Endocrine System
** DM for exam; type 1 and 2
-drawing up more than one insulin
-admin of insulin
-
Functions
- Differentiation of reproductive system in CNS in fetus
- Stimulation of growth and development
- Coordination of male and female reproductive systems
- Maintenance of internal environment
- Adaptation of emergency demands
-
o Are excreted by kidneys or deactivated by liver
or cellular by liver or cellular mechanisms
Regulations of hormone release
o Hormones are released:
 In response to an alteration in the
cellular environment
 To maintain a regulated level of certain
substances or other hormones
 Hormones are regulated by chemical,
hormonal, or neural factors
 N- feedback
 Hormones are released into **
-glucose fuels cells in the body; but cannot go into cell
without insulin = without insulin glucose stays in
bloodstream not being used – stored in liver as
glycogen
The liver
- Sensitive to insulin levels
- High BS and insulin = liver will cause the body to
absorbed extra glucose – turn it into glycogen
- Low glucose and insulin = liver will release stores of
glycogen and turn into glucose
Hormones
- General characteristics
o Specific rates and rhythms of secretion
o Operate withing feedback system
o Affect only target cells with appropriate
receptors
The Pancreas
- Both endocrine and exocrine gland
- Islets of Langerhans
o Secretion of glucagon and insulin
o Cells:
 Alpha- glucagon
 Beta- insulin and amylin
 Delta- somastatin and gastrin
 F cells- pancreatic polypeptide
-
Endocrine Pancreas
- Insulin
o Synthesized from proinsulin
o Secretion is promoted by increased blood levels
of glucose, amino acids, GI hormones
o Facilitates the rate of glucose uptake in the cells
of the body
- Amylin
o Peptide hormone co-secreted with insulin
o Relays nutrient uptake
o Suppresses glucagon secretion
- Glucagon
o Secretion is promoted by decreased blood
glucose levels
o Causes liver to release glycogen to be turned
into glucose
o Stimulates glycogenolysis, gluconeogenesis and
lipolysis
Pancreatic somatostatin
o Possible involvement in regulating alpha and
beta cell secretions
Gastrin, ghrelin, and pancreatic polypeptide
Review of Some Important Hormones
- Glucagon
o Hormone formed in the pancreas that promotes
the breakdown of glycogen to glucose in the
liver
o Produced by alpha cells of the pancreas
o Raises the concentration of glucose in
bloodstream
- Cortisol
o Steroid hormone produced by the adrenal glands
o Released in response to stress and low blood
glucose concentration
o Functions to increase blood sugar through
gluconeogenesis, to suppress the immune
system and to aid in the metabolism of fat,
protein, and carbs
o Elevated levels, if prolonged, can lead to
proteolysis and muscle wasting and promotes
the breakdown of fat
o Counteracts insulin and has detrimental effects
of on the immune system and wound healing
and acts as a diuretic
- Catecholamines
o Are hormones made by the adrenal glands
o They are released into the blood when a person
is under physical or emotional stress s
o Main catecholamine are dopamine,
norepinephrine and epinephrine
Normal feedback loop
- Ate high glucose food -> pancreas releases insulin in
reponse -> insulin causes reuptake of glucose into cells
(left over will be stored in liver)
- Low blood sugar -> pancreas will release glucagon ->
cause liver to release glycogen -> turn into glucose =
increase in blood sugar
What happens in DM?
- Body cannot get access to glucose you’re eating- no
insulin or insulin resistance
- Hyperglycemia results
- Sugar affects organs
- Body starts to metabolize fats (type 1) for energy or
there is enough insulin (doesn’t use carbs; carbs
metabolism
Dysfunction of Endocrine Pancreas: Diabetes Mellitus
NB: common imbalance manifestation = metabolic acidosis
-type 2:
-type 1: complete destruction of beta cells
-dx: ketones in urine, weight loss- suspect possible DMglucose tolerance testing
- Is a metabolic disease, disorder of carbohydrate
metabolism characterized by hyperglycemia resulting
from defects in insulin secretion, insulin action or both
- Sustained hyperglycemia, polyuria, polydipsia,
ketonuria and weight loss
Types
- T1DM
o
o
o
o
-
5% - 10% of all cases
Also called IDDM
Or called juvenile-onset DM
Primary defect is destruction of pancreatic beta
cells
T2DM
o Most prevalent form of diabetes
o Also called NIDDM
o Adult onset diabetes mellitus
o Obesity is almost always present
o Insulin resistance and impaired insulin secretion
Classification of diabetes
-
Diagnosis
- Excessive plasma glucose is dx
- Pt must be tested on two separate days, and both test
must be p+
- Three test:
o FPG
o Casual plasma glucose
o OGTT
 Eval of hypoglycemia
 Normal fasting glucose: 4-6 mmol/L
 30 minutes after glucose – normal is <11
mmol/L
 1 hr <11
 2 hrs <7
 3hrs ***
 High = problem in insulin response
HbA1c, OGGTT
Confirmatory test required
- In the absence of symptomatic hyperglycemia, if a
single lab test result is in the diabetes range, a repeat
confirmatory lab test (FPG, A1C, 2hPG in a 75 g
OGTT) must be done on another day
- Repeat the same test (in a timely fashion) to confirm
- But a random PG in the diabetes range in an
asymptomatic individual should be confirmed with an
alternate test
- If results of two different tests are available and both
are above the diagnostic thresholds, the diagnosis of
diabetes is confirmed
Prediabetes
-
Impaired fasting plasma glucose between 100 and 125
mg/dL
- Impaired glucose tolerance test
- Increased risk for developing type 2
- Many reduce risk with diet and exercise and possibly
oral antidiabetic drugs
DX prediabetes
tests
results
Prediabetes
category
FPG (mmol/L)
6.1-6.9
IFG
2h PG in a 75g
7.8-11.0
IGT
OGTT (mmol/L
A1C (%)
6.0-6.4
Prediabetes
Recommendation 1:
- Diabetes should be diagnosed by any of the following
criteria:
- FPG ≥7.0 mmol/L [Grade B, Level 2]
- A1C ≥6.5% (for use in adults in the absence of factors
that affect the accuracy of A1C and not for use in those
with suspected type 1 diabetes) [Grade B, Level 2]
- 2hPG in a 75 g OGTT ≥11.1 mmol/L [Grade B, Level
2]
- Random PG ≥11.1 mmol/L [Grade D, Consensus]
- In the presence of symptoms of hyperglycemia, a single
test result in the diabetes range is sufficient to make the
diagnosis of diabetes.
- In the absence of symptoms of hyperglycemia, if a
single laboratory test result is in the diabetes range, a
repeat confirmatory laboratory test (FPG, A1C, 2hPG in
a 75 g OGTT) must be done on another day
- It is preferable that the same test be repeated (in a
timely fashion) for confirmation, but a random PG in
-
the diabetes range in an asymptomatic individual should
be confirmed with an alternate test.
If results of two different tests are available and both
are above the diagnostic cut-points, the diagnosis of
diabetes is confirmed [Grade D, Consensus]
To avoid rapid metabolic deterioration in individuals in
whom type 1 diabetes is likely (younger or lean or
symptomatic hyperglycemia, especially with ketonuria
or ketonemia), the initiation of treatment should not be
delayed in order to complete confirmatory testing
[Grade D, Consensus]
Type 1 DM
- Is a slowly progressive autoimmune T-cell mediated
disease that destroys beta cells of the pancreas
- Destruction of beta cells is related to genetic
susceptibility and environmental factors
- These gene-environment interactions results in the
formation of autoantigens that are expressed on the
surface of the pancreatic bet-cells and circulate in the
bloodstream and lymphatics
- Cellular immunity (T-cytotoxic cells and macrophages)
and humoral immunity (autoantibodies) are stimulated,
resulting in beta cell destruction and apoptosis
- Over time, insulin synthesis declines and
hyperglycemia develops
- For insulin synthesis to decline such as hyperglycemia
occurs, 80%-90% of insulin secreting beta cells of the
islet of Langerhans (group of pancreatic cells that
secrete insulin and glucagon) must be destroyed
- Normally, insulin suppresses the secretion of glucagon
(which is the hormone produced by the alpha cells of
-
-
the islets and acts in the liver to increase blood glucose
by stimulating glycogenolysis and gluconeogenesis
There is also a decrease secretion of amylin, another
beta cell hormone that is needed to suppress glucagon
release from the alpha cells therefore
Both alpha cells and beta cell function are abnormal,
both lack of insulin and a relative excess of glucagon
contribute to hyperglycemia in T1DM
Affects the metabolism of fat, protein, and
carbohydrates. Glucose accumulates in the blood and
appears in urine (osmotic diuresis and polyuria and
thirst( due to lack of insulin; protein and fat breakdown
in weight loss
Increased metabolism of fats and proteins leads to high
levels of circulating ketones- can lead to DKA
Clinical manifestations:
o Polydipsia, polyuria, polyphagia (hungry and
craving food; due to burning of fats) , weight
loss
o Patient will present as: thin, young, sudden..
ketones in urine
Type 2 DM
- A genetic-environmental interactions appears to be
responsible for T2DM
- Risk factors include: age, obesity, HTN, physical
inactivity, family hx
- Pathophysiology
o Genetic abnormalities (ie. Genes that code for
beta cells and their function (ability to sense
blood glucose levels, insulin synthesis and
insulin secretion) insulin receptors, synthesis of
glucose, glucagon synthesis etc
o Thereby insulin resistance and decreased insulin
secretion by beta cells
o Insulin resistance-suboptimal response of
insulin sensitive to insulin. It is associated with
obesity-role of obesity in type 2 (adipokines,
increase in FFA, inflammatory cytokines
o There is insulin present (resistant); pancreas
thinks that body needs more insulin due to sugar
levels = over secretion of insulin
o Clinical manifestations:
 Polydipsia (due to polyuria)
 Polyuria (osmosis; water moves from
low concentration to high concentration;
water shifts into blood = high fluids –
kidneys start to filter and excrete;
usually reuptakes glucose but too much
in blood = glycosuria)
 Present will present as: overweight,
happens over time, adult age, rare for
ketones to be present
 Non-specific symptoms including
fatigue, pruritus, recurrent infections,
visual changes, symptoms of neuropathy
S
Slow wound healing
U
Blurry vision
Damage to eyes
G
Glycosuria
Kidney leaking sugar
Acetone
Acetone breath
breath
-Burning of ketones
R
Rashes on skin
Repeated vaginal infection (excess sugar)
-
Acute Complication
- Hypoglycemia
o <60mg/dL
o Side effect of too much insulin or oral
antihyperglycemic
o Present as sweaty, cold, clammy (give me some
candy- simple carbs), lightheaded, double vision
o If unconscious = IV d5w or d50
- Organ problem
o Too much sugar = arteriosclerotic issues
(glucose will stick to proteins of vessels = hard
and form plaques)
 Affects heart, strokes, hypertension,
neuropath, decreased wound healing
(especially on feet), eye problem,
infections
Diabetic ketoacidosis
o Severe manifestation of insulin deficiency – NO
insulin
o No insulin= fat breakdown = ketones ->
hyperglycemia, ketosis, acidosis
o Symptoms evolve quickly -period of hours or
days
o Most common complication in pediatric pts and
leading cause of death
o Altered glucose metabolism:
 Hyperglycemia
 Water loss
 Hemoconcentration: water loss = blood
viscos- blood clots; HTN
o Altered fat metabolism
 Production of ketoacids
o Tx:
 Insulin replacement
 Bicarbonate for acidosis
 Water and sodium replacements – loss
water, loss sodium
 K+ replacements
 Normalization of glucose levels
NB: stress = increase in catecholamines and cortisol;
someone with type 1 having flu can develop
o Typically associated with type 1
o DKA is a serious complication related to
defiency of insulin and an increase levels of
insulin counter regulatory hormones
(catecholamines, cortisol, glucagon and growth
hormone)
o Causes:
 Undiagnosed diabetes
 Body needs more insulin than normal:
illness, stress, medications
(corticosteroids, thiazides)
 Skipping meals or not eating – body
goes to starvation mode – burn fats =
ketones
 Not taking insulin as scheduled =
glucose is not controlled
o Predisposing factors: stressful situations such as
infection, accident, trauma, emotional stress,
omission of insulin
o Slow onset
o What happens?
 Insulin normally stimulates lipogenesis
and inhibits lipolysis thus, preventing fat
catabolism
 In DKA, with defiency of insulin,
lipolysis is enhance and there is an
increase in the amount of free fatty acids
delivered to the liver, thus leading to
increased gluconeogenesis contributing
to hyperglycemia and production of
ketones
 Accumulation of ketone bodies cause a
drop in pH = metabolic acidosis
o Clinical manifestations

Hyperglycemia: intracellular to
extracellular shifting (water)- pulls
electrolytes with it
 Ketones in blood: blood pH drops,
weight loss, electrolyte shifting,
metabolic acidosis, fruity breath
 Metabolic acidosis
 Malaise, dry mouth, headache
 Polyuria
 Polydipsia
 weight loss
 dehydration
 Nausea, vomiting, pruritus, abdominal
pain, lethargy: due to increase blood
sugar and ketones in body
 SOB, Kussmaul respirations -rapid and
deep resp (d/t metabolic acidosis)
 Fruity or acetone odour to breath (due to
ketones)
o Nursing
 Education
 Monitor and prevent
 Need to monitor glucose and
urine ketones in urine every 4 hr
when sick
 If they cant eat or drink –
 Drink every hour
 If BS >300 = notify MD
 Notify MD if excessive urination,
thrist, abdo pain, fruity breath
 Pharmacological
 Goal hydrate, decrease BS,
monitor K+ levels and for



cerebral edema, correct acid-base
imbalance
IV fluids – may start with
isotonic NS, then to 0.45 NS
(hypotonic; go into cells- watch
for cerebral edema)- sometimes
D5W is added with ½ NS with
glucose 250-300 (gradually drop
BS because brain can’t cope and
H2O will be moved from blood
to CSF -> cerebral edema –
increase ICP
Administering insulin
o IV with regular only
o Check potassium level
(>3.3; with DKA levels
are either normal or
elevated due to osmosis
from cell to blood; insulin
will cause shift back to
cell = hypokalemia )
o Priming for tubing for
insulin drip- insulin
absorbed into plastic
lining --- waste 50-100 cc
of insulin to prevent
Other meds:
o Potassium IV solution -to
keep K during insulin –
watch for phlebitis (K is
hard on veins. EKGs,
renal function – renal
issues = decreased k
clearance)
-
Acute Complication: Hyperglycemic Hyperosmolar
Nonketotic Syndrome (HHNKS)
o Uncommon but significant complication of type
2 – EXTREME hyperglycemia
o No breakdown of ketones- no breakdown of fats
(body has just enough insulin)
o Occurs most often in elderly individuals who
have other comorbidities (ie infections, CV and
or renal disease)
o Differs from DKA in the degree of insulin
deficiency (more profound in DKA) and the
degree of fluid deficiency (more marked in
HHNKS)
o Glucose levels are much higher in HHNKS than
in DKA because of volume depletion
o Causes:
 Main cause = illness or infection (esp.
older adults)
o Clinical manifestations include:
 Severe dehydration
 Loss of electrolytes (including K+)
 Neurological changes such as strupor
(confusion, coma, seizures)
 Heavy duty Hyperglycemia (>600)
 Polyuria (due to high glucose in bloodosmotic diuresis)
 Polydipsia (due to polyuria)
o Similar to DKA but different
 Little or no change in ketoacid
 Little or no change in blood pH
 No sweet or acetone like smell to urine
or breath
 Mostly with Type 2 with acute infection,
illness or some other stress
o Large amount of glucose excreted in urine
o Dehydration and loss of blood volume
o Increases the blood concentrations of
electrolytes and nonelectrolytes (particularly
glucose) also increases hematocrit
o Blood “thickens” and becomes sluggish
o Can evolve slowly (warning signs: extreme high
BS, polyuria, polydipsia)
 Metabolic changes begin a month or two
before signs and symptoms become
apparent
o If untreated, can lead to coma, seizures and
death
o Nursing:


-
Goal: hydrate and decrease BS
Correct hyperglycemia with IV insulin,
fluid (similar to DKA), electrolyte
Acute complication: Hypoglycemia
o Occur in type 1 and type 2 diabetes (although
those with type 2 are less at risk)
o Pallor, tremor, anxiety, tachycardia, palpitations,
diaphoresis, headache, dizziness
o Treatment requires immediate replacement of
glucose (PO or IV)
o Prevention: individualized management of
medication and diet, blood glucose monitoring
and education
-
Somogyi effect
o Combination of hypoglycemia followed by
rebound of hyperglycemia
o Asleep 2-am to 3 am
-
o Drop of blood sugar- body release cortisol,
catecholamines, growth hormone to increase
sugar
 To counteract- eating bed time snack or
decrease bed time dose
Dawn Phenomenon
o An early morning rise in blood glucose – 5-8 am
concentration with nor hyperglycemia at night
o Related to nocturnal elevation of growth
hormone which decrease metabolism pf glucose
by muscle and fat
o Body increases extra glucose
 Night time dose of NPH
Relevant Lab Values, Indications and Critical Values
Blood
Adult: 4-6 mmol/L, critical
glucose
values
Glucose
tolerance
Glycosylated -refers to the permanent
hemoglobin attachment of glucose to
HbA1c
hemoglobin molecules and
reflects the average plasma
glucose exposure over the life
of a red blood cell (~120days)
Normal findings:
-non diabetic adult/childe:
4%-5.9%
-good diabetic control: less
than 7%
-fair diabetic control: 8%-9%
-poor diabetic control: greater
than 9%
Hemoglobin
Calcium
Potassium
BUN
-male: 140-180 mmol/L
-female: 120-160 mmol/L
-pregnant women, children
and adolescents
8.8-10.5 mg/dL
3.5-5.0 mEq/L (mmol/L)
3.6-7.1 mmol/L
-critical values >35 mmol/L =
serious impairment of renal
function
7.35-7.45
pH
Sodium
Bicarbonate
Ketone
glucose
Chronic complications of diabetes
- -Macrovascular damage
o Heart disease
o Hypertension
o Stroke
o Hyperglycemia
o Altered lipid metabolism
- Microvascular damage
o Retinopathy
o Nephropathy
o Neuropathy
o Gastroparesis
o Amputations secondary to infections
o Erectile dysfunction
- Infection
Nursing
-
Educate, administering medication , assessing,
monitoring
- Diet:
o Individual: depends on activity and how they eat
o Carbs (45-60%) grains, starchy vegetable (corn,
potatoes- sweets contain hidden sugar
o Fat (<20%) limit saturated fats/cholesterol (in
lard, gravy, whole mill, fatty meats- encourage
healthy fats (monosaturated/poly): avocado,
olives, nuts
o Proteins (15-20): meats don’t increase glycemic
index- avoid red meat
- Exercise
o Aerobic is best (helps body use insulin)
o Check BS prior to exercising- < 100 eat a small
snack (simple carbs)
o Teach signs of decreased BS
o If planning to exercise for a long time- check BS
before, during, after- a lot of glucose
o If glucose > 250 with ketones in urine- avoid
exercising until remove- body is burning
ketones- exercise will burn more ketones ->
DKA
o Teach signs of hyperglycemia (3 p)- im hot and
dry I must be on a sugar high
- Oral Medications
o Usually with type 2 with poor management with
diet and exercise
Sulfonylureas
*most common
-ie. Glyburide, glipizide, diabinese,
Amaryl
-generic name ends with ides
-stimulate beta cells to make insulin
-will cause hypoglycemia (pancreas)
-no alcohol – will experience extreme
hypoglycemia (ETOH already causes
extreme hypoglycemia)
-adverse: hypoglycemia and weight gain
Meglitidinides
-end in glinide
-stimulate beta cells to make insulin
-take with first bite of food*
Biguanides
-metformin
-decreases liver stores of glucose and
increase tissue response to insulin
-held 48 hrs prior to surgery/procedure
(heart cath*)dyes in cath do not interact
well = renal failure (watch renal
function)
-adverse effects: GI symptoms: appetite,
nausea, diarrhea + lactic acidosis
Alpha glucoside
-precose, glyset (starch blockers)
inhibitors
-blocks BS by breaking down starchy
foods in gut; delay carbohydrate
digestion and absorption – decreasing
the postprandial rise in blood glucose
-take with first bite of food
-adverse: GI: flatulence, cramps.
Abdominal distention, borborygmus
Thiazolidinedione -TZD
-gltiztizone
-decrease glucose production in liver ;
(decrease insulin resistance) increase
glucose uptake by muscle and adipose
tissue
-watch for liver and heart function
(increase risk of Mis
-
-adverse: hypoglycemia (w/ excessive
insulin); HF; bladder cancer, fractures
(in women); ovulation (unintended
pregnancy
o Meds that can cause hypoglycemia
 Beta blockers (olol)- mask symptoms of
hypoglycemia
 Alcohol
 ASA
 Sulfonylureas
 MAO inhibitors (depression drugs)
 Backin (antibiotics)
o Meds that can cause hyperglycemia
 Thiazides
 Glucocorticoids
 Estrogen therapy
Insulin
o Only insulin IV = regular insulin
o Rotate sides – no use same site more than once
in a 2-3 week periods
 Risk of developing lipodystrophy” pitting of fat
o Abdo, armpit or thighs
o Don’t massage or heat – increase absorption
(increase chances of hypoglycemia)
o Mixing “clear to cloudy” – R to N
o Rapid, Short, Intermediate, Long
H
U
M
Rap I d
L
O
G
N
S
ovolog
hort
E
G
Hum U lin
P
H (intermediate)
L ong
Levem I r
La N tus
o Peak = pt is more at risk for hypoglycemia
Rapid
-onset: 15 minutes
-peak: 1hr
-duration: 3 hrs
“15 minutes feels like an hour during 3
rapid responses”
Short
-onset: 30 minutes
-peak: 2 hrs
-duration: 8hrs
“short staffed nurses went from 30
patients 2(to) 8 patients”
intermediate -onset: 2 hrs
-peak: 8 hrs
-duration: 16 hrs
“nurses play hero 2 (to) eight 16 year
olds”
Long acting -onset: 2 hrs
-peak: none
-duration: 24hr
“the two long nursing shifts never
peaked but lasted 24 hrs”
Insulin use
•
•
•
•
Indications
• Principal – diabetes mellitus
• Required by all type 1 and some type 2 patients
• IV insulin for DKA
• Hyperkalemia – can promote uptake of
potassium
• Tight glucose control
Dosage
Dosing schedules
• Conventional therapy
• Intensive conventional therapy
• Continuous subQ infusion
Achieving tight glucose control
Insulin complications
• Hypoglycemia
• Lipodystrophies
• Allergic reactions
• Hypokalemia
• Drug interactions
• Hypoglycemic agents
• Hyperglycemic agents
• Beta adrenergic blocking agents
Glucagon for insulin overdose
• -Preferred treatment is IV glucose
• Immediately raises blood glucose level
• Glucagon can be used if IV glucose is not available
• Delayed elevation of blood glucose
Exercise teaching
Case Study
- Lab values to monitor: hemoglobin (hydration), calcium
(, potassium, BUN
- No insulin before exercise = exercise may cause
hypoglycemia