Care of NRS 4 Acute endocrine and neurologic disorders (1).pptx

Department Of Nursing
Care of patient with acute conditions of endocrine disorders
For PG adult Health Nursing students
By: Diriba Mulisa ( BSC,Msc in AHN)
diribamulisa@yahoo.com
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 What do you know about
endocrine gland?
Brain storming

Session objectives
At the end of this sections the student will able to:-
 Define endocrine glands
 Identify types of glands present in our body
 Mention some function of endocrine glands
 Identify common endocrine disorders
 Identify acute complication of diabetes mellitus
 Identify common disorders of thyroid gland

Introduction to Endocrine gland
Glands
• It is secreting cell mas that secretes a specific substance that is called
hormone.
• Specialized cell mas that can produce hormone
• There are two kinds of glands in our body
 Exocrine glands!
 Endocrine glands
 Example :- Exocrine glands are :-
Sweat/sebaceous glands
Salivary gland
Lacrimal gland (tear g)
Digestive glands.
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Endocrine System
The word endocrine derived from Greek words :
Endo- within
Crinis – to secrete
 They are glands which has no duct and these secretes substances
into surrounding blood vessels.
 The hormone secreted by those glands go to the target
organs by blood and lymphatic systems
 They surrounded by highly vascularized area

Anatomic and Physiologic Overview of EG

Hormone
 Often described as the body’s chemical messengers
 Chemical that transfers information and
instructions between cells.
 The secretion of hormone in our body controlled by
two ways.
1) Hormonal control and
2) Neural control
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Characteristics of hormone
1. Needed in very small amounts (potent);
2. Produce long-lasting effects .
3. Regulate metabolic processes (maintain homeostasis)
4. Regulated by negative-feedback mechanisms;
5. Has target organ which has its receptors

Hormone….
1. Amino acid derivatives
• Dopamine
• Catecholamine, and
• Thyroid hormone
2. Small neuropeptides (hydrophilic)
Gonadotropin-releasing hormone
Thyrotropin-releasing hormone
Somatostatin, and
Vasopressin

Hormone….
3. Large proteins
Insulin,
 luteinizing hormone (LH), and
 PTH
4.Steroid hormones (Hydrophobic)
Cortisol and
Estrogen
5. Vitamin derivatives
Retinoid (vitamin A) and vitamin D

Function of Endocrine glands
 The function of endocrine system is to main homeostasis.
 Secreting the hormone that integrate body systems, in
combination with the nervous system
 Those hormone secretion must be in normal range
But in some condition there may be occurrence of:-
1. Hypo secretion
2. Hyper secretion

Functions of the endocrine glands….
Regulating metabolism
Regulating reproduction
Controlling the balance of extracellular fluid and
electrolytes (sodium, potassium, calcium, and
phosphates)
Maintaining an optimal internal environment such as
regulation of blood glucose levels
Stimulating growth and development during
childhood and adolescence
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Mechanisms of hormone release
i. Humoral: in response to changing levels of ions or
nutrients in the blood
ii. Neural: stimulation by nerves
iii. Hormonal: stimulation received from other hormones

Principles of hormonal action
1. Endocrine - produced substances (hormones) are
distributed via blood to the target cells
2. Paracrine - hormones influence directly surrounding
near by cells
3. Autocrine - hormones regulate directly the cells which
produced them
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Comparisons of NS and ENS
NS
 Network of nerves
 Localized response &fast
 Duration of responses is
temporary and reversible.
 Neurotransmitters transmit
electrical signals
 Transmit through neurons
 The whole system is physically
contact
Endocrine system
 Collection of glands,
 The response is spread widely& slow
 Duration of responses is permanent
 Hormones transmit chemical signals
 Transmit through blood stream
 The whole system is not physically
contact
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What are those endocrine gland ?

Pituitary gland
 Is a pea sized gland in the center of the brain that acts as
a “control center” of other hormone
 Commonly referred to as the master gland
 Because it produces hormones that control many
functions of other endocrine glands.
 Divided into anterior and posterior lobes (extension of
the hypothalamus)
 Its secretion is controlled by hypothalamus
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Mechanisms of actions of pituitary gland
• First a signal is sent from the hypothalamus to the
pituitary as "releasing hormone," which stimulates the
pituitary to secrete a "stimulating hormone" into the
circulation.
• The stimulating hormone then signals the target gland
to secrete its hormone.
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Mechanisms of actions of pituitary gland….
• As the level of this target organ hormone rises in the
circulation, the HPT and the P gland shut down secretion
of the RH and the SH respectively, which in turn slows the
secretion by the target gland.
• This system results in stable blood concentrations of the
hormones that are regulated by the pituitary gland

Mechanisms of actions of pituitary gland …..

Hormones Regulated by the Hypothalamic/Pituitary System
Stimuli Hypothalamic
Releasing
Hormone
Pituitary
Stimulating
Hormone
Target
Gland
Hormone Effects
Low
T3/T4(Low
energy)
TRH TSH Thyroid
gland
T3/T4 Increase T3
/T4 (Energy
increased)
Low
glucose
Corticotropin
-releasing
factor (CRF)
ACTH Adrenal
gland
Cortisol Increase
glucose
(burn)
Desire to be
matured for
reproductio
n
(LHRH) or
(GnRH)
FSH/LH Ovary and
testis
Estrogen or
testosterone
2nd sexual
characteristic
s
Desire for
maturation
/growth
GHRH Growth
hormone
Muscle… Insulin like
growth factor-I
(IGF-I)
Growth
increases

A. The anterior pituitary gland
Secrete 6 different hormones:
1. Human growth hormone (HGH)
 Controls growth of the body.
 Targets the bone, muscle and adipose tissue.
 Hypo secretion dwarfism
 Hyper secretion gigantism
2) Thyroid stimulating hormone (TSH)
• Targets thyroid gland.
 Controls the secretion of hormones by the thyroid gland;

The anterior pituitary gland….
3. Adrenocorticotropic Hormone (ACTH)
• Targets the outer portion of the adrenal gland (cortex).
 Controls the secretion of hormones by the adrenal cortex;
4. Prolactin (PRL)
• Targets the mammary glands
 Stimulates the production of milk by the mammary
glands

Anterior pg...con’d
5. FSH also called gonadotropins
 Targets the primary sex organs (ovary & testis)
 In females, stimulate maturation of an ovarian follicle and ovum
 In males stimulates the maturation of sperm in the testes.
6. Luteinizing Hormone (LH) also called gonadotropins
• Targets ovaries & testes
 In females, causes ovulation
 In males, causes secretion of testosterone (secondary sexual
characteristics in the male)
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B. Posterior Pituitary
 located behind the anterior pituitary gland.
 continuous with nerve fibers :-
 Supraopticohypophyseal tract of the hypothalamus
 Does not actually produce hormones
Here hormone produced by HP
But stores them until it is stimulated to release them.

Posterior PG...con’d
A. Anti-diuretic hormone (ADH):
 Targets the kidney tubules
 Causes the kidney tubules to reabsorb water.
 Controls water balance and blood pressure.
B. Oxytocin (OT)
 Targets uterine smooth muscle and breasts
 Uterine muscle contraction during labor and
 Milk production.

Hypothalamus
• The hypothalamus is located in the lower central part of
the brain.
• Located in diencephalon parts of the brain
• It is Part of the brain and Present in the posterior part of
the forebrain
• Connects the midbrain with the cerebral hemisphere

Functions of hypothalamus
 Concerned mainly with homeostasis of the body
 It regulates many vital functions of the body like:-
– Endocrine functions,
– Visceral functions,
– Metabolic activities,
– Hunger,
– Thirst,
– Emotion,
– Sexual functions, etc
Again it secretes hormones that stimulate or suppress
the release of hormones in the pituitary gland.

Hypothalamus....Con’d
♠ HT serves as the major link between the nervous and
endocrine systems..
It connects the nerve systems to the endocrine systems
It receives process signal from other brain region and pass
ways and translate them into hormone.
Synthesizes two hormones that is exports to posterior
pituitary for storage and later release.
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Hypothalamus....Con’d
 contains special cells called neurosecretory cells
Neurons that secrete hormones
These hormones flow to PG which is connected to the
hypothalamus by the infundibulum.
It regulates:-
 Hormonal out put of anterior pituitary
• Many of these hormones are releasing hormones, which
are secreted into an artery (the hypophyseal portal
system) that carries them directly to the pituitary gland

HT And PG Are:-
Command and control
center :-
 They directing
hormone to:
Other glands and
Throughout the body

Hypothalamic Control of the Anterior Pituitary
• It is hormonal control rather than neural.
• Hypothalamus neurons synthesize :
Releasing Hormones And
Inhibiting Hormones.
• Hormones secreted into the hypothalamo-
hypophyseal portal system regulate the secretions
of the anterior pituitary

Hypothalamic Control APG... con’d
 Corticotrophin-releasing hormone(CRH)
 Regulating carbohydrate, protein, and fat metabolism as
well as sodium and water balance in the body
 Gonadotropin-releasing hormone(GnRH)
 Helps control sexual and reproductive functions,
including pregnancy and lactation (i.e., milk production)
 Thyrotropin-releasing hormone(TRH)
 Controls the metabolic processes of all cells and which
contributes to the hormonal releases from thyroid gland

Hypothalamic Control APG... con’d
 Growth hormone-releasing hormone (GHRH)
 Is an essential component of the system
promoting the organism’s growth
 Somatostatin
♠Affects bone and muscle growth but has the
opposite effect as that of GHRH

 E.g. GH secretion is regulated by GHRH or
GHIH
Hyper secretion…..?
Hypo secretion…..?
E.g. 2.Thyrotrophin-releasing hormone (TRH)
 Secreted by the hypothalamus.
 Causes the release (TSH, or thyrotropin) from
the pituitary.

Feedback Control of Hormone secretion
• Anterior pituitary and hypothalamic secretions are
controlled by the target organs they regulate.
Secretions are controlled by:-
 Negative feedback inhibition by target gland
hormones.
E.g. release of TSH controlled by T3 and T4
 Hypothalamus has indirect control over the endocrine
organs.

Negative feedback
The target gland
hormone can act on :-
1. Hypothalamus and
inhibit secretion of
releasing hormones.
2. Anterior pituitary and
inhibit response to the
releasing hormone.

Negative ...con’d

Positive Feedback Loop
Called positive because it accelerates the original
process
Can ensure that the pathway continues to run
Can speed up its activities.
 Few positive feedback loops in the human endocrine
system.
– Example: milk release from the mammary glands

Positive...con’d

Hypothalamic Control of Posterior Pituitary
 Hypothalamus neuron cell
bodies produce:
1. ADH: supraoptic nuclei.
2. Oxytocin: paraventricular
nuclei.
• Transported along the
hypothalamo-hypophyseal tract.
• Stored in posterior pituitary.
 Release controlled by
neuroendocrine reflexes

Care of patient with acute conditions of
Pancreatic gland disorders

Pancreatic gland
• The pancreas (pan= all , kreas = flesh) is a gland that is
partly exocrine and partly endocrine.
• It participating in both the digestive and in the endocrine
system. .
• As endocrine: – producing important hormones as
insulin, glucagon and somatostatin
As exocrine: – Secreting pancreatic juice containing
digestive enzymes that pass to the small intestine. –
Enzymes: trypsin, chymotrypsin, aminopeptidase,
amylase, lipase, phopholipases

Pancreatic gland….
• J shaped organ
• It is soft, lobulated and elongated organ.
 It is gland located beyond the stomach and duodenum
 It is located in the first portion of small intestine
• It is about 15-20 cm long
• 2.5-3.8 cm broad and 1.2-1.8 cm thick and weighs about
90 g

Pancreatic...con’d
• The pancreas is divided (from right to left )
into the head , the neck, the body and
tail.
 Head is enlarged and lies within the
concavity of the duodenum.
 Tail reaches the hilum of the spleen.

Pancreatic...con’d
• The exocrine pancreas lobules made up of small acini,
the walls of which consist of secretory cells.
 The endocrine portion of the pancreas takes the form of
many small clusters of cells called islets of
Langerhans or, more simply, islets.
 Humans have roughly one million islets.
 Islets are seen as relatively pale-staining groups of
cells embedded in a sea exocrine tissue of pancreas

Anatomy of the pancreas

Three major cell types of Pancreatic islets
1. Alpha cells (A cells 20%) secrete glucagon hormone
2. Beta cells (B cells75%) produce insulin and are the most abundant
of the islet cells.
3. PP cells(1%)=pancreatic polypeptide hormone.
– Has role in appetite, as well as in the regulation of pancreatic exocrine and
endocrine secretions
4. Delta cells (D cells 4%) secrete the hormone somato statin
 It is an inhibitor and is important to balance hormone levels in
the body and stop the effects of over-production of certain
hormones.
suppress the release of glucagon and insulin

Diabetic mellitus
A chronic multi-system disease related to:-
– Abnormal insulin production or
– Impaired insulin utilization
Result in elevation of glucose in the blood.
Refers to a group of common metabolic
disorders that share the phenotype of
hyperglycemia

Diabetic mellitus….
 As a general DM is a clinical syndrome
characterized by hyperglycemia due to:-
a) Deficiency of insulin or
b) Diminished effectiveness of insulin

Diabetic mellitus…
 Factors contributing to hyperglycemia include:
1.Reduced insulin secretion,
2.Decreased glucose utilization, and
3.Increased glucose production.
֍In all types of DM there is abnormal glucose
homeostasis

Diabetic...con’d
• It is a GROUP of metabolic disease characterized by
chronic hyperglycemia with DISTURBANCE in the :-
Carbohydrate,
Fat &
Protein metabolism
 Resulting from :-
• DEFECTS in insulin secretion,
• Insulin action or both .
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Prevalence of diabetic mellitus
 As WHO report of 2019 out of 10 top leading causes of deaths 7 of
them were non-communicable diseases
– All non-communicable diseases together accounted for 74% of
deaths globally in 2019.
• As this report Diabetic mellitus was the 9th cause of death
record
– Again as systematic review and MA indicated, incidence of
type 1 diabetes was 15 per 100,000 people/year (Majid
Mobasseri,2019)
 Pooled Prevalence of DM in Ethiopia 6.5% (Melkamu A. 2021)

Why it called metabolic disorder ?
ALTERED
PROTEIN
METABOLISM
 Insulin

Protein Catabolism

 Gluconeogenesis
(amino acids  glucose)

Hyperglycemia

 Weight Loss and
Fatigue
 ALTERED FAT
METABOLISM
 Insulin

 Lipolysis

 Free fatty acids + ketones

 Acidosis + Weight Loss
ALTERED CHO
METABOLISM
 Insulin

 Glucose Utilization
+
 Glycogenolysis

Hyperglycemia

Glucosuria
 (osmotic diuresis)
 Polyuria*
(and electrolyte imbalance)

Polydipsia*
 Hallmark symptoms of
diabetes
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Insulin and glucagon
Hormones secreted by islet cells within the pancreas
 Stimulus for insulin is
high blood glucose levels
 Stimulus for glucagon is
low blood glucose levels

Normal physiology how glucose is maintained in normal range
within the body
 In human blood glucose is maintained in the normal range by
balance between factor which increase blood sugar and factor
which decrease blood sugar.
Factor which increase BS
 Intestinal absorption after meal
 Gluconeogenesis and
 Glycogenolysis in liver by glucagon and in muscle by epinephrine

Factor which decrease glucose blood sugar
• Uptake by peripheral tissue particularly by skeletal muscle.
 Glucolysis and glycogenesis
 When blood glucose is high there is stimulation of insulin secretion
from pancreases which facilitate peripheral glucose up take by the
liver and skeletal muscle.
 When intestinal glucose upsorption decline between meals hepatic
glucose out put:-
• Gluconeogenesis and glycogenolysis is increased in response to low
insulin level and increased level of counter regulatory hormones
(glucagon and adrenaline)
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Classification of diabetic mellitus
There are several different types of diabetes mellitus.
The major classification includes:-
 Type I DM
 Type II DM
 Gestational DM
 Diabetes mellitus associated with other conditions
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Type 1 DM
• This is previously called IDDM
 Caused due to insulin deficiency (Beta cell destruction
leading to absolute insulin deficient).
 Results from the body's failure to produce insulin and
requires the person to inject insulin.[insulin-dependent
diabetes mellitus (IDDM)].

Pathophysiology
• Type 1 DM is result from lymphocytic infiltration and
destruction of beta cells of the islets of Langerhans in the
pancreas.
• As beta-cell mass declines, insulin secretion decreases
until the available insulin no longer is adequate to
maintain normal blood glucose levels.
• After 80-90% of the beta cells are destroyed,
hyperglycemia develops and diabetes may be diagnosed.

Pathophysiology….
• Patients need exogenous insulin to reverse this
• Autoimmunity play major role in the pathophysiology of type
1 DM.
• There is triggering agent for this auto antibody development.
• In a genetically susceptible individual, viral infection may
stimulate antibodies that trigger an autoimmune response
against antigenically similar beta cell molecules

Pathophysiology...con’d
 Studies of the autoimmune process in humans and in animal
models of type 1 DM (NOD mouse and rat) have identified the
following abnormalities in the humoral and cellular immune
system:
1. Islet cell autoantibodies
2. Activated lymphocytes in the islets, peripancreatic lymph
nodes, and systemic circulation;
3. T lymphocytes that proliferate when stimulated with islet
proteins; and
4. Release of cytokines within the insulitis

Type 2 DM
֍Most prevalent type of diabetes, accounting for
approximately 90% to 95% of patients with diabetes.
֍Heterogeneous group of disorders characterized by:
 Insulin resistance
 Impaired insulin secretion
 Excessive hepatic glucose production
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Type 2 DM …
 It is condition in which cells fail to use insulin properly,
sometimes combined with an absolute insulin deficiency.
Formerly referred to as non-insulin-dependent diabetes
mellitus (NIDDM).
Ω How can impaired insulin secretion will occurred?

Type 2 DM...con’d
 This types of DM may range from predominantly insulin
resistance with relative insulin deficiency to a insulin
secretory defect with insulin resistance.
• There is a combination of resistant to action of the insulin in
the muscle and liver , together with impaired pancreatic β cell
function leading to relative insulin deficiency.
In the beginning there is increased insulin secretion to counter
act insulin resistance but as the disease progress there is
progressive β cell failure and insulin deficiency develops.

Pathophysiology of TIIDM
As a general Four pathophysiologic mechanisms of
TIIDM
1. Resistance
2. Decreases insulin secretion
3. Inappropriate glucose production by the liver
4. Altered production of hormones and cytokines by
adipose tissue (adipokines)

Pathogenesis of type II DM
.
Late stage PANCREASE
Impaired insulin Secretion
Gastrointestinal
absorption glucose
Hyperglycemia
LIVER
Increased basal
Hepatic glucose
production
MUSCLE
Decreased insulin stimulated
glucose uptake

Risk factors for DM
A. Genetic
• Family history of diabetes (i.e.parent or sibling with Type IIDM
B. Environmental factors
• Obesity (BMI 25 kg/m
2
)
• Physical inactivity
• Race/ethnicity (e.g., African American, Latino, Native American,
Asian American,
• Previously identified with IFG, IGT, or an A1C of 5.7–6.4%
• History of GDM or delivery of baby >4 kg
• HDL cholesterol level <35 mg/dL (0.90 mmol/L) and/or a
triglyceride level >250 mg/dL (2.82 mmol/L)
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Action of Insulin
• Transports and metabolizes glucose for energy
• Stimulates storage of glucose in the liver and muscle (in
the form of glycogen)
• Signals the liver to stop the release of glucose
• Enhances storage of dietary fat in adipose tissue
• Accelerates transport of amino acids (derived from
dietary protein) into cells
• The average amount of insulin secreted daily by an adult
is 40 to 50 U, or 0.6 IU/kg of body weight

Risk ...con’d

Insulin resistance
• Resistance of action of insulin in the liver and muscle lead to
Over production of glucose and
Under utilization of glucose leading it to hyperglycemia.
 Type IIDM is often associated with central or visceral obesity,
HTN, dyslipidemia( elevated LDL cholesterols and triglyceride, low
HDL cholesterol)
– Coexistence of these cluster of condition is called insulin
resistance syndrome or metabolic syndrome.
• This metabolic syndrome predispose to cardiovascular disease

Some reasons for insulin resistance
1. Central obesity especially intra abdominal fat cause
insulin resistance because large quantity of FFA released
by adipose tissues compete with glucose to be utilized
with peripheral tissue.
2. Adipose tissue also release money hormone (e.g cortisol,
adipokines) which may decrease sensitivity of insulin
receptors.
• The two main adipokines believed to affect insulin
sensitivity are adiponectin and leptin

Risk ...con’d
3. Lack of exercise increase insulin resistance by down regulation of
insulin sensitive kinase and by the accumulation of FFAs within
skeletal muscle.
 Exercise allow noninsulin dependent glucose up take in to muscle.
• In Pancreatic βcell failure there is progressive reduction in the
beta cell mass.
– Disposition of amylin around beta cells which form
insoluble fibrils of amyloid leading to destruction of β cells.
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Comparisons of Type I and Type IIDM

Comparisons of Type I and Type IIDM
Type 1 type2
prevalence Uncommon(5-10%) Common >80%diabete case
Typical age at onset <40yrs >40 yrs
Duration of symptom weeks Month to years
wt. Normal or low obese
ketoacidosis yes rare
Rapid death without rx with
insulin
yes no
Auto antibody yes no
Diabetic complication at dx no 25%
Family history of DM uncommon common
Other autoimmune disease common uncommon
Insulin secretion Absence/severly decreased Increased/decreased

IGT /IFG
• It is period of abnormal glucose homeostatis
• Those abnormal states are impaired fasting glucose
(IFG) or impaired glucose tolerance (IGT).
• It is intermediate states of abnormal glucose regulation
that exist between normal glucose homeostasis and
diabetes
• IFG it is elevated fasting plasma glucose (FPG)
concentration (≥100 and <126 mg/dl)

IGT /IFG....con’d
• IGT 2-h plasma glucose concentration (≥140 and <200
mg/dl) after a 75-g glucose load on the oral glucose
tolerance test (OGTT) in the presence of an FPG
concentration(>100 to <126 mg/dl )
• This is used to identify population under risk

Gestational diabetes:.
• Gestational diabetes: is when a pregnant woman, who
has never had diabetes, has a high blood glucose level
during pregnancy.
• It may precede development of T2DM.
Ω During pregnancy insulin sensitivity decreased by the
action of placental hormones and there is increase insulin
demand
• Beta cell may be unable to met this demand which lead to
development of gestational DM.

Other Specific Types Dm
Genetic defect of β-cell function( earlier called MODY
maturity onset diabetes in the young)
Genetic defect of insulin action
Pancreatic disease
Drug induced (corticosteroid, thiazide diuretics)
Viral infection(congenital rubella mumps)

Other Specific Types Dm...con’d
A) Genetic defects of beta cell function characterized by mutations
in:
1. Hepatocyte nuclear transcription factor (HNF) 4 (MODY 1)
2. Glucokinase (MODY 2)
3. HNF-1 (MODY 3)
4. Insulin promoter factor-1 (IPF-1; MODY 4)
5. HNF-1 (MODY 5)
6. NeuroD1 (MODY 6)
7. Mitochondrial DNA
8. Subunits of ATP-sensitive

Other Specific Types Dm...con’d
B. Genetic defects in insulin action
1. Leprechaunism
 Inherited in an autosomal recessive pattern insulin resistance
brings growth delay
2. Rabson-Mendenhall syndrome
 An inherited disorder associated with the inability to
regulate blood sugar.
3. Lipodystrophy syndromes
 Heterogeneous group of diseases, characterized by selective
absence of adipose tissue

Other .....con’d
C) Diseases of the exocrine pancreas—pancreatitis,
pancreatectomy, neoplasia, cystic fibrosis,
D) Endocrinopathies—acromegaly, Cushing's syndrome,
E) Drug- or chemical-induced—glucocorticoids,
F) Infections—congenital rubella, cytomegalovirus,
G) Other genetic syndromes sometimes associated with
diabetes Down's syndrome, Turner's syndrome,

Clinical manifestation of DM
• Common presenting symptoms of DM include:3 poly
ῤ Polyphagia
ῤ Polydipsia,
ῤ Polyuria,
 Weight loss
 Fatigue/weakness
 Blurred vision
 Frequent superficial infections, and poor wound healing.

Criteria to diagnosis dm.
 Include one of the following:
1. Fasting plasma glucose(FBG) ≥126 mg/dl.
2. 3polly plus random blood glucose concentration ≥ 200mg/dl
 IFG for fasting plasma glucose level of 100-125mg/dl
 IGT for plasma glucose level of 140-199mg/dl 2hrs after
75 g oral glucose load.
– Individuals with IGT and IFG do not have DM but are
at risk for development of type 2 DM and other CVD in
the future.

Criteria to diagnosis dm...con’d
Diagnosis of DM suspected when classical symptom of
DM or 3poly and unexplained wt losses is observed.
In such case RBS≥200 is enough for dx of DM.
Urine glucose test should never be used alone WHY????
• If RBS values are ambiguous, further dx should be
performed.
 FBS measurement is the most convenient test ( after 8
hours of fasting)

Glycated hemoglobin a1c(HBA1c)
 HbA1c, is a form of hg that is bound to glucose.
 It is test that measures how much glucose is bound.
 This method is used for screening purpose and also for
diagnosis ( sometimes)
 RBC cells live for about 3 months, so the test shows the
average level of glucose in the blood for the past 3
months.

Glycated hemoglobin a1c(HBA1c)….
 The normal range for level for hemoglobin A1c is less
than 7%.
 HbA1c is typically measured to determine how well a
type I or type II treatment plan including:-
 Medications,
 Exercise , or
 Dietary changes)
is working.

Criteria to diagnosis dm……….

Treatment Of DM
 Aims of management:-
Normalize insulin activity
Normalize blood glucose levels
 Reduce the development of long term complications
Maintain patient’s usual life style and activities.

Treatment Of DM based on STG 4th Edition 2021 GC
 There are five components of diabetes mgt:
A. Nutritional mgt
B. Exercise
C. Monitoring glucose level
D. Education
E. Pharmacologic therapy
F. Pancreas or Islet cell transplantation

A. Nutritional mgt
• Focus on supporting the patient on choosing healthy eating
behaviors.
• Consider the literacy of the individual, access to food, and
willingness.
• Respect and address the individual preferences, cultural, and
religious choices.
• Be nonjudgmental
• Be practical
• Limit food choices when only supported by scientific evidences
• Help overweight and obese individuals to decrease body weight
• Help attain individualized glycemic, blood pressure, and lipid goals
• Dividing meal into four to six equal parts helps in achieving
stability in some cases
STG 4th Edition 2021 GC

General advice (Nutrition)….
֍ Avoid refined sugars: soft drinks with sugar, or adding
sugar/honey to teas/other drinks.
֍ Carbohydrate
- Reduce overall carbohydrate intake
- Carbohydrate sources high in fiber and minimally
processed are preferred :
 whole grains, non-starchy vegetables, fruits, and
dairy products
 Be encouraged to have complex carbohydrates

General advice (Nutrition)……..
֍Fat
- Reduce saturated fat (animal fat) intake: butter, fatty cuts of
meat, cheese.
- Reduce Trans-fat (hydrogenated oil): solidified vegetable oils
- Mono-saturated and polyunsaturated vegetable oils are preferred
֍Protein
- Should be left to the individual choice.
- When there is chronic kidney disease, reduction (not stopping)
protein intake.

B. Exercise
 Regular moderate-intensity aerobic physical activity : for at
least 30 minutes at least 5 days a week (at least 150 min/week)
 Encourage resistance training three times per week.
• It is extremely important for lowering blood glucose and
reducing cardiovascular risk factors
C. Weight management
 For obese and overweight individuals
- Eating plans (focusing on reduction of overall carbohydrate
intake) and exercise

Exercise precautions
 The Patient who requires insulin should be taught to eat a 15 gram carbohydrate
snack fruit exchange or a snack of complex carbohydrate with a protein before
engaging in moderate exercise- to prevent unexpected hypoglycemia.
 Toward post exercise hypoglycermia that occurs after strenuous or prolonged
exercise, the Pt may need to eat snack at the end of the exercises.
 Patients who have:
– Blood glucose levels > 250 mg/dL
– Ketones in their urine
• There must be a person there around by information (being DM Pt)
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should not begin
exercising until :-
urine test results are
negative for ketones and
the blood glucose level is
closer to normal

Exercise precautions …
• Ideally, a person with diabetes should exercise at the same
time (preferably when blood glucose levels are at their
peak) and in the same amount each day.
• Regular daily exercise, rather than sporadic exercise,
should be encouraged.
• Exercise recommendations must be altered as necessary
for patients with diabetic complications.

D. Stop smoking
E. Moderation of alcohol intake
 A maximum one drink for women and two drinks for
men.
 One drink is roughly equivalent to a bottle of beer, a glass of
wine, or a unit of spirit.
Screening for micro and macro vascular
complications

F. Monitoring glucose level
Self monitoring of blood glucose (SMBG) enables people
with diabetes to :-
Adjust the Rx regimen,
obtain optimal blood glucose level..
 Today its use is limited to patients who cannot or will not
perform SMBG.

G . Education
Areas of Patient Education
– Patients should understand DM & the needs of lifelong
treatment and follow up
– Goal of treatment should be set together with the patient
– To avoid excess alcohol intake and, avoid smoking
– Benefit of weight reduction, diet and regular exercise
– Proper foot care
– Hypoglycemia causes , symptoms and simple first aid management
– Complications of diabetes
– Insulin injection technique
– Self glucose monitoring
– How to store insulin ( if taking it)

Pharmacologic therapy
A) Oral ant diabetic agent
• Oral drug is only effective for type 2DM
B/c most of them are used to stimulate endogenous
insulin secretion which is absent in type 1DM.
• That is in type 1 there is no chance of insulin secretion
from the liver and there is no insulin resistance

Sulphonyl ureas
1) First generation :ex Tolbutamidee, chlorpropamide.
2) Second generation glibenclamide, gliclazide.
They are differ by their:-
 Potency
Duration of action and
Cost
 First generation rarely used b/c availability of second
generation.

Sulphonyl ureas …
 Mechanisms of action of sulphonyl urea.
 It stimulate the release of insulin from the pancreatic beta
cells. i.e. it is insulin secretagogue
 When those regime failed it called primary failure
 When beta cell are completely exhausted insulin secretion
stopped and now sulphonylurea cannot act this is called
secondary failure.
 Glibenclamide cause sever hypoglycemia so it used
rarely.

Glibenclamide
֍ Starting dose is 2.5-5mg/day, 30 minutes before
breakfast.
Titrate dose slowly to maximum of 20mg/day
When 10mg/day is needed, divide the total dose into two,
with the larger dose in the morning.
Avoid in the elderly and patients with renal impairment

Biguanides
• Metformin is the only biguanides available.
Mechanims of action of metformin
1. Increase glucose sensitivity and peripheral glucose up
take.
2. Impair glucose up sorption by GIT
3. Inhibits hepatic gluconeogenesis.
 It does not stimulate insulin secretion from liver so it
cannot cause hypoglycemia.
 It not associated with wt gain so preferred in obese type
2DM.
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Metformin
 It is first line medication for blood glucose lowering
 Because its efficacy (1–2% decrease in HbA1c),
 Initial dose 500mg to 1 000mg/day daily or in two
divided doses with meals.
 Titrate dose every two weeks depending on the fasting
blood sugar
 Maximum dose = 2000mg/day (1 000mg BID)
• Split dose to twice per day if the daily dose is
greater than 500 to 850 mg per day

Metformin side effect
 The major side effects of metformin are GIT intolerance:
 bloating, abdominal discomfort, and diarrhea.
• This can be reduced by gradually increasing the dose.
• Metformin is contraindicated in patients with
– advanced chronic kidney disease (eGFR <30ml/min),
– advanced liver disease, and hypoxia
Alternative to Metformin
 If Metformin is contraindicated a sulfonylurea can be
started

Metformin….
 If glycemic target is not achieved by metformin alone after three
months, add either of the following.
 Sulfonylureas : Glibenclamide, Glimepiride, Gliclazide
OR
 Basal insulin
Initiating two oral agents at diagnosis:-
 Patients with severe hyperglycemia at presentation (Fasting blood
sugar > 250mg/dl or HbA1 C>1 0%) and prefer oral agents than
insulin, need to be started on a combination of metformin and
sulfonylurea.

Combination of oral agent
 More effective than every drug used alone.
 If the blood sugar is not controlled either by
sulphonylurea or metformin ;combination of them is
better.
 If again the blood sugar cannot be controlled insulin
must be combined with oral drug( given together).

Insulin therapy
Indications for insulin therapy
• Failure to control blood glucose with oral medicines
• Temporary use for major stress, e.g. surgery, medical
illness
• Severe kidney or liver failure
• Pregnancy
• In patients difficult to distinguish type 1 from type 2
diabetes
• Ketonuria

Indications for insulin therapy…..
• Unexplained weight loss accompanied by poorly controlled blood
sugar
• Initial therapy for a patients presenting with very high blood sugar
– HbA1 C >1 0% or fasting blood glucose >250 mg/dl or random
glucose consistently >300 mg/d
 Type 1DM.
 DKA or HHS.
 Present of current illness or concurrent infection as MI, Pancreatic or
stroke.
 Major surgery
 Pregnancy. all pregnant woman with DM either gestational or
previous history of DM whose disease do not controlled by diet
alone should be treated with insulin.

Insulin therapy ……
Because the body loses the ability to produce insulin in
type-1 diabetes, exogenous insulin must be administered
for life.
• In type 2 diabetes, insulin may be necessary on long-term
basis to control glucose level.

Classification of insulin preparation
• Short acting
Regular/ plain insulin
Insulin lispro.
Insulin aspart.
 Intermediate
 NPH insulin( neutral protamine hagedron/ isothene insulin)
Lente insulin(insulin zink suspension).
 Long acting
Ultralente ( extended insulin zink suspension)
Insulin glargine and insulin detemir

Insulin ( with preparation)
preparation time of
Action
Time of
Action
Time of Action
Short-acting, subcutaneous Onset hour Peak hour Effective duration
Lispro <0.25 0.5–1.5 3–4
Aspart <0.25 0.5–1.5 3–4
Glulisine <0.25 0.5-1.5 3–4
Regular
Short-acting, inhaled
Inhaled regular insulin
0.5–1
<0.25
2–3
0.5–1.5
4–6
4–6
Regular insulin have to
injected 20-30 minute
before meal since
duration of onstet is
from15-60min.

Long-acting
NPH 1–4 6–10 10–16
Detemir 1–4 6-14 12–20
Glargine 1–4 minimal 24

Site of injection of insulin
 SC in the :-
Anterior abdomen
Upper arm
Outer thigh and
Buttock
 Implanted in subcutaneous tissue
 Intravenous while treating acute complication of DM as
DKA and HHS.

Site of injection of insulin…

NPH and lenten insulin
• Both are intermediate acting insulin
• NPH produced from regular insulin and protamine
protein which is protein of fish origin and trace amount
of Zink.
• It is poorly soluble at physiologic PH and it is so slowly
absorbed from subcutaneous tissue.
Lenten insulin is produced from regular insulin and Zink
which prolong its action.

Dosing basal insulin in type 2 diabetes
֍If started on as an add on therapy to Metformin
 Starting dose = NPH 10 units at bed time
 A higher dose might be started for higher blood glucose
 Dose increment 2-4 units in 3-7 days with self-monitoring
of blood sugar
֍If started as a replacement for oral agents
 Starting dose = NPH 15 -20 units at bed time
 A higher dose might be started for higher blood glucose

Dosing basal insulin in type 2 diabetes…..
• For doses above 20units divided in two ( about 2/3 in
the morning and 1 /3 in the evening)
• Dose increment 2- 4 units in 3-7 days with self-
monitoring

Dosing basal insulin in type 2 diabetes…..
Addition of prandial regular insulin
 Indications to start regular insulin before meal
1. If FBS is well controlled but HbA1 c is above target
2. If HbA1 c is above target despite increasing basal insulin to >0.5
unit/Kg/day
 Dosing prandial regular insulin
 Starting dose of prandial insulin : Regular insulin 4units
– Preferred time : before the largest meal of the day
– Dose increment 1 -2 units in 2-3 days with self-monitoring of
the next pre-meal blood glucose

Con…d
In general, pts with type 1 DM require 0.5–1.0 IU/kg per
day of insulin divided into multiple doses.
Pts with type 2 DM may be managed with
– Diet and exercise alone or
– Conjunction with oral glucose-lowering agents
(diet+exercise+oral glu] OR
– Insulin, or
– A combination of oral agents and insulin.

As summary regular Insulin and NPH in combination
 0.5-0.7 IU/KG of regular insulin And NPH will be given for pt with
TYPE 1DM.
 The aim of this combination is to manage hyperglycemia immediately
and later (prepradial and post pradial mgt of hyperglycemia)
 Out of 0.5-0.7iu/Kg of insulin 30% must be RI and 70% must be NPH.
 These must be given in the morning and evening as 2/3 in the morning
and 1/3 in the evening.
֍ QQQQQQQQQQQQQQQQQQQQQQQ

Insulin therapy can be
1. Conventional insulin therapy
- These include single daily injections, or two
injections per day (including a combination short-
acting and -NPH insulin)
2. Intensive insulin therapy
- It describes treatment with >3 injections/day or
continuous insulin infusion
- It requires frequent monitoring of blood sugar:
fasting, before lunch, before dinner & before bed.

Insulin therapy can be …
 Conventional IT also requires the following
 Counting and recording carbohydrates.
 Adjusting insulin doses in response to given glucose
patterns.
 Coordinating diet, exercise, and insulin therapy.
 Responding appropriately to hypoglycemia

Insulin therapy can be …
3. Designing insulin therapy
 Total insulin dose per day Initiation, 0.2 to 0.4
units/kg/day
 Maintenance – highly variable roughly 0.6 to 0.7
units/kg/day
 Regimen options-with NPH and regular insulin

Why High Blood Sugar Levels in the Morning
 There are two proposed reason for this case !
1.Dawn phenomenon
2. Somogyi effect (Rebound hyperglycemia)
• Not enough diabetes medications.
• Body change during sleep and reactions that happen while you
are sleeping.
A. Dawn phenomenon
• To wake up body need extra energy (Preparation,3-8 am ????)
• Body releases hormones that reduce your sensitivity to insulin.
• Wearing off previous diabetes medication
B. Somogyi effect (Rebound hyperglycemia)
• Mid night glucose decrease Then body release glucose from
storage site This phenomena is beyond expectation in
Diabetic mellitus patients (That is tooo high glucose is
releaseed from liver

Complication of insulin THERAPY
metabolic
• Hypoglycemia
• Wt. gain.
• Insulin edema.
Local
 Lipoatrophy
 Lipohypertrophy
 Local alergic rxn
Systemic
• Altered pharmakokinetics
Immune insulin resistance
• Insulin Resistance-If a daily
insulin requirement of 200
units or more
Causes: - obesity and high level of
antibodies
1. Mgt; - Administration of more
concentrated insulin
2. Prednisone is given to block the
production of antibodies

Complication...con’d
Insulin Lipodystrophy:-is localized reaction, in the form
of either lipoathrophy or lipohypertrophy, occurring at the
site of insulin injection
 Lipoatropy: - is loss of subcutaneous fat.
Lipohypertrophy:- is development of fibro fatty masses
at the injection site
• Causes -Repeated use of an injection site
 Mgt: - rotation the injection site

Complications of DM
• If not manage appropriately the DM can leads to
diabetic complication.
֎2 types of complications:-
A) Acute complication diabetic
i. Ketoacidosis (DKA) And
ii. Hyperglycemic Hyperosmolar States(hhs)
iii. Hypoglycemia

DKA
• It is complication of diabetes that occurs when our body
produces high levels of blood acids called ketones.
• It is caused by an absence / markedly inadequate amount
of insulin.
• Major cause of morbidity and mortality in pt. with dm.
• Many undiagnosed pt. can come for the first time with
DKA.
• Occurred in in type I DM patients b/c.........................

DKA…
• It has feature of :-
– Hyperglycemia,
– Ketosis acidosis, and
– Dehydration

Pathogenesis of DKA

Pathogenesis of DKA…
 IT usually occur rapidly within 24 hrs.
 Two hormonal abnormality play a great role in the
formation of DKA ,
1. Insulin deficiency and
2. Glucagon excess.
 Occurred at blood glucose greater than 300 mg/dL.

Patho....cond
 Due to the lack of insulin, tissue such as muscle and the liver are
unable to take up glucose.
 Even though the blood has an extremely amount of circulating
glucose, the cells are starving.
 Blood brain barrier does not require insulin for glucose to diffuse
across, so brain cells are receiving more than an adequate amount
of glucose.
 Basically, the general body tissue is starving while the brain has
more than an adequate supply of glucose.
 Thus, the patient does not experience the sudden onset of signs
and symptoms

Patho....cond
• Three major pathophysiologic syndromes associated with
an excessively elevated blood glucose level in DKA:
A. Metabolic acidosis
B. Osmotic diuresis
C. Electrolyte disturbance

Patho....cond
1) Metabolic acidosis
 Starvation of cell leads release of:-
– Glucagon and
– Other counter-regulatory hormones
1. Promote the breakdown of triglycerides into free fatty acids
and
2. Initiate gluconeogenesis to produce more glucose
 Body uses protein and fat to produce glucose

Patho....cond
• Free fatty acid circulated in the blood and this metabolized
into:-
1. Aceto-acetic acid and
2. B-hydroxybutric acid
 Those two are organic acid and called ketones
 An increase in ketone production and a decrease in
peripheral cell use lead to metabolic acidosis
– This is also called ketoacidosis

Patho....cond
2) Osmotic diuresis
 Increment of glucose in the blood lead to osmotic diuretics leads DHN
3) Electrolyte disturbance
 Because ketones are strong organic acids, they must be buffered with
Sodium.
 where sodium goes, water follows and aggravate DHN/volume
depletion
 The loss of large amounts of fluid also leads to the excretion of other
electrolytes, such as potassium, calcium, magnesium and
phosphorous.
 This produces electrolyte imbalance and disturbances.

Possible reasons for DKA happening
Previously undiagnosed and untreated diabetes
Omission of anti-diabetic therapy
Stress of intercurrent illness
e.g.
Infection
Myocardial infarction
Stroke
Surgery
Complicated pregnancy

Clinical manifestation of DKA
Due to hyperglycemia
 Polyuria
 Polydypsia
 Wt Loss
Neurologic deficit as lethargy, focal deficit and
obtundation which lead to coma.
Due to dehydration
• Los of skin turgor
• Cold extremities.
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Clinical manifestation of DKA...con’d
Due to methabolic acidosis
Cusmal breathing.
Acetone smell breathing
Nausea ,vomiting and abdominal pain(delay empting
time of stomach and acidosis)
• Alert lethargic or comatose

Investigations for DKA
 Random blood glucose : usually >300mg/dl)
 Urine glucose (usually >3+)
 Urine ketones (usually >2+)
 BUN and Creatinine
 Serum electrolytes, particularly serum potassium
 Investigations for precipitants:
• CBC,
• Blood film for malaria parasites and others
based on the suspected precipitating factors
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Management of DKA
Objectives of treatment
1. Replace fluid losses
2. Replace electrolyte losses and restore acid-base balance
3. Replace deficient insulin
4. Seek the precipitating cause and treat appropriately

Management of DKA…
1. Replace fluids
 Individualize fluid needs based on the patient hydration
status
 The following is a guide to severely dehydrated patients.
A. Initial fluid
 1 000ml NS the first hour.
 Reassess for hydration status:
 If still severely dehydrated, give another 1 000ml NS over the
next 01 hour.

Replace fluids..
B. Subsequent fluid
 Depends on the hydration status and urine output of the patient.
 On average give about 250 mL/hour (1 000ml over 04 hour) in
the first 24 hours or until patient is able to take enough oral
fluids.
 Reassess the patient hydration status to decide subsequent Iv
fluid needs.
C. Changing fluid
 Change the NS to 5% DW9D when plasma glucose reaches 250
mg/dl in DKA and 300mg/dl in HHS.
 HHS requires more fluid.
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2. Administer short-acting insulin
֍Regular Insulin
 1 0units IV and 1 0 units IM, stat,
֍Then:-
– 5 units, I.M, every hour.
֍Goal:-
- Reduce serum glucose by 50 to 70 mg/dl in the 2-3 hours
- If the drop is <50mg/dl in 2-3 hours, double the regular
insulin.
- If the drop is faster, reduce the dose by half for continuous
infusion and give the IM insulin every 2 hour.
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3. Potassium
All patients with DKA have potassium depletion
irrespective of the serum K+ level.
If the initial serum K+ is <3.3 mmol/l, do not
administer insulin until the K is corrected.
 If the initial serum K + is >5.3 mmol/l, do not
supplement K until the level reaches < 5.3.
If K+ determination is not possible delay initiation of K
replacement until there is a reasonable urine put(>50
ml/hr)

3. Potassium…
 Add intravenous KCl in the IV fluids
Add 40–60 mmol/l of IV fluid when serum K+ < 3.7
mmol/l
The serum potassium should be maintained between 4.0
and 5.0 mmol/l

4. Precipitant identification and treatment
 Infection, trauma, infarction. Initiate appropriate
workup for precipitating event (cultures, CXR, ECG)
5. Follow up of response
 Blood glucose every 1 –2hrs
 Urine ketones every 2- 4hr
 Electrolytes (especially K+) every 6 h for first 24 h

6. Continuation of treatment
 The above treatment should continue until the
patient is stable, clinically acidosis improves, and
patient is able to take oral feeding.
 The urine ketone might still be positive, as it usually
lags behind the improvement of acidosis

7. Transition
Once the patient is able to take oral feeding and clinically
the acidosis improved.
 Reduce regular insulin : 2-3 units hourly
 Overlap regular insulin with subcutaneous NPH insulin
for 2-3 hours
If previously on insulin: start the pre DKA or pre HHS dose

Summary mgt
 Correction and treatment of precipitating factors must be done simultaneously
with the treatment of ketoacidosis.
 As the pt. admitted give NS fast up to 4 bag. A total fluid given may be as high
as 10 liters depending on the patient’s response and urine output.
 Give K replecement 20mEq/10m/ ampoule of KCL.
 If RBS <250mg/dl change NS to dextrose.
 Give 20 IU of RI 10 IM 10 IV followed by 5 IU Im Q hrs in adult ( if child
0.1IURI/kg/hr)
-Check RBS q1hr
-Check ketone q 2 hrs
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Mgt of DKA...con’d
• If after the 1st two hours the blood glucose level has not fallen
significantly, dose of IM insulin can be doubled
• When the patient is completely out of ketoacidosis, regular insulin
is given 4 hourly subcutaneously according to the random blood
sugar (RBG) level :
 If RBG > 250mg/dl 12 Units
 If RBG - 180-250mg/dl 8 Units
 If RBG - 120-180mg/dl 4 Units
 If RBG < 120 mg/dl 0 Units
?????

Hypoglycemia
• It occurs when the blood glucose falls less than 50-
70mg/dl
• Sulfonylureas and insulin are the most common causes
of hypoglycemia.
• A value <70mg/dl is agreed as alert level to define
hypoglycemia in diabetes.
• It should be remembered some patients might be
symptomatic at levels>70mg/dl and some might not
develop symptoms at level <70mg/dl.
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Causes of hypoglycemia in patients taking insulin
• Missed, delayed or inadequate meal
• Unexpected or unusual exercise
• Errors in oral anti-diabetics or insulin
dose/schedule/administration
• Poorly designed insulin regimen
• Lipoatrophy at injection sites
• Breasting feeding by DIABETIC mother

Hypoglycemia…
• When plasma glucose drops below 70 mg/dL, counter
regulatory hormones are released and the autonomic nervous
system is activated.
• Suppression of insulin secretion and production of glucagon
and epinephrine provide defense against hypoglycemia.
• Epinephrine release causes manifestations that include
shakiness, palpitations, nervousness, diaphoresis, anxiety,
hunger, and pallor.
• Because the brain requires a constant supply of glucose in
sufficient quantities to function properly, hypoglycemia can
affect mental functioning

Hypoglycemia…
• Hypoglycemic symptoms may occur when a very high blood
glucose level falls too rapidly
– e.g., a blood glucose level of 300 mg/dL falling quickly to
180 mg/dL
• Although the blood glucose level is above normal
the sudden metabolic shift can evoke hypoglycemic
symptoms.
– Too vigorous management of hyperglycemia with
insulin can cause this type of situation

Clinical manifestations
 Grouped in two adrenergic symptoms and central nervous
systems symptoms.
A. Mild hypoglycemia
The blood glucose level falls, the sympathetic nervous
system is stimulated, resulting in a flow of epinephrine
and norepinephrine.
S/s sweating tremor,
Tachycardia, palpitation
Nervousness, hunger
It occur as a result of sympathetic nervous system
stimulation

B. Moderate hypoglycemia
 In moderate hypoglycemia, the fall in blood glucose level
deprives the brain cells of needed fuel for functioning.
Signs of impaired function of the CNS may include:
– Inability to concentrate,
– Headache,
– Lightheadedness,
– Confusion,
– Memory lapses,
– Numbness of the lips and tongue,
– Slurred speech,
– Impaired coordination,
– Emotional changes,
– Irrational or argumentative behavior,
– Double vision, and
– Drowsiness

C. Sever hypoglycemia
• In severe hypoglycemia, CNS function is so impaired that
the patient needs the assistance of another person for
treatment of hypoglycemia.
• Symptoms may include:
– Disoriented behavior,
– Seizures,
– Difficulty arousing from sleep, or
– Loss of consciousness

Hypoglycemia unawareness
• It is a situation where symptoms of hypoglycemia are not
felt by the patient in spite of having low blood glucose
levels.
• It is a common and challenging problem is patients with
long standing diabetes

Investigations and diagnosis
 A documented blood glucose level <70mg/dl
 Presence of symptoms /sign of hypoglycemia
 If symptoms /sign improve with treatment

Management of hypoglycemia
Objectives of treatment
 Reverse hypoglycemic symptoms
 Prevent brain damage
 Prevent recurrence

Management ……………..
• The mainstay of therapy for hypoglycemia is glucose.
• Manage underlying cause
• Dietary therapy may be effective for improving symptoms
in patients with fasting hypoglycemia.
• Frequent meals/snacks are preferred, especially at night,
with complex carbohydrates

Non-pharmacologic
֍ The main stay of management of level 1 -2 (mild to moderate) and
level-3 (severe) hypoglycemia with preserved consciousness taking
or providing glucose rich food/drinks(sweets).
֍ Pure glucose is preferred but any carbohydrate rich food can
be used
- Give 04 teas spoon of sugar diluted in water
- Monitor blood sugar every 20-30 minutes
- If no improvement repeat the above
- Once blood sugar improves, the patient must take a meal or snack
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Non-pharmacologic…
֍ Alternatives: regular soft drinks
- 200ml of Mirinda or Cola, contains about 20gram sugar
can replace the above.
֍Avoid protein rich foods as they increase insulin
response

Pharmacologic
In patients who present to health facilities with decreased
level of consciousness from severe hypoglycemia:-
 40% Dextrose (20ml vial)
- Give 03 vials IV, fast
- Monitor blood sugar every 20-30 minutes
- If blood sugar is <70mg/dl, give another 03 vials of 40%
dextrose and start 5-1 0% dextrose infusion.
 Continue to monitor blood sugar every 20-30 minutes.
- When the patient can take orally give regular meal or snack.

Hyperosmolar Hyperglycemic Syndrome
• It is a life-threatening syndrome that can occur in the
patient with diabetes who is able to produce enough insulin
to prevent DKA
– but not enough to prevent severe hyperglycemia,
osmotic diuresis, and extracellular fluid depletion
• HHS is a hyperglycemic emergency that occurs in type II
DM due to :-
– Relative insulin deficiency and
– Inadequate fluid intake.

Hyperosmolar Hyperglycemic Syndrome….
• HHS is less common than DKA.
• It often occurs in patients over 60 years of age with
type 2 diabetes
• Apart from acidosis the manifestations, risk factors
and management of HHS is similar to DKA
• It most often occurs in type 2 DM, often in the setting
of physiologic stress.

HHS…
Has feature of :-
I. Extreme hyperglycemia and
II. Dehydration
– Unable to excrete glucose as quickly as it enters the
extracellular space
– When sum of glucose excretion plus metabolism is
less than the rate which glucose enters
extracellular space

HHS…
Rare 1% and more severe than DKA(10-15% severity)
֍It is characterized by sever:
 Hyper glycaemia >600 mg/dL
 Hyper osmolality and
 Dehydration in the absence of significance ketosis.
 More common in type 2 DM

Pathogenesis
• The same as DKA
 In DKA there is complete or sever deficiencies of insulin which
leads to formation of KETONE BODIES AND ASIDOSIS.
 IN HHS some amount of insulin is present which is enough to
prevent fat acid oxidation and formation of ketone bodies.
 Hence in HHS significant ketosis and acidosis is absent.
 Dehydration and hyper glycaemia is more sever than in DKA

Pathophysiology of HHNS

Pathophysiology of HHNS …………

Precipitating factor of HHS
 The same as DK
concomitant illness that leads to reduced fluid
intake, as in elderly institutionalized persons with
decreased thirst perception and reduced ability to
drink water.
Infection is the most common preceding illness, but
many other conditions, such as stroke or myocardial
infarction, can cause this state

Precipitating factor OF HHS…
Urinary tract infections,
Pneumonia,
Sepsis,
Any acute illness, and
Newly diagnosed type 2 diabetes.
HHS is often related to impaired thirst sensation
and/ or a functional inability to replace fluids.

Clinical manifestation of HHS
Most common elderly in
T2DM
Symptoms
 Polyuria,
Altered mental state
Lethargy, obtundation,
seizures, possible coma
Weight loss
 Diminished oral intake
of fluids
Profound dehydration
Tachycardia
Hypotension
 Differentiated from DKA
(No nausea and vomiting,
no abdominal pain, and
Kussmaul breathing)
Laboratory: Very high
serum blood glucose level
(may range from 600-
1200mg/dl)

Comparisons of DKA and HHS

Management of HHS
• The same as DKA but more fluid may be require and
change NS to DNS when glucose level is <300mg/dl.
• Give attention to give adequate fluid

Pancreas Transplantation
• Pancreas transplantation can be used as a treatment
option for patients with type 1 diabetes.
• Done for patients who have end-stage kidney disease
and have had or plan to have a kidney transplant.
• Kidney and pancreas transplants are often performed
together, or a pancreas may be transplanted after a
kidney transplant.

Pancreas Transplantation
• If renal failure is not present pancreas transplantation be
considered only for patients who exhibit the following three
criteria:
1. Having history of frequent, acute, and severe metabolic
complications (e.g.,hypoglycemia, hyperglycemia, ketoacidosis)
requiring medical attention;
2. clinical and emotional problems with the use of
exogenous insulin therapy that are so severe as to be debilitating;
3. consistent failure of insulin-based management to prevent acute
complications.

Pancreatic islet cell transplantation
• The islets are infused via a catheter through the upper
abdomen into the portal vein of the liver.
• With only the islets transplanted, pain and recovery
time are diminished compared with whole pancreas
transplants.

Nursing intervention
• Assess for risk factors for prediabetes and type 1 and type 2 DM
• Teach the patient and caregiver about self-management of DM,
including self-monitoring of blood glucose (SMBG), insulin, noninsulin injectables,
OAs, nutrition, physical activity, and recognition and management of hypoglycemia.
• Develop a plan to avoid hypoglycemia or hyperglycemia in the patient with DM who
is acutely ill or having surgery.
• Assess for acute complications and implement appropriate actions:
hypoglycemia, diabetic ketoacidosis (DKA), and hyperosmolar hyperglycemic
syndrome (HHS).
• Assess for chronic complications of diabetes, including cardiovascular disease,
retinopathy, nephropathy, neuropathy, and diabetic foot
complications.
• Teach patient and caregiver about prevention and management of
chronic complications of diabetes

Nursing intervention…
• Administer OAs and routinely scheduled insulin regimens.
• Monitor the diabetic patient for symptoms of hypoglycemia, DKA,
and HHS.
• In the ambulatory or home setting, monitor patient self-
management of insulin, OAs, nutrition, and physical activity.
• Check capillary blood glucose (CBG) levels (after being trained
and evaluated in this procedure) and report values to the RN.
• Report changes in patient vital signs, urine output, behavior, or
level of consciousness
• Ad more……………………

Thyroid Gland

Thyroid Gland
• It is the largest EG located
in the front of the neck
anterior to trachea
• Butterfly shaped
• Two lobes connected by an
isthmus.
 Secretes hormones that
control many function
 Weight ranges from 12 to
30 g
 Has 2 types of cell
1. Follicle cells
2. Para follicular cells

Function of the thyroid glands
A. Fetal and neonatal growth and development
 Promote growth and development of the brain during fetal
life and for the first few years of postnatal life
 Essential for the secretion of GH
B. Normal functioning of nervous system in adults
- reflexes and alertness (amplifies the effect of SNS )
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Function of the thyroid glands …
C. Stimulates carbohydrate metabolism
 Rapid uptake of glucose by the cells
 Enhanced glycolysis, enhanced gluconeogenesis
 Increased rate of absorption from the gastrointestinal tract
 Increased insulin secretion
D. Increases lipids mobilization
 Decreases the fat stores of the body
 Decreases the free fatty acid concentration in the plasma
 Accelerates the oxidation of free fatty acids by the cells
E. Increases basal metabolic rate
 Increased oxygen consumption
 Increased heat production
 The metabolic rate can increase from 60%–100% when blood thyroid
hormones are elevated

Thyroid Hormones
Hormones Function Stimulated by
T3/T4  Metabolism i metabolism
Calcitonin i blood calcium
concentration
i the reabsorption of Ca
and Ph from bones to
blood
Calcitonin “tones” down
serum Ca levels
 blood Ca
levels

• T4 (thyroxine) or tetraiodothyronine and
Inactive form
has four iodine atoms
Produced 20 times as T3
• T3 also called triiodothyronine, is the
Active hormone.
has three iodine atom

Thyroid hormones...con’d
 T4: (Thyroxine) is made exclusively in thyroid gland
 Ratio of T4 to T3 ; 5:1
 Potency of T4 to T3; 1:10
 T4 is the most important source of T3 by peripheral tissue
deiodination “ T4 to T3 “
• T3(Triiodothyronine) is the most important because more than
90% of the thyroid hormones physiological effects are due to the
binding of T3 to Thyroid receptors in peripheral tissues.

Cell and hormone in thyroid glands
1. Follicle cells:
Produce and secrete thyroid hormone
produce and regulate the storage of thyroglobulin
Thyroglobulin glycoprotein in thyroid gland:
 a glycoprotein that is stored in the thyroid gland and
contains the amino acid tyrosine, which combines
with iodine to form thyroid hormones .

2. Para follicular cells
Produce and secrete calcitonin
 Calcitonin
1. Secreted in response to elevated calcium levels
2. Reduces blood calcium levels
3. Facilitate deposition of calcium in bones

• Both thyroid hormone are stored as thyroglobulin
colloid in the lumen of the follicles.
• The follicular cells produce and regulate the storage
of thyroglobulin.
• They also breakdown and the release of T4 and T3
into the bloodstream.

T4 and T3 are taken into target cells and into the
nucleus where T3 activates genes which control
cellular metabolism.
Target cells convert T4 to T3.
These hormones are controlled by TSH from the
adenohypophysis in response to TRH from the
hypothalamus.

The stimulus for increased T4 and T3 production is
↑↑energy demanding activities.
Then hypothalamus sends out more TRH.
 TRH then increases the TSH produced by the
adenohypophysis.
 TSH in turn increases the production of hormones by
the thyroid.

Hormone Loop
DECREASED Metabolic rate Detected by
hypothalamus (TRH) Stimulates anterior pituitary 
Secretes TSH Blood stream  target organ  thyroid
to secrete T3/T4  Blood stream  target organs 
adrenal medulla Secretes Epinephrine &
Norepinephrine  INCREASED Metabolic rate

Control center for thyroid hormone

COMMON THYROID GLAND DISORDERS

Thyroid gland disorders
Divided into:
֍hyperthyroidism
Overproduction of thyroid hormones
֍Hypothyroidism
 Underproduction of thyroid hormones
֍ Goiter
֍Neoplastic processes
Beningn
Malignant

Hyperthyroidism
• It is hyperactivity of the thyroid gland with sustained
increase in synthesis and release of thyroid hormones
Occurs due to hormone overproduction
Results in the metabolic imbalance hyperthyroidism
Thyrotoxicosis refers to the physiologic effects or clinical
syndrome of hypermetabolism that results from excess
circulating levels of T4, T3, or both.
 Graves’ disease, the most common cause of hyperthyroidism
High T3/T4 in blood

 Primary hyperthyroidism
Causes:
 Tumour of thyroid gland
 Grave’s disease
• T3 and T4 increased
Pathophysiology
210

Pathophysiology...con’d
Secondary hyperthyroidism
– Problem with HT or pituitary gland  high T3/T4
– tumors
– Pituitary  high TSH  high T3/T4

• Toxic diffuse goiter (graves
disease)
• Toxic uninodular or
multinodular goiter
• Painful sub-acute
thyroiditis
• Silent thyroiditis
• Iodine and iodine-
containing drugs and
radiographic contrast agents
• Exogenous thyroid
hormone ingestion
Causes for hyperthyroidism
212

Symptoms
• Hyperactivity
• Irritability
• Heat intolerance & sweating
– Palpitations
– Fatigue & weakness
– Weight loss with
increased appetite
– Diarrhea
– Polyuria
– Sexual dysfunction
signs
• Tachycardia
• – Atrial fibrillation
• – Tremor
• – Goiter
• – Warm, moist skin
– Muscle weakness
– Lid retraction or lag
– Gynecomastia
 Exophtalmus
 Pretibial myxedema
Symptoms/signs
213

 The first step is to get HX
 Wt loss
 Rapid pulse
 Elevated BP
 Protruding eye
 Enlarged thyroid glands ?!
Hyperthyroidism Diagnostic Tests

Laboratory evaluation
 TSH normal, practically excludes abnormality
 If TSH is abnormal, next step: Total & Free T4 & T3
 TSI (Thyroid Stimulating Ig)
 Serum Tg (Thyroglobulin)
 Radioiodine uptake & Thyroid scaning
 FNA, Fine-needle aspiration

• Radioiodine (I123) uptake and
• Thyroid scan –clarifies size of gland and detects presence
of hot or cold nodules.
Testing TSH AND T3, T4
216

Goal
 Normalize serum TSH levels
 Reversecorrect clinical signs & symptoms and metabolic
derangements.
Forms of managements
Beta-blockers
Antithyroid medication
I-131
Surgery
Medical Management

A. Antithyroid medication
• Ant thyroid that interfere with:-
 Synthesis of thyroid hormones and
 Agents that control manifestations of hyperthyroidism.

Antithyroid medication…
֍Carbimazole
 First line
Initial dose 30-40mg/day divided in 2-3 doses
Maximum dose 60mg/day
Maintenance dose : variable but commonly 5-15mg/day
Titrated down the dose based on thyroid function tests:
 In the initial few months based on Free T4 levels and T3
 After the first few months follow up is based on TSH

Antithyroid medication…
֍Propylthioracil / PTU
– Inhibits synthesis of thyroid hormones
– blocks thyroid gland oxidation of iodine
– Prevents peripheral conversion of T4to T3

Antithyroid medication….
֍PTU is the first line in pregnant women
 Initial dose: 300 - 400mg/day in 3 divided doses
 Maximum dose 900mg/day
 Maintenance dose: Variable but commonly 1 00-
200mg/day
Agranulocytosis is a rare but serious adverse effect of
PTU.
It should be suspected if patients develop fever, sore
throat or other features of infection

Antithyroid medication….PTU
Duration of treatment with anti-thyroid drugs
depends on the specific cause of the
hyperthyroidism
In Grave’s disease: hyperthyroidism generally resolves
in 1.5 - 2 years;
• Hence, if euthyroid state is achieved the anti-thyroid drug
needs to be discontinued in 1.5 to 2 years.
In toxic multinodular goiter or toxic adenoma: treatment
should continue until thyroidectomy or radioiodine
therapy is done

Iodine
• Iodine is used with other antithyroid drugs to prepare
the patient for thyroidectomy or for treatment of
thyrotoxicosis.
• The administration of iodine in large doses rapidly inhibits
synthesis of T3 and T4 and blocks the release of these
hormones into circulation.
• It also decreases the vascularity of the thyroid
gland, making surgery safer and easier.
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Iodine….
• The maximal effect of iodine is usually seen within 1
to 2 weeks.
• Because of a reduction in the therapeutic effect, long-
term iodine therapy is not effective in controlling
hyperthyroidism.
• Iodine is available in the form of saturated solution of
potassium iodine (SSKI) and Lugol’s solution

B. Adjunct pharmacologic treatment
Beta blockers: for symptom control until euthyroid state is
achieved.
⇊sympathetic nervous system
 Propranolol, 20-40mg, PO every 8-1 2 hours
OR
 Atenolol 25-1 00mg, PO, daily
OR
 Metoprolol 25-1 00mg, PO, daily or in two divided doses

C. Radioactive iodine
 Radioactive iodine has replaced surgery for treatment of
hyperthyroidism
 Produces thyroid ablation without surgery
 Treatment of choice for grave’s disease and toxic nodular
goiter
Higher dose increases success rate but higher chance of
hypothyroidism

D. Surgery
• Thyroidectomy is indicated for individuals who have
1. large goiter causing tracheal compression,
2. been unresponsive to antithyroid therapy, or
3. Thyroid cancer
 Subtotal thyroidectomy-most common
 Total thyroidectomy is for large goiter or severe disease

Thyrotoxicosis (Thyroid Storm,Thyrotoxic Crisis)
 It is a form of severe hyperthyroidism, usually of
abrupt onset.
 Exacerbation of hyperthyroidism
• It´s a life-threatening exacerbation of thyrotoxicosis, a
companied by fever, confusion, seizures, coma, vomiting,
diarrhea, jaundice.
 Pt critically ill and requires smart observation.
 It occurs in patients with preexisting thyrotoxicosis
 Mortality rate is high (10-75%) despite treatment
Complication of hyperthyroidism
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• Adrenergic receptor activation is a hypothesis.
• Sympathetic nerves innervate the thyroid gland, and
catecholamines stimulate TH synthesis.
• In turn, increased THs increase the density of betaadrenergic
receptors, thereby enhancing the effect of catecholamines
• When TH increase in response to any of the precipitating
factors , systemic adrenergic activity increases.
• This results in epinephrine overproduction and severe hyper
metabolism, leading rapidly to cardiac and sympathetic
nervous system disturbance.
Pathophysiology
3/7/2024 229

 Onset is almost always abrupt, evoked by a stressful
event, such
 Trauma,
 Surgery, or
Infection.
sudden discontinuation of antithyroid drug therapy
initiation of radioiodine therapy
Precipitating factors

• Thyroid storm is characterized by:
High fever above 38.5°C (101.3°F)
 Extreme tachycardia (more than 130 beats/min)
 Exaggerated symptoms of hyperthyroidism with
disturbances of a major system—for example, GI
Altered neurologic or mental state, which frequently
appears as drowsiness or coma
Clinical Manifestations

vomiting
 Irritability and restlessness
Visual disturbance such as
diplopia
Tremor and weakness
Fever
Shortness of breath,
Cough, and
palpitation
Clinical Manifestations…..

 Immediate objectives are:-
 Reduction of body temperature and Heart rate
and Prevention of vascular collapse.
A hypothermia mattress or blanket,
A cool environment
Acetaminophen.
 Humidiﬁed oxygen is administered to improve tissue
oxygenation and meet the high metabolic demands.
 Arterial blood gas levels or pulse oximetry may be used
to monitor respiratory status.
Management
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 Intravenous ﬂuids containing dextrose are administered .
 Porpylthiouracil /Methimazole is administered to
obstruct formation of thyroid hormone and block
conversion of t4 to t3
 Iodine is administered to decrease output of T4 from the
thyroid gland.
 Propranolol has been effective in reducing severe cardiac
symptoms.
Cont…

 This is an autoimmune diseases
 caused by abnormal thyroid stimulating immunoglobulin
of IgG
 class which has long acting thyroid gland stimulating
effect.
 Can be associated with other autoimmune diseases
 The body produces an antibody called Thyroid
stimulating immunoglobulin (TSI ) that mimics the action
of TSH
• Also known as toxic diffuse goiter
• It is the most common cause of hyperthyroidism 80%
Graves disease (Toxic diffuse goiter)

• No negative feedback relationship b/n TH and TSI
• Elevated levels of thyroid hormone, suppressed levels of TSH
(caused by antibodies to TSH receptors).
• Graves' disease accounts for 60–80% of thyrotoxicosis

Risk factors for graves diseases
• Insufficient iodine supply,
• Infection, and
• stressful life events
may interact with
genetic factors to cause
Graves’ disease

• It is associated with a diffuse, symmetrically enlarged
thyroid gland, with normal to slightly smooth in
consistency
• Bruit/thrill may be heard over it.
Typical feature
i. Ophthalmopathy ,
ii. Dermatopathy and
iii. Pretibial myxedema
Features specific to Graves’ disease

Serum T3 and T4 level (free or total ) may be raised
• Ant thyroid antibodies:
Ant microsomal antibody and
An follicular cell antibody,
Ant thyroglobulin antibody,
Thyroid-stimulating antibody; elevated especially in
autoimmune thyroiditis
Diagnosis

• Ant thyriod drugs inhibit the oxidation of iodine and
coupling of iodotyrosines, thus decrease the synthesis
of thyroid hormone.
• PTU in addition decreases the conversion of T4 to T3
in peripheral tissues
• Propylthiouracil (PTU)100–200 mg Qid or Tid or
• Methimazole: 10–20 mg Tid or Bid , once-daily
dosing
Treatment for graves’ disease

• I131,Radioactive iodine-to destroy the overactive thyroid cells
• About 70 -85% of patients are cured by one dose of radioactive
iodine
• causes a decrease in function and size of the thyroid gland in 6-
12 weeks
• Those who are still thyrotoxic after 12 weeks are given a second
dose. Additional dose can be given if needed
• Eventually, almost all patients are cured
Surgery
• Subtotal thyroidectomy

Nursing Intervention
• Administer medications as ordered
• Provide supportive therapy,
– monitoring for cardiac dysrhythmias and decompensation,
(failure of the heart to maintain adequate circulation )
– Ensuring adequate oxygenation, and
– Administering IV fluids to replace fluid and
electrolyte losses

Nursing Intervention ……
• Provide a calm, quiet room
– increased metabolism and sensitivity of the sympathetic
nervous system causes sleep disturbances.
• placing the patient in a cool room away from very ill
patients and noisy, high-traffic areas;
• using light bed coverings and changing the linen frequently
if the patient is diaphoretic

Nursing intervention..
• Encouraging and assisting with exercise involving large
muscle groups (tremors can interfere with small-muscle
coordination) to allow the release of nervous tension and
restlessness.
• It is important to establish a supportive, trusting
relationship to facilitate coping by a patient who is
irritable, restless, and anxious
• Tell the patient that talking is likely to be difficult for a
short time after surgery

Postoperative Care
• Postoperative complications include hypothyroidism, hypocalcemia,
hemorrhage, injury to the recurrent or superior laryngeal nerve,
thyrotoxicosis, and infection.
• Recurrent laryngeal nerve damage leads to vocal cord paralysis.
• If both cords are paralyzed, spastic airway obstruction will occur,
requiring an immediate tracheostomy.
• Place the patient in a semi-Fowler’s position and support
the patient’s head with pillows.
• Avoid flexion of the neck and any tension on the suture lines
• Control postoperative pain by giving medication

Hypothyroidism

• IT is a disease that occurs as a result of insufficient
synthesis of thyroid hormone.
• Disorder with multiple causes in which the thyroid fails to
secrete an adequate amount of thyroid hormones
• It is the most common thyroid disorder.
• Usually caused by primary thyroid gland failure.
• Also may result from diminished stimulation of the
thyroid gland by TSH.
Hypothyroidism
247

• Hypothyroidism is
associated with lack
of dietary iodine
Primary hypothyroidism

• Lack of TSH or TRH
• Negative effect on the size
of the thyroid gland
• Low T3 and T4 level
• No goiter
Secondary hypothyroidism

• Chronic lymphocytic thyroiditis(Hashimoto’s thyroiditis)
• Atrophy of thyroid gland with aging
• Iodine deficiency
• Therapy for hyperthyroidism (Thyroidectomy, Anti
thyroid medications)
• Radiation to head and neck for treatment of head and neck
cancers, lymphoma
Causes of hypothyroidism

• Hypothyroidism frequently develops following
treatment of Graves’ disease with I131therapy or
thyroidectomy
• Idiopathic hypothyroidism
– It is one of the commonest causes of hypothyroidism
• Developmental defects and TSH or TRH deficiency are
less common causes
• Drugs, iodine deficiency, and inherited defects in
thyroid hormone synthesis are rare causes
Without thyroid enlargement

Symptoms
• Tiredness
• Weakness
• Dry skin
• Sexual dysfunction
• Hair loss!
• Difficulty concentrating
Signs
 WT gain
 Slow heart rate
 Bradycardia
 Dry coarse skin
 Puffy face, hands and feet
 Diffuse alopecia
 Delayed tendon reflex
relaxation
 Carpal tunel syndrome
Clinical manifestation of hypothyroidism

• Family & personal medical history
 Hypothyroidism
 Interviews patient
Physical exam
• Laboratory tests
• TSH test
• A measure of free T4
Diagnosing hypothyroidism

Physical examination
Inspection
Palpate
• The thyroid gland is difficult to palpate.
• Supply the person with a glass of water and first inspect
the neck as the person takes a sip and swallows.
• Thyroid tissue moves up with a swallow.
• Abnormal- Look for diffuse enlargement or a nodular
lump.

Physical examination ….
• To palpate move behind the person.
• Ask the person to sit up very straight and then bend
the head slightly forward and to the right.
• Use the fingers of your left hand to push the trachea
slightly to the right.
• Then curve your right fingers between the trachea
and the sterno-mastoid muscle, and ask the person to
take a sip of water.

Palpation...con’d
• The thyroid moves up under your fingers with the
trachea and larynx as the person swallows.
• Reverse the procedure for the left side. (One hand
displaces and the other hand palpates).
• Usually you cannot palpate the normal adult thyroid.
– If the person has along thin neck you sometimes will
feel the isthmus over the tracheal rings.

Palpation...con’d
• The lateral lobes usually
are not palpable check them
for enlargement,
consistency symmetry and
the presence of nodules.
• Abnormal – enlarged lobes
that are easily palpable
before swallowing or is
tender to palpation, or the
presence of nodules or
lumps.

Auscultate the Thyroid
• If the thyroid gland is enlarged, auscultate it for the
presence of a bruit.
• This is a soft, whooshing, blowing sound heard best
with the bell of the stethoscope.
• Bruit is not present normally.
• Abnormal – present with accelerated blood flow,
indicating hyperplasia of the thyroid
• Ex. Hyperthyroidism

Study Finding
 Serum T3 Low
 Serum T4 Low
 Radioactive iodine uptake ⇊below 10% in 24 hrs)
 Serum cholesterol Increased
 Serum TSH - High in primary hypo thyroidism
 TRH stimulation test - Low in secondary disease
Laboratory tests

֍Medical management
 The primary objective in treating hypothyroidism is the
 Restoration of an euthyroid or Normal thyroid
function state.
 General management includes
Gradual replacement of thyroid hormone and a
Low calorie diet to promote weight loss and
reduction in cholesterol level.
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