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Aortic Stenosis

Aortic Stenosis is the narrowing of the left ventricle of the heart (where the aorta
begins), such that problems result. It may occur at the aortic valve as well as above and
below this level. It typically gets worse over time. Symptoms often come on gradually
with decreased ability to exercise often occurring first. If heart failure, loss of
consciousness, or heart related chest pain occurs due to AS the outcomes are worse.
Signs of heart failure include shortness of breath especially when lying down, at night,
or with exercise, and swelling of the legs.

PATHOPHYSILOGY OF AORTIC STENOSIS

Progressive decrease in the area of the


aortic valve

Decrease ante grade velocity when


velocity when aortic area decrease at
least by half

Adaptation by hypertrophy

Early Changes Late Changes

Diastolic Dysfunction Systolic Function

Atrial
Fibrillation
Decreased compliance Myocardial ischemia
Increased left
Ventricular diastolic Myocardial Fibrosis
Mitral
pressure Abnormal wall motion
Regurgitation

Unchanged Decreased Contractility


contractility:
Decreased stroke
Normal stroke volume volume

Heart Failure
Guillain-Barre Syndrome
Guillain-Barre Syndrome is a disorder in which the body’s immune system attacks part
of the peripheral nervous system. The first symptoms of this disorder include varying
degrees of weakness or tingling sensations in the legs.

Pathophysiology of Guillain-Barre Syndrome

Campylobacter jejuni

Enters the body by the use of multifenestrated


cells or other mechanism Precipitating
Predisposing Factors:
Factor:
Innate immune response results in the uptake of the >Post infection to
>Age pathogens by immature antigen presenting cells. Campylobacter
>Sex jejuni
>Poor hygiene
Migration to lymph nodes, a mature, >Stress
differentiated antigen presenting cell can present >Diet
in major histocompatibility complex molecules >Lifestyle
and activate CD4 T cells that recognize antigens
from the infectious pathogens.
Pathogen and host have
homologous or identical
B cells can be activated as well by newly
amino acid sequences,
activated Th2 cells. This produce a cell
antigens in its capsule are
mediated and humeral response against the
shared with nerves.
pathogen.

Antibodies will be produced, leading


to activation of the complement Molecular mimicry
system and phagocytosis of the
bacteria. Immune responses directed against the capsular components
produce antibodies that cross-react with myelin.

Lymphocytes and macrophages circulate in the blood and


eventually find myelin

Lymphocytic infiltration of spinal roots and peripheral nerves,


followed by macrophage-mediated, multifocal stripping of
myelin and axonal damage.

Defects in the propagation of electrical nerve impulses, with


eventual conduction block.

Guillain-Barre syndrome

Sensory changes Dull aching pairs Clinical nerve


Acute progressive
paraesthesias or of lower tuck, involvement facial droop
ascending weakness
>Dysarthria
numbness in >lower limbs flank, proximal >Dysphagia
feet/hands. >upper limbs legs. >Difficulty with
>hypareflexia
protruding
If Treated: If not Treated:

>Plasma Exchange Extensive axomal


destruction
>Intravenous
immunoglobulin

>Physical therapy and Ascending weakness


exercise
Progresses
>medication

Weakening of the
diaphragm and the
respiratory muscles.
Good Prognosis

Respiratory Distress
Syndrome

Bad Prognosis

Respiratory Arrest

Shock

Death
Multiple Sclerosis
Multiple Sclerosis is a potentially disabling disease of the brain and spinal
cord (CNS). In MS, the immune system attacks the protective sheath (myelin) that
covers nerve fibers and causes communication problems between your brain and the
rest of your body.

Age: 20-40 y/o PATHOPHYSIOLOGY OF MULTIPLE SCLEROSIS


Gender: Female Exposure to:
Race: Whites >Epstein-Barr virus
Location: Colder climates >Measles
Genetic susceptibility: >Rubella
>HLA-DRB1 gene >Other Herpes strains
>IL7R gene Sensitized T-cells cross the blood-
Low levels of Vit. D brain barrier

T-cells attach to myelin sheath receptors

Interferon gamma
T-cells attach to T-cells release cytokines
Activates
macrophages macrophage

An inflammatory response is started

Macrophage release of tissue necrosis


factor

Myelin is attacked

Destruction of the myelin sheath

Olgodendracytes produce myelin in attempt to


repair the damaged myelin

T-cells, macrophages and interferon gamma works to attack the


myelin sheath as it was identified as non-self

T-cells, macrophages and interferon gamma works to attack the


myelin sheath, oligodendrocytes and axon as non self

Axon becomes demyelinated

Plaques of sclerotic tissue appear on


demyelinated axon

Interruption of impulse transmission

Manifestation depending on
involved neurons
Myasthenia Gravis
Myasthenia Gravis is a chronic autoimmune neuromuscular disease that causes
weakness in the skeletal muscles, which are responsible for breathing and moving parts
of the body, including the arms and legs. The name Myasthenia Gravis, which is Latin
and Greek in origin, means “grave, or serious, muscle weakness.”

PATHOPHYSIOLOGY OF MYASTENIA GRAVIS

Normal neuromuscular transmission begins with action potential


traveling down the motor neuron

Action potential reaches the nerve terminal and activates Ca+


channels

Increase Calcium synaptic vesicles containing ACh to be


released into synaptic cleft

Unknown initiating event

Associated Risk Factors include:


>Autoimmune disease
>Thymus abnormalities
>Genetic Unit

T cells process produces ACh receptor antibodies which


reduce normal neurotransmission:
MYASTHENIA GRAVIS

3 mechanisms:

1. Directly alters function of receptor by blocking Ach


binding and Ach receptor activation activation
2. Promote endocytosis of Ach resulting to degradation of
Ach R
3. Destroy post synaptic surface leading to decrease
number of Ach R

Decrease neuromuscular transmission to skeletal muscle

Muscle weakness and fatigue with repetitive use =


myasthenic fatigue due to continuous muscle contraction

Clinical Presentation of MG:


>Diplopia
>Ptosis
>Snarling Expression
>Dysphagia
>Nasal Speech
>Proximal Limb Weakness
>Respiratory Muscle Weakness
Spinal Cord Injury
Spinal Cord injury is damage to the spinal cord that causes changes in its function,
either temporary or permanent. These changes translate into loss of muscle function,
sensation, or autonomic function in parts of the body served by the spinal cord below
the level of the lesion.

PATHOPHYSIOLOGY OF SPINAL CORD INJURY

Spinal Cord Injury

Hemorrhages, thrombosis and vasospasms


of injured area

Hypoperfusion, hypoxia and ischemia of


neurons and non-neuronal cells

Reperfusion of ischemic area Invasion of injured area by neutrophils,


leads to free radicals macrophages and monocytes

Peroxidation of neuronal lipid


membranes leads to Production of cytokines
pathological depolarisation and (TNF-a,1B and 1L-6), Microglial
glutamate/GABA release chemokines (CX3CL1 and activation
CCL2) and neurptrophic
factors (NGF and BDNF)

Rise in Excess
cytoplasmic Ca2 stimulation of
triggers cascade NMDA/AMPA/Kai Further
Neurophatic
of lytic enzymes nite receptor inflammatory
pain
(calpains,phosph leads to Na influx damage
olipase A, and and
lipoxygenase) repolarisation
failure
Nogo-A, MAG, OMG
prevents axonal
Disruption of growth and
mitochondrial regeneration
function

Further
production of
free radicals Excitotoxicity Glial scar
and neuronal
malfunction

Neuronal death
Ventricular Septal Defects
A ventricular septal defect, a hole in the heart, it is a common heart defect that’s present
at birth (congenital). The hole occurs in the wall that separates the heart’s lower
chambers and allows blood to pass from the left to right side of the heart.

PATHOPHYSIOLOGY OF VENTRICULAR SEPTAL DEFECTS

During Systole, bypasses the RV cavity

Left-Right shunt

Increased Pulmonary blood flow


(shear stress/circumferential stretch)

Endothelial dysfunction and vascular remodelling


Smooth muscle cell proliferation, increase in extracellular
matrix, intravascular thrombosis

Increase in PVR

Inverted shunt: right-to-left

Cyanosis (Eisenmenger syndrome)


Cardiogenic Shock
Cardiogenic shock is a condition in which your heart suddenly can’t pump enough blood
to meet your body’s needs. The condition is most often caused by a severe heart attack,
but not everyone who has a heart attack has cardiogenic shock. Cardiogenic shock is
rare, but it’s often fatal if not treated immediately.

PATHOPHYSIOLOGY OF CARDIOGENIC SHOCK

Initial Insult

Decreased Myocardial
Contractility

Decreased stroke volume

Decreased left ventricular


Increased heart rate
emptying

Decreased coronary artery


Left ventricular dilatation and perfusion and collateral blood
backup of blood
flow

Increased preload Myocardial hypoxia

Pulmonary Congestion Decreased Cardiac Output

Compensation

Decompensation and death

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