13 May 2019 leMaN 06 1

MS. CATHERINE C. MARIBBAY

RN, MSN
 1. Pasteur’s Germ theory – specific microorganism was
capable of causing an infectious disease
2. Biochemical model – explain disease as a result of
malfunctioning organs or cell
 Focuses on the cause and effect relationships but
tends to ignore the psychological components of
disese.

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 HOMEOSTATIC THEORIES OF THE
CAUSES OF DISEASE
1. Claude Bernard laid the foundation of
homeostatic theories.
 Describe the internal milieu
 He hypothesized that if an organism is to live, it
must have the capacity to maintain its internal
environment
 Defined health as the ability of the living organism
to maintain its internal environment in a constant
state despite the variations placed on it by the
external environment
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  Disease as an adaptive effort by the body to restore its
balance
Appropriate to illness but incorrect in magnitude

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 2. Walter Cannon – developed the concept of
feedback mechanism
 Coined the term “homeostasis”
 Homeostasis as a dynamic equilibrium
 Developed the concept of “fight or flight”

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13 May 2019 leMaN 06 7
  Pathos – disease
 Physiology – deals with the functions of the human
body.
Focuses on the mechanisms of the underlying disease
and provides the background for preventive as well as
therapeutic health care measures and practices

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 2. Disease – is an interruption, cessation, or
disorder in the function of a body organ or
system that is characterized usually by a
recognized etiologic agent/s, an identifiable
group of s/s, or consistent anatomic alterations.
3. Etiology – the causes of the disease
4. Pathogenesis – is the sequence of cellular and
tissue events that take place from the time of
initial contact with an etiologic agent until the
ultimate expression of a disease.

13 May 2019 leMaN 06 9

 5. Symptom – is a subjective complaint that
is noted by the person with a disorder
6. Signs – is a manifestation that is noted by
the observer
7. Syndrome – is a compilation of s/s
8. Complications – are possible adverse
extensions of a disease or outcomes from
treatment
9. Sequelae – are lesions or impairments that
follow or a caused by a disease.
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 10. Diagnosis – is the designation as to nature or cause
of a health problem
11. Clinical course – is the evolution of a disease
Acute disorder
Chronic disease
Subacute disease
 Preclinical
 Subclinical
 Clinical
12. Carrier – refers to an individual who harbors an
organism but may have few or no laboratory or
clinical manifestations

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 13. Epidemiology – is the study of disease in
populations
14. Incidence – is the number of new cases
arising in a population during a specified
time
15. Prevalence – is the number of people in a
population who have a particular disease at a
given point in time/period.
16. Prognosis – refers to the probable outcome
and prospect of recovery from a disease

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 17. Incubation period – is the phase
during which the pathogen begins
active replication without producing
recognizable symptoms in the host
18. Prodromal stage – is the initial
appearance of symptoms in the host

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 HOST

ENVIRON
MENT AGENT

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 FAILS TO MULTIPLY
Low pathogenecity of agent
ENTERS Small numbers of agent
TISSUES
unsuitable environment
INFECTIOUS
MULTIPLIES IN TISSUE
AGENT
1. Cellular damage
2. Inflammatory and immune response

FAILS TO ENTER TISSUE

Non pathogenic agent
Anatomic barrier
Destruction by alveolar
phagocytes
NO DISEASE

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 1. Primary prevention is directed at keeping
disease from occurring by removing all risk factors
2. Secondary prevention – detects disease early
when it is still asymptomatic and treatment
measures can affect a cure.
3. Tertiary prevention – is directed at clinical
interventions that prevent further deterioration or
reduce the complications of a disease once it has
been diagnosed.

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  An unpleasant sensory and emotional experience
associated with actual or potential tissue damage or
described in terms of such damage
(IASP)
 It is a subjective symptom of an unpleasant sensation
that is uniquely experienced.

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13 May 2019 leMaN 06 18
 1. NOCICEPTIVE STIMULI
 Algesic substances surrounding
nociceptors
 Distention and contraction of hollow
organs
 Stretching of organ capsule
 Muscle ischemia
 Compression of ligaments and vessels
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 1. CUTANEOUS PAIN- superficial somatic pain
from skin or mucous membrane injury
2. DEEP SOMATIC PAIN – originates from
muscles, bones, joints and other connective
tissue due to mechanical trauma or build up of
chemicals
3. VISCERAL PAIN – arises from internal organs,
possibly being felt on the skin or in location
distant from its nociceptive site

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 1. HOMEOSTASIS – is defined as the
maintenance of static or constant
conditions in the internal environment of
the body
2. ADAPTATION – is defined as adjustment
of an organism to a changing environment
3. MALADAPTATION – is disruptive, a
disordering of the physiologic response.

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 WHAT IS STRESS?
 As a non specific response of the body on any
demand placed on it.

 Stressor is a tension producing stimuli that

potentially could cause disequilibrium

 Described by Hans Selye

 General Adaptation Syndrome (GAS)

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Fig

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 1. ALARM STAGE – generalized stimulation of the
sympathetic nervous system
 Stressor causes an initial activation of the defensive
abilities of the body
 Hypothalamus is activated, releasing corticotropin-
releasing hormone, which stimulates the
adenohypophysis to release ACTH
 Glucocorticoids are release

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 STAGE OF RESISTANCE
 Increased levels of
corticosteroids, thyroid hormones,
glucagon and aldosterone

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 STAGE OF EXHAUSTION
Resistance to stressor is depleted
Death may occur
Lack of immunologic defense

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 STRESSOR

Increased secretion Increase SNS activity and Vasodilatation in heart and

of ACTH secretion of skeletal muscles
catecholamine
Increased secretion of Vasoconstriction in skin,
corticosteroid viscera and kidneys
Increased heart rate,
Decreased inflammatory
increased force of cardiac
response
contraction
Increased BP
Increased blood
glucose Increased vasoconstriction

Altered CHON & fat Hypertension

metabolism
Cardiac failure
Decreased immune Decreased
response resistance to
stressors Renal failure

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 LOCAL ADAPTATION TO
STRESS

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13 May 2019 leMaN 06 29
 Mediated through the hormones catecholamine

Decreased GI Peripheral Vasodilatation of Bronchial Increased

motility, vasoconstriction of skeletal and cardiac dilatation
rate and force
contraction of skin, viscera, muscles of cardiac
sphincter and kidneys
contraction
decreased
secretions

Increased glycogenolysis
and glucogeneogenesis
by liver

13 May 2019 leMaN 06 30

 IMMUNE EFFECTS OF STRESS

INCREASE SECRETION OF ADRENAL CORTEX

HYPERTROPHY OF ADRENAL CORTEX

INCREASE CIRCULATING GLUCOCORTICOIDS

THYMIC ATROPHY

DECREASED NUMBER OF T LYMPHOCYTES

DECREASED LYMPHOCYTES
DECREASED EOSINOPILS DECREASE
DECREASED BASOPHILS INFLAMMATION
DECREASED ACTIVITY OF
MACROPHAGES
INCREASED SPREAD
OF INFECTION

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 HORMONE EFFECTS OF STRESS
INCREASED HYPOTHALAMIC
RELEASING FACTOR

INCREASED INCREASED
ADH ALDOSTERONE
INCREASED
INCREASED
ACTH
TSH
CONSERVATION RETETENTION
INCREASED OF H2O OF NA
INCREASED
CORTISOL THYROXINE

INCREASED INCREASED INCREASED BLOD

BLOOD SUGAR BMR PRESSURE
DECREASED
INFLAMMATION

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 CAD
ANGINAL PAIN
HEART ATTACK, HTN

BACKACHE,
ASTHMA, STRESS CANCER
HEADACHE

DUODENAL ULCER,
CONSTIPATION,
DIARRHEA, CROHN’S
DISEASE, ULCERATIVE
COLITIS

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 LOCAL AND SYSTEMIC
EFFECTS OF INFLAMMATION
1. Lympadenopathy – results when the
local lymph nodes and vessel drain in the infected
material, which become enmeshed in the follicular
tissue of the nodes.
 A sign of severe, localized infection.

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 2.Fever – caused by
released of endogenous
pyrogens from macrophages
3. Leukocytosis

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13 May 2019 leMaN 06 36
 4. Exudates

 A fluid or matter collecting in a cavity or tissue space.

 Serous exudate – a protein rich fluid

that escapes into the tissues

 Purulent exudate

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 ABERRANT WOUND
HEALING
1. Keloid – excessive deposition of collagen at the
wound site
 Elevated levels of propylhydroxylase

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13 May 2019 leMaN 06 39
 2. Dehiscence and
evisceration
 Dehiscence is the surface disruption
that results in the bursting open of a
previously closed wound

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13 May 2019 leMaN 06 41
 Evisceration refers to the internal
organs moving through a
dehiscence

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13 May 2019 leMaN 06 43
 3. Adhesions

 When serous or mucous membrane surfaces are

inflamed, the exudate may cause scar tissue to bind
or adhere to adjacent surface

 May cause intestinal obstruction

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GROUP ACTIVITY (1)
 A 21 YEAR OLD COLLEGE STUDENT
NOTICES THAT SHE FREQUENTLY
DEVELOPS “COLD SORES” DURING
STRESSES INVOLVED IN FINAL
EXAMINATION WEEK.
QUESTIONS:
WHAT IS THE ASSOCIATION OF STRESS
AND IMMUN SYSTEM
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 GROUP 2
 A 75 YEAR OLD WOMAN WITH CHF COMPLAINS THAT
HER CONDITION GETS WORSE WHEN SHE WORRIES
AND IS UNDER A LOT OF STRESS

QUESTIONS:
1. RELATE THE EFFECTS OF STRESS ON THE
NEUROENDOCRINE CONTROL OF
CARDIOVASCULAR FUNCTION AND ITS POSSIBLE
RELATIONSHIP TO WORSENING CHF
2. SHE TELLS YOU THAT SHE DEALT WITH MUCH
WORSE STRESSES WHEN SHE WAS YOUNG AND
NEVRE HAD ANY PROBLEM. HOW WOULD YOU
EXPLAIN THIS?

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 GROUP 3
 A 30 YEAR OLD WOMAN WHO WAS RESCUED
FROM A COLLAPSING BUILDING HAS BEEN AVING
NIGTMARES RECALLING THE EVENT, EXCESSIVE
ANXIETY, AND LOSS OF APPETITE, AND ITS
AFRAID TO LEAVE HER HOME FOR FEAR
SOMETHING WILL HAPPEN.
QUESTION:
1. GIVEN HER HISTORY AND SYMPTOMS, WHAT
IS THE LIKELY DIAGNOSIS

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  A 25 YEAR OD MAN WAS SEEN IN THE
EMERGENCY DEPARTMENT BECAUSE OF
INTERMITTENT DIARRHEA,COLICKY PAIN
USUALLY IN THE LRQ, MALAISE AND LOW GRADE
FEVER
QUESTIONS:
1. WHAT IS LIKELY THE DIAGNOSIS OF THE
CLIENT
2. RELATE THE EFFECT OF STRESS IN THE
DEVELOPMENT OF THIS CONDITION
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 FLUIDS AND ELECTROLYTE
BALANCE
 Healthy adult half of body weight is water
 Babies weight are about 75% water
 Old age is about 45% water

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 FLUID COMPARTMENT
1. Intracellular – about 2/3 of body
fluid

2. Extracellular – 1/3 of body fluids

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 EXTRACELLULAR FLUID
1. Interstitial fluid (15%) fluid located in the extra
vascular spaces between the tissues
2. Intra-vascular (5%) – plasma located within the
vessels of the body
3. Transcellular fluid
 Cerebrospinal, intraocular, GIT fluids
4. Lymph – an alkaline fluid found in the lymphatic
vessels

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 FLUID PRESSURE
 Body fluids shift between the interstitial space and the
vascular space in the capillary as a result of difference
in hydrostatic pressure and the oncotic (colloid
osmotic) pressure
 Hydrostatic pressure is the pressure due to water
volume in the vessels.
 Oncotic pressure is the pressure exerted by the plasma
proteins

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13 May 2019 leMaN 06 53
 REGULATOR OF FLUID
BALANCE
1. THIRST
 Thirst is activated by the an increase in ECF
osmolality
 May result from hypotension, polydipsia, and fluid
depletion.
 Hypo-osmolality of the ECF inhibits the thirst
mechanism

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 HORMONAL INFLUENCES
1. ADH
2. ALDOSTERONE

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 REGULATION F BODY FLUID VOLUME

HYPERVOLEMIA HYPOVOLEMIA

INHIBITS STIMULATES

ADH ALDOSTERONE ADH

THIRST THIRST ALDOSTERONE
RELEASE RELEASE RELEASE

CONTRIBUTE TO
CONTRIBUTE TO
INCREASED URINATION
OF DILUTE URINE INCREASED URINATION
OF DILUTE URINE

NORMAL FLUID VOLUME RESTORED

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13 May 2019 leMaN 06 57
 3. LYMPHATIC SYSTEM
4. KIDNEYS
5. NERVOUS SYSTEM
 When the ECF volume increases, mechanoreceptors
in the wall of the left atrium respond to atrial
distention, increasing cardiac stroke volume and
triggering a sympathetic response in the kidney

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 MOVEMENT OF BODY FLUID

1. OSMOTIC FORCES IN WATER DISTRIBUTION

 Osmotic forces are the principal determinant of
water distribution in the body.
 Osmotic pressure is the movement of fluid from area
of higher concentration to area of lower
concentration through a semi permeable membrane

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13 May 2019 leMaN 06 60
 1. EXTRACELLULAR FLUID VOLUME DEFICIT
 An ECFVD is a decrease in intravascular and interstitial
fluids
 ECFVD can lead to cellular fluid loss owing to fluid
shifting from the cells to the vascular fluid to restore
fluid balance
 Two major types
a. Hyperosmolar fluid volume deficit (fluid loss is
greater than the solute
b. Iso-osmolar fluid volume deficit ( equal proportion of
fluid and solute loss

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ETIOLOGY AND RISK FACTORS
 ECFVD commonly occurs with severe vomiting or
diarrhea, traumatic injuries with excessive blood loss,
third space fluid shifts and insufficient fluid and
sodium intake
 Persons at risk include
1. Confused and debilitated
2. Diabetic ketoacidosis
3. Loosing larger volume of blood
4. Receiving over abundance of IV glucose without
saline or hypertonic feeding

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 OTHER CAUSES
1. Excessive GI fluid losses
 Vomiting
 Diarrhea
 GI suctioning
 Draining GI fistula
2. Excessive renal losses
 Diuretic therapy
 Adrenal insufficiency (Addison’s disease)

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 3. Excessive skin losses
 Fever
 Burns
 Exposure to hot environment
4. Third space losses
 Intestinal obstruction
 Edema
 Ascites

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 CLINICAL PATHOPHYSIOLOGIC BASIS
MANIFESTATIONS
Cells shrink, stimulating “THIRST” osmoreceptors in
THIRST the hypothalamus

DECREASED SKIN Decreased interstitial fluid causes skin tissue to “STICK

TURGOR TOGETHER”
Dry mucus membrane, dry, Water tension in eyeballs decreased, cerebral
cracked lips or tongue, eyeball dehydration, less fluid for evaporation
soft and sunken
apprehension, tachycardia,
elevated temp
Postural systemic blood Plasma volume is inadequate
pressure fall >15 mmhg and
diastolic > 10 mmhg
Narrowed pulse pressure, Decreased venous return
decrease CVP and PCWP,
flatenned neck vein in supine
position, weight loss and
oliguria
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 LABORATORY
FINDINGS PATHOPHYSIOLOGIC BASIS

Increased osmolality Due to hypo-osmolar fluid loss (more fluid than solute is
lost
Increased BUN Because of hemoconcentration
(> 25 mg/dl)

Hyperglycemia Sugar increases serum osmolality causing diuresis and

(>120 mg/dl) water loss

Elevated hematocrit hemoconcentration

Increased specific gravity Increase solute to solvent ration

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 EXTRACELLULAR FLUID
VOLUME EXCESS
 Increased fluid retention in the intravascular and
interstitial spaces
 ECFVE frequently occurs in heart disease, renal
diseases, cirrhosis of the liver, increased ingestion of
foods containing high in sodium and excessive
administration of IVF containing sodium
 Cushing’s syndrome, hyperaldosteronism, and used of
glucocorticoids, CHF and renal failure

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13 May 2019 leMaN 06 68
 OTHER CAUSES
1. Excessive sodium intake in relation to output
 Excessive dietary intake
 Excessive ingestion of sodium- containing
medication or home remedies
 Excessive administration of sodium-containing
parenteral fluids
2. Excessive fluid intake in relation to output
 Ingestion of fluid in excess of elimination
 Administration of fluid or blood at an excessive rate

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 INCREASED HYDROSTATIC PRESSURE IN
ARTERIAL END OF CAPILLARY

INCREASED PERIPHERAL VASCULAR

FLUID MOVEMENT INTO TISSUES
RESISTANCE

INCREASED LEFT VENTRICULAR

EDEMA
PRESSURE

INCREASED LEFT ARTERIAL

PRESSURE

PULMONARY EDEMA

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 LYMPHATIC OBSTRUCTION
DECREASE ABSORPTION OF INTERSTITIAL
FLUID

DECREASED TRANSPORTATION OF
CAPILLARY FILTERED PROTEIN

INCREASED TISSUE ONCOTIC

PRESSURE

EDEMA

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 TISSUE INJURY
INCREASED CAPILLARY
PERMEABILITY

MOVEMENT OF PLASMA PROTEIN

INTO TISSUES

INCREASED TISSUE ONCOTIC

PRESSURE

EDEMA

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 DECREASE SERUM AND
ALBUMIN
DECREASED PRODUCTION
OF PLASMA PROTEINS

DECREASES CAPILLARY
ONCOTIC PRESSURE

EDEMA

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 S/S PATHOPHYSIOLOGICAL BASES

RESPIRATORY S/S
•Constant, irritating cough •Fluid accumulation in the alveolar sacs
•Dyspnea •Due to fluid congestion
•Crackles in lungs •Alveoli are congested with fluid owing to increased
hydrostatic pressure
•Cyanosis •A late symptoms of pulmonary edema

CARDIOVASCULAR S/S

•Neck vein engorgement in
semi-fowler’s position
•Hand vein engorgement
•Bounding pulse, elevated
BP
•Pitting edema of the lower
extremities
•Weight gain
•Due to fluid overload and delayed right sided
heart emptying/filling
•Due to peripheral vascular overload
•Due to peripheral vascular fluid overload
•Osmotic pressure exceeds interstitial pressure
•Due to fluid retention (for every 2.2 lb gained, 1L of
fluid is retained

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NEUROLOGIC S/S PATHOPHYSIOLOGICAL BASES

Change in LOC Malaise, confusion and headache, and

lethargy are due to cerebral edema

LABORATORY
FINDINGS
•Serum osmolality •Indicates a diluted body fluid in which
≤275 mOm/kg there are fewer solutes in proportion to
water volume
•Serum sodium ≤135
mEq/l
•Decreased •Due to hemodilution
hematocrit
•Specific gravity •Solvent in urine exceed solute
below 1.010
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 EXTRACELLULAR FLUID VOLUME
SHIFT: THIRD SPACE FLUID
 A change in the location of ECF between the
intravascular and the interstitial spaces
 Two types of fluid shifts
1. Vascular fluid to interstitial space
2. Interstitial fluid to vascular
 Fluid that shifts into the interstitial space and
remains there is referred to as 3rd space fluid

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 ETIOLOGY
1. From vascular to interstitial spaces:
 Crushing injuries, extensive burns,
intestinal obstruction, lymphatic
obstruction, perforated peptic ulcers

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 Tissue injury releases histamine, and
bradykinin

Capillary permeability

Fluid, protein and other solutes to

escape
Burns

Increased tissue Fluid shifts out of the vessels

oncotic pressure into the injured tissue space

Edema Hypotension

After 24 to 72 hours capillary

permeability is restored

Kidney function Fluid shift from interstitial to

intravascular space

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 CLINICAL
MANIFESTATIONS
1. From vascular to interstitial
 skin pallor, cold extremities, weak and rapid pulse,
hypotension, oliguria and decreased LOC
2. From interstitial to vascular
 Bounding pulse, crackles, engorgement of peripheral
and jugular veins and increased blood pressure

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 LABORATORY ASSESSMENT
 Elevated hematocrit
 Elevated BUN

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DIABETES INSIPIDUS
 “Tasteless diabetes”
 Caused by a deficiency in ADH or decreased response
to ADH
 It is characterized by excessive urination of a dilute
urine (greater than 2L/day) and polydipsia

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 2 TYPES OF DI
1. Central or neurogenic diabetes insipidus occur
because of defect in the synthesis or release of ADH
2. Nephrogenic diabetes insipidus occurs because the
kidneys fail to respond to ADH

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 ABSENCE OR DECREASE OF
ADH

OSMOLALITY KIDNEYS FAIL TO CONSEVE OR

REABSORB WATER

SPECIFIC GRAVITY
EXCRETION OF LARGE AMOUNT OF POLYURIA
OF 1.001 TO 1.005
DILUTE URINE

THIRST CELLULAR DEHYDRATION

PERSON DRINKS DECREASE BP AND

HYPERNATREMIA

HYPOVOLEMIC SHOCK

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 DIAGNOSTIC
ASSESSMENT
1. Water deprivation test
 Test results are positive
if the urine remains
dilute
 Client with
nephrogenic diabetes
insipidus do not
respond to ADH

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 MANAGEMENT
 Replacement of ADH or Vasopressin

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 SYNDROME OF
INAPPROPRIATE ADH
 Results from failure of the negative feedback system
that regulates the release and inhibition of ADH
 Is a disorder associated with excessive amounts of
ADH, resulting in water intoxication
 It can be caused by medication
1. Increase hypothalamic production and release
2. Act directly in the renal tubules to enhance ADH
action

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 Small cell lung MEDICATIONS (AMITRIPTYLINE,
cancer (SCLC) FLUOXATINE, VINCRISTINE,
CYCLOPHOSPHAMIDE, MAOI,
CARBAMAZEPINE, FLUPHENAZINE,
Secretion of substances HALOPERIDOL
(hormone) by tumor itself

INCREASED ADH PRODUCTION

ADH ACTH PTH

WATER REABSORPTION

SIADH HYPERCALEMIA ECF OSMOLALITY SODIUM

CUSHING SYNDROME

DILUTIONAL
WATER HYPONATREMIA
CEREBRAL EDEMA
INTOXICATION
ABSENCE OF THIRST GI FUNCTION
SEIZURES

URINE OUTPUT

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 SODIUMHOMEOSTATIC
MECHANISMS
 Sodium balance is regulated by afferent and efferent
mechanism
 Afferent mechanisms are found in the atria, carotid
sinus, liver and kidneys
 Efferent mechanisms include the glomerular filtration
rate in the kidney
 The glomerulus filters 1000 mEq of sodium every hour
and about 90% of this is reabsorpbed back by the
renal tubules

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  Hormonal factors
1. RAAS mechanisms
2. Prostaglandin
3. Kallikrein are high molecular weight proteins
produced by the distal convulated tubule and secrete
kinin
4. Kinin is a potent renal vasodilator and increases
renal excretion of sodium

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 HYPONATREMIA
 Is a serum sodium below 135 mEq/L

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 ETIOLOGY CLINICAL CONDITIONS AND DISORDERS

HYPOVOLEMIC RENAL LOSS OF SODIUM FROM DIURETIC

HYPONATREMIA THERAPY, ALDOSTERONE DEFICIENCY, EXTRA-
RENAL LOSS OF SODIUM FROM SWEATING,
DIARRHEA, VOMITING AND BURNS

EUVOLEMIC SODIUM DEFICIT FROM SIADH

HYPONATREMIA

EDEMATOUS DISORDERS RSULTING IN SODIUM

HYPERVOLEMIC DEFICIT: CHF, CIRRHOSIS OF THE LIVER,
HYPONATREMIA NEPHROTIC SYNDROME AND CRF

REDISTRIBUTIVE HYPERGLYCEMIA, HYPERLIPIDEMIA

HYPONATREMIA

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 CLINICAL MANIFESTATIONS
GIT MANIFESTATION
NAUSEA, VOMITING, DIARRHEA,
HYPERACTIVE BOWEL SOUNDS,
ABDOMINAL CRAMPS
CARDIOVASCULAR MANIFESTATIONS:
DCREASE DIASTOLIC PRESSURE,
TACHYCARDIA, PROFOUND
ORTHOSTATIC HYPOTENSION, WEAK
PULSE
PULMONARY MANIFESTATIONS
CHANGES IN RATE OF RESPIRATIONS
ADVENTITIOUS LUNG SOUNDS
NEUROLOGIC MANIFESTATIONS
HEADACHE, APPREHENSION, LETHARGY,
CONFUSION,DECREASED DTR
13 May 2019 leMaN 06
PATHOPHYSIOLOGIC BASIS
SODIUM IS ABUNDANT IN THE GIT.
LOSS OF GIT SECRETIONS CAUSES
A SODIUM LOSS
LOSSES OF SODIUM AND WATER
DECREASES THE CIRCULATING
FLUID VOLUME
DUE TO CHANGES IN CNS
FLUID OVERLOAD, CONGESTIVE
HEART FAILURE
DILUTED BODY FLUIDS MOVE
INTO THE BRAIN CELLS AFFECTING
BOTH COGNITION AND REFLEXES,
EXCITABLE MEMBRANES ARE LESS
RESPONSIVE TO STIMULI
92
 CLINICAL MANIFESTATIONS
INTERGUMENTARY MANIFESTATIONS
DRY SKIN, PALE , DRY MUCOUS
MEMBRANE
LABORATORY FINDINGS
SERUM SODIUM ≤135 mEq/L
URINE SODIUM ≤40 mEq/L
SERUM OSMOLALITY ≤275 mOsm/KG
13 May 2019 leMaN 06
PATHOPHYSIOLOGIC BASIS
DECREASED INTESTINAL FLUIDS
COMPENSATORY DECREASE IN
EXCRETION OF SODIUM
SODIUM LOSSES RESULT IN A
DEREASED CONCENTRATION OF
SODIUM IN BODY FLUID
93
 ECF CONCENTRATION OF SODIUM DECREASES

ECF AND ICF DECREASES

WATER IN THE ECF MOVES BY OSMOSIS INTO THE CELLS

LESS SODIUM TO MOVE ACROSS THE EXCITABLE MEMBRANE

DELAYED MEMBRANE DEPOLARIZATION

DECREASED EXCITABILITY OR MEMBRANE IRRITABILITY

DIMINISHED DTR
CEREBRAL
EDEMA

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 DIAGNOSTIC ASSESSMENT
 Based on clinical manifestation
 Serum laboratory values

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 HYPERNATREMIA
 Is a serum sodium above 145 mWq/L

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 ETIOLOGY CLINICAL CONDITIONS AND
DISORDERS

HYPOVOLEMIC RENAL LOSSES: SEVERE HYPERGLYCEMIA

HYPERNATREMIA EXTRA-RENAL LOSSES: PROFUSE
DIAPHORESIS, DECREASED THIRST
DIARRHEA WITH INADEQUATE FLUID
REPLACEMENT

EUVOLEMIC HYPERNATREMIA HYPODIPSIA IN THE ELDERLY AND

INFANTS
DIABETES INSIPIDUS

HYPERVOLEMIC ADMINISTRATION OF CONCENTRATED

HYPERNATREMIA SALINE SOLUTIONS, HYPERTONIC
FEEDINGS, EXCESS
MINERALOCORTICOID, COMMERCIALLY
PREPARED SOUPS AND CANNED
VEGETABLES

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 HYPEROSMOLALITY OF ECF

SHIFT OF FLUID FROM CELL TO THE ECF BY OSMOSIS

CELLULAR DEHYDRATION

MORE SODIUM MOVE ACROSS CALCIUM MOVES FOR CARDIAC

THE EXCITABLE MEMBRANE CONTRACTION AND COMPETE
WITH SODIUM CHANNEL
EARLY MEMBRANE DEPOLARIZATION
DEPRESS MYOCARDIAL
IRRITABILITY CONTRACTILITY

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 CLINICAL MANIFESTATIONS PATHOPHYSIOLOGIC BASIS

GIT MANIFESTATIONS
FLUID RETENTION IN GASTRIC
ANOREXIA, NAUSEA, AND VOMITING CELLS
INTERGUMENTARY MANIFESTATIONS DECREASE OF INTERSTITIAL
SKIN DRY AND FLUSHED, MUCOUS FLUID IN TISSUES
MEMBRANES DRY AND STICKY
THIRST, TONGUE DRY AND ROUGH, BT LESS INTERSTITIAL FLUIDS TO
ELEVATED COOL BODY BY EVAPORATION
NEUROLOGIC MANIFESTATIONS NEUROMUSCULAR IRRITABILITY
RESTLESSNESS, LETHARGY, AGITATION,
IRRITABILITY, MUSCULAR TWITCHING,
HYPER-REFLEXIA, SEIZURES
CARDIOVASCULAR MANIFESTATIONS MYOCARDIAL DEPRESSION AS
TACHYCARDIA, ERRATIC HEART RATE SODIUM COMPETES WITH
CALCIUM
LABOARATORY FINDINGS
INCREASE SERUM SODIUM MORE THAN 145
mEq/L
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 DIAGNOSTIC ASSESSMENT
 CLINICAL MANIFESTATIONS
 LABORATORY FINDINGS

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 POTASSIUM IMBALANCES
 96% is in the ICF and 4% in the intravascular
compartment
 Plentiful in the GIT
 Normal value is 3.5 to 5.0 mEq/L

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 FUNCTIONS OF POTASSIUM
 Assists in the regulation of intracellular osmolality
 Promotes the transmission and conduction of nerve
impulses
 Contraction of skeletal, cardiac and smooth muscles
 It promotes enzyme action for cellular metabolism,
promote glycogen storage in the liver
 Assists in the maintenance of acid-base balance
 80-90% is excreted through the kidneys and the
remainder excreted in feces

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13 May 2019 leMaN 06 103
 HORMONAL INFLUENCE
 Insulin, promotes potassium uptake
 Glucagon increases the level of potassium
 Adrenocortical hormones such a cortisol promote
potassium excretion and sodium retention
 Beta-adrenergic agonists promote cellular uptake of
potassium
 Alpha -adrenergic stimulation increases plasma
potassium concentration

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 HYPOKALEMIA
 Is a serum potassium level of less than 3.5 mEq/L
 People at risk include:
1. Client taking potassium-wasting diuretics
2. Severe tissue injury
3. Decrease dietary intake of potassium

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 ETIOLOGY CLINICAL CONDITIONS AND DISORDERS

GASTROINTESTINAL LOSSES VOMITING, DIARRHEA, NASOGASTRIC

SUCTIONING, INTESTINAL FISTULA, LAXATIVE
ABUSE, EXCESSIVE TAP WATER ENEMA
DIETARY CHANGES MALNUTRITION, STARVATION, POTASSIUM FREE
INTRAVENOUS SOLUTIONS

MEDICATIONS POTASSIUM WASTING DIURETICS, STEROIDS,

GENTAMICIN, AMPHOTERICIN, DIGITALIS
PREPARATION, AND BETA-ADRENERGIC
PROMOTE POTASSIUM LOSS
REDISTRIBUTION OF INSULIN MOVES GLUCOSE AND POTASSIUM
POTASSIUM BACK INTO CELLS; POTASSIUM LOSS FROM
OSMOTIC DIURESIS, ALKALOSIS CAUSES
POTASSIUM TO SHIFT INTO CELL IN EXCHANGE
FOR HYDROGEN ION
DISORDERS CUSHING’S SYNDROME, DIURETIC PHASE OF
ACUTE RENAL FAILURE, ALCOHOLISM,
HYPERALDOSTERONISM

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 WHEN POTASSIUM IS DECREASED

INCREASED POTASSIUM GRADIENT BETWEEN THE CELL AND

THE PLASMA
INCREASED RESTING MEMBRANE POTENTIAL

REDUCED MEMBRANE EXCITABILITY

CONTRACTION OF MUSCLE IS SLOW

RESPIRATORY MOVEMENT AND

VENTILAION IS SLOWED
SLOW CARDIAC
CONTRACTION

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 CLINICAL MANIFESTATION PATHOPHYSIOLOGIC BASIS

GIT MANIFESTATION
ANOREXIA, VOMITING, DIARRHEA SMOOTH MUSCLE
CONTRACTION IS SLOWED

MUSCULOSKELETAL MANISFESTATION SLOWED MUSCLE AND

MUSCLE WEAKNESS,PARALYSIS, LEG SKELETAL CONTRACTION
CRAMPS, MUSCLE FLABBINESS

CARDIOVASCULAR MANIFESTATION INCREASE IN CELL

PROMINENT U WAVE, SLOW, WEAK EXCITABILITY,
PULSE, POSTURAL HYPOTENSION PROLONGATION OF
MYOCARDIAL
REPOLARIZATION

RESPIRATORY MANIFESTATIONS
SHALLOW RSPIRATIONS, SHORTNESS OF WEAKNESS OF THE
BREATH RESPIRATORY MUSCLES

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 DIAGNOSTIC ASSESSMENT
 CLINICAL MANIFESTATION
 SERUM POTASSIUM LEVEL

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 HYPERKALEMIA
 Is an elevated potassium level over 5.0 mEq/L
 Person at risks:
1. Burns
2. Client with ARF

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 ETIOLOGY CLINICAL CONDITIONS AND DISORDERS

RETENTION OF RENALINSUFFICIENCY, RENAL FAILURE,

POTASSIUM DECREASED URINE OUTPUT AFTER SURGERY,
ADRENAL INSUFFICIENCY, ADDISON’S DISEASE,
HYPOALDOSTERONISM, POTASSIUM-SPARING
DIURETICS

EXCESSIVE RELEASE OF SEVERE TRAUMATIC INJURIES, CRUSHING

CELLULAR POTASSIUM INJURIES

EXCESSIVE EXCESSIVE AND RAPID ADMINISTRATION OF

INTRAVENOUS OR POTASSIUM
ORAL ADMINISTRATION
OF POTASSIUM

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 HYPERKALEMIA

DECREASE CELL MEMBRANE’S THRESHOLD

CELL MEMBRANE BECOME EXCITABLE

INCREASED MUSCLE AND NERVE IRRITABILITY

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 CLINICAL MANIFESTATION
CV MANIFESTATIONS
FIRST TACHYCARDIA AND THEN
BRADYCARDIA, ECG CHANGES:
PEAKED, NARROW T WAVES,
WIDE QRS COMPLEX, DEPRESSED
ST SEGMENT
GIT MANIFESTATIONS
NAUSEA, EXPLOSIVE DIARRHEA,
INTESTINAL COLIC,
HYPERACTIVE BOWEL SOUNDS
NEUROMUSCULAR
MANIFESTATIONS
PARESTHESIA, MUSCLE
WEAKNESS AND LATER FLACCID
MUSCLE PARALYSIS
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PATHOPHYSIOLOGIC BASIS
DISTURBANCES IN CARDIAC CONDUCTION
ESPECIALLY THROUGH THE PURKINJE
FIBERS AND AV NODE WHICH MAY LEAD
TO ECTOPIC BEATS
INCREASE SMOOTH MUSCLE
CONTRACTION, INCREASED PERISTALSIS
INCREASED NEUROMUSCULAR
IRRITABILITY OF THE SKELETAL MUSCLES
ELEVATED POTASSIUM LEVELS CAUSE THE
MUSCLE TO BECOME WAK OWING TO A
DEPOLARIZATION BLOCK IN THE MUSCLE
113
 CLINICAL MANIFESTATIONS PATHOPHYSIOLOGIC BASIS

RENAL MANIFESTATIONS

OLIGURIA AND ANURIA USUALLY DUE TO PRE-EXISTING RENAL

DYSFUNCTION

LABORATORY FINDINGS

INCREASE SERUM POTASSIUM

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 SERUM CALCIUM LEVELS
NORMAL = 9-11 MG%

INCREASED IN LEVEL OF DECREASED LEVEL OF

CALCIUM CALCIUM

DECREASED SECRETION OF PTH INCREASED SECRETION OF

PTH

INCREASE URINARY EXCRETION OF DECREASED URINARY

Ca. DECREASED GI ABSORPTION EXCRETION OF CA AND
BONE RESORPTION

RESTORED NORMAL LEVEL OF CALCIUM

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  Calcium has a normal serum range of 4.5 to 5.5 mEq/L
or 9-11 mg/dl
 Calcium acts as a catalyst in the transmission and
conduction of nerve impulses and stimulates the
contraction of skeletal, smooth, and cardiac muscles.
 Calcium maintains normal cellular permeability
 It promotes coagulation of blood
 It promotes absorption and utilization of vitamin B12
 Calcium is excreted in the urine

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  Vitamin D promotes calcium absorption from the GIT
whereas phosphorus inhibits its absorption

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 HYPOCALCEMIA
 Is a serum calcium level below 4.5 mEq/L

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 ETIOLOGY CLINICAL CONDITIONS AND DISORDERS

INADEQUATE DIETARY INTAKE OF Ca, VITAMIN

DIETARY CHANGES D DEFICIENCY OR BOTH, EXCESS INTAKE OF
PHOSPHORUS COMBINES WITH CALCIUM

RENAL FAILURE WITH HYPRPHOSPHATEMIA,

ACUTE PANCREATITIS, HYPOPARATHYROIDISM,
DISORDERS ACCIDENTAL REMOVAL OF PARATHYROID
GLAND DURING THYROIDECTOMY

MAGNESIUM SULFATE, NEOMYCIN INHIBIT PTH

MEICATIONS SECRETION, ASPIRIN , ANTICONVULSANTS,
ESTROGEN ALTER VITAMIN D METABOLISM

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 LACK OF PTH SECRETION DECREASED Ca.

DECREASED OSTEOCLAST ACTIVITY

NERVE FIBERS BECOME MORE EXCITABLE

TETANY OR SPASM

SPASMS OF THE MUSCLE OF LARYNX INTERFERE

WITH RESPIRATION
INCREASE CAPILLARY
PERMEABILITY
DEATH
BONE IS STIMULATED TO
RLEASE Ca. NEUROMUSCULAR EXCITABILITY OF
SKELETAL, SMOOTH AND CARDIAC
MUSCLES AND DECREASED
FRACTURE AND OSTEOPOROTIC
COAGULATION
DYSRHYTMIAS AND BLEEDING

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 CLINICAL MANIFESTATIONS
TETANY SYMPTOM, TWITCHING
AROUND MOUTH, TINGLING AND
NUMBNESS OF FINGERS,
CARPOPEDAL SPASMS,
LARYNGOSPASM
PRESENCE OF TROUSSEAU’s AND
CHVOSTEK SIGNS
DYSPNEA, LARYNGEAL SPASM
INCREASED PERISTALSIS,
DIARRHEA
PROLONGED QT INTERVAL,
PALPITATION
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PATHOPHYSIOLOGIC BASIS
HYPOCALEMIA CAUSES INCREASE
NEUROMUSCULAR
IRRITABILITY/EXCITABILITY,
PRODUCING HYPERACTIVITY OF TH
MOTOR AND SENSORY NERVES
INCREASED NERVE CONDUCTION
LEADING TO TETANY
CALCIUM ABSORPTION IN THE
INTESTINE IS DECREASED;
DECREASED CALCIUM INCREASES
SMOOTH MUSCLE CONTRACTION
INCREASE IN CELL’S EXCITABILITY
121
 CLINICAL MANIFESTATIONS PATHOPHYSIOLOGIC BASIS

PATHOLOGIC FRACTURES CALCIUM LOSS FROM THE BONE DUE

TO OSTEOPOROSIS CAUSES BONE TO
BE BRITTLE

PROLONGED BLEEDING TIME INSTRINSIC PATHWAY FOR BLOOD

COAGULATION IS INHIBITED

DECREASED SERUM CALCIUM

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 HYPERCALCEMIA
 Serum level over 5.5 mEq/L
 Three most common causes are:
1. Metastatic malignancy (lung, breast, ovary, prostatic,
bladder, multiple myeloma, head and neck)
2. Hyperparathyroidism
3. Thiazide diuretic therapy
 Other causes: immobilization, excessive intake of
calcium supplement and vitamin D

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 CLINICAL MANIFESTATIONS PATHOPHYSIOLOGIC BASIS

ANOREXIA, NAUSEA, VOMITING, SLOWED GIT TRANSIT TIME,

CONSTIPATION, DECREASED INCREASED CALCIUM ENHANCES
PERISTALSIS AND DISTENTION HCL, GASTRIN, AND PANCREATIC
ENZYME RELEASE

WEAKNESS, FATIGUE, NEUROLOGIC DEPRESSION

DEPRESSION, DIFFICULTY IN
CONCENTRATING, LETHARGY,
DEPRESSED SENSORIUM,
CONFUSION AND COMA

HEART BLOCK, SHORTENED ST DELAYED TRANSMISSION DUE TO

SEGMENT AND LENGTHENED QT PROLONGED REPOLARIZATION
INTERVAL, DIGITALIS TOXICITY
AND CLINICAL CARDIAC ARREST

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 CLINICAL MANIFESTATIONS PATHOPHYSIOLOGIC BASIS

POLYURIA, KIDNEY STONES, RENAL DECREASE THE GLOMERULAR

FAILURE FILTRATION RATE

BONE PAIN, FRACTURE DECREASED CALCIUM IN THE BONE

INCREASED CALCIUM
ABG’s

pH≤7.45
HCO3 >26 ACIDOTIC STATE INHIBITS CALCIUM
EXCRETION FROM THE KIDNEYS

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