B.

Synthesis of the disease

B.1. Definition of the disease (Book based)
Hyperthyroidism is characterized by loss of normal regulatory controls of TH secretion.
Because the action of TH on the body is stimulatory, hypermetabolism results with increased
sympathetic nervous system activity. Excessive amounts of TH stimulate the cardiac system and
increase the number of beta-adrenergic receptors, leading to tachycardia and increased cardiac
output, stroke volume, adrenergic responsiveness, heartrate, and cardiac contractility.
Preeclampsia is the result of generalized vasospasm. The underlying cause of vasospasm
remains a mystery, but some of the physiologic processes are known. In a normal pregnancy,
vascular volume is significantly increased, and cardiac output is increased. Despite these
factors, blood pressure does not rise in a normal pregnancy, probably because pregnant
women develop resistance to effects of vasoconstrictors such as angiotensin II. Moreover, a
decrease in peripheral vascular resistance occurs from effects of certain vasodilators, such as
prostacyclin (PGI2), prostaglandin E2 (PGE2) and endothelium-derived relaxing factor (EDRF).
In preeclampsia, however, peripheral vascular resistance increases because of the
sensitivity of some women to angiotensin II and a decrease in vasodilators. Vasospasm reduces
the diameter of blood vessels, which results in impeded blood flow and elevated blood
pressure. As a result, circulation to all body organs, including the kidneys, liver, brain, and
placenta, is decreased.
Decreased renal perfusion reduces the glomerular filtration rate. Consequently, blood
urea nitrogen, creatinine, and uric acid levels rise.
Glomerular damage secondary to reduced renal blood flow allows protein to leak across
the glomerular membrane
Loss of protein from the kidneys reduces colloid osmotic pressure and allows fluid to
shift to interstitial spaces. This fluid shift may result in relative hypovolemia, which
causes increased viscosity of the blood and a rise in hematocrit. Generalized edema
often occurs.
In response to hypovolemia, additional angiotensin II and aldosterone are secreted to
trigger the retention of both sodium and water. The pathologic processes spiral:
additional angiotensin II results in further vasospasm and hypertension; aldosterone
increases fluid retention, and edema is worsened.
Decreased circulation to the liver impairs liver functions and leads to hepatic edema and
subcapsular hemorrhage, which can result in hemorrhagic necrosis. This process is
manifested by elevated liver enzyme levels in maternal serum. Epigastric pain is a
common symptom.
Vasoconstriction of cerebral vessels leads to pressure-induced rupture of thin-walled
capillaries, resulting in small cerebral hemorrhages. Signs and symptoms of arterial
vasospasm include headache and visual disturbances, such as blurred vision and spots
before the eyes, as well as hyperreflexia.
Decreased colloid oncotic pressure can lead to pulmonary capillary leaks that result in
pulmonary edema. Dyspnea is the primary symptom.
Decreased placental circulation results in infarctions that increase the risk for abruption
placentae and HELLP (which stands for hemolysis, elevated liver enzymes, and low
 platelets) syndrome. In addition, the fetus may experience IUGR and persistent fetal
hypoxemia.

B.2. Predisposing/ Precipitating Factors

Modifiable
Obesity
Presence of vascular disease (e.g chronic hypertension, diabetes mellitus, renal disease)-
increases risk of preeclampsia
Smoking- can cause vasoconstriction
Alcohol consumption- can stimulate RAS to secrete more aldosterone causing
vasoconstriction
Low Socio-economic status- poor nutrition

Non-Modifiable

Age- preeclampsia is seen more often in teenagers and in women over age 35.
Primigravidity- most likely to occur in first pregnancy
Personal History- women who had prior pregnancies without hypertension are more
likely to have preeclampsia if a new partner has previously fathered a pregnancy in
another woman that was complicated by the disorder.
Race- African-Americans with positive family history and with chronic hypertension or
renal disease.
Family History- follow-up to 3 generations has shown that there may be a single
recessive trait in preeclampsia giving an expected frequency of 2% for daughters and
about 4% for sibling sister. About 1/3 of primigravidas who had eclampsia develops
hypertension in about 20% of subsequent pregnancies
Nulliparity- nulliparas are 6-7x more prone to develop preeclampsia than multipara
Gender- Female
Multiple pregnancy- increases progressively with the number of fetuses.

B.3 Signs and Symptoms

Gestational Hypertension
a. Hypertension -Blood pressure is 140/90 mmHg or systolic pressure elevated 30 mmHg
or diastolic pressure elevated 15 mmHg above prepregnancy level; Due to
vasoconstriction
b. no proteinuria or edema;
c. blood pressure returns to normal after birth.
Mild Preeclampsia
a. Hypertension- Blood pressure is 140/90 mmHg or systolic pressure elevated 30 mmHg
or diastolic pressure elevated 15 mmHg above prepregnancy level; Due to
vasoconstriction
b. Proteinuria of 1+ - 2+ on a random sample; Increased permeability of glomerular
membrane, allowing serum proteins albumin and globulin to escape into the urine.
 c. Weight gain over 2 lb/wk in second trimester and 1 lb/wk in third trimester; Indicates
abnormal tissue fluid retention is occurring
d. Mild edema in upper extremities or face; Due to protein loss, sodium retention, and
lowered glomerular filtration rate.
Severe Preeclampsia
a. Hypertension- Blood pressure is 160/110 mmHg; due to vasoconstriction
b. Proteinuria 3+ - 4+ on a random sample and 5 g on a 24-hr sample; Increased
permeability of glomerular membrane, allowing serum proteins albumin and globulin to
escape into the urine.
c. Oliguria (500ml or less in 24 hr or altered renal function tests; elevated serum creatinine
more than 1.2mg/dl); degenerative changes also result in decreased glomerular
filtration, so there is lowered urine output and clearance of creatinine.
d. Cerebral or visual disturbances (headache, blurred vision); due to cerebral edema
e. Extensive peripheral edema; Due to protein loss, sodium retention, and lowered
glomerular filtration rate.
f. Epigastric pain; abdominal edema or ischemia to the pancreas and liver has occurred
g. Nausea/ Vomiting; abdominal edema or ischemia to the pancreas and liver has occurred
Eclampsia
a. Either seizure or coma accompanied by signs and symptoms of preeclampsia are
present; when cerebral irritation from increasing cerebral edema becomes so acute that
a seizure occurs
b. Poor fetal prognosis; due to hypoxia, possibly caused by the seizure, with consequent
fetal acidosis

Synthesis of the disease

Definition of the disease (Client-centered):
The patient was diagnosed with preeclampsia related to pre-existing hyperthyroidism
on July 18, 2017 when Mrs. Wans blood pressure was taken and recorded as 130/70mmHg and
quickly decreased to 90/70mmHg after 5 minutes. She wasnt aware of her condition since she
wasnt experiencing any signs of hypertension such as nausea/vomiting. Although, the patient
already has edema on her lower extremities.

B.2. Predisposing/ Precipitating Factors

Modifiable Factors:
a. Low socio economic status- the clients poor nutrition may be a result of the
increased intake of high sodium food.

Non-modifiable:
b. Gender- Female

B.3 Signs and Symptoms

a. Hypertension (blood pressure of 130/70)- A very slight decrease in the diameter of the
arteriole causes a major increase in peripheral resistance, reduces the capacity of the system
and increases the diastolic pressure or afterload substantially.
b. Edema on the lower extremities- As sodium retains fluid, edema results. Edema is further
increased because, as more protein is lost, the osmotic pressure of the circulating blood falls
and fluid diffuses from the circulatory system into the denser interstitial spaces to equalize the
pressure.
c. Delayed capillary refill time of 4 seconds- As decreased blood volume available for perfusion
is shunted away from the extremities to feed more vital organs.
 A. Schematic Diagram:
Hyperthyroidism:

Low blood levels of T3 and T4 stimulate hypothalamus

Hypothalamus increases TRH secretion

Pituitary increases TSH secretion

TSH stimulates the thyroid gland

Increased TSH leads to enlarged gland

Goiter

Hypermetabolic Increased sympathetic Cardiac effects

state activity

Wide gaze, lid lag, Increased Peripheral

Increase general heart rate and
diarrhea, nervous, vasodilation due
metabolic rate contractility
irritability, tremor to heart load

Increase overall Increased cardiac Hypermetabolic

BMR output state

Heat
intolerance Skin becomes Palpitation and
and soft, warm, and tachycardia
increased flushed
sweating
 Preeclampsia:

Vasospasm

Vascular effects Kidney effects Interstitial effects

Vasoconstriction Decreased glomeruli

filtration rate and
increased permeability
of glomeruli membranes

Diffusion of fluid
Poor organ perfusion from blood stream
into interstitial tissue
Increased serum blood
skjl
urea nitrogen, uric acid,
and creatinine

Increased blood pressure Edema

Decreased urine output

and proteinuria
Bibliography:

Books:
Pilliteri, Adelle. Maternal and Child Health Nursing; Care of the Childbearing and Childrearing
Family. Lippincoh Williams and Wilkins, 2007

London, Marcia. Maternal and Child Nursing Care 2nd Edition. 2007

McKinney et al. Maternal-Child Nursing 4th Edition. 2013

Black, Joyce. Medical-Surgical Nursing; Clinical Management for Positive Outcomes 8th
Edition. 2009

Doeneges, Marilynn. Nurses Pocket Guide. F. A. Davis Company 11th ed. 2008

Pillitteri, A. (2007). Maternal and child health nursing: Care of the childbearing &
childbearing family. Fertilization: The beginning of pregnancy. 183-197

VanPutte, C., et al. (2016) Seeleys anatomy and physiology (9th ed.)