DIABETES MELLITUS.ppt

Presentation

1. DIABETES MELLITUS
PRESENTER
PC Mukubesa

2. Definition
•It is a chronic metabolic disorder
associated with a disturbance in the
metabolism of carbohydrates, proteins
and fats due to defects in insulin
secretion, insulin action, or both
resulting in a state of hyperglycaemias.

3. Classification
•Currently diabetes is classified in two
major categories as recommended by
the American Diabetes Association in
1997
•This system of classification reflects
both the etiology and pathophysiology
of diabetes
•The two major categories are as
outlined below;

4. Classification cont
•TYPE 1 DIABETES MELLITUS: This
was formally known as juvenile onset
diabetes mellitus or insulin dependent
diabetes
•TYPE 2 DIABETES MELLITUS: This
was also known as non insulin
dependent diabetes mellitus or mature
onset diabetes mellitus

5. Type I diabetes mellitus
•This is due to inadequate or no insulin
production by the islets of Langerhans
•Onset is generally before the age of 30
although it may occur at any age
•Sudden on set of symptoms
•Since the pancreas can not produce
adequate insulin, treatment is usually by
artificial insulin or exogenous insulin (hence
the name insulin dependent diabetes

6. Type I diabetes mellitus cont
•Sufferers are usually lean, rarely
obese
•More prevalent in Caucasians than
black Africans
•Prone to ketosis

7. Type I diabetes mellitus cont
•85-90% there is one or more of the
following autoimmune anti bodies:
Islet cell auto antibodies
Insulin auto antibodies etc.
Strong Human leukocyte antigen
(HLA) association
•There is a weak link to family history of
diabetes

8. Type II diabetes
•There is impaired utilization of insulin by the
cells
•Gradual onset of symptoms
•Onset is usually after the age of 40
(Adult onset diabetes)
•The absolute need for insulin is episodic
•No requirement for exogenous insulin to
sustain life at least initially (non insulin
dependent diabetes)

9. Type II diabetes cont
•There is a strong family history of
diabetes
•No autoimmune or HLA association
•80-90% of sufferer are obese
•More common in African Americans
and Hispanics than Caucasians
•Treatment is with Insulin, diet,
hypoglycemic agents and exercises

10. Predisposing factors to type II
•Presence of insulin antagonist like;
Growth hormone
Adrenaline
Cortico steroids
Hyperthyroidism
•Liver diseases e.g. liver cirrhosis
cancer of the liver and hepatitis
•Obesity due to increased demand for
insulin

11. Gestational diabetes mellitus
•This the type of diabetes occuring
during pregnancy
•Gestational diabetes mellitus (GDM)
resembles type2 diabetes in several
respects, involving a combination of
relatively inadequate insulin secretion
and responsiveness.
•It occurs in about 2%–5% of all
pregnanciesand may improve or
disappear after delivery.

12. Gestational diabetes mellitus
cont
•Gestational diabetes is fully treatable
but requires careful medical
supervision throughout the pregnancy.
•About 20%–50% of affected women
develop type2 diabetes later in life
•Even though it may be transient,
untreated gestational diabetes can
damage the health of the fetus or
mother.

13. Gestational diabetes mellitus
cont
•Risks to the baby include:
macrosomia(high birth weight),
congenital cardiac and central nervous
system anomalies, and skeletal muscle
malformations.
Increased fetal insulin may inhibit fetal
surfactantproduction and cause respiratory
distress syndrome.
Hyperbilirubinemiamay result from red
blood cell destruction.
In severe cases, perinatal death may occur,
most commonly as a result of poor placental
perfusion due to vascular impairment

14. Gestational diabetes mellitus
cont
•In severe cases, perinatal death may
occur, most commonly as a result of
poor placental perfusion due to
vascular impairment
•Inductionmay be indicated with
decreased placental function.
•A cesarean sectionmay be performed
if there is marked fetal distress or an
increased risk of injury associated with
macrosomia, such as shoulder
dystocia

15. Pathophysiology
•The islets of Langerhans in the pancreas
are the endocrine portion of the pancreas
which has two types of cell that are
important for glucose control
•The alpha cells produce glucagon which is a
major counter regulatory hormone of insulin(
its action is opposite to that of insulin)
•It causes the release of glucose from cell
storage sites whenever blood glucose levels
are low.

16. Pathophysiology cont
•The Beta cell on the other hand
secrete insulin
•Insulin allows the body cells to use
carbohydrates, and store fats and
proteins
•Insulin allows glucose in the blood to
move into the cell to provide energy
•It acts like a key that opens the cell
membrane to glucose, thereby
promoting uptake of glucose by the
cells.

17. Pathophysiology cont
•The liver promotes glucose production and
storage of glycogen (glycogenesis) at the
same time it inhibit glycogen break down
into glucose (glycogenolysis)
•Insulin also promote protein and lipid
synthesis
•It inhibits tissue break down by inhibiting
glycogenolysis, ketogenesis (conversion of
fat to fatty acids) and gluconeogenesis (
conversion of protein to glucose)
•Insulin therefore keeps glucose and blood
lipids within normal range.

18. Pathophysiology cont
•In the absence of insulin the cell can not
take up glucose for energy
•The body therefore starts using other
method to make glucose such as
gluconeogenesis, ketogenesis, and
glycogenolysis.
•This process contribute to the rise in blood
sugar levels
•However the absence of insulin make it
difficulty for the cell to take up glucose.
•This lead to elevated blood sugar levels
(hyperglycaemia)

19. Pathophysiology cont
•Hyperglycaemia causes fluids to shift
from the extra vascular spaces into the
intra vascular system.
•This in turn causes fluid and electrolyte
imbalance
•The hyperglycaemia leads to
glucoseuria
•It also leads to polyuria

20. Pathophysiology cont
•Excess fluid loss leads to dehydration
which in turn leads to polydipsia
•There is also excessive hunger which
is called polyphagia in an attempt to
find other sources of energy
•Because of the glucoseuria there will
be glucose on the glans penis causing
balanitis in males and pruritus vulvae
in women

21. Pathophysiology cont
•The break down of fat lead to
formation of ketone bodies which may
accumulate causing metabolic acidosis
because of the increase in carbon
dioxide and H+
•There will be stimulation of the
respiratory control centre to increase
the rate and depth of the respirations
causing what is called KUSSMAULS
RESPIRATIONS

22. Pathophysiology cont
•All these event will lead to the classic
signs and symptoms of
hyperglycaemia, that is;
Polyuria
Polydipsia
Polyphagia
Glucoseuria

23. Sign and symptoms
•Polyuria
•Polyphagia
•Polydipsia
•Glucoseuria
•Pruritus vulvae or balanitis in men
•Dry skin and mucous membrane due
to dehydration

24. Signs and symptoms cont
•Kussmaul’s respiration due to acidosis
•Lassitude (Tiredness) due to
electrolyte imbalance
•Weight loss
•Fatigue
•Visual blurring
•Late signs and symptoms include
coma and chronic complications

25. Investigation
•History may reveal classic signs and
symptoms e.g. polyuria ,polydipsia,
polyphagia, etc.
•Clinical feature will demonstrate dry skin
and mucous membrane, Acetone breath will
be present
•Urinalysis will show glucoseuria
•Blood for fasting blood sugar will be
elevated above 126mg/dl
•Random blood sugar will be high

26. Management
•Management of type 1 diabetes
involve a triad:
Insulin
Diet and
Exercise
Because there is inadequate insulin in
type 1.insulin replacement is the first
management component

27. Management cont
•Types of insulin include:
Short acting insulin (e.g. Soluble (regular)
insulin, Lispro, Aspart)
Intermediate acting insulin (e.g. NPH. Lente)
Long acting insulin ( e.g. Ultralente,
glargine)
Before a patient is put on a regular dose he
must be stabilized using a sliding scale

28. Management cont
The choice of insulin will depend on
whether the patient is new, old and
how the patient responds to a
particular insulin
•For instance rapid acting also used in
hyperglycemic coma
•Dosage may range from patient to
patient e.g. 10-24iu
•This is done to ensure that the patient
attains a euglycemic state

29. Management cont
•Diet must be coordinated with insulin
injection in order to ensure insulin is
available for optimal use when food
that has been taken is absorbed, and
so that glucose is available when
insulin is acting to prevent
hypoglycemia.

30. Management cont
•Encourage regular mild exercises
•Exercises when combined with diet,
and insulin help to manage the
hyperglycemia.

31. Management cont
•TYPE 2 DM:
Here there is impaired utilization of insulin therefore
hypoglycemic agent are used together with diet and
exercise
Hypoglycemic agent reduce insulin resistance and
promote insulin sensitivity (Metformin also called
glucophage)
Others increase production of insulin and action
(sulfonylurea such as glybenclamide)
Examples of hypoglycemic agent are;
Glybenclamide and metformin

32. Management cont
•The dosage for glybenclamide is 5mg qid
Glybenclamide reduces hepatic glucose
secretion while increasing insulin secretion
Because of this it can cause hypoglycemia
•Metformin on the other hand reduces
hepatic glucose production while increasing
skeletal muscle glucose utilization
Because it does not increase insulin
production it is most unlikely to cause
hypoglycemia when used as monotherapy

33. Complications
•The damage to small blood vessels
leads to a microangiopathy, which can
cause one or more of the following:
Diabetic retinopathy, growth of friable
and poor-quality new blood vessels in
the retinaas well as macular edema
(swelling of the macula), which can
lead to severe vision lossor blindnes.

34. Complications cont
Diabetic neuropathy, abnormal and
decreased sensation, usually in a
'glove and stocking' distribution starting
with the feet but potentially in other
nerves, later often fingers and hands.
Diabetic myotrophyis muscle
weakness due to neuropathy.

35. Complications cont
•Diabetic nephropathy, damage to the
kidneywhich can lead to chronic renal
failure, eventually requiring dialysis.
Diabetes mellitus is the most common
cause of adult kidney failure worldwide
in the developed world.
•Diabetic cardiomyopathy, damage to
the heart, leading to heart dysfunction
and eventually heart failure.

36. Complications cont
Macrovascular diseaseleads to
cardiovascular disease, to which
accelerated atherosclerosisis a
contributor:
Coronary artery disease, leading to
anginaor myocardial infarction("heart
attack")
Stroke(mainly the ischemic type)

37. Complications cont
Peripheral vascular disease, which contributes to
intermittent claudication(exertion-related leg and
foot pain) as well as diabetic foot.
Diabetic foot (ulcer formation due to microvascular
impairement
Diabetic myonecrosis('muscle wasting')
Complication related to treatment include
Hypoglycemia.

38. Differences between hyperglycemia and
hypoglycemia in diabetes mellitus
Hyperglycemia Hypoglycemia
Caused by skipping an
insulin dose or too much
carbohydrate intake
Caused by insulin over
dose or skipping a meal
Skin is dry due to
dehydration
Skin moist due to
sweating
Urinalysis will show
glucoseuria
No glucoseuria when
urinalysis is done
To be treated with insulinTreatment is by giving
glucose

39. Differences between hyperglycemia and
hypoglycemia in diabetes mellitus
Hyperglycemia Hypoglycemia
There is Kussmaul's
respirations
Kussmaul’s respirations
absent
Gradual onset Sudden on set of
symptoms

40. Nursing Care
•AIMS:
•To attain euglycemic state
•To prevent complications
•To educate the patient on the skills of
self management and help him accept
the condition

41. Environment
•The patient will be nursed in a stress
free environment
•Patient will be nursed at the acute bay
for close observation
•The room should be well ventilated to
allow free air circulation
•The room should be well lit for easy
observation

42. Position
•If my patient is unconscious nurse him
in supine position with the neck hyper
extended and turned to one side to
promote a patent air way and promote
free flow of secretion
•As condition improve nurse him in any
position of comfort

43. Rest
•I will nurse the patient in a quiet room to
promote rest
•I will play the radio at low volume to avoid
disturbing the patient
•I will answer all phone calls promptly to
prevent disturbing the patient there by
promote rest
•I will do related procedures at the same time
to give more time for patient to rest
•I will administer prescribed analgesics to
relieve headache there by promote rest
•I will ensure that squeaking trolleys a oiled
to prevent noise and there by promote rest

44. Observation
•I will do vital sign to act as base line data in
order to know if the condition is improving or
deteriorating
•I will do urinalysis to see if there is any
improvement in the glucoseuria and report
to the physician for proper management of
the patient.
•If my patient is unconscious I will use the
Glasgow come scale to note the level of
consciousness

45. Observations cont
•I will observe for the level of hydration and if
my client is dehydrated I will give more fluids
to rehydrate the patient
•I will observe the skin folds for signs of
abscess formation and report to the
physician
•I will also watch out for possible
complications such as diabetic foot, diabetic
neuropathy
•I will observe strict intake and out put to
monitor renal functions.

46. Psychological care
•I will explain the disease process in
order to raise the knowledge levels
and thereby alley anxiety
•I will encourage the patient to ask
question and I will answer accordingly
those I cant answer I will refer to the
physician
•I will explain all procedures to my
patient in order to allay anxiety

47. Psychological care cont
•I will involve the patient in his own care
to promote self esteem and gain
coorperation
•I will allow the loved one to visit him for
him to feel loved and not neglected
•I will offer diversional therapy to shift
the patient’s mind from his condition

48. Hygiene
•I will bath the patient and pay
particular attention to the skin folds to
prevent accumulation of dirt which can
lead to development of an abscess
•I will do mouth care to prevent halitosis
•I will do nail care to prevent auto
infection because nail may harbor
microbes.

49. Elimination
•I will offer a bed pan if he is confined to
bed to ensure bowel movement
•I will ensure strict intake and output of
fluids and record on the fluid balance
chart.

50. Nutrition/Fluids
•I will offer food such as inshima to provide
energy to the patient
•I will restrict foods like cakes to prevent
worsening the condition of the patient
•I will offer foods rich in vitamins like
vegetables to boost the immunity and
stimulate appetite
•I will give copious oral fluids to treat
dehydration

51. Medication
•I will administer the prescribed insulin at the
right time in order to promote quick recovery
•I will ensure that if the patient is on iv fluids
they are running at the correct rate to
prevent circulatory over load
•I will explain the side effects of the drug
•I will also sign the treatment chart for
continuation of care

52. Patient education
•I will educate the patient about his
condition to raise the knowledge level
and promote self care and recognition
of complications
•I will teach the patient on what foods to
take liberally and those to avoid like
cakes in order to prevent worsening of
the condition
•I will teach how to inject the insulin to
promote self care at home

53. Patient education cont
•I will advise the patient to pay thorough
attention to the skin folds to prevent
abscess formation
•I will advise my patient to take meals
before injecting himself to prevent
complications such as hypoglycemia
•I will advise my client to rotate the site
of insulin injection to avoid hardening
of the site which may impair absorption

54. Patient education cont
•I will advise the patient to carry the
identity band for recognition in case he
become unconscious due to
hypoglycemia or hyperglycemia and
goes into unconsciousness for proper
management
•I will advise my patient to initiate
weight reducing exercises if he is
obese to control the disease

55. Patient education cont
•I will advise the patient to always adhere to
treatment in order to manage or control the
disease
•I will encourage the patient to keep the
review date in order to monitor his condition
and prevent complications
•I will teach the patient how to recognize the
signs and symptoms of hypo and
hyperglycemias for quick intervention and
prevention of complications

56. THE END
THANK
YOU
56