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Medical Surgical Nursing Pathophysiology
Medical Surgical Nursing Pathophysiology
Purpose
Mechanism
Increased
blood Increased
glucose level
energy
breakdown;
increased
breakdown
adipose
triglycerides
of
tissue
Mental Acuity
Alert state
Increased amount of
blood shunted to the
brain
from
the
abdominal
viscera
and skin.
Dilated pupils
Increased
coagulability
blood
of
d. Hormonal stimulation
e. Innervation
o Example
Secondary sex organs in aging person
Extremity immobilized in cast
Disuse of a body parts
o Often associated
immobilization
with
the
aging
process
and
Hyperplasia
o Increase in the number of new cells in an organ or
tissue
o Tissue mass enlarges
Cells multiply
Subjected to increased stimulation
Reversible when stimulus is removed
o May be hormonally induced
Increased size of the thyroid gland caused by thyroid
stimulating hormone
o Increase in number of new cells
o Increase in mitosis
o Stimulus: hormonal influence
o Example
Breast changes of girl in puberty or of a pregnant
woman
Regeneration of liver cells
New blood cells in blood loss
Neoplasia
o Malignant growth
o Continues growing of cells even though stimulus is
removed
Dysplasia
o The change in the appearance of cells after they have
been subjected to chronic irritation
o Dysplastic cells
Have the tendency to become malignant
o Seen commonly in epithelial cells in the bronchi of
smokers
Genetic Disorder
Inflammation
Inflammation- is a defensive reaction intended to neutralize,
control, or eliminate the offending agent and to prepare the
site for repair.
Types of Inflammation
o Acute Inflammation- is characterized by local vascular
and exudative changes and usually lasts less than 2
weeks.
o Chronic Inflammation- develops if the injurious agent
persists and the acute response is perpetuated.
o Subacute Inflammation- falls between acute and
chronic inflammation.
Cellular Healing
o Regeneration
o Replacement
Primary Intension Healing- wound is clean and dry
and the edges are approximated.
Secondary Intension Healing- the wound or defect
is larger and gaping and has necrotic or dead
material.
Nursing Management (STRESS)
Pain
Pain- is whatever patient says it is and whenever the patient
says it does.
o It is an unpleasant sensory and emotional experience
resulting from actual or potential tissue damage.
Types of Pain
o Acute Pain-usually recent onset and commonly
associated with a specific injury.
Usually last for seconds to 6 months
o Chronic Pain- is constant or intermittent pain that
persists beyond the expected healing time and that can
seldom be attributed to a specific cause of injury.
o
o
o
o
o
o
Distractions
Relaxation
Guided imagery
Hypnosis
Music therapy
Acupuncture
*Intractable pain
*Neurosurgery
Rhozotomy- destruction of sensory nerve roots
Cordoctomy- cutting of spinal pathways in the spinal
cord.
Pathophysiology
(Stress, Inflammation, Pain, CHF, Angina Pectoris, Myocardial
Infarction)
Stress
Stress
o Changes in Environment
Sympathetic Nervous
System
Adrenergic-E/N
Fight or Flight- user of
energy
Aggressive or Avoidance
Increased Activity
Parasympathetic Nervous
System
Repose, vegetation
Cholinergic-Ach
Decreased activity-source
of energy
Organs
SNS
PNS
Blood Vessels
Constriction
Dilation
Vital Signs
Increased
Decreased
Pupil
Dilate
Constrict
Airways
Dilate
Constrict
Constrict
Dilate
Salivation
Decreased
Increased
Sphincters
Contract
Relax
Blood Glucose
increased
No effect
Pathophysiology:
STRESS
STIMULATION OF THE ANS
Stimulation of the hypothalamus
SNS
PPG
APG
SAMR
Adrenal Medulla
Adrenal Cortex
release of ADH
Increased ADH
N/E
Glucocorticoid
Mineralocorticoid
ACTH
StimulatiIncreased
on of the
adrenerg
Release of
angiotensinogen ic
receptor
Tachycardia
in the
Convert to
angiotensin
I
ConvertInflammation
to
vasoconstriction
angiotensin
II
Inflammation
BP and Increased P
cortosol
Release of
aldosterone
Reabsorption
catabolism
of Na+
CHO
CHO
N
Bld. Vol.
Water
reabsorption
Fats
Increased Bld.
vol
Glucose
BP
Pathophysiology:
Inflammants
(physical, chemical, biological)
Injury
Vasoconstriction
Release of chemical mediators
(PGE, H, serotonin, bradykinin, leukotrienes)
Vasodilatation
Increased capillary permeability
hyperemia
Swelling (Tumor)
Warmness
(Calor)
Redness
(Rubor)
Pain (Dolor)
Loss of Function (function laissa)
Systemic manifestation:
Fever
Leukocytosis
Increased erythrocyte sedimentation
Headache
Fatigue
Malaise
Anorexia
Pain
Pain- is what every person or experiencing person say it
existing whenever the person say it does.
IASP- Pain is the 5th vital sign
Set of sensory and emotional response to actual or
potential tissue damage.
Pathophysiology:
Stimulus
-acute
Nociceptors - - - - - - - - - - - - a-delta
C-fiber
-chronic
-slow
unmyelinate
d
-fast
Myelinate
d
Secondary Neuron
Spinal Cord
Afferent neuron
Thalamus (slow)
Response
CV D/O
CAD
o CHF
o MI
o Angina Pectoris
Etiology: Atherosclerosis- hardening and narrowing of
the BV
Risk Factors:
Non-modifiable
(predisposing
factors)
Gender
Age
heredity
Modifiable
(precipitating
factors)
Environment
Diet
Condition
Aggravating
Stress
Lifestyle
Obesity
o CHF
o Decreased supply and increased demand of bld.
o Decreased bld. Vol.
o Compensatory mechanism
Tachycardia
Ventricular dilatation
Ventricular hypertrophy
o S/Sx
DOB
Rales
Cough
Sputum
Tympanic
Pathophysiology:
Increased residual vol.
CO
O2
Tissue hypoxia
hypertrophy
preload
atrial dilatation
atrial
Increased atrial
pressure
Backward flow of bld. Towards
lungs
Pulmonary
congestion
Left sided heart
failure
Increased pulmonary
pressure
Backward flow of bld.
Towards right ventricle
Increased pressure
in the right ventricle
Right ventricular hypertrophy
Right ventricular
dilatation
Increased pressure
in the Right atrium
Right atrial dilatation
Right atrial hypertrophy
S/Sx of RCHF
Increased CVP
JVD
CNS Depression
Increased ICP
Hepatomegaly
Slpeenomegaly
Anorexia
N/V
Ascites
Portal
hypertension
edema
Management:
Short acting- nitroglycerine
Long acting- Isosorbide Dinitrate
Nsg. Mngt when giving patches:
Non hairy part
Angina Pectoris
Pain in the chest wall
Myocardial ischemia- due to decreased o2
Pathophysiology:
Atheroma
Platelet aggregation
narrowing
PGE
O2 hypoxemia
Vasospasm
Pain
metabolism
cardiac hypoxia
platelet aggregation
anaerobic
MI
Sudden occultation/obstruction of coronary artery leading to
necrosis
Pathophysiology:
Atheroma
Blockage/ obstruction
No O2 supply
Necrosis
Intense pain
S/Sx:
1. Intense pain
2. Hypotension
3. Tachycardia
4. Tachypnea
5. Fever
6. Indigestion
increased isoenzymes
Lactic
Increased:
Myoglobin
Dehydrogenase
Troponin
CPK-MB
(creatine
phospokinase
7. Increased ESR
8. Anxiety
Management:
Morphine SO4 for pain