N-204: ADVANCED PATHOPHYSIOLOGY FMA #2

A. Differentiation of Edema
Increased capillary permeability (burns, nephritic syndrome)

Decreased production of plasma proteins (hypoalbuminemia) Loss of plasma proteins (hypoalbuminemia)

(malnutrition, hepatic failure) (renal failure)

decreased capillary oncotic pressure increased tissue oncotic pressure

EDEMA

Decreased transport of capillary filtered protein

Increase Na and Water retention Lymph Obstruction (Cancer)

Fluid movement into tissues Decreased absorption of interstitial fluid

Increased capillary hydrostatic pressure

(Venous congestion, salt and water retention: CHF. Pregnancy and Renal Failure)

Disease/ Congestive Heart Failure Nephrotic Syndrome Renal Failure Severe Burns
Condition
Causes of Increase capillary pressure (Porth, Increased capillary permeability Sodium and Body Water Excess, Decrease colloidal osmotic
Edema 2002) Decrease Colloidal Osmotic pressure, Increase Hydrostatic Pressure pressure,
(Porth, 2002) (Bullock, 1996) Increase capillary permeability
Decrease in Colloid Osmotic (Porth, 2002)
Pressure (McCance and Huether,
2004)
Physiologic During CHF, there is inability to In Nephrotic Syndrome, there is Kidneys cannot adequately In burns, large areas of the
Rationale pump blood to meet body’s needs due increase Permeability of glomerular excrete the solute load and skin are injured. This also includes
to pump impairment. This results to capillaries to protein due to hypervolemia results. Decreased capillary/ blood vessel injury. When
decrease in CO resulting to decrease Glomerular injury. This causes sodium and water excretion by the the capillary wall is damaged,
BP. Proteinuria that leads to kidneys leads to an increase in capillary colloidal pressure is
 However, due to compensatory hypoproteinemia (Albumin <3g/100 extracellular volume with an decreased and capillary permeability
mechanisms of the body: (SNS and ml). increase in capillary volume and is increased. When this happens,
Renal Compensation) there is Hypoprotenemia then leads to pressure with subsequent plasma proteins and other
vasoconstriction and increase in decrease in plasma colloid osmotic movement of fluid in the tissue osmotically active particles leak into
amounts of aldosterone causing pressure. This in turn leads to the ff: spaces. (Porth, 2002) the interstitial spaces, increasing the
abnormal retention of Na and Water.  Fluid escapes into the tissues In protein losing kidney tissue colloidal osmotic pressure
This in turn leads to increase in  Plasma volume decreases. diseases, plasma proteins are lost. and thereby contributing to the
plasma volume that increases SNS and Renal Compensation This causes increase in decreased accumulation of interstitial fluid.
intravascular capillary pressure. The Occurs: increase in colloid osmotic pressure that causes (Porth, 2002)
Failing Heart is unable to pump Aldosterone secretion which fluid to shift into the interstitial
increase venous return resulting to causes Na and Water spaces causing edema. (McCance
fluids being forced in the interstitial retention and Huether, 2004)
spaces. (Bullock, 1996) Fluid is lost in the interstitial spaces.
 Left Sided: due to inability of (GENERALIZED EDEMA) (Porth,
the heart to pump increase in 2002)
venous return, blood dams
back to the pulmonary veins
and capillary bed. Fluid then
passes across to pulmonary
capillary membrane to
interstitial spaces around
alveoli and into the alveoli.
(PULMONARY EDEMA)
 Right Sided: blood dams back
from Right Ventricle to the
Right Atrium causing increase
pressure in the Peritoneal
Vessels. Fluid then moves into
the interstitial spaces.
(SYSTEMIC PERIPHERAL
EDEMA)
Description  Pulmonary and Systemic  Manifestations of generalized  Generalized and pulmonary  Because plasma proteins are
of Edema Peripheral Edema edema (Porth, 2002) edema (Porth, 2002) evenly distributed throughout
 LSHF- dyspnea on exertion,  Initially, in the dependent parts the body and are not
increase in RR, orthopnea, of the body (such as lower affected by the force of
rales, anxiety, weak rapid extremities) but becomes more gravity, edema due to
pulse, increase venous generalized as the disease decreased colloidal osmotic
pressure, skin cool and moist/ progresses pressure tends to affect
ashen gray/ cyanotic, frothy  complications include dyspnea tissues in nondependent as
white/pink-tinged/ bloody due to pulmonary edema, well as dependent parts of
sputum pleural effusions and the body. There is swelling of
 RSHF- peripheral/ dependent diaphragmatic compromise the face as well as the legs
 edema, jugular vein distention,
hepatomegaly, splenomegaly
(Porth, 2002)
 This edema may lead to the ff:
LSHF- Cardiac Asthma, Paroxysmal
Nocturnal Dyspnea
RSHF- respiratory impingement,
organ dysfunction, jaundice/
Coagulation problems, ascites, pleural
effusion
Disease/ Hepatic Failure
Condition
Causes of Decreased Colloidal Osmotic
Edema Pressure (Bullock, 1996)
Physiologic Since the liver is an important site
Rationale for protein synthesis, In liver diseases,
there is decreased production of
plasma proteins (specifically albumin).
(McCance and Huether 2004). Lack or
inadequacy of plasma proteins result
to decrease in capillary osmotic
pressure that causes fluid to escape
into the interstitial spaces. This
causes edema. (Porth, 2002)
Description  generalized edema
of Edema
The effect that edema exerts on the body function is determined by its location, cerebral edema can be a life-threatening situation, but swollen feet can be a normal
discomfort that accompanies hot weather.
can develop
Malnutrition
Decrease Colloid Osmotic pressure
(Porth 2002)
In starvation and malnutrition,
edema develops because there is lack
of amino acids needed in plasma
protein synthesis. Due to inadequate
production of plasma proteins
(albumin, globulins and fibrinogen),
there is decreased colloidal osmotic
pressure. Fluid therefore leaks into
the interstitial spaces causing edema.
(Porth, 2002)
 Because plasma proteins are
evenly distributed throughout
the body and are not affected
by the force of gravity, edema
tends to affect tissues in
nondependent as well as
dependent parts of the body.
There is swelling of the face as
well as the legs and feet.
Cancer
Obstruction of Lymphatic Flow
(Porth, 2002)
Osmotically active plasma
proteins and other large particles
that cannot be reabsorbed through
the pores in the capillary membrane
rely on the lymphatic system for
movement back into the circulatory
system. However due to presence
of malignant obstruction of the
lymphatic structures, lymph flow is
impaired. (Porth, 2002)
 Lymphedema or localized
and dependent on area of
malignant tumor (Porth,
2002)
and feet. (Porth, 2002)
Pregnancy
Increase capillary hydrostatic
pressure (Porth, 2002)
Decrease Colloid Osmotic Pressure
(Olds et. al., 1992)
Physiologic edema is caused
by the increased movement of fluid
out of the intravascular hemodiluted
blood with its decreased colloid
osmotic pressure, into the
extracellular spaces. This movement
is aided by increased hydrostatic
pressure in the venous capillaries of
the dependent limbs due to pressure
of the gravid uterus in the inferior
vena cava. (Olds et. al., 1992)
 Physiologic edema:
Dependent Edema (Legs
and ankles etc.)
 In PIH: generalized edema
(face, ands and abdomen;
pitting edema; weight gain)
(Wong et. al., 2002) with
possible Pulmonary edema
and cerebral edema. (Olds et.
al., 1992)
B. Hypertension

RENAL FAILURE PHEOCHROMOCYTOMA

Disruption in RENIN- ANGIOTENSIN- ALDOSTERONE system secreting tumor of chromaffin

Hypervolemia N circulation increase volume increase secretion of Epinephrine and norephinephrine

Normal SVR increase SVR increase SVR

Increase contractility increase SVR

HYPERTENSION
(Increase BP)

damage to the arcuate arteries and afferent arterioles increase pressure in capillaries of the brain
dilatation of the intracerebral arteries

progressive hyaline sclerosis leakage of water and electrolytes into brain tissues

arteries rupture
ischemic death of nephrons INCREASED INTRACRANIAL PRESSURE

vessels repair
contracted kidneys

thickening of endothelium
RENAL FAILURE

Obstruction of blood flow to the brain

STROKE

Renal Failure and Pheochromocytoma are contributing factors to hypertension. Renal Failure may also be a consequence of hypertension as well as stroke and
increased intracranial pressure (Bullock, 1996).
C. Anemia

Causes:
1. Renal Disease: a decrease in the number of hemoglobin in patients with liver disease results from a short life span of RBCs that because of altered plasma and
reduced erythropoietin because of decreased renal formation and inhibition from uremia (Bullock, 1996).
2. Leukemia: anemia is common due to replacement of erythrocytic bone marrow with leukemic elements. Anemia is also present due to bleeding: nosebleeds,
ecchymosis and petechiae usually results from decreased platelet formation (Bullock, 1996).
3. Aplastic Anemia: Due to decreased bone marrow function, a drop in the levels of all blood elements occurs, including decrease in RBCs (Bullock, 1996).
4. Acid Peptic Disease: This cause gastrointestinal bleeding that results to blood loss. This leads to anemia: Iron deficiency anemia. (Porth, 2002)

References

Bullock, B. L. (1996). Pathophysiology: Adaptations and Alterations in Function.4th edition. Philadelphia: Lippincott- Raven Publishers.

McCance, K. L. and Sue E. H. (1994). Pathophysiology: The Biologic Basis for Disease in Adults and Children.2nd edition. USA: Mosby yearbook Inc.

Olds, Sally et. al., (1992). Maternal and Newborn Nursing: A Family Centered Approach. 4th edition. California: Addison- Wesley Nursing.

Price, S.A. and Wilson, L.M. (1992). Pathophysiology: Clinical Concepts of Disease Processes. 4th edition. USA: Mosby yearbook Inc.

Porth C. M. (2004). Essentials of Pathophysiology: Concepts of Altered Health Status. Philadelphia: Lippincott Williams and Wilkins.

Wong, Donna L. et al., (2002). Maternal Child Nursing Care. 4th edition. USA: Mosby, Inc.