NCM 101A

Endocrine Signs and Symptoms

Fever with diaphoresis and tachycardia. Impaired cognition accompanied by lethargy and edema. Polyuria along with
polydipsia. A cluster of signs and symptoms like this should alert you to critical endocrine balances and possible serious
disorders in your patients. To uncover the cause of these signs and symptoms, your assessments must be fast, accurate,
and highly focused. To help identify the most likely cause and provide life-saving treatments and nursing care.

Assessing Fever, Diaphoresis and Tachycardia

Debra Welson aged 48, was just admitted from the emergency department with a fever of 102.5 oF (39oC). Along with
severe diaphoresis and palpatations. You know you must perform a rapid, focused assessment when you found that she
has tachycardia with a heart rate of 150bpm. So begin with checking her other vital signs. Ms. Wilson’s temperature has
risen to 103oF (39.4oC). Such a high temperature, can stem from an infection or a heightened metabolic condition, such
as thyrotoxic crisis. Her blood pressure is 140/50mmHg. Her pulse pressure. The difference between the systolic and
diastolic pressures is 90 mmHg, which is widened.

An excess of the thyroid hormone Triiodothyronine (T3) or thyroxine (T4) can increase cardiac contractility and lead to
vasodilation. In turn, this can increase stroke volume. The amount of blood ejected with each heartbeat, and decrease
peripheral vascular resistance. The arteries’ resistance to blood flow. Which widens the gap between the systolic and
diastolic pressures. When this gap exceeds 50 mmhg, a widened pulse pressure exists. Next, auscultate the patient’s
heart. In the 5th intercostal space on the left, you detect an extra heart sound. To hear this sound better, turn the patient
on her left side. Switch to the bell of the stethoscope, and listen closely. Because this extra heart sound is soft, and
occurs just after S2 at the end of diastole, its most likely S3 which is also called a ventricular gallop. This sound
commonly results from increase blood volume and tachycardia. In this condition, blood rapidly fills the ventricles causing
the walls to vibrate which produces S3.

Next, observe the patient’s general appearance. Ms. Wilson looks extremely anxious and diaphoretic, despite a
comfortable room temperature. Anxiety and diaphoresis occur when sympathetic nervous system trigger the release of
catecholamine such as epinephrine and norepinephrine. In thyrotoxic crisis, cell receptors sensitivity to catecholamine
rises and increase sweat gland activity causing severe diaphoresis. When expecting the patient’s face, check for
periorbital edema, which is absent with this patient. Then stand behind and above the patient. Gently pull up her upper
eyelids and observe for the protrusion of the eye orbits. Protrusion of one or both eyes indicates exophthalmos; which
Ms. Wilson doesn’t have. Now, ask your patient to hyperextend her neck slightly. Then inspect looking for asymmetry or
bulging. To help visualize the thyroid gland, shine a light down from the patient’s chin as you look below the cricoid
cartilage. Then have the patient swallow so you can observe her thyroid gland movement. To help her swallow, provide
a glass of water.

Now prepare to palpate the thyroid gland. To assess its size and texture, and to detect any nodules or thrills. To palpate
from the front, face your patient and use the finger pads or your right hand to feel the left lobe. Also, using your left
hand, gently press the sternocleidomastoid muscle medially to trap the gland between your fingertips and palpate it.
Then, switch hands. Using your, left finger pads to palpate the right lobe. And using your right hand, press on the
muscle. If you are having difficulty feeling the gland, ask the patient to flex her neck forward, to relax her neck muscles.
Avoid pressing too hard. Otherwise, you may not feel nodules or thrills, and you could cause a sudden release of thyroid
hormones. Now feel the thyroid gland’s movement. To do this, palpate on both sides of the cricoid cartilage until you
feel the thyroid isthmus. Then, ask the patient to swallow so you can feel the gland move.
If you prefer, use a posterior approach to palpate the thyroid gland. Standing behind the patient, palpate as you would
from the front. Feeling the thyroid gland’s lobes and isthmus. Usually, the thyroid gland feels smooth and rubbery and
rises easily with swallowing. Its normally 4cm across and the right lobe is slightly larger than the left one. For Ms. Wilson,
the gland feels smooth and moves easily however, its larger than normal. And enlarged thyroid gland suggests
hypertrophy; which may result from over production of T3 and T4. Ms. Wilson’s thyroid gland, has a palpable thrill or
vibration over its lobes. To assess this further, auscultate the thyroid gland, using the bell of your stethoscope, to detect
a low pitch bruit. Press the bell gently over each lobe and listen for the soft rushing sound of a bruit. Ms. Wilson has a
bruit that lasts throughout systole and diastole. A thyroid bruit usually signifies accelerated blood flow through an
enlarged thyroid gland. To differentiate between a bruit and a venous hum, occlude the jugular vein. if the sound
disappears, it’s probably a venous hum.

Next, inspect the patient’s abdomen. Ms. Wilson’s abdomen has no pulsations or distension. So begin to auscultate it
using the diaphragm of your stethoscope to detect high pitch bowel sounds. Ms. Wilson’s bowel sounds are hyperactive
and audible even without a stethoscope. Next, palpate the patient’s abdomen. Although Ms. Wilson denies feeling pain
or tenderness, she reports that she’s been having diarrhea and nausea. Hyperactive bowel sounds, diarrhea, and nausea
can reflect increased peristalsis. Which can occur with hunger, GI bleeding, or a heightened metabolic state such as a
thyrotoxic crisis.

Assessment Findings
 Fever
 Severe diaphoresis
 Tachycardia
 Widened pulse pressure
 S3 heart sound
 Anxiety
 Enlarged thyroid gland
 Thyroid thrill and bruit
 Hyperactive bowel sounds
 Diarrhea and nausea
After you discuss your assessment findings with the physician, he suspects the probable cause is a thyrotoxic crisis. An
exacerbation of hyperthyroidism. A thyrotoxic crisis can be given when immunoglobulins or other factors, attack the
thyroid gland and cause chronic overproduction of T3, T4, or both. Then an infection or other stressor triggers the
sudden release of these hormones into the blood. In all body cells, T4 converts to T3. When T3 engages with receptors
on mitochondria, it increases cell metabolism by forcing mitochondria to consume more oxygen. And increases their
production of adenosine triphosphate. On cell membranes, excess thyroid hormones may increase the number or
sensitivity of catecholamine receptors. And this produces adrenergic symptoms such as tachycardia, anxiety and
diaphoresis. Eventually, the overwork thyroid gland enlarges. Resulting in hypertrophy.

Test Results in Thyrotoxic Crisis

 Decreased TSH level
 Increased FT  level
4

 Increased FT  level
3

Immediate Interventions
 I.V. fluids to replace fluid due to diaphoresis
 Beta blocker to reduce tachycardia and other adrenergic symptoms
 Radioactive iodine
 Thyroid hormone inhibitor such as propylthiouracil
 Plan to monitor the patient v/s atleast every 4 hrs
 Provide a calm, quiet environment to reduce her anxiety
ASSESSING IMPAIRED COGNITION, LETHARGY AND EDEMA

This morning, Linda Webster aged 52, was admitted with impaired cognition and lethargy. she also report generalized
edema. Her medical history includes hyperthyroidism although she usually takes levothyroxine for this disorder. She
stopped taking it several weeks ago when an illness caused nausea and vomiting. So you prepare for a focused
assessment. Beginning with her vital signs. Ms. Linda Webster’s temperature is 96 oF (35.5oC). This low temperature or
mild hyporthermia can result from a thyroid hormone deficiency. Normally, T3 increases energy production in cells
which increases their oxygen consumption. This boost in cell metabolism generates heat and a higher body temperature.
Without sufficient T3, cell metabolism falls along with body temperature. Mrs. Webster’s blood pressure is 110/90
mmHg signaling, a narrowed pulse pressure. A decreased thyroid hormone level can reduce cardia contractility and
output and cause vessel constriction. And this effects can decrease stroke volume and increase peripheral vascular
resistance. Reducing the difference between systolic and diastolic pressure. If the difference is less than 30 mmHgthe
patient has a narrowed pulse pressure.

Next, auscultate the patient’s heart sound. Mrs. Webster’s heart rate is only 52bpm. Her heart rate may be slow because
a decrease thyroid hormone level can reduce myocardial cell receptor sensitivity to catecholamines. Ms. Webster’s heart
sounds seem faint and distant this may result from pericardial effusion which is a collection of fluid in the pericardial
sack. Here’s how it can develop. A thyroid hormone deficiency allows mucopolysaccharide accumulate in cardiac and
other tissues. As these carbohydrates accumulate, they draw fluid and protein with them. When the fuild collects in the
pericardial space, it dampens heart sound transmission to the chest wall. During your assessment notice your patient’s
mental status. She has difficulty concentrating and is lethargic. Her impaired cognition and decrease level of
consciousness may mean brain metabolism has slowed. Also, assess the patient’s skin which unusually dry and coarse
and appears edematous. Especially around her eyes, and on her hands and feet. This finding may result when decreased
catecholamine sensitivity reduces sweat glands activity. Next, inspect and palpate the thyroid gland. This patient;s gland
is normal in size, texture and movement. Continue by inspecting the patient’s abdomen for palsations and distension.
Which she doesn’t have. Then auscultate for bowel sounds. For this patient, auscultation reveals hypoactive bowel
sounds. Now, palpate the abdomen which causes no pain or tenderness for the patient, However, she reports
constipation. Hypoactive bowel sounds and constipation reflect decrease peristalsis which is common in hypothyroidism
ad myxedema.
Assessment Findings Test Results in Myxedema
 Hypothermia  Normal FT3 level
 Narrowed pulse pressure  Decreased FT4 level
 Bradycardia  Increased TSH level
 Distant heart sounds
 Impaired cognition and lethargy Immediate Interventions
 Edema and dry, coarse skin  Immediately administer an IV or Synthetic
 Hypoactive bowel sounds Thyroid hormone such as Levothyroxine
 Constipation  Plan to monitor your patient’s V/S every 4 hours
 Re-orient her as needed if she becomes
confused
 Provide a warm environment to prevent heat
loss and slowly raise her body temperature

Test Results in Myxedema

 Normal FT  level
3

 Decreased FT  level4

 Increased TSH level

Immediate Interventions
 Synthetic Thyroid hormone

Now, review your assessment findings with the physician and discuss their probable cause which may be an acute
exacerbation of hypothyroidism called, myxedema. I myxedema, inflammation atrophy or another factor, greatly
reduces the thyroid gland production of T3 T4 or both. Without these hormones, cell metabolism slows and cells
become less sensitive to catecholamine. Reduced catecholamines sensitivity, decreases cardiac contractility, reduces
cognition and level of consciousness and causes other symptoms.

ASSESSING POLYURIA AND POLYDIPSIA

Jason Cooper aged 26 has had type 1 diabetes mellitus for 10 years. 2 days ago, he developed a viral infection with a
fever of 102oF (39oC). Today he was admitted with polyuria and polydipsia. So you draw blood for electrolyte and glucose
levels and artetrial blood glas analysis and prepare for a focused assessment of his signs and symptoms. To evaluate the
patient’s polyuria, not the urine’s color and amount before spending a specimen to the laboratory. Mr. Cooper is voiding
large amounts of dilute urine. Which may signal osmotic diuresis caused by hyperglycemia. In the kidneys, glucose rich
blood, move through paratubal capillaries to reach the nephrons. There, glucose moves into the renal tubules, taking
large amounts of water with it. And producing large amounts of dilute urine. Also, use a dip stick to test the urine for
glucose and ketones. Which Mr. Cooper has. Glucose is detectable in the urine; when the blood glucose level exceeds
beyond 180 mm/decileter. This level represents the renal threshold. The point at which the nephrons can no longer re-
absorb glucose. Which then moves into the distal tubules for excretion in the urine. Ketones form when the liver breaks
down free fatty acids (FFA) into glucose for energy. This process, creates ketones as a by product.

Next, ask the patient about his polydipsia or excessive thirst. He says he consumes gallons of water over the past 2 days.
Polydipsia usually results from dehydration. When the kidney excretes massive amounts of urine, the blood volume falls.
Decrease blood volume triggers the thirst center in the hypothalamus to prompt the patient to drink more. Now chedk
the patient’s V/S. Mr. Cooper’s respiration are unusually deep and fast at 28bpm (Kussmaul’s respirations). And his
breath smells sweet and fruity. Typically results in metabolic acidosis, In metabolic acidosis, the level of acidosic ketones,
rises; while the level of basic bicarbonate falls. Together, these changes lower the blood pH. To compensate, the brain’s
medulla signals the lungs to breathe faster and deeper to exhale more CO2; because CO2 is an acid. This raises the blood
ph. At the same time, ketones give the breathe a characteristic sweet, fruity odor. Mr. Cooper’s apical heart rate is rapid
110 bpm. And his bp is low 90/50 mmhg. Low bp occurs when the blood volume and cardiac output, fall. To
compensate, the adrenal glands try to raise the cardiac output and bp by secreting catecholamines, which stimulates the
heart to beat faster. Next, assess the skin because this patient’s skin seems particularly dry, check his skin turgor.
Tenting indicates poor skin turgor,probably caused by interstitial fluid loss through dehydration.
If time permits, assess your patient for long-term complications of diabetes mellitus. Such as diabetic retinopathy and
peripheral vascular disease. To perform an opthalmoscopic examination, first dilate the pupils, then dim the lights and
then ask the patient to stare at a point across the room. With the ophthalmoscope lens indicator set to 0, approach the
patient form the side. When your about 15 inches form his pupil, look for an orange glow called the red reflex. Which
Mr. Cooper has. Loss of the red reflux, may signify that the lens has been clouded by a diabetes induce cataract.
Normally, the thinner light red arteries converge with the thicker dark red veins in the optic disk, where they cross their
borders, appear crisp and intact, without narrowed areas. If you see new, blood vessel growth, suspect diabetic
retinopathy. In this disorder, reduced blood flow to the retine prompts new vessel formation to supply blood and
oxygen to retinol tissue. This new vessels are weak and may rupture. Also, the retina may develop dot shaped
hemorrhages. Hard exudates which are sharply defined, bright yellow spots. and soft exudates which are dull yellow
spots with poorly defined borders. Next, check for signs of peripheral vascular disease by assessing the color and
temperature of the legs and feet. Looking for skin breakdown, especially foot ulcers. And palpating the peripheral
pulses. Mr. Cooper’s legs are warm and dry. His skin is intact and his pulses are strong.

Assessment Findings
 Polyuria
 Glycosuria and ketonuria
 Polydipsia
 Kausmaul's respirations
 Sweet fruity breath
 Tachycardia
 Hypotension
 Poor skin turgor

Blood Test Results

 Glucose: 520 mg/dl
 pH: 7.26 (acidosis)
 Bicarbonate: 14 mEq/liter (reflecting bicarbonate loss through buffering)
 Potassium: 5.2 mEq/liter (reflecting potassium movement out of ceels caused by acidosis)

To determine the probable cause of your patient’s signs and symptoms, discuss them with the physician. Based on the
assessment findings and test results, the physician diagnosis: diabetic ketoacidosis (DKA). This complication of diabetes
mellitus can occur when the stress of illness increases epinephrine and norepinephrine secretion by the adrenal glands
and glucagon secretions by the pancreas. This substances raise the blood glucose level by reducing glucose movement
into muscle cells or increasing glucose production. Then glucose builds up in the blood because it can’t enter the cells
without insulin. And because insulin isn’t produced in type 1 diabetes. Soon. the cells become starved for glucose to fuel
their metabolism. So the brain signal the alpha cells in the pancreas to produce the hormone glucagon which converts
glycogen into glucose in the liver. When the glycogen stores are depleted, the liver converts free-fatty acids and amino
acids into glucose, releasing the blood glucose even further. The conversion of free fatty acids into glucose creates
ketones as a by product. Because ketones are acidic, they disturb the acid base balance when they accumulate in the
blood. Eventually, ketones accumulation and hyperglycemia lead to DKA (a life threatening type of metabolic acidosis).

Immediate Interventions
 Isotonic I.V. fluids (normal saline solution to replace loss fluid)
  Electrolytes (Potassium to correct imbalance that maybe detected after fluid replacement)
 Regular insulin (move glucose into the cells for energy)

Also plan to check your patient’s blood glucose and electrolytes every hour until his conditions
stabilizes. During treatment be alert for signs and symptoms for hyperglycemia such as tremors,
weakness and diaphoresis. This can result from a too rapid reduction of the blood glucose levels and
measure the patient;s V/S particularly noting his bp and heart rate every 4 hours or more frequently.