Host PATHOPHYSIOLOGY OF HYPERTENSIVE Environment

ARTERIOSCLEROTIC CARDIOVASCULAR DISEASE –

L.P, 89 yrs. old, NOT IN FAILURE
female, with HFD of
Hypertension on Agent
both sides.

Injury of blood vessels

due to advance age

Damage to endothelial
layer

Inflammatory
response

Cytokine Serotonin Specialized chemicals

s that promote healing

Macrophages
gather in the area Collagen formation is
Platelet aggregates stimulated
and fibrin to site
Phagocytosis of fat
and cholesterol Collagen replaces
molecules normal epithelial cells

Foam cells
Decreased
elasticity

Substances harden in
the blood vessels
A

Plaque
formation Arterioscleros
is
Artherosclero
A

SlightBinjury
Decreased cardiac
to
Decreased cardiac Weakness
Increased Ischemic
in
Troponin chest
I and Decrease
Obstruction ofoxygen
Anaerobic
Lactic
Angina
acid
coronary
Increased peripheral
resistance

Increase in blood
pressure
(hypertension)

Heart beats harder

to maintain output

Cardiac muscles
start to hypertrophy

Increase oxygen
demand

Activation of RAA Release of

mechanism cathecholamines

Sympathetic effect on the

Retention of
body

Heart beats
Heart
Further harder
Cardiac
Death andload
arrest
Ventricular
compensates
Decreased
Increase heart
increase cardiac
work faster
ventricular
Decrease
Decrease stretching
contractility of
of muscle
 Host PATHOPHYSIOLOGY OF BENIGN PAROXYSMAL Environment
POSITIONAL VERTIGO SECONDARY TO MENIERE’S
L.P, 89 yrs. old, DISEASE
female

Agent
 Fluctuating Genetic Inner ear injury /
pressure of fluid Predisposition
in the inner ear
 C
Macrophage action Leukocyte secrete Arachidonic acid
(phagocytosis) and histamine, serotonin and cascade starts
Endolymphatic secretion of like a kinins
duct may be Membranous labyrinth dilates
Increase in cytokines
balloon (colony
narrow at birth stimulating factor) Fatty acids
Constriction of small
converted to
Formation of endolymphatic veins and arteriole
arachidonic acid in
hydrops dilation in the area of
plasma membrane
Increased bone injury
Blockage of the Endolymphatic
marrow production
drainage system AA converted to
of WBC and histamine,
attracted to site of leukotrienes,
Swelling of endolymphatic sac and other tissues in
prostaglandins,
Sensation of fullness or pressure Trigger new Increased serotonin, and
blood vessel neutrophil action
Damage to the inner ear
growth (phagocytosis)
structures Furthers
Damage to the Damage to the inflammation
vestibular system Exudate formation cochlear System
(Balance) Scar tissue (sanguinous,
serous, pus)
Capillary Warmth Increased
Mechanical leakagehair cells and
Cochlear blood flow and
Unilateral
Loss of normal
(plasma leaks
(stereocilia) gradually redness
die nutrients to the
progressive
tissue function
to tissue) hearing loss
Dilation of utricle and
saccule which normally Activates some neurons
Swelling/ede
contains calcium then toma
some auditory parts
carbonate crystals of the brain
C Increased pressure
and Gives
irritation of
some
Damage to utricle Tinnitus
Migration of otoconia perception of
to the semicircular and saccule
(otolith organs) Pain
canals (posterior
canal is most
commonly affected Sudden activation of vestibular reflexes due to
due to anatomical Nausea and
deformation of otolith apparatus Vomiting
Pain
D E Overpowering sensation of tilting or falling although they
may be straight
Person attempts to reconcile the sensation with external reality
(repositioning) an

F
 D E F

When head is reoriented Crystals adhere to Otolithic crisis of

relative to gravity, heavier semicircular canal cupula Tumarkin or “Drop
otoconial debris within the Attack”
affected semicircular canal
move to direction of Cupula is rendered
Person falls to the
gravity heavier than surrounding
ground uncontrollably
endolymph
and suddenly
Abnormal endolymph
displacement When head is reoriented
(canalithiasis) relative to gravity, Person may strike Persistence of Overwhelming
cupula is weighted down his head on a hearing loss after sense of exhaustion
by dense particles hard surface (risk acute attack after attack
for injury)
Necessitates
Induces immediate and several hours of
maintained excitation of sleep
semicircular afferent nerves
(cupulolithiasis)

Benign
paroxysmal
positional

Vertigo lasting Nause Rotatory nystagmus Pre-syncope Emes

only for seconds (30 seconds to a (feeling faint) or is
to minutes Syncope
(fainting)

Top of the eye rotates May have difficulty

towards the affected ear in reading or seeing
a beating/twitching fashion during attack
which has latency and can
be fatigued