Diabetes Mellitus Pathophysiology and Treatment

A condition characterised by high glucose either lifestyle or congenital

1. Diabetes
Mellitus

2. Learning objectives
1.Define “Diabetes Mellitus”
2. Identify two types of Diabetes Mellitus
3. Explain the causes for Diabetes Mellitus
4. Discuss the diseases process for Diabetes
Mellitus and explain how it can influence
other body systems
5. Explain the disease process create the 4
cardinal signs of Diabetes Mellitus.
6. Identify and explain potential and acute
chronic complications from diabetes Mellitus.

3. Learning objectives
7. Explain common medical treatment for
Diabetes Mellitus for
-Type 1 Diabetes Mellitus
-Type 2 Diabetes Mellitus
•8. Discuss the nursing care plan for clinical nursing of a
patient with diabetes Mellitus (Type 1 or 2)
•Compile a health education programmefor a patient with
Diabetes Mellitus and his/her family with regards to the
following aspects:
-Diet
-Self-injection of insulin
-Foot care

4. Key players
•Glucose
•Insulin
•Glucagon
•pancreas
•Liver

5. Glucose
•“Sugar” (the body needs it to survive) fuels the cells
of your body so they can work properly, BUT IT
CAN NOT ENTER THE CELL WITHOUT THE
HELP OFINSULIN
•It is stored mainly in the liver in the form of
glycogen

6. Insulin
•“deals with high blood sugar levels”
•A hormone that helps regulate the amount of glucose in
the blood (too much glucose is very toxic to the body).
•It allows your body to use glucose by allowing it to enter
the cells (without insulin glucose would just float around
in your body)
•Secreted by theBETA cells of the pancreas from the
islets of Langerhans

7. Glucagon
•“deals with low blood sugar levels”
•A peptide hormone that causes theliver to turn
glycogen into glucose…does the opposite as
insulin.
•Also secreted by the pancreas

8. Pancrease
•Releases insulin and glucagon

9. Liver
•Sensitive to insulin levels and stores and turns
glycogen into glucose when the pancreas secretes
glucagon.Example: (if the body has increased blood
glucose/increased insulin in the blood the liver with
absorb and store the extra glucose for later….if there
is low blood sugar/low insulin levels the liver will
release glycogen which turns into glucose to help
increase the blood sugar level)

10. Glucagon and Insulin Feedback
Loop
•Increased blood sugar -> pancreas releases insulin ->
causes glucose to enter into the cells to be used or be
saved as glycogen for later (stored mainly in the liver)
•Decrease blood sugar -> pancreas release glucagon -
> causes the liver to release glycogen which turns
into glucose to increase the low blood sugar level

11. What happens in diabetes mellitus?
•The body is unable to use glucose due to either theabsence of
insulinorthe body’s resistance to use insulin. Therefore,
the patient becomesHYPERGLYCEMIA (the glucose just
hangs out in the blood stream which affects major organs of
the body)
•The body starts tometabolize FATSfor energy (since it can’t
get to the glucose…remember glucose can NOT enter the cell
without the help of INSULIN)….which happens in Type 1
diabetics OR there is a moderate amount of insulin to deal with
fats and proteins BUT carbs cannot be used (Type 2).

13. Diabetes Mellitus
What is diabetes?
•A metabolic disease characterized by high blood sugar (glucose)
levels above the normal level of 6.5mmol/L (hgt) 7.0 (fasting)
•Diabetes Mellitus is caused by a lack or insufficient insulin, or
from lack of action of insulin, or both.

14. Types of Diabetes
Mellitus
Type 1: Insulin dependent
•no or little insulin secreted due to destruction of the pancreatic
beta cells
Type 2: Non-insulin dependent
•Insulin resistance (decreased tissue sensitivity) eg(obesity,
pregnancy, infection, stress ect)and impaired insulin secretion
Gestational Diabetes
•any degree of glucose intolerance with onset during pregnancy
(placenta hormones →insulin resistance).

15. INSULIN: ITS ACTIONS
•Insulin is a hormone secreted by beta cells (Islets of
Langerhans) in pancreas to lower blood sugar. When a
person eat a meal, insulin secretion increases and moves
glucose from blood into muscles, liver and fat cells.
•Stimulates storage of glucose in the liver and muscle in
form of glycogen
•Signals the liver to stop the release of glucose
•Transports and metabolizes glucose for energy
•Inhibits the breakdown of stored glucose, protein and fat.

16. Pathophysiology or the diseases process for DM
•Type 1:No insulin produced (destruction of beta cells)
•Type2: Insulin is produced but no action of insulin
•In both cases, there is no;
Transports & metabolize of glucose for energy
•The glucose remains higher in the blood(
hyperglycemia) and leads to Glycosuria
•Hyperglycemia causes hyperosmolarityand polyuria
(production of large volume of urine).
•Polyuria causes dehydration

17. Pathophysiology or the diseases process fir DM
•Lack of energy, causes demand for energy, hunger
polyphagia (excessive eating)
•Lack of energy, causes the body to catabolize its own fat
tissues and protein to provide energy.
•Ketone (acids) is produced from catabolism of fats & protein
ketonuria
•Catabolism of fats & protein causes loss of weight.

18. Pathophysiology or the diseases process for DM
Four (4) signs of Diabetes Mellitus
Because of lack of energy, hyperglycemia,hyperosmolarity
the patient presents with:
•Hunger and eats more –Polyphagia.
•Glucose in the urine –Glucosuria.
•Frequent urinationof large volume of urine-Polyuria.
•Thirsty and drinks frequently: Polydipsia

19. Pathophysiology or the diseases process for DM
•In the long-term, hyperglycemia (elevated
blood glucose of 7mmol/L and more)
causes atheromasin the blood vessels and
subsequent gangrene.
Atheromas: degeneration of the walls of the
arteries due to the formation of fatty
plagues and scar tissue. (limit blood
circulation)

20. Pathophysiology or the diseases process for DM
•The conceptual problem for Diabetes Mellitus is a lack of ATP
(adenosine triphosphate)energy.
ATP is a coenzyme that cells use for energy storage. ATP
is present in every cell's cytoplasm and nucleus because it
is necessary for essential life functions in a body.
Therefore:
•Lack of ATP energy causes low systemic output of all
(different) the body systems.

22. Diagnostic studies and the likely findings
1. HGT: more than 6.5 mmol/L
2. An 8 hours fasting blood glucose level:
(NSG≥7mmol/L)
➢No food or drink except water for 8 hours
➢Antidiabetic be postponed till after sample is blood
drawn.

23. Diagnostic studies and the likely findings
3. A random blood glucose or Oral glucose test: 11.1
➢Balanced diet for 3 days prior to the test
➢Fasting for 8h hours prior to test.
➢Take a fasting blood glucose at the start of the test.
➢Instruct the patient to take specific amount of glucose.
➢Draw blood glucose every 30 minutes for 2 hours.

24. Diabetes Mellitus (Medical Treatment)
•Type 1 Diabetes Mellitus: Insulin (Actrapid,
Actraphine& Lantus)
Site to inject (abdomen (right &left lumbar), thigh, back of the upper arm)
•Type 2 Diabetes Mellitus: Oral Anti-diabetes mellitus
(e.g.) metformin, glibenclamide, gliclazide

25. •General measures
NSTG PAGE 662-683

26. Where to inject

27. Diabetes Mellitus (Complications)
ACUTE COMPLICATIONS
1.Hypoglycemia:
Question: What causes hypoglycemia in a diabetic patient?
Question: What are the signs of hypoglycemia?
Immediate management
•Dextrose intravenous
•Monitoring of blood glucose (HGT)

28. answers
•Taking too much insulin or diabetes medication
•Not eating enough
•Postponing or skipping a meal or snack
•Increasing exercise or physical activity without eating
or adjusting your medications
•Drinking alcohol
•Shakiness, Dizziness, Sweating, Hunger, Irritability or
moodiness, Anxiety or nervousness, Headache

29. Diabetes Mellitus (Complications)
2. Keto-acidosis: metabolic acidosis by ketone and acids.
Question: What causes keto-acidosis?
Question: What are the signs of keto-acidosis?
(increased production of acids eglactic,fatty,kettoneand loss of blood bicarbonate→
low PH and low plasma bicarbonate concentration)
Immediate management
•Give N/S for 2hrs once sugar level drops to 14 then
5%Dextrose iv, then Insulin
•Sodium Bicarbonate intravenous (reduce acid)
•Keep pts warm, catheterize, monitor electrolytes

30. ANSWERS
•Not getting enoughinsulin, severe infection anddehydration. It can occur in
people who have little or noinsulinin their bodies (mostly people withtype 1
diabetes but it can happen withtype 2 diabetes, especially children) when
theirblood sugar levelsare high.
•When the body can not use sugar (glucose) as a fuel source because there is no
insulin, instead it use fat as a fuel. When fat is broken down to fuel the body,
chemicals called ketones build up in the body
Higher blood sugar with the following symptoms:
•Flushed, hot,dry skin, Blurredvision, Feeling thirsty and urinating a lot,
•Drowsiness or difficulty waking up. Young children may lack interest in their
normal activities.
•Rapid, deep breathing.
•A strong, fruity breath odor.
•Loss of appetite, belly pain, andvomiting.
•Confusion.

31. Diabetes mellitus (complications)
3. Hyperglycemic hyperosmolar syndrome
Type 2 diabetes metabolic disorder from insulin deficiency
initiated by an illness that raises the demand for insulin.
Persistent hyperglycemia causes osmotic diuresis→ losses of
water and electrolytes→ glycosuria & dehydration
Immediate management
Fluid replacement, correction of electrolytes imbalances
and insulin administration.

32. Diabetes Mellitus (Chronic Complications) (2)
As a result of atheroma and atherosclerosis (fatty plaques
develop in arteries inner walls→ obstruction of blood flow)of arteries &
capillaries which supply body organs:
•Diabetic gangrene: Obstruction of the femoral and
tibialarteries results into gangrene.

33. Diabetes Mellitus (Complications) (2)
•Obstruction of the renal arteries results into
Diabetic Nephropathy: and renal failure.
•Diabetic retinopathy:Obstruction of the retinal
arteries results into paralysis of the optic nerve
and blindness
•Diabetic neuropathy: Obstruction of the arteries
causes nerve damage.
•Obstruction of the coronary arteries results into
ischemic heart diseases.
•Diabetic sclerosis: Obstruction of the cerebral arteries
results into Cerebral Vascular Accident.

34. Diabetes Mellitus (Complications)

35. Diabetes Nursing Management
•Nurse’s role: educating, monitoring, and
administering (medications)
•Teach patient to follow the Triangle of Diabetes
Management
•

36. •Diet, exercising, oral medications,
giving insulin (peak times), drugs that
increase blood glucose and lower
glucose, etc.
•DIET: Diets are individualized due to
physical activity and medication therapy.

37. •Carbs(45-60%) grains, vegetables with starches
potatoes, corn, sweets…cookies, soda, dried beans,
milk)
•Fats(<20 %)….limit unhealthy fats saturated, trans
fats, cholesterol: lard, gravies, whole milk, bologna,
hot dogs, sausage, processed foods hydrogenated
oils…concentrate on mono & polyunsaturated
avocadoes, olives, peanuts, nuts
•Proteins(15-20%) meats don’t increase the glycemic
index: meats chicken, turkey, fish, plant-based beans,
peas, low-fat cheese, eggs whites

38. •Exercising Management
•Exercise: Aerobic is the best (helps
the body use insulin) ex: cardio running,
walking, swimming, etc.

39. Nursing care for a Diabetic patient
•Vital signs monitoring (what and why?)
•HGT monitoring (why?)
•Body fluids monitoring & adjustment (what and why?)
•Skin integrity (what and why?)
•Infection control (what and why?)

40. Nursing care for a Diabetic patient
•Activity tolerance & exercises (what and why?)
(it lowering blood glucose and reducing cardiovascular risk factors)
•Diet (what and why?)
•Foot care (what and why?
•Medication self-administration by the patient(what and
why?)
•Self-monitoring of blood glucose by the patient(what and
why?)

41. Health Education to the patient and family for
palliative care at home
Self-monitoring
❖HGT
❖Urine test
❖Body fluid
❖Diet
❖Adherence to treatment & follow-up treatments
❖Hygiene
❖Activity tolerance & rest

42. Read Further
Medical management;
✓nutritional therapy ; nutrition, meal planning, weight
control, alcohol consumption
✓Exercise-↑ uptake of glucose by muscles & improving
insulin utilization
✓monitoring glucose levels and ketones
•Health education re: self care, foot care etc
•Nursing care plan (Mosby’s, Clinical Nursing, Thompson)

43. Foot care
•Control your diabetes (medicine, diet, exercise)
•Inspect your feet every day
•Wash your feet (warm, dry)
•Keep the skin soft and smooth (skin lotion)
•Smooth corns and calluses
•Trim your toenails each week/ when needed
•Wear shoes and socks all times
•Protect your feet from hot and cold
•Keep blood flowing to your feet

44. Question time

45. Diabetes insipidus (DI)

47. Diabetes insipidus (DI)
•Disorder of the posterior lobe of the pituitary gland
as a result of Antidiuretic Hormone (ADH).
•Condition characterized by large amounts of dilute
urine and increased thirst. Up to 20 liters per day.
•Function of ADH= stimulation of water retention
by the kidneys. Regulate & balances the amount of
water in your blood.

48. two types of diabetes insipidus,
•Cranial diabetes insipidus is a condition in which
the hypothalamus does not produce enough anti-
diuretic hormone.
•Nephrogenic diabetes insipidus = kidneys fail to
respond to anti-diuretic hormone.

49. Predisposing factors
•Occur secondary to head trauma, brain tumor,
surgical ablation or irradiation of the pituitary gland.
(direct disruption of the hypothalamus or pituitary)
•Infections of the central nervous system (meningitis,
encephalitis) or tumors

50. Clinical manifestations
•Large volumes of dilute urine-due to no action of ADH
on the distal nephron (kidney)
•The urine contains no abnormal substances such as
glucose or albumin
•Excessive thirst (polydipsia) (2-20 L of fluids)
•Hydration status (poor skin turgor, dry skin, weight loss)
•Bowel function (constipation)
•Electrolytes imbalance

51. Assessment and diagnostic
studies
•History taking
•Fluid deprivation test-withhold fluids for 8 until 5% of body
weight is lost. Weigh the patient hourly. perform plasma and
urine osmolality studies 4hrly. If there is no ↑ in SG and
osmolality of the urine then =DI. (NB tachycardia, excessive weight
loss/ hypotension)

52. Medical management
•Objectives –to replace ADH (long term), to ensure adequate
fluid replacement and identify the underlying intracranial
pathology
•Medication:
❑Desmopressin= A synthetic analogue of antidiuretic hormone
(ADH). nasal, oral, iv and im
❑Vasopressin= has vasopressor and ADH activity. im/ iv.
❑Chlorpropamide= promotes renal response to ADH.
❑Hydrochlorothiazide= is a thiazide diuretic that decreases
urinary volume in the absence of ADH