endocrinology course2
TRANSCRIPT
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Endocrinology Course Content
Semester (5)Clinical Pharmacy Course
Randa AlMahdi
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Course Content
For each disease disorder there will be asystematic approach to: Terminology of thedisease, general approach to therapeutics,epidemiology, pathology, aetiology, clinicalmanifestations, investigations
used, prevention, pharmacological treatment and non
pharmacologicaltreatment of diseases.
Cases from real patients will be discussed andsolved as pharmaceutical care provission
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Lectures topics include
1. Problem ±Oriented approach: Problem list & SOAP notes
Subjective data, Objective data, Assessment & Plan
Important abbreviations used in patients¶ records (cases: howto go through patients¶ medical records)
2. Adrenocortical Dysfunction: HPA Axis normal control, disorders& abnormalities, management
3. Adrenocortical Dysfunction: disorders.
4. Diabetes Mellitus: Type 1 pathophysiology and therapeutics ,drugs used, drugs in special populations.
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Lectures topics include
5. Diabetes Mellitus: Type 2 pathophysiology and therapeutics ,drugs used, drugs in special populations.
6. Diabetes Mellitus :Monitoring parameters, patient education7. Thyroid disorders: Hyperthyroidism, drugs used in both cases,
monitoring, complications
8. Hypothyrodism, drugs used in both cases, monitoring,complications
9. Parathyroid Disorders: hyperparathyroidism &hypoparathyrodism: treatment approach.
10. Hormonal Contraception & hormonal replacement therapy.
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Discussion of Endocrinology
Discussions of true endocrinology cases.
Group seminars
Assingments.
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³1´
Problem Oriented
Approach
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Definition
How to use, read the medical record?
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Components of POM
1) Problem list
2) SOAP Note
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Medical record
Chief complaint
History of present illness
Past medical history History
- Family
- Social
- Medication
Review of systems
PE
Radiography
Laboratory data
SOAP notes
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Problem list
Numbered
Described as precisely as possible Arranged according to acuity
Resolved or inactive
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SOAP notes
Subjective
Objective Assessment
plans
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Implementation of plan
Diagnostic
Therapeutic Educational
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Follow up progress
SOAP notes
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Sample SOAP
Case --------------- Problem --------------------
-----------------------------------------------------------
S:
-----------------------------------------------------------
O:
-----------------------------------------------------------
A:------------------------------------------------------------
P:
------------------------------------------------------------
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A: Assessment
Etiology
Indications for therapy
Assessment for therapy
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P: Plan
Therapeutic plan
Drugs to be avoided Goals
Therapeutic Monitoring
Toxicity Monitoring Education plan
Future plan
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Abbreviations used in medical records
VS: Vital Signs
HEENT: Head, ear, neck & trachea
COR: CoronaryCHEST: Chest
ABD: Abdomen
GU: Gentiurinary
WNL: Within Normal
RECTAL: Rectal
EXT: ExtremitiesNEURO:Neurological
BP: Blood pressure
RR: Respiratory rate
Oriented X 3: oriented to time, place & person
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Adrenocortical Disorders
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Contents
Normal Control of HPA Axis
Disorders include:1- Cushing¶s Syndrome
2- Addison¶s Disease
3- Hyper & Hypoaldosteronism
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Regulation of Hormone Secretion
Higher control by Corticotropin Releasing
Factor CRF from the median eminence of the hypothalamus.
This stimulates secretion of
adrenocortictropic hormone from the anterior
pituitary (see the flow chart)
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Hormonal control
CRF release
ACTH release
Cortisol release
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CRF
From Median eminence of hypothalamus
Other neurotransmitters can stimulate as well:1) 5 hydroxytryptamine 5HT
2) Norepinephrine NE
CRF stimulates ACTH from pituitary
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Anterior Pituitary
ACTH then stimulates the adrenal cortex of
the adrenal gland to secrete CORTISOL andto a lesser extent aldosterone and
androgens.
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Cortisol
Rising cortisol level inhibits the secretion of
CRF and ACTH in a negative feed backmechanism.
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Aldosterone
Renin Angiotensin Aldosterone system RAA
responses to electrolyte and volumechanges to either increase or decrease
aldosterone secretion.
This RAA system is stimulated or inhibited by
factors
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RAA system stimulators
Low blood pressure
Salt depletion B adrenergic stimulation
CNS excitation
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RAA system Inhibitors
Salt loading
Angiotensin II Vassopressin
Potassium ion
Calcium ion High blood pressure
Drugs
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Cushing¶s Syndrome
Hypercortisolism
Either overproduction of endogenous cortisolfrom the gland or exogenous adminstration
of the hormone.
High ACTH ADRENAL HYPERPLASIA
(cushing¶s disease) accounts for 70% of cushings cases.
Pituitary adenomas account for 85% of these
70%.
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Cushing¶s Syndrome
The remainder of cases (30%) are divided
equally as 15% each between adrenaladenomas and carcinomas and ectopic
ACTH secreting tumors.
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Cushing¶s Syndrome
Diagnosis
Cushingnoid features if long standing
hypercortisolism Documentation of hypercortisolism
Elucidation of the etiology of hypercortisolism
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Cortisol level Measurement
High levels are also in:
StressPregnancy
With some drugs: Heparin- Spiranolactone-
Ethanol- Lithium - Naloxone
To overcome interference measure indirectly:
urine 17 OHCH if > 12 mg/ 24 hours
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Dexamethsone suppression test
1 mg dexamethasone given at the night
17 OHCH in urine is measured in themorning if suppressed to < 5
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Clinical manifestations
Hyperglycemia
Obesity, moon face, baffallo Hump Myopathy
Osteoporosis
Psychological changes Hypertension
Acne
Impotence
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Cusgingoid Features
Buffalo Hump
Moon face
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Laboratory Investigations
Erythrocytes count > 6,000,000
hemoglobin > 18 mg/dlPolycythemia
WBC : Decreased lymphocytes ± decreased
esinophils
Electrolytes: Calcium -Potassium
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Treatment
Adrenocortical adenoma and adrenocortical
carcinoma: surgical removal of the involvedgland
Inoperable patients: chemotherapy
Ectopic ACTH producing tumors: surgical
excision or radiotherapy.
Cushing¶s disease: Pituitary irradiation
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Addison¶s Disease
Chronic insufficiency in the production and
secretion of cortisol and aldosterone fromthe adrenal cortex .
Destruction of the gland results from
infections
Autoimmune and infiltrative process
Or iatrogenic causes
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Causes
Tuberculous infection
Ideopathic Addison¶s Iatrogenic disease: removal or irradiation
Withdrawal of chronic use exogenous
glucocorticoid
Reported cases of: Hydrocortisone 100 mg
X3 days or Prednisone 30 mg X 5 days. Or
Prednisone 20 mg X 7 days: all have induced
HPA axis suppression.
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HPA axis supression
Physiologic doses of 20-30 mg
hydrocortisone or equivalent can causesupression if adminstered in the afternoon,
evening or night.
Chronic use of glucocorticoid and withdrawal
may be recovered over 10 months
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Clinical manifestations
Vague no-specific symptoms: fatigue ,
malaise, nausea, dizziness and anorexia Hypotension
Diarrhea
Hyperpigmentation in body creases due to
chronic increased level of ACTH
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Laboratory abnormalities
Neutropenia
Esinophilia Lymphocytosis
Hyponatremia
Hyperkalemia Sodium/ potassium ratio is < 30
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Radiography
Small heart
Adrenal calcification
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Acute insufficiency
Same clinical manifestations developing over
short period Percipitated by stress
Best treatment is to prevent occurance
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Treatment
Replacement of the cortisol and aldosterone
1) Hydrocortisone 20-30 mg or cortisoneacetate 25- 37.5 mg , titrate dose according
to individual patient
How dosed?
Give 2/3rd of the dose early morning & 1/3rd
late afternoon.
Or 3 equally divided doses at: early morning,
noon & 4 PM
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Treatment
2) Aldosterone replacement:
By Fludrocortisone orally 0.05- 0.2 mg/ dayOr Desoxycortisoterone IM
3) Patients must be educated not to stop
corticosteroid therapy of their own and wear
bracelets or carry cards as warning.
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Clinical Pharmacy
Services
Diabetes Milletus
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Definition of DM
It¶s a series of complex and chronic metabolic
heteroginous disorders characterized bysymptomatic glucose intolerance
All diabetic patients show abnormalities of
insulin secretion and disease complications:
Vascular & neurologic abnormalities.
Or cellular resistance to insulin in Type II DM.
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Burden of the disease
Huge economic burden both direct and
indirect costs. Drugs therapy for life ± Follow ups-
Hospitalizations ± Infections- Laboratory
work-ups
Blindness- End organ damage- Exteremitiesamputations
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Pathogenesis of Type I DM
10% of all diabetics
Absolute lack of insulin Develops in children or early adulthood
Patients are usually thin.
Development of ketoacidosis is common Causes: viruses, heredity (little), autoimmune
reaction.
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Pathogenesis of Type II DM
90% of all diabetics
Usually obese More genetically linked than type I.
Patients may have: High insulin, normal
insulin or low insulin levels.
Insulin receptors may be inactive,
desensitized or inadequate insulin action.
May be further classified to insulin sensitive
or resistant.
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Difference between the two types
Characteristic Type I Type II
Age of onset Childhood- early
adulthood
Age 40 or older
Rapidness of onset Usually abrupt Usually gradual
Family history Little Usually +ve
Etiology Unknown(
postulations)
High heredity
association
Body weight Usually thin Usually obese
Insulin Diminished ± absent Low- normal or high
Ketosis Common Uncommon (stress)
Symptoms 3 Ps + weight loss Asymptomatic (3 Ps
may or may not show)
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Other types of DM
Secondary DM:
1- Increased ACTH or increased Cortisol levels2- Drug induced: Thiazide diuretics
3- Gestational DM: 24- 28 weeks gestation.
4- Impaired glucose tolerance test: high blood
glucose level but not diagnostic of DM.
Have 40% increased risk of developing DM in
10 years time.
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Normal metabolism & utilization
of carbohydrates
Carbohydrates CHO glucose
Processes of taking glucose into blood andstoring glucose in liver as glycogen and as
triglycerides and fat in adipose tissue
facilitated by insulin.
Insulin is secreted at a 0.5- 1 U / hour, andmore is secreted at a blood glucose level of >
100 mg/ dl
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Normal metabolism & utilization
of carbohydrates
Insulin is cleaved (metabolized by the liver ,
peripheral tissue and the kidneys. Glucose in blood is maintained at 60- 160
mg/dl Normal metabolism & utilization of
carbohydrates
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Counter Regulatory Hormones
1. It increases glycogenolysis and
gluconeogenesis in the liver.2. Growth Hormone: Secreted from the
anterior pituitary , it interferes with body¶s
ability to utilize glucose.
3. Somatostatin: Secreted by the cells of thepancreas, it reduces both insulin and
glucagon and also suppresses growth
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Counter Regulatory Hormones
hormone and hence decrease blood glucose ,
reduces absorption of glucose from the gut.4. Epinephrine : from the adrenal medulla , it
stimulates conversion of glycogen to glucose
in liver, (same action like ephedrine and
phenylprapronalamine)5. Glucorticoides: increase gluconeogenesis
and liver glycogen.
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Counter Regulatory Hormones
6. Thyroid Hormone: Increase glucose
absorption from the GIT
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Clinical Presentation of DM
The 3 Ps:
Polydipsia dehydration from osmoticdiuresis
Polyurea from osmotic diuresis
Polphagia due to hunger from low blood
sugar (more in type I).
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To assess a diabetic patient
1- Screen those at risk
2- Diagnose3- Classify type
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Screening tests
+ve family history (more with type II)
Markedly obese Women who gave birth to 9 pounds babies.
All pregnant ladies at 24- 28 weeks gestation
All patients with recurrent urinary tact, skin
or genital infections
Elderly > 65 years age in places where DM
is highly prevalent (Sudan)
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Diagnosis
OGTT
Positive screening testsSigns and symptoms of high blood sugar
High random blood sugar
OGTT:
Fasting blood glucose < 115
1 hour postprandial: < 200
2 hours postprandial: < 140
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Treatment of DM
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Goals of treatment
Answering the questions:
Does tight sugar control preventcomplications?
Does it stop progression into end organ
damage ?
The Diabetes Control and ComplicationsTrial DCCT
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DCCT
Large clinical trial 1440 subjects treated for
6.5 years Results have shown important findings
which had great impact on treatment plans
Trial had compared tight sugar control to
conventional one
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DCCT
Treatment parameter Conventional Intensive
Insulin 1-2 day injections 3 or >, pump
Testing Daily, urine or blood Blood tests severaltimes/ day
Diet + exercise Quarterly Monthly
Follow up exam Quarterly Monthly
Care contact PRN by patient Weekly b y nurse
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Results of DCCT
Complications Reduction %
> Step sustained retinopathy 63
Macular edema 26
Severe retinopathy 47
Laser treat5ment 51
Urinary albumin excretion mg/ day
40
> 300
39
54
Clinical neuropathy at 5 years 60
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Important measures
Patient education :
Diet : 500- 1000 k cal/ dayExercise
Self monitoring
Blood & urine testing
Medications
Hyperglycemic symptoms
Hypoglycemic symptoms
Com lications
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Monitoring glucose level
Plasma glucose levels are 15% less than
whole blood glucose Conversion of mmol/ l to mg/dl?
Multiply by 18
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Glycosylated hemoglobin
Offered accurate assessment of glucose
control over a period of time Must be kept at 6.5 ± 7 %
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Management of Diabetes Mellitus
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Complications of Diabetes
Diabetic ketoacodosis
Diabetic ketoacidosis (DKA) is an acutemetabolic complication of diabetes
characterized: hyperglycemia,
hyperketonemia, and metabolic acidosis.
DKA occurs mostly in type 1 diabetes.It causes nausea, vomiting, and abdominal
pain and can progress to cerebral edema,
coma, and death.
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Pathophysiology of DKA
Insulin deficiency the body to metabolize
triglycerides and muscle instead of glucosefor energy.
Serum levels of glycerol and free fatty acids
(FF As) rise because of lipolysis as does
alanine from muscle catabolism. Glycerol and alanine provide substrate for
hepatic gluconeogenesis, which is stimulated
by the excess of glucagon that accompanies
insulin deficiency.
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Pathophysiology of DKA
ketogenesis proceeds in the absence of
insulin. The major ketoacids produced, acetoacetic
acid and -hydroxybutyric acid metabolic
acidosis.
Acetone derived from the metabolism of acetoacetic acid accumulates in serum and
is slowly disposed of by respiration.
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Complications of Diabetes
Diabetes is a strong risk factor for
cardiovascular diseases. High uncontrolled blood sugar is associated
with macrovasular and microvascular
changes.
Macrovascular changes, no effect.
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Complications of Diabetes
Microsvascular changes: retinopathy,
proteinurea & neuropathy, these can beimproved by glycemic control.
Tight control of blood pressure in diabetic
patients reduces mortality
Other risk factors include: smoking,hypertension, obesity & hyperlipidemia.
Use of Aspirin + lipid lowering agent + ACEI
are recommended
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Insulin
Is a polypeptide hormone of complex
structure synthesized and secreted by the cells of the islets of Langerhans in the
pancreas
Is a vital hormone essential to life.
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Insulin Types
Three basic types:
- Short acting with rapid onset: Soluble insulin,Insulin Lispro & Insulin aspart.
- Intermediate acting Insulins: isophane
insulin & Insulin zinc suspension.
- Those with slower onset and last for longperiods: Insulin zinc suspension.
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Insulin Therapy
Duration of a particular type varies from
patient to another. Doses must be individualized for each
patient
Gradually the dose is increased avoiding
hypoglycemic reactions
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Insulin Indications
All patients with diabetic ketoacidosis
Patients with rapid onset of symptoms Weakness
Ketonurea
All children with diabetes
Type II diabetics when other methods fail to
achieve good control
Pregnant diabetics
Peri-operatively.
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Injection technique
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Examples of recommended
regimens
Short acting + Intermediate acting twice daily
before meals
Short acting + Intermediate acting before
breakfast, short acting before evening meal
& intermediate acting at bed time.
Short acting three times before meals +intermediate acting at bed time
Type II may need intermediate acting with
or without short acting in morning or
evenin
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Recommended insulin regimens
Regimen (!) Morning Noon Evening bedtime
Regimen (1) Short acting
+intermediate
acting
Short acting
+Intermediate
acting
Regimen (2) Short acting
+
intermediate
acting
Short acting
insulin
Intermediate
acting insulin
Regimen (3) Short acting
insulin
Short acting
insulin
Short acting
insulin
Intermediate
acting insulin
Regimen (4) Intermediate
actin insulin
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Insulin use
Insulin requirements may be increased
during stress, infection
Insulin injection techniques may include:
syringes, pens & insulin pumps
Dose may be given by: IM ± IV (soluble only),
SC IV route is reserved for urgent cases, surgery
or seriously ill
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Insulin injections sites
Arms
Thighs Buttocks
Abdomen
Hypertrophy at injection site is a common side
effect
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Insulin delivery devices
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Insulin delivery devices
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Pharmaceutical Issues
Insulin storage
- Must be kept in refrigerator to stay untilexpiry date shown on bottle. Do not freeze.
- Once punctured a vial is stable for one
month at room temperature.
- Cold insulin is painful when injected keepbottle in use at room temperature.
- When mixing 2 types withdraw soluble first.
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Oral Hypoglycemic Agents
For type II only
60-70 % patients have initial response5-20% experience secondary failure?
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Oral Hypoglycemic Agents
Sulfonylureas
Biguanides Thioguaine triodinase inhibitors
Alpha glucosidase inhibitors.
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Oral tretment measures
Fasting blood sugar > 150, Hgb A1c> 8%
Acarbose or sulfonylurea or metformin If FBS < 110 & Hgb A1c <7 monotherapy
adequate
If FBS > 150 & Hgb A1c > 8% sulfonylurea
+ Metformin
If FBS < 110 & Hgb A1c <7 continue
If still FBS > 150 & Hgb A1c > 8% adding