1. immune response. Paracrine acts on adjacent cells

1.      Compare the structure and function
of mitochondria with the endoplasmic reticulum (ER) and Golgi apparatus.

Mitochondria
has an outer membrane that acts as its skin. The inner membrane has many folds
that creates layered structures called cristae. The mitochondria contain fluid
from within that is called the matrix. Mitochondria is the power house of the
cell generating energy in the form of ATP. The ATP helps ribosomes create
proteins. Proteins are the building blocks of the body that are made from amino
acids. Endoplasmic reticulum (ER) structure is made up a network of membranes
and is connected to the nucleus.  Rough
endoplasmic reticulum (RER) has ribosomes attached to its membrane thus giving
it its name “rough” from the attached ribosomes. The ribosomes on RER allows
for protein synthesis to occur in the RER. The structure of Golgi apparatus is
stacks of flatten membrane that contain numerous vesicles containing secretory
granules. The Golgi apparatus helps the proteins that are made in the RER to be
packed into sealed droplets called vesicles and able the vesicles to be
secreted out of the cell. The quick version is mitochondria generates ATP to
make the ribosomes on the RER to conduct protein synthesis and the Golgi
apparatus packages it real nice, so it can be shipped out of the cell.

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2.      Compare autocrine, paracrine and
endocrine cell stimulation.

Autocrine,
paracrine and endocrine ultimately all act on cells in one way or another.
Autocrine acts on itself, sending signals to self-stimulate.   An example of autocrine stimulation will be
cytokines during an immune response. Paracrine acts on adjacent cells stimulating
cells around itself. Example of paracrine stimulation is getting a group of
cells stimulated while adjacent cells are sending signals that triggers the
group. Endocrine acts on cells in different sites after traveling through the
blood stream. Example of endocrine stimulation is when cells produce a signal
that must travel through the blood stream until it hits its target at a
different site.

 

3.      Compare atrophy with hypertrophy and
hyperplasia and give clinical examples of each condition.

Atrophy
is the decrease in size of cells, tissue, and/or organ. Hypertrophy is the
opposite of atrophy it’s the increase in size
of cells, tissue, and/or organ. Hyperplasia increase in size of cells, tissue,
and/or organ due to the cells reproducing. a woman’s uterus goes through
hyperplasia and hypertrophic during pregnancy alone. During pregnancy the
uterus will increase in size from the increase of cell size and increase of
cell production. After a woman goes through menopause the uterus will become
atrophic. Due to the lack of hormones of a postmenopausal woman the uterus will
shrink in cell size.

4.      The two main forms of cell death are
necrosis and apoptosis. Describe and explain how these two forms of cell death
are different.

Necrosis
is a form of cell death, but it’s not a neat or controlled process. When cells
go through necrosis it will have adverse effects to the cells around them or
the body itself. Necrosis is caused from external factors such as infections
from bacteria or viruses causing the cells to die from the pathogen itself or
by the body’s immune system destroying cells while it’s trying to control or
get rid of the infection. Injury can cause necrosis while some injuries in
different parts of the body can have a greater loss of cells easier than other
sites. Apoptosis is a controlled and highly regulated process in the body. When
apoptosis does not work properly drastic results follow such as cancers forming
from the lack of apoptosis. The lack of apoptosis can even cause physical
deformities of a human still developing in utero. Overall apoptosis is a vital
function of the body to function properly even though it’s a type of cell
death.

5.      Summarize the vascular changes (the
circulatory and vessel wall changes) that occur during the process of acute
inflammation.

At
the beginning of acute inflammation, the blood vessels dilate to allow blood to
rush in to the targeted site. The dilation of the blood vessels explains
redness, swelling, and warmness of tissue during acute inflammation. Because
there is more blood in the area than there should normally be this is called
hyperemia. The distribution of blood elements changes, for example RBC’s move
to the middle of the blood flow making a rouleaux formation which is RBC’s stacking
on each other. The WBC’s marginalize and attach to the endothelium during this
phase. WBC’s can do this with surface adhesion molecules that is activated
through the action of cytokines. Last but now least soluble mediators of
inflammation is released by endothelial cells, leukocytes, platelets and
macrophages in the adjacent connective tissue. Examples of Soluble mediators in
inflammation are interleukins (IL’s) or tumor necrosis factor (TNF).

 

6.      Explain the role of
polymorphonuclear neutrophils (PMNs) in acute inflammation.  How do they immigrate to the site of injury
or infection, and what do they do when they get there?

Polymorphonuclear
cell (PMN) has a segmented nucleus with several sections from two to five and
they count for 60% to 70% of circulating WBC’s. PMNs are very mobile which
helps them to get to tight spaces and makes them to be great first responders
in acute inflammation (first line of defense). PMNs have a short life span. PMNs
immigrate from the blood vesicles to infected site by first adhesion to the
endothelial cells. Eventually the PMN will pass through the basement membrane
to travel to the ground zero for the inflammation site. Chemotactic substances
stimulate the PMN’s to move towards the main site of inflammation based on the concentration
of the substance.   When PMNs get to their site of inflammation if
need be they can ingest bacteria and other cellular debris. PMNs can release
various mediators of inflammation if they are unable to get the job done right
away. These various mediators can be from recruiting new leukocytes or cause
systemic symptoms.  

7.      Describe and provide clinical
examples of these three forms of inflammation: serous, fibrinous and purulent.

Serous
inflammation is the mildest of the three types of inflammation. Serous fluid
resembles serum and is made up of proteins and water. An example will be a burn
where a blister is formed. A liquid will fill up the blister with
non-viscous serous fluid that contains serum.

Fibrinous
inflammation is when fluid from the circulatory system goes to the site of
inflammation and is rich in fibrin. Fibrinous inflammation is commonly seen in
bacterial infections. Example of this is fibrinous pericarditis.

Purulent
inflammation is typically caused by puss forming bacteria. The puss is thick
yellow fluid. The puss is made up of dead and dying PMNs and dead tissue
debris. A localizes collection of puss within an organ or tissue is called an
abscess.

8.      The process of wound healing is
often broken down into three phases: the inflammatory, the proliferative and
the remodeling. The first phase (acute inflammation) prepares the wound site
for healing.  Summarize what happens
during the next two phases – the proliferative and remodeling. (Refer to the
video: Wound Healing Process.)

Proliferative
phase the wound begins to rebuild the tissue with granulation tissue.
Granulation tissue is rich in macrophages, myofibroblasts, angioblasts, and
fibroblasts. Myofibroblasts come in the first few days of healing to reduce the
defect and holds the margins of tissue in close approximation. Angioblasts are
precursors to blood vessels that appears day 2 to 3 and by day 5 to 6 the
entire field is permeated with newly formed blood vessels. Fibroblasts is
important for the extracellular matrix that contains fibronectin and collagen.
Fibronectin is important for the formation of scaffold, the provision of
tensile strength and the ability to stick other substances and cells together.
Fibroblasts synthesizes type III collagen by the end of this whole process will
be replaced by type I collagen. The structure will be predominantly type I
collagen that will be called a scar. The scar is then remodeled from replacing
the disorderly formed collagen with collagen that is indistinguishable from
that in normal skin.