4. Cont…
The endocrine system consists of the glands that
secrete hormones.
Ductless glands because they secrete directly
into the blood stream.
Hormones help to regulate organ function in
Conjunction with the nervous system.
Hypothalamus helps to provide the link b/n the
endocrine & nervous system.
The nervous system and the endocrine system
are the two main coordinating and controlling
systems of the body.
5. Cont….
There are several differences between
these two systems.
The nervous system acts by means of
electric impulses and chemical stimuli
The endocrine system has more
widespread, slower, and longer lasting
effects.
The endocrine system also has more
generalized effects on such activities as
6. Hormones
Chemical messengers released by the glands of the
endocrine system.
Hormones are released directly into the bloodstream
and carried to the tissues they affect.
These tissues may be far from where the hormone is
produced.
Only certain cells respond to specific hormones
These responding cells are unique in that they have
receptors to which the hormones attach.
Only cells that have receptors for a given hormone
will respond to that hormone( target tissue)
Hormone concentration in the blood stream is
regulated by feedback control mechanism.
7. Cont…
Hormones fall chemically into two
categories:
Proteins:- most hormones are proteins
or related compounds composed of
amino acids.
All hormones except those of the
adrenal cortex and the sex glands are
proteins.
Steroids:- hormones derived from lipids
and produced by the adrenal cortex &
8. Function of hormones
Growth & differentiation
Maintenance of homeostasis
Reproduction
9. Pancreas
Has both exocrine & endocrine gland function
Endocrine Pancreas
Islets of langerhans are the cells involved in the
endocrine function
Composed of 3 distinct types of cells
- Alpha cells secret glucagons
- Beta cells secret insulin
- Delta cells secret somatostatin
-Glucagons & insulin have significant effect on
carbohydrates, protein & lipids metabolism
10. Cont…
Insulin – lowers blood glucose level
Anabolic hormone bse it stimulates
the synthesis of glycogen, protein &
lipid
It inhibits degradation of these
substance.
Glucagon – raise the blood glucose level
Catabolic hormone
11. Diabetes mellitus(DM)
A group of metabolic disorder characterized by
elevated levels of glucose in the blood
(hyperglycemia) resulting from defects in insulin
secretion, insulin action, or both.
In diabetes the body’s ability to respond to insulin
may be decreased or the pancreas may stop
producing insulin entirely.
Normally a certain amount of glucose circulates in the
blood.
The major sources of glucose
Absorption of ingested food in the gastrointestinal
(GI)
Formation of glucose by the liver from food
substances.
12. Diabetes Mellitus(DM)
Carbohydrate, lipid & protein
metabolism abnormality resulting from
relative or absolute absence of insulin
or its cellular metabolism effect.
Insulin:- controls the level of glucose in
the blood by regulating the production
and storage of glucose.
This leads to hyperglycemia, which
results in
13. Cont…
Acute metabolic complications such as
diabetic ketoacidosis (DKA) and
hyperglycemic hyperosmolar nonketotic
syndrome (HHNS).
Long-term effects of hyperglycemia
contribute to macrovascular
complications (coronary artery disease,
cerebrovascular disease, and peripheral
vascular disease), chronic microvascular
complications (kidney and eye disease),
and neuropathic complications (diseases
14. Classification
A - Type I or insulin dependent (IDDM)
B - Type II non insulin dependent(NIDDM)
C - Gestational diabetes mellitus (GDM) Onset during
pregnancy, usually in the second or third trimester.
Due to hormones secreted by the placenta, which
inhibit the action of insulin
D -Diabetes mellitus associated with other conditions
or syndromes-
Accompanied by conditions known or suspected to
cause the disease: pancreatic diseases, hormonal
abnormalities, medications such as corticosteroids
and estrogen-containing preparations
15. Type I
5 to 10% of people with DM have type
I/ insulin dependent diabetes.
In this form the beta cells of the
pancreas that normally produce insulin
are destroyed by an autoimmune
process.
It is characterized by sudden onset
usually before the age of 30yrs.
16. Type II
~ 90 to 95% of people with diabetes
Results from decreased amount of
insulin production
Occurs most frequently in people who
are older than 30yrs of age and obese.
17. Normal Physiology
Insulin is secretary by B cells of
pancreases
Insulin is an anabolic or storage
hormone it has the following effects.
Stimulate storage of glucose in the liver
and muscle (in the form of glycogen)
Enhance storage of dietary fat in
adipose tissue.
Accelerates transport of amino acids in
to cells
18. Pathophysiology of Diabetes
Type I Diabetes
Inability to produce insulin because pancreatic
beta cell has been destroyed.
Fasting hyperglycemia
Post prandial (after meal) hyperglycemia
Glucose in the urine since the concentration is
high in the blood
Excess glucose excreted in the urine
Excessive loss of fluids and electrolytes
Osmotic diuresis – Polyuria
Polydipsia
19. Insulin deficiency
Impaired metabolism of protein and fats
-Weight loss
Polyphagia – because of the decreased
storage of calories
Further hyperglycemia from – Glycogenolysis
- Gluconeognesis
Fat break down
Production of ketone bodies leads to
diabetic Ketoacidosis (DKA)
20. Type II – Diabetes (pathophysiology)
Impaired insulin secretion
Insulin resistance -decreased sensitivity
of the tissue to insulin
To overcome insulin resistance and to
prevent the buildup of glucose in the
b/d there must be an increased in the
amount of insulin secretion.
If the B cells are unable to keep up
with the increased demand for insulin,
the glucose level rises.
21. Cont…
DKA does not occur in type II diabetes
Occurs most commonly in people >
30yrs
For most pt’s the problem is detected
incidentally
Long term Complications are common
Wt reduction is the primary Rx of type II
DM and also exercise and diet.
22. Etiology
Type I diabetes
- Genetic
Combination of - Immunology
- Environmental factors
An abnormal response in which
antibodies are directed against normal
tissue of the body responding to tissue
as if they are foreign.
23. Type II Diabetes
Exact mechanisms that leads to insulin
resistance and impaired secretion in
type II DM are unknown.
But genetic factors play a role in
addition age (>65 yrs), obesity, family
history and ethnic group.
24. Diagnostic Evaluation
The presence of abnormally high blood
glucose level on at least two occasions
Fasting plasma glucose > 126mg /dl
Random plasma glucose >200mg/dl
Oral glucose tolerance test >200 mg/dl
25. Management
The main goal of the Management
To normalize insulin activity and b/d
glucose
To reduce development of the vascular
and neuropathic complications
26. Cont…
Normal blood glucose level without
hypoglycemic and without seriously
disrupting the pt usual activity patterns.
Diet
Medication
Exercise
Education
Monitoring
27. Dietary Mxt
Constitutes the foundation of diabetes
Mxt
Has the following goals
Provision of all the essential foods
Meeting energy needs
Decrease of blood glucose lipid levels.
For obese pts wt loss is the key to Rx
28. Cont…
Important objective in dietary Mxt of
diabetes is control of total calorie intake
to attain or maintain a reasonable body
wt and control of blood glucose level.
In a young pt with type I diabetes,
priority should be given to provide a
diet with enough calories to maintain
normal growth & dev’t.
29. Insulin Therapy
Insulin lowers blood glucose level after meals by
facilitating the uptake & utilization of glucose by
muscles, fat and liver cells.
During periods of fasting insulin inhibits the
breakdown of stored glucose, protein & fat.
In type I diabetes exogenous insulin must be
administered.
In type II diabetes insulin may be necessary and a
long term bases to controll glucose levels if diet and
oral agents have failed.
30. Insulin Preparation
A number of insulin preparations are
available
Vary according to four major
characteristics
Time course of action
Concentration
Species and source
Manufactures
31. Time Course
May be grouped into three main
categories based on onset, peak and
duration.
Short Acting Insulin
- Regular insulin (marked “R”)
- Onset of regular human insulin action is
½ to 1hr, peak 2 to 3 hrs duration 4 to
6hrs
- Clear in appearance given 20 minutes
before food.
32. Intermediate Acting
NPH insulin (neutral protamin hagodorn)
Lente insulin (“C”)
Onset 3-4 hrs, peak 4-12 hrs duration 16-
20 hrs.
White and milky in appearance
It is important for the pt to have eaten
some food arrived the time of the onset
and peak of these insulin
33. Long Acting Insulin
Ultra lente Insulin (UL)
Sometimes referred to as “peak less”
b/c it tends to have a long, slow,
sustained action rather than sharp
peaks in action
• Onset 6-8hrs , duration 20-30hrs
34. Concentration
The most common conc. of insulin is U-
100
This means 100 units of insulin per ml)
also U-40 & U-80 are used
Species
In the past all insulin were obtained
from beef (cow) and pig pancreas.
Now human insulin is widely available.
35. Insulin regimen
Vary from one to four injections per
day.
Usually these are a combination of a
short acting and long acting insulin
There are two general approaches to
therapy.
36. Conventional Regimen
Simplifying the insulin regimen as much
as possible with the aim of avoiding the
acute complications.
This approach would be appropriate for
Terminally ill
The elderly with limited self care
abilities
Pt completely unwilling or unable to
engage in self management.
37. Intensive Regimen
Uses a more complex insulin regimen
to achieve as much control over bgl is
safe.
Allows pts more flexibility to change
their eating and activity patterns.
Pts who may not be appropriate
candidate
Persons with autonomic neuropathy to
have hypoglycemic awareness
with permanent, irreversible
38. Problems with Insulin
1. Local allergic reaction
Redness, Swelling, tenderness and
indurations at the site of injection
Usually occur during the beginning
stages of therapy and disappear with
continued use of insulin.
2. Systemic Allergic Reaction
First, an immediate local skin reaction
that gradually spread into severe &
generalized.
39. 3. Insulin lipodystrophy
Lipodystrophy refers to a localized
reaction, occurring at the site of insulin
injections.
Lipoatrophy is loss of subcutaneous fat
and appears as slight dimpling or more
serious pitting of subcutaneous fat.
The use of human insulin has almost
eliminated this disfiguring complication.
40. Cont…
Lipohypertrophy, the development of
fibrofatty masses at the injection site,
caused by the repeated use of an
injection site.
If insulin is injected into scarred areas,
absorption may be delayed.
41. 4. Insulin Resistance
Clinical insulin resistance is a daily
insulin requirement of 200 units or
more.
Immune antibodies develop and bind
the insulin, thereby decreasing the
insulin available for use.
All animal insulins, as well as human
insulins to a lesser degree, cause
antibody production Rx:- administering
a more concentrated insulin
preparation, such as U500
Prednisone is needed to block the
42. 5. Morning hyperglycemia
An elevated blood glucose level upon
arising in the morning caused by an
insufficient level of insulin
1.The dawn phenomenon:- relatively
normal bgl until approximately 3 a.m.,
when bgl begin to rise.
The phenomenon is thought to result
from nocturnal surges in growth
hormone secretion that create a greater
need for insulin in the early morning
hours in patients with type 1 diabetes.
43. Rx:-Change time of injection of evening intermediate-
acting insulin from dinner time to bedtime.
2. Insulin waning :-the progressive
increase in blood glucose from bedtime
to morning.
Rx:-Increase evening (predinner/bedtime)
dose of intermediate or long-acting
insulin
3. Somogyi Effect:-Normal or elevated
blood glucose at bedtime, a decrease at
2–3 a.m.to hypoglycemic levels, and a
44. Cont…
Rx:- Decrease evening (predinner or
bedtime) dose of intermediate acting
insulin
or increase bedtime snack.
Administering Insulin Injection
- Selection and rotation
- The four main area for injection are the
abdomen, arms, thighs and the hip.
- Speed of absorption is in the abdomen
45. Cont…
Systematic rotation of injection site
with anatomic areas is recommended to
prevent localized changes in fatty
tissues (lipodystrophy)
46. Oral Anti diabetic/hypoglycemic Agents
Are effective for type II diabetic pts.
They cannot be used during pregnancy.
Oral agents include – Sulfonylurea
-Biguamides
Sulfonylurea
Exert their primary action by directly stimulating
pancreas to secret insulin
Additionally improve insulin action at the cellular
level
Also decrease glucose production by the liver
47. Acute complications
Three major acute complications of
glucose imbalance
Hypoglycemia
DKA
Hyperglycemic Hyperosmolar non
ketotic syndrome.(HHNKS)
48. Hypoglycemia (Insulin Reaction)
Occurs when bgl falls below 50 to 60 mg /dl
Can be caused by
Too much insulin, oral hypoglycemic agents
Too little food
Excessive physical activity.
Occurs at any time of the day or night
Hypoglycemia can be Mild
Moderate
Severe
49. Severe hypoglycemia
CNS function is so impaired that the pt needs the
assistance of another person for Rx
Disoriented behaviors, seizures, difficulty arousing
from sleep or loss of consciousness.
Immediate Rx must be given
Usual recommendation 10 to 15 gm of fast acting
sugar orally.
N.B Golden advice – diabetic pts must carry some
form of simple sugar with them all the times
50. Severe Hypoglycemia
For unconscious pt
40 % DW Iv
Injection glucagon 1gm IM
Simple sugar dissolved (NGT)
Patient Education
Pt should follow regular pattern of
eating, administering insulin and
exercise.
Routine blood glucose tests
51. Impaired function of CNS
Inability to concentrate
Headache, light headedness
Confusion, memory lapses
Numbness of the lips & tongue
Slurred speech to coordination
Emotional Change
Irrational Behavior
Double vision & drowsiness
Mx – Fast Acting Sugar
52. Diabetic Ketoacidosis
Caused by an absence or markedly inadequate
amount of insulin
Result in disorder of metabolism of CH2O, Protein &
fats.
Cause of DKA
Decreased or missed dose of insulin
Illness or infection
Initial manifestations of undiagnosed and
untreated diabetes.
53. Cont…
The three main clinical features of DKA
- Dehydration
- Electrolyte loss
- Acidosis
Pathophysiology of DKA
Break down of fat / lipolysis /
Free fatty acid & glycerol
Ketone bodies (Acid)
Metabolic acidosis
57. Rehydration
Rehydration is important for maintaining tissue
perfusion.
Enhances the excretion of excessive glucose by the
kidneys.
Requires 6 -10 liters of IV fluid to replace fluid
losses caused by polyuria, hyperventilation,
diarrhea, and vomiting.
Initially, 0.9% NaCl is administered at a rapid rate(
0.5-1 L /hour for 2 to 3 hours.
(0.45%NaCl) hypotonic used for patients with
hypertension or hypernatremia or those at risk for
heart failure.
58. Cont…
After the first few hours, half-normal
saline solution is the fluid of choice for
continued rehydration,if BP is stable and the
sodium level is not low.
Moderate to high rates of infusion (200 to
500 mL/ hr) may continue for several more
hrs.
When the bgl reaches 300 mg/dL or less, the
IV fluid may be changed to dextrose 5% in
water (D5W) to prevent a precipitous decline
in the blood glucose level
59. Cont…
Monitor fluid volume status involving
frequent measurement of
- Vital sign (BP,PR,RR)
- Input & out put
- Lung assessment
60. Restoring electrolytes
The major electrolyte of concern during treatment
of DKA is potassium.
Although the initial plasma concentration of
potassium may be low, normal, or even high, there
is a major loss of potassium from body stores and
an intracellular to extracellular shift of potassium.
Further, the serum level of potassium drops during
the course of treatment of DKA as potassium re-
enters the cells
61. Factors related to treating DKA that reduce the
serum potassium concentration
Rehydration leads to increased plasma volume
Rehydration leads to increased urinary excretion of
potassium.
Insulin administration, which enhances the
movement of potassium from the extracellular fluid
into the cells.
Cautious but timely potassium replacement is vital to
avoid dysrhythmias.
Up to 40 mEq per hour may be needed for several
hours.
62. Acidosis
Ketone bodies accumulate as a result
of fat breakdown.
The acidosis that occurs in DKA is
reversed with insulin, which inhibits fat
breakdown, thereby stopping acid
buildup.
Insulin is usually infused intravenously
at a slow, continuous rate 5 units per
hour).
Hourly bgl values must be measured.
63. 3 . Hyperglycemic hyperosmolar nonketotic syndrome
HHNS is a serious condition in which
hyperosmolarity and hyperglycemia
predominate, with alterations of sensorium.
The basic biochemical defect is lack of
effective insulin.
The patient’s persistent hyperglycemia
causes osmotic diuresis, resulting in losses of
water and electrolytes.
To maintain osmotic equilibrium, water shifts
from the intracellular fluid space to the
extracellular fluid space.
64. Cont…
With glucosuria and DHN,
hypernatremia and increased osmolarity
occur.
HHNS can be traced to a precipitating
event such as an acute illness (eg,
pneumonia or stroke), medications that
exacerbate hyperglycemia (thiazides).
65. Cont…
Patients may tolerate polyuria and
polydipsia until neurologic changes or
an underlying illness (or family
members or others) prompts them to
seek treatment.
Because of possible delays in therapy,
hyperglycemia, dehydration, and
hyperosmolarity may be more severe in
HHNS.
66. Clinical Manifestations
Hypotension
Profound DHN (dry mucous
membranes, poor skin turgor)
Tachycardia
Variable neurologic signs (eg, alteration
of sensorium, seizures, hemiparesis).
The mortality rate ranges from 10% to
40%, usually related to an underlying
illness.
67. Assessment and Diagnostic Findings
Serum osmolality
The bgl is usually 600 to 1,200 mg/dL
The osmolality exceeds 350 mOsm/kg.
Electrolyte and BUN levels are consistent with the
clinical picture of severe dehydration.
Mental status changes, focal neurologic deficits, and
hallucinations are common secondary to the cerebral
dehydration that results from extreme
hyperosmolality.
Postural hypotension accompanies DHN
68. Medical Management
The overall approach to the treatment of
HHNS is similar to that of DKA:
Fluid replacement
Correction of electrolyte imbalances, and
Insulin administration.
Close monitoring of volume and electrolyte
status is important for prevention of fluid
overload, heart failure, and cardiac
dysrhythmias.
69. Cont…
Fluid treatment is started with 0.9% or 0.45%
NS, depending on the patient’s sodium level
and the severity of volume depletion.
Potassium is added to IV fluids when urinary
output is adequate
Extremely elevated bgl drop as the patient is
rehydrated.
Insulin plays a less important role in the
treatment of HHNS because it is not needed
for reversal of acidosis.
70. Cont…
Insulin is usually administered at a continuous low
rate to treat hyperglycemia
Replacement IV fluids with dextrose are
administered when the glucose level is decreased to
the range of 250 to 300 mg/dL
Treatment is continued until metabolic
abnormalities are corrected and neurologic
symptoms clear. It may take 3 to 5 days for
neurologic symptoms to resolve
Treatment of HHNS usually continues well beyond
the time when metabolic abnormalities are
resolved.
71. Long-Term Complications of Diabetes
Steady decline in the number of deaths of
diabetic patients attributable to ketoacidosis
and infection
An alarming rise in the number of deaths
from cardiovascular and renal complications.
Long-term complications are becoming more
common as more people live longer with
diabetes.
The long-term complications of diabetes can
affect almost every organ system of the body.
72. Cont…
The general categories of chronic diabetic
complications are macrovascular disease,
microvascular disease, and neuropathy.
Increased bgl may play a role in neuropathic
disease, microvascular complications, and
risk factor contributing to macrovascular
complications.
HTN may also be a major contributing factor,
especially in macrovascular and
microvascular diseases.
73. Macrovascular complications
Result from changes in the medium to large
blood vessels.
Blood vessel walls thicken, sclerose, and
become occluded by plaque that adheres to
the vessel walls. Eventually, blood flow is
blocked.
Coronary artery disease, cerebrovascular
disease, and peripheral vascular disease are
the three main types of macrovascular
complications that occur more frequently in
the diabetic population.
74. Cont…
Myocardial infarction is twice as common
in diabetic men and three times as
common in diabetic women.
Coronary artery disease may account for 50%
to 60% of all deaths in patients with diabetes.
One unique feature of coronary artery
disease in patients with diabetes is that the
typical ischemic symptoms may be absent.
This lack of ischemic symptoms may be
secondary to autonomic neuropathy .
Cerebral blood vessels are similarly affected
by accelerated atherosclerosis.
75. Cont…
Occlusive changes or the formation of an
embolus elsewhere in the vasculature that
lodges in a cerebral blood vessel can lead to
transient ischemic attacks and strokes.
Atherosclerotic changes in the large blood
vessels of the lower extremities are
responsible for the increased incidence (two
to three times higher than in nondiabetic
people) of occlusive peripheral arterial
disease in patients with diabetes.
76. Signs and symptoms
Diminished peripheral pulses
Intermittent claudication (pain in the
buttock, thigh, or calf during walking).
The severe form of arterial occlusive disease
in the lower extremities is largely responsible
for the increased incidence of gangrene and
subsequent amputation in diabetic patients.
Neuropathy and impairments in wound
healing also play a role in diabetic foot
disease
77. Management
Prevention and treatment of the commonly accepted
risk factors for atherosclerosis.
Diet and exercise are important in managing obesity,
hypertension, and hyperlipidemia.
The use of medications to control hypertension and
hyperlipidemia .
Smoking cessation is essential.
Control of bgl may reduce triglyceride levels and can
significantly reduce the incidence of complications.
78. Cont…
When macrovascular complications do
occur, treatment is the same as with
nondiabetic patients.
In addition, patients may require
increased amounts of insulin or may
need to switch from oral antidiabetic
agents to insulin during illnesses.
79. Microvascular complications
Unique to diabetes
Diabetic microvascular disease is
characterized by capillary basement
membrane thickening.
The basement membrane surrounds the
endothelial cells of the capillary.
Two areas affected by these changes are the
retina and the kidneys.
Diabetic retinopathy is the leading cause of
blindness in both type 1 and type 2 diabetes.
80. Cont…
About one in every four individuals
starting dialysis has diabetic nephropathy.
Retinopathy is caused by changes in the
small blood vessels in the retina, the area
of the eye that receives images and sends
information about the images to the brain.
Retina is richly supplied with blood vessels
of all kinds: small arteries and
veins,arterioles, venules, and capillaries.
81. Cont…
Nearly all patients with type 1 diabetes
and more than 60% of patients with
type 2 diabetes have some degree of
retinopathy after 20 years.
Changes in the microvasculature
include microaneurysms, intraretinal
hemorrhage, hard exudates, and focal
capillary closure.
82. Nephropathy
Renal disease secondary to diabetic
microvascular changes in the kidney, is a
common complication of diabetes.
People with diabetes account for nearly
half of new cases of endstage renal
disease (ESRD) each year and about a
quarter of those requiring dialysis or
transplantation each year.
About 20% -30% of people with type 1
or type 2 diabetes develop nephropathy,
83. Cont…
Patients with type 1 diabetes frequently show
initial signs of renal disease after 10 to 15
years, whereas patients with type 2 diabetes
develop renal disease within 10 years of the
diagnosis of diabetes.
Many patients with type 2 diabetes have had
diabetes for many years before it was
diagnosed and treated. They have evidence of
nephropathy at the time of diagnosis.
• There is no reliable method to predict
whether a person will develop renal disease.
84. Medical Management
To achieving and maintaining near-
normal bgl, management for all patients
with diabetes include careful attention
to the following:
Control of hypertension (use of [ACE]
inhibitors, captopril
Prevention or vigorous treatment of
UTI
Avoidance of nephrotoxic substances
Adjustment of medications as renal
85. Cont…
If the patient has already developed
microalbuminuria and its level exceeds
30 mg/24 hours on two consecutive
tests, an ACE inhibitor should be
prescribed.
Lower BP and reduce microalbuminuria
and therefore protect the kidney.
In chronic or end-stage renal failure:
Hemodialysis and transplantation from
a relative or a cadaver.
86. Diabetic neuropathies
Refers to a group of diseases that affect all
types of nerves, including peripheral
(sensorimotor), autonomic,and spinal
nerves.
The disorders appear to be clinically diverse
and depend on the location of the affected
nerve cells.
The prevalence increases with the age of the
patient and the duration of the disease and
may be as high as 50% in patients who have
87. Cont…
Elevated bgl over a period of years have been
implicated in the etiology of neuropathy.
The pathogenesis of neuropathy may be
attributed to either a vascular or a metabolic
mechanism or both.
Capillary basement membrane thickening
and capillary closure may be present.
Demyelinization of the nerves, which is
thought to be related to hyperglycemia.
Nerve conduction is disrupted when there
are aberrations of the myelin sheaths.
88. Cont…
Control of bgl to normal or near-normal
levels was shown in the study to
decrease the incidence of neuropathy
by 60%.
The two most common types
Sensorimotor polyneuropathy
Autonomic neuropathy.
Cranial mononeuropathies, for example,
those affecting the oculomotor nerve, also
occur in diabetes, especially among the
89. Cont…
Peripheral neuropathy most commonly affects
the distal portions of the nerves, especially the
nerves of the lower extremities.
It affects both sides of the body symmetrically and
may spread in a proximal direction.
Decreased sensations of pain and temperature
place patients at increased risk for injury and
undetected foot infections.
Deformities of the foot may also occur with
neuropathy-related joint changes .
These joint deformities result
90. Autonomic Neuropathies
Results in a broad range of dysfunctions
affecting every organ system of the body.
Three manifestations of autonomic
neuropathy are related to the cardiac, GI, and
renal systems
Cardiovascular symptoms range from fixed,
slightly tachycardic heart rate; orthostatic
hypotension;and silent, or painless,
myocardial ischemia and infarction.
Delayed gastric emptying may occur with the
typical symptoms of early satiety, bloating,
nausea, and vomiting.
91. Cont…
Urinary retention, a decreased sensation of
bladder fullness, and other urinary symptoms
of neurogenic bladder result from autonomic
neuropathy.
Patients with a neurogenic bladder are
predisposed to developing urinary tract
infections due to inability to completely
empty the bladder.
This is especially true in patients with poorly
controlled diabetes, because hyperglycemia
impairs resistance to infection
92. Hypoglycemic unawareness
Autonomic neuropathy of the adrenal medulla is
responsible for diminished or absent adrenergic
symptoms of hypoglycemia.
Patients report that they no longer feel the typical
shakiness, sweating, nervousness, and palpitations
associated with hypoglycemia.
Strict blood glucose monitoring is recommended for
these patients. Their inability to detect and treat
these warning signs of hypoglycemia puts them at
risk for developing dangerously low bgl.
93. Sexual dysfunction
Impotence in men, is a complication of
diabetes
The effects of autonomic neuropathy on
female
sexual functioning are not well documented.
Reduced vaginal lubrication , decreased
libido and lack of orgasm.
Vaginal infection, increased in incidence in
women with diabetes, may be associated
with decreased lubrication and vaginal
itching and tenderness.
