Diabetes Mellitus (Type II): Pathophysiology, Symptoms, Treatment and Relevance to Nursing Practice

This presentation provides an overview of Diabetes Mellitus (Type II) including its pathophysiology, symptoms, treatment options, and relevance to nursing practice. It also discusses the role of metformin and rosiglitazone in treating the disease.

DIABETES MELLITUS (TYPE II)
Name of the student:
Name of the university:
Author note:

Brief overview of disease
 Diabetes mellitus is a group of
metabolic disorder characterized by
hyperglycemia which resulted from a
defected secretion of insulin from the
body.
 Approximate 27 million people in
Australia are suffering from the
diabetes mellitus.
 Courcoulas et al. (2015). highlighted
that because of environmental factors
such as overweight, family history,
having a sedentary lifestyle prediabetic
causes insulin resistance and defected
beta cells of body which further give
rise to the type II diabetes.
Figure : diabetes mellitus
type ii
source: (Rubino et al.,
2016)

Homeostasis of the system in
diabetic patient
 Homeostasis is defined as a state of the steady
internal condition mentioned by living things. The
dynamic state of equilibrium is the condition
optimum for the body which varies organism to
organism as well as body conditions such as
temperature and fluid balance of the body (Marso et
al., 2016).
 Insulin stimulates the glycogen formation from
glucose which further help in balancing the blood
glucose level.
 Patient with diabetes are failed to produce and thus
their blood glucose level is not at homeostasis that
further started affected other organs of body.
 To maintain the homeostasis , patient is required to
inject insulin, consume medications and exercise to
maintain homeostasis of the body.
Figure : diabetes
mellitus type ii
source: (Rubino et
al., 2016)

Pathophysiology
The pancreases secrete insulin in
the bloodstream where it circulates
in the blood to lower the blood
sugar level through inducing
glucose metabolism.
glucose level increased in the blood
due to glycogen metabolism the
insulin-producing beta cells in the
pancreases started secreting more
insulin (Forslund et al., 2015)
Obesity, prediabetic
symptoms
sedentary
lifestyle
Fast food or
high sugar /fat
containing food
family
history
cells become impaired
to meet the demand of
Give rise to diabetes
mellitus and affected
other organs

Diagram of pathophysiology
Figure: pathophysiology of diabetes
Source : (Forslund et al., 2015)

Symptoms:
 Excessive Urination
 Excessive Thirst
 Dry Mouth
 Fatigue
 Increased Hunger
(Papademetriou et al., 2017)
 Loss Of Consciousness
 Blurry Vision
 Excessive Sweating
 Slurred Speech
Figure : diabetes
Source :
(Papademetriou et al.,
2017)

Affected body organs and
complications
 Diabetes dramatically
increases the risk of heart
disease (Nowotny et al.,
2015).
 High blood pressure and
narrowing the blood vessels
 diabetic retinopathy
 diabetic neuropathy or nerve
disorders
Figure : affected body
part
Source : (Nowotny et al.,
2015).

Treatment
Medications of diabetes:
 Biguanides ( metformin)
 Thiazolidinedione(Rosiglitazone)
 Alpha-glucosidase inhibitors
( acarbose)
 Dopamine agonist
 DPP-4 inhibitors
Other interventions:
 Exercise
 diet modifications
Figure : medications
Source : (Nowotny et al., 2015).

METFORMIN
 DESCRIPTION : biguanide anti-
hyperglycemic agent used for treating
blood glucose level. It improves glycemic
controls by decreasing hepatic glucose
since work on liver and decrease glucose
absorption as well as glucose mediated
uptake (Nowotny et al., 2015).
 Associated condition :
Diabetes mellitus ii and polycystic ovary. Figure : affected body
part
Source : (Nowotny et al.,
2015).

Mode of action and
pharmacodynamics of metformin
 Pharmacodynamics: the drug decreases hepatic glucose
production, increase uptake of peripheral glucose which
improves insulin sensitivity. Unlike the drug such as
sulfonylureas, metformin doesn't produce hypoglycemia and
hyperinsulinemia. With the influence of the drug, the insulin
secretion remain unchanged while plasma insulin decreases.
 Mechanism of action: It is unique from any other classes of
oral antihyperglycemic drugs. Asmat, Abad and Ismail
(2016), highlighted that metformin inhibits the mitochondrial
complex I. Another study highlighted that it inhibits hepatic
gluconeogenesis in a redox-dependent manner. Therefore, it
reduces the production of hepatic glucose and maximizes
hepatic cytosolic redox state.

Pharmacokinetics of metformin
 Absorption: it administrated under fasting condition, where absorption is 50% to
60% and without food 40% lower mean peak plasma concentration..
 volume of distribution : It is less likely to bind to the GI tract when administrated
intravenously (Koivusalo et al., 2016).
 metabolism : Metformin is negligibly bound to plasma proteins and does not
undergoes hepatic metabolism metabolism.
 route of elimination: no biliary excretion and in oral administration 90% of the
drug eliminated via renal route.

Route of administration and side
effects
 Route of administration : oral in majority of cases , in few cases they uses.
 toxicity: Acute oral toxicity
 Indication: it is indicated as an adjunct to diet and exercise for improving
glycemic control.
 Contraindication: infection, pituitary hormone deficiency, alcohol
intoxication, liver problem and heart attack.
 Side effects: Diarrhea, drowsiness, weakness, dizziness, malaise
(Koivusalo et al., 2016)
 Precautions:
Age , sex and any other associated health conditions is required to evaluate
before administrate the drug to the patient.

Rosiglitazone
 Description : it is anti-diabetic drug in the
thiazolidinedione class of drugs. It is
administrated to the patient with type II
diabetes mellitus in combination with
metformin. It is induced by activation of
the intracellular receptor class of the
peroxisome proliferator-activated
receptors(Koivusalo et al., 2016).
 Associated condition : Diabetes mellitus
Figure :
thiazolidinedione
Source: (Koivusalo
et al., 2016)

Mode of action and
pharmacodynamics of Rosiglitazone
 Pharmacodynamics: when it is used as a monotherapy, the combination
with other drugs increases LDL and HDL. It is associated with decreases
in fatty acid of the body. After two months of therapy, LDL/HDL ratio
peaked ratio shows the highest peak then decreased over time.
 Mechanism of action: it acts as highly selective and potent antagonist
peroxisome proliferator-activated receptors in tissues such as skeletal
muscles, adipose tissue, hepatic tissue. The activation of receptors
regulates the transcription of genes involves in glucose production,
transport, and utilization. Consequently enhances the sensitivity of the
tissue (Koivusalo et al., 2016).

Pharmacokinetics of Rosiglitazone
 Absorption : Bioavailability of the drug is 90% . After1 hour plasma
peak observed in patient.
 Volume of distribution : the oral volume distribution is 17.6 L (Watts et
al., 2016).
 Metabolism : it primarily bound to the albumin. The metabolism is
hepatic where it metabolized into the inactive metabolite where it
conjugated with glucouronic acid.
 Elimination: approximately 64% of the drug is eliminated through urine
and feces.

Route of administration and side
effects.
 Route of administration : oral and intravenous administration
 Toxicity: congestive heart failure and liver disease.
 Indication: it is indicated as an adjunct to diet and exercise for
improving glycemic control.
 Contraindication: visible water retention, abnormal liver function, Broken
Bone, Macular Edema (Watts et al., 2016)
 side effects: Diarrhea, drowsiness, weakness, dizziness, malaise.
 Precautions:
 age , sex and any other associated health conditions is required to
evaluate before administrate the drug to the patient.

Relevance to practice
Relevance to the nursing practice :
 The study will highly relevant to in the field of nursing
since it would help nurses to gain the understanding the
pathophysiology of diabetes mellitus type II and therapy
associated with the diabetes.
 It will also help nurses to provide safe and responsive care
to the patient, support patient in self care management.
 Pharmacology of the treatment would assist nurses to
conduct thorough assessment (Watts et al., 2016)
Figure : diabetes
Source :
(Papademetriou
et al., 2017)

Conclusion:
 Thus, it can be concluded that diabetes mellitus is a group of metabolic
disorder which increases global burden of disease. It is characterized by
the condition where insulin resistance because of high blood glucose
level and defected beta cells of the body which further give rise to the
type II diabetes. The potential treatments are Biguanides ( metformin),
Thiazolidinedione(Rosiglitazone).
 An important consideration, in this case is exercises and dietary
modifications which are required for leading a quality life.

References :
Asmat, U., Abad, K., & Ismail, K. (2016). Diabetes mellitus and oxidative stress—a concise review. Saudi
Pharmaceutical Journal, 24(5), 547-553.
Courcoulas, A. P., Belle, S. H., Neiberg, R. H., Pierson, S. K., Eagleton, J. K., Kalarchian, M. A., ... & Jakicic, J. M.
(2015). Three-year outcomes of bariatric surgery vs lifestyle intervention for type 2 diabetes mellitus
treatment: a randomized clinical trial. JAMA surgery, 150(10), 931-940.
Forslund, K., Hildebrand, F., Nielsen, T., Falony, G., Le Chatelier, E., Sunagawa, S., ... & Arumugam, M. (2015).
Disentangling type 2 diabetes and metformin treatment signatures in the human gut
microbiota. Nature, 528(7581), 262.
Koivusalo, S. B., Rönö, K., Klemetti, M. M., Roine, R. P., Lindström, J., Erkkola, M., ... & Andersson, S. (2016).
Gestational diabetes mellitus can be prevented by lifestyle intervention: the Finnish Gestational
Diabetes Prevention Study (RADIEL): a randomized controlled trial. Diabetes care, 39(1), 24-30.
Marso, S. P., Bain, S. C., Consoli, A., Eliaschewitz, F. G., Jódar, E., Leiter, L. A., ... & Woo, V. (2016).
Semaglutide and cardiovascular outcomes in patients with type 2 diabetes. New England Journal of
Medicine, 375(19), 1834-1844.

Referecences:
Nowotny, K., Jung, T., Höhn, A., Weber, D., & Grune, T. (2015). Advanced glycation end
products and oxidative stress in type 2 diabetes mellitus. Biomolecules, 5(1), 194-222.
Papademetriou, V., Lovato, L., Tsioufis, C., Cushman, W., Applegate, W. B., Mottle, A., ... &
ACCORD Study Group. (2017). Effects of high density lipoprotein raising therapies on
cardiovascular outcomes in patients with type 2 diabetes mellitus, with or without renal
impairment: the Action to Control Cardiovascular Risk in Diabetes Study. American
journal of nephrology, 45(2), 136-145.
Rubino, F., Nathan, D. M., Eckel, R. H., Schauer, P. R., Alberti, K. G. M., Zimmet, P. Z., ... &
Amiel, S. A. (2016). Metabolic surgery in the treatment algorithm for type 2 diabetes: a
joint statement by international diabetes organizations. Surgery for Obesity and
Related Diseases, 12(6), 1144-1162.
Watts, N. B., Bilezikian, J. P., Usiskin, K., Edwards, R., Desai, M., Law, G., & Meininger, G.
(2016). Effects of canagliflozin on fracture risk in patients with type 2 diabetes
mellitus. The Journal of Clinical Endocrinology, 101(1), 157-166.

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