats three times a day, favorite food is potato salad, also loves chips and fish
crackers, drinks about 4 – 6 glasses of water per day with 2 – 3 cups of coffee and 1
can of soda as regular intake every day. She complains of constipation at times but
no history of digestive disorders reported.
 Weight = 58 kilograms, height = 5’4” BMI ???

3. Elimination Pattern
 Bowel habits sometimes irregular

4. Activity – Exercise Pattern

 uses the computer and cellular phones often as they are needed for work purposes
 kulang
5. Cognitive – Perceptual Pattern
 Early today she was in the “office doing computer works when I felt headache in
increasing intensity. My vision was blurry so it was useless to continue working. I
had to rest but the pain persisted so I called my husband to take me home”.
 had been on prescription glasses for being “myopic” since she was in high school.
Recent visual acuity revealed OD-20/100, OS-20/40, OU-20/70.

6. Sleep – Rest Pattern

 Usually works overtime in most cases,
 comes home late, sleeps 4 – 5 hours per night,
 sometimes spends extra time until morning to finish some work

7. Self – Perception Self – Concept Pattern

 Husband claimed: “She is a very workaholic; she sometimes forgets she has a
family”.

8. Role – Relationship Pattern

 Accountant in a private firm for 12 years now
 Married for 8 years, she has 2 children who are 6 and 4 years old, all boys

9. Sexuality – Reproductive Pattern

 Has “regular, monthly menstruation” with no reports of any unusual bleeding
 She delivered her 2 sons normally in the hospital. She underwent appendectomy
when she was 16 years old. No other history of surgery reported.

10.Coping – Stress – Tolerance Pattern

 ???????

11.Value – Belief Pattern

 Roman Catholic but seldom goes to church. “God is everywhere, I don’t have to go to
church to find Him”.
 CEPHALO CAUDAL ASSESSMENT

General Appearance
She was responsive and oriented and could answer questions correctly.
Head
The patient hair is completely distributed on the head and dyed brown. There are no signs of
dandruff, lesions, scars, and wounds noted. And there was no offensive smell noted.

Eyes
The patient is wearing eyeglasses +2.0 since 16 years old. The pupil in the right eye was semi-
dilated, while the pupil in the left eye revealed PERRLA. Corneal blinking reflexes are present in
both eyes and sclerae appeared pinkish. There is slight peri-orbital edema noted on the right eye,
and complaining of “blurring, glaring and crooked letters” and cannot correctly identify letters in
the magazine when shown to her.

Ears
The patient ear canal is intact, with minimal dry cerumen noted. There are no discharges, and an
unusual odor noted. During the whisper test, the patient was able to repeat the words correctly as
what the nurse said.

Nose and Sinuses

The patient's nasal passageways are patent, and the septum was in place. Upon illumination, the
sinuses revealed faint red color. And the patient was able to identify the scent of mild cologne
when introduced.

Mouth and throat

The patient's lips appeared chappy, with minimal cracks in the tongue. The mouth was clean, with
missing right upper molar 1. No odor was noted from the mouth, the uvula was intact, and the
tonsils are not inflamed. The patient was able to drink well from a cup and speech was clear.

Neck
The patient neck is aligned with no complaints of discomfort claimed. The thyroid was
hardly palpable, no bruit or abnormal sounds identified. The large vessels were intact and
not swollen, and the carotid pulse rate was 108 b/min.

Anterior thorax
The patient anterior thorax showed no evidence of lesions. Both breasts showed no signs of mass
or discharges during palpation, and breath sounds were clear, RR -23 br/min.

Posterior thorax
The patient posterior thorax showed no evidence of scars or wounds. Percussion sounds
showed no abnormal results. There are no lesions nor masses palpated. Breath sounds
were clear. RR – 23 br/min.

Abdomen
The patient's abdomen was soft; no scars and lesions were noted. Bowel sounds were heard at 1-
2x per minute in all four quadrants. Percussion sounds were tympanic at the epigastric region and
dull at hypochondriac regions. There are no masses palpated and no unusual findings noted.

Extremities
Extremities showed muscle strength 3+ scores in both upper and 4+ scores in both lower areas for
resistance. Can raise arms & legs independently and can identify dull and sharp stimulations in all
four limbs.

Genital
The patient's genital area appeared intact. There are no discharges, hemorrhoids and any sign of
abnormality noted with inspection and palpation. And there are no complaints of discomfort in the
area.

Cranial Nerves
The patient verbalized blurred vision and difficulty moving the eyes to sides or to an up-down
motion. (needs further data)
 MECHANISM OF INDICATION CONTRADICTION ADVERSE NURSING
DRUG NAME ACTION EFFECTS RESPONSIBILITIES
DRUG STUDY

Generic name: Prednisolone PRED PRED - elevation -Advise patients that if eye
prednisolone acetate acetate is FORTE® is FORTE® suspension of intraocular inflammation or pain
ophthalmic a glucocorticoid t indicated for is contraindicated in pressure (IOP) persists longer than 48
suspension hat, on the basis the treatment acute untreated -possible hours or becomes
of weight, has 3 of steroid- purulent ocular development aggravated, they should
to 5 times the responsive infections, in most of glaucoma and consult a physician.
anti- inflammation viral diseases of infrequent optic -Advise patients that to
Brand name: inflammatory of the the cornea and conju nerve damage prevent eye injury or
Pred Forte potency palpebral nctiva including epit - contamination, care should
of hydrocortisone and bulbar helial herpes posterior subcap be taken to avoid touching
. Glucocorticoids conjunctiva,  simplex keratitis (de sular cataract for the bottle tip to eyelids or to
DOSAGE: one to two inhibit the cornea, ndritic keratitis), vac mation, and any other surface -Keep
drops edema, fibrin dep and anterior  cinia, and varicella, delayed wound bottle tightly closed when
osition, capillary  segment of and also in healing. not in use. Keep out of the
dilation, and the globe. mycobacterial reach of children.
Frequency: two to
phagocytic infection of the eye -Advise patients that PRED
four times daily.
migration of the and fungal diseases FORTE® 
ROUTE: acute inflammato of ocular structures. suspension contains
conjunctival sac ry response, as PRED benzalkonium chloride,
well as capillary FORTE  suspension
®
which may be absorbed by
proliferation, is also soft contact lenses. Contact
Classification: deposition contraindicated in lenses should be removed
corticosteroids. of collagen, and individuals with prior to application of PRED
scar formation. known or suspected FORTE® and may be
hypersensitivity to reinserted 15 minutes
any of the following its administration.
ingredients of this
preparation and to
other corticosteroids.
DRUG NAME MECHANISM OF INDICATION CONTRADICTIO ADVERSE EFFECTS NURSING RESPONSIBILITIES
ACTION N

Generic DIAMOX is an For adjunctive Hypersensitivity CNS: Paresthesias, -Establish baseline weight before
name: enzyme inhibitor treatment to sulfonamides sedation, malaise, initial therapy and weigh daily
acetazolamid that acts of: chronic si and derivatives disorientation, thereafter when used to treat
e specifically on mple (open- (e.g., thiazides), depression, fatigue, edema.
carbonic angle) glauco marked renal muscle -Monitor for S&S of: mild to severe
Brand anhydrase, the ma, secondary and hepatic weakness, flaccid metabolic acidosis; potassium loss
name: enzyme that glaucoma, and dysfunction; paralysis.  which is greatest early in therapy
Diamox catalyzes the preoperativel Addison's GI: Anorexia, nausea, (see hypokalemia in Appendix F).
reversible y in acute disease or other vomiting, weight loss, -Monitor I&O especially when used
DOSAGE: reaction angle-closure types of dry mouth, thirst, with other diuretics.
The involving the glaucoma whe adrenocortical diarrhea.  -Lab tests: Blood pH, blood gases,
recommende hydration re delay insufficiency; Hematologic: Bone urinalysis, CBC, and serum
d dosage is 1 of carbon of surgery is hyponatremia, marrow depression electrolytes (initially and
capsule (500 dioxide and the desired in hypokalemia, with agranulocytosis, periodically during prolonged
mg) dehydration of order to hyperchloremic hemolytic anemia, therapy or concomitant therapy
carbonic acid. In lower intraoc acidosis; aplastic anemia, with other diuretics or digitalis).
Frequency: the eye, this ular pressure. prolonged leukopenia, pancytopen Patient & Family Education
1 capsule is inhibitory action DIAMOX is administration ia.  -Maintain adequate fluid intake
administered of acetazolamide also indicated to patients with Metabolic: Increased (1.5–2.5 L/24 h; 1 liter is
in the decreases the for the hyphema or excretion of calcium, approximately equal to 1 quart) to
morning and secretion prevention chronic potassium, magnesium, reduce risk of kidney stones.
1 capsule in of aqueous or amelioratio Non congestive and sodium; metabolic -Report any of the following:
the evening. humor and n of angle-closure acidosis; numbness, tingling, burning,
ROUTE: results in a drop symptoms glaucoma. Safety hyperglycemia; drowsiness, and visual problems,
 PO in intraocular associated during hyperuricemia.  sore throat or mouth, unusual
pressure, a with acute pregnancy Urogenital: Glycosuria, bleeding, fever, skin or renal
Classificatio reaction mountain (category C) or urinary frequency, problems.
n: considered sickness despi lactation is not polyuria, dysuria, -Eat potassium-rich diet and take
carbonic desirable in cases te gradual established. hematuria, crystalluria.  potassium supplement when taking
anhydrase of glaucoma and ascent Other: Exacerbation of this drug in high doses or for
inhibitors even in certain gout, hepatic prolonged periods.
non- dysfunction -Do not breast feed while taking
glaucomatous this drug without consulting
conditions. physician.

MECHANISM OF INDICATION CONTRADICTION ADVERSE EFFECTS NURSING RESPONSIBILITIES

DRUG NAME ACTION

Generic name: Acute or chronic -Anorexia, Assessment:

METFORMIN Metformin lowers Metformin is used metabolic acidosis -Nausea,
your blood sugar with a proper diet with or without -Vomiting, History: Allergy to metformin;
levels by improving and exercise coma (including -Diarrhea, diabetes complicated by fever,
Brand name: the way your body program and diabetic -Weight loss severe infections, severe trauma,
GLUCOPHAG handles insulin. It's possibly with other ketoacidosis). -Weakness major surgery, ketosis, acidosis.
E usually prescribed medications to
for diabetes when control high blood Renal failure, -Headache Intervention:
diet and exercise sugar. It is used in severe renal or -Light headedness,
DOSAGE: alone have not been patients with type hepatic -Indigestion Monitor urine or serum glucose
850mg enough to control 2 diabetes impairment, acute -Abdominal levels frequently to determine
your blood sugar controlling high conditions which discomfort effectiveness of drug and dosage.
levels. blood sugar helps may affect renal
Frequency: prevent kidney function and WARNING: Arrange for transfer
850 mg PO damage, blindness, dehydration, to insulin therapy during periods
once daily nerve problems, severe infection or of high stress (infections,
Decreases hepatic loss of limbs, and shock. surgery, trauma).
ROUTE: glucose production; sexual function
PO decreases GI glucose problems. WARNING: Use IV glucose if
absorption; Metformin works severe hypoglycemia occurs as a
increases target cell by helping to result of overdose.
Classification: insulin sensitivity. restore your
Antidiabetics, body's proper Teaching point:
Biguanides response to the
insulin you Do not discontinue this
naturally produce. medication without consulting
It also decreases your health care provider.
the amount of
sugar that your Monitor urine or blood for
liver makes and glucose and ketones as
that your prescribed.
stomach/intestines
absorb. Swallow extended-release
tablets whole; do not cut, crush,
or chew.

Avoid using alcohol while taking

this drug.

Report fever, sore throat,

unusual bleeding or bruising,
rash, dark urine, light-colored
stools, hypo- or hyperglycemic
reactions.
NCP??????
LEARNING PLAN??????
CONCLUSION??????
 DOCUMENTATION

First meeting : May 5, 2021

REFERENCES (later)