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DIABETES

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

Insulin dependant or IDDM


NIDDM
Comparison
Ketones are normal
Hyper..and Hyper
Ketones elevated
Excessive insulin Skipping insulin dose
Blood glucose Blood glucose
less(<3.3mmol/l) elevated(>6.7mmol/l)
Onset symptoms Onset of symptoms slow
rapid Treatment:insulin,IV
Treatment:candy,50% fluids.
Dextrose(this table
needs to be verified)
Nutrition
Imbalanced nutrition less than
body requirement related to
hyper metabolic state due
inadequate food intake, weight
loss, weakness and increased
ketones.
Individualised meal plan to
control weight, glucose and lipids
Modest CHO,
Protein double the amount
needed
Alternative sweeteners
Omega-3 fatty acids is given to
offer some protection against
type 1 diabetes.
Rest
Procedures done in blocks to
provide periods of rest
Bed should be clean and crease
free
Hygiene
Daily bed bath
Oral care 2 hourly to prevent
oral infection particularly gum
infections
Lubricate lips after oral care
Clean nostrils and lubricate
them
Keep hair groomed
Infection prevention
Risk of infection related to high
glucose levels in body tissues
that attract microorganisms.
Psychological care
Fear of managing medication
and hypoglyceamia counsel
patient and facilitate learning
Provide brief clear explanations
about what to do in case of
hypoglycaemia
Psychological carecont
Counsel the patient to assist
him/her grieve and adapt to
living with a chronic disease
Assist the individual to cope
with the new disease.
Elimination
Nasogastric tube passed in all
drowsy and unconscious
patients to prevent aspiration
Catheterised and urine bag
emptied hourly
Drugs
Administer fast acting insulin
intravenously by pump
Monitor capillary blood glucose
hourly to check if it is returning
to within normal range
PATIENT TEACHING
Life style modification Some of
changes that need to be done are:
Smoking
Alcohol intake
Dietary control
Exercise
TEACHINGCONT
Care of skin and feet
Eye care
Screening
Treatment teach patient on urine
testing.
Insulin administration
As soon as the need for insulin has
been established, the patient should be
instructed on the technique of self
injection.Insulin is injected in four
main area which are the abdomen,
upper arm(lateral
aspect),thighs(anterior and lateral
surface).
TEACHINGCONT
All the requirements for insulin
administration should be assembled
when teaching about insulin
administration.
After preparation of insulin, the patient
should be instructed on the method of
administration.
TEACHING CONT
Diabetic Association The patient
should join diabetic Association so that
they can gain additional information
from the fellow patient and counselor.
Signs of complication
Identification
Control of Diabetes at home
TEACHINGCONT
Community collaboration and support
groups
Nursing of diabetic clients is not the
responsibility of the Hospital health care
workers alone. The care needs community
collaboration and various support groups.
The patients themselves need to be
involved in their own self care.
Prevention
Maintenance of normal body
weight through regular physical
exercise and
Health nutrition habits which
include adequate protein intake,
high fibre intake, and avoidance of
sweet foods
Prevention of hyperglycaemic
states
Once the crisis has passed with
the patient identify the events
that led to the crisis and analyse
where action might have been
taken to avert the crisis or
obtain help at an earlier stage
Avoid over nutrition and obesity
Avoid excessive alcohol intake
Avoid diabetogenic drugs like
oral contraceptives
Reduce factors that promote
artherosclerosis for instance
smoking, high blood pressure,
elevated cholesterol and high
triglyceride levels
Mass education and screening
For early detection of the
condition to prevent its
complications
Diabetes insipidus
Clinical features
Deficiency of ADH leads to:
polyuria, nocturia and plasma
osmolarity
Polydipsia
Dehydration due to urinary out
put of 15 or more liters/day
Management: investigations
Urinalysis: urine will be dilute
Plasma osmolality will show
high concentration (normal
plasma osmolality is 285-295
mmol/kg)
Treatment
Synthetic vasopressin 10-20mg
TDS, subcutaneous or
intamuscular or intranasal
REFERENCES
Haist A.S.Robbins,B.J (2005),Internal medicine on
call,Fourth Edition,Sydney.Toronto.
Lemone P.& Burke c.(2004)Medical surgical
nursing,critical thinking in client care,third
Edition,NewJersey
Gulanick.H.Myers G.(2007),nursing care
plans,nursing diagnosis and Interventions.sixth
Edition,Loius.Missouri.
Polaski A.L.& Tatro S.E.(1996),Medical surgical
nursing,Saunders company.philadelphia,London.
THANK YOU
FOR YOUR
ATTENTION.
Thyrotoxicosis
Thyrotoxicosis is a syndrome
that can originate in a variety of
ways that include the following:
Thyrotoxicosis is a
hypermetabolic state caused by
elevated circulating levels of
free T3 and T4
1. Disorders associated with
thyroid hyperfunction:
Excess production with thyroid
hyperfunction
Abnormal thyroid autonomy:
graves disease and
trophoblastic tumor
Intrisic thyroid autonomy:
hyperfunctioning adenoma and
toxic multinodular goiter
11. Disorders not associated
with thyroid hyperfunction:
Disorders of hormone storage:
subacute thyroiditis and chronic
thyroiditis with transient
thyrotoxicosis
Extra thyroid source of hormone
Thyrotoxicosis factitia
Ectopic thyroid tissue: struma
ovarii and functioning follicular
carcinoma
Complications
Cardiac disease:
hypermetabolism of the tissues
increases both metabolic and
non metabolic circulatory
overload
Effects of thyroid hormone on
the myocardium include
increase in force, velocity and
rate of ventricular contraction
As a result there is increased
cardiac work and output
There is also enhancement of
atrial irritability leading to
atrial fibrillation
Treatment: iodine and large
doses of digitalis
Thyrotoxicosis crisis or storm
This causes a fulminating
increase in the signs and
symptoms of thyrotoxicosis
Treatment:
Iodine and humidified oxygen
Chronic hyperthyroidism result
in osteoporosis and a high risk
of fractures
Hepatomegally due to fatty
changes in the hepatocytes
Clinical features: skin
Excessive levels of thyroid
hormone result in an increase in
the basal metabolic rate.
Skin is soft, warm and flushed
due to increased blood flow and
peripheral vaso dilation
Excessive sweating due to
higher levels of calorigenesis
Increased basal metabolic rate
also result in weight loss despite
increased appetite
Heat intolerance
Increased blood flow and
peripheral vasodilation may also
result in fever
Cardiac manifestations
Increased cardiac output owing
to increased contractility and
increased peripheral oxygen
requirements this may lead to:
Tachycardia, palpitations and
cardiomegally
Neuromuscular system
Over activity of the sympathetic
nervous system produces
tremor, hyperactivity,
nervousness, emotional lability,
inability to concentrate,
insomnia
The thyroid gland producing
too much thyroxine lead to
proximal muscle weakness with
decreased muscle mass or
muscle wasting especially in
shoulders and hips (thyroid
myopathy)
Ocular changes
Wide, staring gaze and lid lag
due to sympathetic
overstimulation of the levator
palpebrae superioris
Gastrointestinal system
Sympathetic hyperstimulation
of the gastrointestinal tract
result in hypermotility,
malarbsorption, hyperfeacation
or diarrhoea
Skeletal system
Thyroid hormone stimulates
bone resoption resulting in
corticol bone becoming
exceedingly porous reduction in
volume of trabecular bone
Management: investigations
Laboratory tests: TSH
Ultra sound
Treatment
Radioactive iodine
Anxious, restless and fidgety
Skin is warm and moist with a
velvety texture
Plummers nail: separation of
finger nail from nail bed
Fine and silky hair
A fine tremour of the fingers
and tongue with hyperreflexia
Oligomenorrhea and
amenorrhea in premenopausal
women
Sympathetic overstimulation will
result in the following ocular
signs:
Stare with widened palpebral
fissures
Infrequent blinking
Lid lag and
Failure to wrinkle the brow on
upward gaze
Cardiovascular findings include:
A wide pulse pressure
Sinus tachycardia
Atrial arrhythmias
Systolic murmurs
HIV
Virus properties
Acellular: do not have
recognisable cellular organelles
Smaller in size than bacteria
Metabolically innate: cannot
carry out metabolism on their
own but they need to enter a
living cell to be functional and
multiply
Genome: have genes
Has a protein coat called capsid
surrounding nucleic acid
Capsid
Help virus move from one cell to
another
Protects the fragile genome
Give virus a structure
Protein in the genome give virus
antigenic properties
Retrovirus
These viruses replicate in a
unique way called reverse
transcription that is why they
are called retroviridae.
The virus that cause AIDS is a
member of this family
Lenti viruses are the HIV 1 and
HIV 2 viruses.
Their unique features are that
they become latent in cells of
macrophage lineage
HIV 1 and HIV 2
Have diploid RNA genome and
it is the only virus with two
molecules
The genes found on the genome
are 3 main ones namely gag, pol
and env
Gag: encodes proteins on the
nucleocapsid
Pol: encodes enzymes
replication
Env: encodes glycoproteins
envelope
On each molecule of RNA at
each end you find a long
terminal repeat called LTR
important for integration
The capsid can have different
shapes
HIV is enclosed in an envelope
that has glycoprotein spikes
Most important is gp120 and gp
141 these have a role of entry
into target cell
Replication
Attachment protein gp120 binds
to receptor molecules on target
cell T helper cell, CD4, or
macrophage
They bind to chemokine
receptors
Different strains bind to
different receptors
Fast strains like HIV 1 type c,
bind to CXCR4 on T cells hence
monocytes/macrophages are
not infected
Slow strains bind to CCR5 and
tend to attack macrophages
rather than T cells
Gp141 mediates fusion of the
virus with target cell membrane
then nucleo capsid enters
Production of virus components
RNA is released in the cell
Once internalised enzyme called
reverse transcriptase change
genome RNA to double stranded
cDNA (proviral DNA) remain in
cytoplasm in quiet T cells
In dividing T cells the cDNA
circularises, enters the nucleus
and is integrated into host
genome. This means that the
viral genome RNA is inserted in
the host DNA hence the human
chromosomes found in target
cell become part of the virus
and may be locked in their for
months or years
This is known as provirus state.
The virus can be in this state
quietly resting for a long time.
When activated the provirus
DNA replicate and is
transcribed into RNA which has
two functions
Functions of the RNA
Serve as messenger RNA which
will be translated into structural
proteins
A new genome to form a new
virus
The new virus is then released
by process called budding
Budding involves taking a piece
of host cell plasma membrane
to escape to the environment
Pathogenesis
Target cells are lymphocytes
particularly the T cells and
monocytes (macrophages,
dendritic cells)
These cells are directly infected or
the Langerhans cells carry the
virus to them
Hence, first cells infected are the
macrophages in genital epithelial
or the T cells (CD4) and
macrophage in blood
Fluid drainage carry the infected
cells to the local lymph nodes and
spleen
Viral replication in lymph nodes
occurs at a fast rate and wide
spread seeding of lymphoid
tissue causing a viral spike in
blood termed viraemia. Immune
system contain situation and
patient goes in clinical latency
Transmission
Sexual contact
Parenteral inoculation
Passage of the virus from
infected mother to their fetus or
newborns
Mechanisms of immune
suppression
Continuous infection of T cells
and viral replication is the
major mechanism by which
viral causes lysis of CD4 cells.
However in the early course of
HIV infection the immune
System manages to replace the
dying cells hence rate of cell loss
is masked.
Eventually the replacement fails
to match the massive T cell loss
from the peripheral blood
The colonisation of lymphoid
organs (lymph nodes, tonsils and
spleen) by HIV in early stage turns
them into reservoirs of infected
cells.
Also destroys the lymphoid tissue
Reverse transcription can be
toxic and cause cell death
Autoimmune destruction of T
cells coated with gp120 from
infected cells
Loss of immature precursors of
T cells by infection of thymic
progenitor cells (since after T
cells are formed in bone marrow
they migrate to the cortex of the
thymus to undergo maturation in
an antigen-free environment for
about one week) or
by infection of accessory cells
that secrete cytokines essential
for T cell maturation
Hence virus inhibition of
cytokine expression and
immune system not functioning
properly
Disruption of Ag presentation
or mutation of virus
Infected and non infected cells
may fuse and form giant cells
The fused cells form a big
balloon up and die within few
hours
Clinical picture
Clinical course of the disease is
very long
Acute infection Sero conversion
illness
Occurs 6 weeks after infection
and patients presents with:
Fever
Sore throat
Lymphadenopathy
These resolve spontaneously
hence this stage can be missed
Clinical latency
Varies in length that is few
months to many years
Patient will be symptomless
although the virus is not
completely sleeping as it is in
provirus state
Clinical stage
The virus is active and
replicating and spreading in
both T cells and macrophages
Gradual erosion of CD4 cells
lead to decline of CD4 cells and
patient develops symptoms.
WHO staging used to find out
the presenting stage and to
monitor the patient who is ART
Principles of ARV therapy
Taking Antiretroviral (ARV)
therapy requires long term
commitment from the patient
Correct and consistent use is
required for the drugs to be
effective
Antiretroviral therapy should be
initiated at an opportune time:
Treating too early may lead to
unnecessary toxicity and
premature development of drug
resistance
Treating too late can increase the
risk of morbidity, mortality and
treatment failure
Use of combinations of three
ARV drugs
Maximise adherence to the ARV
regimen
Rational sequencing of ARV
drugs
Avoiding resistance
Five goals of ART
Reduce the amount of HIV
viruses in the body
Support and help the immune
system
Improve quality of life
Reduce HIV related illness and
deaths
Reduce risk of HIV transmission
to others
Prerequisites for administration of
ARV therapy
Appropriate drugs are available
Drug supply can be sustained
Basic clinical and laboratory
measures are used to determine
need for treatment
The patient understands the
importance of near perfect
adherence
Health care providers have been
trained in the use of ARV
therapy
Diagnosing HIV
Antibody detection tests
Abbot Determine
If positive confirm: Unigold
If unigold negative break tie:
Biolin
Patients readiness to start ARV
Stage of the disease
Likelihood of adequate
adherence
Ability of the patient to return
for regular and reliable follow
up and consistently get drugs
Baseline: clinical
ART history, current medication
Counseling and education
Risk reduction
Adherence
Complaints, fears, new illness
and urinalysis for protein
Laboratory
Creatinine
ALT/AST
Haemoglobin
CD4
Blood glucose, cholesterol,
triglycerides
Other labs
Blood for RPR (repeat yearly)
Hepatitis
PAP smear or cervical cancer
screening
Pregnancy test
Adherence counseling: purpose
To educate and counsel patients
eligible to ART about HIV
disease and ART
To asses the patients readiness
to start ART and adhere to the
prescribed medication regimen
To identify patient needs for
additional medical and support
services.
NB: adherence counseling should be
recorded on the adherence forms
and attached to the patients file
First adherence session
Patients knowledge assessed
Educate on HIV and correct
misconceptions
Second adherence session
Assess patients knowledge of
HIV and goals of ART and
Cotrimoxazole prophylaxis
With the patient identify any
difficulties and potential
barriers to keeping medical
appointments, taking the
medications, and adhering to
the medications
Review the patients medication
regimen, including:
Schedule of each medication
Dose of each medication
Stress the importance of 100%
medication adherence
Explore ways of living positively,
the importance of a positive
attitude, social support, healthy
food and spiritual aid
Identify need (the patients and
the households) that have not
been addressed before, provide
referrals to appropriate services
Discuss ongoing prevention,
including specific strategies to
prevent transmission of the
virus to sexual partner(s) and
possible reinfection
Identify the patients needs for
other services, including
nutrition, housing, couples
counseling and legal aid, with
the patients consent, make
appropriate referrals
Schedule an appointment for
the third counselling session,
two weeks from the first session,
preferably to include a family
member or friend to whom the
patient has disclosed her/his
HIV status and who will agree to
attend the remaining
counseling sessions
Direct the patient to the
laboratory for baseline
laboratory tests as ordered, and
to the pharmacy for dispensing
of medications including CTX
Third counseling session
Assess patients knowledge of
HIV
The goals of CTX prophylaxis,
review importance of
medication adherence
With the patient identify any
difficulties and potential
barriers to keeping medical
appointments, taking
medications and adhering to
the medications
Review the patients CTX
schedule including:
Time taking CTX
Dose of CTX
Stress the importance of 100%
medication adherence (CTX
prophylaxis prepares patient for
ART)
Discuss possible side effect:
Which side effects to report to
health staff immediately
Which side effects can be
managed at home and how to
do so
To continue taking medications
despite side effects
Explore ways of living positively,
the importance of a positive
attitude, social support, health
food and spiritual aid
Identify needs (patients and
the households) that have not
been addressed before, provide
referrals to appropriate services
Discuss ongoing prevention,
including specific strategies to
prevent transmission of the
virus to sexual partner(s) and
possible reinfection
Identify the patients needs for
other services, including
nutrition, housing, couples
counseling and legal aid, with
the patients consent, make
appropriate referrals
Direct the patient to the
laboratory for baseline
laboratory tests as ordered, and
to the pharmacy for dispensing
of medications including CTX
Subsequent adherence counseling
Review the previous counseling
session and answer patients
questions
Discuss the role of the family
member/friend regarding social
support and ART adherence
Obtain commitment from the
patient and family member/
friend to ART,
Discuss that ART is not a cure
and does not prevent
transmission of the virus,
ongoing prevention is essential
Discuss benefits, risks, and side
effects of ARVS
Jointly develop strategies that
will help the patient adhere to
the ARV regimen
Schedule an appointment for
the next counselling session on
the day of the next visit to the
MO to begin ART
Direct the patient to the
laboratory for baseline
laboratory tests as ordered, and
to the pharmacy for dispensing
of medications
Deferral
A patient with an acute/severe
opportunistic infection should
be treated before starting ART
A patient who is not ready to
begin ART or is unwilling to
adhere come for follow up
Exclusion criteria
Severe or end stage liver failure
Severe or end stage renal failure
Severe cardiomyopathy or
advanced stage cardiac disease
Urgent ART initiation
The patient has been assesses to
be in WHO stage 3 and 4 and
has been treated for Ois
The patient has no acute
condition requiring immediate
treatment
Drug selection to initiate therapy
When deciding to initiate
therapy consider the following:
Potential for serious adverse
effects and toxicity
Side effects and tolerability
Cost and availability
Considerations for drug selection
Effectiveness of regimen
Convenience: number of pills,
dosing frequency, food and
refrigeration requirements
Considerations for drug selection
Potential for interaction with
other drugs
Potential for treatment options,
should the initial drug
combination fail
Presence of other illness
Considerations for drug selection
Presence of pregnancy or the
risk of becoming pregnant
Presence of tuberculosis and
other illness
Rationale for new regimens
Ability to lower viral loads to
undetectable levels
Ability to raise CD4 count
Less risk for serious adverse
effects and toxicity
Fewer side effects and
intolerability
More treatment options should
the initial drug combination fail
Recommended for initial therapy
First line regimen include two
NRTIs + an NNRTI
First line recommendations are
for individuals who are nave
Fixed dose combinations have
less pills hence lead to better
adherence
Monitoring and follow up
The purpose is to:
Assess the effectiveness of
therapy
Evaluate potential side effects
Assess and reinforce adherence
Evaluate for the development of
other HIV related illness
Minimum clinical assessment
Signs and symptoms of possible
drug toxicity
Assessment of adherence
Assessment of response to
therapy
Weight and basic labs
Return visits
1st visit at 2 weeks after ART
2 nd
visit at 4weeks
Monthly visits for 2months
3 monthly till stable
6 monthly when stable
During return visits
Make any necessary changes to
the plan of care
Provide more ARVs
Care for side effects or concerns
Provide care and support
Assess for opportunistic
infections or
Need for referral
Assess and reinforce adherence
Show empathy
Ask patient to bring remaining
drugs
Ask patient to show you which
pills they take and at what times
during the day
Ask patients to tell you how
they take their pills and what
they eat, starting in morning of
a typical day
Assess effectiveness
Assess success of therapy by
assessing the following
CD4
Viral load
Ask the following:
Has patient gained weight
Is patient able to do more daily
tasks
Does patient feel better
Has not developed
opportunistic infection
If patient is not responding you
may need to change the
regiment when:
Patient was taking the drugs
Patient was adhering to the
drug regimen
IRIS
At 2-12weeks of therapy patient
may become sicker for a short
time as their immune system
improves that is immune
reconstitution syndrome (IRIS)
IRIS is an exaggerated
inflammatory reaction from a
re-invigorated immune system
presenting as:
unmasking of previously sub-
clinical opportunistic infections
Clinical deterioration of pre-
existing opportunistic
infections OR
Development of autoimmune
disease
Risk factors
Initiating ART close to
diagnosis of an OI
Initiating ART when CD4 is less
than 50 cells/mm3
Rapid fall in HIV-1 RNA level in
response to ART in low CD4
IRIS management
If ART continuation is
impossible, temporarily
interrupt ART and restart same
regimen after OI or
inflammatory condition is
treated
Corticosteroid in moderate and
severe cases: prednisolone
0.5mg/kg/day for 5-10 days
Indications for changing treatment
Intolerance or unresolved and
prolonged side effects
Failure: clinical, immunologic
or virologic
Toxicity such as anaemia or
peripheral neuropathy
Poor adherence: to simplify
dosing schedule to improve
adherence
Occurrence of an active TB and
possibility of rifampicin
interaction
Occurrency of pregnancy: if the
regimen has EFV
Treatment failure
There are three types of
treatment failure namely
Virological failure
Immunologic failure
And then clinical failure
Factors leading to treatment
failure
Poor adherence to treatment
Prior exposure to ART with
development of resistance
Primary viral resistance
(infected with resistant strain of
HIV)
Inadequate drug absorption
Suboptimal dosing (for instance
sharing drugs, cutting dose
because of side effects, drug
interaction with rifampicin
Inadequate/inconsistent supply
Virologic failure
After 6 months of therapy
plasma HIV viral load >400
copies/ml
Repeat viral loads performed to
confirm the failure
When viral load is undetectable
in a patient with treatment
failure consider undiagnosed OI
or other concomitant illness
Viral load monitoring
One of the goals of HAART is to
suppress the viral load below
the level of detection, and
durable viral suppression is
highly associated with long
term treatment success
Viral load testing measures the
number of HIV viral copies
present in sample of blood
Virologic treatment failure is the
earliest sign of eventual
immunologic and clinical failure
Immunologic and clinical
markers are the primary means
for determining treatment
failure in patients on the first
line regimens that include TDF
and ABC
Immunologic failure
A fall of 50% of CD4 count from
the peak value on treatment OR
A decline to pre-therapy baseline
or below OR
Persistent CD4 levels below 50
cells/mm3 after 12 months on ART
If CD4 increase is less than 50 at
6 months review consider
treatment failure though in
advanced disease it may take
longer to see immunologic
improvement
Total lymphocyte count has
been shown to be effective in
assessing for failure or
effectiveness of therapy
Clinical failure
Clinical disease progression
signalled by new or recurrent
WHO stage 3 and 4 when art
has been given for at least 6
months
It is often associated with
weight loss and drop in
haemoglobin
Resistance
Specific mutations in the
genome of a virus that are
associated with antiretroviral
resistance
Cross resistance
The same mutations that cause
primary resistance to certain
ARV drugs can also cause cross
resistance to several other drugs
in the same class
Mutations lead to resistance
Virus may continue to replicate
in the presence of AZT or d4T
progressive mutations develop
that may compromise future
treatment options
Transitioning patients from
previous regimens
Key questions:
Is patient stable and doing well
on current regimen?
Is child transitioning to adult
care?
Is combination irregular?
Continue current regimen in
stable patient without signs of
toxicity or clinical failure
Switch to proposed regimen in
patient with signs of toxicity,
but NOT clinical failure
Switch regimen in patient with
signs of clinical failure
In paediatric patient
transitioning to adult care
follow recommendation for
stable patient
Nursing care
Home based care when very sick
due to fully blown AIDS or
opportunistic infections
Palliative care for patients
admitted in hospital
Prevention and control
Use the traditional ABC
PEP for those exposed through
inoculation and sexual abuse
PMTCT for positive mothers
and exposed newborns
Medical aspects
To raise public awareness of the
dangers of contracting HIV
To make condoms and other
barrier methods available,
accessible to all sexually active
individuals
To only provide safe and secure
blood and blood products
To diagnose, treat and prevent STI
and/or HIV
To minimise vertical transmission
of HIV from mother to child
To prevent and control TB
To diagnose and treat Ois
To avail ARVs to everyone who
needs them
To care and support PLWHA
legal aspects
Law enforcement for those who
deliberately infect others
All sexually abused and their
abusers tested for HIV for
prevention through PEP and
punishment of abuser
Law provides for protection of
citizens from being abused by
criminals or terrorists
Ethics as related to STI, HIV/AIDS
Confidentiality of patients HIV
status and who is on ART
Avoid participating in unethical
procedures like HIV testing
without consent
Forcing a person to do an HIV
test for instance mandatory HIV
test except where it involves a
sexual abuser
Counselor should encourage
patients to disclose HIV status
to partner
Infectious disease ordinance
Post exposure prophylaxis readily
available and accessible to health
workers and persons who are
sexually abused
Universal precaution guidelines
observed in all the health care
settings as part of IP
Infection prevention practices
Use of the following in care of
patients:
Gowns
Gloves
Goggles particularly in theatre
Sharps disposal
Infection prevention practices
At personal level:
Abstinence
Being faithful
Consistent use of condoms
ART in positive pregnant
woman
Protection of human rights
To ensure that rights of HIV
infected and affected people are
protected and stigma and
discrimination are eliminated
the HIV/AIDS/STI/TB policy
includes:
Encourage voluntary counseling
and testing for all persons and
insist on the maintenance of
confidentiality by HCW and
employers
Legalise mandatory testing in
cases of persons charged with
sexual offences that could
involve the risk of HIV
transmission
Not encourage anonymous HIV
(without consent) testing
Discourage mandatory testing
for scholarships and
employment
Legislate against individuals
who deliberately and knowingly
withhold their HIV status from
their partners or spouses
Legislate against wilful
transmission of HIV/AIDS
Educate about the need to
eliminate stigma and
discrimination against PLWHA
Promote positive living among
PLWHA
Clients rights
Information to enable patient
make an informed decision
Privacy
Confidentiality
Dignity
Respect
Decision making
Movement
Association (can join PLWHA)
Basic needs of life that include
clean water, education
Public health ACT
HIV/AIDS is an infectious
disease however it is not
notified as other infectious
diseases because of the
increased levels of stigma and
discrimination associated to it
Public health ACT
To prevent and suppress an
infectious disease the following
must be done: inspection of
premises and patient this is not
done as it may lead to stigma
Surveillance or isolation of
persons exposed to infection
Conveyance of infection an
offence
No person shall publish any
advertisement or statement
intended to promote the sale of
any medicine, appliance
or article for the alleviation or
cure of any venereal disease or
of any complaint or infirmity
arising from or relating to
sexual intercourse.