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PANCREAS
FUNCTIONS OF THE PANCREAS
The pancreas has two main
functions namely:
An exocrine function that
helps in digestion and
An endocrine function that
regulates blood sugar
Roles of insulin
Allows the liver to take up and
process glucose, amino acids and
fats
Promote glucose storage: In the
presence of insulin the liver stores
glucose in the form of glycogen
Lowers blood sugar and
increase protein synthesis:
Insulin acts on the receptors on
the surface of cells to allow for
the entry of glucose for
them to be used by the cells and
amino acids to be stored by the
cells
Prevents fat break down
Roles of glucagon
Glycogen in the liver and
muscles is used for energy
Increases lipolysis: Fat cells
release lipids and these are
transported to the liver where
they are metabolised for energy
Increases protein breakdown
Effects of deficiency of insulin
Hyperglycaemia occurs due to
the following:
Effects of deficiency of insulin
Glucose is not taken up from the
portal vein by the liver hence
glucose remains in the general
circulation
Amino acid uptake and synthesis in
muscles is impaired
Glycogenesis (formation of
glycogen from glucose) is inhibited
Owing to cellular starvation the
liver continues to produce glucose
via glycogenolysis
Skeletal muscle and adipose tissue
do not extract glucose from blood
as they normally would hence the
muscle cells metabolise their own
glycogen supply and the break
down protein.
DIABETES MELLITUS
Definition
This is the complex disorder of
carbohydrate, fat and protein
metabolism, that is, primarily a result
of a deficiency or complete lack of
insulin secretion of the beta cells of
the pancreas or defects of insulin
receptors. (Phipps et al. 2003).
A heterogenous group of disorders
of carbohydrates, fat and protein
metabolism charecterised by chronic
hyperglycaemia, degenerative
vascular changes and neuropathy
due to decreased or ineffective
insulin
EPIDEMIOLOGY
According to the International
Diabetic Federation(IDF)
Diabetes mellitus is a serious
condition worldwide.
EPIDEMIOLOGY.CONT
In 2007 it was estimated that 246
million people worldwide had the
condition, with 46% of the affected
being between the age of 40 to 59
years old.
EPIDEMIOLOGYCONT
Type ll diabetes accounts for 85 to
95% of all diabetic cases in
developed countries and accounts
for even higher percentage in
developing countries.
EPIDEMIOLOGYCONT
Its also estimated that 7.3% of
adults 20 to 29 in all countries have
diabetes mellitus, prevalence varies
with race and ethnic background.
Incidence is greater in women than
in men.
classification of diabetes mellitus
Diabetes mellitus is divided into two
categories namely primary and
secondary. Primary implies that no
disease is associated to its occurrence
while in secondary there is a condition
that causes or allows a diabetic
syndrome to develop
Classificationcont
Primary category is subdivided into
insulin dependent diabetes
mellitus (IDDM) or type 1 diabetes
and non insulin dependent
diabetes mellitus (NIDDM) or type
2.
Classificationcont
IDDM in this classification means
that the patient is at risk of
developing ketoacidosis in the
absence of insulin
NIDDM do not develop
ketoacidosis but are at risk of
hyperglycaemia
TYPE I (IDDM)
This type accounts for about 5
to 10 % of all cases. It occurs
twice as frequently in women as
in men. Individuals in this
group are usually non obese.
Pathogenesis
Step 1: genetic susceptibility to
the disease must be present.
The susceptible gene resides on
the sixth chromosome. It is
responsible for making a person
susceptible to autoimmune
disease
Pathogenesis.cont
Step 2: An environmental event
initiates the process in a
genetically susceptible person.
Viral infections of the pancreas
that preceed episodes of:
mumps, hepatitis, congenital
Pathogenesis.cont
rubella, infectious
mononucleosis,
encephalomyocarditis and
coxsackievirus infection.
The virus causes inflammatory
disruption of islets and/or
Pathogenesis.cont
Induce an immune response
Step 3: insulitis occurs due to
the inflammatory response in
the pancreas.
Pathogenesis.cont
The inflammatory process
includes infiltration of the
affected area with activated T
lymphocytes
Step 4: there is activation of
autoimmune response due to
Pathogenesis.cont
Due to increased levels of T
lymphocytes infiltrating the
area in response to a virus.
The beta cells under go an
alteration that allows them to
function in antigen form.
Pathogenesis.cont
The antigen presentation results
in the cells being recognised as
non self or foreign antigens.
Consequently the beta cells are
destroyed and the stimulus to
the immune response disapears
Pathogenesis.cont
Step 6: The Beta cell destruction
usually leading to absolute
insulin deficiency and
The person developing IDDM
with onset of polyuria,
hyperglycaemia & ketoacidosis
Pathogenesis.cont
The onset of the disease is
sudden as the name implies a
person who has this type of
diabetes requires injections of
exogenous (from outside the
body)
Pathogenesis.cont
Insulin to maintain life because
they produce no endogenous
insulin or too little insulin on
their own.
TYPE II (NIDDM)
This type of diabetes accounts for
90% of the total diabetic
population. The individuals with
this type are generally obese.
Pathogenesis.cont
There is a positive history of
NIDDM in the family found on
chromosome 11.
This predisposes the person to
developing islets cells
abnormality
Pathogenesis.cont
The person has two physiologic
defects namely: impaired insulin
secretion and resistance to
insulin action in target tissues.
Acquired insulin resistance may
also occur in obesity
Pathogenesis.cont
The alpha cell population is
increased and the beta cell
population is intact.
This accounts for the excess of
glucagon relative to insulin that
charecterises NIDDM
Pathogenesis.cont
In general NIDDM has a
tendency to develop later in life
than IDDM, and these patients
rarely develop diabetic
ketoacidosis, but they develop
hyperinsulinism as well as
Pathogenesis.cont
requirement for exogenous
insulin to sustain life initially.
Classificationcont
There are schools of thought
who classify Diabetes mellitus
in four types namely:
Insulin dependent Diabetes
mellitus (IDDM)or Juvenile
onset type I,
Classificationcont
Non insulin dependent diabetes
mellitus(NIDDM) TYPE II,
Other specific type III, and
gestational Diabetes mellitus.
OTHER-TYPE III
This type of diabetes involves
individuals with diabetes mellitus
associated with the other identified
causes including pancreatic disease,
hormonal disorders (Cushings
syndrome) drug or chemical causes,
insulin receptor abnormalities and
certain genetic syndromes.
OTHER-TYPE III/Secondary forms
Type 111 or Secondary forms of
diabetes mellitus includes a lot
of conditions namely:
Classificationcont
Pancreatic disease particularly
chronic pancreatitis in
alcoholism. The cause is
destruction of the beta cells
Classificationcont
Hormonal abnormalities (due
to impairment of insulin release
and induction of insulin
resistance):
they include
pheochromocytoma,
acromegaly, Cushing's
syndrome and therapeutic
administration of hormones
Stress hyperglycaemia, this is
associated with burns or burns
Acute myocardial infarctions and
other life threatening illnesses:
due to endogenous release of
glucagon and catecholamines
Drugs: a number drugs can lead
to hyperglycaemia though most
drugs cause impaired glucose
intolerance
Genetic syndromes: are
associated with impaired glucose
tolerance or hyperglycaemia
GESTATIONAL DIABETES MELLITUS
Gestational diabetes is any
degree of glucose intolerance
with onset during pregnancy.
GESTATIONALCONT
Hyperglyceamia develops during
pregnancy because of the
secretion of placental hormones
which causes insulin rsistance.
It results from the following:
GESTATIONALCONT
An unidentified pre existing
disease.
The unmasking of a
compensated metabolic
abnormality by the added stress
of pregnancy.
GESTATIONALCONT
A direct consequence of the
altered maternal metabolism
stemming from changing
hormonal levels.
AETIOLOGY OF DIABETES
MELLITUS
The exact cause of diabetes
mellitus is idiopathic .At least
four factors influence the
development of D.M and these
include the following:
AETIOLOGYCONT
Genetic factors
Immunological factors
Microbiological factors
Metabolic factors
Genetic factors
The clients with a family history
of diabetes are at risk of
developing diabetes especially
NIDDM .
Genetic factors..cont
Diabetes mellitus runs in family
even though research has not
yet pinpointed the responsible
gene.
Offspring of diabetic
pregnancies are at risk
Immunological factors
In IDDM there is evidence of an
autoimmune response, this is an
abnormal response in which
antibodies are directed against
normal tissue of the body
responding to these tissues as if
they are foreign.
Microbiological factors
Infectious agents like viruses
predispose individuals to
diabetes, especially IDDM
resulting from dysfunctioning
of beta cells, for example
Coxsackie virus, mumps, rubella
Microbiological factorscont
Viral infection can and often
attack the pancreas, and many
viral infections are
characterized by the
inflammation of pancreatic beta
cells.
Metabolic factors
Factors involved are many and
complex in the etiology of the
disease, emotional or physical
stress can un mask an inherited
predisposition to diabetes,
Metabolic factors..cont
probably as a result of
gluconeogenesis induced by
increased production of
hormones from the adrenal
cortex especially glucocorticoid
Risk factors
Sedentary life style: lack of
exercise
Diet: high saturated fat intake
risk impaired glucose tolerance
and higher fasting glucose and
insulin levels
Higher levels of unsaturated
fatty acids in serum lipid or
muscle phospholipid have been
associated with fasting insulin,
lower insulin sensitivity and a
higher risk of type 2 diabetes.
Dietary fiber: high intakes of
dietary fiber results in reduced
blood glucose and insulin levels,
and impaired glucose tolerance
Malnutrition: PEM in early
infancy and childhood may
result in partial failure of beta
cell function
Alcohol: Excessive alcohol
damages pancreas and liver by
causing obesity.
Obesity may reduce insulin
receptors on target cells
Central obesity is a risk factor as
it causes insulin intolerance
CLINICAL MANIFESTATIONS
There are four cardinal signs
and symptoms of DM which are
related to hyperglycaemia
The first event may be an acute
metabolic decompensation
resulting in diabetic coma.
Glycosuria
Blood glucose level reaches a
threshold of 180mg/dl in normal
kidney, exceeding the capacity of
the renal tubules to reabsorb it
from the glomerular filtrate.
Since the kidney fail to keep up
with reabsorption glucose is lost in
urine and it attracts water osmotic
diuresis resulting in polyuria
Polyuria
Polyuria increased urination
leading to excess loss of fluid
and electrolytes particularly
sodium chloride, potassium and
phosphate associated with
osmotic diuresis.
Polydipsia
Polydipsia occurs as a result of
excess loss of fluid associated
with osmotic diuresis to try and
compensate with increased
urine output.
Polyphagia
Polyphagia (excessive hunger)
is caused by tissue loss and a
state of starvation which result
from the inability of the cells to
utilize the blood glucose.
Weight loss
Weight loss is seen in IDDM
type I, its due to the use of fat
and proteins for energy, thereby
causing muscle wasting.
Fatigue and weakness
It is due failure to utilise glucose for
energy
This is due to muscle wasting
caused by fat and protein
mobilisation for energy.
Pruritus of the vulva
Fungi thrive on glucose deposits
from urine on the female genitalia.
The vulva becomes swollen and
inflamed
Other symptoms
Sudden vision changes
Dry skin
Tingling or numbness in hands
or feet.
Skin lesion
Recurrent fungal infection
CHRONIC COMPLICATIONS:
MACRO VASCULAR
Atherosclerosis: there is
tendency to develop atheroma in
young age and with both types of
diabetes. This is because of
elevated blood lipids and clotting
factors. Blood platelets tend to be
Stickier and platelet
aggregation is often increased
Obesity, smoking and
hypertension increase the risk
Heart disease
Cardiomyopathy
Coronary artery disease
Stroke
Hypertension
Congestive cardiac failure.
MICRO VASCULAR
i)Eye
Diabetic retinopathy: results
from changes in the small blood
vessels of retina causing
oedema, bleeding and exudates
and resulting in visual loss
cataracts and glaucoma may
also occur and result in blind
ii)Kidney
Diabetic nephropathy
Renal failure occurs due to renal
function impairment
Nervous system
Diabetic neuropathy:
accumulation of metabolites
of glucose leads osmotic
swelling and subsequent
damage to the Schwann cells
results in demyelination of some
nerve areas and impairs conduction
of nerve impulses causing the
following conditions:
Peripheral neuropathies, poly and
mono neuropathy, autonomic
neuropathy
Muscle
Diabetic myonecrosis
muscle wasting.
Diabetic foot
Diabetic foot is often due to a
combination of sensory
neuropathy(numbness)and
vascular damage. It increases
the rate of skin ulcers and
infection, in serious cases
necrosis and gangrene.
Diabetic gangrene
Diabetic gangrene is death of
tissue due to long standing
effects of diabetes.
Medical management:
Investigations
History of diabetes in the
family and clinical features.
History of clinical features of
diabetes: polyuria, polydipsia
and polyphagia
Investigations.cont
Random blood sugar: Readings
above 10mmol/l with presence
of any classic symptoms is
indicative of diabetes.
Oral glucose tolerance test:
(<7.8mmol/l)
Investigations.cont
Fasting blood sugar: 3.9 -
6.1mmol/l
Urine: ketone levels and
glucose levels raised
Postprandial blood glucose:
28mmol/l
Investigations.cont
Blood for serum lipids:
triglycerides greater than
200mg/dl
Haemoglobin
Oral Hypoglycemic
Some clients with NIDDM may
require oral hypoglycemic
agents for lowering blood
glucose levels, these drugs lower
the blood sugar by stimulating
the pancreatic beta cells to
release insulin.
a).sulfonylurea
These are mostly used; they act
mainly by augmenting insulin
secretion and consequently are
effective only when some
residual pancreatic beta cell
activity is present, during
Sulfonylureacont
long term administration they
also have an extra pancreatic
action
Chloprapamide
It stimulates insulin release
from pancreatic beta cells and
reduces glucose output by the
liver. It also exerts an
antidiuretic effect in client with
diabetes insipidus.
b).Biguanide
Metformin Hydrochloride
It is the only biguanide available
with a different mode of action
from the sulfonylureas, and is
not interchangeable with them.
Biguanide..cont
It decreases intestinal absorption
of glucose and improves insulin
sensitivity (glucose uptake and
utilization).
INSULIN THERAPY
In type I diabetes mellitus the
pancreas cannot produce insulin,
so insulin must be replaced daily
for survival.
INSULIN THERAPY..cont
Insulin promotes the transport
of glucose into the cell.
It inhibits the conversion of
glucose and amino acids into
glucose.
Types of insulin
Short- acting insulin
Intermediate acting insulin
Long acting insulin
Route of administration
Insulin is injected under the
skin into the fat layer, usually in
the arm, thigh or abdominal
wall. Small syringes with very
thin needles make the injection
nearly painless.
Route of administrationcont
It can also be given IV/IM for
severe ketoacidosis or diabetic
coma.
Insulin in cells
Transports and metabolizes
glucose for energy
Stimulates storage of glucose in
the liver and muscle(in form of
glycogen)
Insulin in cells.cont
Signals the liver to stop the
release of glucose.
Enhances storage of dietary fats.
ACUTE COMPLICATIONS
There are two acute
complications namely
hypoglycaemia and
hyperglycaemia.
Hypoglycemic coma
Its abnormally low blood
glucose level to less than 50 to
60mg/dl. It can be caused by
too much insulin or too little
food or excessive physical
activity
Fasting blood glucose is lower
than 3.5 mmol/l
Symptoms of hypoglycaemia
mostly occur when blood
glucose level falls 3mmol/l
Aetiology
There are 3 main causes of
hypoglycaemia namely:
Excessive dose of insulin (high
dose, wrong type) or oral
hypoglycaemic agents or
prolonged action of these drugs
Too little food intake (delayed or
skipped meal), delayed gastric
emptying, vomiting or diarrhoea
Excessive (or unusual) exercise or
activity in relation to food intake
and insulin or oral hypoglycemic
agent doses
Other causes
Kidney disease
Liver disease
Ingestion of alcohol particularly
when hungry
Stress such as hypothermia
Clinical features
Increased sympathetic nervous
system activity resulting in the
following:
Perspiration, nervousness,
weakness, pallor, pilo-erection,
Tachycardia (full bounding
pulse), palpitation,
Hunger pangs,
Trembling butter flies in the
stomach and irritability
Deprivation of the CNS of glucose
causing the following:
Convulsions, headache, blurred
vision, diplopia, impotence
Fatigue, numbness of lips, tongue
Emotional changes, incoherent
speech, mental confusion
Coma
Deprivation of the CNS of glucose
causing the following:
If hypoglycaemia occurs during the
night particularly in those on
multi-dose insulin regimens the
only symptoms that may occur will
be: nightmares, sweating and
headache on rising
Management of hypoglycaemia
Investigations
Blood glucose test
Treatment
When symptoms subside
give a snack: complex
carbohydrate and protein or
if the next meal is soon due
give it instead of a snack
Intravenous infusion commenced
and give 50% dextrose if patient is
unconscious
Injection Glucagon im/iv given to
mobilise the liver convert glycogen
to glucose
Glucocorticoids to promote
gluconeogenesis
Oxygen therapy as hypoglycaemia
interferes with oxygen
consumption of nervous tissue
Admit if on oral hypoglycaemics
or unconscious
NURSING MANAGEMENT
Environment
Barrier nurse as they are
susceptible to infection.
Isolate to prevent infection
Practice scrupulous hand
washing at critical times
Resuscitation
Nil orally
Insert cannula for drugs
Give injection glucagon 1mg
subcutaneously if not available
50% dextrose 30-50ml, iv slowly
in 10-15 minutes
10-20% dextrose 1 liter will be
commenced
Catheterise the patient
If patient is too drowsy to eat or
drink: give injection glucagon
1mg subcutaneously or
intramuscularly to raise blood
glucose levels
The conscious patient: give
rapidly absorbed glucose with a
more gradually absorbed form
of carbohydrate.
For instance, dextrose sweets/gel
tablets followed by a glass of
milk or fruit juice and a biscuit
or sandwich
If a meal has been skipped it
should be taken
Observations
Two hourly measurement of
capillary blood glucose to
monitor the condition
Glasgow coma scale to monitor
patients conscious levels
Urinalysis hourly
Position
Recovery position till
consciousness is regained
Hygiene
Daily bath
Oral care 6 hourly
Regular evaluation of feet and
teeth to prevent/ detect
complications
Hyperglycemic coma/Diabetic
ketoacidosis (DKA)
This is an elevated blood
glucose level to more than
6.6mmol/l due to failure of
transportation of glucose due to
lack of insulin.
Pathophysiology
Accelerated glucogenesis and
glycogenolysis cause
hyperglycaemia, which in turn
results in osmotic diuresis,
electrolyte disruption and
dehydration
Increased fat breakdown
(lipolysis) results in the
formation of ketone bodies
which are weak acids and
cause metabolic acidosis
Management: investigations
To monitor dehydration: check
blood urea, electrolytes and
plasma osmolality 2hourly
To monitor acidosis: check arterial
or venous blood gases and
hydrogen ion concentration 2hrly
Venous blood glucose
Plasma potassium measured
2hourly
Catheter specimen of urine
Throat swab and sputum
urea, electrolytes to monitor
Ketosis and renal function.
To detect underlying infection:
Chest x-ray
Blood culture
Treatment
Broad spectrum antibiotics
Anticoagulants: heparin 5000 iu
subcutaneous, BD
Rapid acting insulin is
administered to lower blood
glucose
Nursing care
Nursing management is
aimed at preventing and
decreasing infection,
improving fluid status,
promoting adequate
nutrition, decreasing fatigue
Resuscitation
Artificial airway inserted and
connected to ventilator
Oxygen therapy administered in
accordance with blood gas
analysis
Orapharyngeal suction prn
Rehydration
Hourly urinalysis to check for
glucose, ketones proteins, and
amount
Continuously monitor colour
Monitor neurological status
hourly
Intravenous infusion: 0.9%
sodium chloride one to two
liters given over the first hour
and then one liter for 2-5
hours
If blood glucose falls below
15mmol/l replace normal
saline with 5-10% dextrose
Electrolytes replacement
Hyperkalemia in early stages
due to severe acidosis.
Administer insulin and
rehydrate the patient
Hypokalemia: 10-30mmol/hr of
intravenous potassium chloride
Maintenance of temperature
Patient has hypothermia due to
vasodilatory response to
acidosis hence:
Space blanket to warm patient
Switch on a heater
Avoid unnecessary exposure
Observations
Glasgow coma scale:
Vital signs hourly to monitor
persistent hypovolaemic shock
Fluid balance chart to prevent
fluid overload
ECG monitoring on vent to
detect hypo and hyperkalaemia
Hypoglyceamic coma Hyperglycaemic coma