Endocrine System Completely Pdf file....

Endocrine glands

1. Endocrinology
Prepared by: Masihullah Omer Mohammadi
ARIANA INSTITUTE OF
HIGHER EDUCATION
Medical faculty

2. General consideration
Special feature of
endocrine illness
History
Physical examination
Laboratory testing
Management

3. General consideration
The endocrine system is concerned
with “internal secretions
ﻪﺑ ت اﺮﺠﺣ زا پ وﺮ ﮏ ﯾ ﺎﯾ و هﺮﺠﺣ ﮏ ﯾ ﻂ ﺳ ﻮﺗ ﻪﮐ ﺖ ﺳ ا یوﺎﯿﻤﯿﮐ هدﺎﻣ نﻮﻣرﻮﻫ
ﺪﻨﮐ ﯽ ﻣ لوﺮﺘﻨﮐ ار نﺪﺑ ﮏ ﯾژﻮﻟﻮﯾﺰﻓ یﺎﻫ ﺖ ﯿﻟﺎﻌﻓ و هﺪﺷ زاﺮﻓا نﺪﺑ ت ﺎﻌﯾﺎﻣ ﻞﺧاد

4. Cont………..
Hormones divided Generally two types
ﻮﻀ ﻋ ت روﺎﺠﻣ رد ﺎﻫ نآ ﺮﻈﻧ درﻮﻣ جﺎﺴ ﻧا ﻪﮐ :Local Hormone•
Actyle Choline, Histamine, GI :ﺪﻨﻧﺎﻣ دراد راﺮﻗ هﺪﻨﻨﮐ ﺢﺷ ﺮﺗ
hormone
نﻮﺧ نارود ﻞﺧاد ﻪﺑ هﺪﻏ ﻂ ﺳ ﻮﺗ نﻮﻣرﻮﻫ ﻪﮐ :General Hormone•
ﺪﻨﮐ ﯽ ﻣ لﺎﻘﺘﻧا ف ﺪﻫ درﻮﻣ یﺎﻀ ﻋا ﻪﺑ نارود ﻖ ﯾﺮﻃ زا هﺪﺷ ﻪﯿﻠﺨﺗ
ﻦﯿﻟﻮﺴ ﻧا : ﺪﻨﻧﺎﻣ

5. Cont………..
The classic members:
Hypothalamus (TRH,CRH,GHRH,GHIH,PIF or dopamine) all are peptide
except dopamine(amine)
Pituitary Gland
Ant Pit( GH,TSH,ACTH,Prolactin,FSH,LH [P]
Post Pit( ADH or vasopressin, Oxytocin )[P]
Endocrine Pancreas( insulin, Glucagon )[P]
Thyroid( Thyroxine T4, Triiodothyronine T3)[P]
Parathyroids( PTH)[P]
Adrenals(cortisol, Aldosterone [S], Epi/ nor epi [A])
Gonads( Testosterone , Estrogen ) [S]

6. Cont………..
Charastrastric of Hormones
Composed of small Molecule easily cross
endothelial cell Membrane
Distance from gland act on target organ
Not permanently in circulation excrete in urine
Role of Hormone
Metabolism of carbohydrate, Protein, lipid
Balance of water, electrolytes , minerals
Control of cellular Metabolism
Growth and development

7. Cont………..
Key Concept One:
For each hormone, what is the target cell
and its receptor?
Single or Multiple Target Cells
Single or Multiple Receptors
Location of Receptors
Cell M ( Proteins , Peptide , Catecholamine)
Cytoplasm ( steroids)
Nucleus ( Thyroids T3, T4)

8. Cont………..
Regulation of Hormone secretion
 Negative Feedback : Insulin secreted by beta cell of
Pancrease response to an increase in blood
glucose by decrease of blood glucose, secretion of
insulin
Positive Feedback: in hypothyroidism which
secretion of thyroid hormone secretion of TSH
increased

9. Special feature of endocrine illness
Delayed Growth
•Hypothyroidism, Hypopituitarism
Excessive growth
•Can be family, Race or physiologic but disease of pituitary gland
cause excessive GH
Obesity
•BMI 25-29 overweight , BMI over 30 called obesity
•Cushing syndrome, hypothyroidism, DM2,
Loss of weight
•4,5 kg or 5% of body weight decreased during 6-12 months
•Metabolic rate no eating can be both in cancer or one in
hyperthyroidism DM1 ,

10. Diabetes Mellitus
Definition of DM
Epidemiology
Classification and pathogenesis
Clinical and laboratory findings
 treatment and management
Indication for hospitalization
And complication

11. Definition of DM
Diabetes Mellitus is a clinical syndrome
characterized by chronic hyperglycemia and
disturbance in carbohydrate , lipid and protein
The disease may result from defect in insulin
secretion , resistance or both

12. Contin…………..
Epidemiologic consideration-
o29.1 million people in the united states have DM which-
1.25 million have Type 1 DM
Most of the rest have Type 2 DM
Some are other specific types of DM
Both type of diabetes progressively increase but DM2 is more
because of obesity and decrease physical activity

13. Classification
Primary diabetes mellitus (Cause unknown)
Type I or insulin dependent ( IDDM)
Type 2 or non – insulin dependent (NIDDM)
Gestational Diabetes Mellitus
When pregnant woman without a previous history of diabetes
develop high blood sugar level
Secondary diabetes
•Consequence of another medical condition

14. Contin……
Pancreatic disease
Pancreatitis
Hemochromatosis
Cystic fibrosis
Panreatectomy
Endocrine disease
Cushing syndrome , Glucagonoma
Acromegaly
Thyrotoxicosis
Pheochromocytoma
Drug induce
Corticosteroid
Thiazide diuretic
Phenytoin

15. Etiology
Type I DM (IDDM): result from autoimmune disease
Genetic susceptibility ( HLA DR4 gene mutation)
Inheritance ( this risk is greater with diabetes father than mother) Child of
diabetic mother has 3% risk of developing but child of diabetic father has
6% risk of developing of DM
Viral infection: Auto antibody to coxsackie virus
Panreatic pathology (pancreatitis,hemosidrosis)
Immunological factor ( IDDM is T-cell mediated autoimmune
disease

16. Contin……
Type 2 DM( NIDDM)
Genetic( twins chance of DM is 70%-90%)
Parents with DM child have more chance for DM
Environmental factor
Life style : obesity which increase resistance to insulin
Pancreatic Pathology
Reduction of insulin secretion
Resistance to insulin
Delayed insulin secretion in response to oral glucose

17. Pathogenesis
Type I DM: outo immune process destroy B cell of
Pancrease
At birth beta cell is natural progressively destroy
Destruction of cell are different in people
70%-80% cell damage after that clinical feature will
occure

18. Contin……….
Type 2 DM:
Insulin secretion , Resistance,over production of glucose.
80% patient are obese ( central obesity)
Causes of resistance against insulin
Insulin receptor in obese patient less than normal , in DM patient
alfa cell more than beta cell
Circulating endogenous insulin is sufficient to prevent
ketoacidosis but is inadequate to prevent hyperglycemia

19. Gastational Diabetes
Hypertrophy and hyperplasia causes resistance against
insulin increased glyconeogenesis and ketogenesis
If there is no enough insulin in pregnancy increase
glyconeogenesis and lipolysis cause ketosis
Esterogen and progesterone increase insulin demand
In third trimester CO increase lots of glucose inter renal tubule
cause glucose urea
Hyperglycemia of mother stimulate secretion of insulin in
fetus cause macrosomia

21. Clinical feature
Polyuria : due to osmotic diuresis
Polydipsia : due to loss of fluid and electrolyte
Weight loss : due to depletion of glycogen ( Type I )
There is no weight loss in type 2 DM
Blurred of vision : it result from exposure of lens and retina to
hyperosmolar fluid
Postural hypotension
Parasthesia
Ketoacidosis

22. Contin…………
Nocturia
Xerostomai
Superfacial infection: Genital candidiasis
Nausea
Headache
Delayed healing
Over eating
Chronic feature of DM neuropathy , Opthalmopathy
Reduced muscle mass (Type I DM)
Many other are asymptomatic initially (Type 2 DM)

23. Contin…………..
Physical Examination:
BMI
Fundoscopy
Orthostatic hypotension
Peripheral puslse
Site of insulin injection
Hypertension over 140/80mmhg in DM

24. Contin…….
Type I DM
Before age of 30 years
Thin body
Need insulin in first treatment
Ketoacidosis
Other outo immune disease ( autoimmune thyroiditis, pernicious
anemia)
Type 2 DM:
Occur after age of 30 years
80% are obese
Maybe at first not be used insulin as first treatment
Other problem ( CVD, Resistance to insulin, )

25. Diagnosis
Glucose Tolerance
Normal Glucose Tolerance
FBS 100mg< Two hours after 75 gr 140mg/dl< HB A1c <5.7
Impaired glucose tolerance (Prediabetes )
100-125mg/dl <140-199mg/dl Hb A1c 5.7-6.4
Diabetes Mellitus
>126mg/dl > 200mg/dl Hb A1c >6.5

26. Contin………
Oral glucose tolerance test-
It done If fasting plasma glucose is less than 126mg/dl and DM is suspected
The stages to perform it include of –
oPatient may be on low carbohydrate diet
o
o
o
o
o
This test is interprete in below form-
o
oDiagnostic- if 2hours value greater than 200 mg/dl
oImpaired glucose tolerance- if 2 hours value 140- 199 mg/dl

27. Contin…………
Glycated hemoglobin(hemoglobin A1)measurement-
It circulate within red blood cells
Reflect the glycemic state over preceding 8-12 weeks
Thereby is method of assessing diabetic control
some condition may affect the value of Hb A1c-
o
survival(e.g splenectomy)
o
survival(e.g hemolysis)
A cutoff value of Hb A1c is 6.5%
Value of 5.7-6.4 should be considered at high risk fpr
developing DM(prediabetes)

28. Contin……..
Urine and blood ketons-
Qualitative detections of keton bodies
Quantitative detection of ketone bodies
Patients with greater than 3 mmol/L equivalent to very
large ketone bodies require hospitalization
Glycosuria
Type 2 DM ( LDL, TG) increased

29. Treatment
Goal of treatment:
Diminish sign and symptoms of hyperglycemia
Maintain Euglycemia
Prophylaxis from hypoglycemia
Treatment of dyslipidemia
Prophylaxis from infection

30. Medical nutrition therapy
ﯽﯾاﺬﻏ ﻢﯾژر
ﯽ ﯾاﺬﻏ ﻢﯾژر ف اﺪﻫا
رد DM2 عوﺮﺷ ﻦﺘﺧاﺪﻧا ﺮﯿﺧﺎﺗ ﻪﺑﺎﯾ و ﻪﯾﺎﻗو MNT لوا ﻪﻠﺣﺮﻣ یﻮﯾﺎﻗو ت ﺎﻣاﺪﻗا
نزو ﺶ ﻫﺎﮐ ( قﺎﭼ)ﺮﻄﺧ ﻪﺑ ض وﺮﻌﻣ داﺮﻓا
ﻖ ﯾﺮﻃ زا ﺖ ﯿﺑﺎﯾد ت ﺎﻃﻼﺘﺧا ﻦﺘﺧاﺪﻧا ﺮﯿﺧﺎﺗ ﻪﺑ ﺎﯾ ﻪﯾﺎﻗو MNT مود ﻪﻠﺣﺮﻣ ف ﺪﻫ
نﻮﺧ زﻮﮐﻮﻠ لوﺮﺘﻨﮐ
" ﯿﺑﺎﯾډ ﻪﺑ ط ﻮﺑﺮﻣ ت ﺎﻃﻼﺘﺧا ﺮﯿﺑاﺪﺗ MNT مﻮﺳ ﻪﻠﺣﺮﻣ ت ﺎﻣاﺪﻗا

31. Contin……
ﯽ=اﺬﻏ?ﻢ<ژر?تﺎﯿﺻﻮﺼ ﺧ
دراﺪz?ﻧ?لﺎﻣرﻮﻧ?ﮏ ﯾدﺰﻧ?ﺎﯾ?لﺎﻣرﻮﻧ?ار?نﻮﺧ?ﺮﮑﺷ
ددﺮ??نﻮﺧ?زﻮ?ﻮﻠ??ﺪﯾﺪﺷ?تاAﯿﻐ?ﻊrﺎﻣ
ﺪﯾاﺮﺴﻠ??یاﺮﺗ?و?لوAﺴﻟﻮ??صﻮﺼ ﺧ?ﮫﺑ?نﻮﺧ?ﻢp'?نﻓر?ﻻﺎﺑ?زا
/s??9A?}h!
Caloric restriction is distributed as follow-
o45-65% carbohydrate
o10-30% as protein
o25-35% Fats
oAnd <30% as total fat (<7% saturated fat) with <300mg/d of
cholesterol
Patient with progressive kidney disease restriction of protein
intake to 0.8g/kg/d

32. Contin……
Weight reduction by caloric restriction is an
important goal in obese and Type 2 diabetic
patients
Insoluble fibers such as cellulose and hemicellulose
increase colonic transition and is efficient on colon
function
Soluble fibers such as gum and pectin tends to
retard nutrients absorption rates so that glucose
absorption is slower in diminish hyperglycemia
High soluble fibers content also have a favorable
effect on blood cholesterol decrease absorption of it

33. Contin…..
:هﺪﺷ ﻢﯿﺴﻘﺗ یرﻮ ﻪﺘﮐ ﻪﺳ ﻪﺑ " ﯿﺑﺎﯾډ نﺎﻀﯾﺮﻣ ﯽﯾاﺬﻏ ﻢﯾژر
ﻪﮐ یﺎﻫاﺬﻏ ،زﻮﮐﻮﻠ ،هرﻮﺑ )ﺪﻨﮐ ﺰﯿﻫﺮﭘ نا زا ﺪﯾﺎﺑ ﻪﮐ یﺎﻫاﺬﻏ
(ﺪﺷﺎﺑ ﻪﺘﺷاد زﻮﮐﻮﻠ ﺮﺘﺸﯿﺑ
،مﺪﻨ ، نﺎﻧ )ﺪﻧﻮﺷ هدﺎﻔﺘﺳا دوﺪﺤﻣ ت رﻮﺻ ﻪﺑ ﻪﮐ یﺎﻫاﺬﻏ
،ﺎﺑرﻮﺷ ،ﻆ ﯿﻠﻏ پ ﻮﺳ ،" ﯿﮑﺴﺑ ،ﮏﯿﮐ ،هﺪﺷ خﺮﺳ نﺎﻧ
،ﻮﻟﺎﭽﮐ ،ت ﺎﺑﻮﺒﺣ ،ﺮﯿﻨﭘ ،ﻢﺨﺗ ،ﯽﻧﺮﻓ ،ﺮﯿﺷ ،ﯽﻫﺎﻣ ،ﺖ ﺷﻮ
(ﮏﺸﺧ و هزﺎﺗ ت ﺎﺟ هﻮﯿﻣ مﺎﻤﺗ و دﻮﺨﻧ ،ﺎﯿﺑﻮﻟ
و هدﻮﺒﻧ حﺮﻄﻣ ﺖ ﯾدوﺪﺤﻣ نآ زا هدﺎﻔﺘﺳا رد ﻪﮐ یﺎﻫ اﺬﻏ
،ﻖﯿﻗر پ ﻮﺳ ،یرﺎﮐﺮﺗ ) ﺪﺷﺎﺑ ﯽﻣ ﺖ ﺑﺎﯾد ﯽﺑﺎﺨﺘﻧا یاﺬﻏ
(هﻮﻬﻗ یﺎﭼ ،ﻮﻤﯿﻟ س ﻮﺟ ،ﯽﻣور نﺎﺠﻧدﺎﺑ
:ش زرو

34. Medical Treatment
1.Medication that primarily stimulate insulin secretion by
binding to the sulfonylurea receptor on the beta cell-
A.sulfonylurea-
Stimulate insulin release from beta cells of pancrease
Increased receptor of insulin in target cell
Inhibit liver glycogenolysis
Contraindicate in liver failure , renal failure , pregnancy, type
1
Using in patients with type 2 diabetes but not in type 1
diabetes
Metabolize in the liver and excrete by kidney
Adverse effects of this drug include hypoglycemia and
weight gain
Mechanism of weight gain include improved glucose control and
increased food intake in response to hypoglycemia
Idiosyncratic reactions are rare with skin rashes and
hematologic toxicity(leukopenia,thrombocytopenia)

35. Contin….
Ther are two generation of sulfonylurea
oFirst generation include-
Tolbutamide
Tolazamide
Acetohexamide
Chlorpropamide
oSecond generation include-
Glyburide
Glipizide
Gliclazide
glimepiride

36. Contin…….
Meglitinide analogs-
Absorbed from intestine and metabolized in the liver
Half life is less than one hour, stimulate insulin from beta cell
Starting dose is 0.5 mg three times a day 15 minutes before
each meal
The dose can be titrated to 16 mg
Like sulfonylurea it can be use in combination to metformin
Side effect are include of hypoglycemia and weight gain
D-phenylalanine derivative-
 Stimulate insulin secretion from beta cell
Rapidly absorbing from intestine and metabolized in the liver
Cause brief rapid pulse of insulin, when given before meal
reduce the postprandial raise of glucose
Starting and maintenance dose is 120mgr three times a day
Like other agents side effects are hypoglycemia and weight
gain
Posterior Anterior

37. Continue-
2.Medication that primarily lower glucose level by their action
on the liver,muscle,and adipose tissue- increase insulin
receptor
A.Metformin-( Biguanide)
Is the first line therapy in the patients with tye 2 diabetes
Inhibit glyconeogensis
Combine with sulfonylurea
Its ineffective in patients with type 1 diabetes
Half life is 1.5-3 hours and is not bind to plasma proteins
,being excreted unchanged by kidneys
Improve both fasting and postprandial hyperglycemia and
hypertriglyceridemia

38. Continue-
Posterior Anterior
This drug is avoided in CKD patients because of lactic
acidosis
In the united states this drug is not recommended at or
above a serum creatinine level of 1.4mg/dl in women and
1.5mg/dl in men
The medication should be stopped if creatinine exceeds
150mcmol/L(1.7mg/dl) or the GFR is below 30ml/min/1.73m
The maximum dose of metformin is 2550 mg
Its important to start from minimal dose and increase
gradually to reduce gastrointestinal upsets
The most frequent side effects of metformin are
gastrointestinal symptoms

39. Continue-
B. thiazolidinedione's-
Two medication of this class rosiglitazone and
pioglitazone are available
Sensitize peripheral tissue to insulin
Like biguanides does not cause hypoglycemia
And is effective as monotherapy and in combination with
sulfonylureas
Increase risk of angina pectoris and myocardial infarction
And also cause edema in 3-4 %
3.Medications that affects absorption of glucose-
Alpha-glucosidase inhibitor that competitively inhibit the
alpha glucosidase enzyme in the gut
Two below agents are most common:
oAcarbose
omiglitole

40. Continue-
4.Incretin –
Oral glucose provokes a threefold to fourfold higher
insulin response than an equivalent dose of glucose
given intravenously
Because oral glucose cause release of gut hormones
principally glucagon-like peptide1(GLP 1) and glucose
dependent insulinotropic polypeptide(GIP1) from L cell of
small intestine,
Infusion of GLP1 stimulate insulin secretion and lower
glucose level, decrease appetite and delayed stomach
emptying and cause weight loss

41. Continue-
Two group of drugs are include in this type-
A.GLP-1 receptor agonists-
oExenatide
oLiraglutide
oAlbiglutide
oDulaglutide
oLixisenatide
B.DPP-4 inhibitors
oSitagliptine
oSaxagliptine
oAlogliptine
oLinagliptine
ovildagliptine

42. Continue-
5.Sodium-glucose co- transporter 2 inhibitor-
90% inhibit glucose from proximal tubule
There are three agents in this group-
oCanagliflozine
oDapagliflozin
oEmpagliflozin
6.others-
oPramlintide
oBromocriptine
ocolesevelam

43. Continue-
Insulin indication :
 Type I DM
Diabetic ketoacidosis
Hyperosmolar state
Gestational diabetes
Type 2 DM not response against oral agent
Type 2 DM patient with liver, renal, heart failure
Patient under large operation and general
anesthesia

44. Continue-
Short acting insulin
Regular insulin
Rapidly acting insulin
Insulin lispro
Intermediate acting insulin
Neutral protamine hagedorn(NPH)
Permixed insulin
•70%NPH, 30% regular 50%NPH , 50% regular
Long acting insulin
Insulin glargine
Insulin determir

45. Complication of insulin
Lipodystrophy
Dystrophy or hypertrophy in the site of injection
Antibody against insulin
Local ( edema, erythema , urticarial ) systemic(
angioedema, anaphylactic shock )
Hypoglycemia
Commonly in type 1DM

46. Chronic complications of DM
2. Diabetic retinopathy-
There are two main categories of diabetic
retinopathy-
oNo proliferative retinopathy- represent the earlier stage of
retinal involvement:
Micro aneurysm
Dot hemorrhage
Exudate
And retinal edema
oProliferative retinopathy- involves the growth of new
capillaries and fibrous tissue within the retina and vitreous
chamber

47. Contin……..
 proliferative retinopathy can occur in both types of
diabetes
oWhich is more common in type 1 diabetes
oDeveloping about 7-10 years after onset of symptoms
oVision threatening retinopathy virtually never appears in type
1 in the first 3-5years
oUp to 20% of patients with type 2 have retinopathy at the
time of diagnosis
oAnnual ophthalmologist consultation must be arranged for
diabetic patients
3.Glaucoma-
oOccurs in approximately 6% diabetic patients

49. Contin……….
B. Diabetic nephropathy-
25-45% of patients with either type developes nephropathy
Is the leading cause of ESRD
And is the major cause of mortality and morbidity
Protein urea 30-299mg 24hr micro protein urea
24hr 300mg overt protein uria
Most common in type 1 than type 2 DM
Protein 0.8mg/kg , treatment of HTN
Captopril 50mg twice daily decrease protein uria
Sulfonylurea and metformin contraindicate in this
condition

50. Contin….
Diabetic Neuropathy :
50% in type 1 and type 2 DM
Poly neuropathy, mononeuropathy, Autonomic
Without CNS effect all other part of nervous system
Commonly bilateral peripheral neuropathy, paresthesia during
night spontaneously disappear
Poly neuropathy of lower limb
“Distal symmetric polyneuropathy”
Progressive loss of sensation: distal proximal
•Severe cases: motor weakness
Glove stocking neuropathy
Generally not reversible
•Glucose control slows progression
•Pain in feet (burning or stabbing)
•SNRIs: duloxetine or venlafaxine
•TCAs: amitriptyline,desipramine or nortriptyline
•AEDs: pregabalin or gabapentin

51. Contin….
Some autonomic neuropathy include of –
Orthostatic hypotension,
CV: orthostatic hypotension, silent ischemia
Intractable nausea and vomiting
Diabetic cystopathy
Chronic , persistent diarrhea , Dysphagia , Gastroparesis
Macro vascular complication of DM include of –
Coronary heart disease
Peripheral vascular disease
 Cerebrovascular disease
50% of type 2 DM patient use antihypertensive drug
Miscellaneous complication of DM include of-
Erectile dysfunction
hypoglycemia

52. Contin…..
Lower extremity complication
Ulcer and infection are common
DM are common cause of non traumatic
amputation of lower extremity
Risk factor
•Neuropathy
•Peripheral vascular disease
•Ischemia
•Diabetic foot ulcer most in male, 10year of DM
history ,smoking , previously have ulcer

53. Contin…..
A.Acute complications-
1.Diabetic ketoacidosis- (Most commonly in type1 DM)
Symptoms
oNausea and vomiting
oThirst and polyuria
oAbdominal pain and shortness of breath
Physical findings-
oTachycardia
oDehydration/hypotension
oTachypnea/kussmaul respiration/respiratory distress
oAbdominal tenderness
oLethargy/edema and possibly coma

54. Contin….
Precipitating events-
oInadequate insulin administration
oInfection(pneumonia/UTI/gastroenteritis/sepsis)
oInfarction(cerebral/coronary/mesenteric/peripheral)
oDrugs(cocaine)
oPregnancy
oStress
Under these circumstance hormonal changes cause
glyconeogenesis
Decrease consumption of glucose in peripheral tissue cause
hyperglycemia
During lipolysis free fatty acid inter to liver synthesis of keton body
cause acidosis

56. Laboratory abnormalities
DKA is characterized by-
oHyperglycemia(serum glucose350-900mg/dl)
oKetosis
oAnd metabolic acidosis(serumbicarbonate<15mmol/L
PH ranges betw 6.8 and 7.3 depending on the severity of
acidosis
Level of potassium 5-8meq/lit , Hyponatremia ,
Hypophosphatemia
Phosphaturia caused by osmotic diuresis
•Loss of ATP
•Muscle weakness (respiratory failure)
•Heart failure (↓
Urine glucose and ketone positive
Hyperlipidemia
Leukocytosis with infection

57. Treatment of DKA

metabolic acidosis )
Patient admitted in ICU
Evaluation of serum electrolyte, renal function test
Serum saline (0.9% 2-3lit ) 1-3 first hr after 0.45% saline
250-500 ml per hr until plasma glucose 250 mgr/ dl
Glucose 5% and saline 0.45% 150-250ml/hr




58. Questions?