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B. Schematic Pathophysiology TETANUS-a Disease Condition Caused by Clostridium Tetani

This document provides a schematic overview of the pathophysiology of tetanus. [1] It is caused by Clostridium tetani bacteria entering the body through a wound. [2] The bacteria produce toxins that travel through the nervous system and block inhibitory neurotransmitters, causing painful muscle spasms. [3] Left untreated, this can lead to respiratory failure and death.

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Stephanie Ann L. Torrecampo
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© Attribution Non-Commercial (BY-NC)
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4K views

B. Schematic Pathophysiology TETANUS-a Disease Condition Caused by Clostridium Tetani

This document provides a schematic overview of the pathophysiology of tetanus. [1] It is caused by Clostridium tetani bacteria entering the body through a wound. [2] The bacteria produce toxins that travel through the nervous system and block inhibitory neurotransmitters, causing painful muscle spasms. [3] Left untreated, this can lead to respiratory failure and death.

Uploaded by

Stephanie Ann L. Torrecampo
Copyright
© Attribution Non-Commercial (BY-NC)
Available Formats
Download as DOC, PDF, TXT or read online on Scribd
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B.

SCHEMATIC PATHOPHYSIOLOGY

TETANUS- a disease condition caused by Clostridium tetani

Precipitating Factors: Predisposing Factors:

 Work (Farming)  Age

 Exposure to bacteria  Gender (Male)


(laceration at left foot)

 No previous history of
tetanus immunization

Clostridium tetani bacteria Tetanus


containing virulence Toxoid
plasmids enter wound
STAT 1 tab
via NGT
Toxins produced by growing
cells

Spores germinate under


anaerobic conditions

Vegetative Spore
growth

Cell lysis
Metronidazole 500
occurs
mg tab BID PO

Cefazolin mg IVTT Release of


q8 bacterial
endotoxins into
Gentamycin 50 mg surrounding
IVTT q8

Tetanolysin Tetanospasmin (potent


neurotoxin)

Potentiating of
infection

Toxin circulated Enter Central Nervous


around the body System (CNS) along
Release of biochemical
through peripheral nerves
mediators of inflammatory
bloodstream and
response (histamine,
lymphatic system
bradykinin) 41
Inflammatory response Toxin not able to
initiated pass through
blood-brain barrier

Increased WBCs such as


capillary neutrophils and Toxin makes its way to
permeability monocytes spinal cord
enter
Increased blood
flow Toxin enters the Baclofen 10
Phagocytosis and
CNS mg TID PO
removal of debris
occur
Toxin taken up by
Swelling Rednes
neuromuscular
junction
Phagocytes release
endogenous pyrogens
Crosses to synaptic
cleft

Stimulation of
Irreversibly binds to
hypothalamus to
gangliosides at
increase body
presynaptic inhibitory
temperature
motor nerve endings
Paracetamol
Fever
STAT 1 amp IVTT
Taken up by
STAT 500 mg tab preganglionic neuron
PO axon through
endocytosis

Blocks the release of


Diazepam 10 inhibitory
mg IVTT q12 neurotransmitters
(glycine and GABA)

Carbamazepi Excitatory activities


ne 200 mg unregulated
Mefenamic tab BID PO
acid 500 Generalized tonic muscle
mg cap TID Pain spasms occur
PO

Pharynx Cranial Facial Masseter Glottis GI


(laryn
Respiratory x,
Aspiration Rapid firing Risus Lockjaw Failure muscles abdo
of oral of impulses sardonicu to minal
secretions s (fixed speak wall)
smile and or cry
Irritability elevated
Chest wall Diaphrag
Pneumonia of neurons eyebrows 42
muscle m
)
Restlessn
Chest wall
rigidity
Ampicillin Sodium &
Sulbactam Sodium 1.5 g IVTT
q8 after ANST (-)
Headache
Penicillin G Benzathine 500 Asphyxiation
“U” q8 IVTT after ANST (-)

Hypoxemia

Cardiac Arrest

DEATH Respiratory
failure

LEGEND:

Clinical manifestations

Disease process manifested by


patient

Disease process not manifested


by patient

Signs and symptoms

Medications

43

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