When the respiratory droplets gets into the respiratory system, it will attack the

alveoli specifically the type 2 pneumocytes which is responsible for producing

surfactant that decreases surface tension and reduces collapsing pressure. The
spikes of the virus binds to specific receptor which is the ACE-2 in the type 2
pneumocytes which made the virus be engulfed inside the cell. Then the virus
releases its single stranded RNA in the cytoplasm and uses the host cell's ribosome
which will undergo translation causing it to synthesize more RNA. This will damage
the type 2 pneumocytes, causing it to release an inflammatory mediators which will
stimulate macrophage that will lead to secretion of cytokines. These cytokines will
go to the bloodstream causing the endothelial cells to undergo dilation.Smooth
muscles will dilate and increases the capillary permeability which will lead to
vasodilation and increased capillary permeability. When this happens, all the fluid
and plasma will start leaking in the interstitial spaces and into the alveoli
causing it to be compressed. When the fluid enter the alveoli, this will lead to
alveolar edema. Production of surfactant will be affected, increasing the surfacing
tension that leads to alveolar collapse which will also lead to hypoxemia.

Coronavirus disease (COVID-19) is an infectious disease caused by a newly

discovered coronavirus

when the virus enters the respiratory system, it affects the ventilation syetem of
the human body. it resulats to inadequate gas exchange due to an increase in carbon
dioxide levels and drop in oxygen resulting in an increased work of breathing
leading to a respiratory failure

when you breathe in the same air as someone with tuberculosis and the gets into
your lungs. it will spread to your lymph as well as to the bloodstream. immune
system will be alerted, B cells will make antibodies against it to attack
ktuberculosis. the body will alert the T-cells which are the natural killers to
directly attack tuberculosis. Macrophage will make a perimeter with T- lymphocytes

if a nurse suspect that a patient has tb, the nurse should put them in a private
negative airflow room so they will be on airborne precaution

Ebola virus enters the patient through mucous membranes, breaks in the skin, or
parenterally and infects many cell types, including monocytes, macrophages,
dendritic cells, endothelial cells, fibroblasts, hepatocytes, adrenal cortical
cells, and epithelial cells.Normally, dendritic cells will activate the killer T
cells and helper T cells that work together with B cells to wipe out the infection
in a matter of days but when ebola strikes, it directly attacks the immune system.
It takes over the dendritic cells which is the brain of immune system. The ebola
virus enters the dendritic cells by binding into receotors for cell transport. Once
it is inside, it dissolves its outer hull and releases its genetic material,
nucleoproteins and enzymes. Basically this virus will take over the cell, disabling
the cells protective mechanisms and reprograms it. the cell now becomes a virus
producing machine and build more ebola viruses. As the virus spreads through the
body, it damages the immune system and organs. Ultimately, it causes levels of
blood-clotting cells to drop. This leads to severe, uncontrollable bleeding.

This virus is transmitted by inhalation or ingestion of infected droplets such as

in sneezing and coughing. The virus has an envelope with spikes of protein called
the H and N protein. Swine flu infects the cells in the respiratory system first
such as the nose, throat and lungs. Once the spike of the virus attached to the
receptors of a healthy cell membrane, this allows the virus to penetrate the cell.
The body forms a membrane around the virus molecule. The virus now travel to the
nucleus as it opens up and releases its' genetic content inside the cell's
cytoplasm. The viral genetic content enters the nucleus and uses the cells
machinery to print copies of itself and it even go to ribosome and causes it to
produce protein like the H and N spikes that are needed to create new virus
molecules. the viral load on the cell causes it to burst and these newly generated
viruses then go on and infect other healthy cells causing the flu.

inform people receiving the vaccine of the possible adverse effects and report them
immediately
instruct patient and/or SO about influenza types when typical outbreaks occur
methods to avoid infection; and
instruct patient and/or SO about newer antiviral drugs, their effects, when to seek
immediate medical attention, and side effects of medications.

When myobacterium enters the lungs, it affects the pulmonary alveoli. As a defense
of the immune system to pathogens, it will alert macrophage. When macrophage detect
the pathogen, it will phagocytose the myobaterium in the cell through the process
of phagocytosis. This cell will now be encapsulated by phagosome. Normally, under a
normal immune response, the lysosome with hydrolytic acid inside the macrophage
fuses with phagosome to form phago-lysosome and the pathogen will be dissolved with
acids and finally be eliminated but in case of tuberculosis, the phago-lysosome is
not formed and the fusion is inhibited and the mycobacterium will remain protected
inside the macrophage without being detected by the immune system. The bacteria
will just replicate inside the macropahges and infection will occur.

Middle East respiratory syndrome (MERS) is a viral respiratory disease caused by a

novel coronavirus (Middle East respiratory syndrome coronavirus, or MERS‐CoV) that
was first identified in Saudi Arabia in 2012.
ypical MERS symptoms include fever, cough and shortness of breath. Pneumonia is
common, but not always present. Gastrointestinal symptoms, including diarrhoea,
have also been reported. Some laboratory-confirmed cases of MERS-CoV infection are
reported as asymptomatic, meaning that they do not have any clinical symptoms, yet
they are positive for MERS-CoV infection following a laboratory test. Most of these
asymptomatic cases have been detected following aggressive contact tracing of a
laboratory-confirmed case.

When the MERS virus enters the body, it infects and replicates in the human airway
epithelial cells and suppresses the production of interferons. Interferons play an
important role as the first line of defense against infections. These are proteins
that are made and released in response to pathogens like viruses, bacteria,
parasites, and cancer cells. this virus interacts with the host DPP4 receptor
through its spike (S) protein after entering the respiratory tract. DPP4 receptors
are present on the epithelial surface of various human organs such as, the lungs,
kidneys, liver, bone marrow, thymus and intestines. The systemic distribution of
DPP4 facilitates the dissemination of virus in the human body.

• MERS-CoV can also induce pro-inflammatory cytokines but lacks in production

of innate antiviral cytokines.

Expression of DPP4 on the respiratory tract is mainly on type I and type II

pneumocytes, endothelial cells, nonciliated bronchial epithelial cells and a few
forms of hematopoietic cells.
• The abundance of the receptor DPP4 is greater on the epithelial cells lining
the lower airways and alveoli and lesser on the epithelial surface of upper
conducting airways and nasal cavity.
• Macrophages are the important phagocytic cells of innate immune system which
help remove the pathogenic substances from the body and present their antigens to
the T cells. The cytokines as well as chemokines produced by the macrophages help
in destroying the pathogens, adjusting the immune system and maintaining tissue
homoeostasis.
• The infection with MERS-CoV of human epithelial cells induces the release of
pro-inflammatory chemokines and cytokines from the monocyte-derived macrophages. It
is believed that these chemokines/cytokines cause inflammatory changes and tissue
injury through infiltration of immune cells in the lower respiratory tract.

people who develop serious symptoms and need to be hospitalized, treatment is

focused on supporting individuals while their body fights the infection and reduce
patient's symptoms.

patients who have trouble breathing mey be given supplemental oxygen

if supplemental oxygen alone is insufficient to help the patient breathe,
healthcare provider may choose to put patient on a mechanical ventilation such as
BiPAP and in some situations they may need to intubate and oxygenate the patient
with conventional ventilators

remdesivir is an antiviral medication that disrupts virus ability to replucate and

spread within the body

recommended for patients who have been hospitalized and require oxygen but are not
in mechanical ventilator

dexamethasone is a corticosteroid that makes adjustments to how immune system

regulates itself
this drug can be used in patients who need oxygen and also for patients on/not on
mechanical ventilation
however, patients who dont need oxygen are not recommended to take dexamethasone as
the side effect may worsen their condition

injecting the blood plasma of people who have recovered from COVID-19 (convalescent
plasma) into patients who are seriously ill with the disease